Immuno suppressants | Crack AIIMS, NEET 2017 with NIME MCQs

All are true for immuno suppressants except: 

A. Sirolimus acts by I cell modification 
B. Tacrolimus inhibits calcineuiin pathway 
C. Mycophenolate acts by inhibiting GMP dehydrogenase 
D. Cyclosporin is integral in transplant rejection regimen.

Ans. C.

Mycophenolate is a prodrug of mycophenolic acid which selectively inhibits inosine monophosphate dehydrogenase thus inhibiting lymphocyte proliferation, antibody production and cell mediated immunity. Available in oral &iv forms. 

• Newer applications are lupus nephritis, RA & some skin conditions. 

Cyclosporin:

Mech. of Action: enters target cells and binds to a protein cyclophilin forming a complex which inactivates calcineurin -1 gene transcription of IL-2/3, INF-alpha) Response of T helper cells to antigenic stimulation fails 

• Selectively increases cell mediated immunity 

• S/E: Nephrotoxicity, increase in BP, Hyperkalemia Hepatotoxicty, pecipitation of OMHirsuitism, gum hyperplasia, tremors 

Uses: 

i. Prevents graft rejection (most effective drug for it) 

ii. Autoimmune diseases (RA, 180 etc) 

iii. Psoriasis 

iv. Aplastic anemia 

Leukotriene receptor antoagonist | Crack AIIMS, NEET 2017 with NIME MCQs

Which of the following acts as a leukotriene receptor antoagonist? 

A. Zafirlukast 
B. Zileuton 
C. Cromoglycan sodium 
D. Deriphylline

Ans. A. 

The lukasts (Zafirlukast/Montelukast) competitively antagonize cys LT1 receptor mediated bronchoconstriction, increased vascular permeability and recruitment of eosinophilis. 

• Used for mild to moderate asthma 

• Headache, rashes, eosinophilia, neuropathy 

Zileuton: S-LOX inhibitor 

• Short duration of action and hepatotoxic potential limit it’s use. 

Filgrastrim | Crack AIIMS, NEET 2017 with NIME MCQs

Filgrastrim is used for: 

A. Neutropenia 
B. anemia 
C. polycythemia
D. Neutrophilia

Ans. A.

• Filgrastrim is recombinant human G-CSF (rHuG-CSE used to mitigate the adverse effects of anticancer drugs. 

- It is a nonglycosylated peptide of 175 aminoacids. 

• rHuGM-CSF has also been developed - called sargramostim. 

• SargramoStim is partly glycosylated peptide of amino acids. 

• Pegfilgrastrim (Pegylated filgrastrim) has much longer half life than filgrastrim and can be used once per chemotherapy cycle. 

Action

• Action mediated via JAKIST AT pathway 

• GM-CSF has broader biological actions than G 

CSF. It affects early & late granulocYtiC progenitor cells, erythroid and megakarYOcY progenitors. 

• GM-CSF also stimulates T cell proliferation (together with IL-2) and causes mobilization of peripheral blood stem cells (this property has therapeutic significance) GCSF>GMCSF. 

Toxicity: 

• G-CSF is better tolerated 

• G-CSF can cause bone pain (reversible on discontinuation) 

• GMCSF cart lead to - fever, malaise, arthratgiaS, myalgias and a capillary leak syndrome (characterized by pleurallpericardial effusions and peripheral edema) 

• Splenic rupture occurs rarely with G-CSF. 

Antiepileptic does not act via sodium channel blockade | Crack AIIMS, NEET 2017 with NIME MCQs

Which antiepileptic does not act via sodium channel blockade? 

A. Vigabatrin 
B. Carbamazepine 
C. Lamotrigine 
D. Phenytoin

Ans. A.

Vigabatrin (y vinyl GABA) - is all inhibitor of GABA 

- transaminase, hence decreases breakdown of GABA and increases its concentration in synaptic cleft. 

• Useful in refractory epilepsy esp partial seizures with/without generalization 

S/E: Behavior changes, depression, psychosis. 

Carbamazepine: Prolongation of sodium channel inactivation 

Lamotrigine: Prolongation of sodium channel inactivation; in addition it may directly block voltage sensitive Na+ channels. 

