Harrison images charts tables for post graduate students

Harrison tables

2. Pulmonary/Respiratory Medicine

4. α1 antitrypsin
deficiency
↑↑ neutrophil
elastase
level
↑↑ alveolar
wall
damage
↑↑COPD

8. •Severe hypoxemia
•Increased PaCO2(>45mmHg)
•TYPE 2 RESPIRATORY FAILURE
•MORE RISK OF Rt. HEART FAILURE
& COR PULMONALE
•Mild to moderate
hypoxemia(PaO2>65mmHg)
•Normal or slightly reduced PaCO2
•TYPE 1 RESPIRATORY FAILURE
•NO RISK OF Rt. HEART FAILURE &
COR PULMONALE

9. •CENTRILOBULAR EMPHYSEMA-
•Smokers
•Upper lobe involvement
•Most common clinical type
•PARASEPTAL EMPHYSEMA-
•Young males
•Higher chance of pneumothorax
•PANACINAR EMPHYSEMA-
•Whole acini is involved
•<45 yrs.
•Emphysema without risk factor/NON-SMOKERS
•α1 ANTITRYPSIN DEFICIENCY
•Basilar or lower lobe involvement
•Associated with vasculitis & liver disease
•Can evolve into BRONCHIECTASIS
•IRREGULAR EMPHYSEMA-
•Most common pathological type

13. FEATURES MILD ASTHMA MODERATE ASTHMA SEVERE ASTHMA IMPENDING FAILURE
BREATHLESSNESS WHILE WALKING
AT REST, LIMITS
ACTIVITY
INTERFERES WITH
CONVERSATION
MUTE
TALKS IN SENTENCES PHRASES WORDS SILENT
ALERTNESS AGITATED AGITATED AGITATED DROWSY & CONFUSED
RESP. RATE ↑↑ ↑↑ >30/MIN >30/MIN
BODY POSITION CAN LIE DOWN PREFERS SITTING UPRIGHT CAN’T RECLINE
ACCESSORY MUSCLES NO COMMONLY USUALLY
PARADOXICAL
BREATHING
(ABDOMINO-
THORACIC)
WHEEZE MODERATE
LOUD; THROUGHOUT
EXHALATION
LOUD THROUGHOUT SILENT CHEST
PULSE <100 100-120 >120
RELATIVELY
BRADYCARDIA
PULSUS PARADOXUS ABSENT
FALL IN SBP OF 10-
25mmHg
FALL IN SBP OF
>25mmHg
ABSENT DUE TO
MUSCLE FATIGUE
PEF NORMAL 40-69 <40 <25
PaO2/PaCO2 NORMAL 60/42 <60/>42 <60/>42

23. Inj. Adrenaline s/c
Oral corticosteroids +
continuous β2 agonist

24. Exercise induced asthma: precipitated by SABA & DOC is ICS
Aspirin sensitive asthma-DOC-inhaled corticosteroids (ICS)
(may be combined with SABA + LTRA)

28. WELL’S SCORING SYSTEM
>4-HIGHLY SUSCEPTIBLE
<4-LOW SUSCEPTIBLE

31. •KERLEY A LINES: extend radially from hilum to upper lobes
•KERLEY B LINES:
•1-2 cm in length in periphery of the lung
•Perpendicular to pleural surface & extend out of it
•Represent sub-pleural thickened interlobular septa & seen
at lung bases
•KERLEY C LINES: don’t reach pleura & go radially away from hila
•KERLEY D LINES:same as KERLEY B LINES but seen on lateral CXR
IN THE RETROSTERNAL AIR GAP

33. A.Schematic of the surface epithelium andsupporting glandular
structure of the human airway.
B.The submucosal glands of a patient with CF are filled with
mucus, and mucopurulent debris overlies the airway surfaces,
essentially burying the epithelium.
C.A higher magnification view of a mucus plug tightly adhering
to the airway surface, with arrows indicating the interface
between infected and inflamed secretions and the underlying
epithelium to which the secretions adhere.
D.CFTR is expressed in surface epithelium and serous cells at
the base of submucosal glands in a porcine lung sample, as
shown by the dark staining, signifying binding by CFTR
antibodies to epithelial structures (aminoethylcarbazole
detection of horseradish peroxidase with hematoxylin
counterstain
Both Band Cwere
stained with
hematoxylin and
eosin, with the
colors modified to
highlight structures.)
Infected secretions obstruct
airways and, over time,
dramatically disrupt the
normal architecture of the
lung
Extrusion of mucus secretion onto the epithelial surface of airways in cystic
fibrosis (CF)

