13. Internal Medicine

7/22/2019 13. Internal Medicine

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Fanconi anemia- a type of idiopathic refractory anemia characterized by pancytopenia,hypoplasia of the bone marrow, and congenital anomalies, occurring in members of the samefamily (an autosomal recessive trait); the anemia is normocytic or slightly macrocytic, macrocytesand target cells may be found in the circulating blood, and the leukopenia usually is due toneutropenia. Congenital anomalies include short stature; microcephaly; hypogenitalism;strabismus; anomalies of the thumbs, radii, and kidneys and urinary tract; mental retardation; andmicrophthalmia.

Fanconi syndromeis a disease of theproimal renal tubulesof the kidney in which glucose,aminoacids, uric acid,phosphateandbicarbonate are passed into the urine, instead of being reabsorbed. !heloss ofbicarbonate results in !ype " or proimal renal tubular acidosis .!he loss of phosphate results inthe bone diseaserickets(even with ade#uate vitamin $ and calcium), because phosphate is necessary forbone development.

%ilirubin occurs in plasma in four forms (&elson 'e Chapter-*+")

free or unbound bilirubin (the form responsible for kernicterus, because it can cross cellmembranes)

unconugated bilirubin tightly bound to albumin

conugated bilirubin (the only fraction to appear in urine). n the liver it is conugated withglucuronic acid by the enzyme /lucuronyltransferase, making it soluble in water.

0 fraction- the fractionof bilirubincovalently boundtoalbumin1 inconventional

methodsit is measured as partof conugated bilirubin. %ecause of its covalent bondduring the recovery phaseof hepatocellular aundice, it may persist in theblood for a

week or more afterurineclears.

2lthough the terms direct and indirect bilirubin are used e#uivalently with conugated andunconugated bilirubin, this is not #uantitatively correct, because the direct fraction includesboth conugated bilirubin and 0 bilirubin.

Hepatorenal syndrome(345) is defined as functional renal failure in patients with end-stageliver disease. !he pathophysiology of 345 is poorly defined, but the hallmark is intense renalvasoconstriction (mediated by hemodynamic, humoral, or neurogenic mechanisms) withcoeistent systemic vasodilation. !he diagnosis is supported by the findings of oliguria (6'm7kgday), a characteristic pattern of urine electrolyte abnormalities (urine sodium of 6'8

m9#7, fractional ecretion of sodium of 6':, urine plasma creatinine ratio 6'8, and normalurinary sediment), absence of hypovolemia, and eclusion of other kidney pathology. !he besttreatment of 345 is timely liver transplantation, as complete renal recovery can be epected.

9levations in serum 2, +< nucleotidase (+


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359 must be distinguished from herpes simple meningitis, which is more commonly causedby 35>-" and which often occurs in association with a concurrent herpetic genital infection.

C!- low density lesions in temporal lobes. 3emorrhage is highly suggestive and seen in laterdisease course.

?4- temporal lobe hyperintense

?etavir 5coring is done for- Chronic heaptits

&atalizumab in multiple sclerosis n Crohn@s as an antibody against alpha A integrin inhibiting !lymphocyte adhesion n migration to lesions in these diseases.

&9B classification liver cancer --DEF$2, C7 primary cause of community ac#uiredpneumonia ---- ?452

albright@s osteodystrophy is &D4?27 calcium, not decreased calcium

Plummer vinson's syndrome- Combination of symptomatic hypopharyngeal webs and rondeficiency anemia in middle aged female. resence of web is in postcricoid1 region. 3emoglobinis low and there is hypochromic microcytic anemia. 2ll cases have a low serum iron and high ironbinding capacity. ron shold be given orally to correct 3b levels.

2trial fibrillation- 9nlarged left atrium and 1increased left atrial pressure.

rocollagen suicide phenomenon seen in- D (Dsteogenesis mperfecta) !he etiologic agent in over G8: cases of post-transfusion hepatitis is hepatitis C. t is also

associated with incidence of chronic active hepatitis upto 'H: and an 1-'8: increase ofcirrhosis or hepatoma or both. C?> infection is not a significant problem in immunocompetentrecipients and hence blood is not routinely tested for C?>. (I-'J /!-J)

Diabetes insipidus(DI) is a conditioncharacterized by ecessive thirstand ecretion of largeamounts of severely diluted urine, with reduction of fluid intake having no effect on the latter.!here are several different types of $, each with a different cause.

!he most common type in humans is central $, caused by a deficiency of argininevasopressin(2>), also known asantidiuretic hormone(2$3). >asopressin acts at the distaltubule and collecting ducts to increase permeability to water not aw electrolytes i.e. freewater. 3ence central $ is aw 1free waterclearence. Fnder normal circumstances, this would

result in the movement of free water from renal tubule to capillary. Fnder conditions ofvasopressin deficiency, as in nephrogenic $ water remains in the tubules, resulting inecretion of dilute urine.

!he second common type of $ isnephrogenicdiabetes insipidus, which is caused by aninsensitivity of the kidneysto 2$3. 5ymptoms are similar to neurogenic $ ecept plasmalevels of vasopressin are increased.

Hyperuricemia- 2 purine rich diet can cause hyperuricemia. Koods high in the purines adenine

and hypoanthinemay be more potent in eacerbating hyperuricemia. 7ow temperature is acommonly reported trigger of acute gout. !his is believed to be due to temperature dependentprecipitation of uric acid crystals in tissues at below normal temperature. !hough asymptomatichyperuricemia does increase the risk of acute gouty arthritis prophyllais is not recommended.

3%e2g negative means-

Chronic carrier low infectivity recore mutant (infective but still 3%e2g negative)

both can be differentiated by >427 7D2$ , 27! 79>97

Fanconi anemia- a type of idiopathic refractory anemia characterized by pancytopenia,hypoplasia of the bone marrow, and congenital anomalies. !he anemia is normocytic or slightlymacrocytic, macrocytes and target cells may be found in the circulating blood, and the leukopeniausually is due to neutropenia. Congenital anomalies include short stature; microcephaly;hypogenitalism; strabismus; anomalies of the thumbs, radii, and kidneys and urinary tract; mentalretardation; and microphthalmia

on!enital hypoplastic anemia- hypoproliferative macrocytic anemia. 2 macrocytic anemiaresulting from congenital hypoplasia of the bone marrow, which is grossly deficient in erythroid

precursors while other elements are normal; anemia is progressive and severe, but leukocyte andplatelet counts are normal or slightly reduced; survival of transfused erythrocytes is normal; minorcongenital anomalies are found in some patients. (5yn congenital nonregenerative anemia,Diamond-Blackfan anemia, familial hypoplastic anemia, pure red cell anemia, erythrogenesisimperfecta,Diamond-Blackfan syndrome.)
http://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Polydipsiahttp://en.wikipedia.org/wiki/Polydipsiahttp://en.wikipedia.org/wiki/Polyuriahttp://en.wikipedia.org/wiki/Vasopressinhttp://en.wikipedia.org/wiki/Antidiuretic_hormonehttp://en.wikipedia.org/wiki/Antidiuretic_hormonehttp://en.wikipedia.org/wiki/Nephrogenic_diabetes_insipidushttp://en.wikipedia.org/wiki/Nephrogenic_diabetes_insipidushttp://en.wikipedia.org/wiki/Nephrogenic_diabetes_insipidushttp://en.wikipedia.org/wiki/Kidneyhttp://var/www/vhosts/wiki/Adeninehttp://var/www/vhosts/wiki/Hypoxanthinehttp://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Polydipsiahttp://en.wikipedia.org/wiki/Polyuriahttp://en.wikipedia.org/wiki/Vasopressinhttp://en.wikipedia.org/wiki/Antidiuretic_hormonehttp://en.wikipedia.org/wiki/Nephrogenic_diabetes_insipidushttp://en.wikipedia.org/wiki/Kidneyhttp://var/www/vhosts/wiki/Adeninehttp://var/www/vhosts/wiki/Hypoxanthine


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"- #hich o$ the $ollo%in! is not an indication o$Digoxin-specific Fab antibodiesin children-& Supraventricular tachycardia------ans verdose * + m!, Serum di!oxin levels * &n!.ml+ Pro!ressive bradycardia

9planation-

!reatment of $igoin toicity-

5upraventricular tachycardia- ECl

Kre#uent >entricular premature beats- 7idocainehenytoin

>entricular tachycardiaKibrillation- Cardioversion$igibind

5econd or third degree heart block- 2tropineCatheteracing$igibind

ndications of digibind are-

'. 2ccidental overdose Amg". 5erum digoin level '8 ngml

*. 7ife threatening rhythm disturbance>entricular arrhythmiasrogressive bradycardia("ndor *rddegreeheart block)

" / + yr old male alcoholic presents %ith a 0 days history o$ bin!e drin1in! Serum chemistry testsreveal the $ollo%in!2Electrolytes- 3a4 &+56 74 56 l- &56 H,- &5reatinine- &5 m!.dl8lucose- &9:he nitroprusside a!ent !ives a minimally positive result ptimal therapy to ameliorate the patient'sacid-base disorder %ould include 5; dextrose in-

'. Bater

". &5-------------------------------------------------ans*. &5, insulin, and sodium bicarbonate

A. '" &5 and insulin$iscussion- 3'J -"G'"G"

?etabolic acidosis dt alcohol (alcoholic ketoacidosis). atients suffering from alcoholic ketoacidosis do well onglucose and saline. &either insulin nor alkali is re#uired unless the acidosis is etreme (bicarbonate 6H to )

" /ll are tests $or stoppa!e o$ circulation E


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fibrosisof the ventricle (eg. post-?)

Congestive 3eart Kailure

7ymphoma of the brain (ususally diffuse large cell) is increasingly common as a sporadic tumor andoccurs fre#uently in immunosuppressed patients, specially those with 2$5. t@s clinical sensitivity toglucocorticoids can mistakenly suggest a diagnosis of multiple sclerosis, and its complete

disappearence or dramatic improvement on C! after steroid therapy is baffling. 4adiosensitivity is awell known feature of most primary C&5 lymphomas, which almost always are of 1%-Cell origin.

Fibromyal!ia- 2 history of sleep distrbances and widespread musculoskeletal pain associated withtrigger points1 (localised area of tenderness on palpation).

/limentary !lycosuria /lycosuria developing after the ingestion of a moderate amount of sugar orstarch, which normally is metabolized without appearing in the urine. 5een in hyperthyroidism.

n 1-alpha-hydroxylasedeficiency deficiency of >it. $ can not be corrected by supplementation.

