Injury to the tibial nerve PGI MCQ

Injury to the tibial nerve results in:

A. Calcaneo-valgus deformity of the foot
B. Foot drop
C. Claw like deformity of the toes
D. Loss of sensation of the sole of the foot
E. Loss of sensation of the lateral aspect of the leg

The Answer is. A. Calcaneovalgus deformity of the foot, C. Claw like deformity of the toes, D. Loss of sensation of the sole of the foot

Injury to the tibial nerve results in calcaneovalgus deformity ofthe foot, claw like deformity of the toes and loss of sensation tothe sole of the foot. The common peroneal nerve providessensation to the anterolateral aspect of the lower leg, includingthe ankle and dorsum of the foot. Injury to the commonperoneal nerve results in foot drop.

Communicating Hydrocephalus | PGI MCQ

Which of the following are communicating hydrocephalus?

A. Choroid plexus carcinoma
B. Post hemorrhagic
C. CSF infection
D. Ventricular wall lesions
E. Raised CSF protein

The Answer is. B. Post hemorrghagic, C. CSF infection, E. Raised CSF protein

Aetiology of hydrocephalus

Obstructive hydrocephalus

1. Lesions within ventricle                  2. Lesions in the ventricular wall     

3. Lesions distant from the ventricle but with a masseffect

Communicating hydrocephalus

1. Post haemorrghagic                        2. CSF infection                   3. Raised CSF Protein

Excessive CSF production (rare)

Choroid plexus papilloma/carcinoma

Anatomy of Esophagus

Which of the following is incorrect regarding anatomy of esophagus?

A. The length of the esophagus is 40cm
B. It is lined throughout by columnar epithelium
C. The proportion of the smooth muscle decreaseson progression from upper to lower end whencompared to skeletal muscle.
D. The lower esophageal sphincter is powerful striated muscle
E. Cricopharyngeal sphincter is located at 15cmfrom upper incisor teeth.

Correect Ans A

The length of the esophagus is 40cm, B. It is lined throughout by columnar epithelium, C. The proportion of the smooth muscle decreaseson progression from upper to lower end when compared to skeletal muscle. D. The lower esophageal sphincter is powerfulstriated muscle. 
The length of the esophagus is 25 cm. It is lined by squamous epithelium throughout and the musculature of the upper esophagus is striated. Thisis followed by a transitional zone of both striated andsmooth muscle with the proportion of the latterprogressively increasing so that in the lower half, there issmooth muscle.Upper sphincter is powerful striated muscle. The lower sphincter is more subtle, created bythe asymmetrical arrangement of themuscle fibres.There is no serosal layer.

The brain tumors is highly vascular in nature

Which one of the following brain tumors is highly vascular in nature? 

A. Glioblastoma 
B. Meningiomas 
C. CP angle epidermoid 
D. Pituitary adenomas

Answer. A. (Glioblastoma) 

• Both glioblastoma and meningioma are highly vascular tumors. 

• Glioblastoma is highly vascular tumor, sometimes so vascular that it resembles an

arteriovenous fistula on angiography. 

Component of Glasgow Coma Scale

All of the following EXCEPT component of Glasgow Coma Scale is 

A. Eye opening 
B. Motor response 
C. Pupil size 
D. Verbal response

Answer. c (Pupil size) 

Glasgow Coma Scale

Best motor response [M]		Best verbal response [V]		Eye opening [E]
Obeys  to verbal Command	6	Oriented and converses	5	Spontaneous	4
Localizes pain to painful stimuli	5	Disoriented and converses	4	To speech	3
Flexion withdrawal	4	Inappropriate words	3	To pain	2
Flexion abnormal	3	Incomprehensible sounds	2	No response	1
Extension	2	No response	1
No response	1
TOTAL (E+V+M)	3 (minimum) – 15 (maximum)

Rupture of a berry aneurysm of the Circle of Willis

Rupture of a berry aneurysm of the Circle of Willis would likely produce hemorrhage into the 

A. Epidural space 
B. Cerebellum 
C. Subarachnoid space 
D. Subduraispace

Answer. C. Subarachnoid space

• Subarachnoid hemorrhage is much less common than hypertensive intracerebral hemorrhage, and most often it results from rupture of a berry aneurysm.

