Monday, 20 March 2017

Autoimmune haemolyticanaemia | Crack AIIMS, NEET 2017 MCQs


Autoimmune haemolyticanaemia is an example of which of the following hypersensitivity disorders? 

A. TypeI
B. TypeII
C. TypeIII
D. TypeIV


Ans. B. Type II Hypersensitivity
Hypersensitivity reactions
Type I Hypersensitivity reactions: IgE Mediated
• Theobald phenomenon
• Prusnitz reaction (PK)
• Casonis Test
• Anaphylaxis
• Local: Asthma, Hay fever, Angloedema, Eczema, Urticaria
Type II Hypersensitivity reactions: IgG or 1gM Mediated
• Grave’s disease (ALSO TYPE V)
• Good Pauster’s Syndrome
• Myasthenia Gravis
• Blood transfusion reactions.
• Immune hemolytic anemia
• Immune Thrombocytopenic purpura
Type III Hypersensitivity reactions: Immune complex mediated
• Arthus reaction
• Serum Sickness
• SLE
• Schiks test
• Post Streptococcal Glomerulonephritis
Type IV Hypersensitivity reactions: Delayed Hypersensitivity
• Tuberculin test
• Lepromin Test
• Contact dermatitis
• Pernicious anemia

Sunday, 19 March 2017

The two nitrogen atoms in urea arise from | Crack AIIMS, NEET 2017 MCQs


The two nitrogen atoms in urea arise from: 

A. Ammonia and glutamine 
B. Ammonia and asp artic acid 
C. Glutamine and glutamic add 
D. Glutamine and alanine





Ans. B. Ammonia and Aspartic acid                                                                               

Urea cycle  
• Takes place in liver and brain.
• 1st two reactions occur in mitochondria.
• 1st two reactions are rate controlling reactions.
• Nitrogen atoms arise from Ammonia and Aspartic acid
• Combination of “Hyperammonemia+ ‘t’Blood Glutaniine+4.Blood urea” suggests defect in Urea Cycle. Lethargy, vomiting, coma are associated. 

Unconjugated hyperbilrubinaemia | Crack AIIMS, NEET 2017


Unconjugated hyperbilrubinaemia is characteristic of; 

A. Rotors syndrome 
B. Dublin johnson syndrome 
C. Chronic active hepatitis 
D. Gilberts diseases 


Ans. D. Gilberts syndrome
Causes of “Unconjugated” hyperbilirubenemia are
• Gilbert’s syndrome
• Criggler najar Syndrome I, Criggler najar Syndrome II
• Hemolytic anemia
• Physiological jaundice
• Hypothyroidism
• Breast milk jaundice
• Excessive RBC Destruction (Rh incompatibility, G6PD Deficency, Spherocytosis, Vitamin K,
Sulfamethaxoole)
Causes of “Conjugated” hyperbffirubenemia are:
• Parenchymal diseases (Rubella, Toxoplasmosis, CMV, Herpes infection)
• Neonatal hepatitis syndrome.
Biliary atresia (Intrahepatic/ Extrahepatic)
• Watson Alaigallie syndrome
• Choledochal cyst
• Dubin Johnson syndrome, Rotor syndrome
• Commonest cause in new born Idiopathic infantile hepatitis





High energy phosphates | NEET Based MCQ


High energy phosphates are not produced in 

A. HMP shunt 
B. Oxidative pathway 
C. TCA 
D. Glycolysis




Ans. A. (HMP shunt)
Explanation 
.•“Hexose Monophosphate Shunt Pathway (HMP) produces NADPH that is required for several synthetic pathways, e.g., for fatty acids and steroid synthesis. However, the NADPH produced is not converted to ATP or used for energy production (unlike NADH produced in glycolysis and TCA cycle)” — Devlin and Rama Rao 
• The HMP shunt or pentose phosphate pathway serves several purposes, including synthesis and degradation of sugars other than hexoses, particularly pentoses is necessary for synthesis of nucleotides and other glycolytic intermediates. 
• Most important is the ability to synthesize NADPH, which has a unique role in biosynthetic reactions. 
• The direction of flow and path taken by G6P after entry into the pathway is determined largely by the needs of the cell for NADPH or sugar intermediates.