/uerbach's re!imeused in treatment of-- ?alignant pheochromocytoma

Sarcoidosis- mostly incidious but presents acutely as-

3eerfordt Baldenstrom syndrome 1- fever, parotid enlargement, anterior uveitis, and facial nervepalsy

7ofgren@s syndrome-erythema nodosum, arthralgias, and bilateral hilar lymphadenopathy

2 normal ?C> within " days after acute bleeding-- because %? has not got enough time to releasereticulocytes(which are larger than mature 4%Cs and could potentially increase the ?C>)

8onococcal urethritis 3on-speci$ic urethritis

/onococcal urethritis presents 1within the firstweek of seual eposure./onococccalurethritis has a thick creamy eudate

&on-specific urethritis is most commonly caused byChlamydia trachomatis. !he is "-*wks followingseual eposure. urulent eudate in non-specificurethritis is thin and watery

atient complain of dysuria and increased fre#uency of urination in both types of urethritis. /ram stain ofeudate in both types has numerous nutrophils, but in gonoccocal urethritis, gram negative diplococci arevisible in the cytoplasm. Chlamydia is not visible on routine gram stains

2llelic hetrogenicity is the phenomenon in which different mutations at the same locus(or gene) causethe same disorder. 9g. %eta-thalassemia

Bilson@s de-- wrong statement-- Ceruloplasmin6'88

$efective copper incorporation into apoceruloplasmin leads to ecess catabolism and low blood

levels of ceruloplasmin. Kew important points-

Chronic fundal gastritis aw pernicious anemia

Chronic antral gastritis aw 3.pylori infection

%arretts esophagus lt adenocarcinoma

2chalasia cardia lt s#uamous cell carcinoma

" / lady on ri$ampicin = %ar$arin develop pulmonary embolism :he best mana!ement is-

')4eplace warferin by long term eparin therapy

")/ive 7?B3

*)4eplace warferin A acetacumarinA)4eplace rifampicin A ethambutol-----------ans given

$iscussion-

') 5ince the lady is on rifampicin she must b suffering frm tb or leprosy...2s rifampicin is cidal drug and most imp

drug in treatmemt regimen of both tb and leprosy, it cannot be replaced by ethambutol, which is a satic drug. 5o i
http://var/www/vhosts/wiki/Fibrosishttp://var/www/vhosts/wiki/Myocardial_infarctionhttp://var/www/vhosts/wiki/Fibrosishttp://var/www/vhosts/wiki/Myocardial_infarction


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think warfarin should be stopped and replaced by 7?B3.

")Mea, u r right. %ut we have no such option in the #uestion. !he second option says that N/ive 7?B3N,,,, not

Nreplace warfarin with 7?B3N. 4ifampin do induce the metabolism of Barfarin in liver and affects &4. !he

induction of metabolism is unpredictable. 7ong term heparin therapy as such carries a lot of risk of complications.

2cenocumarin also interact with 4ifampin. 5o, the Ath Dption is the best option among all of these. soniazid is also

a -Cidal drug, so shd be there in therapy too.

"- Di!italis act in atrial $ibrillation by-

')increasing 2> node refractoriness

")decreasing atrial contractility

*)inhibiting &aOEO2!ase

A)inhibiting &aO3O2!ase

$iscussion- 2ns is -')

%asic mechanism to &aOEO2!ase inhibition h,then why the ans. s ')...

$igitalis also acts on the >agus nerve through the same channel, and increases its discharge(i.e., it increases vagus

tone). ncreased vagus tone in turn inhibits 2> node and make it refractory.5o, it prevents the impulses generated inatria to reach >entricles, control ventricular rate and improves hemodynamic stability in 2trial fibrillation.

" Dama!e to cate!orial hemisphere usually leads to-

a.normal speech

b.increased speech

c.decreased speech answer

d.senseless fluent speech

$iscussion- ans given for this in aa is PdQ

also causes $ysleia which is a broad term applied to impaired ability to read, due to an inherited abnormality.Causes of $ysleia

4educed ability to recall speech sounds, so there is trouble translating them mentally into sound units (phonemes).

!here is a defect in the magnocellular portion of the visual system that slows processing and also leads to phonemic

deficit. !here is decreased blood flow in angular gyrus in categorical hemisphere in both cases.

" >ost sensitive dia!nostic test + den!ue is-

a.g? elisab.complement fiation testc.neutrilization test answer... routinely done at airports in china n taiwand.electron microscopy

$iscussion- Kamous by name nsst......igm elisa was usedd to b... now it is nsst G+: sp n GG: sn...

Primary Immunode$iciency disorders

rimary ?-cell diseases include panhypogammaglobulinemia (?ruton disease) , an R-linkeddeficiency of all three maor classes of immunoglobulins, as well as other selectivedeficiencies of the immunoglobulins or their subgroups. !his condition presents after *months of age (after maternal antibodies wane) with recurrent and often simultaneous boutsof otitis media, pneumonia, diarrhea, and sinusitis.

:-cell 2mong the !-cell diseases is $i/eorge anomaly, in which defective embryologic

development of the third and fourth pharyngeal pouches results in hypoplasia of both thymusand parathyroid glands. 2ssociated findings with $i/eorge anomaly include C2!C3 C for

cardiac, 2 for abnormal faces, ! for thymic hypoplasia, C for cleft palate, and 3 forhypocalcemia.

ombined ? and :-cell diseases


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R-linked recessive Biskott-2ldrich syndrome of mild !-cell dysfunction, diminished

serum g?, marked elevation of g2 and g9, eczema, recurrent middle-ear infections,lymphopenia, and thrombocytopenia.

5evere combined immunodeficiency disease (5C$), have deficient !- and %-cells.Conse#uently, they are both marked lymphopenia and agammaglobulinemia, as well as

hypoplasia of the thymus.

2taia telangiectasia and chronic mucocutaneous candidiasis.

Complication of malaria (C327&)

Cerebral malaria Coma

3ypoglycemia

2naemia

ulmonary edema

7actic acidosis

nfections

&ecrois of renal tubules (2!&)

wind swept deformity of hands------rheumatoid arthritis

wind swept deformity of knee------rickets

most common cause of pyometra in india---carcinoma cervi

in western(developed)countries-----senile endometritis

when nothing mentioned ,,we should choose whats commoner in india and hence choose cancercervi as the answer.

n PD

?ronchitis has ?... so they are called N?lue bloatersN. Cyanosis is characteristic finding.

emPhysema has P...so they are called NPink uffersN.

?ehcet's syndrome-

'. 4ecurrent genital ulcers

". 5kin lesions

*. 9ye lesions

A. athergy test

Supraventricular tachycardia treatment 2%C$9

2denosine

%eta-blocker

Calcium channel antagonist

$igoin

9citation (vagal stimulation)

@entricular tachycardia treatment 72?%

7idocaine


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2miodarone

?eiltene ?agnesium

%eta-blocker

&eurofibromatosis diagnositic criteria (type-') C2K9 5D!

-Cafe-au-lait spots-2illary-nguinal-Kreckling Kibroma-9ye lisch nodules-5keletal (bowing leg, etc)-edigree ositive family history-Dptic !umor (glioma)

" #hich o$ the $ollo%in! is true re!ardin! /sthma-2) 4educed K4C, 4educed 4esidual >olume

%) 4educed K4C, ncreased 4esidual >olume

C) ncreased K4C, 4educed 4esidual >olume

$) ncreased K4C, ncreased 4esidual >olume-------------ans

&ecrobiosis lipoidica diabeticorum-- found over anterior surface of legs

ersons with > usually have diminished cerebral blood flow and are particularly at risk fordeveloping thrombotic complications. Kunctional platelet abnormalities may cause boththrombotic and bleeding problems(gi tract is common site of bleeding), and affected persons are

fre#uently iron-deficient. ! wave inversion of the anterior leads especially >'->A seen in--pulmonary embolism. /eneva

score is used in pul. embolism

/nti mitochondrial antibody Primary biliary cirrhosis

2nti smooth muscle antibody 2utoimmune hepatitis

Coma vigil--akinetic mutism--a state in which patient lies with eyes open, yet unresponsive tothe outside world--seen in typhoid

>ycoplasma pneumoniae--diagnosis is confirmed by Cold agglutinins. 2s in other atypical pneumonias,radiographic abnormalities may be more prominant than would be predicted by auscultation of chest (normalor nearly normal)

7issencephaly--smooth brain (lack development of gyri and sulci)

"- ?reath sounds are decreased in all except-

'. 7obar pneumonia-------ans". leural effusion*. neumothoraA. 2telectasis

9planation- $ue to consolidation in lobar pneumonia, high pitched bronchial breadth sound and whisperingpectorilo#uy are present

"#hich o$ the $ollo%in! is true re!ardin! Aheumatoid arthritis - (/l B+)a) !ypically involves small and large oints symmetrically but spares the cervical spineb) Causes pleural effusion with low sugarc) ulmonary nodules are absentd) 9nthesopathy prominent


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$iscussion- /3S I3 //2ns. is @a@ i.e., !ypically involves small and large oints symmetrically but spares thecervical spine

CD449C! 2&5 %-- 32445D& 'J,"8J-- leuropulmonary manifestations, which are more commonlyobserved in men, include pleural disease, interstitial fibrosis, pleuropulmonary nodules, pneumonitis, and arteritis.9vidence of pleuritis is found commonly at autopsy, but symptomatic disease during life is infre#uent. !ypically, the

pleural fluid contains very low levels of glucose in the absence of infection. leural fluid complement is also lowcompared with the serum level when these are related to the total protein concentration

" Hyperbaric oxy!en is use$ul in the treatment o$ all6 except2

'. CD poisoning". /as gangrene*. 2telectasis-----------------ansA. Cyanide poisoning

9planation- n atelectasis alveolar collapse leads to shunting of the desaturated blood at the alveolar capillary leveland thus the desaturated blood is not available for oygenation.

lasma levels of many polypeptide hormones(parathyroid hormone, insulin, glucagons, 73 and

prolactin) rise with renal failure. Fremic patients are also resistant to the action of insulin. !heglucose intolerance of uremia results mainly from this peripheral resistance to the action of insulin.

Fanconi Syndromeis characterised by glycosuria, aminoaciduria, and phosphaturia(mnemonic8/P). 2minoaciduria is generalised and other associated abnormalities may be bicarbonaturia,hyperkaluria, uricosuria, and sodium wasting. Clinical features are linear growth failure and vitamin $deficiency rickets. 5ymptoms typically appear in 'stsi months of life and consists of vomiting,polydipsia, polyuria and constipation.

>ycosis $un!oides-- Cutaneous !-Cell lymphoma(&37)-- name mycosis fungoidesis somewhatmisleading--it loosely means Nmushroom-like fungal diseaseN

$uring immediate *8 min postictal period serum prolactin level rises. !his does not happen inpeudoseizure-- hence used to differentiate the two

2sthma may be aggravated by Chlamydia or mycoplasma pneumoniae. !reatment with macrolide

antibiotics benefits patients with %2. n asthma airway obstruction is reversible, ?ultiple sclerosis also causes facial palsy but taste is not lost unlike in bellLs palsy

2 lesion to the left prefrontal area produces depression and uncontrollable crying. n contrast acomparable lesion to the right prefrontal area may produce laughter, euphoria and a tendency to okeand make puns.

M decent and 5* are produced in the rapid filling phase of cardiac cycle. !hatLs why 5* is also knownas filling sound.

?ineral deficiency-o Cinc de$iciencyis characterised by alopecia, a maculopapular rash around the mouth and

eyes, taste dysguesia and smell abnormalities and problems with healing of wounds.o Essential $atty acid de$iciencyis characterised by an eczematous rash and

thrombocytopenia.o >a!nesium de$iciencyis associated with resistence to activity of parathormone with

subse#uent hypocalcemia and tetany. ?uscle weakness, irritability, delirium andconvulsions are also noted. 2lcoholism is the most common cause of hypomagnesemia

o opper de$iciencyis associated with iron deficiency anemia, dissecting aortic aneurysm

and kinky hair syndrome

%ecause helper ! cells are integral to normal cellular immunity(type > hypersensitivity) tests thatevaluate cellular immunity are impaired in 3>. !his lack of immune response is called anarchy. nvitro stimulation of !-cell response to phytohemagglutinin, a potent !-cell mitogen is also impaired.

