June 2013 Medicine Paper

1.Scenario: Lady with dry eyes and dry mouth... diagnosis is

a.Sjogren(Ans)

b.Milkulicz syndrome?

2 Smooth and co-ordinated movement by

a. basal ganglia(Ans)

b. spinocerebellar

3.Scenario: elderly,diplopia,granuloma,raised b.p

a. giant cell arteritis(Ans)

b. takayasu disease

c. wegeners Granulomatosis

November 2013 Gynae Obs

1 epidural bupuvacaine

2 local anesthetic bupivacaine

3 thiopental.. redistributed in body

4 remnant of allontois..

5 remnant of paramesonephric duct.. appendix testis

6 whip like cilia.. fallopian tube

7 partly ciliated tubular.. fallopian tube

8 tubular structure,lymhpoid tissue..

appendix

9 true abt sacroiliac joint.. plain synovial joint

10 pain radiating to medial malleolus...

November 2013 Surgery Paper

1. A Female during delivery loses blood and requires blood. Her blood sample is reactive blood agglutinates with anti-sera B and anti-sera D. which blood is suitable for transfusion.

A.  A+

B.  B RH Positive

C.  O +

D.  AB +

E.  .

2. arches over left lung root.

A.  Thoracic duct

B.  Arch of aorta

C.  Azygos vein

D.  .

E.  .

3. Patient IVC is blocked just above the emergence of azygos vein, where blood will divert.

A.  Right gastric artery

B.  Hepatic vein

Syllabus and important topics for FCPS (PAPER-I)

Candidate for the fellowship of the college are expected to have a sound working knowledge of the structure and function of the human body and various mechanism  whereby these structures and functions are altered leading to diseased states.The emphasis in the FCPS Part 1 examinations is on comprehension of the various mechanisms by which body works and adjusts to external and internal changes. Concepts of the integration and interrelationship of various parts of the body are to be given more importance than finer details of structures and functions.

The outline of various topics given in this syllabus is a guide to what at the moment are considered to important topics which the candidate is expected to know.This is to help both the candidate and the examiner in defining the minimum boundaries of FCPS Part 1 examination.