S/E: Sleepiness, dizziness, diplopia, ataxia, Rash. Phenytoin: Prolongation of sodium channel inactivation.

Gabapentin: Lipophilic GABA derivative which crosses to the brain and enhances GABA release, but doesnot act as agonist at GABA receptor. 

• It is now the first line drug for pain due to diabetic neuropathy and post herpetic neuralgia. 

• Topiramate: Weak carbonic anhydrase inhibitor; has broad-spectrum anticonvulsant activity. 

Also has other mechanisms of action like prolongation of Na+ channel inactivation, GABA potentiation by a post- synaptic effect and antagonism of certain glutamate receptors. 

S/E - Sedation, ataxia, Wt loss(wt gain by vaiproate), renal stones. 

Tiagabine - Inhibits GABA transporter GAT - (which removes synaptically released GABA into neurons and glial cells.) 

Which pathologic processes is an example of dysplasia | Crack AIIMS, NEET 2017 with NIME MCQs

Which of the following pathologic processes is an example of dysplasia? 

A. Actinic keratosis 
B. Chronic cystitis 
C. Chronic bronchitis 
D. Ulcerative colitis

Ans. A.  

Actinic keratosis is a form of dysplasia in sun-exposed skin. Histologically, such lesions are composed of atypical squamous cells, which vary in size and shape. They show no signs of regular maturation as the cells move from the basal layer of the epidermis to its surface. Dysplastic epidermis shares many features with squamous cell carcinoma, and untreated actinic keratosis often gives rise to invasive cancer. Chronic cystitis and bronchitis may result in foci of metaplasia, but these tend to be composed of differentiated cells that show no nuclear atypia. Squamous metaplasia of the columnar epithelium of the bronchi or the transitional epithelium of the urinary bladder may become dysplastic, but this transition is unpredictable. Therefore, these metaplastic lesions should not be grouped together with actinic keratosis, which is often referred to as “squamous cell carcinoma, one half.” Although dysplasia and even neoplasia can occur in the colonic mucosa affected by ulcerative colitis or in the columnar epithelium of Barrett’s esophagus, by itself neither ulcerative colitis nor Barrett’s esophagus should be classified as dysplasia.

Squamous metaplasia | Crack AIIMS, NEET 2017 with NIME MCQs

Squamous metaplasia occurs typically in 

A. bronchi of chronic smokers. 
B. skin exposed to sunlight. 
C. chronic gastritis
D. Barrett esophagus.

 Ans. A. Long-term smoking irritates the normal columnar bronchial epit helium, which undergoes squamous metaplasia (i.e., it transforms into stratified squamous epithelium). Skin cannot undergo squamous metaplasia, because it is already lined by stratified squamous epithelium. The term callus refers to thickening of the skin (e.g., as would be caused by ill-fitting shoes); it is an example of hyperplasia rather than metaplasia. Barrett’s esophagus represents a form of glandular metaplasia in which the normal squamous epithelium of the esophagus changes into gastric or intestinal epithelium. In chronic gastritis the normal gastric mucosa changes into intestinal epithelium but is not converted into squamous epithelium. 

Hypertrophic heart muscle cells | Crack AIIMS, NEET 2017 with NIME MCQs

Hypertrophic heart muscle cells contain increased amounts of 

A. water in the sarcoplasmic reticulum. 
B. smooth endoplasmic reticulum.
C. peroxisomes. 
D. Messenger RNA.

Hypertrophic cardiac myocytes, which are larger than normal, have more cytoplasm and larger nuclei than normal cells. The enlarged nuclei contain more DNA and RNA than their normal counterparts and generate more messenger RNA. The cytoplasm of hypertrophic myocytes contains more myofilaments and mitochondria, but the number of other cytoplasmic organelles is not increased. Water influx, which is typical of hydropic swelling, is not found in hypertrophy. 

