3rd Year Pathology

GENERAL
PATHOLOGY
KMU PAST PAPERS SOLVED SEQS
SALMAN KHAN | REHMAN MEDICAL COLLEGE

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Contents 1
CELL INJURY, CELL DEATH, AND ADAPTATIONS 2
HEMODYNAMIC DISORDERS, THROMBOEMBOLISM, AND SHOCK 12
INFLAMMATION AND REPAIR 19
NEOPLASIA 29
DISEASE OF IMMUNE SYSTEM 36
CLINICAL BACTERIOLOGY 46
GENERAL BACTERIOLOGY 61
PARASITOLOGY 66
References
1. Robbins Basic Pathology (9th Edition)
2. Goljan - Rapid Review Pathology (4th edition)
3. Harsh Mohan Textbook of Pathology (7th Edition)
4. Levinson- Review of Microbiology and immunology (13th edition)
KMU Past Papers Solved SEQs
Cell Injury, Cell Death, and Adaptations 2
Q-1. Questions regarding necrosis.

a) Define necrosis.
b) Enumerate its types. Give example of each
c) Which type is the most common and name the organ affected by it?
d) What are the morphological features of a necrotic cell?
e) Define the nuclear changes seen in necrotic cell nuclei
f) Write the morphology of each type of necrosis
ANS:
a) DEFINITION:
Necrosis is the type of cell death that is associated with loss of membrane integrity and
leakage of cellular contents, largely resulting from the degradative action of enzymes on
lethally injured cells. The leaked cellular contents often elicit a local host reaction, called
inflammation that attempts to eliminate the dead cells. The enzymes responsible for
digestion of the cell may be derived from the lysosomes of the dying cells and lysosomes of
leukocytes that are recruited in inflammatory response.
b) TYPES OF NECROSIS:
1) Coagulative necrosis, solid organs heart kidney
2) Liquefactive necrosis, central nervous Brain
3) Gangrenous necrosis, lower leg, abdominal viscera
4) Caseous necrosis, tuberculous infection i.e. lungs
5) Fat necrosis, pancreas (may be traumatic or enzymatic)
6) Fibrinoid necrosis, blood vessels wall.
c) MOST COMMON TYPE AND THE ORGAN AFFECTED BY IT:
Coagulative necrosis is the most common type of necrosis and the most affected organs are
the solid organs except the brain.
d) MORPHOLOGICAL FEATURES OF A NECROTIC CELL
i) Cytoplasmic changes.
1) Necrotic cells show increased eosinophilia (i.e., pink staining), due to increased
binding of eosin to denatured cytoplasmic proteins and in part to loss of the
basophilia
2) More glassy due to loss of glycogen
3) Myelin figures are more prominent
4) Discontinuation of plasma and organelle membranes
5) Dilation of mitochondria
6) Disruption of lysosomes
7) Intra-cytoplasmic myelin figures
ii) Nuclear changes
1) Karyolysis (break down of DNA and chromatin by DNase activity)
2) Pyknosis (nuclear shrinkage and increased basophilia; the DNA condenses into a solid
shrunken mass)
3) Karyorrhexis, (the pyknotic nucleus undergoes fragmentation.)
4) Nucleus disappear in 1-2 days
iii) Other
Dead cells may be replaced by myelin figures which is either phagocytosed by other cells
or further degraded to fatty acids, fatty acids then bind to calcium salts and ultimately
become calcified.
e) NUCLEAR CHANGES SEEN IN NECROTIC CELL NUCLEI:
1) Karyolysis (break down of DNA and chromatin by DNase activity

2) Pyknosis (nuclear shrinkage and increased basophilia; the DNA condenses into a solid
shrunken mass)
3) karyorrhexis, (the pyknotic nucleus undergoes fragmentation.)
f) MORPHOLOGY OF EACH TYPE OF NECROSIS.

i) Coagulative necrosis
1) Underlying tissue architecture is preserved
2) Injury denatures structural proteins as well as enzymes, thereby blocking the
proteolysis of the dead cells
3) Eosinophilic, anucleate cells may persist for days or weeks.
4) Leukocytes are recruited to the site of necrosis, and digested dead cell through its
lysosomal enzymes.
5) The cellular debris is then removed by phagocytosis.
6) Coagulative necrosis is characteristic of infarcts (areas of ischemic necrosis) in all of
the solid organs except the brain.
ii) Liquefactive necrosis
1) Hypoxic death of cells within the central nervous system often evokes liquefactive
necrosis
2) Seen in focal bacterial or, occasionally, fungal infections,
3) The dead cells are completely digested, transforming the tissue into a liquid viscous
mass.
4) Eventually, the digested tissue is removed by phagocytes.
5) In case of acute inflammation, as in a bacterial infection, the material is frequently
creamy yellow and is called pus.
iii) Gangrenous necrosis
1) It usually refers to the condition of a limb, generally the lower leg that has lost its
blood supply and has undergone coagulative necrosis involving multiple tissue layers.
2) When superimposed by bacterial infection,
3) Coagulative necrosis is modified by the liquefactive action of the bacteria and the
attracted leukocytes (wet gangrene).
4) Gangrenous necrosis may be Dry gangrene, Gas gangrene and Wet gangrene as
mention above.
iv) Caseous necrosis
1) Encountered most often in foci of tuberculous infection i.e lung
2) Caseous means “cheese-like,” yellow-white appearance of the area of necrosis
3) Collection of fragmented or lysed cells with an amorphous granular pink appearance.
4) Unlike with coagulative necrosis, the tissue architecture is completely obliterated and
cellular outlines cannot be discerned.
5) The area of caseous necrosis is often enclosed within a distinctive inflammatory
border (granuloma)
v) Fat necrosis
1) Refers to focal areas of fat destruction, typically resulting from release of activated
pancreatic lipases into the substance of the pancreas and the peritoneal cavity
(pancreatitis).
2) pancreatic enzymes liquefy the membranes of fat cells in the peritoneum, and lipases
split the triglyceride esters
3) The released fatty acids combine with calcium to produce grossly visible chalky white
areas (fat saponification)
4) The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic
calcium deposits, surrounded by an inflammatory reaction.
vi) Fibrinoid necrosis