41. ACUTE EOSINOPHILIC PNEUMONIA CHRONIC EOSINOPHILIC PNEUMONIA

42. ACUTE EOSINOPHILIC PNEUMONIA

44. COAL WORKER’S PNEUMOCONIOSIS

47. For primary lung abscesses, the recommended regimens are ----
(1)clindamycin (600 mg IV three times daily; then, with the disappearance of fever and clinical
improvement, 300 mg PO four times daily) or
(2)an IV-administered β-lactam/β-lactamase combination, followed—once the patient’s condition is
stable—by orally administered amoxicillin-clavulanate.
This therapy should be continued until imaging demonstrates that the lung abscess has cleared or
regressed to a small scar. Treatment duration may range from 3–4 weeks to as long as 14 weeks.
One small study suggested that Moxifloxacin (400 mg/d PO) is as effective and well tolerated as
Ampicillin-sulbactam.
Notably, Metronidazole is not effective as a single agent: it covers anaerobic organisms but not the
microaerophilic streptococci that are often components of the mixed flora of primary lung abscesses.
•In secondary lung abscesses------
Antibiotic coverage should be directed at the identified pathogen, and a prolonged course (until
resolution of the abscess is documented) is often required.
Treatment regimens and courses vary widely, depending on the immune state of the host and the
identified pathogen.
Other interventions may be necessary as well, such as relief of an obstructing lesion or treatment
directed at the underlying condition predisposing the patient to lung abscess.
Similarly, if the condition of patients with presumed primary lung abscess fails to improve, additional
studies to rule out an underlying predisposing cause for a secondary lung abscess are indicated.
•An abscess >6–8 cm in diameter is less likely to respond to antibiotic
therapy without additional interventions.Options for patients who
do not respond to antibiotics and whose additional diagnostic
studies fail to identify an additional pathogenthat can be treated
include SURGICAL RESECTION AND PERCUTANEOUS DRAINAGE OF
THE ABSCESS(especially when the patient is a poor surgical
candidate).
•Possible complications of percutaneous drainage include bacterial
contamination of the pleural space as well as pneumothorax and
hemothorax.

57. Nephrology

59. FUNCTIONS OF KIDNEY
EXCRETORY URINE FORMATION
HOMEOSTASIS
•WATER BALANCE
•ACID BASE BALANCE
HORMONAL
•ERYTHROPOIETIN SYNTHESIS
•VIT-D ACTIVATION

102. GOLDBLATT KIDNEY MODELS

110. (--) BARTTER

125. Rheumatology

143. OCT, 2019 EULAR CRITERIA FOR SLE

147. ANTI-ERYTHROCYTE Ab (DIRECT COOMB’S TEST)
NOT THERE IN NEW CRITERIA

149. ACR(1982;
REVISED IN
1997)
SLICC, 2012EULAR, 2019
SENSITIVITY 85 97 98
SPECIFICITY 95 90 96

171. Schaumann
bodies
Asteroid
bodies

172. SCADDING SCORING/ STAGING
SYSTEM OF PULMONARY
SARCOIDOSIS

173. HEERFORDT-WALDENSTROM’S
SYNDROME

180. Cardiology

181. Jugular venous pressure and waveforms

182. •Jugular venous pulse is the oscillating top of the distended proximal portion of
the internal jugular vein and represents volumetric changes that faithfully
reflect the pressure changes in the right heart.
•Right atrial pressure during systole and right ventricular filling pressure during
diastole.
•Window into the right heart, providing critical information regarding its
hemodynamics.

183. 1.Anatomy
2.JV pressure measurement
3.Causes of elevated JVP
4.Normal wave pattern
5.Abnormal wave pattern
6.Kussmauls sign and hepatojugularreflux
7.Specific conditions

184. The internal jugular vein begins just medial to the mastoid process at the base of the skull. The
internal jugular vein runs directly inferior from the mastoid process,.it joins the subclavian
vein, to form Rtinnominate which continue as superior vena cava and then into the right
atrium.