Examples of atrophy | Crack AIIMS, NEET 2017 with NIME MCQs

All the following are examples of atrophy except 

A. skeletal muscle, following transection of its motor neuron
B. skeletal muscles, following long-term immobilization of the broken extremity in a cast
C. ovary following hypophysectomy
D. endometrium following long-term administration of estrogen

Ans. D. All answers except for D are examples of atrophy. Atrophy of skeletal muscles can result from a loss of innervation due to spinal cord or peripheral nerve trauma. Inactivity, as is often seen following the long-term immobilization of an extremity in a cast, has the same effect. Hypophysectomy is accompanied by atrophy of the thyroid, adrenal cortex, and ovary, which are all organs that depend on stimulation by pituitary trophic hormones. The brain atrophies with advancing age. Estrogen exerts trophic effects on the endometrium, causing hyperplasia rather than atrophy. Endometrial atrophy occurs following ovariectomy or after the menopause, when the ovaries no longer produce estrogen. 

Allergic bronchopulmonary aspergillosis diagnotic criteria | PGI May 2017 Preparations MCQ

Allergic bronchopulmonary aspergillosis diagnotic criteria are 

A. Peripheral eosinophilia> 0.1 x l07
B. Central lower lobe bronchiectasis 
C. ↑ IgG 
D. Detection of Aspergillus in sputum 
E. Asthma is always present

Ans. B. Central lower lobe bronchiectasis; (D) Detection of Aspergillus in sputum 

* In Allergic Bronchopulmonary Aspergillosis (ABPA), upper lobes are most likely to be affected for unknown reasons. ABPA occurs in atopic asthmatic (particularly Glucocorticoid dependent) individuals of age 20-40 years. Sometimes, may present without previous history of Asthma. It can occur in non-Asthmatic individuals, e.g. cystic fibrosis.

True about meningitis | PGI May 2017 Preparations MCQ

True about meningitis is /are 

A. Epidemic is caused by H influenzae 
B. E. coli, Group B Streptocci is the MC caused in neonatal period 
C. Haemophilus-B vaccine is effective in prevention of meningitis. 
D. Epidemics caused by Meningococcus group B
E. None of the above.

Ans. B. Gr ‘B’ streptococci, E. coli are MC cause in neonatal period; (C) Hib vaccine is effective in prevention of meningitis.

The most common organisms causing meningitis are: 

- Neisseria meningitidis 

- Streptococcus pneumoniae

- Haemophillus influenzae. 

* The epidemic of meningitis is caused by meningococcus. 

- Gr. A in —> Sub Saharan Africa 

- Gr. B in — Europe, Latin America, Newzealand 

-Gr. C&w 135 type. 

• Group B streptococci, str. Agalactiae was previously responsible for meningitis predominantly in neonates but it has been reported with increasing frequency in individuals >50 yrs, particulary those underlying diseases. 

• The frequency of H influenzae type b meningitis is declinect in children dramatically since the introduction of Hib conjugate vaccine. 

• Epidemics of H. influenzae disease have not been observed, although clusters of cases are seen 

in households, day care centers, and facilities for care of chronically ill children.

Pulmanary flow is decreased | PGI May 2017 Preparations MCQ

Pulmanary flow is decreased in 

A. Fallot’s tetralogy 
B. Ebstein’s anomaly 
C. Common atria 
D. TGV with intact septum 
E. Postoperative TGV correction

Ans. A. Fallot’s tetralogy ; (B) Ebstein’s anomaly.

• The route of blood flow in complete Transposition of great vessels (TGA) results in two separate circulation and survival depends on mixing that occur at a trial, ventricular or great vessel level. In TGA with intact septum, mixing occurs through foramen ovale and being small, the mixing is poor. Pulmonary plethora is seen. 

• In corrected TGA, route of blood flow is normal. Haemodynamics depend on associated anomalies.

• Normal or Decreased pulmonary blood flow with cyanosis is seen in

- Tricuspid atresia 

- Ebstein’s anomaly with atrial shunt 

- Pulmonary atresia with intact ventricular septum

- Pulmonic stenosis or atresia with VSD 

- Pulmonic stenosis with right to left atrial shunt

- Complete TGA with pulmonic stenosis 

- Double — out left ventricle with pulmonic stenosis 

- Single ventricle with pulmonic stenosis 

- Pulmonary AV fistula 

- Vena cava to Lt atrial communication. 

• Pulmonary blood flow increased in common artria. 