1) Immune reactions in which complexes of antigens and antibodies are deposited in the
walls of arteries.
2) The deposited immune complexes, together with fibrin that has leaked out of vessels,
produce a bright pink and amorphous appearance on H&E preparations called
fibrinoid
3) The immunologically mediated diseases (e.g., polyarteritis nodosa) in which this type
of necrosis is seen.
Q-2. Questions regarding cell injury

a) What is cell injury?
b) Enumerate the causes of cell injury.
c) Describe various mechanism of cell injury
d) Describe the morphology of reversible cell injury.
e) What do you mean by free radical? Simply enumerate the circumstances under which free
radicals are formed.
f) Give a brief account of the role of free radicals in cell injury.
ANS
a) CELL INJURY
Cell injury results when cells are stressed so severely that they are no longer able to adapt or
when cells are exposed to inherently damaging agents or suffer from intrinsic abnormalities
(e.g., in DNA or proteins). Cell injury may be reversible or irreversible (cell death).
b) CAUSES OF CELL INJURY: (A-COPING)
1) Oxygen Deprivation: Hypoxia, interferes with aerobic oxidative respiration
2) Chemical Agents: poisons, air pollutants, insecticides, CO, asbestos and therapeutic drugs
3) Infectious Agents: viruses bacteria, fungi, and protozoans
4) Immunologic Reactions: autoimmune reactions and allergic reactions against
environmental substances
5) Genetic Factors
6) Nutritional Imbalances: Protein–calorie insufficiency specific vitamin deficiencies obesity
7) Physical Agents Trauma, extremes of temperature, radiation, electric shock, and sudden
changes in atmospheric pressure
8) Aging
c) VARIOUS MECHANISM OF CELL INJURY
1) Depletion of ATP—failure of energy dependent function i.e. Transport, protein synthesis,
aerobic glycolysis
2) Mitochondrial Damage and Dysfunction— leads to decreased ATP and increased ROS
formation.
3) Influx of Calcium—causes activation of intracellular enzymes and increased
mitochondrial permeability
4) Accumulation of Oxygen-Derived Free Radicals (Oxidative Stress)— causes lipid
peroxidation, protein modification, DNA damage
5) Defects in membrane permeability— due to decreased phospholipids synthesis,
membrane degradation by enzymes, ROS lipid peroxidation and cytoskeletal damage.
6) Damage to DNA and Proteins—triggers apoptosis and leads to cell death
d) MORPHOLOGY OF REVERSIBLE CELL INJURY.
Grossly, when it affects many cells in an organ, it causes some pallor (as a result of
compression of capillaries), increased turgor, and increase in weight of the organ.
Microscopically, Cellular swelling the first manifestation of almost all forms of injury to cells,