DI- 2ntithrombin levels may be low due to the combination of increased consumption anddecreased synthesis. Dther findings- 3ypofibrinogenemia, !hrombocytopenia, Kibrin degradationproducts and prolon!ed prothrombin time

hermittes si!n also known as barber chair sign is an electrical shocklike sensation (induced byfleion or other movements of neck) that radiates down the back into the legs. 4arely it radiates intothe arms. Kound in >S, Cervical spondylosis S posterior column lesion.

D@:-4isk factorso !3(Tmnemonic)-

&3, olycythemia


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!hrombophilia-- activated protein C resistance, protein C and 5 deficiency

3ematological, 3yperviscosity syndrome, Homocysteinuriao 2utoimmune-2ntiphospholipid syndrome

o $rugs-

2ntipsychotics(recent evidence)

DC *

rd

/ "

nd

/

Pierre Aobin Syndrome- isolated cleft palate, retrognathia, and a posteriorly displacedtongue(glossitis) and is associated with early respiratory and feeding difficulties

-curve phenomenon- point beyond which blood pressure reduction in hypertensivesubects is nolonger beneficial and possibly even deleterious. Clinical trials have found no evidence of U-curvephenomenonL at blood pressure reductions achieved in clinical practice.

Channelopathy of Sodium, potassium and calcium are autosomal dominant

linical Aelapse- n type /hepatitis once the patient is fully cured he may again develop symptomsof fever, malaise, anoreia and vomiting without aundice. !he 7K! is normal.

" / + yrs old lady under%ent cholecystectomy $or !all stones + hrs a$ter the sur!ery she

became con$used and developed tachycardia n examination lun!s %ere clear Her arterial blood!as analysis sho%ed p G 56 pG 6 pHG9+B :he most important next investi!ation toestablish the cause o$ her deterioratin! condition %ould be-

'. Chest roentgenogram". %lood culture*. 9C/A. 7ung scan------------ans

$iscussion- $evelopment of repiratory distress, hypoia and confusion following surgery; without anyobvious reason should make one to suspect P:E. Dther risk factors for !9 are Obesity, Pregnancy,OCPs etc. un! scannin!is the principal imaging test for diagnosis of !9, which detects perfusiondefect indicating decreased or absent pulmonary blood flow. Chest R-4ay is normal or near normal inmost cases of !9 and a normal or near normal chest R-4ay in a dyspoenic patient suggests 9. Bell

established abnormalities include focal oligemia(#estermar1s si!n), a peripheral wedged shapedopacity above the diaphragm(1Homptons hump), or an enlarged right descending pulmonaryartery(Pallas si!n). !he 9C/ is often abnormal in 9, but findings are not sensitive, not specific. 9C/changes include sinus tachycardia1, new onset atrial fibrillation or flutter and 5'I*!* (it is a sign ofacute cor pulmonale). 2ny cause of acute cor pulmonale (9, !R, bronchospasm, etc) can result in the5'I*!* finding on the electrocardiogram. /nterior : %ave inversionssuggest the diagnosis of massiveor sub-massive 9. Overall the greatest utility of the EC in the patient with suspected PE is ruling outother potential life-threatening diagnoses such as !"#

ericarditis in renal failure(acute or chronic) is an indication to initiate haemodialysis, becauseuntreated uremic pericarditis may progress to pericardial temponade. Dther indications forhaemodialysis include encephalopathy, volume overload, and intractable hyperkalemia. 2lso %?

depression, mainly due to reduced erythropoietin combined with mildly reduced red cell half-life,causes hematocrit to fall almost universally in renal failure(acute and chronic). !his does notdetermine need for dialysis.

Causes of %ide pulse pressureo 24

o 3yperthyroidism

o regnancy

o 5evere anemia

o agetLs disease

o %eri-beri

!hese are also found in (are causes of) Bater hammer pulse 5ystolic 3!

Dementia(??59 6"A) Delirium

nset nsidious 2cute

ourse Fsually protracted Fsually recover in ' week

onsciousness & Clouded


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rientation & $isturbed

>emory mmediate retention and recall normal4ecent memory disturbed4emote memory disturbed only in late stages

mmediate retention and recall disturbed1

4ecent memory disturbed

omprehension mpaired only in late stages mpaired

Sleep-%a1e cycle & $isturbed

/ttention andconcentration

& $isturbed

Diurnal variation -nt ?arked, Sundo%nin! 4nt--* Dnset oreacerbation of delirium during theevening or night

Perception 3allucinations may occur >isual illusions and hallucinations verycommon

Kirst sign seen in hypoglycemia-- loss of fine motor skills

#ernic1e's encephalopathy- classic triad(/D2)-o /lobal confusion

o Dphthalmoplegia

o 2taiaBhen the diagnosis is suspected thiamine should be administered before glucose since glucose canprecipitate worsening of the disease. ?any of the patients who recover from the acute encephalopathy willbe left with a profound defect in memory and learning ka 7orsa1o$$'s psychosis.

$rugs that can be cleared with-

3emodialysis- ?/S:

%arbiturate

7ithium

2lcohol(includes-- methanol, ethylene glycol)

5alicylates

!heophylline(charcoal hemoperfusion preferred) 2cid diuresis- , "ueens P/:

Iuinine

Iuinidine

ChloroIuine

hencyclidene

2mphetamine

Cocaine

!C2, !ocainide

2lkaline diuresis- >S PDF

?t

5alicylate, 5ulfonamide

Chlorpropamide

henobarbitone

$iflunisal

Kluorine

5aline diuresis- /? FI>

2lcohol

%r

Ca

Kluorine

&3

7i

?eprobamate 3emoperfusion- ?E8 P>:

%arbiturates

9thchlorvynol

/lutethimide
http://en.wikipedia.org/wiki/Ophthalmoplegiahttp://en.wikipedia.org/wiki/Ataxiahttp://en.wikipedia.org/wiki/Ophthalmoplegiahttp://en.wikipedia.org/wiki/Ataxia


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Chloramphenicol

henytoinrocainamide

?eprobamate?etha#ualone

!heophylline

$rugs which can-notbe cleared with hemodialysis-ABCDs

%nti-cholinergic&'C% ( Organophosphates) *en+odia+epines, *eta blockers

Compound like kerosene oil

$extropropoxyphene&Co-proxamol)

$igoxin

!he psycho!enic stuporcan be differentiated from organic stupor by-o !he dollLs head eye phenomenon or oculocephalicrefle-- absentin psychogenic stupor

o Dculovestibularrefle-- present

o rotective reflees-- present

o 4esistence to eye opening-- present

%ruit is found in hepatoma-- highly vascular tumor

4elative polycythemia (due to relative decrease in plasma volume)-- seen in den!ue hemorrha!ic $ever >it. 2 causes rupture of lysosomal membranes (but carotenoids do not cause toicity ecept a

reversible yellow discolouration of skin)

/ADI8Hypertension

& >r Sharma +0 years old has ?P o$ &5.& he has-

'. &ormal %". re hypertensive*. 5tage 3!

A. 5tage 3!---------------ans$iscussion- &ew classification of 3ypertension(V&C >)

lassi$ication Systolic Diastolic

&D4?27 6'"8 and 6 8

re-hypertension '"8-'*G andor 8-G

Sta!e & &+-&5B and.or B-BB

5tage " 'H8 andor '88

"solated systolic'

1./ and 0 /

o Cuff width should be *.,Jof arm circumference

o $iastolic pressure disappearance of sounds (Eorotkoff >1)-- 2/9 "88o seudohypertension- seudohypertension is when blood pressure measurements are elevated

but the blood pressure is actually normal. 5een in elderly dt arterioloscerosis(notatherosclerosis)

8oldblatt hypertension is seen in-

'. 4enovascular disease----------------ans". $rug induced*. 2drenal medulla tumorA. Children

$iscussion-

4enovascular disease (4enal artery stenosis)-- 8old ?latt 1idney ?ost fre#uently atheromatous(elderly, cigarette smokers with peripheral vascular disease) or

$ibro muscular dysphasiaJin young ladies

!he kidney with 425 becomes 1small and shrunken. !he decrease in bloodflow to the kidneywith 425 (/oldblatt@s kidney) causes hyperplasia of V/ appratus and increased renin production


12/61

which lead to retention of sodium and also produces 3! but escapes the effects of 3! dt stenosis.!he other kidney however shows microscopic shanges of benign nephrosclerosis (hyalinearteriolosclerosis) dt effects of 3!.

425, can occur in :a1ayasu disease but it does not occur in 2&

3ote %est screening test for 425 is /adolium enhanced ?4 angiography.(&.I)reviously it used to be

34C!. ?ost con$irmatorytest for 425 is conventional angiography.(K2I)

Krom copy-ncreased renin-

'. 4. 4enal 2rtery". 4. 4enal >ein-------------ans*. 7. 4enal 2rteryA. 7. 4enal >ein

, /ll are causes o$ hypertension %ith hypo1alemia except-

'. %ilateral 425". C4K-----------------------ans(hyperkalemia)

*. Conn syndromeA. Crushing syndrome

$iscussion-

3! also occurs in 24K2c. /lomerulonephritis?C cause of sec. 3!-- 4enal

" ?P in pheochromocytoma-

'. 5ustained 3!". 5ustained 3! with post. hypo*. 9pisodic 3!A. 9pisodic 3! with post. hypo---------------ans(post.-- ostural Ck)

$iscussion- (T""HG 3'J)K&2C not done in pheochromocytoma because-- 3ighly vascularheochromocytoma-- 5 -- % decreases-- give &5

Hypertension >ana!ement2

?P G ardiac output() x Peripheral resistance(PA)

G Heart rate(HA) x Stro1e volume(S@)

5o, ?P G HA x S@ x PA

2. Dru!s %hich reduce HA- %eta blockers%. Dru!s %hich reduce stro1e volume-

'. ?eta bloc1ers2 beta blockers have negative inotropic S negative chronotropic effects (so betablocker should be used with caution or should be avoided in HFJ with 3! )

". Diuretics !hey reduce blood volume so they reduce the preload1*. 3itrate!hey primarily dilate the venules thereby cause peripheral pooling of blood. 5o they

reduce the preload.C. Dru!s %hich reduce the peripheral resistance-

1# %lpha blockers2# Calcium channel blockers3# %CE-"4A. $irect vasodilators W3ydralazine, alpha-?ethyl $opa, 5odium &itroprusside(2O>), indapamideX

+. %osentan (&ew I)-- 9ndothelial receptor blocking drug (ri. ul. 3!, 4aynaud@s de)

&ew drugs for 3!- 2liskiren, Kendolpam3ever use sublin!ual ni$edipineJ to reduce ?P (bi! drop in ?P and increase stro1e ris1 )(3")nection frusemide should not be used in severe 3! %ut can be used in severe 3! in 7>K.(&I)

% T CD 4 --


13/61

'. 5ystolic". $iastolic*. ?2----------------ansA.