185. •The internal jugular
vein is Lateral to
carotid artery & deep
to sternomastoid
muscle.
•External jugular is
superficial to
sternomastoid.

186. SHOWS THE VERTICAL COURSE OF THE IJV
WHICH PASSES IN BETWEEN THE TWO HEADS
OF THE STERNOCLEIDOMASTOID UNDER THE
MEDIAL END OF CLAVICLE.

187. Examination of JVP
•Right IJV is usually assessed both for waveform and estimation of venous
pressure
•Transmitted pulsations to overlying skin between two heads of sternomastoid
•Unlike EJV pulsations it is not possible to see IJV pulsations directly as it is deep.
We actually see the transmitted pulsations to the overlying skin b/w the two
heads of sternomastoid.
•Right IJV Preferred :Why?
•Straight line course through innominate vein to the svc and right atrium
•Less likely extrinsic compression from other structures in neck
•Why not EJV
•No or less numbers of valves in IJV than EJV

188. IJV Carotid pulses
•Superficial and lateral in the
neck
•Deeper and medial in the neck
•Better seen than felt •Better felt than seen
•Has two peaks and two troughs•Has single upstroke only
•Descents >obvious than crests•Upstroke brisker and visible
•Digital compression abolishes
venous pulse
•Digital compression has no
effect
•Jugular venous pressure falls
during inspiration
•Do not change with respiration
•Abdominal compression
elevates jugular pressure
•Abdominal compression has no
effect on carotid pulse

189. Measurement of JV Pressure
•Sternalangle or angle of Louis -reference point
•Found approximately 5 cm above the center of the right atrium
•Sternal angle –RA: Fixed relationship

190. Position of Patient
•Patient should lie comfortably and trunk is inclined by an angle of
45º to bed, which permits best view of the upper level of the
venous pulsations
•Elevate chin and slightly rotate head to the left
•Neck and trunk should be in same line
•When neck muscles are relaxed, shine the light tangentially over the
skin and see pulsations
•Simultaneous palpation of the left carotid artery or apical impulse
aids in timing of the venous pulsations in cardiac cycle
•Inclination is required as level go below mandible in high JVP or
below clavicle in low JVP.
•So start with 45ºthen tilt pt. appropriately up or down.
•In patients with low jugular pressure , a lesser (<30º) inclination is
desirable
•In patients with high jugular pressure ,a greater (60-90º) inclination
is required to obtain visible pulsations

191. Measurement of JVP
•Two scale method is commonly used
•Normally JV pressure does not exceed 3-4 cm above
the sternalangle
•Since RA is approximately 5 cm below the sternal
angle , the jugular venous pressure
corresponds to 9 cm =7mmHg
•Elevated JVP : JVP of >4 cm above
sternal angle .

193. Kussmaul'ssign
•Normally mean JVP falls during inspiration ..as a result of
impaired RV compliance, so the increased venous return can
not be accommodated by the RV, resulting in an elevated JVP
•Mean jugular venous pressure increases during
inspiration : Kussmaul'ssign
•Constrictive pericarditis
•Severe right heart failure
•RV infarction
•Restrictive cardiomyopathy
•Impaired RV compliance.

194. Abdominal-Jugular Reflux/Hepato-jugular reflux
•Apply firm pressure to periumbilical region X10-15 sec
•Normally JV pressure rises transiently to < 1cm
while abdominal pressure is continued
•Abdominal compression forces venous blood into thorax.
•A failing/dilated RV not able to receive venous return without
rise in mean venous pressure.
•If JV pressure remains elevated >1cm until
abdominal pressure is continued: Positive
AJR
•Positive AJR
•Incipient (impending) and/or compensated RVF
•Tricuspid regurgitation
•COPD

195. Normal JVP
•Normal JVP reflects phasicpressure changes in RA during systole and RV during
diastole
•3 visible positive waves ( a, c and v) and 2 negative troughs ( x and y)
•Consists of 3 positive waves
•a, c & v
•And 3 descents
•x, x’ & y