1) Small, clear vacuoles may have revealed within the cytoplasm, these represent
distended and pinched-off segments of the endoplasmic reticulum (ER).
2) This pattern of nonlethal injury is sometimes called hydropic change or vacuolar
degeneration.
3) Fatty change is manifested by the appearance of lipid vacuoles in the cytoplasm. It is
principally encountered in cells participating in fat metabolism (e.g., hepatocytes,
myocardial cells) and is also reversible.
4) Injured cells may also show increased eosinophilic staining,
5) The intracellular changes associated with reversible injury include
i) Plasma membrane alterations such as blebbing, blunting, or distortion of microvilli,
and loosening of intercellular attachments;
ii) Mitochondrial changes such as swelling and the appearance of phospholipid-rich
amorphous densities;
iii) Dilation of the ER with detachment of ribosomes and dissociation of polysomes;
and
iv) Nuclear alterations, with clumping of chromatin. The cytoplasm may contain
phospholipid masses, called myelin figures, which are derived from damaged
cellular membranes.
e) FREE RADICAL AND CIRCUMSTANCES UNDER WHICH FREE RADICALS ARE FORMED:
Free radicals: are chemical species with a single unpaired electron in an outer orbital. Such
chemical states are extremely unstable, and free radicals readily react with inorganic and
organic chemicals; when generated in cells, they avidly attack nucleic acids as well as a
variety of cellular proteins and lipids.
Circumstances under which free radicals are formed
1) The absorption of radiant energy (e.g., ultraviolet light, x-rays). Ionizing radiation can
hydrolyze water into hydroxyl (•OH) and hydrogen (H•) free radicals.
2) Administration of high concentrations of O2 produces superoxide FRs.
3) The enzymatic metabolism of exogenous chemicals (e.g., carbon tetrachloride)
4) NADPH oxidase reaction generates superoxide FRs in neutrophils and monocytes in
phagolysosomes during Inflammation
5) Xanthine oxidase acting upon xanthine (degradation product of ATP) produces
superoxide FRs, which are important in reperfusion injury in a myocardial infarction
6) Other condition:
i) Drugs acetaminophen
ii) Chemicals carbon tetrachloride (CCl4)
iii) Nitric oxide (NO)
iv) Low-density lipoprotein (LDL)
f) BRIEF ACCOUNT OF THE ROLE OF FREE RADICALS IN CELL INJURY:
Reactive oxygen species cause cell injury by three main reactions
1) Lipid peroxidation of membranes. Double bonds in membrane polyunsaturated lipids are
vulnerable to attack by oxygen-derived free radicals. The lipid–radical interactions yield
peroxides, which are themselves unstable and reactive, and an autocatalytic chain
reaction ensues
2) Cross-linking and other changes in proteins. Free radicals promote sulfhydryl-mediated
protein cross-linking, resulting in enhanced degradation or loss of enzymatic activity.
Free radical reactions may also directly cause polypeptide fragmentation.
3) DNA damage. Free radical reactions with thymine in nuclear and mitochondrial DNA
produce single-strand breaks. Such DNA damage has been implicated in cell death, aging,
and malignant transformation of cells.

Q-3.
a) Enumerate the various cellular adaptations to environmental stresses.
b) Write the causes of atrophy.
ANS:
a) CELLULAR ADAPTATION TO ENVIRONMENTAL STRESSES:
1) Atrophy
2) Metaplasia
3) Hypertrophy
4) Hyperplasia
b) CAUSES OF ATROPHY.
1) Decreased workload (e.g., immobilization of a limb to permit healing of a fracture),
2) Loss of innervation (e.g. Damage of lower motor neuron in polio)
3) Diminished blood supply,
4) Inadequate nutrition,
5) Loss of endocrine stimulation,
6) Aging (senile atrophy).
Q-4. Define fatty change. List three organs in which fatty change may occur. What is the
mechanism of accumulation of triglyceride in fatty liver?
ANS:
Fatty Change (Steatosis) Fatty change refers to any abnormal accumulation of triglycerides
within parenchymal cells.
 Organs:
1) Liver (most often seen)
2) Heart
3) Skeletal muscle
4) Kidney
 Causes:
1) Toxins (alcohol)
2) Protein malnutrition
3) Diabetes mellitus
4) Obesity
5) Anoxia.
 Mechanism:
Fatty liver is most often caused by increased synthesis of TGs and less commonly by
problems with the packaging of TGs into VLDL or its secretion into blood.
A. Increased synthesis of TGs is caused by increased conversion of Dihydroxyacetone
phosphate (DHAP) to Glycerol 3 phosphate (G3-P), which occurs with
kwashiorkor and excessive alcohol consumption
1) In kwashiorkor, there is increased intake of carbohydrates (CHO) and little
to no intake of proteins. Increased CHO intake increases the amount of
DHAP produced during glycolysis, therefore providing more substrate for
synthesizing TGs.
2) In alcohol excess, increased production of NADH from alcohol metabolism
accelerates conversion of DHAP to G3-P. (NADH is coenzyme for the
conversion of DHAP to G3-P)

3) An additional factor enhancing TG synthesis in alcohol excess is increased

availability of fatty acids (FAs) to combine with G3-P to form TGs.
a. Recall that acetyl CoA is used for synthesizing FAs and since acetyl CoA
is the end product of alcohol metabolism, it is available to synthesize
more FAs.
b. Alcohol increases the mobilization of FAs from TG stores in adipose
tissue by activating hormone sensitive lipase, which hydrolyzes TG into
FAs and glycerol.
c. β-Oxidation of FAs in the mitochondrial matrix is reduced, because
NAD+, which is required for the oxidation process, NAD+ less
availability is due to its conversion to NADH in alcohol metabolism.
B. Decreased packaging of TG into VLDL and secretion into the blood, resulting from
decreased synthesis of apoB-100, causes fatty liver.
1) In kwashiorkor, because of decreased protein intake, apoB-100 synthesis
is decreased.
2) TGs that are synthesized in the hepatocyte remain in the hepatocyte
producing fatty change.
Q-5.
a) Name two types of cell death. Tabulate the salient features of both.
b) Define apoptosis.
c) Enumerate causes of apoptosis.
d) Describe mechanism of apoptosis.
e) Write examples of apoptosis.
f) Write morphological features of apoptotic cell.
ANS:
a) FEATURES OF NECROSIS AND APOPTOSIS:
b) APOPTOSIS
Apoptosis is a pathway of cell death in which cells activate enzymes that degrade the cells’
own nuclear DNA and nuclear and cytoplasmic proteins.
c) CAUSES OF APOPTOSIS
1. Growth Factor Deprivation
2. DNA damage
3. Accumulation of misfolded proteins
4. Apoptosis of self-reactive lymphocytes
5. Cytotoxic T-lymphocyte mediated apoptosis