9nd diastolic volume-- '"8 ml 9nd systolic volume-- A8 ml

5troke volume-- mlJ

9K-- "* (HH:)

&9K-- H+-J": (Ck)

5ingle best test to calculate 9K-- 9chocardiography

$iuretic not used in which 3!-

heochromocytoma (already dehydrated)

also olycythemia(3'J -*H")

HF+ Earliest si!n o$ @F-

'. 5*". %asal crepitation*. !achycardia-------------------ansA. 4aise V>

$iscussion-(3'J -'AA*)

7>K- of choice-- 9K

'. 4esting tachycardia1 (9arliest feature of 7>K-- !achycardia)

". ulsus alternans1*. 2uscultation S, !allop1 (%est feature of 7>K but heard normally in Children, regnancy)

5igns of 4>K Aaised @P, 9dema 2scites , 3epatomegaly

&5 Pulsus alternans is seen in-'. 2ortic regurgitation". 3ypertrophic cardiomyopathy*. 2-> blockA. 5evere 7>K----------------ans

$5CF55D&5-

?is$eriens pulse(!wo systolic peaks)- 241, 24 with 251, 3DC?1 (%isferiens pulse is best

assessed in 1branchial.radial artery)

Dicrotic pulse (!wo waves Dne is systole and one is diastole)-$ilated cardiomyopathy4.

Pulsus alternans(regular alteration of amplitude with regular rhythm)- 5evere 7>K1. (5-* isfound with ulsus alternans)

Pulsus paradoxus (decrease in systolic arterial pressure during inspiration)- ericardialtamponade1, 5evere CD$, %ronchial 2sthma1, 5>C obstruction

5 #hich is not a maKor Framin!hams criteria in HF-

'. Cardiomegaly". aroysmal nocturnal dyspnea*. 5-* gallopA. 3epatomegaly-----------------ans

$iscussion-Framin!ham criteria $or dia!nosis o$ HF

?aor criteria-'. aroysmal nocturnal dyspnea


14/61

". 4aised V>*. CrepitationsA. Cardiomegaly+. 2cute pulmonary edemaH. 5-*J. ncreased venous pressure('Hcm 3"D)

. ositive hepatougular reflu

?inor criteria-'. 9tremely edema". Drthopnea(night cough)*. $yspnea on ecretion.# epatomegaly+. leural effusionH. >ital capacity reduced by '* from normalJ. !achycardia ('"8m)-- Earliest criteria even though a minor criteria

2t least one maor and two minor criteria are re#uired1

0 #hich o$ the $ollo%in! is not seen in HF-

'. ncrease serum sodium--------------------------ans(2/ "88J)". ncrease catecolamines*. ncrease blood ureaA. edal edema

$iscussion-ompensatory mechanism-

'. ncrease epinephrine t leads to tachycardia". ncrease no r- epinephrine t leads to increase peripheral resistance, there-by blood supply to

muscles and skin is reduced but blood supply to heart and brain is normal*. 4educe renal blood flow t lead to prerenal azotemia and hyperaldosteronism

A. ncrease aldosterone t leads to more &a and water retention but primary &aO gain is eceededby secondary water gain....(5ee ?E >ol-' -"G8 for more)

ercentage of blood flow to Eidney- "8:

C3K (Cold etemities-- 7ess blood to skeletal muscle and skin)

C3K decreased bood flow to kidney-- hyperaldosteronism but dilutional hyponatremia

3yponatremia without edema 52$3

&ew drugs for C3K-

9pleremone-- 2ldosterone receptor blocker

&esiritide

9 #hich o$ the $ollo%in! a!ents does not reduce mortality in patients %ith con!estive heart $ailure-

'. $igitalis----------------ans(E$! T+8')". Kurosemide*. 9nalaprilA. %eta blocker

$iscussion-%asic principle of drug therapy in C3K(3'J -'AAG)-

'. $rugs to reduce preload T &D*, diuretic". $rug to increase pumping of myocardium T digoin*. $rug to reduce after load T 2C9-

(9tra Iuestion- Controversial #uestion)" #hich o$ the $ollo%in! a!ents is contraindicated in patients %ith HF-

'. $igitalis". Kurosemide*. 9nalaprilA. %eta blocker-----------------ans(5ee eplanation to I-*)


15/61

ardiomyopathy-- -'A' 3'J

ardiomyopathy is seen in all except-'. ompeLs disease". KriedrichLs ataia

*. 7owe syndrome--------------------------ans (/II>S 3ov 9)A. $uchenne ?uscular dystrophy$iscussion-Dilated cardiomyopathy2 re-disposing conditions

& /lcoholJ". $rugs doorubicin(causes irreversible dose dependent cardiomyopathy), Cyclophosphamide1,

Cocaine(also vasoconstriction-- ?), matinib,trastuzumab*. 2utoimmuneA. eri- or postpartum1+. 5elenium deficiency1H. $uchenne myopathy1J. KreidrichLs ataia. /lycogen storage disease(ompeLs disease)

B S/> is seen in-

'. 3DC?---------------------ans". Constrictive pericarditis*. $C?A. 4estrictive C?

$iscussion- 52? 5ystolic 2nt. ?ovement of ?itral valve

Hypertrophic cardiomyopathy(H>)2'. 2utosomal dominant inheritance1

". J8: have mutations in genes encoding beta-myosin, alpha-tropomyosin, and troponin-!*. Kamily history of sudden death may be there

Symptoms = si!ns2'. 5udden death(2lso in 25,?,?>)". Verky carotid pulsation1(K2I)*. @a@ wave in V>A. $ouble ape beat1(K2I)+. 5A heart soundH. 3arsh eection systolic murmurJ. !he intensity of murmur increases on standing and >alsalva1(most commonly asked #uestion in

world)-- also see I-'J

9cho 52?-- 5ystolic anterior movement of mitral value1.

4 5eptal myomotomy-- surgical or chemical with 1alcohol(absolute alcohol)

$rugs contraindicated $igoin(absolutely), &itrates, %eta agonist, $iuretics

Pericardial diseases

&& Pulsus paradoxus is seen in-'. Cardiac tamponade--------------ans". ulmonary oedema*. 5-*A. C

$iscussion-

ardiac tamponade-

Si!ns pulsus paradoxusJ,Ewart sign is positive4, 53 is absent4, 6 descent is never prominent4


16/61

Dia!nosis ?ec1s triad-

'. Kalling %". 4ising V>*. 5mall, #uiet heart

E82 Electrical alternansJ6 lo% volta!e E8J

Echo is dia!nos tic 2 echo-free +one around the heart

& #hat is not seen in P(onstrictive Pericarditis)-

'. &ephrotic syndrome". rotein losing enteropathy*. 5-* ---------------------------------ansA. Eussmaul sign

$iscussion-Constrictive pericarditis does notoccur in rheumatic pericarditis(K2I)

Clinical Keatures !hese are mainly of right heart failure with raised V>;Kussmauls signis positive(V> rising paradoically with inspiration).Prominent ! descent4, 5-3 absent, diastolic pericardial

1noc1J, hepatosplenomegaly, ascites and oedema. !he apical pulse is reduced and may retract insystole(?roadbents si!n)

&% $iastolic pericardial knock is also heard in early diastole. 5-* is also heard early diastole but 3arrison'Je !able "*"-", age &o. 'AG' mentions that 5-* is absent in C.

Complications-'. &ephrotic syndrome1". rotein loosing enteropathy

" / ,5 yrs old male . substernal chest pain a!!ravated by inspiration and relieved by sittin!up He has a H. :? un! $ields are clear to auscultation6 and heart sound are some%hat distant

entricular premature contractions

$5CF55D&- 5ystolic but not pansystolic. nasystolic murmur is seen in !4.


17/61

>itral valve prolapse-

t is the commonestvalvular lesion in the world. t is seen in 1+-J: of the young girls. Occurs alone orwith7 %5$, P$%, Cardiomyopathy, 'urner8s syndrome,"arfans syndrome#Osteogenesis imperfecta,Pseudoxanthoma elasticum, 9P9 syndrome

5ignsa. &on eection!id-5ystolic click4b. 2 late systolic murmur4. ("ntensity of the murmur increases on standing and :alsalva4)

& e$t ventricular hypertrophy is not seen in-'. ?5-------------------------ans". 25*. 2ortic incompetenceA. 9ssential hypertension

$5CF55D&- (K2I)>S(3'J -'AH+)-

Presentation $yspnoea1 on eertion (main symptom); hemoptysis1, 3oarseness of voice

(2utner syndrome)

n auscultation;oud 5-14< Opening snap4&pliable valve4)< rumbling mid-diastolic murmur4,7oud ". /raham steel murur of 4 and Car$ello sign&murmur is loud during inspiration) alsofound#

Severity is indicated by- 7onger the diastolic murmur, the closer the opening snap to 2-"

Echocardio!raphy dia!nostic. 4educed 9K slope is characteristic1

7>3 and 5* not found in ?5.

&B >itral re!ur!itation may occur in-'. ?itral valve prolapse

". 4upture of papillary muscle*. 4upture of chordae tendineaeA. 2ll----------------------------------------ans

$5CF55D&->itral re!ur!itation(3'J -'AHG)-auses

a. Kunctional(7> dilatation)b. 2nnular calcification(elderly)c. 4heumatic feverd. nfective endocarditise# !itral valve prolapsef# =upture chordae tendinea

g# Papillary muscle dysfunction>ruptureh. Connective tissue disorder(Ehlers-$anlos,!arian8s)i. Congenital(may be associated with other defects.eg 25$,2> canal)

Symptoms 9asy fatigability1 (commonest symptom)

Dancin! carotids is also 1no%n as-

'. 3illLs sign". IuinckeLs sign*. CorriganLs sign----------------------ansA. !raubeLs sign

$5CF55D&-(2?5 ?ay "88+)/A- eripheral signs 1-

'. /ustin Flint murmurJ may be heard in severe 24". ollapsin!(water hammer) pulseJ*. orri!ans si!n1 (carotid pulsation)A. de >ussets si!n1 (head nodding)+. DuroLieLsi!n1 ($emoral diastolic murmur as blood flows backwards in diastole)


18/61

H. Hill Si!n-% difference in upper and lower limb-- (F7677)J. "uinc1es si!nJ(capillary pulsations in nail beds). :raubes si!nJpiston sound over femoral arteriesB #ide pulse pressureJ

& Hepatome!aly %ith liver pulsations indicates-

'. !4------------------------------ans". ?4*. ulmonary hypertensionA. ?5

$5CF55D&- (2/ "88G):ricuspid re!ur!itation2auses-

'. Kunctional (Commonest cause of !4) seen in cor-pulmonale1". ulmonary hypertension

Si!ns2 iant ?v? waves4,rominent?y? descent4in V>,Pansystolic murmur4, arvallos si!n, ulsatilehepatomegaly1, aundice, ascites

H/E7 does not include-

'. 3aemophilus influenze------------ans". 2ctinobacillus*. CardiobacteriumA. 9ikenella

$5CF55D&- (2?5 ?ay "88J)

32C9E

aemophilusspecies &aemophilus parainfluen+ae, aemophilus aphrophilus, aemophilus

paraphrophilus)

%ctinobacillus actinomycetemcomitans

Cardiobacterium hominis

Eikenella corrodens @ingella

Commonest cause of native endocarditis-- 5.aureus(3'J)

E8

, Prolon! ": interval is seen in(>:A)-'. C4K----------------ans". Cirrhosis*. CD$

A. &one$5CF55D&- (5ee I-*")3ormal ":2 ,0-++ secJProlon!ed ": intervalJ 9lectrolyte imbalance (3ypokalemia1, 3ypocalcemia1, 3ypomagnesemia1),Class '2 anti arrhythmic drugs(Auinidine1) bradycardia, head inury, hypothermia, sotalol4,antihistamines, macrolides4(eg erythromycin), amiodarone1,Phenothia+ine4, 'ricyclic1, !orse $eointes(caused dt hypokalemia)

Short ": interval 3yperkalemia, 3ypermagnesemia, Class '% anti arrhythmic drugs, $igoin, 2cute ?

