1. This document provides guidance on examining patients and summarizing key clinical findings. It discusses differential diagnoses for masses in the upper quadrants, mechanisms of pes cavus, cardiovascular examination findings, complications of renal failure, and signs of cirrhosis among other topics.
2. Details are given on potential examination findings for different disease processes, including surgical scars that may indicate prior procedures. Subtle exam signs are noted, and correlating exam findings with a patient's history is emphasized.
3. Pathophysiology behind common complications of conditions like chronic kidney disease are reviewed, along with treatments for diseases such as renal transplantation. Normal exam findings and important details to remember are also provided.
1. This document provides guidance on examining patients and summarizing key clinical findings. It discusses differential diagnoses for masses in the upper quadrants, mechanisms of pes cavus, cardiovascular examination findings, complications of renal failure, and signs of cirrhosis among other topics.
2. Details are given on potential examination findings for different disease processes, including surgical scars that may indicate prior procedures. Subtle exam signs are noted, and correlating exam findings with a patient's history is emphasized.
3. Pathophysiology behind common complications of conditions like chronic kidney disease are reviewed, along with treatments for diseases such as renal transplantation. Normal exam findings and important details to remember are also provided.
1. This document provides guidance on examining patients and summarizing key clinical findings. It discusses differential diagnoses for masses in the upper quadrants, mechanisms of pes cavus, cardiovascular examination findings, complications of renal failure, and signs of cirrhosis among other topics.
2. Details are given on potential examination findings for different disease processes, including surgical scars that may indicate prior procedures. Subtle exam signs are noted, and correlating exam findings with a patient's history is emphasized.
3. Pathophysiology behind common complications of conditions like chronic kidney disease are reviewed, along with treatments for diseases such as renal transplantation. Normal exam findings and important details to remember are also provided.
1. Large spleen that you felt, might not be a spleen! Must know Ddx of Left Upper quadrant mass: Spleen, kidney, Colon/pancreratic/gastric mass, adrenal mass. Right Upper quadrant mass: Liver, kidney, Gallbladder, Colon, adrenal mass.
2. What is the mechanism behind pes cavus?
Definition: High arch on the foot that does not flatten when the patient weight bears. In CMT disease, the distal weakness usually affect the anterolateral compartment. Hence the anterior tibialis and peroneus muscle are weak . Then the posterior tibialis muscle and peroneus antagonizes these muscles and pull harder causing the imbalance and hence pes cavus.
3. Sometimes sign can be so subtle, example is if you only find pes cavus. Two Ddx: CMT disease) sometimes you are expecting bilateral leg sensory deficit and weakness, sometimes they only only present at unilateral site! n Fredreich’s ataxia.
4. Cardiovascular: Approach to a midline median sternotomy scar in elderly, middle age, young adults…… If mediasternotomy scar (CABG? Valve replacement? Valve repair? Congenital heart repair eg. VSD,ASD, TOF/Coarctation repair absence of left radial pulse etc) + laparatomy scar (ischaemic bowel) + venous graft: sapheneous vein or radial artery harvest scar/site (CABG).
5. Scenario of median sternotomy scar with a permanent pacemaker >>> aortic valve replacement complicated by complete heart block.
6. Scenario of aortic valve replacement in young patient with Marfanoid features. AVR secondary to aortic regurgitation.
7. In CV examination : look for Marfanoid features, Turner’s, Down’s syndrome.
8. Common cause of death of Marfan’s syndrome is aortic dissection, aortic root aneurysm and aortic regurgitation are major causes of death and is because of cystic medial necrosis of the tissues. Autosomal dominant condition due to mutation to the fibrillin 1 gene which is essentially the build up of extracellular matrix protein.
9. Abdominal Ex: If multiple surgical scars, with ? healing fistula…PEG tube, ileostomy bag? Colostomy bag? (how to differentiate both) Vague mass at LIF or RIF (no evidence of AV fistula to suggest ESRF) >>> likely a chronic relapsing remitting abdominal disease such as Crohn’s or UC. The vague mass could be inflammatory masses due to IBD. Might also have a roof top/Chevron scar suggestive of liver resection, or liver transplant (IBD associated with PBC. PSC, hepatitis, cholangitis, cirrhosis) Reason for multiple scars > multiple laparatomy done due to CROHNS: intestinal obstruction/perforation/abscess/fistula UC: Toxic megacolon, flare not responding to medical Rx after 3 days etc.
10. Polycystic kidney disease:
Remember there could be multiple scars! Rt AVF (Make sure roll up sleeve: could be a BCF instead of RCF.) Parathydectomy scar/ reimplantation of parathyroid gland at hand, neck. Could have hepatomegaly due to cyst formation Could have only one ballatoble kidney? Will b confused with spleenomegaly ( but look if pt not anaemic with AVF likely to b kidney) The contralateral site not ballatoble but with a nephrectomy scar and a RIF scar with a palpable smooth firm non tender mass > renal transplant.\
11. Ddx of lone hepatomegaly: If no stigmata of CLD> still can b early cirrhosis, especially in alcoholic liver disease, Fatty liver (NAFLD), HCC, primary n secondary malignancies etc. If have jaundice (with +/- hepatomegaly +/- spleenomegaly but without stigmata of CLD >>> ve to think about haemolytic anaemia, causes include thalassemia, sickle cell anaemia etc)
11. Pathophysiology of kidney disease
12. Causes of failed kidney transplant:
Acute rejection (T cell mediated, antibody mediated); Graft versus host disease; Glomerulonephritis; Infection such as polyomavirus nephropathy; Drug toxicity
IF the AVF still have a strong palpable thrill with sign of puncture mark : failed kidney transplant?
13 . Patient with high blood pressure, during abdominal examination, should look hard for…..polycystic kidney disease, renal artery stenosis > listen to bruit ; triple A (expansile mass etc)- due to correlation of high BP with IHD and generalized atheromatous disease.
14. Remember they will ask u to examine the heart..then the pt have a laparatomy scar? Ask u what is the correlation? IF pt in AF> ischaemic bowel leading to bowel resection, or if evidene of ischaemic heart disease, may have generalized atheromatous disease with an abdominal aortic aneurysm repair.
15. Cirrhosis might not necessary present with peripheral stigmata of CLD!!!
16. If have sign of CLD, + hepatoslenomegaly+ANAEMIA >>>> if asked bout differential diagnosis: apart of CLD with portal hypertension, must always mention about hematological malignancy: such as myeloproliferative disease or lymphoproliferative disease! 17. Read about CML! Philadelphia chromosome. Cytogenetics of CML:
The Philadelphia chromosome present in 90-95% of CML. Chromosomal translocation, fusion of
abl gene on chromosome 9 and bcr gene of chromosome 22. Lead to increase oncogene activity, dysregulation of thyrosine kinase signaling eventually CML. Detection of philadelphia gene, mRNA of bcr-abl gene is use for diagnosis and monitor disease activity. TKi such as Imatinib and Nilotinib as monoclonal antibodies has been introduced.
18. Read about pathophysiology of complication of renal failure
Why anaemic? Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production.
Any condition when pt is not anaemic? PKD associasted with polycythemia
Why hypertensive? Salt and water handling by the kidney is altered in chronic kidney disease. Extracellular volume expansion and total-body volume overload results from failure of sodium and free water excretion. As kidney function declines further, sodium retention and extracellular volume expansion lead to peripheral edema and, not uncommonly, pulmonary edema and hypertension
Why hypocalcaemia? Why secondary hyperparathyroidism? Why need parathyrodectomy?
Hypocalcemia develops primarily from decreased intestinal calcium absorption because of low plasma calcitriol levels( due to inhibition by high phosphate) and possibly from calcium binding to elevated serum levels of phosphate. Low serum calcitriol levels, hypocalcemia, and hyperphosphatemia have all been demonstrated to independently trigger PTH synthesis and secretion. As these stimuli persist in chronic kidney disease, particularly in the more advanced stages, PTH secretion becomes maladaptive and the parathyroid glands, which initially hypertrophy, become hyperplastic. The persistently elevated PTH levels exacerbate hyperphosphatemia from bone resorption of phosphate. If serum levels of PTH remain elevated, a high bone turnover lesion, known as osteitis fibrosa, develops. This is one of several bone lesions, which as a group are commonly known as renal osteodystrophy. These lesions develop in patients with severe chronic kidney disease and are common in those with ESRD.
Why renal transplant?
ESRF patient for variety of reason. Reduce medical expenses in a long run. Reduce long term risk of death Better quality of life
>50% will still be hypertensive, due to 1. Diseased native kidneys, Immunosuppresants eg. cyclosporins, or 3. dysfunction of graft
What medication can be used for hypertension after transplant?
The antihypertensive drugs usually used after kidney transplantation are diuretics, calcium channel blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and β – blockers. Most emphasis is given lately to ACEIs/ARBs and β – blockers because of their cardioprotecive effect.
19. Remember in a renal transplant patient…sometimes pancreas-kidney transplantation for pt
with ESRF secondary to DM. Hence we see a Ruttherford Morission scar at RIF as well as a roof top Chevron scar at the bilateral subcostal region. Sometimes even a median sternotomy scar! Because of increase Cv risk> IHD in CKD patient.
20. Last minute ve to remember L4,L5,S1 dermatome always forget.
21. Pls remember liver span is more important than how many finger breath below costal margin ( think about emphysematous lung or flatten diaphragm). Normal male is 10cm . Female is 7 cm
22. Must read about Crohn’s disease and ulcerative colitis!
23. What is spider naevi? Central red spots which are essentially dilated arterioles with reddish extension that radiates outwards (small veins that carry away free flowing blood). Blanching and fill up from central to peripheral. >5 is abnormal.
24. What is the histopathological features of cirrhosis? Fibrosis+ scarring surrounding the hepatocytes with abnormal regenerating nodules (micro or macronodules)
25. What is bronchial breathing?
26. What is ESR? What is rheumatoid factor?
27. Must read about cystic fibrosis! Western disease, can come out in abdominal station- because can present with cirrhosis, distal ileal obstruction causing ileostomy….. OR respiratory station!
28. Need to know the pathophysiology of ascites and edema in cirrhosis!
Indicate decompensation, poor prognostic factor.
Following development of portal hypertension, lead to vasodilation of the splanchnic circulation.
Causing decrease in systemic vascular resistance and hence decrease in travascular volume, then lead to activation of the renin angiotensin aldosterone system and the end result is the avid sodium and water retention propagating the development of ascites and edema.
29. Read about Hereditary Haemochromatosis:
- Bronze, slate grey, metallic grey pigmentation of the skin/face - koilonychias - Hepatomegaly +/- features of cirrhosis - Diabetes mellitus - Atropathy (pseudogout) * Remember DM + Cirrhosis = Non alcoholic fatty liver disease or haemochromatosis
Ix: Features of iron overload: Transferrin saturation >45%; liver Bx- Parenchymal deposition of iron Diagnosis of HH: Genetic testing >autosomal recessive trait Rx Venesection Iron chelators 3-6 monthly USG and AFB Screen for dilated cardiomyopathy : Cardiac MRI : Failure Rx Screen for hypogonadism : Iron deposition at pituitary gland.
30. Read about Priary Billary Cirrhosis
-Cirrhotic features - Middle age lady - Xantholasma - Tendon Xanthomata - Pruritus = excoriation mark - Association with other autoimmune disease Dx: AMA, liver biopsy: portal tract granuloma> cirrhosis Mx: -Vitamin ADEK supplement - Statin to treat hypercholestrolaemia - Due to lack of absorption of vitamin D> hence low calcium > hence bone disease : Rx with supplement, biphosphonate etc - Ursodeoxycholic acid, Cholestyramine > reduce prupritus, improve liver profile etc - Liver transplant for intractable pruritus and refractory fatigue.
31. Remember respiratory station that might come out : pulmonary fibrosis with systemic sclerosis, restrictive lung disease secondary to marfan syndrome ( can have apical bulae/pneumothorax, fibrosis or bronchiectasis) or secondary to muscular dystrophy (with pacemaker!)
32. In pulmonary fibrosis, can be 7th nerve palsy! (sarcoidosis)
33. In pulmonary fibrosis, if upper zone , must ask about bird, pigeon , farm exposure.
34. Examiner will ask can u elaborate more on idiopathic pulmonary fibrosis? - chronic lung disease characterized by inflammation and fibrosis of the lung parenchyma. - Also known as cryptogenic fibrosing alveolitis - After other causes have been excluded. - ATS/ERS classify 7 types of interstitial pneumonia, UIP : restrictive lung pattern, dyspnea, bilateral interstitial lung infiltrates. 35. Learn about cystic fibrosis!
36. Learn about celiac diseae!
37. Purse lip breathing: Splinting the airway open during expiration
38. In COPD blue bloaters (chronic bronchitis) vs pink puffers (emphysema)
39. In COPD centri acinar (reduce breath sounds at upper to middle zone) vs pan acinar (reduce breath sounds at lower zone)
40. Remember use the word breath sounds! NOT air entry.
41. COPD might not be just COPD could be with underlying lung infection ? Rt LZ pneumonia, but rather unlikely in PACES exam.
42. Must remember surgical management of COPD : bullectomy, lumg volume reduction surgery, lung transplantation.
43. Criteria for LTOT
44. Remember polymyositis and dermatomyositis can come out in respiratory station as well for pulmonary fibrosis, so watch out for proximal muscle weakness and tenderness, or heliptrope rash on eyes, Gottrons papules at hands!
45. Facts about bronchiectasis:
- Coarse crackles alter with coughing - Not necessarily present with clubbing - 30% of pt with COPD have bronchiectasis - More commonly a local process, involving a certain lobe. It can also be diffuse where crackles are generalized. - REMEMBER in productive cough + coarse crackles + clubbing can be : 1. Brochiectasis (with inspiratory clicks) 2. Lung CA (look for nicotine staining, LN enlargement, cachexia) 3. Lung abscess (fever, very sick) 4. Pulmonary fibrosis ( crackles r less coarse, usually dry cough) - Pathophysiology: Abnormal bronchial wall associated with wall dilation, destruction and transmural inflammation - Ix: FBC, CXR, sputum C+S, HRCT (signet ring sign: bronchial diameter greater than adjacent vessel diameter), - Lung function test (usually obstructive pattern, but in severe cases due to scarring and atelectasis, may cause restrictive pattern, or if got underlying pulmonary fibrosis. - Bronchiectasis can cause metastatic cerebral abscess - Mx: 1. General measure: stop smoking, adequate nutrition, vaccination, LTOT 2. Antibiotics 3. Postural drainage an physiotherapy 4. Bronchodilators 5. Anti-inflammatory steroids 6. Surgery: resection, tumour removal, lung transplant in cystic fibrosis
46. Marfan syndrome can present with brochiectasis > hence respiratory system!!!!!!!!
47. Need to read up on cystic fibrosis!!!!!!!!!! (Can come out in abdominal case, in respiratory case)
In respiratory station> come out as part of bronchiectasis! + lobectomy scar + beware with bilateral thoracotomy scar!: Bilateral lung transplant! (In that case no more coarse crackles) Other important points: - Patient are usually young adults, thin, underweight, cachexic, pale, short stature but good appetite! - Pt is a young adult, who looked pale, thin, short stature. He is breathless at rest, with a productive cough. There is an inspiratory click with expiratory wheeze hear with an unaided ear. He has clubbing. Trachea is not deviated, there is no cervical LN palpable. Ex of the chest review a right lower zone coarse crepitation/crackles which altered with coughing. There is also generalized wheeze. - Usually patient might have wheeze! - Can look for sign of glucose pin prick : DM - Can look for GI related complications: Steatorrhoea, rectal prolapse, distal ileal obstruction (meconium ileus equivalent), cirrhosis, gallstones > so look for scars, at RUQ, laparatomy , sign of cirrhosis etc. - Respiratory: Nasal polyps, Asthma, Pneumonia, Bronchiectasis, pneumothorax, Haemoptysis, ABPA. - CV: Cor pulmonale. - Pathophysiology: Autosomal recessive condition associate with a defect in chromosome 7 that encodes the CFTR (CF Transmembrane regulator) chlorine channel. So a defect in chloride transport to the airway causing increase in viscosity and tenacity of the airway secretion - Ix: sweat sodium test (>60mmol/L) - Usual lung infection, bacteria type is ifferent: staphy aureus, pseudomonas, H.influenza etc. - Management: 1. General measures: Stop smoking, adequate nutrition, pancreatic enzymes, multivitamins, low fat diet, LTOT, immunisation 2. Antibiotics, nebulised tobramycin for pseudomonas infection 3. Postural drainage and physiotherapy, use of nebulised recombinant DNAse to decrease thickness of airway secretion. 4. Bronchodilators 5. Surgery: Lung/heart-lung transplantation.
Specific for cystic fibrosis: high dose ibuprofen, nebulised tobramycin for pseudomonas infection, nebulised recombinant DNAse, inhalation of hypertonic saline. Heart-lung transplantation. 48. In respiratory cases, sometimes maybe no findings at all…only two small dots marks : radiation burn , or radiotherapy mark! > that suggestive have pt having a lung CA under radiotherapy
49. Sometimes, think laterally, must think of SE of drugs as the cause of clinical presentation. Eg. Pt who has bradykinesia, rigidity, tardive dyskinesia>>>>> must think about drug induced parkinsonism….use of dopamine antagonist such as Neuroleptics: Phenothiazines, Chlorpromazine, prochloperazine, methyldopa, sodium valproate etc.!!!! Use causing parkinsonism in pt who has underlying Huntington’s disease!!!! chorea!!!
Extrapyramidal symptoms:
Acute dystonic reactions: muscular spasms of neck – torticollis, eyes – oculogyric crisis, tongue, or jaw; more frequent in children Akathisia: A feeling of motor restlessness Pseudoparkinsonism: drug-induced parkinsonism (cogwheel rigidity, bradykinesia/akinesia, resting tremor, and postural instability; more frequent in adults and the elderly). Although Parkinson's disease is primarily a disease of the nigrostriatal pathway and not the extrapyramidal system, loss of dopaminergic neurons in the substantia nigra leads to dysregulation of the extrapyramidal system. Since this system regulates posture and skeletal muscle tone, a result is the characteristic bradykinesia of Parkinson's. Tardive dyskinesia: involuntary asymmetrical movements of the muscles, this is a long term chronic condition associated with long term use of antipsychotics
50. Failed renal transplant, fresh puncture mark at the fistula, with very strong thrill at AVF.
51. HARRT related lipodystrophy: Side effect of drugs causing symptoms! / Clinical presentation >>>> lead to underlying diagnosis.
52. Must read about HIV related complications!!!! Lipodystrophy etc…
53. Your differential diagnosis must always include drug induced SE>>> which can later lead to the diagnosis of the condition!!!!!
54. If trachea deviated, listen to the front of chest 1st, look for apices changes
55. Trachea usually not deviated in lower zone lobectomy
56. Signs of collapse/lobectomy can be quite similar especially for upper zone ( reduced breath sounds, dullness on percussion, reduced chest expansion, trachea deviation) except for the thoracotomy scar.
57. Remember rheumatoid lungs can present with a mixed of symptoms! (Apical or basal fibrosis; bronchiolitis obliterans > wheezes!!! ; Pleural effusion ; Bronchiectasis) 58. Think laterally……..mixed of respiratory signs! Pleural effusion with bronchiectasis eg….etc etc.