• Berry aneurysms are saccular aneurysms that result from congenital defects in the media of arteries.

• They are not the result of atherosclerosis. Instead, berry aneurysms are called congenital, although the aneurysm itself is not present at birth.

• Berry aneurysms are most commonly found in the circle of Willis.

• The chance of rupture of berry aneurysms increases with age (rupture is rare in childhood).

• Rupture causes marked bleeding into the subarachnoid space and produces severe headaches, typically described as the worst headache ever.” Additional symptoms include vomiting, pain and stiffness of the neck (due to meningeal irritation caused by the blood), and papilloedema and death.

Neuronophagia of anterior horn neuron

Neuronophagia of anterior horn neurons is characteristic of 

A. JC virus infection 
B. Treponema pallidum infection 
C. Poliovirus infection 
D. St. Louis encephalitis

Answer.  C. poliovirus infection

> Poliomyelitis is caused by an enterovirus that causes a nonspecific gastroenteritis and then secondarily invades the anterior horn motor neurons of the spinal cord. Microscopy reveals characteristic neuronophagia of anterior horn neurons; the dorsal roots are not affected. Infection causes acute muscular paralysis (atrophy, fasciculations, fibrillation, and hyporeflexia).

> Postpolio syndrome occurs more than 25 years later, with progressive weakness, decreased muscle mass, and pain. Progressive Multifocal Leukoencephalopathy (PML)

• In contrast, progressive multifocal leukoencephalopathy (PML) is a viral infection of oligodendrocytes that causes demyelination and symptoms of dementia and ataxia.

• The pathognomonic feature of PML is oligodendrocytes in areas of demyelination having a “ground-glass” appearance of their nuclei. PML occurs as a terminal complication in immunosuppressed individuals. 

GLP-1 agonist

Which of the following is a GLP-1 agonist? 

A. Pramlintide 
B. Exenatide 
C. Sitagliptin 
D. None of the above

Answer. B. Exenatide

Alpha–Glucosidase inhibitors	¯Glucose absorption	Acarbose, Miglitol
Dipeptidyl peptidase IV inhibitors	Prolong endogenous GLP-1 action	Sitagliptin
GLP-1 agonist	­Insulin, ¯Glucagon, slow gastric emptying	Exenatide
Amylin agonist	Slow gastric emptying, ¯Glucagon	Pramlintide

TPN develops deficiency of:

A pt. on TPN develops deficiency of: 

a. Folic acid 
b. Iron 
c. Vitamin B-12 
d. Copper 
e. Fatty acids

Ans (A) Folic acid; (B) Iron; (C) Vitamin B-12; (D) Copper; (E) Fatty acids;

• Metabolic complications of total Parenteral nutrition (TPN):-

First 48 hr onwards	First 2 Wk	3 months onwards
Fluid overload	Cardiopulmonary failure	Essential fatty acid deficiency
Hyperglycemia	edema	Iron deficiency
Hypophosphatemia Hypokalemia	Hyperosmolar non-ketotic hyperglycemic coma Acid balance imbalance Electrolyte imbalance	Vitamin deficiencies TPN metabolic bone disease TPN liver disease Zinc,Copper Chromium, selenium, Molybdenum Deficiency

Characteristic of intravascular hemolysis

Markedly decreased blood levels of which one of the listed substances are most characteristic of intravascular hemolysis?