+ / 9, year old patient develops acute renal $ailure secondary to bladder obstruction His serumcreatinine is m!; %ith potassium o$ 05 meM. :he patient had an electrocardio!ram6%hich

revealed pea1ed : %aves as the only abnormality It the hyper1alemia %ere not corrdcted 6%hat%ould be the expected next electrocardio!raphic abnormality-

'. !-wave inversion". 4 prolongation and -wave flattening------------ans*. rolongation of the I45 interval

A. Bidening of the I45 interval


19/61

$5CF55D&-(2/ "88) K2I

Hyper1aliemia !all, tented ! wave1, rolong 4, -Bave disappear, Bide I45 (Usine %aveL appearance)Hypo1aliemia ! wave become smaller and then disappear, prominent F waves1, prolong 4, 5! segment sagging.

5 E8 chan!es in >obitL type I is-

'. rogressive 4 interval prolongation with a wave followed by dropped I45-------ans

". I45 wide with 5! and ! directed opposite to I45*. 4 interval is 8.H" secA. 4 and ! phenomenon

$5CF55D&-(Confusing #uestion)rogressive 4 interval prolongation with a wave followed by dropped I45

0 First E8 chan!e in acute >I is-'. 5! segment elevation". 7oss of 4 wave*. nverted ! waveA. !all peaked ! wave-------------------ans

$5CF55D&- (Confusing #uestion) / $ec "88H?

Bithin minutes the ! wave may becomepeaked4 (9arliest features)1

Bith "-* hrs 5! segments may begin to rise(Pardees sign)1

Bithin -'" hrs the ' wave inversion4

Bithin "A-Ahrspathological B waves4begin to form. I waves usuallypersist in old !"4

:all :is the earliest manifestation of acute ?.(K2I)

/D

9 / + year old man6 smo1er6 complains o$ epi!astric pain since an hour n electrocardio!raphic

examination he is $ound to have S: elevations su!!estin! an in$erior %all in$raction 3ext step in themana!ement %ould be-

'. 2spirin---------------------------ans". !hrombolytic therapy*. antoprazoleA. %eta-blockers

$5CF55D&- (Confusing #uestion) 2?5 &ov "88J

%est method to diagnose angina-- 3istory

2dd beta-blocker in all cases of angina if no C eists

5ee net #uestion

Initial treatment o$ choice $or a patient o$ anterior %all >I %ith cardio!enic shoc1 is-'. !C2--------------------------------------------ans". ntra aortic balloonpumping(2%)*. 5treptokinaseA. $opamine drip

$5CF55D&- 2/ "88 (Confusing #uestion)--3'J -'+'A

?asic concept o$ mana!ement o$ >I (oncept o$ Aeper$usion therapy and concept o$ myocardiumsalva!e)>ana!ement o$ acute coronary syndrome (/S)-

& /spirin

". :hrombolysis (if no contraindication) or primary angioplasty*. %eta-blockerA. 2C9-inhibitor=ole of %CE" in acute !" !o control %, !o control 7>K.!o help in the

remodelling of infarct tissue

AolaLapine-t is new angina drug useful for refectory angina (&ew $rug)


20/61

Extra " (/II>S >ay ) Dru! used to per$orm stress EH-a. !halliumb. $obutamine-------------ansc. $opamined. 2denosine

B >ost important pro!nostic $actor in an in$arct case is-

'. 9ection fraction------------------ans". CE*. >entricular tachycardiaA. 7eft main coronary artery obstruction

$5CF55D&- 7illip's lassi$icationfor assessing the prognosis of a case of ?. t is based on degree of7> dysfuction)-

Feature >ortality

Class - &o signs of pulmonary or venous congestion +-'8:

Class - Crepts at lung bases, 5*, tachypnea 8-"+:Class - 5evere heart failure, ulmonary edema, systolic % G8 +8-H8:

Class >- Cardiogenic shock, systolic % 6 G8 mental confusion, cyanosis 8-G8:

, #hich dru! is used to prevent restenosis in stent-

'. 5irolimus-----------------ans". Cyclosporin*. rednisoloneA. 9rythromycin

$5CF55D&- (&ew Iuestion)Percutaneous transluminal coronary an!ioplasty (P:/)involves balloon dilatation of the stenoticvassel(s). Stentin! reduces restenosis rates $rug-coated stents reduce restenosis. $rug use israpamycin4, sirolimus, paclitael(?CI)

redisposing factors for ventricular free-wall rupture after ? include advanced age as well

as the first ?, probably dt lack of coronary collaterals. ?ost commonly seen bn '-A daysafter ?. 7ateral and anterior walls are most often involvedand it is typically seen with large

? involving "8: of the ventricle. 4upture typically occurs at the unction of infarct withthe normal tissue. atients are diagnsed by 9C/ and treatment involves operative treatment

if possible.

/rrhythmias,& / + year man is admitted to N %ith an acute in$erior >I :%o hours a$ter admission6 his ?Pis 0.5 m!H!O his pulse is +.mt %ith sinus rhythm#hich o$ the $ollo%in! %ould be the mostappropriate initial therapy-

'. mmediate insertion of a temporary transvenous pacemaker". > administration of atropine sulfate, 8.H mg--------------------ans*. 2dministration of normal saline, *88ml over '+ minA. > administration of dobutamine, 8.*+ mgmin

$iscussion- (2?5 &ov "88)2tropine-- unsucessful-- 5aline

, :orse-de-pointes is caused by-'. 3ypermagnesemia". 3ypokalemia-------------------ans*. 3yperkalemiaA. 3ypercalcaemia

$5CF55D&-


21/61

3ypokalemia (commonest cause)

rolonged I!c interval1

9C/ oscillates along baseline--

Causes- Common causes for torsades de pointes include diarrhea,hypomagnessemia andhypokalemia.$rug interactions such aserythromycinor moifloacin, taken concomitantly with inhibitors likenitroimidazole, dietary supplements, and various medications like methadone,lithium, tricyclicantidepressants orphenothiazines may also contribute.

!reatment->a!nesium sul$ate

ardiac 3eoplasm

,, :rue statements re!ardin! cardiac neoplasms include-'. 7ymphoma is the most common malignant neoplasm that primarily involves the heart". !he most common site for a myoma is the right atrium*. ?yomas may arise as part of a familial syndrome that also includes pigmented skin lesions and

endocrine abnormalities--------------------ans(A. 2 midsystolic YplopZ typically indicates the presence of a cardiac myoma

$5CF55D&(3'J -'AG+)- Cardiac myoma is a rare benigncardiac tumour in 1left atriumusually sporadicJ, may be $amilialJ (autosomal-dominant)J t may mimic infection endocarditis(fever, weight loss, clubbing, raised 954), or mitral stenosis4 (left atrial obstruction, systemic emboli, 2f).2 Utumour plopL may be heard, and signs may changed according to posture. 3istologically they arecomposed of stellate cells in a loose myoid background.n contrast Ahabdomyomasare the most common primary cardiac tumors in infants and childrenand

often occur in aw tuberous sclerosis. 3istologically the so-called spider cells may be seen. apillaryfibroelastosis usually are incidental lesions found at the time of autopsy and are probably hamartomasrather than true neoplasms.

arney complexcomprises-'. myomas (cardiac1, skin, andor breast),". lentigines andor 1pigmented nevi, and*. endocrine overactivity (primary nodular adrenal cortical disease with or without Cushing@s

syndrome, testicular tumors, andor pituitary adenomas with gigantism or acromegaly).

Certain constellations of findings have been referred to as the &2?9 syndrome (nevi, atrial myoma,myoid neurofibroma, and ephelides) or the 72?% syndrome (lentigines, atrial myoma, and blue nevi),

although these likely represent subsets of the Carney comple.

!ests 9nchocardiography!reatment 9cision

Aheumatolo!y

,+ :3F- alpha is involved in the patho!enesis o$ %hich o$ the $ollo%in! disorder-

'. 42-------------------ans". 579*. soriasisA. &one

$5CF55D&-(?aheshwari -"AA) !&K-alpha is involved in the pathogenesis of 42Dia!notic criteria o$ A/-Four of seven criteria are re#uired1

'. !orning stiffness- lasting ' hour before maimal improvement". %rthritis of 3 or more oint areas-'A possible oint areas are right or left , ?C, Brist, 9lbow,

Enee, 2nkle, and ?! oints
http://var/www/vhosts/wiki/Diarrheahttp://var/www/vhosts/wiki/Hypokalemiahttp://var/www/vhosts/wiki/Erythromycinhttp://var/www/vhosts/wiki/Moxifloxacinhttp://var/www/vhosts/wiki/Methadonehttp://var/www/vhosts/wiki/Lithiumhttp://var/www/vhosts/wiki/Tricyclic_antidepressantshttp://var/www/vhosts/wiki/Tricyclic_antidepressantshttp://var/www/vhosts/wiki/Phenothiazineshttp://var/www/vhosts/wiki/Magnesium_sulfatehttp://var/www/vhosts/wiki/Magnesium_sulfatehttp://var/www/vhosts/wiki/Diarrheahttp://var/www/vhosts/wiki/Hypokalemiahttp://var/www/vhosts/wiki/Erythromycinhttp://var/www/vhosts/wiki/Moxifloxacinhttp://var/www/vhosts/wiki/Methadonehttp://var/www/vhosts/wiki/Lithiumhttp://var/www/vhosts/wiki/Tricyclic_antidepressantshttp://var/www/vhosts/wiki/Tricyclic_antidepressantshttp://var/www/vhosts/wiki/Phenothiazineshttp://var/www/vhosts/wiki/Magnesium_sulfatehttp://var/www/vhosts/wiki/Magnesium_sulfate


22/61

*. 2rthritis of hand ointsA. 5ymm etrical arthritis+. 4heumatoid nodules1H. ositive 5erum rheumatoid factor1J. 4adiographic changes- erosions(3allmark) or une#uivocal bong decalcification localized in or

most marked adacent to the involved oint.

%ackache never a symptom of 42.......

,5 False positive Aheumatoid $actor can be associated %ith all except-

'. nflammatory bowel disease--------------ans(5ee I-*J)". 3bs2g*. >$47A. Coombs test-- diagnose 579

$5CF55D&-7aboratory findings in 42- 42 factor(g?) is positive in J+: patients of 42 though it is found in +: ofhealthy persons. 2nti P antibody are also seen.