59. Remember recurrence of secondary pneumothoraces is highest in cystic fibrosis! If present
with bronchiectasis, clubbing, young boy, reduced breath sounds at one zone, , small chest tube scar > must think of pneumothorax!!!!!!
60. Avoid pleurodesis in pt with CF, bcos need to prep them for lung transplant.
61. Remember when examining the lungs, if have rheumatoid hands…..can hear coarse crackles : bronchiectasis, fine crackles : fibrosis, , dull at bases/reduce breath sound: pleural effusion. Prolonged expiratory phase, wheeze: bronchiolitis obliterans…..a mixture of respiratory symptoms!!!!
62. Contraindication for renal transplant: Active infection, HIv, cancer, severe heart disease. 63. Pre transplant workup: Counselling Make sure no abnormal urinary tract-urodynamic studies Consider pancreatic transplant in DM patient Make sure CAD identified, revascularization done prior t o transplant Hepatitis B, Hepatitis C, HIV, Cytomegalovirus, TB, Zoster. Compliance issue. Coagulopathies, eg. on warfarin etc.
64. Ddx of superior vena cava obstruction (must look at radiation mark at the chest!!!!!) – edematous, plethoric upper limb and face, JVP raised and fixed, Dilated superficial veins of upper chest, upper limb and face.
65. Cardiac cases:
- Think about, if I see a median sternotomy scar, what is my approach?
- Think about, If I see a thoracotomy scar, what is my approach?
- Think about if I see clubbing and central cyanosis, what is my approach?
- Think about if I hear irregularly irregular rhythm, what is my approach? Ddx of
irregularly irregular rhythm.
- Think about if I hear a loud pan systolic murmur all through out the precordium, how to differentiate between a tricuspid regurgitation, a mitral regurgitation or a VSD. Can it be a mixed disease?
- Must always think about syndromic features associated with valve disease, Marfan syndrome, Turner’s, Myotonic dystrophy? 1. Marfan Syndrome: Aortic dissection, aortic regurgitation 2. Turner’s symdrome: COarctation of aorta, bicuspid valve (AS/AR) 3. Myotonic dystrophy: Heart block>pacemaker, cardiomyopathy> heart failure 4. Klinefelter’s syndrome: MVP
- Because doing PACES in Glasgow centre, if heard an AORTIC REGURGITATION murmur,
MUST think about associated symptoms such as AS/Psoriatic athropathy, RA/SLE, Marfan’s syndrome (blue sclerae but tall with kyphoscoliosis) , weird weird condition such as Osteogenesis imperfecta (watch out for hearing aids, blue sclera but short stature with kyphoscoliosis) Pseudoxanthoma elasticum (loose skins over neck and axilla) Ehlers-Danlos (blue sclera, hyperextensible skin and joints, poor skin healing, purpura>>>>> can be MArfan’s Syndrome as well)
- Indication for AVR-
1. AS: a) Symptomatic severe AS (>50mmHG) b) Asymptomatic: if going for CABG, EF impaired, abnormal BP response, VT, <0.6cm2 2. AR: a) Symptomatic (angina , heart failure) b) Asymptomatic but EF<50%, LV dilated, LVESD>55mm, aortic root dilatation >50mm - Indication for MVR- For MR/MS 1. MR: a) NYHA III b) LV dysfunction, EF<60% c) Left ventricular end systolic diameter >45mm 2. MS: a) Symptomatic + heart failure b) Pulmonary hypertension c) Haemoptysis d) Recurrent thromboembolic event due to AF
- Indication/contraindication for PTMC
INDICATION: Multiple comorbids where open heart surgery will be of high risk; temporary measure before MVR. CONTRAINDICATION: MR, Left atrial appendage thrombus, non mobile valve with calcification of the valve and subvalvular apparatus
- Indication for SBE prophylaxis
- How to differentiate between Teratology of Fallot with Eisenmenger Syndrome?
- Think about if there is an absent of radial pulse, what is my approach?
- Sign of severity of aortic stenosis, mitral stenosis, aortic regurgitation, mitral
regurgitation 1. Sign of severity of aortic stenosis: - small volume pulse - slow rising pulse - narrow pulse pressure - systolic thrill - soft second heart sound - late peaking of the murmur - sign of pulmonary congestion - sign of pulmonary hypertension Mx: ECG (LVH), CXR(post stenotic dilation of proximal ascending aorta, pulmonary congestion), ECHO (LV size, fn, aortic valve area), Coronary angiogram Patient education, regular f/up if asymptomatic, SBE prophylaxis Symptomatic Rx: if in heart failure> diuretics, beta bocker Surgical Rx: AVR, TAVR
2. Sign of severity of mitral stenosis:
- Low voume pulse - Increase length of murmur* usually the same for all diastolic urur eg. aortic regurgitation - Sign of pulmonary hypertension - Sign of pulmonary congestion - Early opening snap (must know the significance!!!) - Graham Steel murmur (Pulmonary regurgitation) Mx - ECG (AF, Bifid P), CXR (Straightening L heart border, pulmonary congestion), ECHO, COROS. - Patient education, regular ECHO f/up, SBE prophylaxis - AF management - Heart failure Mx - Surgery: PTMC, open heart valve repair, MVR
A couple of pointers when presenting MS
- If malar flush, must have sign of pulmonary hypertension (malar flush due to pul HPT leading to low cardiac output) - If AF> mention irregularly irregular rhythm (NOT AF!) Ddx including: AF, ventricular ectopics, atrial flutter with variable block, second degree heart block etc - lateral thoracotomy scar =mitral valvotomy scar? For mitral valve repair? - Apex beat undisplaced, tapping quality-palpable 1st heart sound (due to loud first heart sound) - Must mention loud first heart sound (but not a sign of severity!) - opening snap at early diastole
3. Sign of severity of aortic regurgitation:
- Wide pulse pressure - Long duration of the murmur - Sign of pulmonary hypertension - Sign of pulmonary congestion - Austin flint Murmur (low pitch mid diastolic murmur) (need to know the mechanism, the artic regurgitant jet flow impinged on anterior mitral leaflet causing ‘functional mitral stenosi’ but without the loud 1st heart sound/opening snap.)
Mx: ECG,CXR,Echo Heart failure Rx Use of vasodilator: Nifedipine, ACEi,ARB ONLY RECOMMENDED for SEVERE AR + LV dilatation but no symptoms AVR
4. Sign of severity of mitral regurgitation:
- Soft first heart sound - Displaced apex beat - Precordial/Systolic thrill - Sign of pulmonary hypertension - Sign of pulmonary congestion
- When describing valvular lesion, use MODERATE TO SEVERE eg. aortic stenosis/mitral regurgitation - Leaning over left hand side is called LEFT LATERAL POSITION -
What is the mechanism of opening snap in MS?
- Opening snap with be heard with a loud first heart sound - Indicates mitral leaflets are mobile and pliable (reduce with calcification) - The earlier the opening snap, the greater the left atrial pressure, hence the greater the severity of mitral stenosis. -
- MUST ALWAYS THINK ABOUT MIXED VALVE LESION< DO NOT SATISFY WITH ONLY ONE VALVE LESION
63. Mitral regurgitation if the cause is functional, due to ischaemic heart disease, if there is an abdominal scar> can be due to a generalized atheromatous disease with a triple A (AAA) repair. If pt in AF, could be ischaemic bowel!
64. Relation of seronegative spondyloarthropathies with AR
65. when describing management of valvular heart disease:
1st: CXR, ECG, ECHO, Coronary angiogram 2nd : Pt education, SBe prophylaxis, Regular symptom n echo f/up 3rd: AF management 4th: Heart failure management 5th : Valve replacement 66. Remember Austin Flint: mid diastolic murmur in severe AR Remember Graham Steel: early diastolic murmur in severe MS
66. In hx taking session , make sure think about MENS, POLYGLANDULAR AUTOIMMUNE SYNDROME (APS-1,APS-2)
Gradual rise in serum creatinine, proteinuria, heamaturia, reduced urine output etc. (chronic)
Lung transplant
Chronic rejection explains long-term morbidity in most lung-transplant recipients,[2][3] the
median survival roughly 4.7 years, about half the span versus other major organ transplants.[4] In histopathology the condition is bronchiolitis obliterans, which clinically presents as progressive airflow obstruction, often involving dyspnea and coughing, and the patient eventually succumbs to pulmonary insufficiency or secondary acute infection.
Airflow obstruction not ascribable to other cause is labeled bronchiolitis obliterans syndrome (BOS), confirmed by a persistent drop—three or more weeks—in forced expiratory volume (FEV1) by at least 20%.[5] BOS is seen in over 50% of lung-transplant recipients by 5 years, and in over 80% by ten years. First noted is infiltration by lymphocytes, followed by epithelial cell injury, then inflammatory lesions and recruitment of fibroblasts and myofibroblasts, which proliferate and secrete proteins forming scar tissue.[6] Generally thought unpredictable, BOS progression varies widely: lung function may suddenly fall but stabilize for years, or rapidly progress to death within a few months.
70. Median sternotomy scar can be lung transplant scar? Yes
71. Must know broad term of management of Rx of each valve disease.
AS
MS
What is the mechanism of opening snap in MS?
- Opening snap with be heard with a loud first heart sound - Indicates mitral leaflets are mobile and pliable (reduce with calcification) - The earlier the opening snap, the greater the left atrial pressure, hence the greater the severity of mitral stenosis.
AR
MR
72. Haematological cases
What will you see in peripheral blood films For ALL AML CML CLL
Remember , even though pt have features suggestive of Grave’s Disease, most of them have features of hypothyroidism, or just simply euthyroid. Because they have thyroidectomy done (watch out for a scar!).
75. Mechanism of lid lag/lid retraction in thyroid?
- Increase sympathetic tone of Muller muscle, proptosis, fibrosis of the levator muscle
76. Mechanism of proximal myopathy in thyroid?
- Due to thyroxine toxicity, there is evidence to suggest that structural changes in motor end plates could lead muscle fiber degradation, muscle fiber weakness, and muscle fiber fatigue.
Iodine excess: Preventing organification of iodide and inhibit thyroid hormone synthesis, usually autoimmune mediated, know as Wolff Chaikoff effect
Iodine excess in population with iodine deficiency or goiter or autonomous thyroid tissue can cause hyperthyroidism, known as Jod Basdeow phenomenon
79. Value of autoantibodies in diagnosing hypothyroidism?
- Antithyroid antibodies such as anti-thyroglobulin or anti-thyroid peroxidase - unhelpful in diagnosis of hypothyroidism BUT helpful in establishing cause of hypothyroid eg. Hashimoto’s disease BUT helpful in predicting progression of disease.
80. What it means by subclinical hypothyroidism?
- TSH high, T4 normal. - Do not treat repeat in 6 months if TSH between 5-10 - IF above 10, Rx to prevent overt hypothyroidism.
81. Reidel’s thyroditis: chronic inflammation of the thyroid tissue parenchyma causing dense fibrosis.
82. Thyroid eye disease happens because of infiltration, edema and fibrosis of the extra ocular muscles.
83. Remember in Graves’ opthalmoplegia , just mention it’s a complex opthaloplegia. But it affects the inferior rectus muscle 1st causing impairment in upward gaze.
84. When considering Grave’s ophtalmoplegia, must always check visual field, visual acuity and the pupils for RAPD. It can cause optic nerve compression!
85. Management of Grave’s disease:
a) symptomatic- beta blocker b) thionamides – carbimazole or PTU (prophytiouracil): Ensure compliance, agranulocytosis, monitor 4-6 weeks time, by 18 months, not responding> failure c) radioactive iodine ablation – 2 weeks away from children and preggers - 4 months before attempting pregnancy - risk of hypothyroidism 2-3% d) surgery
86. Rx of Grave’s exopthalmos:
Eye patch/lubricants Smoking cessation Lateral tarsorrhaphy Sleep upright with eye taped close
87. Graves’ malignant exophtalmos: Severe inflammation and congestion of the eye that lead to severe pain and can lead to blindness due to optic nerve compression. Rx: Systemic steroids, orbital decompression, radiotherapy. 88: Graves’ disease: Autoimmune disease characterized by the presence of TSH autoantibodies that bind to TSH receptors and stimulate the production of excessive thyroid hormone.
89. Sequence of examination for acromegaly (Station 5)
1. Joint pain? 2. Headache 3. Loss of vision at the extremities 4. Change in finger size. Able to put on your ring? 5. Change in shoe size. 6. Change of appearance 7. Changes in jaw, dentures 8. LOW/LOA/fever 9. Tingling of hands 10. Polyuria/Polydipsia 11. Chest pain, SOB?
Ex: Check the hands: large spade like fingers, sweaty large hands Check BP Check the face/ears: prominent supraorbital ridges, enlarged nose/lips Check the mouth/jaw/tongue: prognathism, interdental separation, macroglossia Check vision: bitemporal hemianopia Check proximal myopathy Check thyroid: maybe diffusedly enlarged Check apex beat: displaced in cardiomegaly n heart failure
90. Sequence of examination for Cushing’s syndrome? (Station 5)
1. Gaining a lot of weight? 2. Skin getting thinner, bruised easily? 3. Any stretch marks, striae at your body? 4. Feeling tired? Weakness when lifting arm? 5. Fever/LOW/LOA?Haemoptysis? (lung CA) Polyuria/Polydipsia?(DM) 6. Traditional meds/ steroids used? 7. vision problem? Headache? 8. Fall? Backpain? Neck pain? 9. Chest pain? SOB? 10. Relevant medical history: asthma/COPD/SLE/RA
Ex: Check the hands: thin skin, purpura, bruises, pigmentation Check the face: plethora, moon face, buffalo hump, acne, hirsutism Check for visual field Check for shoulder: supraclavicular infrascapular fad pad, proximal myopathy Check abdomen: Striae purple Palpate the adrenal gland/ look for adrenelectomy scar Check for complications of Cushing’s: cataract, hypertension, diabetes mellitus, osteoporosis 91. Two main differentiating features between pseudo cushing syndrome and cushing syndrome is ; Cushing syndrome usually will have proximal myopathy and dermatological manifestation ( purpura, purple striae, acne, hirsutism, hyperpigmentation, acanthosis nigricans etc)
92. Nelson’s syndrome: Condition where after bilateral adrenalectomy, the pituitary tumour enlarges, associated with the elevated serum ACTH and hyperpigmentation. Patient sometimes can present with bitemporal hemianopia due to the rapidly enlarging pituitary tumour.
93. If patient have cushingoid features, have elevated serum calcium, with gastritis symptoms, need to think about MEN1 (pituitary adenoma, pancreatic tumour-gastrinoma, hyperparathyroidism)
94. Need to read up on Cushing’s syndrome, what test to order
For screening: Urinary free cortisol x3, overnight/low dose dexamethasone suppression test
For localizing ACTH dependent or independent : ACTH level
If ACTH low, do adrenal imaging > adrenal adenoma/carcinoma
If ACTH high, do high dose dexamethasone suppression test > ectopic ACTH or pituitary/Cushing’s disease
Why not go straight to MRI pituitary, because 50% of <1cm microadenoma is not picked up by MRI scans.
95. Addison’s disease (station 5)
Hx taking: Energy level? Loss of weight? Loss of appetite? Feel dizzy/fainting Abdominal pain Constipation Nausea/vomiting Notice your skin changing colour? Notice you feel giddy when you stand up? Depressed Hx of TB Family Hx of gland problems Previous surgical hx
Examination: Look at the hands: Hyperpigmentation at the palmar creases Look at chest/face: Loss of axillary/body/facial hair (women), gynaecomastia (men) hyperpigmentation at the buccal mucosa, candidiasis at tongue Look at elbows, knee etc Check postural blood pressure Look for other associated autoimmune disease: APS1 candidiasis, addison’s, hypoparathyroidism low calcium) APS2 DM type 1, hypothyroidism, Addisons
Addison’s disease: The adrenal glan does not work properly. It is a gland above the kidney that produce hormones that r essential to life, making sure our blood sugar level are alrite, out blood pressure r alrite. The body produce these antibodies that turn back and attack our own body.
Ix: Morning cortisol at am, if abnormal, short synacthen test
Rx: Replacement of the hormones Educate patient, ensure compliance, advice during episodes of stress, sickness, trauma, operation Medic alert bracelet.
96. The difference between oral glucose tolerance test (OGTT) +GH: to diagnose acromegaly
vs
insulin tolerance test (ITT) + GH +cortisol: to diagnose panhypopituitarism
97. If you suspect hypopituitarism, MUST ALWAYS mention primary hypogonadism as your differential diagnosis because it is more COMMON!!!
98. Remember if there is loss of axillary hair, facial hair + loss of body musculature + gynacomastia : either chronic liver disease (in abdominal station) OR Addison’s disease, primary hypogonadism (must look hard for Klinfielter’s syndrome), hypopituitarism (mostly in station 5)
99. In hypopituitarism, symptoms depending on which hormone is lacking, generally symptoms
are GH,gonadrophins (LH,FSH) affected first followed by TSH and ACTH.
Might have eye symptoms> bitemporal hemianopia> headache
Hypopituitarism (Station 5 ! Station 5! Lost of pubic , axillary , facial hair- think bout hypopit, addison’s Only in female because androgen produce by adrenal cortex, primary hypogonadism) Hx: Pale-ACTH Tiredness-ACTH Dizziness-ACTH Lost of weight (ACTH deficiency stronger than TSH deficiency) Abdominal pain-ACTH Cold intolerance-TSH Slow speech, slow movement, bradycardia-TSH Short stature-GH Lost of muscle, lost of axillary hair, lost of facial hair, gynaecomastia –LH/FSH Ask about history of surgery, radiotherapy, PPH in the past
Ex: As per hypothyroid Lost of muscle, lost of axillary hair, lost of facial hair, gynaecomastia REMEMBER USUALLY NOT MUCH CLINICAL FINDINGS EXCEPT -DRY, WRINKLED AND PALE SKIN - DECREASE BODY HAIR, PUBIC HAIR, AXILLARY HAIR, FACIAL HAIR, GYNAECOMASTIA -Testicular volume - Postural hypotension - Slow releasing deep tendon reflex - Bitemporal hemianopia
Ix: FT4,TSH, LH, FSH, testosterone, estrodiol, prolactin Short Synacthen Test Insulin tolerance test (ITT) +GH+ cortisol -2nd line, C/I: epilepsy, heart disease, adrenal failure (* Pituitary stimulation test: either ITT, metyrapone, or Short Synacthen test: preferred) Rx: Replace hydrocortisone (No need to replace fludicortisone, bcos mineracorticoids not affected, still produce and regulated by rennin angiotensin system) Replace thyroxine Replace testosterone Replace oestrogen Replace GH (if QOL affected)
100. In station 5, if you see a scar at forehead, can be very faint!!!!!!! Think about acromegaly, Cushing’s disease (pituitary adenoma), prolactinoma, hypopituitarism
101. Klinefelter’s syndrome:
- predominant karyotype of 47XXY, with others being mosaic forms - If in station 5, saw a patient with hypogodanism, must ask to examine the testes and look for associated features such as: SLE, RA, Sjogren’s, Diabetes, mitral valve prolapse (pansystolic murmur), varicose veins.