November 2013 medicine paper

PAPER 1

1. Estrogen containing contraceptives…thrombo embolism

2. Highest renal clearance…PAH

3. Dec Hb dec MCV dysphagia (target cell confusing)…..IRON DEF ANEMIA

4. Arches over root of left lung….ARCH OF AORTA

5. Dorsal rami of spina nerve…SUPPLY EXTENSER TRUNK MUSCLE

6. Primary artiagenous joint……COSTOCHONDRAL JOINT

7. Sarcomere is between…..Z-LINES

8. Moves k+ out of cell and hyperkalemia….STERNOUS EXERCISE

9. Trigeminal ganglia…MIDDLE CRANIAL FOSSA CLOSE TO CAVERNOUS SINUS

10. RBCs….DESTORY BY SPLEEN WHEN OLD

11. Hyperplasia…INCREASE NO. OF CELLS AND…

12. Vomiting center is in….MEDULLA

13. Dec venous return…SKELETAL MUSCLE PARALYSIS

14. True about thyroid…EPITHELIUM CHANGE WITH SERETARY ACTIVITY

15. Good interaction between doc and patient…ACTIVE LISTENING

PATHOGNOMONIC SIGNS

HYPOCALCEMIA .. Chvostek & Trosseaus sign
ULCERATIVE COLITIS .. Recurrent bloody diarrhea
LYME’S DSE .. Bull’s eye rash
GLAUCOMA .. Painfull vision loss, tunnel/gun barrel/halo vision (Peripheral Vision Loss)
CATARACT .. Painless vision loss, Opacity of the lens, blurring of vision
RETINO BLASTOMA .. Cat’s eye reflex (grayish discoloration of pupils) 
ACROMEGALY .. Coarse facial feature 
DUCHENNE’S MUSCULAR DYSTROPHY ..Gowers’ sign
GERD .. Barretts esophagus (erosion of the lower portion of the esophageal mucosa) HEPATIC ENCEPHALOPATHY .. Flapping hand tremors
HYDROCEPHALUS .. Bossing sign (prominent forehead)
INCREASE ICP .. Cushing’s Triad (HYPERBRADY) HYPERtension BRADYpnea BRADYcardia
SHOCK ..(HYPOTACHYTACHY) HYPOtension TACHYpnea TACHYcardia
MENIERE’S DiSEASE .. Vertigo, Tinnitus MYASTHENIA GRAVIS ..Descending muscle weakness
GUILLAIN BARRE SYNDROME ..Ascending muscle weakness
DVT .. Homan’s Sign
CHICKEN POX ..Vesicular Rash
ANGINA .. Crushing stubbing pain relieved by NTG
CROUP ..Inspiratory stridor
EPIGLOTITIS .. 3Ds’ Drooling, Dysphonia, Dysphagia
HODGEKIN’S DISEA SE/LYMPHOMA .. Reedstenberg Cells
INFECTIOUS MONONUCLEOSIS ..Hallmark: sore throat, cervical lymph adenopathy, fever
PARKINSON’S DISEASE .. Pill-rolling tremors
FIBRIN HYALIN ..Expiratory Grunt
CYSTIC FIBROSIS .. Salty skin
DIABETES MELLITUS .. Polyuria, polydypsia, polyphagia
DIABETIC KETOACIDOSIS (DKA) .. Kussmauls breathing
BLADDER CANCER .. Painless hematuria BENIGN PROSTATIC HYPERPLASIA .. Reduced size & force of urine
RETINAL DETACHMENT .. Visual Floaters, flashes of light, curtain veil like vision TUBERCULOSIS .. Low-grade afternoon fever
PNEUMONIA .. Rusty sputum
ASTHMA .. Wheezing on expiration EMPHYSEMA .. Barrel chest
KAWASAKI SYNDROME .. Strawberry tongue
PERNICIOUS ANEMIA .. Red beefy tongue 
DOWN SYNDROME .. Protruding tongue 
CHOLERA .. Rice watery stool
MALARIA .. Stepladder like fever with chills 
TYPHOID .. Rose spots in abdomen 
DIPTHERIA .. Pseudomembrane
MEASLES .. Koplik’s spots
SYSTEMIC LUPUS ERYTHEMATOSUS ..Butterfly rashes
LIVER CIRRHOSIS .. Spider like varices 
LEPROSY .. Lioning face
BULIMIA NERVOSA Chipmunk face 
APPENDICITIS .. Rebound tenderness 
DENGUE .. Petechiae or (+) Herman’s sign 
MENINGITIS .. Kernig’s sign (leg flex then leg pain on extension), Brudzinski sign (neck flex = lower leg flex
TETANY .. Hypocalcemia (+)
Trousseau’s sign/carpopedal spasm; Chvostek sign (facial spasm) 
TETANUS .. Risus sardonicus
PANCREATITIS .. Cullen’s sign (ecchymosis of umbilicus); (+) Grey turners spots 
PYLORIC STENOSIS .. Olive like mass PATENT DUCTUS ARTERIOSUS .. Machine like murmur
ADDISON’S DISEASE .. Bronze like skin pigmentation
CUSHING’S SYNDROME .. Moon face appearance and buffalo hump HYPERTHYROIDISM/GRAVE’S DISEASE .. Exopthalmus
INTUSSUSCEPTION .. Sausage shaped mass, Dance Sign
MULTIPLE SCLEROSIS ..Charcot’s Triad (IAN)

KINDEY & ACID BASE BALANCE IMP POINTS

• Epithelium of Thin loop of henle has flat attenuated cells
• Epithelium of thick ascending loop of henle has coboid cells
• Walls of afferent arterioles have rennin secreting JG cells. At this point the tubular epithelium Is modified to form macula densa. 
• JG clls, macula densa and LACIS cells near them are collectively called JG apparatus
• PCT have distinct brush border while DCT do have few microcilli but no distinct brush border
• The pressure in glomerular capilleries is higher than other capillary bed because
1. Afferent arterioles are short
2. Efferent arterioles have higher resistance
• Loop of henle is counter current multiplier
• Vasa recta are counter current exchanger
• Counter current exchange is passive process. It depends upon the movement of water.
• Sympathetic nerves have no role in micturition… they have role in preventing retrograde ejaculation.
• Major buffer of the body is bicarbonate system
• Major interstitial buffer is bicrab
• Major buffer in the blood is also bicarb
• Major intrcellular buffer is protein
• Major defense of tonicity of body fluids is by ADH and thirst mechanisms.
• Major defense for the volume is angiotensin II coz it stimulates aldosterone, thirst and constricts vessels