197. WIGGER’S DIAGRAM

198. a-Wave
•due to right atrial
contraction
•Effective RA contraction is needed for
visible a wave
•Dominant positivewave in JVP and
larger than v-wave

199. x-descent
which

200. C Wave

201. x’-Descent


202. v-Wave

203. y-Descent

204. h-wave

205. •Tricuspid stenosis or atresia
•RA myxoma
•RVH
•Pulmonary stenosis
•Pulmonary hypertension of any cause
•Restrictive cardiomyopathy
•RV infarction
•Acute pulmonary embolism

206. Regular cannon a wave

209. (causes
blood stasis)

217. •JVP is usually elevated
•y descent is diminished or absent
•x wave is normal
•Kussmaul'ssign---usually negative

218. •JVP is elevated
•a wave is usually normal
•v wave is usually equal to a wave
•x descent –prominent
•y descent –rapid descent
•Kussmaulssign is usually positive

219. •JVP is usually elevated
•Both a and v wave equal
•Kussmaul’smay be positive

220. JVP may be elevated
a wave is prominent
a and v wave prominent
v wave larger than a wave
x descent is diminished or
absent
Rapid y descent due to TR

224. Systemic HTN (ESH-2018 Guidelines)

245. because thiazide/thiazide-like
diuretics are much less effective/ineffective when eGFR
is reduced to this level.

246. •MRA, mineralocorticoid receptor antagonist.
c.MRA (spironolactone or eplerenone)

250. ECG FLASH CARDS

269. Gastroenterology

283. TRUELOVE-
WITT’S SEVERITY
CRITERIA FOR UC
MAYO’S SCORING
SYSTEM

284. TRUELOVE-WITT’S SEVERITY CRITERIA FOR UC

290. •SULFASALAZINE ARE NOT USED NOWADAYS DUE TO COMPLICATIONS OF SULFAPYRIDINE
•INSTEAD MESALAMINE IS USED EITHER ORALLY/TOPICALLY

291. RISK OF CA COLON: UC>CD
RISK OF LEUKEMIA &
LYMPHOMA: CD>UC

292. ANTIBODIES IN CD SIGNIFICANCE
ASC-A (Anti-Saccharomyces Cerevisae) SCREENING; MARKER OF EARLY COMPLICATIONS; ALSO SEEN
IN BEHCET’S DISEASE
OMP-C (Outer Membrane Protein)
APB (Anti Pancreatic Ab)
Anti-flagellin
Anti-I2 CORRELATE WITH RISK OF SURGERY
ANTIBODIES IN UC SIGNIFICANCE
ANTI-GOBLET CELL Ab
P-ANCA CORRELATE WITH RELAPSE OF UC

324. Wilson’s disease
KF RING
SUNFLOWER CATARACT

325. HEMOCHROMATOSIS

352. PPT BY DR RAHULNIKUMBHE
Malabsorption
Which of the following is not required forabsorption
offat?
A.Conjugatedbile
B.Lipase
C.SGLT1
D.Lymphatics

353. PPT BY DR RAHULNIKUMBHE
Malabsorption
Breath test is usedfor
A.Monosaccharidemalabsorption
B.Fatmalabsorption
C.Vitamin B12malabsorption
D.Polysaccharidemalabsorption

354. PPT BY DR RAHULNIKUMBHE
Malabsorption
Schilling’s test is a testfor
A.Proximalintestine
B.Distalintestine
C.Fatmalabsorption
D.Monosaccharidemalabsorption

355. PPT BY DR RAHULNIKUMBHE
Malabsorptionsyndrome
Whichofthefollowingisnotamalabsorptionsyndrome?
A.Whipple’sdisease
B.Coeliacdisease
C.Tropicalsprue
D.Tangier’sdisease

356. PPT BY DR RAHULNIKUMBHE
Malabsorption
•Non-absorption of fat soluble vitamins is dueto
A.Steatorrhea
B.Pancreaticinsufficiency
C.Cirrhosis ofliver
D.All ofthese

357. PPT BY DR RAHULNIKUMBHE
Malabsorption
PositiveD-xylosetestindicatesallofthefollowingEXCEPT
A.Pancreaticinsufficiency
B.Small intestinal mucosaldisease
C.Impaired carbohydrate absorption in smallintestine
D.Pyloricstenosis