ACE inhibitor induced cough | PGI May 2017 Preparations MCQ

ACE inhibitor induced cough is mediated by. 

A. Bradykinin 
B. Substance - P 
C. Prostaglandin 
D. Serotonin 
E. Renin

Ans. A. Bradykinin ; (B) Substance—P ; (C) Prostaglandin

•About 5-20% of patients taking ACE inhibitors develop a non-productive cough. Onset is usually within 1 week of starting the drug but can be delayed up to 6 months. Mechanism is not known with certainty, but may be due to accumulation of bradykinin, substance-P, and / or prostaglandin which are degraded by ACE. 

• Treatment:Cough disappears within 4 days if stoppage. Sometime require cessation of therapy. 

• Thromboxane antagonism reduces ACE inhibitor induced cough. 

Fasciculation | PGI May 2017 Preparations MCQ

Fasciculation is seen in 

A. UMN type of lesion 
B. LMN type of lesion 
C. Myoneural junction 
D. Peripheral neuropathy
E. Anterior horn cell pathology

Ans. B. LMN type of lesion ;E. Anterior horn cell pathology.
• A fasciculation is a visible or palpable twitch within a single muscle due to spontaneous
discharge of one motor unit. The pathology lies in the anterior horn cells.
• Causes MND, Spinomuscular atrophy, poliomyelitis, syringomyelia, diabetic amyotrophy, hyperglycemia, hypoxia, organophosphorous poisoning.

HMB-45 is immunohistochemistry marker | Crack AIIMS, NEET 2017 with NIME MCQs

HMB-45 is immunohistochemistry marker for 

A. Melanoma 
B. Schwannoma 
C. Neurofibrorna 
D. Rhabdomyosarcoma

Ans. A. Melanoma.

Explanation 

• HMB-45 is immunohistochemical marker for melanoma

• HBN-45 is a monoclonal antibody originally, obtained from extract of malignant melanoma, which identifies an oncofel3l glycoconjugate associated with immature melanosomes and probably related to the tyrosinase engymatic system

• Originally thought to be specific for activated neoplastic melanocytes, it is now known to be expressed by other neural crest derived tumors, angiomyolipomas of the kidney and other sites, other components of tuberosus sclerosis complex (“PEComas”) and occassional carcinomas and other neoplasms. 

Malignant hypertension | Crack AIIMS, NEET 2017 with NIME MCQs

Which of the following changes do not occur in malignant hypertension? 

A. Segmental dilation of vessels 
B. Fibrinoid necrosis of arteriol 
C. Intimal thickening of arteriol 
D. Hyaline arteriosclerosis

Ans. D. (Hyaline arteriosclerosis)

Explanation
• Malignant nephrosclerosis is the form of renal disease associated with the malignant or accelerated phase of hypertension.
1. Fibrinoid necrosis of arterioles: In malignant hypertension, small muscular arteries show segmental dilation due t necrosis of smooth muscle cells. Endothelial integrity is lost in these regions and increased vascular permeability leak to entry of plasma proteins into the vessel wall, deposition of fibrin, and an appearance termed as fibrinoid necrosis.

2. In the interlobular arteries and arterioles, there is intimal thickening caused by a proliferation of elongated, concennically arranged smooth muscle cells, together with fine concentric layering of collagen and accumulation of pale stainii material that likely represents accumulations of proteoglycans and plasma proteins. This alteration has been referred s as onion-skinning (hyperplastic arteriolopathy) because of its concentric appearance. Other changes include necrotisir. glomerulitis and glomerular thrombotic microangiopathy.

3. In benign nephrosclerosis, on histologic examination of kidney, there is narrowing of the lumens of arterioles and sm arteries, caused by thickening and hyalinization of the walls (hyaline arterioloselerosis) 

Antiphospholipid antibody syndrome | Crack AIIMS, NEET 2017 with NIME MCQs

Antiphospholipid antibody syndrome is characterized by all of the following EXCEPT 

A. Recurrent abortions 
B. Arterial thrombosis 
C. Thrombocytopenia 
D. None of the above

Ans. D. (none) Explanation

• Individuals with the antiphospholipid antibody syndrome present with an extreme variety of clinical manifestations;

A. These are typically characterized by recurrent venous or arterial thrombi

B. Repeated miscarriages

C. Cardiac valvular vegetations

D. Thrombocytopenia

E. Venous thromboses occur most commonly in deep leg veins, but renal, hepatic, and retinal veins are also susceptible.
F. Arterial thromboses typically occur in the cerebral circulation, but coronary, mesenteric, and renal arterial occlusion have also been described.