d) MECHANISM OF APOPTOSIS
Apoptosis results from the activation of enzymes called caspases, balance between
production of pro- and anti-apoptotic proteins. it is the loss of this balance that determines
survival or death of a cell.
 Withdrawal of normal cell survival signals e.g. absence of certain hormones,
growth factors, cytokines.
 Agents of cell injury e.g. heat, radiation, hypoxia, toxins, free radicals.
After the cell has been initiated into self-destruct mode, cell death occurs by two pathway
1. The Mitochondrial (Intrinsic) Pathway of Apoptosis
2. The Death Receptor (Extrinsic) Pathway of Apoptosis
finally, mediators of cell death are activated caspases, caspases are a series of proteolytic or
protein-splitting enzymes which act on nuclear proteins and organelles containing protein
components
The Mitochondrial (Intrinsic) Pathway of Apoptosis

1. This pathway of cell death signalling is due to increased mitochondrial permeability and
is a major mechanism.
2. Bcl-2 sensors are members of the Bcl-2 family called “BH3 proteins” turn activate pro-
apoptotic proteins, Bax, Bak and Bid and form channels in mitochondrial membrane and
lead to Cytochrome C Escape
3. Cytochrome C, activates caspase-9 and block the activities of caspase antagonists. The net
result is the activation of the caspase cascade
4. If cells are exposed to growth factors and other survival signals, they synthesize anti-
apoptotic members of the Bcl-2 family, the two main ones of which are Bcl-2 itself and
Bcl-xL. These proteins antagonize Bax and Bak, and thus limit the escape of the
mitochondrial pro-apoptotic proteins.
Extrinsic (cell death receptor initiated) pathway:

1. This signalling pathway of cell death is by activation of death receptors on the cell
membrane. An important cell death receptor is type 1 tumour necrosis factor receptor
(TNF-R1) and a related transmembrane protein called Fas (CD95) and its ligand
(FasL), a membrane protein expressed mainly on activated T lymphocytes.
2. Signals from plasma membrane receptors lead to the assembly of adaptor proteins
into a “death-inducing signalling complex,” which activates caspases 8 and 10,
3. caspase 8 and 10 may cleave and activate a pro-apoptotic member of the Bcl-2 family
called Bid, combined activation of both pathways delivers a lethal blow to the cell.
4. Here a caspase antagonist called FLIP, can block activation of caspases downstream of
death receptors.
The dead apoptotic cells develop membrane changes which promote their phagocytosis.

e) EXAMPLES OF APOPTOSIS
A. Physiologic Conditions
1. Programmed destruction of cells during embryogenesis
2. Involution of hormone dependent tissues upon hormone deprivations i.e. regression
of lactating breast.
3. Cell lose in proliferations cells populations i.e. intestinal epithelium
4. Elimination of cells that served their useful purposes
5. Elimination of potentially harmful self-reactive lymphocytes
6. Cell death induced by cytotoxic T-lymphocytes
7. Involution of the thymus in early age
B. Pathologic Conditions
1. Cell death in tumours exposed to chemotherapeutic agents.
2. Cell death by cytotoxic T cells in immune mechanisms such as in graft versus-host
disease and rejection reactions.
3. Progressive depletion of CD4+T cells in the pathogenesis of AIDS.
4. Cell death in viral infections e.g. formation of Councilman bodies in viral hepatitis
5. Pathologic atrophy of organs and tissues on withdrawal of stimuli e.g. prostatic
atrophy after orchiectomy, atrophy of kidney or salivary gland on obstruction of
ureter or ducts, respectively.
6. Cell death in response to low dose of injurious agents involved in causation of
necrosis e.g. radiation, hypoxia and mild thermal injury.
7. In degenerative diseases of CNS e.g. in Alzheimer’s disease, Parkinson’s disease, and
chronic infective dementias.
8. Heart diseases e.g. in acute myocardial infarction (20% necrosis and 80% apoptosis).
f) MORPHOLOGIC FEATURES OF APOPTOTIC CELL

1. Apoptotic cells are round to oval shrunken masses of intensely eosinophilic cytoplasm
containing shrunken or almost normal organelles.

