Q1. Commonest site of Hypertensive bleed is in the (Bihar/AYUSH)Homoeo/MO/QP):
b) Frontal lobe
d) Temporal lobe
Note Out of above given variables (a) Thalamus – is suggested.
Stem: Hypertensive bleed
Hypertensive Intracerebral Hemorrhage results from rupture of small, penetrating arteries. Hypertensive angiopathy (small vessel disease) stiffens vessel walls and makes them fragile. This, in conjunction with increased pressure from within the lumen, causes vascular rupture and hemorrhage. Hypertensive hemorrhage is parenchymal and its most frequent sites of are the basal ganglia and thalamus. Less commonly, it involves the cerebellum, the pons, and occasionally the subcortical white matter. Ref: http://neuropathology-web.org/chapter2/chapter2cCerebralhemorrhage.html
Review of variables
Hypertensive intracerebral haemorrhages to their typical locations in order of frequency are: Basal ganglia (especially the putamen), Thalamus, Pons and Cerebellum. Ref: Dr Henry Knipe and Dr Frank Gaillard et al.
Frontal Lobe -NA-
Temporal Lobe -NA-
Ref: Golwalla – NA-
Q.2. Xeroderma pigmentosa is produced as a result of a defect in? (Bihar AYUSH Homoeo/MO/ QP/2014):
a) DNA polymerase I
b) DNA polymerase II
c) DNA exonuclease
d) DNA ligase
Note From the variables given above the most suitable choice is (c) DNA exonuclease.
Stem: Xeroderma pigmentosa
Review of variables
(a) DNA polymerase I: DNA Polymerase I (or Pol I) is an enzyme that participates in the process of DNA replication. Ref: http://en.wikipedia.org/wiki/DNA_polymerase_I
(b) DNA polymerase II: DNA polymerase II (also known as DNA Pol II or Pol II) is a prokaryotic DNA polymerase most likely involved in DNA repair. Ref: http://en.wikipedia.org/wiki/DNA_polymerase_II
(c) DNA exonuclease: Exonucleases are enzymes that work by cleaving nucleotides one at a time from the end (exo) of a polynucleotide chain.
Xeroderma pigmentosum is caused by a defect in the exonuclease (or any of 8 other genes) which removes pyrimidine dimers.
Ref: Chapter 28: DNA Structure, Replication and Repair-Biochemistry 461
(d) DNA ligase: In molecular biology, DNA ligase is a specific type of enzyme, a ligase, (EC22.214.171.124) that facilitates the joining of DNA strands together by catalyzing the formation of a phosphodiester bond. It plays a role in repairing single-strand breaks in duplex DNA in living organisms, but some forms (such as DNA ligase IV) may specifically repair double-strand breaks (i.e. a break in both complementary strands of DNA). Ref: http://en.wikipedia.org/wiki/DNA_ligase
Q.3. The following is NOT TRUE about montoux test (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) It is a specific test
b) It is only tool available for estimating prevalence of TB in a community
c) Induration of 10mm indicates positive test
d) New cases occur more commonly in patients who are tuberculin reactors
Note Out of the variables given above (a) It is a specific test is suggested for-NOT TRUE.
Review of variables
(a) It is a specific test
Mantoux test is a widely used test for latent TB. (The problem with using it in countries with high rates of TB infection is that the majority of people may have latent TB.) It was developed by Koch in 1890 but the intradermal technique currently in use as described in 1912 by Charles Mantoux, a French physician who developed on the work of Koch and Clemens von Pirquetto to create his test in 1907. However, various factors both in the host and inherent in the test lower both its specificity and sensitivity. Due to the test’s low specificity, most positive reactions in low-risk individuals are false-positives. A false-positive result may be caused by non-tuberculous mycobacteria or previous administration of BCG vaccine. Prior vaccination with BCG may result in a false-positive result for many years later. Ref: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481914/
(b) It is only tool available for estimating the prevalence of TB in a community
Epidemiologists have used it extensively for assessment of tuberculosis situation in different communities. In clinical practice, it is used to find out the presence or absence of tuberculous infection. Articles%5CIPTUVI01.pdf
(c) Induration of 10mm indicates positive test
A reaction with induration between 10 to 14 mm could be attributable to infection with tubercle bacilli or due to cross-sensitivity to environmental mycobacteria and/or BCG-induced sensitivity Articles%5CIPTUVI01.pdf
(d) New cases occur more commonly in patients who are tuberculin reactors
Most persons who are exposed to a person with active TB and become infected do not develop active disease, but rather have latent, asymptomatic infection for long periods of time. Active TB is usually the result of reactivation of latent infection. The symptoms of active disease include fatigue, fever, weight loss, cough, pleuritic chest pains, and hemoptysis. TB is, however, a treatable disease. Ref: http://www.ncbi.nlm.nih.gov/books/NBK64733/
Q4. Diseases in which herd immunity does not protect an individual is (Bihar/AYUSH/Homoeo/MO/ QP/2014):
Note Out of the variables given above the (c) Tetanus – is suggested for-Herd immunity does not protect from tetanus.