102. When seeing patient with tall stature and long limbs, think about ?acromegaly Klinefelter’s syndrome, Marfan’s syndrome (what are the differentiating features)
103. When seeing pt with primary hypogonadism- usually testes are small, and will have gynaecomastia. MUST think about drug causes!!!! Radiotherapy! Chemotherapy! Other drugs such as spironolactone, ketoconazole, cimetidine etc.(inhibit testosterone synthesis) 104. Secondary hypogonadism usually will NOT have gynaecomastia because no LH/FSH to stimulate testicular aromatization of testosterone to estradiol.
105. Ddx of secondary hypogonadism (testosterone low, LH/FSH low):
105. Turner’s syndrome = Noonan’s syndrome (but normal genotype)
- short stature, short neck, webbed neck, shortening of fourth metacarpal(Archibald sign= absence of fourth knuckle, dimpling of knuckles), nail dysplasia, multiple naevi. - Medical condition associated with Turner’s a) Primary ovarian failure b) CV: Bicuspid aortic valve, coarctation of aorta, sometimes dissection c) Kidney: horse shoe kidney d) Eye: Cataract, ptosis, strabismus e) Hypothyroidism f) Type 1 diabetes
a) Review drugs b) Look for causes> start with testicular tumours, adrenal tumours c) Look for salient features, eg, Klienfelter’s? d) If still unable to find out, check bloods, hCG, LH, testosterone, oestrogen, > can determine primary or secondary hypogonadism.
108. Cardiovascular examination:
Make sure do not forget: Radial-radial delay Radial femoral delay When auscultating heart, HAVE TO PALPATE THE CAROTID PULSE AT ALL TIMES! Always listen to the quality of the first and second heart sound> loud 1st heart sound > MS; soft second heart sound > AS; fixed splitting of second heart sound > ASD
Conversation: ‘ I want to examine your heart, check your pulses.’ ‘ Is it alright for you to take your top off, roll your trousers up to your knees’ ‘ I will have a look at your chest’ ‘ Just get you turn your head slightly to your left’ ‘ Feel your neck pulse’ ‘ I will just get you to lift your left arm above your head, and roll towards your left hand side’ ‘ I will just get you to sit and lean forward’
I would like to complete the examination by
1. Checking patient’s BP 2. Do a urine dipstick. 3. Check all the peripheral pulses.
During presentation: MUST COMMENT ON HEART SOUNDS EG. loud 1st heard sound, soft second heart sound etc.
108. Respiratory examination:
Make sure do not forget: Take deep breath in and out + cough Feel lymph nodes cervical Look for flapping tremor TO TAP THE CLAVICLES AND AUSCULTATE THE APICES
Conversation: ‘ I am just going ot stand at the end of the bed and have a look at you.’ ‘ Just want to have a feel of your wind pipe’ Start examining the back of the lungs. However, if trachea is deviated, to start from the front.
I would like to complete the examination by
1. Checking patient’s BP, looking at the temperature chart 2. Look at the sputum pot 3. Check for patient’s peak flow. 4. Listen to the heart, check for peripheral edema to look for sign of right heart failure> cor pulmonale.
110. Abdominal examination:
Make sure do not forget: Palpate the lymph nodes Look at the upper limb from hands to forearm to arms!!!! >>>fistula!!!! Look at the neck for parathyroidectomy Sit up the patient, look at the back for scars!!!!!! BALLOT the kidney (look at the proper way of balloting the kidney) LOOK for flapping tremor
Conversation: ‘ Swing your leg over and lie your self flat.’ ‘ Just lie on your back again’
I would like to complete the examination by
1. Checking patient’s vital sign, including the temperature 2. Do a genital examination 3. Check for the hernia orifices. 4. Do a per rectal examination
109. Need to differentiate between osteogenesis imperfecta vs Paget’s disease
Because both also have hearing aids, SCARS consistent with previous surgery of long bones
However OI got short stature with kyphoscoliosis.
110. Systolic thrill is palpable at the aortic area for aortic stenosis. 111. must remember it is always alright to say it’s a mixed aortic/mitral valve disease. As long as you can pin point the predominant lesion. The other less dominant lesion can b there or not there, just say it’s a soft murmur. Examiner themselves might miss it.
112. Basic things!!! Listen to the heart sounds….1st heart sound loud with an opening snap!!? MS, 1st heart sound soft? MR………soft second heart sound ?AS
113. It is not wrong to say mixed mitral valve disease! Severe MR will have some mid diastolic murmur anyway due to increase forward flow across mitral valve..!!!! The important thing is to mention the predominant lesion!
114. Sometimes, it will be unclear which one is the predominant lesions eg. loud 1 st heart sound with displaced apex beat or small volume pulse with non displaced apex beat….
Just say its quite difficult to ascertain which one is the predominant lesion> I will conform my diagnosis by the use of ECHO or cardiac catheterization.
115. Apical systolic thrill = sign of severity in MR
116. Since going to Glasgow, need to read about coarctation of aorta, HOCM, MVP but only last minute because clinical signs not easy to pick up …can only use as part of differential diagnosis.
117. Must remember mechanism of S3 S4
118. Prosthetic aortic valve replacement always will have an ejection systolic murmur (soft)
119. Look hard for AVR associated with pacemaker insertion (due to calcified conduction system with AS, or during surgery, injury to the conduction system leading to PPM insertion because of CHB)
120. Anaemia with prosthetic valve?
- Blood loss due to anticoagulation - Endocarditis - Haemolysis
121. Remember when you are given a prosthetic valve case, look for all these!!! Complication of prosthetic valve -thromboembolic event eg. stroke - endocarditis - haemolysis - bleeding due to anticoagulation - valve dysfunction, leakage,dehiscence, calcification, thrombosis etc
123. Starr Edwards, ball and cage in MVR will have two clicks..but loudest at the mitral area. 124. Remember it is very difficult to diagnose a VSD by its own. Because your clinical finding is a pansystoic murmur, if loud throughout the whole precordium> it can be very severe mitral regurgitation.
However there r some subtle differences in VSD,
1. loud through out but does not change with respiration, 2. 2apex beat not displaced??? (not really because they will b displaced when there is a significant left to right shunt) 3. Does not radiate to axilla ( hard to say) 4. A parasternal systolic thrill!!! > more suggestive of VSD 5. Have a good discussion with the examiner providing Ddx of pansystolic murmur …
125. Additional information about Hallark for VSD during presentation
- Parasternal systolic thrill - Pansystolic murmur (but apex beat not displaced!-unless haemodynamically significant) --apparently loudest at the lower LSE? Difficult to ascertain
Classification of VSD: Perimembraneous, supra cristal, muscular, posterior
- Mechanism of spontaneous closure: hypertrophy of the muscular septum, formation of fibrotic tissue - Complications: IE, Pulmonary hypertension, LV dysfunction, Eisenmenger, aortic regurgitation - Ix: CXR (cardiomegaly, pulmonary congestions, increase markings); ECG (LVH, RVH, LA enlargement); ECHO - Mx: 1. Reassurance, SBE prophylaxis, normal life, yearly eCHO and r/v 2. Rx heart failure 3. Rx pulmonary hypertension 4. VSD closure: indication > Increase pulmonary: systemic blood flow Qp:Qs 2:1 > LV dilatation/dysfunction > Recurrent endocarditis > Development of aortic regurgitation - Absolute contraindication for VSD closure: irreversible pulmonary hypertension NOT Eisenmenger. 126. Atria septal defect: -Hallmark when presenting : 1. Fixed wide splitting of the second heart sound (SO listen carefully at the heart sound, NOT just murmur!) 2. Ejection systolic murmur at the upper left sternal edge (pulmonary area) bcos shunt L > R causing increase abnormal flow at the pulmonary valve.
127. I think this two (ASD & VSD) will seldom come out as separate entity, unless its in a young patient, and if with association with Eisengmenger syndrome or TOF. YOUNG PT!!!!
128. Complication of ASD: AF, Pulmonary hypertension, Eisenmenger’s syndrome IE,
129. remember if you think it’s a septal defect…look at the patient carefully for syndromic features. Down’s Syndrome and Turner’s syndrome r associated with ASD or VSD.
130. Sometimes , you might see a special scar for ASD closure below the breast line.
131. Since I will be going to a hard station like royal infirmary Glasgow! Must learn about Eisenmenger Syndrome vs TOF
132. ASD usually has AF
Approach to patient (at cardiac station) with:
1. Central cyanosis 2. Clubbing Ddx either 1. Eisenmenger Syndrome (+ pulmonary hypertension) or 2. Cyanotic congenital heart disease eg. Teratology of Fallot.
Tips: If there is a median sternotomy or a thoracotomy scar, chances are it is a repaired TOF.
If there is a absence or unequal left radial pulse, chances are TOF with Blalock Taussig shunt.
If there is a ejection systolic murmur at the upper left sternal edge (pulmonary area) and a pulmonary systolic thrill, chances are TOF (due to pulmonary stenosis)
If there are signs suggestive of pulmonary hypertension (eg. raised JVP, parasternal heaves, palpable second heart sound) chances are it is a Eisenmenger Syndrome!
If there are other extra murmur such as early diastolic murmur at the upper left sternal edge (pulmonary area) OR a pansystolic murmur at the lower left sternal edge (tricuspid area)> indicative of either a pulmonary regurgitation or a tricuspid regurgitation, ,all indicative of functional right heart dilatation> chances are it is a Eisenmenger Syndrome! If you think it is Eisenmenger Syndrome, you need to localize the lesion-remember the murmur you heard will not be the murmur of the lesion: 1. Single loud second heart sound : VSD (sometimes associated with aortic regurgitation) 2. Fixed wide splitting second heart sound: ASD 3. Reverse splitting of second heart sound: PDA 4. Aortopulmonary window (shunt between aorta and pulmonary arteries)
133Complication of TOF: - Cyanotic spells (syncope) - IE - Right heart failure - Polycythaemia - Thrombosis - Cerebral abscess - 134 Other info on TOF - What precipitate cyanotic spells: Exercise, fever, stress, dehydration, hypoxia, acidosis - Pathophysiology of cyanotic spells: Infundibular spasm and decreased systemic vascular resistance lead to increase RVOT> lead to right to left shunt ++ cyanosis - CXR: Boot shape heart, ECG: RBBB, RVH - Blalock Tausig shunt? An anastomosis of left subclavian artery to pulmonary artery to bypass the RVOT - Rx of TOF: Eliminate precipitating factor for cyanotic spells, total correction under cardiopulmonary bypass, Blalock taussig shunt.
135. Complications of Eisenmenger Syndrome:
- Haemoptysis (due to pulmonary hypertension and increase bleeding tendencies due ot dysfunctional platelet). - RV failure - Paradoxical embolism - IE - Sudden death - Polycythaemia - Thrombosis - Bleeding
136. Principle of management of Eisenmenger Syndrome:
- Patient education - Avoid dehydration and hot n humid conditions - Contraception, avoid pregnancy - IE prophylaxis - Oxygen - Anticoagulation - Heart failure Rx - Venesection if Hct >65 - Surgical repair if demonstrable reversibility of pulmonary hypertension - Heart lung transplantation
137. Read up on rare diseases:
Cluster of disease: Osteogenesis imperfecta vs Paget’s disease of the bone > both have similarities: of bowing of tibia, multiple previous healed long bone fractures with corrective surgery, hearing aids > differences: blue sclerae, joint hyperextensibility, kyphoscoliosis, short stature in> osteogenesis Enlarge skulls, hyperdynamic high output failure in Paget’s disease
Remember if there is a median sternotomy scar, a hearing aid!!! Think about osteogenesis imperfecta causing aortic regurgitation
138. Cluster of diseases due to defective collagen matrix (connective tissue disease):-blue sclera, joint hyperextensibility, Aortic regurgitation)
- Marfan Syndrome (tall stature, disproportionately long limbs)
- Osteogenesis Imperfecta (short stature, bowing tibia, hearing aid due to osteosclerosis)
- Ehlers Danlos Syndrome (thin skin, hyperextensibility, skin fragility, cigarette paper scars, fish mouth wounds, GI bleed)
Station 4: Communication skills and ethics
1. Remember you can say words like ‘I have got some of the information about your condition here, just to check and confirm whether they are correct, do you mind telling me again what happened?’ Delay with investigation management 2. Delay with investigation management: apologize: ‘I apologise on behalf of my team for the shortcoings that had occurred > let them vent> try to tell them what could be the reasons> promise them you would definitely look it up> file an incident report if finding fault in the system> offer options to the pt: will get a date as soon as possible, I will go down personally, have a word with the radiology specialist to get the earliest date + have a word with the respiratory physician how would this affect pt’s condition> ‘are you okay with my arrangement?’ ‘How do you feel about my arrangement?’still not happy? Offer to speak to the consultant, or provide contact of the patient liason service> apologise again> Ask whether patient have any concerns or worries? 3. Requesting for postmortem: if it’s a coroner’s postmortem? Can family member object? 4. Requesting for postmortem: - ‘Sorry for your loss, sorry to hear about the death of your father, it’s a big loss to the family, how are you coping so far?’ - Obviously your dad was quite sick, but his death yesterday was a bit sudden. - After discussion, we would like to suggest for a post mortem. - Explain on nature, types, indication, purposes of post mortem. - Any advance directive : has your dad ever expressed any objections towards post mortem? - This must be very difficult for you. Would you like to think about it first before making the decision? ‘HOW DO YOU FEEL ABOUT THAT?’ - Any special concerns or worries? a) funeral not necessarily delayed b) 2-3 days time, 3 hours c) Organ might be retained with your permission of course d) Results of post mortem will be informed via an appointment with the consultant.
5. Refusal of blood products in Jehovah’s witness
- Assess understanding of illness and explain seriousness of illness> need blood transfusion - Explore about religious view of not wanting blood transfusion - Respect decision but need to reinforce can potentially be fatal. Could die from this - Explore about use of other blood products, IV NS, IV Pantoprazole - Reassure during procedure, will make a mark at the consent form, not for blood transfusion & - Reassure pt apart from the blood transfusion, will not treat patient differently. - Offer to contact Jehovah’s Witness Hospital Liason Service, 24 hr help line. - Suggest patient to talk to religious leaders, family friends , an yone else who has similar experience - Lastly, ,will have to speak to consultant, consultant should speak to patient.
Where to patient/carer stands legally if he declines blood transfusion??
PATIENT HAS THE ABSOULTE RIGHT TO REFUSE TREATMENT! BUT THEY MUST BE COMPETENT, HAVE THE CAPACITY TO MAKE THE DECISION.
Offer option to discuss together with Jehovah’s Witness hospital liason service Offer option such as IV NS, EPO, IV iron therapy, hematinics (Vitamin B12, folate), use of other blood products such as albumin, haemophilia concentrates etc. ??? clotting factors: purified blood coponent (FFP. Cryoprecipitate)
Potentially be fatal if you bleed further. You could die from this.
I need you to be informed about the implications of your decision. You need the oxygen from the red blood to be used by all the tissues Don’t jus focus on why do not want blood transfusion!!!!!!!! Need to discuss about the nature of his disease, what happened up to this point>>> HOPC of melena, the procedure endoscopy!!!
Advance directive???
Have you been into this situation before? Any of your family? Friends have had that experience
When we fill in the consent form > about endoscopy , we will specify that you do not have any blood transfusion, packed cells.
I respect your wishes completely. Rest be reassured that although you do not wish to have any blood product/blood transfusion, we will still give you other treatment as usual. We will not treat you differently from the others.
I am pretty sure we have a 24 hour advice line specifically to deal with Jehovah’s Witness in this hospital. I need to double check this.
Jehovah’s Witness Hospital Liason service
I encourage you to discuss about this with your religious leader, your wife and the help line as well..
I need to talk to my consultant about this, so that you can talk to the consultant as well because he is doing the procedure.
6. We would like to discuss with you the treatment that we would like you to consider.
7. When staring conversation, a couple of things must be said:
Introduction: ‘Hi, I am Dr Leong the senior house officer today.’
Consent: ‘I have been asked to talk to you about the reason why you are here today. Is that okay with you?’ Offer for 3rd party presence: ‘Would you like anyone else to be present during our conversation?’ Assess understanding: ‘Just to check whether I have got all the information correct and correct me if I am wrong’ ‘Before I go on, how much have you been told about your condition?’ ‘Would you like to know more about your/your father’s condition?’
8. Explaination on brain stem death +Do not resuscitate + organ donation:
First of all, I am sorry to hear about your dad’s condition. How are you coping at the moment? Always a good 1st liner ‘I a afraid I ve got soe bad news to share with you.
‘Irreversible brain damage at an area that control the consciousness and breathing activity, eg. brain stem. ‘Brain stem death equates with the death of an individual.’
‘I am afraid that is the case for your father. We have done a few confirmatory test.’
‘ I am sorry to say that the chance of a meaningful recovery is very small. And there is only a very slim chance for him regaining consciousness.’>>this is before brain stem death is confirmed
******‘IT is important for me to stress that ventilation is not withdrawn to allow your father to die but because continued ventilation is inappropriate for a patient who is already dead. It will only prolong his agony and suffering’
****** If his heart stops, we will not attempt chest compression as well as he is technically brain dead and this would only prolong his agony and suffering.’ ‘How do you feel about that?’ ‘Have your father ever discussed about that issue?
******’It is also important for you to know that this decision is made by our medical team and don’t feel that you are responsible and actually causing the death of your father by allowing the ventilator to be stopped/ or by allowing us to withhold chest compression
****** I know this is a difficult time to discuss about this. Although your father’s brain is severely damaged, all his other organs are still in good condition. In such scenario, usually for all the other patients that we encounter, we would explore about the concept of organ donation. Has your father ever mentioned about his intention to donate his organs? We will give you more time to think about this. Feel free to talk to us about this. We will get you in touch with the transplant team for further information.
‘I am sure this must be difficult for you.’ ‘Your father is still young’ ‘but if he is already brain dead’, ‘holding on ventilators would only prolong his suffering and agony’, and ‘there might be some other patients who has potential for recovery and need the ventilator for support.’
‘If I were you, I would feel the same’
‘Are you okay?’ ‘Would you like to have more time to think about this, and perhaps talk to your other family members, or religious leaders in that sense?’
9. When breaking bad news, have to explore about social circumstances,
-are you working? - May I know who are you staying with at the moment? - How many of you in the family? - How many children? - Economic wise? Sole breadwinner? 10. Breaking bad news:: - Introduce yourself - Ask for consent - Check whether correct pt - Offer for anyone else to be present in the conversation : before I begin, would you like anyone else to present? - Ask how is the patient??? - Check patient’s understanding - Check how much he wants to know - Give warning shot: I am afraid I ‘ve got some bad news to share with you. - Break the bad news: I am Afraid it is a cancer. How you heard about lymphoma? - Express empathy: I am sure this is difficult for you. If I were in your shoes, I would feel the same. Would you like a moment alone? Would you want me to contact any one of your family members? How do you feel now?
‘Is it cancer?’ I am afraid it is cancer. ‘Are you sure?’ Yes, I have double checked it. I am afraid so. ‘Am I going to die?’ a) Chances of recovery unfortunately are slim, but that doesn’t not mean that there is nothing that we can do. b) Cancer does not equal to death, because there is treatment to control the disease and sometimes cure.