2. Nuclear chromatin is condensed under the nuclear membrane i.e. pyknosis,

ultimately, karyorrhexis at the molecular level this is reflected in fragmentation of
DNA into nucleosome-sized pieces
3. The cell membrane may show blebs or projections on the surface.
4. There may be formation of membrane-bound near-spherical bodies containing
condensed organelles around the cell called apoptotic bodies.
5. Characteristically, unlike necrosis, there is no acute inflammatory reaction around
apoptosis.
Q-6.
a) Define pathological calcification.
b) Differentiate between metastatic and dystrophic calcification.
c) Write down the causes of metastatic calcification.
ANS:
a) PATHOLOGICAL CALCIFICATION.
it implies the abnormal deposition of calcium salts, together with smaller amounts of iron,
magnesium, and other minerals. When the deposition occurs in dead or dying tissues, it is
called dystrophic calcification it occurs with normal serum levels of calcium.
In contrast, the deposition of calcium salts in normal tissues is known as metastatic
calcification and is almost always secondary to some derangement in calcium metabolism ie
hypercalcemia.
b) DIFFERENCES BETWEEN METASTATIC AND DYSTROPHIC CALCIFICATION.
A. Dystrophic
1. Dystrophic calcification is encountered in areas of necrosis of any type.
2. The pathogenesis of dystrophic calcification involves initiation (or nucleation) and
propagation
3. formation of crystalline calcium phosphate
B. Metastatic
1. Metastatic calcification can occur in normal tissues whenever there is hypercalcemia.
2. Destruction of bone
3. Vitamin D–related disorder
4. Renal impairment
c) CAUSES OF METASTATIC CALCIFICATION.
1. Increased secretion of parathyroid hormone, due to either primary parathyroid tumors or

production of parathyroid hormone–related protein by other malignant tumors;
2. Destruction of bone due to the effects of accelerated turnover (e.g., Paget disease),
immobilization, or tumors (increased bone catabolism associated with multiple myeloma,
leukemia, or diffuse skeletal metastases);
3. Vitamin D–related disorders including vitamin D intoxication and sarcoidosis (in which
macrophages activate a vitamin D precursor); and
4. Renal failure, in which phosphate retention leads to secondary hyperparathyroidism.
Q-7. What are pigments? classify it and give examples.
ANS:

Pigments are colored substances that are either exogenous, coming from outside the body,
such as carbon, or endogenous, synthesized within the body itself, such as lipofuscin,
melanin, and certain derivatives of hemoglobin
Classification:
1. Carbon coal dust, blacken the draining lymph nodes and pulmonary parenchyma
(anthracosis)
2. Lipofuscin “wear-and-tear pigment (particularly the heart, liver, and brain)
3. Melanin brown-black pigment that is synthesized by melanocytes located in the
epidermis
4. Hemosiderin hemoglobin-derived granular pigment that is golden yellow to brown and
accumulates in tissues when there is a local or systemic excess of iron. hemosiderosis

Hemodynamic Disorders, Thromboembolism, and Shock 12
Q-1.
a) Give the definitions of Embolus and Thrombus
b) What is the outcome of a thrombus?
ANS:
a) DEFINITION:
Embolus: An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the
blood to a site distant from its point of origin.
Thrombus: A clot of blood formed within a blood vessel and remaining attached to its place
origin
b) OUTCOME OF A THROMBUS:
1. Propagation. The thrombus enlarges through the accretion of additional platelets and
fibrin, increasing the odds of vascular occlusion or embolization.
2. Embolization. Part or all of the thrombus is dislodged and transported elsewhere in the
vasculature.
3. Dissolution. If a thrombus is newly formed, activation of fibrinolytic factors may lead to
its rapid shrinkage and complete dissolution. With older thrombi, extensive fibrin
polymerization renders the thrombus substantially more resistant to plasmin-induced
proteolysis, and lysis is ineffectual.
4. Organization and recanalization. Older thrombi become organized by the ingrowth of
endothelial cells, smooth muscle cells, and fibroblasts into the fibrin-rich thrombus
Q-2.
a) Enumerate the major categories of shock.
b) List causes of hypovolemic shock.
c) Discuss pathogenesis of septic shock
ANS:
a) CATEGORIES OF SHOCK
1. Hypovolemic
2. Septic
3. Cardiogenic
4. Septic
5. Neurogenic
6. Anaphylactic
b) CAUSES OF HYPOVOLEMIC SHOCK.
1. Hemorrhage
2. Inadequate blood or plasma volume
3. Fluid loss (e.g., vomiting, diarrhea, burns, trauma)
c) PATHOGENESIS OF SEPTIC SHOCK
1. Septic shock results most often from Gram-negative bacteria entering the body from
genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Gram-
positive bacteria.

2. Microbial products activate endothelial cells and cellular and humoral elements of the
innate immune system
3. In septic shock, there is immune system activation and severe systemic inflammatory
response to infection.
4. The net result of above mechanisms is vasodilatation and increased vascular permeability
and decreased tissue perfusion in septic shock.
5. Profound peripheral vasodilatation and pooling of blood causes hyper-dynamic
circulation in septic shock, in contrast to hypovolemic and cardiogenic shock.
6. Increased vascular permeability causes development of inflammatory edema.
7. Disseminated intravascular coagulation (DIC) is prone to develop in septic shock due to
endothelial cell injury by toxins
8. There is microvascular thrombosis tissue ischemia which causes multi organ failure and
adrenal insufficiency (Waterhouse Friderichsen Syndrome)
Q-3.
a) Define thrombosis
b) describe the pathogenesis of thrombosis and give the salient features of Virchow’s Triad.
ANS:
a) THROMBOSIS:
A condition in which the blood changes from a liquid to a solid state and produce a blood clot