ARTERIAL SUPPLY OF HEART

RCA:Right Coronary Artery
• Arises from anterior aortic sinus. It goes almost vertically in right AV groove crosses the inferior border of heart to continue posteriorly and anastomose with LCA
• It supplies RA, RV and parts of LA and LV and AV septum
BRANCHES are

- Right conus artery
- Anterior ventricular branches. The marginal branch is largest and reach upto apex
- Posterior ventricular branches
- Posterior inter ventricular artery: runs towards apex and gives branches to right and left vemtricles. It supplies the posterior part of ingter ventricular septum but NOT TO THE APEX. A large septal branch supplies AV node
- Atrial branches. Branch to SA node supplies SA node and right and left atria

LCA:Left Coronary Artery
• Usually larger than RCA and supplies the major part of heart.
• Supplies greater part of LA, LV and interventricular septum
BRANCHES are

- Anterior interventricular artery( in most of the people it supplies the APEX of heart) left diagonal artery is major branch
- Circumflex artery. Left marginal art is major branch

SUPPLY OF CONDUCTIVE SYSTEM
• SA node, AF node AV bundle are supplied by RCA
• RBB is supplied by LCA(right is wrongO
• LBB is supplied by both LCA and RCA(left doghla hota hai )

SUMMARY:
• RCA supplies all of RV(except for small area to the right of anterior nterventricular groove), variable part of diaphragmatic surface of LV, posteroinferior 3rd of ventricular septum, RA, part of LA, SA node and AV node. Small branches to LBB are also given
• LCA supplies most of LV, small area of RV to the right of Interventricular groove, anterior 2/3rd of ventricular septum, most of LA, RBB, and LBB