Stem: Herd Immunity
Unimmunized persons are protected—indirectly—against some infectious diseases by being surrounded by immunized persons. This is known as community (or “herd”) immunity.
Community immunity only applies to diseases transmitted from person to person, such as measles, smallpox, rubella, and chickenpox, among others. Tetanus, on the other hand, is not spread from person to person but acquired from the environment, so there can be no community immunity—only the immunized person is protected.
Community immunity can only be achieved when the vast majority of the population is immune. In other words, a population needs high immunization rates to reap the benefits of community immunity. Ref: http://www.immunizationinfo.org/issues/general/community-immunity
Review of variables
Diphtheria: Community (or “herd”) immunity protects from Diphtheria.
Measles: Community (or “herd”) immunity gives protection form Measles.
Tetanus: The Herd immunity does not protect in the case of tetanus. Ref: https://pgblazer.com/spm-mcq-89-herd- immunity-for-infectious-diseases/
Mumps: Community (or “herd”) immunity help protect Mumps.
Q5. The earliest change in iron deficiency anaemia is (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Decreased serum iron
b) Decreased serum ferritin
c) Decreased TIBC
d) Decreased Haemoglobin
Note Out of above given variables (b) Decreased serum ferritin – is suggested.
Stem: The earliest change in iron deficiency anaemia
Serum ferritin: The single most sensitive tool for evaluating the iron status is by measurement of serum ferritin. It reflects the size of iron stores in the body. It is the most useful indicator of iron status in a population where the prevalence of iron deficiency is not high. Values below 10 mcg/l probably indicate an absence of stored iron (25).
Three stages of iron deficiency have been described:
The first stage characterized by decreased storage of iron without any other detectable abnormalities
An intermediate stage of “latent iron deficiency”, that is, iron stores are exhausted, but anaemia has not occurred as yet. Its recognition depends upon measurement of serum ferritin levels. The percentage saturation of transferrin falls from a normal value of 30 per cent to less than 15 per cent. This stage is the most widely prevalent stage in India.
The third stage is that of overt iron deficiency when there is a decrease in the concentration of circulating haemoglobin due to impaired haemoglobin synthesis (59). Ref: Pg-493, 19th Ed Park and Park
Review of variables
(a) Decreased serum iron: Normal: Iron: 60-170 mcg/dl (micrograms per deciliter): Lower-than-normal levels may mean: Long-term digestive tract bleeding Heavy menstrual bleeding Intestinal conditions that cause poor absorption of iron Not enough dietary iron Pregnancy Anemia of chronic disease. Ref: http://www.nlm.nih.gov/medlineplus/ency/article/003488.htm
(b) Decreased serum ferritin: Ferritin is the major iron storage protein of the body. Ferritin levels can be used to indirectly measure the iron levels in the body. Normal ferritin levels are: -For Males-12-300 nanograms per milliliter of blood (ng/ml) -For Females-12-150 ng/ml for females. Value: Subnormal levels of ferritin can be detected when iron stores are exhausted, but before the serum iron level has become affected. Ferritin thus represents the most sensitive index of early iron deficiency. Ref: http://www.australianprescriber.com/magazine/20/3/74/6
(c) Decreased TIBC: Total iron-binding capacity (TIBC): Normal: TIBC: 240-450 mcg/dl TIBC is usually higher than normal when the body’s iron stores are low. This can occur with: -Iron deficiency anaemia -Pregnancy (late) Ref: http://www.nlm.nih.gov/medlineplus/ency/article/003489.htm
(d) Decreased haemoglobin: The haemoglobin test is a blood test that measures haemoglobin in blood. Normal results for adults vary, but in general are: -Male: 13.8 to 17.2 grams per deciliter (g/dl) -Female: 12.1 to 15.1 g/dl Low hemoglobin level may be due to: -Anemia due to red blood cells being destroyed earlier than normal (hemolytic anemia) -Anemia (various types) Bleeding from digestive tract or bladder, heavy menstrual periods Chronic kidney disease Bone marrow being unable to produce new blood cells. This may be due to leukemia, other cancers, drug toxicity, radiation therapy, infection, or bone marrow disorders Poor nutrition; Low level of iron, folate, vitamin B12, or vitamin B6 Other chronic illness, such as rheumatoid arthritis Ref: http://www.nlm.nih.gov/medlineplus/ency/article/003645.htm
Q6. Myocardial injury in acute myocardial infarction as a result of sudden occlusion of the coronary artery is an example of: (NHMC/MD/Ent/2014):
a) Coagulative necrosis
b) Liquefactive necrosis
c) Fat necrosis
d) Fibrinoid necrosis
Note Out of the variables given above (a) Coagulative necrosis-is suggested.