!he presence of 4heumatoid factor in 42 correlates with etraarticular menifestation of thedisease

ther conditions in %hich A/ $actor is positive are- SE, 5ogrenLs syndrome, nterstitial pulmfibrosis, Hepatitis ?, 7eprosy, 5ubac. bacterial endocarditis, Chronic liver disease, 5arcoidosis, ?&,!uberculosis, Syphilis,>isceral leishmaniasis, ?alaria

:reatment o$ A/ (7D: P-)-

'. &52$5 - !o control the symptoms and signs of local inflammatory process. !hese drugs haveminimal effect on the progression of the disease.

". $isease modifying antirheumatic drugs - !hese drugs alter the course of 42. !hese drugs haveminimal effect on the inflammation. 5o are not useful as analgesics. !hese drugs should be usedearly1 in the course of the disease as they slow the progression of disease. !he most commonlyused $?24$ is ?ethotreate.'. Immunosuppressants- !he immunosuppressive drugs used are ?ethotreate, 2zathioprine,

leflunomide, cyclosporine and cyclophosphamide

". Dther drugs- d-penicillamine, and sulfasalazine, /old , 3ydroychloro#uine*. %iological response midifiers-

& :3F alpha neutraliLin! a!ents-

'. >onoclonal antibodyto !&K alpha (In$liximab)". !&K-alpha type [ receptor antagonist (Etanercept)(&ew $rug)*. /dalimumab(3uman antibody to !&K)(&ew $rug)

". I-&4eceptor antagonist T 2&2E&42 I (&ew $rug)A. 2duvent drugs - Corticosteroids+. /ene therapy - /enes which intercept the pathway of inflammatory cascade reaction are usedH. 5urgery - 5ynovectomy, tenosynovectomy, arthroplasty and total oint replacements

,0 Aituximab (/nti-D antibody) is used in all except-

'. 579". 42*. &3----------------ansA. &37

$5CF55D&- (2?5 &ov "88) Aituximab(anti D antibody)-- C77 also

,9 Serone!ative arthritis include-

'. 25

". 4eiterLs arthritis*. soriatic arthritisA. all------------------------ans

$5CF55D&-


23/61

Spond ylo -/rthrosis

t is a group of disease which include-'. 2nkylosing spondylitis". 4eiterLs disease*. 4eactive 2rthritis(Mersinia,5almonella,/onococcus)

A. soriatics arthritis+. Vuvenile rheumatoid arthritis(V42)Wnot adult rheumatoid arthritis which is $BA$4AX

Keatures'. 5eronegativity". 372 ?9 associated*. 2ial arthritis athology in spine (5pondylo-)and sacroilias (5) oints(%ackache is the presenting

symptom)A. 2symmetrical large-oint oligoarthritis(i.e. 6+ oints) or monoarthritis+. 9nthesitis nflammation of the site of insertion of tendon or ligament into boneH. 9tra-articular manifestations eg. anterior uveitis, aortic regurgitation, CrohnLs or FC

AEI:EAS DISE/SE(Imp)2t is characterised by a triad of-1# 5eronegative oligoarthritis42# Conunctivitis*. Donspecific urethritis, '-* weeks following bacterialdysentery(epidemic form) or eposure to

seually transmitted disease2rthritis occurring alone following seual eposure or enteric infection is known as reactive arthritis.4eiterLs disease can occur in epidemic1 form(K2I) 2?5 &ov "88 9am

Etiolo!y- 9nterpathogenic %acteria in 4eactive 2rthritis 5almonella,5higella,Campylobacter,MersiniaChlamydia

linical Features-

'. t presents with monoarthritis of a knee or an asymmetrical inflammatory arthritis ofinterphalangeal oints

". atient can have heel pain.2chilles tendinitis or plantar fasciitis with presence of circinatebalanitis. (resence of rash of keratoderma blennorrhagia(2?5 &ov "88) is diagnostic of4eiterLs disease in the absence of classical traid.)-- Ck printed matter

*. Dcular involvement (mild bilateral conunctivitis)

9tra #uestion-" ircinate balanitis is seen in(/IP8 9)-

'. 42". 579*. 4eiterLs disease----------ans

A. /out

" #hat is not seen in Aeiters syndrome(/II>S 3ov )

'. 5ubcutaneous nodules---------------------ans". Eeratoderma blennorrhagicum*. Circinate balanitisA. Dral ulcers

, Schirmer test is positive in-'. 5ogrenLs syndrome------------------ans". %ehcetLs syndrome*. 579

A. BhippleLs diseaseDiscussion-

S8AE3S S3DA>E-

De$inition- Chronic, slowly progressive autoimmune disease characteried by lymphocytic infiltration of


24/61

the eocrine glands resulting in erostomia and dry eyes.

Causes of secondary 5ogren@s syndrome-

'. 4heumatoid 2rthritis(most common cause)". 579*. 5clerodermaA. ?ied connective tissue disease+. rimary biliary cirrhosisH. >asculitisJ. Chronic active hepatitis. olymyositisG. 3ashimoto@s thyroiditis'8. nterstitial pulmonary fibrosis

2ntibodies to Ao.SS-/ and a.SS-? anti!ens; 2ntibodies to alpha-$odrin-- a salivery gland specificprotein

&37 common in 5ogren ans also in 3>........

linical >eni$estations(:riad)-

'. $ry eye". $ry mouth*. %7 arotid enlargement

,B Sudden renal $ailure occurs in-

'. 579". 55---------------------ans*. 42A. 25

$5CF55D&-

SS:E>I SEASIS-

$efinition- !his is a generalised disorder of connective tissue characterised by fibrosis and degenerativechanges in the skin (scleroderma) and many internal organs$iagnosis 2ntibodies seen are-

'. %ntinuclear antibodies(2&2)". 2ntibodies to single stranded 4&23# %nti-5cl-/

art of Crest 5yndrome(2nticentromere 2b)

+ #hich radiolo!ical $eature is most important to help di$$erentiate rheumatoid arthritis %ithSE-

'. 9rosion---------------------------ans". Vuta articular osteoporosis*. 5ubluation of ?C ointA. 5welling of oint

$5CF55D&-aboratory $indin!s in a cause o$ SE 2ntibodies. !he antibodies seen in 579 are-

'. 2ntinuclear antibodies (2&2) - ?ost sensitive test

". 2nti ds D&2- most speci$icJfor 579. 3igh titres are associated with nephritis and disease activity.*. 2nti 5m [ 2lso specific for 579

A. 2nti- 4o (55-2) [ 2ssociated with subacute cutaneous lupus and%D% negative lupus+. 2nti-7a (55-%) [ 4isk for nephritis is low if present

H. 2nti-histone - ?ore fre#uent in drug induced 79.J. N&A3P ab -5een in mi connective tissue disorder. Bhich include 579,55 and polymyositis

+& >ost speci$ic dia!nostic $indin! in !out is-

'. 4aised serum uric acid


25/61

". Fric acid crystals in urine*. resence of monosodium urate crystals in synovial fluid under polarized microscopy---------ansA. resence of calcium pyrophosphate crystals in synovial fluid under polarized microscopy

$5CF55D&-

8out-

'. >ales females. 8reat toe, /rade +tenderness". resence of monosodium urate crystals in synovial fluid under polarized microscopy (5erum uric

acid level may be normal)*. Kor acute pain [ colchicine, indomethacin (%ut aspirin is contraindicated)A. Kor prophylais- 2llopurinol+. Fricosuric drugs- robenecid, 5ulphinpyrazone

+ -/3/ /b are seen in-

'. Begener@s granulomatosis----------------ans". 2&*. Chrug-5traussA. 579

$5CF55D&-(2?5 ?ay "88J) -/3/antibodies are seen in #e!eners !ranulomatosisthese are directed against

proteinase-,

-2&C2 antibodies are seen in ?icroscopic polyangitis, Churg-5trauss syndrome, Crescenticglomerulonephritis, /oodpastureLs 5yndrome

+, A/S is seen in all except-'. 2&------------------------------ans". !akayasu*. 2therosclerosisA. Kibromuscular dysplasia

++ :rue about !iant cell arteritis are all except-'. 3igh dose steroid is drug of choice". 954 is usually elevated*. nternal carotid artery is particularly susceptibleA. ?ainly affect people below age of A8 years-----------------------ans

$5CF55D&-

:emporal arthritis(olymyalgia rheumatica fre#uently occur with !emporal arteritis)-

?ainly effect people above age of H8 years

3eadache

nternal carotid artery is particularly susceptible

>isual disturbance can occur (affects retinal 2.-- branch of nt. Carotid)

954 is usually elevated

3igh dose steroid is drug of choice

+5 /ll o$ the $ollo%in! are true about 7a%asa1i disease except-

'. 4ash". 7ymphadenopathy*. 9tremities edemaA. urulent conunctival congestion----------------ans

$5CF55D&5- (2/) 3'J -"'*8'. 4ash". 7ymphadenopathy (does not respont to antobiotics)*. 9tremities edemaA. Conunctival congestion it is non-purulent

4 >g

+0 /nti o-& antibody = /nti synthetase antibody are seen in-

'. 5ystemic lupus erythematosus


26/61

". 5ystemic sclerosis*. $ermatopolymyositis----------------------ansA. $ermatitis herpetiformis

$5CF55D&-n polymyositis eye muscle are not involved and biopsy is confirmatory.

+9 >ali!nant A/ occur i$ there is severe involvement o$-'. 9ye". 5kin------------------ans*. &erveA. Voint

$iscussion- t is a very simple and easy #uestion\\\\

3ENA8

4efresh your knowledge of neuroanatomy to understand &eurology much better....

erebral Hemisphere

+ / , year6 male c.o headache $or last & year = !radually pro!ressive paraparesis $or last &month >ost li1ely cause-

'. 2C2 infarct". ?eningioma----------------ans*. !% spineA. ?C2 infarct

(Extra "uestion) >/ in$arct leads to contralateral-'. 7eg paralysis

". 2rm paralysis*. %oth------------------ansA. &one

+B #hich statement re!ardin! 8erstmanns syndromeJ is true-

'. 2ffected patients have difficulty distinguishing right from left----------------ans". t results from a lesion of the nondominant parietal lobe*. ?otor deficit is a prominent featureA. 2praia is common

$iscussion- ($/ "88H)

Parietal lobe-

/ Dominant parietal lobe

Disease /artsman syndrome1

Features2'. 2calculia". 2graphia*. Kinger anomia(can not name finger)A. $ifficulty in ri!ht and le$tdifferentiation

Extra points

F rontal lobe Disease Koster Eennedy syndrome1. psilateral optic atropy and contralateralpapilledema. t results from the simultaneous presence of raised intracranial pressure and opticnerve compression secondary to tumor [ classically due to a meningioma of the olfactory grooveor more commonly due to a meningioma of the sphenoid wing.

ccipital lobe disease Cortical blindness1


27/61

:emporalJ lobe disease Eluver %ucy syndrome1(%ilateral temporal lobe involvement)

5 I$ #ernic1es area is dama!ed in the dominant hemisphere6 it %ill result in-'. rrelevant and rapid speech------------------------------------ans". 5enseless speech and difficulty in outflow of words*. 5peech with difficulty in outflow of words

A. 5peech with difficulty in naming obects

$iscussion-

Speech-

/natomy = Physiolo!y-

%rocaLs area T 7ies in dominant inferior frontal gyrus1. t is motor speech area(5peech outflow isdisturbed in inury)

BernickeLs area T 7ies in dominant temporal lobe1. t is sensory speech area

2rcuate fibres T !hey connect the two speech areas

Physiolo!y o$ speech2 5poken words -- /o to ears -- /o to auditory area in temporal lobe via th

nerve-- /o to BernikeLs area where speech is understood-- ?essage go to %rocaLs area via 2rcuatefiber-- %rocaLs area is a motor speech which gives command to vocal cord and lip area in the motorcorte-- speech is spoken

Diseases2

%rocaLs area involvement-- 5peech out flow and fluency is lost

BernickeLs area involvement-- 5peech understanding is lost. atient speaks senselessly

3ominal aphasia (/nomic aphasia) is seen in metabolic encephalopathy It is an early $eature

o$ /lLeimers diseaseJ

Nrinary bladder-


28/61

/natomy

3erve supply-

5ympathetic- !''-7" (3ypogastric &)-- 5upply !rigone

arasympathetic- 5", 5*, 5A (elvic &)1-- 5upply $etrusor

5omatic [ 5", 5*, 5A (udendal nerve)1-- 5upply Ext Sphincter

Physiolo!y 2fferent by all three nerves i.e. elvic, 3ypogastric, udendal nerve. 9fferent mainly bypelvic nerve. $etrussor muscle is uni#ue-- does not follow starling@s law. 2rea of social behaviour andpersonality lies in $rontal lobe.