IMPORTANT POINT FOR FCPS 1

Here is a list of commonly tested facts in Part 1 exam. They are listed in order of importance - highest first.
1. Acromegaly – Diagnosis: OGTT followed by GH conc.
2. Cushings – Diagnosis: 24hr urinary free cortisol. Addisons --> short synacthen.
3. Rash on buttocks – Dermatitis herpetiformis (coeliac dx).
4. AF with TIA --> Warfarin. Just TIA's with no AF --> Aspirin
5. Herpes encephalitis --> temporal lobe calicification OR temporoparietal attentuation – subacute onset i.e. Several days.
6. Obese woman, papilloedema/headache --> Benign Intercanial Hypertention.
7. Drug induced pneumonitis --> methotrexate or amiodarone.
8. chest discomfort and dysphagia --> achalasia.
9. foreign travel, macpap rash/flu like illnes --> HIV acute.
10. cause of gout --> dec urinary excretion.
11. bullae on hands and fragule SKIN torn by minor trauma --> porphyria cutanea tarda.
12. Splenectomy --> need pneumococcal vaccine AT LEAST 2 weeks pre-op and for life.
13. primary hrperparathyroidism --> high Ca, normal/low PO4, normal/high PTH (in elderly).
14. middle aged man with KNEE arthritis --> gonococcal sepsis (older people -> Staph).
15. sarcoidosis, erythema nodosum, arthropathy --> Loffgrens syndrome benign, no Rx needed.
16. TREMOR postural,slow progression,titubation, relieved by OH->benign essential TREMOR AutDom. (MS – titbation, PD – no titubation)
17. electrolytes disturbance causing confusion – low/high Na.
18. contraindications lung Surgery --> FEV dec bp 130/90, Ace inhibitors (if proteinuria analgesic induced headache.
21. 1.5 cm difference btwn kidneys -> Renal artery stenosis --> Magnetic resonance angiogram.
22. temporal tenderness--> temporal arteritis -> steroids > 90% ischaemic neuropathy, 10% retinal art occlusion.
23. severe retroorbital, daily headache, lacrimation --> cluster headache.
24. pemphigus – involves mouth (mucus membranes), pemphigoid – less serious NOT mucosa.
25. diagnosis of polyuria -> water deprivation test, then DDAVP.
26. insulinoma -> 24 hr supervised fasting hypoglycaemia.
27. Diabetes Random >7 or if >6 OGTT (75g) -> >11.1 also seen in HCT.
28. causes of villous atrophy: coeliac (lymphocytic infiltrate), Whipples , dec Ig, lymphoma, trop sprue (rx tetracycline).
29. diarrhoea, bronchospasm, flushing, tricuspid stenosis -> gut carcinoid c liver mets.
30. hepatitis B with general deterioration -> hepaocellular carcinoma.
31. albumin normal, total protein high -> myeloma (hypercalcaemia, electrophoresis).
32. HBSag positive, HB DNA not detectable --> chornic carier.
33. Inf MI, artery invlived -> Right coronary artert.
34. Autosomal dominant conditions: Achondroplasia, Ehler Danlos, FAP, FAMILIAL hyperchol,Gilberts, Huntington's, Marfans's, NFT I/II, Most porphyrias, tuberous sclerosis, vWD, PeutzJeghers.
35. X linked: Beck/Duch musc dyst, alports, Fragile X, G6PD, Haemophilia A/B.
36. Loud S1: MS, hyperdynamic, short PR. Soft S1: immobile MS, MR.
37. Loud S2: hypertension, AS. Fixed split: ASD. Opening snap: MOBILE MS, severe near S2.
38. HOCM/MVP - inc by standing, dec by squating (inc all others). HOCM inc by valsalva, decs all others. Sudden death athlete, FH, Rx. Amiodarone, ICD.
39. MVP sudden worsening post MI. Harsh systolic murmur radites to axilla.
40. Dilated Cardiomyopathy: OH, bp, thiamine/selenium deficiency, MD, cocksackie/HIV, preg, doxorubicin, infiltration (HCT, sarcoid), tachycardia.
41. Restrictive Cardiomyopathy: sclerodermma, amyloid, sarcoid, HCT, glycogen storage, Gauchers, fibrosis, hypereosinophilia Lofflers, caracinoid, malignancy, radiotherapy, toxins.
42. Tumor compressing Respiratory tract --> investigation: flow volume loop.
43. Guillan Barre syndrome: check VITAL CAPACITY.
44. Horners – sweating lost in upper face only – lesion proximal to common carotid artery.
45. Internuclear opthalmoplegia: medial longitudinal fasciculus connects CN nucleus 3-4. Ipsilateral adduction palsy, contralateral nystagmus. Aide memoire (TRIES TO YANK THE ipsilateral BAD eye ACROSS THE nose ). Convergence retraction nystagmus, but convergence reflex is normal. Causes: MS, SLE, Miller fisher, overdose(barb, phenytoin, TCA), Wernicke.
46. Progressive Supranuclear palsy: Steel Richardson. Absent voluntary downward gaze, normal dolls eye . i.e. Occulomotor nuclei intact, supranuclear Pathology .
47. Perinauds syndrome: dorsal midbrain syndrome, damaged midrain and superior colliculus: impaired upgaze (cf PSNP), lid retraction, convergence preserved. Causes: pineal tumor, stroke, hydrocephalus, MS.
48. demetia, gait abnormaily, urinary incontinence. Absent papilloedema-->Normal pressure hydrocephalus.
49. acute red eye -> acute closed angle glaucoma >> less common (ant uveitis, scleritis, episcleritis, subconjuntival haemmorrhage).
50. wheeles, URTICARIA , drug induced -> aspirin.
51. sweats and weight gain -> insulinoma.
52. diagnostic test for asthma -> morning dip in PEFR >20%.