- MUST ASK ABOUT SOCIAL HISTORY!!!!
- DO YOU have any questions or specific worries at this point of time?
- Plan: What we do now is, refer you to oncologist, get you a scan, propably plan for chemo or radiotherapy. Let your GP know, so that can provide you with support as well. - Can I continue to work? Yes, after you feel fit and upon completion of your chemotherapy. - Follow up/closure: This must be a great shock for you. You would definitely need time for all these to sink in. I suggest that we meet again in a few days so I can answer all your questions. Menawhile I have this contact number that you can. - 11. Consent from patient who does not have capacity to give consent –PEG tube insertion - make sure understand what is the definition of informed consent! - Consist of: A) Pt must have capacity to give consent (capacity: able to understand the nature, indication, pros and cons of the procedure and able to express it out-clearly explain it out to us) B) C) Pt is not coerced into making the decision
- So is the patient’s next of kin have the right to refuse PEF tube even though its deemed necessary? If she disagree?? The ethical issue behind this? Necessity vs (Patient’s ) best interest? Can a consultant overright him/her. Or should be respect his autonomy. Do no harm? . To confer benefit?
Steps: - I introduce yourself, ask for consent to speak to pt’s son/daughter - Clarify that the pt’s son/daughter is the carer with legal authority/ nominated next of kin to make the decision.
- Assess pt’s son/daughter’s understanding
- Explain to him/her about the father’s condition
- Why a PEG tube is recommended? Poor swallowing, risk of aspiration pneumonia, not compliant to NG tube
- Pros: less uncomfortable/irritating as compare to NG tube, can give adequate nutrition, avoid aspiration pneumonia
- Cons: Bowel, organ perforation, infection at the skin where the PEG tube is, PEG tube displacement
- How izit done?: give sedation, done in daycare OT, special tube pass throught the mouth , the lights can be seen from the skin through the stomach, a needle and wire is put through the skin to the stomach via the light, the scope can then catch and pull the tube into position.
- Ask how he/she feels?
- IF agrees, what now? PLAN:…
- IF disagree, what are the reasons? Concerns? Query
- Offer time for patient to think about it, perhaps discuss with his/her family members - Offer to discuss with my consultant or ask for second opinion
- Reassure that do not hesitate to contact us back if have any questions or doubt.
12. Dealing with poor compliance Very very common in station 4
- Introduce yourself
- How are you? How are your symptoms?
- How do you find taking your tablets? Do you have any problems with them?
- If yes> what are the problems? Any specific concerns? Worries about side effects?
- If no/ deny, saying everything is fine > Say that there does not seem to be any improvement in your symptoms, the most common reason that a lot of my patient encounter is that the pills have not been taken correctly. - I am also aware that you have not been picking your medications (DO NOT TELL WHO THE WHISTLE BLOWER ARE!)
- Explore about social history (Very important! In breaking bad news, dealing with compliance, Explaining DNR, Brain death, Organ donation etc). Work as? Shift work? Nature of work? Supportive environment? Supportive family?
- Explain about the importance of compliance to medication. For health, for avoiding drug resistance.
- Explain about ways of improving his compliance:
a) Family members as reminder b) Smart phones as reminder c) Try to fixed a specific time, when u r least busy , and take your pills d) Try combined pills e) Try directly observed therapy DOT, need to discuss with your health supervisors f) Suggest for social service to change jobs etc
- Can always come back and discuss further.
- Ask the pharmacy to have a word with you. They have better suggestions, educations
13. Deliberate self harm:
Must have a fall back, if patient is speaking very very softly. Refuse to have eye contact with you. Refuse to answer your questions. What are the fall back questions/actions that you can ask? ‘I am sorry that you are in the hospital now. It must be very difficult to have to deal with all these.’ ‘I will try to help as much as I can, alright? How are you feeling at the moment?’ ‘I realize that this is really painful and difficult for you. Let me reassure you that I am here to help you.’ ‘How are you feeling?’ ‘IS there anything that you would like to tell me?’ ‘Would you like to do this at a different time?’ ‘Would you like to have a cup of tea?’ ‘Or do you prefer to have a doctor or nurses of a different gender to be present?’ ‘Would you like to have someone else to be present during our conversation, like your close friend or family members to be around?’
The same go to dealing with angry patients/family. What are your fall backs?? ………
- Introduce yourself. Check if it’s the correct patient.
- Would you like someone else to be present in our conversation here today? - Unless there are some exceptional circumstances, our conversation is strictly private. So feel free to tell me about your difficulties. I will try to help as much as I can. - First of all, I mean I am sorry that you are in the hospital today. It must be very difficult to have to deal with all these at the moment. - Would you like to tell me what happen? - How are you feeling now? Physically (nausea, vomiting, abdominal pain?). Mentally. - Incident:What happen? How many tablets? Together? Separately? With drinks? What happen before that? Did you call/inform anyone else? Any suicide notes? When does it happen? Were you alone in the house? - Reason for incident: I know this must be very difficult and painful for you to tell me this. I mean is there any specific reasons why you try to harm yourself. You can always talk to me about it and I will try to help as much as I can. Family problems? Financial problems? Alcohol and drug problems? Any previous psychiatric history? - Screen for suicide risk: Feeling depressed now? Loss of appetite, weight, energy, concentration? Feeling of worthlessness, hopelessness? Any more suicidal thoughts? Psychotic symptoms such as delusions or hallucination? Insight: Do you think you need help? - - Explore past medical/psychiatric history: - Explore social history: Family and social support
- Reassure that you are here to help & help is available readily
- What plan of action next: I guess now the important thing is to make sure that you are well physically. Make sure you are not nauseous, having abdominal pain and we will arrange for some blood tests as well.
- Next, I think you would benefit from seeing our psychiatric doctors.
- They might want to start you on a medication and perhaps to protect you from further self harm. - Referring you to a psychiatric doctors does not mean that you have a psychiatric illness. Obviously, there are lots of things happening in your life at the moment. - Perhaps the psychiatric doctors can help you with some sort of advice or counseling. And give you some constructive advice as to how you can cope and deal with all these stress. Does not necessarily mean that you have a psychiatric illness.
Read about detaining patient under 1. COMMON LAW 2. MENTAL HEALTH ACT
14. Deep vein thrombosis in pregnancy
Read about anticoagulation in pregnancy: For prosthetic heart valve, dvt etc
- Introduce yourself - Check correct patient - ALWAYS Show sympathy: I know this is a difficult time for you. You must be quite concern about the leg swelling , and how it will affect your pregnancy. - Assess understanding - Explain what has been done and what are the results and Break the news: - Explain what is DVT? Why it happens? Pregnancy is 4-50 times more prone to DVT. - How is the pain now? Any SOB, pleuritic chest pain> PE - ALWAYS Ask some medical questions: How long ago is the swelling? Any hx of trauma/ blood clot? Miscarriages? Any family history of blood clot - Reassurance: We know what is happening now. We can treat it. It is treatable with anticoagulation to thin the blood. - Plan of action: a) Anticoagulation: warfarin (tablet-cross placenta) vs s/c heparin (injection-did not cross placenta) : Duration : 3 months b) Warfarin: contraindicated due to risk of fetal/placental bleeding c) Safest option: subcutaneous injection of heparin (LMWH) :tinzaparin- once daily; dalteparin-once daily or enoxaparin- twice daily d) During term, will stop the injection 24 hr prior while OnG induce labour. e) After delivery, started back on LMWH and warfarin, overlap over 5 days until therapeutic for another 4 to 6 weeks f) Safe for breastfeeding? YES. g) Explain about still a small chance of bleeding -Reassure again it is treatable, stresses on the importance of compliance, to come back for follow ups, if unwell come straight to emergency.
- Will refer to hematologist and OnG specialist for further opinion n management
- Any more questions and worries
- Welcome any questions anytime.
15. Fitness to drive ( usually after an epileptic fit –most frequent; or after a heart attack or stroke) - Introduce yourself - Check correct patient - BEFORE YOU DIVE INTO fulfilling your task given, make sure you must spend a little bit of time explaining of THE MEDICAL CONDITION , THE HOPC, SOME RELEVANT SOCIAL N FAMILY N MEDICAL HISTORY. - How are your since you are discharge? How are you so far? - I just want to check how much do you know so far about what has happened to you? What tests have been done? What have the doctors told you about your condition, the results of your scans or EEG?? - Explain about condition. - ‘That’s right, that’s good news that we did not see anything abnormal in the scans or the EEG.’ - Are you having any more fitting episodes since you are discharged from the hospital? - ‘It is very pleasing that you have not had any more of these fitting episodes.’ - Have any doctors explained to you about some of the precautions that you might have to take for the time being since you have a fit a while ago? - Some activities that might be harmful and endangering you and other ppl if you happen to have a fit again eg. swimming, operating heavy machinery, on a motorcycle etc. - But the main thing I want to talk to you about this DRIVING. Because there is a risk of hurting yourself, the passengers, other pedestrians other drivers etc if you happen to fit again. Professionally, legally, you are not allowed (don’t use ban) to drive for 6 months to a year. And you must notify the DVLA and comply with their guidelines. - Do you drive? What do you do for a living? - How are things financially if you don’t drive? - The important thing is that we see a lot of ppl in these situation. - You can feel very well in between your fitting episode, that’s obviously what is happening now that you are feeling completely well now, but the fit can come out all of a sudden/ out of the blue. - I have seen a lot of ppl in your situation before, felt completely well, gone out and it happens again. - The consequences of driving and having the fit at the same time would be devastating to yourself, to your passenger or to other ppl. - PATIENT WILL DEFINITELY BY ANGRY AT THIS TIME: show sympathy ‘I can understand this must be difficult for you, obviously it involves your lifelihood’ ‘Most ppl in your shoes will feel the same as well’ ‘Perhaps there is a way that we can go around it?’ - This is very unfortunate but you have to let the local driving authority knows about this because if something were to happen, your insurance will not be valid. - ‘ I mean now the DVLA does not know what is happening now, and I m afraid it is your duty to inform them about your situation now. That you have a fit’ - ‘I understand that this has major financial repercussion to you and your family but we can do everything that we can , to minimize this.’ - THIS IS VERY IMPORTANT: PLS USE THIS STATEMENT!!!!! WHO IS GOING TO FEED ME AND MY CHILDREN IF I DON’T DRIVE??? ‘You can use your discharge summary, with all your information, and I will contact your GP, directly we can work out some form income support and we can make sure of any kind of benefit that you are legible for, you can get’
‘At the mean time, your GP can know about this, and so that they can get you some financial support to support you as much as possible’
‘ I know that is really bad news, but there might be a small chance that this maybe epilepsy, and maybe we should think about other ways of making money apart from driving taxi’
‘ I DO NOT WANT TO CALL UP THE DVLA AND INFORM THEM ABOUT THIS AND I WILL CONTINUE DRIVING’
MY RESPONSE: I have to be very clear that the law is very clear that if we have already warn you about the potential risk of fitting on the wheels and which leads to accident, and that happens , all your insurance + license will be invalid and you will be legally accountable for what that has happened.
It is not our duty to directly inform the dVLA about this, it is your responsibility. It is your legal duty unfortunately. And I think you have to inform them right from the start. That’s still the wisest and best strategies and the DVLA will provide you with more information and perhaps way how you can go around doing this. In terms of getting some financial support etc. I am sorry it’s such a bad news, I understand that this is awful as this is your income. I m sorry about what that has happened.
It is a blessing in a way that your fitting episode does not happen when you are on the wheel or you might be injured and fortunately that has not happened.
IF PT STILL INSIST SO:
- Perhaps you can take a moment to think about this.
- Or perhaps discuss with your other close friends or family members. - I understand this is such a bad news. But there are things that we can do to help and if you have any concerns or worries feel free to let us know and we can help you as much as we can. We are here to help you. Thinking for your best interest. etc - So my advice is still no driving at the moment.
IF PT STILL INSIST SO:
Perhaps you would like to talk to my consultants about this. Or if you are not happy with my explanation, we can always get you in touch with another medical personnel, for a second opinion.
IF PT STILL INSIST SO:
Legally, it is quite clear that you cant drive. So if there is any evidence that you still continue driving , I m sorry I have to do this as I m legally obliged to do so. I will disclose this to the DVLa. I will let your GP n you yourself know about this disclosure of information in writing.
- Introduce yourself - Check is it the correct patient - Check and offer if patient wants someone else to present during the conversation eg. spouse,close family members - Firstly, say that: ‘I am glad that you have come and talk to us about this. Some patient’s relative and family does not have the courage to come and discuss with us about their worries’ - ‘I am also sorry to hear that your father was just recently diagnosed with Huntington’s disease. This probably has come as a shock in the family.’ - HoW CAN I HELP YOU TODAY? - In genetic testing :must ask: FOR FAMILY TREE - Assess about understanding on huntington’s disease: How much do you know about huntington disease? - It is a condition where part of the nerve cells in the brain die. It causes people to move in odd ways, and also affect people’s mood, memory and thinking. It runs in the family, due to a mutation in gene of your body and hence, 50-50 chance if either one of your parents are affected. - There is a genetic test that we can do to determine the illness, but we will discuss in more details about it. - IT IS A DISEASE WITH NO CURE AND THERE IS NO WAY OF PREVENTING IT UNFORTUNATELY. However, some of the symptoms we can try to control and to improve the quality of life. But essentially, to be honest with you, it is a progressively deteriorating illness, and eventually people will die from it or due to its complications. - Just before I move on to talk about genetic SCREENING. - Do you mind me asking YOU THE REASON FOR WANTING THE TEST? (make sure they are not forced into it) - I can understand your dilemma and I can assure you that most people who has family history of Huntington’s disease will have such thoughts’ - Now lets talk about the genetic test: 1. The nature of it: a blood test to look at your genetic work up (mutation at 2. chromosome 4: number of repeat of CAG>40 –confirmed) 2. Sometimes we may need your family’s blood as well to confirm the diagnosis 3. It is not 100% accurate. Sometimes you can get an inconclusive result. False positive and negative 4. The impact if the test being positive: ppl can be certain: start to write own will, do the things they like etc; can feel depressed> suicidal, how about your insurance? Employement? Social security? ; If the test is wrong! 5. The impact if the test is negative: relief! Guilty! False negative???? 6. The test will not show you the age of onset, and the severity and progression of the illness.
- Action plan: I will give you time to think about it. You can come back and talk to us anytime you want. I would advice you not to just race into it. There are some pamplets that are available I can get hold of them and pass it to you If you decide to go ahead with it: Then I would refer you to the regional genetic centre. (where they will involve consultants they will do a full neurological examination, pretest counseling, follow up, psychiatric assessment etc) - any other questions? - any other worries? - There is no right or wrong answers though for your question.
17. HIV TESTING
- Introduce yourself - Ensure confidentiality with patient - Do you know why you are here today? - MAKE SURE again you ask about the patient’s medical problems, eg. still coughing? Fever? Night sweats etc. - Assess understanding: What have your GP told you so far - You proceed to give your explanation - ‘Have you ever considered the possibility of HIV infection?’ - ‘Have you ever heard of HIV infection?’ Explain that it’s a virus that attacks and weakened the body’s immune system causing a wide range of symptoms, one of them being pneumonia, thrush, cancers, lymphomas etc. HAVING HIV DOES NOT EQUATE WITH HAVING AIDS. Need to clarify that.
- Explore about risk factors for HIV : sexual promiscuity-unprotected sex, IV drug use- sharing needles, blood transfusion - ‘Have you ever had a HIV test before?’ - Explain about HIV test: ‘Would you like to have one?’ It involves taking a blood test, detecting the virus, NOT AIDS. It will be strictly confidential - Pros: If positive> can start treatment (now there are strong medications that can be used to control the illness, reduce the symptoms, can have a near normal life for years) , prevent your partner from getting it If negative> reassurance, feel less anxious, will adopt a better health habits about STDs - Cons: If positive> Increase anxiety, depression, if let it slipped, lost your job, insurance, social security, finances etc - But need to bear in mind that the test is not 100% accurate, might need to retest, sometimes there is a window period when it is not detected but your body still has it. 3-6 months window period. - Explore about social hx: regular partner? Work? Family? - Prevention counseling: Safe sex now, avoid IVDU etc. - Express empathy: I understand that this must be very difficult for you. - Plan of action/Safety net: a) Do not need to make a decision now, have a think about this, discuss with your partner if you want to. We will take consent. Confidentiality. b) There is a full counseling service available c) Don’t hesitate to contact us as well if you have any queries: Contact number d) Leaflets available e) Any other concerns that have not been addressed.
18. Industrial benefit:
- Introduce yourself - Ask about his medical condition. ALWAYS DO THAT!!! HOW ARE YOU? HOW ARE YOUR SOB? - Assess patient’s understanding. What do you know so far about your condition? What test has been done? Have anyone of my colleague spoken to you about your condition? - Explain: The test shows that essentially you have scarring of your lung tissues. - There are thickening of the lining of your lungs in addition to harden patches around them. > Suggestive of asbestos lung disease. Due to your previous exposure to asbestos. And it usually take years to develop upon exposure. - Explore about occupational history - Any questions so far? - The good news is its not cancer - Break bad news+ express empathy: However, the lung scarring that you are experiencing is not reversible. They are permanent. This might come as a shock for you. How are you feeling now? - The reason of the lung scarring is because of the asbestos. - Have you ever heard of any industrial benefit that you might be able to apply because of your illness? - Get in touch with your local social security office. Fill up a form B1. Pass it up then the medical officer from the department will assess your disability and provide compensation as required. - If you are not happy, you can always appeal. - If you would like to sue the company, you can ask for legal assistance. But chances are ..not high because of expenses, company , employer might not be around anymore. - Any questions?
19. INFORMED CONSENT FOR AN EMERGENCY PROCEDURE: no such things, decision lies on the consultant in charge if it is a life threatening situation where delaying treatment with definitey cause death - Introduce yourself - Confirm that the pt’s family is the next of kin /daughter of the pt. - Express empathy. I am sorry for what has happened to your dad. You must be devastated and is in shock. How are you feeling now?’ - How much do you know about your father’s condition as of now? - Explain about condition::::: - Explain about what needed to be done::: including the risks and benefit - Clarify whether advance directive or a living will is available?