G. Depending on the vascular bed involved, the clinical presentations can vary from pulmonary embolism (due to a low extremity venous thrombus), to pulmonary hypertension (from recurrent subclinical pulmonary emboli), to stroke bowel infarction, or renovascular hypertension. 

Ferruginous bodies | Crack AIIMS, NEET 2017 with NIME MCQs

Ferruginous bodies are seen in 

A. Silicosis 
B. Asbestosis 
C. Bagassosis 
D. Byssinosis (lung)

Ans. B. (Asbestosis)

Explanation
• Asbestosis is marked by diffuse pulmonary interstitial fibrosis, which is indistinguishable from diffuse interstitial fibrosis resulting from other causes, except for the presence of asbestos bodies.

• Asbestos bodies appear as golden brown, fusiform or beaded rods with a translucent center and consist of asbestos fibem coated with an iron-containing proteinaceous material.

• They arise when macrophages attempt to phagocytose asbestos fibers; the iron is presumably derived from phagocyte ferritin.

• Other inorganic particulates may become coated with similar iron protein complexes and are called ferruginous bodies. Sometimes asbestos bodies can be found in the lungs of normal people, but usually in much lower concentratioi and without interstitial fibrosis. 

Peripheral edema in CCF | PGI May 2017 Preparations MCQ

Peripheral edema in CCF is due to: 

A. Increased sympathetic tone 
B. ANP (atrial natriuretic peptide) 
C. Increased hydrostatic pressure 
D. Pulmonary hypertension
E. All of the above

Ans. A. Increased sympathetic tone; (C) Increased hydrostatic pressure :

* Oedema in CCF is due to :

— Activation of Renin angiotensin system. 

---- Increased sympathetic tone via intrinsic renal mechanism. 

— Increased capillary hydrostatic pressure. 

— Chronic hypoxia may cause injury to capillary wall causing increased capillary permeability. 

* Atrial Natri-uretic peptides released from atria in response to volume expansion This peptides cause increasedGFR and inhibit sodium reabsorption.

— Circulating units of ANP and BNP are elevated in CCF but obviously not sufficient to prevent edema formation and they evoke compensatory response tending to reduce cardiac load (preload and after load) by vasodilatation and by enhancing sodium and water excretion.

---- In oedematous state there is abnormal resistance to actions of Natriuretic peptides

Superior vena cava obstruction | PGI May 2017 Preparations MCQ

In superior vena cava obstruction following are true.

A. Dyspnea 
B. Palpitation 
C. Oedema of the head and neck 
D. Enlarged dilated veins on anterior chest wall 
E. ↑ed JVP

Ans. (A) Dyspnea (C) Oedema of head and neck; (D) Enlarged dilated veins on anterior chest; (E) ↑ed JVP: 

• Symptoms of superior vena cava syndrome (SVCS) : Swelling of face and neck, dyspnea, and cough, hoarseness, tongue swelling, headaches, nasal ongestion, epistaxis, hemoptysis, dysphagia, pain, dizziness, syncope and lethargy, visual disturbances, stupor, 

• Signs of SVCS : Non-pulsatile distension of neck veins, oedema and cyanosis of head, neck, hands and arms, dilated anastomatic veins on ant. chest wall. In more severe cases proptosis, glossal and laryngeal edema, and obtundation. 

• CXR : Superior mediastinal widening, most commonly on right side. 

Note : Causes of SVCS:

— Malignancy (90%) like lung cancer (particularly small cell and squamous cell carcinoma accounts 85% of all malignancies), lymphoma and metastatic tumours. 

— Benign lesions: Chronic fibrotic mediastihum (e.g. T.B. histoplasmosis, pyogenic infections, drugs), thrombophlebitis, aneurysm of aortic arch, constrictive pericarditis. 

• Rx of SVCS : Radiation therapy is primary Rx for SVCS caused by Ca Lung. 