• When more NADPH than ribose 5-phosphate is required, the pathway leads to complete oxidation of G6P to CO2 and resynthesis of G6P from ribulose 5-phosphate.
•Alternatively, if more ribose 5-phosphate than NADPH is required, G6P is converted to fructose 6-phosphate and glyceraldehyde 3-phosphate by the glycolytic pathway.
•The distribution of the pentose phosphate pathway in tissues is consistent with its functions. It is present in erythrocytes for production NADPH, required to generate reduced glutathione, which is essential for maintenance of normal red cell structure.
• It is also active in liver, mammary gland, testis, and adrenal cortex, sites of fatty acid or steroid synthesis that also require the reducing power of NADPH. 

High energy phosphates are not produced in 

A. HMP shunt 
B. Oxidative pathway 
C. TCA 
D. Glycolysis




Ans. A. (HMP shunt)
Explanation 
.•“Hexose Monophosphate Shunt Pathway (HMP) produces NADPH that is required for several synthetic pathways, e.g., for fatty acids and steroid synthesis. However, the NADPH produced is not converted to ATP or used for energy production (unlike NADH produced in glycolysis and TCA cycle)” — Devlin and Rama Rao 
• The HMP shunt or pentose phosphate pathway serves several purposes, including synthesis and degradation of sugars other than hexoses, particularly pentoses is necessary for synthesis of nucleotides and other glycolytic intermediates. 
• Most important is the ability to synthesize NADPH, which has a unique role in biosynthetic reactions. 
• The direction of flow and path taken by G6P after entry into the pathway is determined largely by the needs of the cell for NADPH or sugar intermediates.

• When more NADPH than ribose 5-phosphate is required, the pathway leads to complete oxidation of G6P to CO2 and resynthesis of G6P from ribulose 5-phosphate.
•Alternatively, if more ribose 5-phosphate than NADPH is required, G6P is converted to fructose 6-phosphate and glyceraldehyde 3-phosphate by the glycolytic pathway.
•The distribution of the pentose phosphate pathway in tissues is consistent with its functions. It is present in erythrocytes for production NADPH, required to generate reduced glutathione, which is essential for maintenance of normal red cell structure.
• It is also active in liver, mammary gland, testis, and adrenal cortex, sites of fatty acid or steroid synthesis that also require the reducing power of NADPH. 

Wednesday, 15 March 2017

Gamma carboxylation of glutamic acid | NEET Based MCQ


Gamma carboxylation of glutamic acid in clotting factors II, VII and protein C is dependent on 

A. Vitamin K 
B. Vitamin C 
C. Vitamin A 
D. Vitamin E

Ans. A. (Vitamin K)
Explanation
•Vitamin K is required for the conversion of several clotting factors and prothrombin precursors to the active state. The mechanism of this action has been most clearly delineated for prothrombin.
•Prothrombin is synthesized as an inactive precursor called pre-prothrombin. Conversion to the active form requires a vitamin K-dependent carboxylation of specific glutamic acid residues to y-carboxyglutamic acid.
•The ‘y-carboxyglutamic acid residues are good chelators and allow prothrombin to bind Ca2.
•The prothrombin—Ca2 complex in turn binds to the phospholipid membrane, where proteolytic conversion to thrombin can occur in vivo.

•Factors 2, 7, 9 and 10 are synthesized in the liver as inactive precursors. They undergo post-translational modification: gamma carboxylation of glutamic residues. This step is Vitamin K dependant. 

Features of essential hypertension | PGI May 2017 Preparations MCQ


Features of essential hypertension 

A. Concentric hypertrophy of LV 
B. Increased heart size 
B. Increased size of the heart muscles 
D. Myohypertrophy 
E. Myohyperplasia


Ans. A. Concentric hypeetrophy of LV; (B) increasedheart size ; (C)  increased Size of heart muscle; (D) Myohypertrophy:
Features of essential hypertension are:-
• There is concentric hypertrophy of the left ventricles due to pressure overload of the heart.
• On physical examination the heart is enlarged.
• The weight of the heart is increased above the normal, often over 500 gm.
• Thickening of the Lt. ventricular wall, increased the ratio of its wall thickness to radius.
• Microscopically the earliest changes of systemic hypertensive heart disease is an increased in transverse myocytes diameter.
• In advanced stage the cellular and nuclear enlargement are prominent.
• There may be multiple minute foci of degenerative changes and necrosis in hypertrophied myocardium,
• Electron microscopy reveals increase in number of myofilaments comprising myofibrils, mitochondrial changes and multiple intercalated discs.