:ypes o$ urinary bladder disturbance2

'. Au tomatic %&ypertonic bladder%Complete spastic 7esion in the spiral segment above 5",5*,5A. 5mallcapacity bladder Kre#uent voiding at interval (%ladder start behaving like a new born bladder.)

". Autonomous%&ypotonic bladder- 17esion at 5", 5*, 5A, 7arge capacity bladder, $istention with overflow

*. Cortical%'ninhibited Bladder-Frontal-nappropriate micturition, loss of social inhibition control

5 Painless burn in hand is a characteristic $eature o$-

'. 5yringomeylia-------------------ans". !halamic syndrome*. Cord compressionA. 579

$iscussion- (3'J -"+GA; "+G Kigure *J"-')

5, #hich is not a $eature o$ extramedullary tumor-

'. 9arly corticospinal signs and descending paralysis". 4oot pain or ?idline %ack-ain*. C5K 2bnormalA. 5acral sparing--------------------ans

$iscussion- (2/ "88)

omparison o$ intramedullary and extramedullary comparison-

Symptoms Intramedullary ExtramedullaryJ

'. 4oot pains Fncommon Common

". >ertebral pain Nncommon ommon

*. ?otor Beakness 7ate 9arly

A. 5arcral nvolvement ate Early-- Commonly involved

Si!ns

'. %rown 5e#uard Fncommon Common

". $issociative sensory loss resent 2bsent

*. %ladderbowel dysfunction 9arly 7ate

Investi!ation


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5ubarachnoid %lock 7ate Sless marked 9arly S marked

Froin syndrome- alteration in the cerebrospinal fluid due to block, which is yellowish andcoagulates spontaneously in a few seconds after withdrawal, owing to its greatly increased protein(albumin and globulin) content; noted in loculated portions of the subarachnoid space isolated

from spinal fluid circulation by an inflammatory or neoplastic obstruction. 5yn loculationsyndrome.

5+ #hich $indin!s are $ound in ?ro%n SeMuard syndrome-

Ipsilateral loss ontralateral loss

' ain and temperature >ibration and motor

" >ibration and motor ain and temperature

* >ibration and ain ?otor S temperature

A ain S vibration !emp. and motor

2nswer- "

?eevor's si!n- 7esion at !G-!'81 paralyse the lower but not the upper abdominal muscles,resulting in upward movement of umblicus when abdominal wall contracts (beevor@s sign)

" /n yrs old male %ith mid alLheimer's disease has been started on donepeLil 5 m! a$ter hecontinued to have di$$iculty in $inancial matters and 1eepin! trac1 o$ the dayo$ the %ee1 and time/$ter , months the $amily $eels that there has been no improvement :here are no complaints o$nausea6 diLLiness or hypotension :he patients %i$e $eels the medicaton is unnecessary :he bestadvice is-

'. $iscontinue the donepezil

". ncrease the donepezil dose to '8 mg*. Continue donepezil to prevent further pla#ue formationA. Continue donepezil for * to H months and reevaluate mental status

9planation- /!-J I-'JA!he best course would be to continue the donepezil and see if it slows progression of cognitive functionloss based on ??59 or family assessment. !he success of the intervention needs to be evaluated over alonger time period realising that success may mean maintainting baselinefunction. !he anticholinesteraseinhibitors do not prevent pla#ue formation. ncreasing dose is rarely helpful and often causes side effects.!here is no datato suggest that one cholinesterase inhibitor works better than another.

ranial nerves = ?rain stem

50 /ll are true about ?enedicts syndrome except-

'. Contralateral choreoathetosis". $ense hemiplegia------------------ans*. 7esion is in mid brainA. psilateral *rd nerve palsy

$iscussion-(2/ "88J) 3'J -"+"+; ?E- -*8"

5ite-- >idbrain2 C2Dcclusion-

#eber's synd C7 hemiparesis O ipsilateral *rdnerve palsy

&othnagel syndrome C7 cerebellar signs O ipsilateral *rdnerve palsy

%enedikt@s syndrome C7 cerebellar signs O ipsilateral *rdnerve palsy

Claude syndrome G *enedikt?s H Dothnagel syndrome

3?- &othnagel syndrome-- 5ame presentation as %enedict@s


30/61

%ilateral infarction in distal C2 produces cortical blindness (blindness with preserved pupillary lightreaction. !he patient is often unaware of the blindness or may even deny it (Anton(s )yndrome)

59 >illard 8ubler Syndrome consists o$ the $ollo%in! E. ?alformation*. %erry aneurysm

A. &one--------------------ans$iscussion- 3'J -'J"H :raumais the mc cause. 2mong options-- *

0& :he site o$ cerebral hemorrha!e in hypertension are all except-

'. ons". nternal capsule-----------------ans*. utamenA. !halamus

$iscussion- 5ite of hypertensive bleed are- Cerebellum, ons, utamen, !halamus

N>3 = >3 esions

0 N>3 lesion is characteriLed by-'. Beakness S spasticity-------------------ans". Kasciculations*. 4igidityA. 7ocalized muscle atrophy


31/61

Diseases causin! dementia

0, /lLheimers disease typically a$$ects-

'. &ucleus basalis of ?eynert-----------------ans

". 2mygdala*. arietal corteA. %asal ganglion

$iscussion- (2?5 &ov 8J) Controversial Iuestion/lLeimer's Disease- (-A8H 4D2?5)

athology 2t autopsy, the most severe pathology is usually found in the hippocampus, temporal

corte, and nucleus basalis o$ >eynert(lateral septum)

?icroscopically - neuritic senile pla#ues and cytoplasmic neurofibrillary tangles. !he neuritic

pla#ue contain%-beta amyloid, proteoglycans, 2po 9, 2lpha-' antichymotrypsin

!acroscopically- $iffuse atropy of cerebral corte with secondary enlargement of ventricular

system

%iochemically - $ecrease in cerebral cortical levels of%cetylcholine, choline acetyltransferase and

nicotinic cholinergic receptors. 4eduction in norepinephrine levels in brainstem nuclei.

:reatment2

!acrine

$onepezil

3e%er dru!s

Aivasti!mine

8alantamine

>emantine

$rugs which reduce progression of 2$-

9strogen replacement therapy1

/inkgo

&52$1

5elegiline

>itamine 9

0+ :riad o$ normalpressure hydrocephalus includes-'. !remor, aphasia dementia". 2taia, aphasia, gait disorder*. /ait disorder, urinary incontinence, dementia---------------------ansA. /ait disorder, urinary incontinence, lower cranial nerve palsy

$iscussion- (3'J -"+AH)

&D4?27 4955F49 3M$4DC9327F5-

t is a triad of abnormal gait &%taxic gait), dementia and urinary incontinence

2 type of communicating hydrocephalous with patent a#ueduct of sylvius

&3 is caused by obstruction to normal flow of C5K over the cerebral conveity and delayedabsorption into the venous system

3D conditions producing scarring of basilar meninges such as meningitis, 523 and head trauma

9nlarged lateral ventricles (3ydrocephalus) with little or no cortical atropy.

C5K- ressure is in high normal range. !7C, $7C, rotein, 5ugar are normal

!reatment- >entricular peritoneal shunt

Extra Muestion(/IP8 9)- #hich o$ the $ollo%in! disease doesnt have autosomal dominantmode o$ inheritance-

'. ?arfanLs syndrome". olycystic kidney disease*. KabryLs disease------------------ans


32/61

A. 3untingtonLs disease$iscussion- 2pha-galactosidase 2 deficiency. R-linked recessive lysosomal storage disease4 9nzyme replacement therapy

/hent@s criteria is used for the diagnosis of ?arfan@s syndrome

Par1insonism(3'J -"+AG)

05 :rue about Aoti!otine-'. t is a non ergot alkanoid-----------------ans". t is a ?2D [ % inhibitor*. t is an anti-oidantA. none

$iscussion-

3e%er dru!s-

Er!ot al1aloid2%romocriptine, Cabergoline, ergolide

3on -er!ot al1aloid ramipaol, 4opinirol, 4otigotine

? of !remors- 2ntimuscarinics-- rocyclidine, %enztropine, %enzheol

4ead whole drug clssification from -A'+ E$!

3europrotective therapy-

'. Chronic use of &52$5 or the use of estrogen replacement in postmenopausal women may delayor prevent the onset for $(also 2lzeimer@s)

". 5elegiline monotherapy delayed the need for levodopa therapy

*. Coenzyme I'8 , an antioidant and a cofactor of comple of the mitochondrial oidative chain,has been shown to have neuroprotective effects

Demyelinatin! disorders

00 :he most common presentin! $indin! o$ multiple sclerosis is-

'. nternuclear ophthalmoplegia". !ransverse mylitis*. Cerebellar ataiaA. Dptic neuritis------------------ans

$iscussion- 3'J -"H''

9cercise induced weakness is a characteristic symptom of ?5

eat sensitivity-o 2ppearance of new symptoms or the worsening of pre-eisting symptoms on eposure to

heato Conduction block which may occur in response to increase temperature or metabolic

derangements

*hermittes symptom- /eneration of ectopic impulsegiving rise to 7hermitteLs 5ympt,paroysmal symptoms or paresthesias

nvestigations-'. >AI--*$awson8s finger sign- 7esion appear to etent from the ventricular surface,

corresponding to a pattern of perivenous demyelination". 9voked responses - !o detect slowed or absent conduction in visual, auditory, somatosensory or

motor pathways*. C5K-

?ononuclear pleocytosis , !7C usually 6"8

"ncrease "g1


33/61

Oligoclonal banding4

!reatment of 2cute 2ttack-'. /lucocorticoid treatment". lasma echange3# !ethotrexate4

A. > g+. ulse cyclophosphamide,2zathioprineH. ulse ?ethyl rednisolone

&ew $rugs forprophylaxis

/latiramer acetate

?itoantrone

K&-beta-'a'b

&atalizumab

Epilepsy = Syncope

09 #hich o$ the $ollo%in! %ould help exclude the dia!nosis o$ seiLure in a patient %ith sudden losso$ consciousness-

'. 2 brief period of tonic [ clonic movements at the time of falling". 2n aura of a strange odor before falling*. 5udden return to normal mental function upon awakening, though with a feeling of physical

weakness-------------------------ansA. Frinary incontinence

$iscussion- (2/ 8H) t. is usually confused following seizure in comple partial seizure

EPIEPS(3-'J -"AG)-

5eizure- aroysmal event due to abnormal,ecessive and hypersynchronous discharges from an aggregateof C&5 neurons.?anifestation of a seizure can include impairment or loss of consciousness andsensory,motor or behavioural abnormalities. !he term epilepsydescribes a syndrome characterised byrecurrent sei+ures.