A. Alkaline phosphatase 
B. Bilirubin
C. Haptoglobin 
D. Lactate dehydrogenase

The answer is c. Destruction of red cells (hemolysis) may occur within the vascular compartment (intravascular hemolysis) or within the mononuclear-phagocyte system (extravascular hemolysis). In both cases, the hemolysis leads to anemia, and the breakdown of hemoglobin leads to jaundice due to increased indirect bilirubin. Intravascular hemolysis releases hemoglobin into the blood (hemoglobinemia); this hemoglobin then binds to haptoglobin. When haptoglobin levels are depleted, free hemoglobin is oxidized to methemoglobin, and then both hemoglobin and methemoglobin are secreted into the urine (hemoglobinuria and methemoglobinuria). Within the renal tubular epithelial cells, hemoglobin is reabsorbed and hemosiderin is formed; when these cells are shed into the urine, hemosiderinuria results. Since extravascular hemolysis does not occur within the vascular compartment, hemoglobin- emia, hemoglobinuria, methemoglobinuria, and hemosiderinuria do not occur. The breakdown of the red cells within the phagocytic cells causes anemia and jaundice, just as with intravascular hemolysis, and, since hemoglobin escapes into the blood from the phagocytic cells, plasma haptoglobin levels are also reduced. Unlike the case with intravascular hemolysis, the erythrophagocytosis causes hypertrophy and hyperplasia of the mononuclear phagocytic system, which in turn may lead to splenomegaly. 

Red cell abnormalities is most indicative of hemolysis

Which of the following red cell abnormalities is most indicative of hemolysis?

A. Target cells 
B.Acanthocytes
C. Schistocytes 
D. Basophilic stippling

The answer is c. Abnormalities of red cells can help to identify a disease process. Schistocytes, which are red cell fragments, indicate the presence of hemolysis, and they can occur in hemolytic anemia, megaloblastic anemia, or severe burns. Red cell shapes characteristic of hemolysis include triangular cells and helmet cells. Target cells (red cells with a central dark area) are the result of excess cytoplasmic membrane material and are found in patients with liver disease, such as obstructive jaundice, or in any of the hypochromic anemias. Acanthocytes are irregularly spiculated red cells found in patients with abetalipoproteinemia or liver disease. Echinocytes, in contrast, have regular spicules (undulations) and may either be artifacts (crenated cells) or be found in hyperosmolar diseases such as uremia. Basophilic stippling of red cells (irregular basophilic granules within erythrocytes) varies from fine granules, seen in young reticulocytes (polychromatophilic cells), to coarse granules seen in diseases with impaired hemoglobin synthesis, such as lead poisoning and megaloblastic anemia. Heinz bodies are formed by denatured hemoglobin and are not seen with routine stains. They are found in patients with glucose-6-phosphatase dehydrogenase deficiency and the unstable hemoglobinopathies.

Megaloblasts result from the impaired synthesis

Megaloblasts result from the impaired synthesis of

A. DNA 
B. RNA
C. Glutathione 
D. β-globin chains

The answer is a. Deficiency of either vitamin B12 or folate results in megaloblastic anemia. Deficiency impairs DNA syn-thesis and delays mitotic division, which in turn causes the nuclei to be enlarged. The synthesis of RNA and cytoplasmic elements is not affected, however, so there is nuclear-cytoplasmic asynchrony. These cellular changes affect all rapidly proliferating cells in the body, but in the bone marrow they result in enlarged erythroid precursors, which are referred to as megaloblasts. These abnormal cells produce abnormally enlarged red cells, which are called macroovalocytes. These megaloblasts also undergo autohemolysis within the bone marrow, resulting in ineffective erythropoiesis. Granulocyte precursors are also enlarged and are called giant metamyelocytes. These abnormal cells produce enlarged hypersegmented neutrophils. The megakaryocytes are large and have nuclear abnormalities, but, although the platelet count is decreased, the platelets are not enlarged. Abnormalities of glutathione production are seen in patients with glucose-6-phosphate dehydrogenase deficiency, while decreased synthesis of β-globin chains is seen in patients with β thalassemia. Abnormalities of decay-accelerating factor are seen in patients with paroxysmal nocturnal hemoglobinuria. 

Immune thrombocytopenic purpura

Antibodies made in the spleen that are directed against the cell surface antigens GpIIb/IIIa or GpIb/IX are characteristically seen in individuals with

A. Cold autoimmune hemolytic anemia
B. Felty’s syndrome
C. Hashimoto’s thyroiditis
D. Immune thrombocytopenic purpura

The answer is d. Idiopathic (immune) thrombocytopenic purpura (ITP) is a major cause of increased peripheral destruction of platelets. Clinically, ITP may be divided into an acute form and a chronic form. The acute form is more commonly seen in children following a viral infection, while the chronic form is more often seen in adult women of childbearing years. Most individuals with ITP are asymptomatic, but if the platelet count drops low enough, they may develop petechial hemorrhages or epistaxis, usually after an upper respiratory infection. Both clinical types of ITP are associated with the development of antiplatelet antibodies, mainly against the platelet antigens GpIIb/IIIa and GpIb/IX.