b) VIRCHOW’S TRIAD
Thrombus development usually is related to
one or more components of Virchow’s triad:
1. Endothelial injury (e.g., by toxins,
hypertension, inflammation, or
metabolic products)
2. Abnormal blood flow, stasis or
turbulence (e.g., due to aneurysms,
atherosclerotic plaque)
3. Hypercoagulability: either primary (e.g.
factor V Leiden, increased prothrombin
synthesis, antithrombin III or protein C,
S deficiency) or secondary (e.g., bed rest,
tissue damage, malignancy)
Q-4
a) Define hemostasis.
b) Name the sequence of events after vascular injury
ANS:
a) HEMOSTASIS:
Normal hemostasis comprises a series of regulated processes that maintain blood in a fluid,
clot-free state in normal vessels while rapidly forming a localized hemostatic plug at the site
of vascular injury
b) SEQUENCE OF EVENTS AFTER VASCULAR INJURY
1. Transient vasoconstriction through Local neuro-humoral factors.
2. Platelets bind via glycoprotein 1b (GpIb) receptors to von Willebrand factor (vWF) on
exposed extracellular matrix (ECM) and are activated, undergoing a shape change and
granule release.
3. Activation of platelets and release of adenosine diphosphate (ADP) and thromboxane
A2 (TxA2) which induce additional platelet aggregation through binding of platelet
GpIIb-IIIa receptors to fibrinogen.
4. Primary hemostatic plug formation through platelet aggregation which fills the
vascular defect, forming the.
5. Local activation of the coagulation cascade (involving tissue factor and platelet
phospholipids) results in fibrin polymerization, “cementing” the platelets into a
definitive secondary hemostatic plug that is larger and more stable than the primary
plug and contains entrapped red cells and leukocytes.

6. Counter regulatory mechanisms, such as release of t-PA (tissue plasminogen activator,

a fibrinolytic product) and thrombomodulin (interfering with the coagulation
cascade), limit the hemostatic process to the site of injury.
Q-5.
a) Define edema
b) What are the pathophysiologic causes of edema?
c) What is the pathogenesis of cardiac edema?
ANS:
a) EDEMA:
Edema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also
collect in body cavities such as the pleural cavity (hydrothorax), the pericardial cavity
(hydropericardium), or the peritoneal cavity (hydroperitoneum, or ascites).
b) PATHOPHYSIOLOGIC CAUSES OF EDEMA
A. Increased Hydrostatic Pressure
i) Impaired Venous Return
1. Congestive heart failure
2. Constrictive pericarditis Ascites (liver cirrhosis)
3. Venous obstruction or compression
4. Thrombosis External pressure (e.g., mass)
5. Lower extremity inactivity with prolonged dependency
ii) Arteriolar Dilation
1. Heat
2. Neurohumoral dysregulation
B. Reduced Plasma Osmotic Pressure (Hypoproteinemia)

1. Protein-losing glomerulopathies (nephrotic syndrome)
2. Liver cirrhosis (ascites)
3. Malnutrition
4. Protein-losing gastroenteropathy
C. Lymphatic Obstruction
1. Inflammatory
2. Neoplastic
3. Postsurgical
4. Postirradiation
D. Sodium Retention
1. Excessive salt intake with renal insufficiency
2. Increased tubular reabsorption of sodium
3. Renal hypo-perfusion
4. Increased renin-angiotensin-aldosterone secretion
E. Inflammation
1. Acute inflammation
2. Chronic inflammation
3. Angiogenesis

c) PATHOGENESIS OF CARDIAC EDEMA

1. Reduced cardiac output causes hypovolaemia
which stimulates intrinsic-renal and extra-
renal hormonal (renin-angiotensin-
aldosterone) mechanisms as well as ADH
secretion resulting in sodium and water
retention and consequent oedema.
2. Due to heart failure, there is elevated central
venous pressure which is transmitted
backward to the venous end of the
capillaries, raising the capillary hydrostatic
pressure and consequent transudation.
3. Chronic hypoxia may injure the capillary
endothelium causing increased capillary
permeability and result in edema this is
called forward pressure hypothesis.
4. Cardiac edema is influenced by gravity and is thus characteristically dependent oedema.
Q-6.
a) Classify embolism.
b) Give a brief account of air embolism.
ANS:
a) CLASSIFICATION OF EMBOLISM:
1. Pulmonary thromboembolism
2. Systemic thromboembolism
3. Fat embolism
4. Amniotic fluid embolism
5. Air embolism (nitrogen)
6. Atherosclerotic debris (cholesterol)
7. Tumor
b) AIR EMBOLISM:
Air embolism may be
A. Venous air embolism Air may be sucked into systemic veins under the following
circumstances:
1. Operations on the head and neck, and trauma
2. Obstetrical operations and trauma
3. Intravenous infusion of blood and fluid
4. Angiography
B. Arterial air embolism Entry of air into pulmo nary vein or its tributaries may occur in
the following conditions:
1. Cardiothoracic surgery and trauma
2. Paradoxical air embolism