‘I do understand your concerns and I completely respect your decision. If I were in your shoes, I might feel the same as well.’ ‘I do understand your feeling with regards to your father’s of never wanting to go through a surgery that might potential make him having a neurological deficit, but unfortunately it is just a verbal thing, not advance directive or living will etc.’ ‘Unfortunately, your dad has not written a living will or an advance directive with a solicitor which we can use as a legal document’. ‘So legally, I mean in order to save your dad’s life, the decision for operation will rest with the consultant in charge’ ‘I mean we as a team, feel that this decision in the best interests of your dad’ ‘I understand that you are frustrated now, perhaps you would like to take a moment to think about this, to talk to your family members. Or perhaps it would be a good idea if you have a talk with my specialist/consultants with regards to this.’ ‘I am sorry for what has happened so far. And I truly believe that both of us wanted the best for you dad.’ 20. Informed refusal of treatment -Introduce self - Check it is patient’s next of kin, check that the father is okay with the doctors telling the daughter about his medical condition. - Check about patient’s daughter’s understanding about the father’s condition - Explain about condition: (make sure you familiarize with this) –Nowadays there are new drugs that does not require regular follow up on INR, eg. dabigatran. But risk of GI bleed or ICB is still there. - Explain about the decision that the father has made - I AM THE NEXT OF KIN, I SHOULD BE ABLE TO MAKE THE DECISION, BESIDES MY FATHER IS OLD. HE CANNOT MAKE HIS OWN DECISION. ‘ I can see that you are quite upset about the whole situation. Would you mind telling me more about it?’ ‘How do you feel? Is there a particular reason that you are upset?’ ‘I do understand that you want the best for your father.’ ‘So did we’ ‘However, we have discussed this in details with you father, with regards to his condition, how we think anticoagulation/blood thinner would be beneficial, the pros and cons of it. Essentially he made an informed decision not to be anticoagulated’ ‘At the same time, we have also tried to counter any possibility of a misunderstanding.’ ‘ There is no misconception about the whole situation and the reasons why he feel that he does not want to be anti-coagulated are….’
I am the next of kin, and he is too old to make this decision
‘I respect how you feel here, that I think you have such feelings because you want the best for your father.’
‘Unfortunately, I think that your father is in his right state of mind to make an informed decision here. He is certainly capable of understanding the nature of his illness, purpose of the treatment and what are the pros and cons of the particular treatment. I can see that he is able to communicate and reilliterate what we have discussed so far and this shows that he truly understanding what is happening and therefore he is making an informed decision here.’
‘Hence, Legally, I am afraid that your father has the right to refuse taking warfarin.’ ‘Unfortunately, not you, not us as doctors can overrule his decision.’
-Reassurance: Aspirin can also reduce the risk of stroke. But less compare to warfarin.
- Any questions? Any other concerns?
- If still not happy? Would you like to speak to my consultants? - Or to seek a second opinion. I can arrange it for you - Thank you. 21. Managing complaints after an adverse incident/medical error: (giving gentamicin despite gentamicin level high; given medication despite knowing allergies to them; emphysema after previous chest tube insertion) - introduce yourself - Explain what has happen - How are feeling now? - Show empathy: - I am afraid so. . - I do apologise for that. It is definitely a mistake, and we will do our best to investigate and find out what exactly has happened. - I understand that you are angry and it is completely appropriate. An error has been made and we will do our best to find out what exactly has happened. - We are not sure about the details yet but we will investigate and find out and I can assure you that along the way, we will be transparent in terms of how we approach this. - Troubleshooting: we have stopped the medication right away. So from that point of view, that will not happen again and we will continue to closely monitor your/your parents’ condition. - It is difficult to pin point who is responsible here . Mostof the time, most likely it’s a error of the system, mistake in the chain of communication, there is a breakdown in terms of communication etc. We will investigate it right away - Again, I am sorry that this has happened. I know this is not a consolation for what has happened but I want to assure you that the whole process will be transparent. - I will definitely let my consultant know about this. We will get an opinion for a consultant, respiratory etc. - I don’t know the statistics of that. I m afraid. - Plan of action: We will get you in touch with the Patient advice liason service if you would like to complaint. I will let my counsultant know. We will let you know the result of our investigation. We will continue to monitor your condition 22. Obtaining consent for a Lumbar Puncture: - Introduce yourself - Anyone else accompanying you? - Assess understanding: What have you been told so far? - Reassurance: The reassuring thing is that your CT scan is normal, it does not show any tumours or bleeding etc. However, it does not exclude conditions such as infection. - Explain about possible diagnosis: - Explain what need to be done to confirm the diagnosis: Have you heard about lumbar puncture before? We need to take some spinal fluids from in between from back bones. (DRAW A DIAGRAM TO EXPLAIN). The indication, how is it done (step by step > clean and drap, lie at your left side, knees towards your tummy neck slightly flexed) , risks involved, after procedure , need to lie on your back for at least 4h etc. - Reassure that it will be aseptic technique, will give LA to minimize pain etc. - How do you feel about this? Any worries or concerns? Would you like to have more time to consider? - Would you like to speak to my consultants about this? Perhaps you would like a second opinion? - Plan of action: Okay. We will get this sorted out as soon as possible. We will do some blood test to check that your blood is not too thin to have this done. Just to check again you are not on any aspirin or blood thinners? Any history of back problems? Spinal problems etc..
23. Postponing an investigation
- Same old consent. Introduction. - Check is it the correct patient - How are you Mr X? - APOLOGIZE: I am so sorry for what has happened. I can see that you are frustrated here. I would feel the same if I were in your shoes. Clearly there is a misunderstanding between you and the consultant previously. - Do you mind telling me what the consultant told you previously? - EXPLAIN the reason why the Ix has to be postponed: …. - SHOW EMPATHY: I can understand that you are worried about your condition. Obviously, this is something regrettable and can be avoided. There appears to be a misunderstanding or perhaps a breakdown in the communication here. I am glad that you pointed it out and I strongly agree with you that something needed to be done, I will provide feedback to the consultant or whoever that is involved in this. - I guess at this point the important thing is for us to avoid anymore complication which might happen if we were to proceed with the lung bx. - ADDRESS ANY CONCERNS?WORRIES: - This must b e very distressing for you to have to go through all these. I will tell u what. I will go down and speak to the consultant radiologist on my own, and hopefully I can get another appt as soon as possible. Would you prefer to stay here until I got the appt? - How many children do you have? Whereabouts do you live? How far is it from the hospital? Would you want me to ask the ambulance to provide you with the necessary transportation? - Once again, I do apologise for this. - The plan now: I will go and get the appt, hopefully can let you know the date ASAP. I will let the consultant in charge know. If you would like to complain, I will provide you will the contact details of the patient liason service. If at any time you felt breathless or coughing out blood etc, please come back to us and we will try our best to assist you. Any other questions?
24. Pregnancy and pharmacy
1. AntiTB drugs - AntiTB is perfectly safe in pregnancy - Also safe in breastfeeding - Complication of stopping antiTB: Risk of TB reactivation; risk of Abx resistance - If you still think uncertain, I will get you to talk to the ID physician, OnG specialist. 2. Antiepileptic drugs (more tricky)
- A two- to three-fold risk of perinatal mortality has been reported in infants born to women with epilepsy compared with controls. (Population values vary widely, however). (See 'Perinatal mortality and miscarriage' above.) - Both major and minor malformations are more common in fetuses exposed to antiepileptic drugs (AEDs) in utero compared with offspring of untreated women with epilepsy and women without epilepsy. The overall risk of major malformations is 4 to 6 percent; valproate is a major contributor to this risk. Polypharmacy and higher AED dose increase the risk. The timing (early versus late in gestation) and dose of exposure are also likely to be important. Valproate should be avoided in pregnancy, if possible. (See 'Fetal and neonatal effects' above.)
- There is increasing evidence that AED exposure in utero may be associated with impaired cognitive development. The evidence for this association is strongest with valproate. (See 'Long-term effects' above.)
- Seizures, particularly convulsive seizures, are believed to be harmful to the fetus. Fetal bradycardia has been documented during maternal seizures. However, studies documenting the risk that seizures pose to the fetus are lacking. (See 'Risk to the fetus of maternal seizures' above.)
Risks associated with pregnancy and epilepsy can be minimized by preconception planning and careful management during pregnancy.
Patients who have been seizure free for two or more years should be considered for AED withdrawal six months or more prior to planned conception. (See 'Necessity for antiepileptic drugs' above.)
Because there are no clear data indicating that any drug is without risk in pregnancy, we suggest that patients planning pregnancy should be managed on the most effective AED for their seizures (Grade 2C). As an exception, valproate should be avoided if an alternate effective AED regimen can be found (Grade 1B).
Monotherapy and the lowest possible drug dose may limit risk of teratogenicity. The AED regimen should be optimized six months prior to planned conception. (See 'Choice of antiepileptic drug' above.)
We suggest NOT making changes to AED regimen for the purpose of reducing teratogenic risk in established pregnancy (Grade 2C). (See 'Choice of antiepileptic drug' above.) Folic acid supplementation (0.4 to 0.8 mg per day) is recommended for all women of child bearing potential (Grade 1A). (See "Folic acid for prevention of neural tube defects".)
For women taking carbamazepine or valproate, or with a previously affected child, we
suggest higher dose folate supplementation, 4 mg per day, prior to conception (Grade 2B). (See 'Folic acid supplementation' above.)
We recommend monitoring both total and free plasma AED levels during pregnancy. A suggested schedule is: at weeks five to six, at week 10, and then at least once each trimester, and again in the first or second postpartum week. Lamotrigine may need to be monitored more frequently. (See 'Drug levels and dose adjustment' above.)
For patients being treated with AEDs, we recommend offering prenatal screening. (See 'Screening for malformations' above.)
We suggest oral vitamin K supplementation, 10 to 20 mg/day, in the last month of
pregnancy for women taking enzyme-inducing AEDs (eg, phenobarbital, carbamazepine, phenytoin, topiramate, oxcarbazepine) (Grade 2C). (See 'Vitamin K supplementation' above.)
AED therapy is not considered a contraindication to breast feeding; however, use of
lamotrigine or sedating drugs may be exceptions. (See 'Breast feeding' above.)
Patient wanting to start a family but is on sodium valproate for epilepsy. Pls counsel.
1. I have been asked to have a chat with you….
2. Introduce yourself 3. Ask for consent to have a chat with patient 4. How are you? 5. Just a bit of background information about your seizure. Can you tell me a bit about it? What type? Since when? On what meds? What investigation? Last seizure? What are the precipitating factors? 6. Check about donts of epilepsy: driving, diving, swimming etc issue of compliance to meds 7. What are your worries? 8. Planning to have a family/pregnancy is a fantastic idea. 9. A few issue to think about: - Refer you back to neurologist, if planning on a pregnancy while you are still on sodium valproate, and the fact that you have just recently have a seizure would mean that your management is a little bit more complicated and we should involve the neurologist - Uncontrolled epilepsy can endanger you and baby ( if you are not taking the medications) - Options: - 1. Continue same medication: Pt must be willing to take the risk - 2. Stopped the medication if fit free for 2 yrs ( stopped for 6 months before considering pregnancy) - 3. Changed to another type of medication with better safety profile but no guarantee of as good as valproate. - to continue sodium valproate, but obviously there is a risk of higher chance of teratogenicity (increase the chance of your child born with abnormalities compare to other drugs: with birth defect-neural tube defect to be exact) to your baby. - However if we were to stop or change the sodium valproate which is obviously very good in controlling your epilepsy, there is a chance that you might ended up having a seizure, despite the fact that if we change to another medication that appears to have a lower risk of causing birth defect, eg. carbamazepine, levetiracetam, lamotrigine. - Are you on the pill at the moment? - - ACTIONS: 1. I will give you some pamplets about the drugs that we can consider. 2. Epilepsy nurses to talk to you. 3. An appointment with the neurologist 4. Put you on folic acid!
Any other concerns???????
25. Refusal to have effective analgesia (Morphine administration in a terminally ill patient) Talking to the patient or the next of kin -Remember when asking about morphine. Establish what are their fears? Fear of addiction? Fear of side effect (constipation, nausea?) Fear of confusion? - Also explore the hidden agenda: fear of the illness? (Is the patient in denial? Depressed), fear of the pain? fear of morphine.
- Introduce yourself - Ask for consent - Check it’s the same patient, ensure confidentiality - Would you like anyone else to be present during our conversation today? - HOW ARE YOU? - How much do you know about your condition/ your mom’s condition? - Explain what has been happening to the pt/ the family’s condition? - This must be difficult for you. We will try our best to offer whatever assistance that we can. OR to answers any queries that you have - How is your pain? Have you been taking the pain killers? - We are worried about the pain that you have? How izit? How often, where? When? Have you been taking the medications? The nurses are abit worried that your pain is not controlled. - SHOW EMPATHY: I do understand your worries. But I will never imagine what you have been through because you are the one experiencing the illness and the pain, as well as the medication. But we do have experience, from our experience of dealing with patients similar like your self. We understand that sometimes patients are worried about the medication that they are taking. In terms of causing addictions, side effects, drowsiness etc. Let me reassure you that it is completely normal to feel such way. Do you experience any of those thoughts? - REASSURANCE: A lot of ppl feel the same. They do not like the idea of addiction, the side effects involved. Hence, they will not take the medication regularly. How about yourself? - Chances of addiction is slim to none because you are experiencing pain, it will relieve the pain but not cause addiction. As for the side effects, there are medications, laxative, anti-vomit drugs that we can prescribe. - The important thing is you are comfortable, not in pain, make sure you can carry on with your daily activities, improve your quality of life, - You/She might be confused, there is a chance> but we can adjust the dosage. But I suppose that’s a trade off. But we can adjust to balance it out between getting sleepy and getting less pain - What she thinks? What you think? Have you spoken to her previously about what she wants/her wishes - Any other concerns of the illness? - Anything else that worries you? - How is your mood? Depressed? Energy level. Apettite? Able to sleep? How are you coping at home? - Social hx? - Anything that you think is important that you would like to discuss with me? - Perhaps if you have any more concerns, I can arrange for you to have a word with our pain specialist, our pain nurses, the McMillan nurses etc. - I appreciate your concerns. - We will make a decision together, not pressuring you to make a decision now. - Plan of action: 1. reassure you that morphine will not cause addiction in your case 2. we can try to help you reduce the side effect 3. I will ask the pain specialist/pain nurses to have a word with you. 4. there are pamplets available that I can pass to you 5. we will see you back in a couple of weeks to discuss further.
26. Resuscitation status in a terminally ill patient
- Introduce yourself - Check correct patient’s family members/ next of kin - Ensure privacy - Do they want anyone else accompanying them? - Tell them it’s confidential, all the discussion. - How are you? I am sorry to tell you that your dad is in a critical condition now. He is very ill now indeed. He has…. - Assess understanding. How much do you know about your father’s condition? - Explain about the father’s condition: This must be a very difficult time for you. This must be very distressing for you. Explain further….? I am sorry to tell you that your dad is in a critical condition now. He is very ill now indeed. He has…. I understand how difficult this must be for you. You must feel very awful. Would you like to have a moment? Would you want me to stop? Hand over tissues? Do you wan to have a cup of tea? Do you want to talk to someone else about this?
YOU CANT JUST LET HER DIE!!!!!!!!!
- He has been very sick . …. - In condition where your dad is this ill, I am sorry but I think we need to discuss about the issue of resuscitation. - How much do you know about the term resuscitation? Have your father ever mentioned this to any one of you? Any advance directive or a living will?
- I have discuss this with my senior medical officers, both of us think that your father’s condition is of guarded prognosis. Reasons are:…
- I think his condition, unfortunately is almost impossible to reverse at this point.
- The team looking after him thinks that any insertion of tube to help him breathing (if he stops breathing), or any chest compression(if his heart stopped beating) would be extremely unlikely to be successful. EVEN IF ITS SUCCESSFUL,It will only prolonged his suffering FOR HOURS and in fact cause more harm.
CAN YOU GIVE HIM ONE MORE CHANCE??
- We will always do our best to help him. But I have to be frank with you, that his condition is too ill, and unlikely that he will pull through,
- From our point of view, chances for recovery is very very slim,
- I know this an enormous amount of information to take in.
- Do you have any particular concerns or worries?
- He should be kept comfortable with perhaps morphine infusion to ease his
breathing or pain, oxygen and fluids if he is not able to swallow .
- He should be kept comfortable with dignity and self esteem.
- I respect your thoughts but I think that this decision is made in the best interests of your father.
I FEEL GUILTY!!!! - hopefully you wont feel that this is your responsibility, that you allow your dad to die. This is a medical decision made by us. But of course your understanding and thought swill be taken into consideration as well.
’It is also important for you to know that this decision is made by our medical team and don’t feel that you are responsible and actually causing the death of your father by allowing the ventilator to be stopped/ or by allowing us to withhold chest compression
- UNFORTUNATELY THIS IS NOT PREVENTABLE AT THIS STAGE.
Plan FOR NOW::
1. He is very sick 2. Active resus is unlikely to be beneficial 3. Make sure he is comfortable 4. Make sure you have time to accompany her 5. Any questions you can ask me 6. Ask the consultant to have a word with you.
27. Self discharge
- Introduce yourself - Assess understanding: What have you been told so far? - Explain further - Explore the reason why wanting self discharge - Acknowledge patient’s reason. Try to solve them. Any hidden agenda!!!?? ALCOHOL-need to explore!!! Could interact with the medications, eg. during TB treatment, SMOKING. - Explain why is it wise to stay in the hospital.
NO WAY NO WAY!!!!! - - If still insist, tell patient they will take full responsibility if something were to happen. - ALWAYS NEGOTIATE FOR COMPROMISE: 1. changing to oral antibiotics 2. would you wanna talk to my consultant 3. arrange for early follow up 4. come back straight if feeling unwell.
28. Smoking Cessation Advice
- unlikely will come out in counseling station - Introduce yourself, ask for consent - Check same patient - Check for understanding - Explain to patient about condition: The test showed that the airway in your lungs are broken down and narrowed, and it is most likely due to smoking - Do you smoke? Have you ever smoke? How much do you smoke? The reason starting smoking? - Acknowledge that smoking is habit forming and a lot of people find it extremely difficult to stop smoking. - Xplore about social history (There is always a hidden agenda: pt might be depressed! No family members around?? That’s why smoking..the only past time…!!!! REMEMBER TO EXPLORE THE HIDDEN AGENDA) - Ask patient CAGE like question: - Ever consider stopping? Why is that? Have anyone asked you to stopped smoking? - Annoyed when ppl ask you to stopped smoking? - Ever tried stopping? What happened? What do you think are the reasons you fail? - Explain about benefits of stopping: CVS, respiratory, cancer risks, social, financial, for the sake of family - Reassurance/Encouragement: Never too late to quit smoking. A lot of people have successfully done so. What are your worries and concerns? Fear of withdrawal? Fear of weight gain? You must have the will to stop smoking! - Ways of stopping: 1. Lifestyle: Stay away from environment that will encourage you to smoke, go to smoke free places, avoid gatherings with friends who are smoking. Distract yourself with gardening, jogging, exercise, social activities with family members etc 2. Nicotine Replacement therapy: Patch, gum, inhalers, lozenges to avoid nicotine withdrawal 3. Medication: Bupropion (Zyban): One week before the actually quting time, gradually increase doses, warning on SE: Neuropsychiatric behaviour, depression, suicidal thoughts, restlessness, agitation, insomnia, tachycardia, headache. Contraindication: PLS check for SEIZURE, MAOI use, LIVER IMPAIRMENT, H/O ANOREXIA, BULIMIA etc. 4. Psychotherapy: CBT, meditation, acupuncture (less effective) - Plan of Action: - 1. Pamphlets - 2. Quit smoking hot line - 3. Follow up with us in 2 weeks time - 4. Contact the smoking cessation specialist clinic/nurse to provide you with more information.