Treatment of DI | PGI May 2017 Preparations MCQ

Treatment of DI 

A. ADH 
B. Thiazide 
C. Loop diuretics 
D. Insulin 
E. Chlorpromazine

Ans. A. ADH; (B) Thiazide
• Desmopressin (DDAVP = desamino-D-arginine-8 vasopressin) acetate is the treatment of choice for central diabetes insipidus. It is a synthetic analogue of AVP that acts selectively at V2 receptors to increase urine concentration and decrease urine flow in dose dependent manner. Lypressin or vasopressin are alternatives.
• Other drugs for DI.
Chlorpropamide for pituitary DI
— Thiazide diuretics for Nepbrogenic DI
— Carbamazipine reduced the urine volume in pituitary DI
— Clofibrate has shown beneficial for nephrogenic DI
— Indomethacin

Herpes simplex encephalitis | PGI May 2017 Preparations MCQ

Herpes simplex encephalitis is diagnosed by 

A. MRI 
B. Biopsy 
C. Corneal scrapping and culture 
D. EEG periodic lateralised 
E. CSF PCR of HSV DNA

Ans. E. CSF PCR for HSV DNA : 

• HSV DNA polymerase chain reaction (PCR) in CSF is a rapid and sensitive and specific tool for early diagnosis and rapidly replacing brain biopsy as the diagnostic standard. 

According to Harrison it is the diagnostic procedure of choice with sensitivity (98%) and specificity (94%), equal or exceed brain biopsy. PCR results are not generally affected  with1 wk of antiviral therapy. 

• Brain biopsy:The isolation of HSV from brain tissue obtained at biopsy was once “gold standard” for diagnosis of HSV encephalitis although with advent of CSF PCR tests for HSV,itis no longer necessary to perform biopsy. Tissue is cultured for virus and examined histopathologically and ultrastructurally. 

•MRI, CT, ECG: Less sensitive than HSV DNA PCR. Approx 10% and 33% of PCR documented cases have normal MRI and CT respectively. CT is less sensitive than MRI. EEG abnormalities occur in >90% of PCR documented cases. HSV encephalitis show focal findings 

(i) Areas of increased signal intensity in frontotemporal, cingulate or insular regions of brain on T2 weighted spino-echo MRI images. 

(ii) Temporoparietal areas of low absorption, mass effect and contrast enhancement on CT. 

(iii) Periodic focal temporal lobe spikes on a back ground of slow or low amplitude activity (flattened) on LEG. BEG finding is non specific. 

• CSF shows lymphocytic pleocytosis, mildly elevated protein, normal glucose, CSF culture for HSV-I encephalitis is invariably negative. 

• Serologic studies and antibodies detection : CSF HSV antibodies and antigen detection are done after 1 week of illness and who are CSF FCR negative for HSV. They are of limited value in 1st week of illness.

The RAS family of oncoproteins | Crack AIIMS, NEET 2017 MCQs

The RAS family of oncoproteins is an example of: 

A. Growth factors 
B. Signal transducing proteins 
C. Growth factor receptors 
D. Transcription factors

Ans. B. Signal Transduction Proteins

• Is a protein subfamily of small GTPases that are involved in cellular signal transduction, and is also used to designate gene subfamily of the genes encoding those proteins.
• Activation of Ras signalling causes cell growth, differentiation and survival.
• Ras is the prototypical member of the Ras superfamily of proteins which are all related in structure and regulate diverse cell behaviours.

Most important route of occupational exposure to lead | Crack AIIMS, NEET 2017 MCQs

The most important route of occupational exposure to lead is: 

A. Ingestion 
B. Absorption 
C. Inhalation 
D. Absorption

Ans. C. inhalation

• Populations are exposed to lead chiefly via paints, cans, plumbing fixtures and leaded gasoline. 

• The intensity of these exposures remains high because of the deterioration of lead paint used into the past and the entrainment of lead from the paint and vehicle exhaust into soil and household. 

• Greatest source of environmental (non-occupational) is gasoline 

• Most common mode of absorption in case of occupational lead poisoning is inhalation of flumes and dust of lead and its compounds

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

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. 

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.