This is the most common type of necrosis caused by irreversible focal injury, mostly from sudden cessation of blood flow (ischaemia), and less often from bacterial and chemical agents. The organs commonly affected are the heart, kidney, and spleen.
Grossly, foci of coagulative necrosis in the early stage are pale, firm, and slightly swollen. With progression, they become more yellowish, softer, and shrunken. Ref: Pg51, 5th Ed, Textbook of Pathology by Harsh Mohan
Review of variables
(a) Coagulative necrosis:
Ischemia in most tissues of the body will cause coagulative necrosis. Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.
The lack of oxygen (hypoxia) causes cell death in a localised area which is perfused by blood vessels failing to deliver primarily oxygen, but also other important nutrients. http://en.wikipedia.org/wiki/Coagulative_necrosis
(b) Liquefactive necrosis:
Liquefaction or colliquative necrosis occurs commonly due to ischaemic injury and bacterial or fungal infections. It occurs due to degradation of tissue by the action “of powerful hydrolytic enzymes. The common examples are infarct brain and abscess cavity.
Grossly, the affected area is soft with liquefied centre containing necrotic debris. Later, a cyst wall is formed. Ref: Pg51, 5th Ed, Textbook of Pathology By Harsh Mohan
In the central nervous system ischemia causes liquefactive necrosis, as there is very little structural framework in neural tissue. Ref: http://en.wikipedia.org/wiki/Coagulative_necrosis
(c) Fat necrosis:
Fat necrosis is a special form of cell death occurring at two anatomically different locations but morphologically similar lesions. These are: following acute pancreatic necrosis, and traumatic fat necrosis commonly in breasts.
The damaged adipose cells assume cloudy appearance when only free fatty acids remain behind, after glycerol leaks out. The leaked out free fatty acids, on the other hand, complex with calcium to form calcium soaps (saponification) discussed later under dystrophic calcification. Ref: Pg52, 5th Ed, Textbook of Pathology by Harsh Mohan
Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes.
In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits. It is usually associated with trauma of the pancreas or acute pancreatitis. It can also occur in the breast, the salivary glands and neonates after a traumatic delivery. Ref: http://en.wikipedia.org/wiki/Fat_necrosis
(d) Fibrinoid necrosis:
Fibrinoid necrosis or fibrinoid degeneration is characterised by deposition of fibrin-like material which has the staining properties of fibrin. It is encountered in various examples of immunologic tissue injury (e.g. in immune complex vasculitis, autoimmune diseases, Arthus reaction etc), arterioles in hypertension, peptic ulcer etc. Ref: Pg52, 5th Ed, Textbook of Pathology By Harsh Mohan
Fibrinoid necrosis is a form of necrosis, or tissue death, in which there is accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin. It is associated with conditions such as immune vasculitis (e.g. Henoch-Schönlein purpura), malignant hypertension, pre-eclampsia, or hyperacute transplant rejection. Ref: http://en.wikipedia.org/wiki/Fibrinoid_necrosis
Q.7. The principal sign of inflammation “rubor” occurs as a result of (NHMC/MD/Ent/2014):
a) Decreased interstitial hydrostatic pressure
b) Decreased vascular permeability of capillaries
c) Vasoconstriction of muscular arteries
d) Vasodilation of arterioles
Note Out of above given variables (d) Vasodilation of arterioles – is suggested.
The traditional names for signs of inflammation come from Latin. The basis of the five cardinal signs are as under:
(a) Rubor (Redness): Increased blood flow due to vascular dilatation gives redness and heat.
(b) Tumor (Swelling): Increased vascular permeability gives oedema causing tissue swelling
(c) Color (Heat): Increased blood flow due to vascular dilatation gives redness and heat.
(d) Dolor (Pain): Certain chemical mediators stimulate sensory nerve endings giving pain. Nerves also stimulated by stretching from oedema.
e) Functio laesa (loss of function): Pain and swelling result in loss of function.
The first four (classical signs) were described by Celsus (ca. 30 BC–38 AD), while loss of function was added later by Galen even though the attribution is disputed and the origination of the fifth sign has also been ascribed to Thomas Sydenham and Virchow. Ref: Pg-5, 5th Ed, Textbook of Pathology By Harsh Mohan
Q.8. Pathogenic mechanisms in tuberculosis are due to (NHMC/MD/Ent/2014):
a) Specific cell adhesion sites
b) Clogging of alveoli by large numbers of acid-fast mycobacteria
c) Toxin production by the mycobacteria
d) Cell mediated hypersensitivity
Note The most suitable choice suggested among above given variables is (d) Cell-mediated hypersensitivity.