53. Causes of SIADH : chest/cerebral/pancreas Pathology , porphyria, malignancy, Drugs (carbamazepine, chlorpropamide, clofibrate, atipsychotics, NSAIDs, rifampicin, opiates)
54. Causes of Diabetes Insipidus: Cranial: tumor, infiltration, trauma Nephrogenic: Lithium, amphoteracin, domeclocycline, prologed hypercalcaemia/hypornatraemia, FAMILIAL X linked type
55. bisphosphonates:inhibit osteoclast activity, prevent steroid incduced osteoperosis (vitamin D also).
56.returned from airline flight, TIA-> paradoxical embolus do TOE.
57. alcoholic, given glucose develops nystagmus -> B1 deficiency (wernickes). Confabulation->korsakoff.
58. mono-artropathy with thiazide -> gout (neg birefringence). NO ALLOPURINOL for acute.
59. painful 3rd nerve palsy -> posterior communicating artery aneurysm till proven otherwise
60 late complication of scleroderma --> pumonaryhypertention plus/minus fibrosis.
61. causes of erythema mutliforme: lamotrigine
62. vomiting, abdominal pain, hypothyroidism -> Addisonian crisis (TFT typically abnormal in this setting DO NOT give thyroxine).
63. mouth/genital ulcers and oligarthritis -> behcets (also eye /SKIN lesions, DVT)
64. mixed drug overdose most important step -> Nacetylcysteine (time dependent prognosis)
65. cavernous sinus syndrome - 3rd nerve palsy, proptosis, periorbital swlling, conj injectn
66. asymetric parkinsons -> likely to be idiopathic
67. Obese, NIDDM female with abnormal LFT's -> NASH (non-alcoholic steatotic hepatitis)
68. fluctuating level of conciousness in elderly plus/minus deterioration --> chronic subdural. Can last even longer than 6 months
69. Sensitivity --> TP/(TP plus FN) e.g. For SLE - ANA highly sens, dsDNA:highly specific
70. RR is 8%. NNT is ----> 100/8 --> 50/4 --> 25/2 --> 13.5
71. ipsilateral ataxia, Horners, contralateral loss pain/temp --> PICA stroke (lateral medulary syndrome of Wallenburg)
72. renal stones (80% calcium, 10% uric acid, 5% ammonium (proteus), 3% other). Uric acid and cyteine stone are radioluscent.
73. hyperprolactinaemia (allactorrohea, amenorrohea, low FSH/LH) -> Da antags (metoclopramide, chlorpromazine, cimetidine NOT TCA's), pregnancy, PCOS, pit tumor/microadenoma, stress.
74. Distal, asymetric arthropathy -> PSORIASIS
75. episodic headache with tachycardia -> phaeochromocytoma
76. very raised WCC -> ALWAYS think of leukaemia.
77. Diagnosis of CLL --> immunophenotyping NOT cytogenetics, NOT bone marrow
78. Prognostic factors for AML -> bm karyotype (good/poor/standard) >> WCC at diagnosis.
79. pancytopenia with raised MCV --> check B12/folate first (other causes possble, but do this FIRST). Often associayed with phenytoin use --> decreased folate
80. miscariage, DVT, stroke --> LUPUS anticoagulant --> lifelong anticoagulation
81. Hb elevated, dec ESR -> polycythaemua (2ndry if paO2 low)
82. anosmia, delayed puberty -> Kallmans syndrome (hypogonadotrophic hypogonadism)
83. diagnosis of PKD -> renal US even if think anorexia nervosa
85. commonest finding in G6PD hamolysis -> haumoglobinuria
86. mitral stenosis: loud S1 (soft s1 if severe), opening snap.. Immobile valve -> no snap.
87. Flank pain, urinalysis:blood, protein -> renal vein thrombosis. Causes: nephrotic syndrome, RCC, amyloid, acute pyelonephritis, SLE (atiphospholipid syndrome which is recurrent thrombosis, fetal loss, dec plt. Usual cause of cns manifestations assoc with LUPUS ancoagulant, anticardiolipin ab)
88. anaemia in the elderly assume GI malignancy
89. hypothermia, acute renal failure -> rhabdomyolysis (collapse assumed)
90. pain, numbness lateral upper thigh --> meralgia paraesthesia (lat cutaneous nerve compression usally by by ing ligament)
91. diagnosis of haemochromatosis: screen with Ferritin, confirm by tranferrin saturation, genotyping. If nondiagnostic do liver biopsy 0.3% mortality
92. 40 mg hidrocortisone divided doses (bd) --> 10 mg prednisolone (ie. Prednislone is x4 stronger)
93. BTS: TB guidlines – close contacts -> Heaf test -> positive CXR, negative --> repeat Heaf in 6 weeks. Isolation not required.
94. Diptheria -> exudative pharyngitis, lymphadenopathy, cardio and neuro toxicity.
95. Indurated plaques on cheeks, scarring alopecia, hyperkeratosis over hair follicles ->>Discoid LUPUS
96. wt loss, malabsoption, inc ALP -> pancreatic cancer
97. foreign travel, tender RUQ, raised ALP --> liver abscess do U/S
98. wt loss, anaemia (macro/micro), no obvious cause -> coeliac (diarrhoea does NOT have to be present)
99. haematuria, proteinuria, best investigation --> if glomerulonephritis suspected --> renal biopsy
100. venous ulcer treatment --> exclude arteriopathy (eg ABPI), control oedema, prevent infection, compression bandaging.
101. Malaria, incubation within 3/12. can be relapsing /remitting. Vivax and Ovale (West Africa) longer imcubation.
102. Fever, lymphadenopathy, lymphocytosis, pharygitis --->EBV ---> heterophile antibodies
103. GI bleed after endovascular AAA Surgery --> aortoenteric fistula