3. Arteriography
4. Coronary or cerebral arterial air embolism may cause sudden death.
C. A particular form of gas embolism called decompression sickness is caused by sudden
changes in atmospheric pressure, caisson disease. divers’ palsy or aeroembolism
Decompression sickness is produced when the individual decompresses suddenly,
either from high atmospheric pressure to normal level, or from normal pressure to
low atmospheric pressure.
Q-7.
a) Define infarction.
b) Classify infarction.
c) Write down common causes of vascular obstruction leading to infarction
d) Why infarction is uncommon both in lung and liver?
e) Write morphological changes of white infarct.
ANS:
a) INFARCTION
Infarcts are areas of ischemic necrosis most commonly caused by arterial occlusion (typically
due to thrombosis or embolization); venous outflow obstruction is a less frequent cause.
b) CLASSIFICATION
A. According to their colour:
i) Pale or anaemic
ii) Red or haemorrhagic
B. According to their age:
i) Recent or fresh
ii) Old or healed
C. According to presence or absence of infection:
i) Bland, when free of bacterial contamination
ii) Septic, when infected.
c) CAUSES OF INFARCTION
1. Most commonly, infarcts are caused by interruption in arterial blood supply, called
ischaemic necrosis.
2. Vasospasm
3. Extrinsic compression by tumor
4. Dissecting aortic aneurysm
5. Compartment syndrome
6. Vessels twisting (testicular torsion)
7. entrapment of vessel in hernia
8. traumatic vascular rupture
9. Venous thrombosis, venous obstruction (termed stagnant hypoxia).
d) REASON FOR, INFARCTION BEING UNCOMMON IN LUNG AND LIVER:
The dual supply of the lung by the pulmonary and bronchial arteries means that obstruction
of the pulmonary arterioles does not cause lung infarction unless the bronchial circulation
also is compromised. Similarly, the liver, which receives blood from the hepatic artery and

the portal vein, and the hand and forearm, with its parallel radial and ulnar arterial supply,
are resistant to infarction.
e) MORPHOLOGY OF WHITE INFARCT:
1. White infarcts occur with arterial occlusions in solid organs with end-arterial circulations
(e.g., heart, spleen, and kidney), and where tissue density limits the seepage of blood from
adjoining patent vascular beds
2. Infarcts tend to be wedge-shaped,
3. The margins of acute infarcts typically are indistinct and slightly hemorrhagic
4. Extravasated red cells in hemorrhagic infarcts are phagocytosed by macrophages, and the
heme iron is converted to intracellular hemosiderin
5. Ischemic coagulative necrosis

Inflammation and Repair 19
Q-1. Define inflammation
ANS:
Inflammation is a protective response involving host cells, blood vessels, and proteins and
other mediators that is intended to eliminate the initial cause of cell injury, as well as the
necrotic cells and tissues resulting from the original insult, and to initiate the process of
repair.
Q-2. Define Acute and Chronic inflammation
ANS:
Acute inflammation is rapid in onset and of short duration, lasts from a few minutes to as few
days, and is characterized by fluid and plasma protein exudation and a predominantly
neutrophil
leukocyte accumulation.
Chronic inflammation is inflammation of prolonged duration weeks to years, in which
continuing inflammation, Infiltration with mononuclear cells including macrophages,
lymphocytes, and plasma cells, tissue injury induced by products of inflammation and
healing, often by angiogenesis and fibrosis, proceed simultaneously.
Q-3. Tabulate differences between the two types of inflammation.
ANS:
Acute inflammation Chronic inflammation
Rapid onset short duration Prolong duration

Lasts for minutes to few days Weeks to years
Infiltration with neutrophils leukocytes Infiltration with mononuclear cells ie macrophages
no healing proceed simultaneously lymphocytes and plasma cells
Healing is proceed simultaneously
Q-4. Enumerate the causes of chronic inflammation
ANS:
1. Persistent infections by microbes that are difficult to eradicate eg Mycobacterium
tuberculosis, Treponema pallidum. fungi Blastomyces dermatitidis, Histoplasma
capsulatum, elicit a T lymphocyte–mediated immune response called delayed-type
hypersensitivity
2. Immune-mediated inflammatory diseases chronic inflammatory diseases due to
autoimmunity, such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis.
Immune responses against environmental substances allergic diseases, such as bronchial
asthma.
3. Prolonged exposure to potentially toxic agents. Examples are no degradable
exogenous materials such as inhaled particulate silica, leads to silicosis, and endogenous
agents such as cholesterol crystals, which may contribute to atherosclerosis