29. STARTING INSULIN THERAPY
- Introduce yourself - Ask patient ‘HOW are YOU?’ - Assess understanding about her diabetes. Ask about her control? How’s her diet like. Sugar level at home. Symptoms: passing more urine, thirsty all the time, losing weight. - Assess family support/social hx. - Break the news: I am afraid your sugar level has been out of control. We checked your HBA1C and it is twice the recommended level. - This literally means that your diabetes is not well controlled, and in a long run , it will lead to serious complications to your eyes, kidneys , nerves etc. - Generally, for all our diabetic patients, once the oral medications are not effective, we will switch them to insulin. - Have you ever had any experience with insulin? Have you ever heard of that? NO NO , I HAVE BAD EXPERIENCE WITH HANDLING INSULIN WITH MY MOM. I AM SCARED OF NEEDLE. - I UNDERSTAND THAT YOU HAVE BAD EXPERIENCE WITH INSULIN. - I am sorry that you have to go through this but from our point of view, insulin is the best option available. And this is made in your best interest. - I know this ay sound horrible and I completely acknowledge that and in fact I would feel the same if I were in your shoes. - Furthermore, I think a lot of ppl would feel the same as well when we started mentioning or exploring about the option of insulin injection. Most of them handled it quite well eventually - Things have changed over the years, there are newer ways and newer techniques to prevent those complications that you have mentioned. - The needles are much smaller now, unlikely to cause bruising, in fact there is a pre filled syringe into a pen like device that you can carry in a pocket. So its quite convenient nowadays. - Offer option: Perhaps you would like to speak to one of our diabetic nurses who has lots of experience in this. They can demonstrate to you the neddle that we are using now and also the newer techniques available. - ANY OTHER WORRIES OR CONCERNS? ANYTHING THAT YOU THINK IT IS IMPORTANT THAT I HAVE NOT EXPLORED? - Plan of action: - You do not need to start insulin right away, have a think about it, talk to your family members. - See our diabetic nurses, you might change your mind about insulin after that - There are some pamplets for you to have alook - Feel free to ask us if you have any questions - See you back in 2 weeks time, perhaps you will change your mind after that.
30. BREAKING THIRD PARTY CONDIFENTIALITY (eg. to tell HIV status of a patient to his/her partner due to risk of infecting the partner as they are having unprotected sex) - Introduce yourself - Ask for consent - Ensure privacy and confidentiality - Tell patient, your priority is him, you owe him a duty of care ; duty of confidentiality. - Assess understanding: How much do you know about your illness? - How are things with you? How’s your social life at the moment? What’s happening in your life at the moment? - How are things with family and friends? - Have you told her about your HIV status? - Have you been practicing safe sex with her? - I appreciate that this must be very difficult for you. Most of the patients we see here would struggle with the same dilemma. Have you ever thought of telling her? OR how you might do this? - ‘Hope you don’t get offended by this, I tell this to all my HIV patients in the clinic that they should tell their partners about their HIV status because they are putting their partner at risk of HIV infection, especially when they have unprotected sex.’ - Is there a specific reason that you chose not to tell your partner? Any specific worries or concerns? - DO YOU REALLY HAVE TO TELL MY PARTNER? - If your partner is my patient, then i would have a clear duty of care to your partner and I would tell him. - But if he is not my patient, I don’t have to tell him. - However, in some circumstances, I am allowed, and will be protected legally, to break the confidentiality if I think that you are putting the lives of others at risk. - I am sure that if you really care about her/he you would have told your partner, because this is in his best interest. And it definitely shows your trust in her. - Furthermore, if you have unprotected sex with your partner and later on he/she finds out that you are HIV positive, he could have you sued for endangering his life. People has been sent to prison because of this.
MY QUESTION: Should I tell the partner in an active way! Contact her and tell her or only if she asks then I tell her.
- Plan of action: - 1. Would you want my help to tell her? You can bring her in, I would be more than happy to tell her. - 2. Would you like to have a word with the specialist nurse or perhaps my consultant as they have more experience in this. - 3. I will see you back in my clinic and we can discuss about this further. - 4. Pls if you have any concerns or worries at all, contact us and let us know.
31. To ventilate or not to ventilate
- *****Remember you are here to explore about the premorbid, patient’s and family’s expectation>>>> Pls read the stem carefully, you are not DNARing the patient just as yet. - The fall back is you will promptly discuss will your consultants and come out with a decision as soon as possible. It is okay not to come out with a decision as of yet. - Introduce yourself - Check correct family members, next of kin - Assess understanding: How much do you know about your father’s condition? - Assess premorbid: housebound? ADL independent? Mode of treatment? Previous hx of admission? - Explain to family members about patient’s conditon: very ill, critical, cannot breathe properly, might need artificial ventilation of the lungs - Pros: Help rest the lungs, wait for the pneumonia to settle , have chance of recovery - Cons: Need to be admitted to ICU, chances of sepsis, infection, deterioration during the intubation. - Explore any wishes from patient before this, advance directive, or living will. - How do you feel now? - Any other concerns or queries? - Plan of action: 1. Give you a moment to think about this, discuss with your family members 2. I will talk to my senior consultant about this, hopefully we can come out with a decision. - Do you need to come out with a decision????????????????????????????????????
32. Withdrawing treatment
*** Pls remember that this is totally different from discussing resus status in a terminally ill pt, or to decide to ventilate or not. This is about withdrawal of treatment!! - Introduce yourself - Check pt;s family is next of kin - Check for understanding - I am sorry that your dad is very ill. - Explain what has been happening. - ‘Despite all our effort, he is not improving.’ - ‘We have discussed among our medical team together with the ICU team, and we strongly feel that his outlook is very poor and that he will eventually die’ - ‘And we feel that any continuous active treatment will not achieve the desirable result of restoring your dad back to his normal health.’ - ‘All our effort will only prolonged his life, his suffering and in fact might cause more harm’. - Have you ever heard of the term withdrawal of treatment? - Have your dad ever mentioned that he is very sick, to withdraw treatment, eg. advance directive or a living will? - Does all the family members know about his condition? - Explain how withdrawal is done: We will first start by tailing down the inotropes which is the medciation that help to pump his heart, he may deteriorate quickly and die soon after. - ‘All these will be done ensuring that your dad is comfortable, painless and not in any distress’ - “””I need to stress that the decision of withdrawing treatment does not reside with you or your family but with our medical team. So please do not feel that as if you are actively causing the death of your father.””””” - Plan of action: 1. You do not need to make a decision right away. 2. Discuss with your other family members. 3. Any enquiries do let us know 4. Perhaps I would arrange for my consultant to have a word with you as well 5. Assure you that your dad will be kept as comfortable , as painless as possible.
Ddx of chronic tophious gout : rheumathoid nodules, tendon xanthomas!!!!!
Undulant fever +Migratory Arthralgia & Myalgia +SPLEENOMEGALY Transmitted by close contact with animals’ secretions, drinking unpasteurized milk, transmission between humans by sex FBC: Leucopenia + Anemia + +ve Bengal rose reaction Blood culture & Detection of antibodies TTT: IM streptomycin 1gm for 14 days + Doxycyline 100 mg twice for 45 days
Causes: CA lung , Legionella Pneumonia ,Lung abscess , Head injury, Sarcoidosis , Carbamazepine , Morphine, Cholropropamide, SSRI , TCA , hypothyroidism Na <134 , Osm <280 TTT: Cause , Fluid restriction , Demeclocycline , Conivaptan (V1 and V2 receptor antagonist)
Bloody diarrhea + Wt. loss + Abdominal Pain + young age = IBD
Back Pain, Eye Pain INV.: Colonoscopy and biopsy TTT: Prednesolone , Mesalazine , Azathioprine , Methotrexate , surgery UC can be complicated by PRIMARY SCLEROSING CHOLANGITIS Fatigue +obstructive jaundice (pale stool , dark urine) + pruritis ERCP: beading of intrahepatic & extrahepatic bile ducts + P-ANCA TTT: Ursodiol , Rifampicin , Cholestyramine , definitve =liver transplantation Crohns Complicated by GALL STONES
Pain & Tingling In The Legs At The End Of Day Relieved By Walking + Normal Examination = RESTLESS LEG SYNDROME Causes: Fe deficiency, polycythemia, Varicose veins, Thyroid disorders, Uremia, D.M, Antidopaminergic drugs, P.N., Familial (AD) INV: NCV, EMG, FBC, TFTs TTT: Cause /Dopamine agonist /Gabapentin
Sudden weakness which resolves in 24 h = TIA
Causes: Athreosclerosis (D.M , HTN , cholesterol), Embolism from Heart, Hypercoagulable state, AF, Risk of stroke is determined by ABCD2 score: Age >60 =1p Blood pressure >140/90 =1p Clinical: speech but no weakness =1p , weakness =2 p Duration < 1h = 1p , > 1h = 2p Diabetes present =1p 1-3 =mild , 4-5 =moderate , 6-7 high risk
Hypercoagulable states: Antiphospholipid Syndrome DVT + Recurrent miscarriage + Stroke (recurrent thrombosis); Lupus anticoagulant, anticardiolipin TTT: Asprin, heparin Pregnancy & OCPs PNH (Hematuria + Anemia) Behcet`s :oral + genital ulcers + Iritis = pethargy test , TTT:Steroids Antithrombin III defiency: AD , Causes heparin resistance increase the dose of heparin Protein C & S deficiency: Nephrotic (Xanthelasma + L.L edema+ Eye puffiness) Factor V Leiden : FH of recurrent thrombosis (AD) , the ratio of time for blood to clot Using 2 samples one with APC and other without, genetic testing Homocysteinuria Nephrotic syndrome Myeloproliferative disorders Headaches by end of day = TENSION HEADACHE Band like Causes: Stress , Sleep depreviation , Eye strain , Irregular meal times TTT: NSAIDs / TCA prevent future attacks Morning Headache + Obesity /OCP + Blurred vision +Vomiting = IDIOPATHIC INTRACRANIAL HTN Causes: OCP, Tetracycline , Vit A , Retinoids, WT.Gain , Steroids INV.: CT scan, MRV to R/O Sinus Thrombosis, Lumbar puncture (inc. opening pressure) TTT: Repeated lumbar puncture, Acetazolamide Wt.loss Unilateral Headache (Around eyes) + No Aura + 2 Autonomic symptoms (Ptosis, Miosis, Rhinorrhea, lacrimation, Flushing, Sweating) on same side = CLUSTER HEADACHE More common in males TTT: Oxygen, Sumatryptan Prevention: CCBs, verapamil Episodes of intense pain in Face for seconds, minutes or hours + triggering area on the Face + Triggered by light touch or air currents = TRIGEMINAL NEURALGIA Any division of V nerve (ophthalmic, maxillary or mandibular) 10% are bilateral Electric , stabbing or burning pain Triggered by: Chewing, brushing teeth, Talking, Shaving, Loud noise (concerts) Cause: Trauma , CPA tumours , Superior cerebellar artery aneurysm , post herpetic neuralgia , MS , Idiopathic TTT: Carbamazepine/Microvascular decompression Anemia (S/S) + Red urine + Vascular thrombosis (Bud Chiari / DVT/ Mesenteric/ Stroke) = PNH INV.: Flow cytometry for CD55 & CD59 TTT: Heparin / blood transfusion + Ecluzimab = B.M transplantation Chronic chest infection + pins and needles in hands/proteinuria (Frothy urine) / L.L edema = BRONCHIECTASIS WITH AMYLOIDOSIS AMYLOIDOSIS: Abdominal pain , Vomiting , Diarrhea , HSM , P.N , CT$, Macroglossia , Hemoptysis , Cardiomyopathy =CCF, Nephrotic = RF INV: CT chest, sputum analysis, Rectal biopsy and staining with congo red for amyloidosis TTT: TTT of cause + Melphalan /Cyclophosphamide ANEMIA + MCV>110 FL = MEGALOBLASTIC ANEMIA Dec. Hb., Macrocytosis, Low reticular count Platelets may be reduced WBC are hyper segmented Howell jolly bodies (Pernicious Anemia) Pernicious anemia is common with auto-immune conditions (Vitiligo) Pernicious anemia is common in the elderly INV:Anti-intrinsic factor abs, anti parietal cell Abs TTT: Cyanocobolamine every week for 4 weeks then every 3 months VIT. B12 DEFIENCY Pernicious Anemia (Autoimmune) Ileal resections Malabsorption $ Gastrectomy FOLIC ACID DEFIENCY Malabsorption & Deficiency of diet Liver disease & Alcohol OCPs, Phenytoin, Metformin Repeated recurrent infections in sinuses, URTIs, LRTIs +Diarrhea (Giardiasis, Cryptosporidium, Helicobacter) = COMMON VARIABLE IMMUNODEFIENCY (Acquired hypogamaglobulinema) Recurrent Sino-pulmonary infections +Joint infections + Giardia/ Cryptosporidium / Helicobacter INV: low immunoglobulin levels in blood TTT: IVIG Fatigue, Dry eye + Joint Pain+ E.N. =SARCOIDOSIS Lupus pernio (Purple rash on nose and cheeks resemble frost bite) Cough + SOB + L.Ns Bilateral VII Palsy Bilateral hilar L.N + E.N = Lofgren syndrome Dry eye + Dry mouth = Mikulicz syndrome Hypercalcemia signs (Polyuria, PUD, Renal stones, depression , constipation) E.N (tender red bumps/rash over shins) Other Autoimmune conditions INV: CXR , CT Scan , Biopsy , Inc. serum ACE , Hypercalcemia TTT: 30-70% no need for TTT Chest changes not healing after 2 months Or Uveitis , Neurosarcoidosis , Hypercalcemia = Steroid / Azathioprine Hypertension in young age + Weight loss = Remember VASCULITIS Maltezers Triad (Purpura +Arthritis+ Myositis) + Constitutional S/S (Fever+ Wt.Loss + Night Sweats) Nose Bleeds, HTN, G.N, Abdominal pain, Bloody diarrhea, Headaches INV: High ESR , biopsy , Angiogram TTT: Cyclophosphamide Bloody diarrhea + Gall stones + fever, Sweating + loss of wt. = IBD (CROHNS) Due to terminal ileitis= Bile salts pool = gall stones Nose problems (Stuffiness , Crusts , Change in shape ) , sinus problems , ear problems (URT problems ) +LRT problems (Hemoptysis , SOB) + Elevated creatinine (Hematuria)= GRANULOMATOSIS POLYANGIITIS Iritis, scleritis, purpura, Arthritis, Rapidly progressive G.N INV: High ESR , C-ANCA , Biopsy TTT: Steroid + Cyclophosphamide + Plasma exchange +Rituximab Repeated Wheezing (shortness of breath) + URT problems + Eosinophilia + Kidney problems (Hematuria, high creatinine) = ESINOPHILIC POLYANGIITIS Mononeuropathy (C.Ns) Montelukast can cause Churg strauss INV: Esinophilia + P-ANCA +Biopsy TTT: Steroids + Cyclophosphamide Dizzy spells + Noisy chest + Flushing + Wt.loss = CARCINOID SYNDROME Hypotension + Tricuspid stenosis + Diarrhea + wheezing + hepatomegaly Enterochromaphain cells tumour with liver metastasis Raised 5HIIA in urine TTT: Cyproheptadine & Octereotide Wt.Loss + Polyuria+ Polydipsia + Infections (UTI, SKIN) = D.M Leg Cramps could happen , Diarrhea FBS > 7 RBS or 2 hr Post prandial > 11.1 Inflammatory Diseases & Auto-Immune Gets Worse At Night & Early Morning Endogenous Steroids increase By Day and Dec. in evening Wheezing and shortness of breath which gets better on holidays away of work = OCCUPATIONAL ASTHMA Isocyanates (painters of automobile & furniture), Wheat (Bakery workers) PEFR, Spirometry AT WORKPLACE , Skin prick test, IgE specific Abs Stop job (occupational therapist) + bronchodilators CHRONIC FATIGUE SYNDROME CRITERIA New onset fatigue in 6 months not related to exertion plus: Memory & conc. Problems Headaches Tender L.Ns Sore Throat Myalgia Irritable bowel $ Textile worker + SOB + Cough = BYSSINOSIS Similar To occupational Asthma From cotton inhalation Constitutional S/S (fever +Night sweats) + ESR>100 + tooth extraction = INFECTIVE ENDOCARDITIS Heart murmur + Inc. Creatinine +Stroke +Gangrene (septic emboli) INV: Transesophageal echo (vegetations)+ blood culture (dukes major criteria), RF, Urine Dip TTT: IV antibiotics (Hospital Protocol) until C&S In people with colon cancer = Streptococus bovis = IV penicillin or IV Ceftriaxone Dukes minor criteria: Immunological (Osler , G.N), Embolic manifestations (Roth , splinter Hemorrhage, Jane way ), IV drug abuser Young Age + HTN +Polyuria + Glycosuria + FH of RCC = VON-HIPPEL LINDU AD on chromosome 3 Genetic diagnosis CNS tumors (Epilepsy, Headaches) + Retinal hemangiblastoma (loss of vision) + RCC (Flank mass + Hematuria) +Pheocromocytoma + Pancreatic neuro endocrine tumors + pancreatic cyst (Glycosuria +Polyuria) + endolymphatic sac tumors. TTT: surgery for tumors, Laser photocoagulation for retina Fever + Myalgia +Body pains + Rash + Recent visit to Queensland = DENGUE FEVER SEROLOGY Supportive TTT Chest pain /Faints + GIT bleeding + Old Age =ANGIODYSPLASIA (HEYDES SYNDROME) AS (Aortic stenosis) causes consumption of Von willibrand = Angiodysplasia =bleeding per rectum/hematemesis INV: Von Willibrand electrophoresis TTT: Desmopressin or Factor VIII/ Aortic valve replacement Increase cholesterol > 4 mmol = HYPERCOLESTEROLEMIA (hyperlipedemia) Primary Hyperlipidemia Secondary Hyperlipidemia Type I: Hyperchylomicronemia (lipoprotein lipase deficiency) Eruptive xanthoma, colic, retinal vein occlusion, pancreatitis, steatosis, organomegaly D.M, Alcohol , Hypothyroidism PBC Type IIa: Familial Hypercholesterolemia Tendon Xanthoma + Xanthelasma + Arcus senilis +Premature CVS events (claudications , Impotence, Infarctions, renal bruits) Beta blockers, Estrogen, Diuretics Type IIb: Familial Combined Hyperlipidemia Hypertriglyceridemia + Hypercholesterolemia Renal Failure Nephrotic Type III: ABETALIPOPROTIENEMIA Palmar xanthoma+ Retinitis Pigmentosa + Steatorrhea Type IV: Familial Hypertriglyceridemia Acute pancreatitis Type V: Familial Hyperchylomicronemia + Glucose Intolerance + Hyperuricemia Treatment Cholesterol =Statins, Ezetemibe, Cholestyramine Triglycerides =Fibrates , Omega 3, Ezetemibe, Niacin Wt.Gain + Cold intolerance + Menorrhagia + Hair loss + Apathy+ Pins & needles in hands (carpal tunnel) + Macrocytic anemia + Hyperlipedemia = HYPOTHYROIDISM Hypersomnia + P.N +Resteless Leg Syndrome+Dry skin Hashimoto/1ry atrophic / radioactive iodine /Thyroidectomy/Lithium & Amiodarone Post partum Thyroiditis ; 30 % will need L.