104. Young girl – suspect Anorexia Nervosa – linugo hair, finctional hypogonadotrophic hypogonadism -> amennorhea. LH and FSH both low. All other hormones are usually normal. Ferritin low.

105. Reiters Syndrome – arthritis, uveitis, urethritis – Chlymidia, campylobacter, Yersinia, SALMONELLA , Shigella. Balanisits.
106. PKD – aut dom Chr 16/4 assoc berry aneurysm, mitral/aortic regurg
107. Porphyria – photosensitivity, blisters, scars with millia, hypertrichosis
108. heart sounds: Aortic Stenosis s2 paradoxical split, length proportional to severity
109. Vitiligo – commonest assoctions pernicious anaemia >>> type 1 DM , autoimmune addisons, autoimmune thyoid dx
110. Gout – blood urate high/low/normal, joint aspirate pos birif, ppt thiazides, NO allopurinol/aspirin in acute phase
111. Peripheral neuropathy – a) B12 – rapid, dorsal columns (joint pos, vibration), sensory ataxia, pseudoathetosis of upperlimbs b) diabetic – slow, spinothalamic (pain, temp?) c)alcohol – slow progressive, spinothalamic d) Pb – motor upper limbs
112. CNS abnormalities in HIV: toxoplaasmosis (ring enhancing), lymphoma (solitary lesion). HIV encephalopathy, progressive multifocal leucoencephalopathy (PML – demylination in advanced HIV, low attenuation lesions)
113. Travellers diarrohea: chronic (>2 WEEKS) giardia (incidious onset rx. Metronidazole), SALMONELLA (serious systemic illness), E.coli (rx. Ciprofloxacin) , Shigella
114. Renal syndrome – minimal change disease, membanous, IgA nephropathy, post-streptococcal.
115. If you see blood on urinalysis forget about RAS
116. Thyroid Malignancy – tend to be non-functional, anaplastic has worse prognosis, local infiltration -> dysphagia, vocal cord paralysis
117.ALMOST Pathognomic for the exam
fatiguability -> myasthenia gravis
fasciculations -> Motor neurone diease
silvery white scale -> PSORIASIS
hypopigmented -> vitiligo/pityriasis versicolor
pretibial myxoedema --> Graves (NOT lid lag, NOT exopthalmus)

CARDIOLOGY EXAMINATION IMP POINTS

S4 heart sound CANNOT be present during atrial fibrillation (atrial kick is required).

A S3 heart sound CANNOT be present in the setting of severe mitral stenosis.

A S3 heart sound can be present in athletes, pregnant females and other young healthy individuals.

A S3 heart sound can indicate severe systolic heart failure.

A S4 heart sound is always pathologic and can indicate diastolic heart failure, left ventricular hypertrophy or active myocardial ischemia.

Factors that increase the intensity of the S1 heart sound include short PR interval, fast heart rate and mild mitral stenosis.

Factors that decrease the intensity of the S1 heart sound include long PR interval, slow heart rate and severe mitral stenosis.

A fixed split S2 heart sound can be from an atrial septal defect.

A paradoxically split S2 heart sound can be caused by aortic stenosis, hypertrophic obstructive cardiomyopathy or a left bundle branch block.

A widened split S2 heart sound can be caused by severe mitral regurgitation, pulmonic stenosis or a right bundle branch block.

Large systolic jugular venous pulsations can be from V waves due to severe tricuspid regurgitation.

A holosystolic murmur at the left lower sternal border louder with inspiration is due to tricuspid regurgitation (Carvallo’s sign).

The aortic stenosis murmur can radiate to the cardiac apex where it sounds holosystolic and can mimic the murmur of mitral regurgitation (Galiveriden phenomenon).

The three physical exam findings that correlate with severity of aortic stenosis include the timing of the murmur peak in systole (late peak is severe), the intensity of the S2 heart sound (soft or absent is severe) and “pulsus parvus et tardus”.

The late diastolic crescendo portion of a mitral stenosis murmur disappears when atrial fibrillation is present due to the loss of the atrial kick.