Autoimmune type-II Liver disease | PGI May 2017 Preparations MCQ


True about Autoimmune type-II Liver disease 

A. Antinuclear antibody 
B. LKM-1 antibody 
C. Anti smooth muscle antibody 
D. Ds DNA 
E. LC-1, & LC-2




Ans. B. LKM-1 antibody ;(E) LC-1, LC-2.

Depending upon the present of antibody in serum, autoimmune hepatitis is of 3 types:-
(1) AIH type I — It is characterised by ANA with or without SMA.
• It is the most common autoimmune hepatitis.
(2) AIH type II — Characterised by anti p 450 and anti UGT autoimmunity.
• LKM-l antibody against — P4502D6 is found.
• This type most commonly leads to fulminant hepatitis.
• Low IgA level also common.
• Common in paediatrics age group.
• Anti LC-1 (Liver cytosol-1) and LC-2 along with LKM-1 found.
(3) AIHtype-III is characterised by absence of ANA, SMA, and LKM-1 and anti SLA/L.P, and ASGPR (asialoglycoprotein receptor) is present.
• Long time result is most important for liver transplantation in type-2.

Anoxia of liver | PGI May 2017 Preparations MCQ


In anoxia of liver, necrosis is seen in: 

A. Centrilobular 
B. Around the periphery 
C. Around the central vein 
D. Around the bile duct
E. around the central artery



Ans. C. Around the central vein:
• The histological hallmark of ischemic hepatitis or shock1iver is zone three necrosis.
• Depending upon the degree of ischemia, a variable degree of architectual collapse around the central vein may occur with severe and prolonged ischemia. Necrosis may extended to the midzonal hepatocytes.
Note: Functions of different zone of liver.

Zone 1 — Glycogen synthesis and glycogenolysis inhibitor-I:
— Main area for protein metabolism
— Formation of plasma protein
— Conjugation of certain drugs.
Zone 3 —* Glycogen storage
Lipid and pigment formation metabolism of certain drugs and chemicals.
Zone 2 -4- Share functions of both zones.
 


Vasculitis | PGI May 2017


Vasculitis is seen in 

A. Burger’s disease 
B. HSP 
C. Gout 
D. Reiter’s disease 
E. Behcets syndrome



Ans. A. Burger’s disease ; (B) HSP; (D) Reiter’s disease ; (E) Behcet’s syndrome
Classification of vasculitis
I. Systemic necrotizing vasculitis
A. Poly arteritis nodosa (PAN)
1. Classic PAN
2.Microscopic polyangitis
B. Allergic angitis and granulomatosis of churg strauss
C. Polyangitis overlap syndrome.
II. Wegener’s granulomatosis.
III. Temporal arteritis
IV. Takayasu’s arteritis
V. Henoch-Schonlein purpura.
VI. Predominantly cutaneous vasctilitis. (hypersensitivity vasculitis)
A. Exogenous stimuli suspected
1. Drugs-induced vasculitis.
2. Serum sickness and serum sickness like reaction.
3. Vasculitis associated with infection disease
B. Endogenous antigen likely involved
1. Vasculitis associated with neoplasm.