-Thyroxine for life Young age + HTN + Headaches + Sweats + Polyuria + Glycosuria = PHEOCROMOCYTOMA (Ask about MENII S/S & Neurofibromatosis) Tachycardia + Flank pain + Wt. loss INV.: 24 hrs urinary catecholamines , metanephrines , Inc. serum chromogranin , CT abdomen TTT: Phenoxybenzamine (non-selective alpha blocker) + Labetalol (alpha & beta blocker) + Surgery MEN II A is AD RET oncogene (Pheocromocytoma +Medullary carcinoma (thyroid swelling) + hyperparathyroidism = hypercalcemia =constipation , polyuria , PU , psychiatric problems , renal stones (hematuria) , fractures MEN II B is AD (Pheocromocytoma +medullary carcinoma + neurofibromas + Marfanoid features) Neurofibromatosis I is AD on chromosome 17 (>6 café au lait patches + Optic glioma + >2 Neurofibromas + Axillary freckling + Lisch nodules + epilepsy + pheochromyctoma , CPA (Cerebellopontine angle) $ , Jugular foramen $) Neurofibromatosis II AD on chromosome 22 Has Acoustic neuroma ( Hearing loss + Tinnitus +Vertigo) History of gall stones/bile duct tumors or intervention + Fever + jaundice + Rt. Quadrant pain = ASCENDING CHOLANGITIS Charcot`s triad + shock (hypotension)+ confusion = Raynold`s pentad INV.: Inc. ESR , increased ALP , bilirubin , GGT , U/S , MRCP , ERCP , blood culture TTT: Usually E.coli =IV fluids = penicillin + gentamycin / ciprofloxacin + metronidazole then ERCP & cholecystectomy May be caused by stones, Benign stricture, Malignant stricture, Ascaris Progressive worsening dyspnea + Antibiotics for recurrent urinary tract infections + Bibasal crackles + Normal FBC, urea & electrolytes = NITROFURANTOIN INDUCED PULMONARY FIBROSIS CT , PFTS , CXR Drugs causing pulmonary fibrosis :Methotrexate, Belomycin, Busulphan, Nitrofurantoin, Amiodarone + Pain in Rt. Upper quadrant = HEPATITIS Jaundice (Back pain) or ASCENDING CHOLANGITIS In hepatitis fever precedes the jaundice In ascending cholangitis fever is with the jaundice Diarrhea + Wt.Loss + Irregular periods + Sweating + Intolerance to hot weather = THYROTOXICOSIS Tremors /L.L swelling/HTN/Palpitations Grave`s = Eye signs (Opthalmoplegia , Exopthalmous) + Acropachy+ pretibial Myxdema +Enlarged gland (TSHR stimulating Abs) Hashimoto`s = Enlarged gland (Anti thyroglobin , Anti thyroid peroxidise) Dequervian = Tender gland Amiodarone Post-partum Thyroiditis =2-12 m post-partum = hyper then hypo = Antithyroid peroxidise= Resolve in months to years , 30% will neeed Lthyroxine INV.: TSH , T3 , T4 , Thyroid Scan , U/S TTT: Propranolol , Carbimazole , Propylthiouracil (pregnancy), Surgery , Radioactive iodine Malabsorption (Pale , Offensive Diarrhea , Floating , Difficult to flush ,Wt.Loss , Vit. deficiencies) + Anemia + Normal colonoscopy = CELIAC DISEASE Wt. loss + Mouth ulcers + Itchy Rash (dermatitis herpitiform) Associated autoimmune disorders (Hypothyroidism , D.M , Microscopic colitis) HLA DQ2 , HLA DQ8 Always ask about diet Vit K defiency (Eccymosis, Petichie , Hematomas) B12 , Folic deficiency=Megaloblastic anemia (SOB, palpitation) Vit D deficiency (osteomalacia) (Bone pain + Muscle weakness + easy fractures +Hypocalcemia + Inc. ALP) IgA nephropathy (Hematuria) Inc. IgA , Anti tissue transglutaminase, Anti-Endomysil Abs, Anti gliadin Abs , endoscopy with jejunal biopsy (villous atrophy) TTT with Gluten free diet (barely, oats, wheat ) .. Rice & maize are ok Dapsone for dermatitis herpitiform Malabsorption + Fever = TROPICAL SPRUE TTT: Tetracycline / cotrimoxazole Malabsorption + Joint pain = WHIPPLE DISEASE INV: Biopsy = PAS organism TTT: Tetracylcine/cotrimoxazole for 1 year Resistant celiac not responsive to gluten free diet = INTESTINAL LYMPHOMA (enteropathy associated T Cell Lymphoma)= TTT: CHOP Diarrhea + Normal colonoscopy + PPIs/NSAIDS over use = MICROSCOPIC COLITIS TTT : Antidiarrheal + Mesalazine Malabsorption (Pale offensive floating, difficult to flush, Vit. Deficiencies, Wt.loss) + History of surgery in bowel (Crohns, Tumors) = SHORT GUT SYNDROME < 2 m of small bowel May be transient condition for intestinal adaptation TTT: Loperamide, Lactase enzyme, PPIs, Vit. injections , Intestinal lengthening surgery, TPN PPIs/fistulas/diverticula/D.M + Malabsorption + Bloating/Nausea /Vomiting = SMALL BOWEL BACTERIAL OVER GROWTH Dec. motility (Scleroderma , Celiac , Bilroth antrectomy (blind loop) , Diverticula) Dec. Immunity (Common variable , D.M , Chronic pancreatitis , immunosuppressive medication) Inc. small bowel bacterial contamination (Crohns (surgery to remove ileocecal valve) , PPIs) Jejunal aspiration = 10^5 bact./ml TTT: Norfloxacin /Co-Amoxiclav for 1 week PPIs Causing Diarrhea Microscopic Colitis Small bowel Bacterial over growth CDIF Alteration of bowel habits + Chr. Pain (bloating) + No alarm signs (age >50 , Bleeding , Wt. Loss , FH of IBD or colon CA) = IRRITABLE BOWEL SYNDROME Usually start after an infection Diarrhea predominant or constipation predominant Urgency for bowel movement + Sense of incomplete evacuation (tenesmus) + GERD + other psychological related problems (chronic fatigue syndrome, fibromyalgia, Headaches, back aches, depression , anxiety) INV. All normal TTT: Psychotherapy, laxatives, Antispasmodics, TCA, SSRIs , Lactobacillus ROME III criteria for IRRITABLE BOWEL SYNDROME Recurrent abdominal or discomfort for 3 days/month for 3 months plus: Relieved by defecation Altered stool frequency Altered stool form Altered stool passage (Urgency/Straining/Tenesmus) Mucus with stool Abdominal pain + Fatigue + Tiredness + Jaundice + Itching = PBC Auto-Immune more in females Xanthelasma + Other Auto-immune disorders (Thyroid , D.M , Vitiligo, RA) INV: Inc. IgM , AMA M2, Inc. ALP , Bilirubin , GGT , U/S , ERCP , Biopsy TTT: Ursodeoxycholic acid , Rifampicin , cholestyramine , Liver transplantation Previous URTI + Chest Pain + CCF (Palpitations + SOB + PND+ Orthopnea + Swollen legs) = VIRAL MYOCARDITIS Other Causes: Rheumatic fever , Parvo virus B19, Coxackie , Doxorobusin , VASCULITIS INV.:ECG , ECHO , CXR TTT: TTT of CCF (Nitrates, ACEIs, Diuretics) CHF signs (Palpitations +SOB+ PND+ Orthopnea + Swollen legs)+ last month pregnancy = PERIPARTUM CARDIOMYOPATHY Last month of pregnancy up to 5 months postpartum Excessive Wt. Gain in last month of pregnancy Dilated cardiomyopathy TTT: Diuretics, ACEIs, Nitrates Recovery takes few months to years Mitral stenosis signs ( SOB , Cough , Orthopnea , PND ) + Palpitations +Wt. Loss + Faints + Murmur = LA MYXOMA Fevers + Chest pain TTT: Surgery / Mitral valve repair > 5 Unilateral headache (Pulsating) + Vomiting, Photophobia, Phonophobia + Aura ( Vision loss, Sensory , Motor symptoms) = MIGRAINE OCP , Pregnancy , Cheese , Tomatoes , Caffeine Classic migraine is with Aura Common migraine without Aura TTT: simple analgesics, sumatryptan, Prevention: BBs , TCA Old female + Sudden back pain + Radiculopathy (Severe shooting pain in dermatome) = COMPRESSION FRACTURE due to OSTEOPOROSIS Could Cause Cauda Equina S/S (Leg pain & weakness (paraparesis) + urinary retention/Incontinence + Saddle Anesthesia +Absent ankle reflex) Osteoporosis itself cause no S/S Repeated fractures = Stooped posture Risks: Alcohol , smoking , under wt. , Cushing , Acromegaly , Anorexia nervosa , hypogonadism , Rheumatoid , Multiple myeloma , Steroids , Glitazones , Anticoagulants, Malabsorptin $ INV.: DEXA scan : T score < -2.5 TTT: Bisphosphonates (Alendronate) + Ca + Vit D Recurrent TIA (Weakness + Normal examination + Resolving) + HTN + Palpitations = AF SOB + Orthopnea + PND + Lightheadedness Alcohol / HTN / MS/ MR/ Thyrotoxicosis/ pericarditis / Congenital Ht.Ds / Lone AF Indication of warfarin CHADSVASC score Rhythm control if Acute AF=Amiodarone/DC Rate control if Chronic AF=CCBs , BBs , Digoxin Epigastri pain Resistant to H2 blockers = PEPTIC ULCER DISEASE H.Pylori / NSAIDs / Steroids Hypercalcemia Gastrinoma (Zollinger elisson=Recurrent ulcers+Unusual places) Part of MEN I Epigastric pain + Wt.Loss + Vomiting +Hematemsis (coffee ground or frank) + Melena ( Black tarry offensive motion) Endoscopy with biopsy (exclude malignancy), H.Pylori fecal Ag , Urea Breath Test, H.pylori Abs , Serum Gastrin Complications of PUD: Hematemsis/Melena =Anemia Perforation Pyloric obstruction TTT: Triple therapy (Clarithromycin/Metronidazole + Amoxicillin+ PPIs) for 14 days Diarrhea + Recurrent PUD (Epigastric pain + Vomiting + Wt.loss + hematemesis/Melena) + Constitutional S/S (Fever +Night sweats+Wt.Loss) = ZOLLINGER ELLISON PUD non responsive to PPIs = Zollinger Ellison or Malignancy Ulcers of esophagus , stomach , duodenum , intestine Gastrinoma of pancereas Part of MEN I (Hypercalcemia +Pit.Tumour+Pacereas Tumour) Fasting Serum Gastrin in 3 occasions/Secretin test TTT: Octerotide+PPIs /Surgery+ Chemotherapy Hemoptysis/Cough for years + Inc. Creatinine/Frothy urine/hematuria+ Anemia = GOOD PASTURE`S SYNDROME Hemoptysis is late (cough for years with anemia due to pulmonary Hemorrhage before hemoptysis appear) Renal failure is late (proteinuria , hematuria are early signs) Preceded by viral infection (Influenza) Type II hypersensitivity= Crescentic G.N , RPGN Anti-glomerular B.M Ab TTT: Steroids + Immunosuppression + Plasmapharesis / Renal transplant Recurrent miscarriage/Pre-eclampsia (proteinuria ,HTN , Edema) + inc. APTT + Thrombocytopenia + Vaso-occlusive S/S = ANTIPHOSPHOLIPID Ab SYNDROME Other Autoimmune disorders / SLE INV:Anticardiolipin , lupus anticoagulant , inc. APTT , Low platelets TTT: Asprin , heparin CA Lung +Severe bone pain (Dull , Constant, Inc. with activity)+Spinal compression +Hypercalcemia S/S (polyuria + polydypsia + PUD+ Depression+ fractures+ Constipation) + Inc. ALP = METASTATIC BONE DISEASE CA Breast , Prostate , Lung TTT: Bisphosphonates /Radiotherapy /steroids Recurrent Joint pain & swelling (hemoarthrosis) + Prolonged bleeding after procedures+ FH = HAEMOPHILIA XL-R , VIII (A),IX (B) INV: Normal bleeding time , platelets , PT , Inc. clotting time , APTT TTT: Factor VIII transfusion , Fresh frozen plasma Easy bruising + Nose bleeds +Bleeding Gums+ Heavy menses + FH = VWBD AD Normal PT ,Platelets , inc. Bleeding time & APTT Measurement of VWB factor TTT: Desmopressin Leg Ulcers + Anemia S/S + Recurrent infection (Autosplenectomy) = SICKLE CELL ANEMIA Strokes Osteomyelitis+ Slamonella enteritis + DI + Choledocolethiasis Vaso-occlusive crisis (Acute chest syndrome , Pain in arms or legs, priapism ,Abdominal pain , Ulcers ) Acute chest crisis(lung infarction) (Fever, Chest pain , SOB, Pulm.infiltrates) Aplastic crisis (Erythema infectiousm parvo virus B19) XL-R , Sickling occurs with Dehydration , Acidosis , Infections INV.: CBC: Anemia with reticulocytosis , howell jolly bodies Hb electrophoresis Sickling test with Sodium Metabisulphite Genetic councelling TTT: blood/penicillin/folic Chest crisis=exchange tranfsuion Vaso-occlusive crisis=Opioids , Oxygen , NSAIDS, IV fluids Bone marrow transplant Recurrent vaso-occlusive episodes (DVT , PE , Budd chiari , Cerebral sinus thrombosis <inc. Intr.Cr. Pr.>/Stroke) + Mouth ulcers = BEHCET DISEASE Oral ulcers +genital ulcers + Uveitis + Vaso-occlusive+ livido reticularis/Erythema nodosum / Pyoderma gangrenosa + Sagittal sinus thrombosis + Hemoptysis + Aseptic meningitis Diagnosis : skin lesion +genital lesions + eye lesions + pethargy test TTT: high dose steroids+ Infliximab+ Azathioprine+ INF if severe IVIG Diarrhea With Normal Colonoscopy Malabsorption Syndromes Microscopic colitis Irritable Bowel Syndrome Common Inherited Cancer Syndrome: HNPCC (Lynch syndrome) Colon , Gastric CA/Endometrial CA/Ovarian CA/Pancereatic (biliary) Keratoacanthomas /Sebaceous adenoma / Skin CA FAP APC gene: Autosomal dominant Gardner syndrome: FAP+Lipomas+osteomas+sebaceous cysts+gatric polyps Turcot $: FAP+Medulloblastomas (CPA $) Peutz Jeghers AD GIT Hamartomas MEN I , MEN II Von Hippel Lindu BRCA I , BRCA II Breat CA / Ovarian CA / Prostate CA Leukemia /Lymphoma Causes Of Abdominal Pain With Normal Initial Investigations: Vasculitis ( PAN) =Mesenteric Ischemia FMF Porphyria Addison`s Working in Hotel/Hospital (A/C) + Cough+ Dyspnea + Hyponatremia + Elevated LFTs + Ataxia + Fever= LEGIONELLA PNEUMONIA Reservoirs : A/C , Cooling towers /Nebulizers/Showers/Hot Tubs INV: LFTS , KFTs , CXR , CT ,Urinary Ag Risks: Immuno compromised/smoking/Chr.Lung Ds TTT: Azithromycin / Levofloxacin Fever + Sorethroat + L.Ns + Wt.Loss + Rash + High Risk Behavior = ACUTE HIV INV.: Abs , CD4 TTT: HAART (2NRTI + 1 PI/NNRTI) (zidovudine+lamivudine+ neverapine) if CD4<350 Coinfection with HBV regardless of CD4 HIV Neuropathy regardless of CD4 Pregnancy regardless of CD4 count Cotrimoxazole if CD4 <200 Ataxia + Urinary Incontinence + Dementia (Mental decline= Apathy, forgetfulness, Inattention) =NORMAL PRESSURE HYDROCEPHALUS No signs of increased intracranial pressure 1ry or 2ry (SAH , Brain infection , tumour , surgery , Trauma) INV: CT brain= enlarged ventricles with convoluted atrophy, Lumbar puncture (improvement =success of ventriculoperitoneal shunt) TTT: Ventriculoperitoneal shunt Seizures (Autism , learning disability) + Hematuria + Skin rash = TUBEROUS SCLEROSIS Autosomal Dominant Commonest brain tumour = Giant Cell astrocytoma Renal =Angoimyolipoma , Renal cysts and rarely RCC Skin: Adenoma sebaceum (butterfly bumps on nose,cheeks of reddish spots) Shagareen patch (lower back or nape pigmented thick skin) Subungal fibroma (small fleshy tumours under nails) INV: renal U/S , CT brain , MRI , fundoscopy , Echo TTT: Supportive Jaundice + Wilson (history of CLD) + Disturbed sleep Rhythm , Agitation,Flapping tremors, personality changes = HEPATIC ENCEPHALOPATHY Bleeding /Constipation/high proteins/benzodiazepines/Alcohol /Infections (UTI,Pneumonia) / Hypokalemia (Diuretics) Due to GABA mediated inhibition , Build up of Ammonia (metabolic toxins) Urgent Admition EEG : Triphasic slow Waves Enema /Lactulose/Metronidazole/Protien restriction Old age + Bone pain (Sternum,back) + Frothy urine = MULTIPLE MYELOMA High ESR Hypercalcemia S/S + Hyperviscosity S/S + Constitutional S/S + Paraprotienemia(P.N) + Amyloidosis(CTS) + Pancytopenia+ Osteoporosis Fractures+spinal cord compression+ RF (hypercalcemia, Uricemia, Fanconi, pyelonephritis) Cancer of plasma cells INV: Protien electrophoresis (polyclonal protein)/B.M examination/Xray bones TTT: steroids/chemotherapy/thalidomide/stem cell transplant CAUSES OF HYPERVISCOSITY PRV MM Waldenstrom Macroglobulinemia Cryoglobulinemia Leukemia TTT: Plasmapharesis Enlarged L.Ns + Hypervicosity of bl.