/SSIFI/:I3-

'. artial seizuresi. 5imple partial-- no alteration in consciousnessii. Comple partial-- transient inability to maintain normal contact with environment.iii. artial seizures with secondary generalization

". rimary generalised seizures

i. 2bsence (etit mal)ii. !onic-clonic(/rand mal)iii. !oniciv. 2tonicv. ?yoclonic

*. Fnclassifiedi. &eonatal 5eizureii. nfantile 5pasm

A. 5tatus epilepticus

24!27 59]F495- 5eizure activity is restricted to discrete areas of cerebral corte.artial seizures areoften associated with structural abnormalities of the brain.n such case C!?4 of brain is mandatory.

'. )imple partial sei+ure- !he consciousness is fully preservedduring the seizure simple partialseizure cause motor,sensory autonomic or psychic symptoms.


34/61

i. ac1sonian march- ?ovements begin in a very restricted region and gradually progressto include a large area(not whole area).

ii. 'odd?s paralysis- 7ocalised paresis in the involvement region-- followed by completerevival

iii. 5eizure partialis continua- 5eizure activity continue for hours to days.". Complex partial sei+ure- %egins with aura. Kocal seizure activity accompanied by atransient

impairement of patient8s abilityto maintain normal contact with the environment*. ,artial sei+ures ith secondary generali+ation- artial seizure can spread to involve both

hemisphere and produce generalised seizure. t is fre#uently observed following simple partialsei+ure#

/9&942759$ 59]F495- 2rise from both cerebra simultaneously .4esult from cellular ,biochemicalor structural abnormalitites

Phases o$ a tonic-clonic seiLure rodromal phase, !onic phase, Clonic phase, ost-ictal phase

0B Dru! o$ choice in absence seiLure-

'. >alproate---------------ans

". henytoin*. CarbamazepineA. !opiramate

$iscussion- (2?5 8)-- $rug table 3'J Chapter-*H*(!able *H*-)4emember-- 5aare dard ki ek dawa hai >alproate

>enin!itis = Encephalitis

9 :he least common complication o$ menin!itis is-'. 3ypernatremia--------------ans(3yponatremia-- dt 52$3)". 3ydrocephalus*. %rain abscess

A. $eath$iscussion- 3'J -"H"'

Causes-

5. neumoniae &. ?eningitidis

Children- 5. 2ureus (-"H"")

Complications of ?eningitis- 4aised C, Cranial nerve palsy, >asculitis, Kocal deficit, 5eizure,3ypocephalus, 52$5, %rain abscess, ?ental retardation, $eath, 5ubdural effusion(very common inchildren with 3. nfluenza infection)

9& #hich is not true about pro!ressive multi $ocal leucoencephalopathy-

'. $egeneration of cortico cerebellar system---------------ans(Ck " in copy)". $ifficulty in speech*. ndolent course over few yearsA. %rain biopsy is definitive diagnosis

$iscussion- 3'J -"H*A

rogressive ?ultifocal 7eukoencephalopathy-

rogressive multifocal leukoencephalopathy(?7) is a rare demyelinating C&5 disorder causedby the reactivation of.C $irus (VC>-- a polyomavirus)

!he virus stays latent in the kidneys and lymphoid organs until reactivation

?7 mainly occurs in adults with impaired cell-mediated immunity, especially 2$5 patients butalso in those with lymphoproliferative and myeloproliferative disorders

VC> causes lytic infection of oligodendrocytes in the hite matter 5ymptoms include altered mental status, aphasia, ataia, hemiparesis or hemiplegia and visual

field disturbances. 5eizures occur in about ':.

C5K-- &ormal

4 4isperidone(-A"+ E$!) and mirtazapine(-A*G E$!)


35/61

9 :rue about /moebic menin!oencephalitis include-

'. 2cute form of meningoencephalitis". Common in tropical countries*. Keco-oral mode of transmissionA. !rophozoites in cerebrospinal fluid is diagnostic--------------ans

$iscussion- 3'J -'"JGnfection caused by the ameba 3ae!leria $o%lerican also cause acute meningoencephalitis (primaryamebic meningoencephalitis), wereas that caused by%canthamoebaand *alamuthiamore typicallyproduces subacute or chronicgranulomatous amebic meningoencephalitis. 3ae!leriathrive in warm,iron-rich pools of water, including those found in drains, canals, and both natural and human-madeoutdoor pools. nfection has typically occurred in immunocompetent children with a history of swimmingin potentially infected water. !he C5K, in contrast to the typical profile seen in viral encephalitis, oftenresembles that of bacterial meningitis with a neutrophilic pleocytosis and hypoglycorrhachia. ?otiletrophozoites can be seen in a wet mount of warm, fresh C5K. &o effective treatment has been identified,and mortality approaches '88:.

>3D

9, >otor neuron disease is characteriLed by-

'. 5ensory loss". 4igidity*. Kasciculation---------------ansA. Kocal seizure

$iscussion- 4iluzole (&ew drug)-- 3'J -"+J"-- read about it

>yasthenia !ravis

9+ 3ot a characteristic $eature o$ myasthenia !ravis-

'. 5ometimes spontaneous regression". roimal muscle involvement*. 2bsent deep reflees----------------------ansA. Katigue with eertion

$iscussion- 3'J -"HJ"

n ?/, the fundamental defect is a decrease in the number of available 2Ch4s at the postsynaptic musclemembrane.

7aboratory testing-'. 9drophonium chloride(!ensilon) -- 5creening test". 2nti-2Ch4 radioimmunoassay ^+: positive in generalised ?/; +8: in ocular ?/. $efinite

diagnosis if positive but negative result does not eclude ?/. ^A8: of 2Ch4 antibody-negativepatients with generalised ?/ have anti-?u5E antibodies

*. 4epetitive nerve stimulation decrement of '+: at *3z highly probableA. 5ingle-fibre electromyography confirmatory, but not specific

4eflees &ormal-- ?/, arkinson@s disease

95 In myasthenia !ravis6 $ace appearance is-

'. 5narling----------------ans". ?ouse like*. ?ask likeA. &one

$iscussion ?ouse like face-- C4K

AESPIA/:A SS:E>


36/61

bstructive.Aestrictive Diseases

99 FE@&.F@; is reduced in all except-'. Chronic bronchitis". %ronchial asthma

*. nterstitial lung disease----------------ansA. 9mphysema$iscussion-

bstructive Aestrictive

FE@-& $ecrease decrease

F@ decrease $ecrease

Aatio $ecrease 3ormal.Increase

decrease-- small decerease$ecrease-- %ig $ecrease

9 In an emphysematous patient %ith bullous lesion %hich is the best investi!ation to measure lun!volume-

'. %ody plethysmography--------------ans". 3elium dilution*. !rans diaphragmatic pressureA. $7CD

$iscussion- (2?5 &ov 8)

4> , K4C, and !7C- Cannot be measured by spirometry because they include the volume of gaspresent in the lungs

!wo techni#ues of commonly used to measure these volumes helium dilutionandplethysmo!raphy

!he helium dilution method may underestimate the volume of gas in the lungs if they are slowly

communicating airspaces, such as bullae. n this situation, lung volumes can be measured moreaccurately with a body plethysmograph, a sealed bo in which the patient sits while pantingagainst a closed mouth piece

9B First to be seen in acute severe asthma is-

'. ulsus paradous--------ans". 3ypercapnia*. 2cidosisA. Cyanosis

$iscussion- (2?5 ?ay 8) 3'J -'+GH

Keatures of Severe attack

'. nability to speak complete sentence in one breathe42# Pulse 12/ per min#*. 4espiratory rate "+min.# Pulsus paradoxus of 1/ mmgI# PEF between 33 to I/J of predicted

Keatures of i$e-threatenin! attack -1# 5ilent Chest42# Cyanosis43# *radycardia4

A. Confusion4(altered sensorium)I# PEF 0 33J of predicted4

False re!ardin! chronic bronchitis is-

'. 3emoptysis". " consecutive years*. roduction cough


37/61

A. Cough for * months in a year---------------ans(2/ @8H)-- * consective months$iscussion- 3'J -'H*G

& SIAS includes all except-'. 3ypothermia". 7eukopenia

*. !achycardiaA. 3ypotension-----------------ans

$iscussion-

De$initions used to describe the condition o$ septic patients

%acteremia resence of bacteria in blood, as evidenced by positive blood cultures

5epticemia resence of microbes or their toins in blood

Systemic in$lammatoryresponse syndrome(SIAS)

(nly this is Imp)

:%o or more o$ the $ollo%in! conditions2

& Fever (oral temperature *,Q) or hypothermia (R,0Q) eu1ocytosis (*&6.)6 leu1openia (R +6.)6 or *&;

bandsO may have a non-in$ectious etiolo!y, :achypnea (*+ breaths.min)+ :achycardiaJ (heart rate *B beats.min)

5epsis 545 that has a proven or suspected microbial etiology

5evere sepsis (similar toNsepsis syndromeN)

5epsis with one or more signs of organ dysfunction _ for eample

'. Cardiovascular 2rterial systolic blood pressure 6 G8 mm3g ormean arterial pressure J8 mm3g that responds to administration ofintravenous fluid

". 4enal Frine output 68.+ m7kg per hour for ' h despite ade#uatefluid resuscitation

*. 4espiratory aD"KD" 6 "+8 or, if the lung is the only

dysfunctional organ, 6 "88A. 3ematologic latelet count 68,8887 or +8: decrease in plateletcount from highest value recorded over previous * days

+. Fneplained metabolic acidosis 2 p3 6 J.*8 or a base deficit +.8m9#7 and a plasma lactate level '.+ times upper limit of normalfor reporting lab

H. 2de#uate fluid resuscitation ulmonary artery wedge pressure '"mm3g or central venous pressure mm3g

5eptic shock 5epsis with hypotension (arterial blood pressure 6G8 mm3g systolic, or A8mm3g less than patient@s normal blood pressure) for at least ' hr despiteade#uate fluid resuscitation;or

&eed for vasopressors to maintain systolic blood pressure G8 mm3g or meanarterial pressure J8 mm3g

4efractory septic shock 5eptic shock that lasts for ' hr and does not respond to fluid or pressoradministration

?ultiple-organdysfunction syndrome(?D$5)

$ysfunction of more than one organ, re#uiring intervention to maintainhomeostasis

or Pulmonale

ardinal si!n $or the dia!nosis o$ chronic corpulmonale is-'. 4aised ugular venous pressure". 4ight ventricular failure*. 7eft ventricular hypertrophyA. 4ight ventricular dilatation----------------ans

7/22/2019 13. In

13. Internal Medicine

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