2. Vasculities associated with connective tissue disease e.g. RA, SLE, sjogren syndrome.
3. Vasculitis associated with underlying disease e.g. SBE, EB virus infection HIV infection, ulcerative coilits ; congenital deficiencies of various complement components, retroperitonial fibrosis and primary biliary cirrhosis. Predominantly cutanous vasculitis with α-antitrypsin deficiency ;intestinal bypass surgery, and relapsing polychondritis.
4. Vasculitis associated with congenital deficiency of complement system.
VII. Other vaculitis syndrome
A. Kawasaki disease
B, Isolated central nervous system vasculitis
C. Thromboangiitis obliterans (Burger’s disease)
D. Behcet’s syndrome
E. Miscellaneous vascutilis
Direct infection related to vasculitis,
Bacterial (e.g. — Neisseria)
Rickettsial (e.g. Rocky Mountain spotted fever)
Spirochetal (e.g. syphilis)
Fungal (e.g. aspergillosis, murmor mycosis)
Viral (e.g. Herpes Zoster, variable hepatitis virus infection)
 → The seronegative arthropathies, amkylbsing spondylitis, Reiter’s Syndrome, Psoriatic arthrits and arthrities associated ulcerative colitis and regional enteritis may be accompained by paricarditis and
Proximal aoritis.

Monday, 27 February 2017

MCQ for tibial plateau fracture



Answer. D. The image shows a fracture of the vertical lateral condyle
Tibial plateau injury:
Fractures of the tibial plateau are caused by a varus or valgus force combined with axial loading (a pure valgus force is more likely to rupture the ligaments). This is sometimes the result of a car striking a pedestrian (hence the term ‘bumper fracture’); more often it is due to a fall from a height in which the knee is forced into valgus or varus.
The fractures are classified based on Schatzker classification.
Type 1: vertical split of lateral condyle
Type 2 – a vertical split of the lateral condyle combined withdepression of an adjacent loadbearing part of the condyle
Type 3 – depression of the articular surface with an intactcondylar rim
Type 4 – fracture of the medial tibial condyle (as shown in the image in MCQ)

Type 5 – fracture of both condyles

Saturday, 28 January 2017

Eosinophiluria | PGI May 2017 Preparations MCQ


Eosinophiluria is seen in :

A. PAN 
B. Microscopic polyangitis 
C. Interstitial nephritis 
D. Atherothrombotic emboli 
E. None




Ans. C. Interstitial nephritis , (D) Atherothrombotic emboli :
• Eosinophiluria (>5% of urine Leukocytes) is a common finding (- 90%) in antibiotic-
induced allergic nephritis
however lymphocytes predominate in allergic interstitial
Nephritis induced by NSAIDS.
Eosinophiluria is a feature of atheroembolic ARF,
• In PAN, Microspic polyangitis, eosinophilia is rare.


Complications of TBM | PGI May 2017 Preparations MCQ


Complications of TBM are :

A. Endarteritis 
B. Hydrocephalus 
C. Deafness 
D. Venoussinus infarct 
E. Mental Retardation


Ans. A. Endarteritis ;(B) Hydrocephalus :E. Mental Retardation

• Complications of TBM (T.B. meningitis)
— Mental Retardation.
— Seizure.
— Motor and cranial nerves palsies.
— Endarteritis (obliterative).
— Hydrocephalus
— Ventricular dilatation.
— Calcification
— Tuberculomas



Thalassemia occurs due to which mutations | PGI May 2017 Preparations MCQ


Thalassemia occurs due to which mutations 

A. Missense 
B. Splicing 
C. Transition 
D. Frame-shift 
E. Truncation


Ans. B) Splicing; D) Frame-shift

Important causes of thalassemia are

• β—thalasssemia : A wide variety of mutations in β—globin gene including deletion, nonsense and Frameshift mutation, and others affecting every aspects of its structure (e.g. splicing sites, promotor mutans)
•α-thalassemias . Mutations in α-globin gene mainly unequal crossing over and large DELETIONS and less commonly nonsense and Frame shift mutations.
• Mutations causing β-thalassernia can affect at any step in the pathway of globin geneexpression transcription, processing of m-RNA precursors, translation and post translational meta bolism of β—gIobin polypeptide chain

• The most common forms arise from mutations that derange SPLICING of mRNA precursor or permenantly terminate translation of mRNA.