358. PPT BY DR RAHULNIKUMBHE
Malabsorption
A41yearoldmalepatientpresentedwithchronicdiarrhoeafor 3
months.AD-xyloseabsorptiontestwasorderedtolookfor
A.Carbohydrate malabsorption due to mucosaldisease
B.Carbohydrate malabsorption due to chronicpancreatitis
C.Fat malabsorption due to mucosaldisease
D.Fat malabsorption due to chronicpancreatitis

359. PPT BY DR RAHULNIKUMBHE
Malabsorption
A D-xylose test was requested on a patient with history of diarrhoea since 2
months. 5 hour urine sample showed < 4 gm excretion after giving 25 gm of D-
xylose. The most likely diagnosisis
A.Chronicpancreatitis
B.Bacterial overgrowthsyndrome
C.Celiacsprue
D.Intestinallymphangiectasia

360. PPT BY DR RAHULNIKUMBHE
Malabsorption
CauseoffalsepositiveD-xylosetestincludeallofthe
followingexcept
A.Renalfailure
B.Ascites
C.Celiacsprue
D.Pleuraleffusion

361. PPT BY DR RAHULNIKUMBHE
Malabsorption
Schilling test is abnormalin
A.Pancreatic endocrineinsufficiency
B.Lipasedeficiency
C.Amylasedeficiency
D.Intrinsic factordeficiency

362. PPT BY DR RAHULNIKUMBHE
Malabsorption
Which of the following grains can be used safely inpatients
with celiacsprue:
A.Rice andcorn
B.Wheat andcorn
C.Rye andwheat
D.Barley andrye

363. PPT BY DR RAHULNIKUMBHE
The presence of anti-Saccharomyces cerevisae antibodyis
a surrogate marker of one of thefollowing:
a.Celiacdisease
b.Crohn’sdisease
c.Ulcerativecolitis
d.Tropicalsprue

364. Bilirubinmetabolism
Ratelimitingstepinbilirubinmetabolismis–
a.Conjugation ofbilirubin
b.Transport of unconjugated bilirubin tohepatocyte
c.Transportofconjugatedbilirubinintobilecanaliculi
d.Transport of conjugated bilirubin intosinusoids
Rate limiting step in bilirubin metabolism is not Conjugation of
bilirubin but rather the transport of conjugated bilirubin intobile
canaliculi. Harrison 20
th
edition page2338
PPT BY DR RAHULNIKUMBHE

365. PPT BY DR RAHULNIKUMBHE
Jaundice
Apatienthasjaundice.Urineforurobilinogenisabsent.Whatisthe
diagnosis?
A.Hemolysis
B.Glucornyl transferasedeficiency
C.Alcoholichepatitis
D.Obstructivejaundice

366. A 40 year old male who is chronic ethanolic comes with jaundice, nausea and
abdominal pain.Labinvestigationsare as shown in the table. What is thedrug
of choice for thiscondition?
A.Ursodeoxycholicacid
B.InjectionThiamine
C.TabletPentoxifylline
D.TabletPrednisolone
PPT BY DR RAHULNIKUMBHE

367. PPT BY DR RAHULNIKUMBHE
NAFLD
Which of the following sentence is false regarding NAFLD?
A.It is because of obesity and increased insulin resistance
B.It causes macronodular cirrhosis ofliver
C.AST:ALT ratio is generally >2
D.Diet modifications and exercise are important part ofmanagment

368. PPT BY DR RAHULNIKUMBHE
AIH
Which of the following is correctlymatched?
A.LKM 1-Autoimmune hepatitis type1
B.LKM-2-Autoimmune hepatitis type2
C.LKM-1-Autoimmune hepatitis type2
D.LKM-2-Chronic hepatitisD
LKM-1 Autoimmune hepatitis2
LKM-2 Drug induced hepatitis
LKM-3 Chronic hepatitisD

369. PPT BY DR RAHULNIKUMBHE
PBC
Antibodies usually elevated in primary biliarycholangitis
are
A.Antiactinantibodies
B.Antinuclearantibodies
C.Antimitochondrialantibodies
D.Antisoluble liver antigenantibody