The murmur of aortic regurgitation is located at the right upper sternal border (aortic post) ONLY if the etiology is aortic root dilation. If valve leaflet pathology is the cause then the murmur is heard at the left lower sternal border.

The best position to hear the murmur of aortic regurgitation is to have the patient lean forward and listen after a forced, held expiration.

As aortic regurgitation worsens, the murmur becomes shorter in early diastole due to the aortic and left ventricular pressure equalizing more quickly.

The two murmurs that can be heard in the patient’s back are mitral regurgitation and coarctation of the aorta.

The Austin-Flint murmur is a diastolic rumble at the cardiac apex in a patient with aortic regurgitation and occurs from the regurgitant jet striking the anterior mitral leaflet.

There are multiple peripheral physical exam findings in patients with severe aortic regurgitation due to the high stroke volume...

When the mitral regurgitant jet is eccentrically directed posterior (anterior leaflet involvement), the murmur radiates to the back. When directed anterior (posterior leaflet involvement), the murmur radiates to the cardiac base.

The murmur of mitral regurgitation increases with handgrip and transient arterial occlusion since these maneuvers increase afterload.

The earlier the opening snap in a patient with mitral stenosis, the more severe it is due to higher left atrial pressures forcing the valve open immediately in early diastole.

The murmur of a small ventricular septal defect (VSD) is very loud a frequently associated with a thrill. This murmur is referred to as “maladie de Roger”

The murmur of an atrial septal defect is a systolic, crescendo-decrescendo murmur at the pulmonic listening post due to increased pulmonic valve flow. There is frequently a fixed splitting of the S2 heart sound.

The murmur of a patent ductus arteriosus is continuous throughout systole and diastole since the aortic pressure (normally 120/80) is ALWAYS higher than the pulmonary artery pressure (normally 25/10) in both systole and diastole.

A right ventricular heave can be present from severe pulmonary hypertension.

Cannon A waves can be seen in the jugular venous pulsations when the atrium contracts at the same time as the ventricle (against a closed tricuspid valve) which occurs in the setting of AV dissociation (complete heart block or ventricular tachycardia).

Roth spots, Janeway lesions and splinter hemorrhages are all peripheral signs of endocarditis.

Unequal radial pulses can be a sign of aortic dissection (with subclavian artery compression) OR from atherosclerotic subclavian arm occlusion.

Always check blood pressure in both arms in acute chest pain patients to help diagnose aortic dissection (will be markedly lower in one arm, usually the left, if the subclavian artery is involved).

ECG IMP POINTS

PR interval is misnomer it is actually PQ interval........

There is no wave for atrial repolarization coz ventricular depolarizaton masks it....

The three irregularly irregular rhythms are atrial fibrillation, atrial flutter with variable conduction and multifocal atrial tachycardia (similar to wandering atrial pacemaker).

AV dissociation occurs in complete heart block (3rd degree AV block) and ventricular tachycardia.

Treat a wide-complex tachycardia like ventricular tachycardia until proven otherwise. Use the Brugada criteria to distinguish ventricular tachycardia from SVT with aberrancy.

If no P waves can be seen and the QRS complexes are irregularly irregular, then atrial fibrillation is present.

ST segment elevation from pericarditis is diffuse (all leads except aVR and V1) and concave upward.

PR segment depression can be from acute pericarditis or an atrial infarction.

Diffuse T wave inversion is stage III of the ECG changes in pericarditis.

Pericarditis can be distinguished from early repolarization by the ratio of the T wave to the ST elevation. If the ratio is > 4, then early repolarization is present (the ST elevation is < 25% of the T wave amplitude).

The ST elevation from early repolarization resolves with exercise while that of pericarditis does not.

Acute myocardial infarction can be diagnosed on an ECG in the setting of a left bundle branch block (LBBB) on occasion using Sgarbossa Criteria or identifying Chapman’s sign or Cabrera’s sign.

The causes of the R wave in lead V1 greater in amplitude than the S wave include right bundle branch block, posterior myocardial infarction, WPW type A, right ventricular hypertrophy, ventricular tachycardia with right bundle morphology and isolated posterior wall hypertrophy occurring in Duchenne’s muscular dystrophy.

An Epsilon wave in lead V1 occurs in Arrhythmogenic Right Ventricular Dysplasia (ARVD) and is described as a “grassy knoll” appearance just after the QRS complex.