(spontaneous bleeding ,visual problems , headaches, vertigo ) + P.N + Hepatomegaly = WALDENSTROM MACROGLOBULINEMIA Monoclonal gammopathy (IgM) B.M sample + flow cytometery +CT+Urine+ESR+KFTS (inc. Creat) TTT: if constitutional S/S Rituximab+Cyclophosphamide+plasmapharesis (hyperviscosity) Smoking + Old Age+ Cough+ Hemoptysis+ Wt.Loss = BRONCHOGENIC CARCINOMA Difficulty swallowing + Clubbing +SOB+Horner (ptosis & myosis)+bone mestastasis Caused by Smoking /Asbestosis Paraneoplastic SMALL CELL CA SIADH (Hyponatremia , Low serum osmolarity) Inc. pigmentation (ACTH) Ataxia (Anti Hu Abs) Eaton Lambarat $ (Anti voltage gated Ca channels) TTT: Steroids/IVIG NSCC HPOA Hypercalcemia (polyuria , constipation,stones,PUD) INV: CXR , CT scan chest , Bronchoscopy with biopsy TTT: Lobectomy , pneumonectomy , radiotherapy , chemotherapy (cisplatin,Etoposide) Old Age > 50 + Pain & stiffness in shoulders + headaches + ESR > 50 + Normal CT = POLYMYALGIA RHEUMATICA TTT Steroids May cause TEMPORAL ARTERITIS (GIANT CELL ARTERITIS) Headaches + Jaw claudication + Pain in scalp + Loss of vision + very high ESR Causes loss of vision (AAION) Loss of pulsations of temporal artery + tender temporal & Scalp areas Temporal artery biopsy for Giant cells infiltrates High Dose steroids Young Age (15-40) + Constitutional S/S (Fever, Wt.loss , Night sweat) + Itching + Painless Lumps = HODGKIN LYMPHOMA Cancer of lymphoctyes Past history of EBV infection/Excessive use of GH Pain In L.Ns after Alcohol consumption INV: Reed sternburg cells on biopsy/CT & PET Scan for staging Stages: STAGE I : Single L.N group STAGE II : 2 or > L.N on the same side of diaphragm STAGE II : Both sides of diaphragm including spleen STAGE IV : extralymphatic spread A: no systemic symptoms B: systemic symptoms TTT: Radiotherapy /chemotherapy (Mustin,vincristine,bleomycin,prednisone) Old Age + Constitutional S/S + Generalized Lumps = NON-HODGKIN LYMPHOMA Skin rash (Mycosis fungoids) EBV(Burkit),HH8 , HTLV , HIV , H.Pylori ,Autoimmune ds (SLE,RA) , Radiation INV: Biopsy/CT TTT: chemotherapy/Radiotherapy/B.M trasnplantaion ESR>100 = T.B, INFECTIVE ENDOCARDITIS , OSTEOMYELITIS, DEEP ABSCESS, GCA , VASCULITIS , METASTAIC CANCERS , WALDENSTROM MACROGLOBULINEMIA Male +Constitutional S/S + Abdominal pain + Joint pains+ elevated creatinine= POLYARTERITIS NODOSA MI + Strokes + HTN + Livedo reticularis +Testicular pain +HBV No lung S/S , No purpura (doesn’t affect small vessels) INV: CBC , ESR , Sural nerve biopsy (rosary beads sign of vessels) TTT: Steroids + cyclophosphamide + Rituximab Previous throat infection/ Impetigo (skin rash ttt with Antibiotics) + Hematuria + Frothy urine + Eye Puffiness =POST STREPTOCOCCAL G.N Oliguria + HTN DPGN : Type III hypersensitivity INV: U&Es/Urine analysis TTT: Steroids D.M + Weakness/Wasting/Pain of thighs/hips/buttocks =DIABETIC AMYOTROPHY Proximal diabetic neuropathy Due damage to the nerve INV: HBA1C , NCV , EMG TTT: Control D.M , Physiotherapy , Diet , Gabapentin Meltzer’s Triad (Purpura + Arthritis + Myositis) + Hematuria (IgA nephropathy) +Abdominal pain = HENOCH SCHENOLIEN PURPRA Platelets are normal or raised History of pharyngitis ( Sore throat) TTT: Steroids + Azathioprine + IVIG Meltzer’s triad (Purpura + Arthritis + Myositis) + Hyperviscosity S/S (spontaneous bleeding of mucous membranes + blurred vision + headaches + vertigo) = CRYOGLOBULINEMIA TYPE I : (Monoclonoal IG) Waldenstrom , Multiple myeloma TYPE II : (Monocloncal IG + Circulating ICs)HCV TYPE III: (Polycloncal IG + circulating ICs) HCV , SLE INV: Cold agglutinins + Cause Inc. ALP + Normal LFTS+ Proximal weakness + Bone Pains/Fractures = OSTEOMALACIA Malabsorption / Dec. intake/RF INV: PTH is high , Low Ca , Low P , High ALP TTT: Weekly Vit D. 10,000 U IM injection for 6 weeks Severe pain after eating by 15 mins + Old age + Atherosclerotic manifestations (stroke/cramps/MI) =CHRONIC MESENTERIC ISCHEMIA Angiography TTT: anticoagulation / Angioplasty / Surgery (endarterectomy) Malabsoprtion + D.M = CHRONIC PANCEREATITIS/Celiac Disease Alcohol, Cystic fibrosis , Idiopathic INV.: X-ray calcified , CT, Dec. fecal elastase ,secretin stimulation test TTT: Replacement (Insulin + Pancereatic enzymes) URTIs (sinusitis, otitis media ) + Chr. Pancereatitis (Malabsorption +D.M)+ Recurrent Chest infection (SOB + Cough+yellow sputum) +Infertility + FH = CYSTIC FIBROSIS Salty tasting skin, ABPA, Pseudomonas inf., Borkholderia inf. INV: Sweat test Cl > 60 mmol , CFTR gene Ch. 7 TTT: Replacement therapy + TTT of complications Dextrocardia + Infertility + recurrent URTIs + Recurrent chest Infections = KARTAGNER SYNDROME Immotile cilia syndrome (AR) Hypoglycemia + HSM + Renomegaly on U/S + Lactic acidosis + Hyperuricemia (Gout) + Infections +bleeding= GLYCOGEN STORAGE DISEASE (VON GIERKES) Autosomal recessive INV: Liver Biopsy , Glucose-6-phosphatase activity TTT: Increase eating starch , glucose/Allopurinol for hyperuricemia BMI 30 + Waist circumference > 94 cm + BP >140/90 +FBG >6.1 mmol + Cholesterol > 4 mmol + Triglycerdies > 2 + HDL <1 mmol = METABOLIC SYNDROME Due to insulin resistance , Endocrine (PCO , Cushing) , Stress , Sedentary life Risks it cause Diabetes Coronary Heart disease Psychosis Rheumatic disease Gout TTT: Life style modification , TTT of cause , surgery Purpra + low platelets + Normal WBC +Abdominal pain+ Normal ESR = IMMUNE THROMBOCYTOPENIC PURPRA Increased bleeding (Gums , Menorrhagia) INV: inc. bleeding time , low platelets , normal PT , APTT , Clotting TTT: Steroids , IVIG, splenectomy ITP + Autoimmune Hemolytic Anemia = EVAN SYNDROME Purpura (Thrombocytopenia) + Headache/hallucinations/confusion +Anemia = TTP Renal impairement might occur Pregnancy , Quinine , Clopideogrel , Cyclosporine , Ticlopedine TTT: Plasma exchange / Steroids + immunosupression if recurrence after plasma exchange Recurrent different neurological deficit+ Uhthoff phenomenon (loss of vision/pins & needles sense with inc. body temp.) = MULTIPLE SCLEROSIS Avoid hot bathes and hot showers, exercises (Uhthoff phenomenon) Heat inc. demyelination May be presented with: Recurrent vertigo Double Vision Pain With Moving Eyes Weakness Unsteadiness Lhermit sign (neck flexion causes pain in back) INV: MRI , VEP , CSF TTT: Steroids Anemia + Inc. Creatinine + Low platelets + Recent bloody diarrhea ( EColi O157:H7) =HUS Medical emergency , most will resolve , small % will have Chr. Kidney ds and need replacement therapy TTT: Antibiotics , Hemodialysis Sudden Weakness in foot & Legs + Ascending pattern (diplopia , dysphagia , dec. resp.) = GUILLIAN BARRE SYNDROME CAUSES: Campylobacter ( diarrhea) , Influenza , CMV (sore throat) Blitaeral VII + Areflexia + Motor more than sensory loss Low Bl.Pr. + Bladder dysfunction may occur in severe cases but is temporary INV: NCV , CSF (inc. protiens) TTT: IVIG , Plasmapharesis Opthalmoplegia + Ataxia + Areflexia = MILLER FISCHER $ Anti GQ1B Abs Malabsorption (offensive diarrhea + difficult to flush) + Wt.loss + fatigue + Itchy rash on elbows = CELIAC DISEASE Low back pain + Dyspnea + Opacities of both upper zones of lungs on CXR = ANKYLOSING SPONDYLITIS Anterior uveitis , AR , Achilis tendinitis , Apical fibrosis , HLA B21 , schober test , X-ray showing scaro-iliitis , bamboo spine , TTT: NSAIDS , Sulphasalazine /methotrexate as disease modifying/ physiotherapy Hypercoagulable state ( DVT , PE , BudChiari , Cerebral Sinus Thrombosis ) + Hyperviscosity + inc. Hb + Itching with hot bath =PRV HSM+Facial Plethora + congested eyes +PUD+ GOUT INV.:Inc. Red cell mass + Jak 2 mutation + Thrombocythemia+Dec. ESR TTT: Venesection , Hydroxyurea , Bone marrow transplant Pregnancy + Dyspnea +Anemia + elevated liver enzymes + low platelets = HELLP SYNDROME Third timester Pregnancy induced HTN or pre-eclampsia Exclude fits = Pre-eclampsia DIC , Renal failure is a complication TTT: Delivery , DIC : Fresh frozen plasma , HTN: labetalol/hydralazine/ Nifidepine Lymphopenia + Hypothyroidism= DIGEORGE SYNDROME Lymphopenia + Albinism + peripheral neuropathy= CHEDIACK HEGASHI SYNDROME Pregnancy + Jaundice + Abdominal Pain + fever = ACUTE FATTY LIVER OF PREGNANCY Third trimester +RF +Pancereatitis +Hepatic encephalopathy Elevated Liver enzymes TTT: Delivery after stabilization (Fluids , Glucose , FFP) Old Age + Sudden Falls + Bradychardia (<40BPM) = COMPLETE HEART BLOCK Causes : Ischemic Ht. Ds , Lyme ds. , Congenital (Anti Ro , la Abs) INV: ECG ,ECHO TTT: Permanent Pacing Recurrent Abdominal pain + Recurrent fevers + PH of laparotomy+ Normal tests =FMF Serositis (pericarditis, pleurisy, effusions) COMPLICATIONS: Amyloidosis & RF INHERITANCE : AR TTT: Colchicine & NSAIDS HYPOGLYCAEMIC UNAWARENESS (hypoglycaemia with no alarm Signs) Occurs in long standing IDDM who always keep their glucose to normal levels Causes: AUTONOMIC NEUROPATHY BRAIN DESENSITIZATION TO HYPOGLYCAEMIA (if repeated attacks the brain increases its receptors to glucose) BETA BLOCKER DRUGS INCREASED FREQUENCY OF HYPOGLYCAEMIA IN IDDM AUTONOMIC NEUROPATHY (Diarrhea , vomiting) BETA BLOCKERS ADDISON DISEASE (pigmentation + postural hypotension) PREGNANCY (Ask about LMP) Imbalance between INSULIN & FOOD (irregular eating pattern) & EXCERCISES RENAL FAILURE INSULINOMA Old Age +Constitutional S/S +Wt.Loss+inc. ESR >100+ Cough + Pain in chest = TUBERCULOSIS Long contact with people with chest infection ( Nurse) Hemoptysis + osteomyelitis + potts ds of spine + cold abscess in skin + L.Ns INV: Sputum analysis with zeil nelson and culture on bactic or lovenstien Jensen TTT: admition , isolation , contact tracing , notify local authority 2 months Rifmpicin , INH , pyazinamide , ethambutol 4 months Rifampicin + INH Constitutional S/S ( Fever +Night sweats + Wt.Loss ) = MALIGNANCY /C.T. DISEASE (vasculitis) / INFECTIVE ENDOCARDITIS /T.B / LYMPHOMA Recurrent Angio-edema (Swelling of the Dermis)+ No Cause= C1 ESTERASE INHIBITOR DEFIENCY Inherited as AD or Acquired First appears after trauma or dental work Abdominal pain and vomiting Stridor or suffocation No Urticaria ACEIs are contraindicated (inc. bradykinin levels) INV: Low C1 inhibitor , Low C2 , C4 TTT: EPI-Pen , Purified C 1 inhibitor, Tranexemic acid Inc. Intracranial pr. S/S (vomiting , headache , blurred vision) + Amenorrhea =PROLACTINOMA Bitemporal hemianopia / Breast discharge INV: Inc. Prolactin , MRI , Ca , PTH , G TTT: Bromocriptine , Surgery Pancereatic problem (Glucagonoma :D.M ,polyuria+polydepsia , Insulinoma : Hypoglycemia Gastrinoma : Recurrent PUD , Vipoma : Diarrhea) + Pituitary adenoma( Prolactinoma (Amenorrhea , breast discharge , Acromegaly ) + Hyperparathyroidsim (Parathyroidectomy , Recurrent renal stones , HTN) = MEN I AD , RET oncogene Hemodialysis + Painful knee =GOUT More in old age / May be +ve FH Metabolic syndrome / Glycogen storage ds/ Chemotherapy / Alcohol / Polycythemia / Psoriasis / Thiazides X-Ray , Aspirate (Needle like –ve Birefringence on polarized microscopy of Mono sodium urate) , Inc. ESR Check KFTS TTT = NSIADS , Steroids , Intra-articular steroids /Colchicine Prophylaxis by allopurinol after 14 days of attack if: 2 attacks/year or Nephropathy Sudden Muscle weakness after exercise + Hypokalemia = HYPOKALEMIC PERIODIC PARALYSIS AD Exercise /High sodium & CHO diet/Excitement /Noise/Infection Often misdiagnosed as conversion disorder TTT: Acetazolamide , Spironolactone & potassium drinks with exercise Sickle Cell Anemia (SCA) + Sudden Pain in arms and legs not responding to analgesia= THROMBOTIC SICKLE CRISIS = B.M Infarction TTT : Hydration, Analgesia, Blood Crisis due to Hypoxia or Infection (UTI =Burning , Polyuria) Other Sickle Crisis: Aplastic Crisis Infection with Parvo virus B19 Decrease reticulocytes Give blood Hemolytic Crisis If with other hemolytic anemia Acute Chest Syndrome SCA +Lung Infection =sickling=Lung infarction= more Hypoxia , Cough , fever , SEVERE CHEST PAIN Exchange transfusion + Antibiotics Knee Pain + IV drug Abuser/Sexually active + Constitutional S/S = SEPTIC ARTHRITIS Any Blood infection / Near by infection / Sexual partners / IV drug user Staph aureus / Gonococcal (Rash on the trunk) / E.Coli (IV drug users) Knee x-ray (soft tissue swelling , erosions , subchondral necrosis) , Knee aspiration (Microscopy, Cytology, Gram Stain , Culture, polarizing microscope) TTT: IV Flucloxacillin + fusidic Acid Exclude Rieter Conjunctivitis , Uveitis , burning urine/Diarrhea, Back Pain , AR , keratoderma blenorrhagica (rash on feet) , Balanitis Campylobacter , Chlamydia, Shigella, Salmonella , chlamydia HLA B27 TTT: NSAID , Steroids , Immuno supressants FH of IHD + Stress /Straining job + HTN + Chest pain = ANGINA PECTORIS must be excluded Stress ECG, Dobutamine stress Echo Recurrent falls with no warning signs (Adam Stock ) + Palpitations + Chest pain +Dizziness = SICK SINUS SYNDROME Worsens with CCBs , BBs , Digoxin Idiopathic fibrosis/Ischemic/Sarcoidosis/Amyloidosis/Chagas/cardiac surgery ECG: sinus bradycardia/sinus arrest/AF/Atrial Tachycardia TTT: Pacing Recurrent falls + Old age + No alarming signs = COMPLTE HEART BLOCK Idiopathic, Ischemic ECG TTT: Pacing Young Age + Syncope during exercise + FH of collapse =HOCM Autosomal Dominant ECG , ECHO TTT: BBs , ICD Fatigue / Tiredness for 6 months+ Ms / Bone pains + Dec. concentration+ Flu like illness =CHRONIC FATIGUE SYNDROME Preceding vial illness Irritable bowel $ / Sore throat / Tender L.Ns /SOB/Chest pain/ Headaches TTT: CBT , Graded exercise ,SSRI Proximal Weakness (Wasting) + Rash on eyes & Fingers + Intact sensations + Arthralgia = DERMATOMYOSISTIS /MIXED CT.DS. (Anti RNP) Dysphagia / Dyspnea Auto-Immune / EBV/ Parvo virus /Malignancy/Breast implants Exclude malignancy ( GIT) Inc. CPK , EMG , Biopsy , Anti Jo-1 , Anti Mi-2 TTT: Prednisolone, IVIG, Plasmapharesis Proximal Weakness + Painful Muscles + Intact sensations + No rash = POLYMYOSITIS Statins/Malignancy/EBV CPK , Biopsy , Anti Jo Abs Weakness of Hand grip + Weakness Of Thighs = INCLUSION BODY MYOSITIS Polymyositis not responding to prednisolone Frequent falls Dysphagia & foot drop are late CPK , EMG ,Biopsy TTT: Supportive + Specialized exercise therapy Dysphagia + Odynophagia + Homosexual + TTT for oral candidiasis = ESOPHYGEAL CANDIDIASIS Preceding sore throat (Cold 3 weeks before) = seroconversion Testing for HIV , CD4 Starting HAART (Zidovudine + Lamivudine +Nelfinavir) Endoscopy TTT: IV Fluconazole Ascites in Old age + No liver disease = Suspect MALIGNANT ASCITIS
Long history of Asthma (Dyspnea) + Chest pain + New development of
L.L edema +FH = PRIMARY PULMONARY HTN CXR: Prominent pulmonary arteries with clear lung fields ECG: Right axis deviation + RVH +strain pattern ECHO Cardiac catheterization to show inc. Pulmonary Pr. >25 mmhg with CWP <15mmhg TTT: Bosentan, Sildenafil, Prostacylins + ANTICOAGULATION Chest Pain Radiates To Throat, Burning , Worse After Meals = GORD Chronic cough worse at night / Lying flat 24 hrs ambulatory PH monitoring TTT: PPIs Recurrent Loss of consciousness/Dizzy spells with SUDDEN TURNING OF HEAD = CAROTID SINUS HYPERSENSITIVITY Occur with Wearing high collars shirts Vasovagal syncope TTT: Life style modification / Dual chamber Pacing Long standing reflux + Dysphagia = BENIGN ESOPHYGEAL STRICTURE , CA ESOPHAGUS
Heparin + Low platelets after 5-14 days =HEPARIN INDUCED
THROMBOCYTOPENIA HIT + Thrombosis = HEPARIN INDUCED THROMBOCYTOPENIA AND THROMBOSIS TTT: Danaproid , Lepirudin, Fondaparinox Causes Of Zigzag Line Vision TIA (Emboli of AF , Carotid Atheroma ) Macular edema Vitrous heamorrhage Retinal detachment Migraine Hypotension Hypoglycemia Surgery in pituitary + Vomiting =ADDISONIAN CRISIS Hyperkalemia ( Gastro-enteritis causes hypokalemia) TTT: IV Fluids & hydrocortisone Causes Of Howell Jolly Bodies On Blood Film Splenectomy Sickle cell anemia (Auto splenectomy) Celiac disease (Hyposplenism) Megaloblastic anemia Severe hemolytic anemia Sjogran (Autoimmune disease) + Elevated Liver enzymes (Rt. Hypochondrial pain + jaundice) = AIH Autoimmune disease could be associated all together WT. gain /Low mood / Depression / Easy bruising /Hirsuitism / Acne = Cushing Syndrome