370. PPT BY DR RAHULNIKUMBHE
PRIMARYSCLEROSINGCHOLANGITIS
Which of the following is not a feature of primary sclerosing cholangitis?
A.It is more common inmale
B.Pruritis is a clinicalfeature
C.It is associated with ulcerativecolitis
D.Biopsy isdiagnostic

371. PPT BY DR RAHULNIKUMBHE
Wilson’sdisease
Allofthefollowingarecharacteristicneurologicmanifestationsof
Wilson’s diseaseEXCEPT
A.Dystonia
B.Sexualdysfunction
C.Severely impairedcognition
D.Dysphagia

372. PPT BY DR RAHULNIKUMBHE
Cirrhosis ofliver
In patient with cirrhosis of the liver the site of obstruction in the portal
system is inthe
A.Hepaticvein
B.Postsinusoidal
C.Extra hepatic portalvein
D.Sinusoids

373. Cirrhosis ofliver
PPT BY DRRAHUL
•A50yearoldmalecamewithabdominaldistension.Clin
NIK
i
U
c
MB
a
HE
l
examinationand USGabdomenconfirmedthediagnosisof
ascites. Lab investigations are as shown in the table. What is
the probable diagnosis?
A.Cirrhosis ofliver
B.IVCobstruction
C.Budd Chiarisyndrome
D.Tuberculousperitonitis

374. PPT BY DR RAHULNIKUMBHE
UGIbleed
A 40 year old male, known case of cirrhosis develops acute episode of
GI bleed. Initial therapy given for 6 hours. Which of the following
procedure isuseful?
A.Nasogastricaspiration
B.Urgentendoscopy
C.Sedation
D.Ultrasound

375. PPT BY DR RAHULNIKUMBHE
UGIbleed
For the treatment of which of the following Sengstaken-Blakemore
tube isused?
A.Epistaxis
B.Urethralinjury
C.Urinaryretention
D.Bleeding from oesophagealvarices

376. PPT BY DR RAHULNIKUMBHE
UGIbleed
WhichofthefollowingisabsentinSengstaken-Blakemore
tube?
A.Gastricballoon
B.Oesophagealballoon
C.Gastric aspirationport
D.Oesophageal aspirationport

377. PPT BY DR RAHULNIKUMBHE
H.PYLORI
DiagnostictestsofH.Pyloriincludeallofthefollowingexcept
A.Urea breathtest
B.Rapid ureasetest
C.Gastricbiopsy
D.SAFAtest
SolubleAntigenFluorescentAntibodytestisusedfordiagnosisof
pulmonary tuberculosis,rabies.

378. PPT BY DR RAHULNIKUMBHE
H.PYLORI
WhichofthefollowingisfalseregardingH.Pyloriinfection
A.Withchronicinfectionureasebreathtestbecome
negative
B.H.pyloriinfectionremainlifelongifuntreated
C.Endoscopy isdiagnostic
D.Toxigenic strains usually causesulcers

379. PPT BY DR RAHULNIKUMBHE
H.PYLORI
ApatientwithH.Pyloriinfectionistreatedwithdrugs.Thepreferred
test to detect the presenceof residual H. Pyloriinfectioninthis
personis-
A.Rapid ureasetest
B.Urea breathtest
C.Endoscopy andbiopsy
D.Serum anti H. Pylorititre

380. PPT BY DR RAHULNIKUMBHE
H.PYLORI
WhichdrugisnoteffectiveagainstH.Pylori?
A.Bismuthsubsalicylate
B.Metronidazole
C.Amoxicillin
D.Erythromycin

381. PPT BY DR RAHULNIKUMBHE
PUD
Allofthefollowingaretrueregardinga patientwithacidpeptic
diseaseexcept
A.MisoprostolisthedrugofchoiceinpatientsonNASIDS
B.DuodenalulcerispreventablebytheuseofsinglenighttimeH2
blocker
C.OmeprazolemayhelpulcersrefractorytoH2blockers
D.Misoprostolisdrugofchoiceinpregnantpatients