Stem: Pathogenic mechanisms in tuberculosis:
Most cases of tuberculosis are caused when patients inhale droplet nuclei containing infectious organisms. While the bacilli are deposited on the alveolar spaces, they do not clog up the alveoli but are engulfed by macrophages. Tissue injury is not a result of toxin secretion but by cell-mediated hypersensitivity, that is, “immunologic injury.” Ref: Raoult, pp 673–674.
Hypersensitivity or allergy, and immunity or resistance, plays a major role in the development of lesions in tuberculosis. Tubercle bacilli as such do not produce any toxins. Tissue changes seen in tuberculosis are not the result of any exotoxin or endotoxin but are instead the result of the host response to the organism which is in the form of development of cell-mediated hypersensitivity (or Type IV hypersensitivity) and immunity. Ref: text Book of Pathology by Harsh Mohan, 5th Ed, Pg-157
Q.9. Lacunar cells (variants of Reed-Sternberg cells) are found in which type of Hodgkin’s Lymphoma? (NHMC/MD/Ent/2014):
a) Mixed cellularity
b) Nodular sclerosis
Note Lacunar cells (variants of Reed-Sternberg cells) are found in (b) Nodular sclerosis type of Hodgkin’s lymphoma
Stem: Lacunar cells
Review of variables
|Histological subtype||Incidence||Main pathology||RS cells||Prognosis|
|Mixed cellularity||22%||Mixed infiltrate||Numerous classic type CD15+, CD30+||Good|
|Nodular sclerosis||70%||Lymphoid nodules, collagen bands||Frequent, Lacunar type, CD15+, CD30+||Very good|
|Lymphocyte- predominate||5%||Proliferating lymphocytes, a few histocytes||Few classic and polyploidy type, CD15-CD-30, CD- 20+||Excellent|
|Lymphocyte-depleted||1%||Scanty lymphocytes, atypical histocytes, fibrosis||Numerous, pleomorphic type, CD15+ CD30+||Poor|
Modified Rye Classification of Hodgkin’s Disease
Ref: P-446, 5th Ed, Textbook of Pathology by Harsh Mohan
Q.10. Invasive carcinoma of the cervix develop in which of the following regions? (NHMC/MD/ Ent/2014):
a) Columnar epithelium
b) Squamo-columnar junction
c) Squamous epithelium
d) Transformation zone
Note Invasive Ca of cervix develops in (d) Transformation zone.
Ref: Pg: 688; Robbin’s Basic Pathology; 9th Edition
Review of variables
(a) Columnar epithelium:
During development, the columnar, mucus-secreting epithelium of the endocervix is joined to the squamous epithelial covering of the exocervix at the cervical os.
(b) Squamo-columnar junction:
Squamo-colmnar junction; is the place where columnar epithelium of the endocervix is joined to the squamous epithelial covering of the exocervix at the cervical os
(c) Squamous epithelium:
Squamous epithelial covering of the exocervix at the cervical os
(d) Transformation zone:
During development, the columnar, mucus-secreting epithelium of the endocervix is joined to the squamous epithelial covering of the exocervix at the cervical os. With the onset of puberty, the squamocolumnar junction undergoes eversion, causing columnar epithelium to become visible on the exocervix. The exposed columnar cells, however, eventually undergo squamous metaplasia, forming a region called the transformation zone.
Invasive carcinomas of the cervix develop in the transformation zone
Ref: https://www.inkling.com/read/ robbins-basic-pathology-kumar-abbas- aster-9th/chapter-18/figure-184
Q.11. The stage in the life cycle of plasmodia responsible for an infection and can be identified with distinctive appearance in thick smears of peripheral blood is: (NHMC/MD/Ent/2014):
Note Out of the given variables the choice suggested is (b) Trophozoite-for identification of plasmodium responsible for an infection with distinctive appearance in thick smear of peripheral blood.
Stem: Stage in the life cycle of plasmodia
The life cycle of plasmodia is complex. As mosquitoes feed on human blood, sporozoites are introduced from the saliva and within a few minutes infect liver cells. Here the parasites multiply rapidly to form a schizont containing thousands of merozoites. After a period of days to several weeks that varies with the Plasmodium species, the infected hepatocytes release the merozoites, which quickly infect red cells. Intraerythrocytic parasites either continue asexual reproduction to produce more merozoites or give rise to gametocytes capable of infecting the next hungry mosquito. During their asexual reproduction in red cells, each of the four forms of malaria develops into trophozoites with a somewhat distinctive appearance. Thus, the species of malaria that is responsible for infection can be identified inappropriately stained thick smears of peripheral blood. The asexual phase is completed when the trophozoites give rise to new merozoites, which escape by lysing the red cells. Ref: Pg-418-419, Robbins Basic Pathology, 9th Ed