An Osborne wave classically occurs in the setting of hypothermia and is seen as a spike at the end of the QRS complex. An Osborne wave can also occur from hypercalcemia.

Hypercalcemia shortens the QT interval.

Dextrocardia shows negative QRS complex in lead I with negative P and T wave in this lead. There is low voltage in leads V4 through V6 (unlike limb lead reversal which has normal voltage in these leads, but negative QRS in lead I).

Hypokalemia causes U waves in the ECG seen as a positive wave just after the T wave.

Hyperkalemia causes peaked T waves initially, then an intraventricular conduction delay with a widened QRS complex, then bradycardia and eventually a “sine wave” pattern ensues.

Hyperacute T waves are large and broadly shaped occurring in the first few minutes of an acute myocardial infarction.

Delta waves occur in Wolff-Parkinson-White Syndrome

Hypertrophic Obstructive Cardiomyopathy (HOCM) is characterized by sharp, dagger-like Q waves in the lateral leads in the setting of left ventricular hypertrophy.

The most common ECG finding of an acute pulmonary embolism is sinus tachycardia, however the classic finding is an S wave in lead I, Q wave in lead III and inverted T waves in lead III (S1Q3T3 pattern).

A bifascicular block is a combination of a right bundle branch block with a left anterior or posterior fascicular block.

A trifascicular block is a bifascicular block with a first degree AV block.

2:1 AV block is a form of second degree AV block that can be type I or type II. If the PR interval of the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second degree type I AV nodal block (Wenckebach). Alternatively, if the PR interval is normal and the QRS duration is prolonged, then it is most likely second degree type II

Carotid massage, atropine administration or exercise can help determine if 2:1 AV block is from second degree type I or second degree type II AV block (see 2:1 AV block review).

A posterior wall MI shows ST depression, not elevation in leads V1 and V2 with an R:S ratio greater that 1 in lead V1.it can b seen by mirror image...

Blocked premature atrial contractions occurring in a pattern of bigeminy can mimic sinus bradycardia.

Coarse “fibrillatory waves” can be seen during atrial fibrillation.

Clockwise atrial flutter causes positively deflected P waves in the inferior leads while counterclockwise atrial flutter causes negative deflected P waves in the inferior leads.

Multifocal atrial tachycardia (MAT) requires 3 different P wave morphologies in 1 ECG with a QRS complex rate of > 100.

Wandering atrial pacemaker (WAP) requires 3 different P wave morphologies in 1 ECG with a QRS complex rate of < 100.

Idioventricular rhythms meet criteria for ventricular tachycardia, but have a heart rate of < 100.

Massive left atrial enlargement causes a notch in the P wave and is termed “P-mitrale”

A left ventricular aneurysm results in chronic ST elevation in the anterior precordial leads.

Low voltage on the ECG can be caused by obesity, COPD, pericardial effusion, severe hypothyroidism, subcutaneous emphysema, massive myocardial damage/infarction, or infiltrative/restrictive diseases such as amyloid cardiomyopathy.

Electrical alternans occurs when every other QRS complex has varying amplitudes and is from the heart swaying within a large pericardial effusion.

Sinus arrhythmia requires a variation of at least 120 milliseconds of the PP interval.

A prolonged QT interval from hypocalcemia has a lengthened ST segment, then normal appearing T wave.

Wellen’s phenomenon occurs from a proximal left anterior descending subtotal occlusion and has 2 types. Type I is deep inverted T waves in the precordial leads and type II is biphasic T waves in V1 through V3.

Digoxin can cause ST depression appearing as a “reverse tick” or “reverse check”.

Bidirectional ventricular tachycardia occurs when every other beat has a different QRS morphology and each morphology meets VT criteria. This is caused most commonly by digoxin toxicity.

Atrial tachycardia with 2:1 AV block is a common rhythm in the setting of digoxin toxicity.

An acute intracranial process (hemorrhage, trauma, carotid endarterectomy etc...) can cause dramatic T wave inversions and a prolonged QT interval on the ECG.

Ostium primum atrial septal defects cause an incomplete right bundle branch block with left axis deviation. Ostium secundum atrial septal defects cause an incomplete right bundle branch block with right axis deviation.
There is a big difference between Pr segment and PR interval................
There is also 15 leads EKG.....