Two specific tests to diagnose Wilson’s disease | PGI May 2017 Preparations MCQ

Two specific tests to diagnose Wilson’s disease are: 

A. KF ring 
B. Liver copper by dry weight of liver < 200 microgm/gm of dry weight 
C. Sr. Ceruloplasmin 
D. 24 hours urine copper after penicillamine 
E. Sr. copper


Ans. A. KF ring ; (C) Sr. Ceruloplasmin

The diagnosis of wilson’s disease is confirmed by demonstration of either
(i) Sr. Ceruloplasmin level <20 mg/dl and K.F. ring
(ii) Serum ceruloplasmin level <20 mg/dl and a concentration of copper in a liver biopsy sample >200 microgm/gm dry weight.
In the question, mentioned copper concentration 200 µgm/g dry wt. So, combined A, C will be the best choice.

Thursday, 26 January 2017

True about naturally occurring amino acids | PGI May 2017 Preparations


True about naturally occurring amino acids: 

A. All are racemic mixtures 
B. Have specific genetic code 
C. 20 in number 
D. All are D-isomers 
E. All are L-isomers



Ans. B. Have specific genetic code ; 
• Of the over 300 naturally occurring amino acids., 20 constitute the monomer units of proteins.

• Both D-amino acids and non a anion acids occur in nature, but only L α — amino acids arepresent in proteins. D-amino acids that occur naturally inclued D-serine and D-aspartate in brain tissue, D-alanine and D-glutamate in cell walls of Gram +ve bacteria and D-amino acids in some non-mammalian peptides and certain antibiotics.
• The genetic code is universal, specific, non-overlapping and degenerate. This universal nature of genetic code has lead to incorporation of 20 amino acids during protein synthesis in cells.
• Racemic mixture has both D and L isomers in equal concentration, thereby optically neutral.

Saturday, 21 January 2017

Naturally occurring amino acids | PGI May 2017 Preparations MCQ


True about naturally occurring amino acids: 

A. All are racemic mixtures 
B. Have specific genetic code 
C. 20 in number 
D. All are D-isomers 
E. All are L-isomers



Ans. B. Have specific genetic code ;
• Of the over 300 naturally occurring amino acids., 20 constitute the monomer units of proteins.
• Both D-amino acids and non a anion acids occur in nature, but only L α — amino acids arepresent in proteins. D-amino acids that occur naturally inclued D-serine and D-aspartate in brain tissue, D-alanine and D-glutamate in cell walls of Gram +ve bacteria and D-amino acids in some non-mammalian peptides and certain antibiotics.
• The genetic code is universal, specific, non-overlapping and degenerate. This universal nature of genetic code has lead to incorporation of 20 amino acids during protein synthesis in cells.
• Racemic mixture has both D and L isomers in equal concentration, thereby optically neutral.


Sunday, 15 January 2017

Pituitary Gland | PGI May 2017 Preparations


Which of the following statements is true regarding the pituitary gland?

A. It is separated from the optic chiasma by the sells turcica 
B. It is situated deep in the sella. 
C. The spenoidal air cells lie inferior to it 
D. It develops from the base of the 31 ventricle form the pars anterior 
E. It is supplied by a branch of the internal carotid artery


Ans. B.  It is situated deep in the sella. ; (C) The spenoidal air cells lie inferior to it.
(E) It is supplied by a branch of the internal carotid artery.

• The pituitary gland lies in the sella turcica or pituitary Fossa also called hypophysis Fossa
• The fossa is roofed by the diaphragmatic sellae over which lies the optic chiasma.
• It is supplied by sup. and inf. hypophyseal arteries which are branches of Internal Carotid Artery.
•Sphenoidal air Sinus lies inferior to it.
• Development of ant. pituitary— From Rathke’s pouch, an evagination of roof of the pharynx.
•Development of post pituitary: Evagination of the floor of the third ventricle in the region of infundibulum

Use of timolol in the eye can cause | PGI May 2017 Preparations


Use of timolol in the eye can cause: 


A. AV block 
B. Bradycardia 
C. Hypertension 
D. Hypotension 
E. Asthma


Ans. A. AV block; (B) Bradycardia; (D) Hypotension; (E) Asthma :
On topical application of β-blocker on eye, there can occur significant systemic absorption, producing systemic adverse effects :
• Bronchospasm
• Accentuation of heart block
• Congestive heart failure especially in elderly
• Bradycardia
• Other adverse effects: depression, anxiety, confusion, drowsiness, loss of libido, skin rashes, diarrhoea, nausea.