382. PPT BY DR RAHULNIKUMBHE
HEPATITIS
Hepatitis B is not transmittedby
A.Saliva
B.Semen
C.Breastmilk
D.Feco-oral

383. PPT BY DR RAHULNIKUMBHE
HEPATITIS
All are transmitted by bloodexcept
A.HepA
B.HepB
C.HepC
D.HIV

384. PPT BY DR RAHULNIKUMBHE
HEPATITIS
All are transmitted by bloodexcept
A.HepA
B.HepB
C.HepC
D.HepE

385. PPT BY DR RAHULNIKUMBHE
HEPATITIS
Non parenteral hepatitisis
A.HepatitisE
B.HepatitisB
C.HepatitisC
D.HepatitisD

386. PPT BY DR RAHULNIKUMBHE
HEPATITISB
Acute infection of hepatitis B virus is diagnosedby
A.IgM antibody ofHBsAg
B.IgM antibody ofHBcAg
C.IgM antibody ofHBeAg
D.IgG antibody ofHBcAg

387. PPT BY DR RAHULNIKUMBHE
HEPATITISB
First virological marker following acute infection with HBV is
A.HBsAg
B.Anti-HBsAg
C.IgM antiHBcAg
D.AntiHBeAg

388. PPT BY DR RAHULNIKUMBHE
HEPATITISB
Diagnosis of acute hepatitis B infection is madeby
A.Presence ofHBeAg
B.Presence of IgManti-HBc
C.Presence ofHBsAg
D.Presence of IgGanti-HBc

389. PPT BY DR RAHULNIKUMBHE
HEPATITISB
Diagnosis of acute hepatitis B infection is madeby
A.Presence ofHBsAg
B.Presence of IgManti-HBc
C.Presence of HBsAg plus IgManti-HBc
D.Presence of IgGanti-HBc

390. PPT BY DR RAHULNIKUMBHE
HEPATITISB
Which of the following is true regarding HBeAg in serum
A.Signals recovery from HBVinfection
B.Indicates viral replication andinfectivity
C.An evidence for successful vaccination against hepatitis B
D.Enhances the severity of HBV and increases the risk of cirrhosis

391. D.Acute hepatitis infection with lowinfectivity
PPT BY DR RAHULNIKUMBHE
HEPATITISB
A 30 year old man presented with nausea, fever and jaundice of 5days
duration. The biochemical tests revealed a bilirubin of 6.7 mg/dl (Conjugated 5
mg/dl) with AST 900 IU/ml and ALT 1400 IU/ml. The serological tests showed
the presence of HBsAg, IgM anti HBC and HBeAg. The most likely diagnosisis:
A.Chronic hepatitis B infection with highinfectivity
B.Acute hepatitis infection with highinfectivity
C.Chronic hepatitis infection with lowinfectivity

392. PPT BY DR RAHULNIKUMBHE
HepatitisC
Hepatitis C is associatedwith
A.Anti LKM-2antibody
B.Scleroderma
C.Cryoglobulinemia
D.Polyarteritisnodosa

393. PPT BY DR RAHULNIKUMBHE
HepatitisC
Most sensitive test for HCV infection is
A.HCVRNA
B.Anti-HCVIgM
C.Anti-HCVIgG
D.Detectable Anti-HCV and absence of HCVRNA
Assays for HCV RNA are the most sensitive tests for HCV
infectionandrepresenttheGoldstandardinestablishinga
diagnosis of hepatitis C. Harrison 20
th2360.

394. Mineral deficiencies

395. Hypothyroidism in sub-Himalayan zone
ESOPHAGEAL CA
USED FOR Rx OF KESHAN’S DISEASE

396. •Pb/cadmium/chromium toxicity–CTID (chronic
tubulo-interstitial disease) variant of CKD
•CHROMIUM TOXICITY: CKD + LUNG CANCER
•PbTOXICITY: CKD + SATURNINE GOUT
•CADMIUM TOXICITY: CKD + SEVERE BONE PAIN (OUCH-OUCH
NEPHROPATHY)

397. •ARSENIC OVERDOSE:
•PEROPHERAL NEUROPATHY
•GARLIC ODOUR
•LUNG CANCERS
•NASAL CANCERS

398. Acid base balance

410. CNS