Adnexal Tumors

All of the following are adnexal tumors, except: 

A.Trichoepithelioma
B. Sebaceous adenoma
C.Trichilemmoma
D. Benign fibrous histiocytoma

Ans. (d) Benign fibrous histiocytoma

• Adenexal Or Appendegeal tumors arise from cutaneous appendages.
• They may serve as markers for internal malignancies.
• They are mostly in the form of solitary or multiple nodules/papules.

Benign fibrous histiocytoma is a benign dermal neoplasm.

Most common presentation is a dermatofibroma.

They are most common in adults with indolent behavior and appear as tan to brown firm papules

To diagnose hyperglycemia of two weeks old

To diagnose hyperglycemia of two weeks old the best investigation retrospectively is 

A. Ketone bodies 
B. Glycosated hemoglobin 
C. Glucose in the blood 
D. Chromosomal study


Ans. (b) Glycosylated HB
• Normal whole blood hemoglobin A₁ is approximately 4 to 6 percent of total hemoglobin; reflect the metabolic
• Control over the preceding 3 months,
• Hemoglobin A₁ may be falsely elevated in patients whose diabetes is unstable when the intermediate
• Precursor is elevated, e.g. in alcoholism and falsely lowered in conditions of shortened red blood cell lifespan, e.g. in anemia and acute or chronic blood loss or in patients with hemoglobinopathies, e.g. sickle cell disease. 

Acid mucinis

Acid mucinis best demonstrated by the stain 

A.Alcian blue 
B. Periodic Acid Schiff (PAS) 
C. Van Gieson 
D.Reficulin

Ans. (a) Alcian blue
Stains:
> Von kossa:                         Calcium
> Toluidine blue:                  Mast cells
>Alician blue:                       Mucins
> Congo red:                         Amyloid
Masons trichome:                 Collagen, connective tissue
Orcein:                                  Elastic fibers

Chioroma

Chioroma is a tumor of: 

A. Soft tissue 
B. Bone 
C.Hemopoietic cell 
D. Ovary

Ans. (c) Hemopoeticcells
• In AML (Leukemia) rarely patients may present with symptoms from a mass lesion located in the soft tissues, breast, uterus, ovary, cranial or spinal dura, gastrointestinal tract, lung, mediastinum,
prostate, bone, or other organs.
• The mass lesion represents a tumor of leukemic cells and is called a granulocytic sarcoma, or chioroma.
• Derived from hemopoetic cells.

Type I helper cells

Type I helper cells secrete:

A. Interleukin-l 
B. Interleukin-2 
C. Interleukin-4 
D. Interleukin-5

Ans. (b) IL -2
• Interleukins are “cytokines”.
• Proteins of usually low molecular weight.
• Regulating important biological processes.
• Interleukins are produced by Monocytes, Macrophages, B and T Lymphocytes, mast cells, neutrophils.
IL1 causes fever
IL2 T cell stimulation
IL3 Bone Marrow stimulation
IL4 IgE Stimulation
IL5 IgA Stimulation 

Lesion in Wernicke’s encephalopathy

Lesion in Wernicke’s encephalopathy occurs in 

A. Mamillary body 
B. Cerebellum 
C. Motor cortex 
D. Substantia nigra

Ans. (a) Mammillary body 

• Psychosis occur in Wernicke Korsakoff syndrome secondary to thiamine deficiency. It is consistent with pathologic changes in the cortex, cerebellum, and mammillary bodiesof the thalamus. 