Combination use of beta blockers and calcium channel blockers | PGI May 2017

Combination use of beta blockers and calcium channel blockers cause 


A. Heart block 
B. Hypertension 
C. Hypotension 
D. Bradycardia 
E. Tachyarrhythimias


Ans. A. Heart block ; (D) Bradycardia :
• When β-blockers given with verapamil or diltiazem, they produce:-
— Additive sinus depression, conduction defects or asystole may occur resulting in marked bradycardia, A-V block.
— Cardiac arrest may occur.
• Nifedipine causes tachycardia, increased contractility and cardiac output due to reflex sympathetic stimulation, propranolol has been safely used with Nifedipine
• Propranolol, initially causes little change in BP (due to blockade of β-mediated vasodilation but on continued use fall in BP due to chronically reduced CO.).
— Verapamil dilates arterioles and some α-blocking activity — BP is only moderately lowered.

Treatment of choice for typhoid fever | PGI May 2017 Preparations

Treatment of choice for typhoid fever is:-

A. Cephalexin 
B. Gentamicin 
C. Co-trimoxazole 
D. Tetracycline 
E. Ciprofloxacin


Ans. (E) Ciprofloxacin:
• Till recently chloramphenicol was drug of choice for typhoid fever. But due to emergence of resistant- strains of S. Typhi, it is no longer used now a days.
• Due to emergence of MDR S. typhi — either quinolones or third-generation cephalosporins (e.g. ceftriaxone) are currently recommended for empirical antibiotic treatment.
• First and 2nd generation cephalosporins and aminoglycosides are ineffective.
• Drugs for chronic carrier — amoxycillin, TMP-SMX, Ciprofloxacin or Norfloxacin — shown 50-80% effective.
• S. typhi is now resistant to chloramphenicol, ampicillin, trimethoprim, Streptomycin, Sulfonamides, tetracycline

Saturday, 14 January 2017

True about Fat absorption | PGI May 2017 Preparations


True about fat absorption 

A. Fat in stool > 6 gm/day indicate malabsorption 
B. C-glycine test is most sensitive test 
C. Major fat absorption occurs in proximal intestine 
D. Steatorrhea means stool fat> 10 gm/day 
E. Steatorrhea is increased fat in stools >20gm/day



Ans. A. Fat in stool > 6 gm/day indicate malabsorption:
(C) Major fat absorption occurs in proximal intestine :
·      Normal fecal fat excretion is less than 6gm/day, more than 6 gm/24 hr indicates malabsorption.
• Fat absorption takes place in small intestine except short chain fatty acids which is absorbed in colon
• Sudan is best for screening but gold standard is quantitative estimation of fecal fat. OraL glycin glycolate test may show bile acid malabsorption, but not best for screening.
- Steatorrhea is defined as stool fatexeeeding 7g/day
- Daily fecal averages 15-25 g with small intestine disease, often exceeds 40 gm with pancreatic disease.


Thursday, 12 January 2017

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Wednesday, 11 January 2017

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Carbon Dioxide Retention | Carck PGI May 2017


Carbon dioxide retention is seen in the following condition 


A. Carbon monoxide poisoning 
B. Lung failure 
C. Drowning 
D. Ventilatory failure 
E. Highaltitude


 Ans. B. Lung failure; (C) Drowning; (D) Ventilatory failure:
• Retention of CO2 in the body (hypercapnia) caused by hypoventilation or circulatory deficiency.
• In Lung failure due to parenchymal causes (e.g. Fibrosis, poor diffusion through the pulmonary membrane or through the tissues); serious hypercapnia usually doesn’t occur because CO2 diffuses 20 times as rapidly as 02. If hypercapnia begins to occur, this stimulates pulmonary ventilation which corrects the hypercapnia.
• Hypercarbia associated with apnea or hypoventilation is less often documented than hypoxia in drowning.
• In CO-poisoning, there is variable PCO2
• Hypercapnia is not concomitant when too little 02 in the air, too little Hb, or poisoning of oxidative enzymes
• In high altitude due to hypoxic stimulation —hyperventilation occurs resulting in fall of PaCO2
produces respiratory alkalosis.