• Parenteral thiamine should be given prophylactically to all chronic alcoholic patients in the emergency room, or as soon as they are admitted, to prevent precipitation of thiamine deficiency after the provision of glucose-containing solutions

Thoracic vertebra and Typical cervical vertebra

Difference between thoracic vertebra and typical cervical vertebra is 
A. Has a triangular body
B. Has a foramen transversarium
C. Superior articular facet directed backwards and upwards
D. Has a large vertebral body

Answer B. Has a foramen transversarium

Cervical vertebra is square shaped with concave superior surface and convex inferior surface. Each transverse process is trough shaped and perforated by a round foramen transversarium. Spinous process is bifid and short; vertebral foramen is triangular shaped. Thoracic vertebra is heart shaped and vertebral foramen is circular having superior and inferior costal facets for articulation with the rib. 

Anterior Interosseous Nerve

All muscle strictly receive nerve supply from anterior interosseous nerve except

A. Pronator quadrates
B. Flexor pollicis longus
C. Flexor digitorum profundus of index finger
D. Flexor digitorum profundus of middle finger

Answer .D. Flexor digitorum profundus of middle finger

·         Flexor digitorum profundus of middle finger is supplied by the ulnar nerve in 20% of the population.

·         Anterior interosseous nerve (AIN),a branch of median nerve, supplies all the deep muscles of the anterior  forearm exceptpart of the flexor digitorum profundus.

·         Flexor digitorum profundus (FOP) gives 4 tendons to the 4 fingers (except finger no. 1 - the thumb!).

·         FDP of Finger no. 2 & 3 are controlled by the AIN and 4 & 5 by the ulnar nerve majority of the population. It is evident that the middle finger is mostly supplied by the AIN.

·         In 20% of the population the ratio is 3:1 (AIN supplying the finger no. 1, 2 & 3, whereas, ulnar supplying only the finger 4). It is evident that even the ring finger is being supplied by AIN here.

·         In 20% of the population the ratio is 1 :3, that is , AIN supplies finger no. 1 and 2, 3, & 4 are supplied by the ulnar nerve. Here it is evident that FDP of middle finger is being supplied by the ulnar nerve.

·         Hence, FDP of middle finger is supplied by the AIN in 80% of the population, but in 20% of the population it is supplied by the ulnarnerve. 

‘Mallet finger’ MCQ

‘Mallet finger’ is a common traumatic lesion resulting in flexion deformity of distal interphalangeal joint. The basic pathology of this condition is 

A. Avulsion fracture of middle phalanx 
B. Rupture of collateral slips of extensor expansion 
C. Rupture of central slip of extensor expansion 
D. Dislocation of distal interphalangeal joint

Answer. B. Rupture of collateral slips of extensor expansion

‘Mallet finger’ describes the characteristic drooping of the finger observed with injury to the extensor digitorum at its insertion at the base of the distal phalanx (the collateral slips). o A mallet finger may result from direct trauma to the finger tip or more commonly, by forcibly bending the finger in extension, for example, when catching a ball – hence, the synonym, ‘baseball finger.” o In older patients, the associated trauma may be minor for example, catching the tip of the finger whilst changing the sheets on the bed.

o The extensor mechanism is disrupted. The finger is held flexed at the distal interphalangeal joint. There is no active movement but passive movement is unimpaired. In time, the proximal phalanx 

may become hyperextended.

o An x-ray should be obtained to look for any associated chip fracture.

o Most injuries are treated conservatively. A mallet finger splint is applied to hold the distal interphalangeal extended whilst permitting movement at the proximal interphalangeal joint.

o If conservative treatment fails then part of the tendon is excised over the terminal phalanx and the joint held extended with a Kirschner wire.

o Extensor expansion (dorsal expansion, dorsal hood) refers to the flattened tendons (aponeurosis) of extensor muscles that run into the back of the hand.

o At the distal end of the metacarpal, the extensor tendon will expand to form a hood, which covers the back and sides of the head of the metacarpal and the proximal phalanx.

o The expansion soon divides into three bands:

* Two lateral bands pass on either side of the proximal phalanx and stretch all the way to the distal phalanx. The lumbricals of the hand, the palmar & dorsal interossei of the hand, also insert on these bands.

* A single median band passes down the middle of the finger along the back of the proximal phalanx, ending at the base of the middle phalanx