4. Mild forms of chronic inflammation in neurodegenerative disorders such as Alzheimer

disease, atherosclerosis, metabolic syndrome and the associated type 2 diabetes in these
conditions the inflammation may be triggered by inflammasome.
5. Response to malignant tumor
Q-5. Enlist the causes of acute inflammation
ANS:
1. Infections (bacterial, viral, fungal, parasitic) are among the most common and medically
important causes of inflammation.
2. Trauma (blunt and penetrating)
3. physical and chemical agents (e.g., thermal injury, such as burns or frostbite; irradiation;
toxicity from certain environmental chemicals)
4. Tissue necrosis (from any cause), including ischemia (as in a myocardial infarct) and
physical and chemical injury
5. Foreign bodies (splinters, dirt, sutures, crystal deposits)
6. Immune reactions against environmental substances or against “self” tissues. Because the
stimuli for these inflammatory responses often cannot be eliminated or avoided, such
reactions tend to persist, with features of chronic inflammation.
Q-6. Enumerate different causes of inflammation giving an example in each case
ANS:
1. Infection Bacterial infections ie staphylococcus mycobacterium tuberculosis
2. Trauma, blunt or penetrating
3. Physical injury from thermal extremes or from ionizing radiation
4. Chemical injury
5. Immunologic injury, hypersensitivity reactions allergic reactions and autoimmune
reactions.
6. Tissue death. Inflammatory changes occur in viable tissue adjacent to necrotic areas.
Q-7. Name the localized cardinal signs of acute inflammation
ANS:
1. Rubor (redness caused by dilation of vessels)
2. Dolor (pain due to increased pressure exerted by the accumulation of interstitial fluid and
to mediators such as bradykinin)
3. Calor (heat caused by increased blood flow)
4. Tumor (swelling due to an extravascular accumulation of fluid)
5. Functio laesa (loss of function)
Q-8. Name the systemic signs of acute inflammation
ANS:
1. Fever in response to exogenous pyrogens (lipopolysaccharide (LPS)) and endogenous
pyrogens (cytokines such as IL-1 and TNF)

2. Elevated plasma levels of acute-phase proteins C-reactive protein (CRP), fibrinogen, and
serum amyloid A (SAA) protein
3. Leucocytosis
4. Increased heart rate and blood pressure; decreased sweating, mainly as a result of
redirection of blood flow from cutaneous to deep vascular beds
5. Rigors (shivering), chills (perception of being cold as the hypothalamus resets the body
temperature),
6. Anorexia, somnolence, and malaise, probably secondary to the actions of cytokines on
brain cells.
7. Metabolic disturbances including acidosis, and hypotensive shock such as DIC
(disseminated intravascular coagulation)
Q-9. Name the sequels of acute inflammation
ANS:
1. Complete resolution of structure and function with regeneration.
2. Tissue destruction Abscess (This is a cavity filled with pus having neutrophils, monocytes,
and liquefied cellular debris). Ulcer (This is the loss of surface epithelium) and Fistula
3. Complete resolution with scarring
4. Transition to chronic inflammation
Q-10. Enumerate types of acute inflammation on the basis of morphology of exudate.
ANS:
1. Serous inflammation  outpouring of a watery, relatively protein-poor fluid (effusion)
2. Fibrinous inflammation fibrinous exudate i.e. pericardium
3. Suppurative (purulent) inflammation  purulent exudate i.e. puss in bacterial infection
4. Ulcer in mucosa of mouth, stomach, intestines
Q-11. Enumerate the cell derived mediators of inflammation
ANS:
A. Preformed mediators
1. Histamine
2. Serotonin
B. Newly synthesized
1. Prostaglandins
2. Leukotrienes
3. Platelet-activating factor
4. Reactive oxygen species
5. Nitric oxide
6. Cytokines (TNF, IL-1, IL-6)
7. Chemokines

8. Neuropeptides
Q-12. What is the role of macrophages in chronic inflammation?
ANS:
1. Phagocytosis like the other type of phagocyte, the neutrophils, ingest and eliminate
microbes and dead tissues by producing ROS and NO. Because macrophages respond to
activating signals from T lymphocytes, they are the most important phagocytes in the cell-
mediated arm of adaptive immune responses
2. Role in repair: initiate the process of tissue repair and are involved in scar formation and
fibrosis through alternative path way induced by cytokines such as IL-4 and IL-13,
produced by T lymphocytes and other cells, including mast cells and eosinophils, to
secrete growth factor that promote angiogenesis and activate fibroblast and stimulate
collagen synthesis
3. Role in inflammation: secrete mediators of inflammation, such as cytokines (TNF, IL-1,
chemokines, and others) and eicosanoids. These cells are therefore central to the
initiation and propagation of all inflammatory reactions.
4. Role in immunity: as an antigen presenting cell it displays antigens to T lymphocytes
and respond to signals from T cells, thus setting up a feedback loop that is essential for
defence against many microbes by cell mediated immune responses. The same
bidirectional interactions are central to the development of chronic inflammatory
diseases.
5. Role in granuloma formation: IFN-γ induce macrophages to fuse into large,
multinucleate giant cells in granuloma.
Q-13. Define granuloma. Name its types, enumerate the causes of granulomatous inflammation.
ANS:
Granulomatous inflammation: specialized form of chronic inflammation characterized by
small aggregates of modified macrophages (epithelioid cells and multinucleated giant cells)
usually surrounded by a rim of lymphocytes
Granuloma: nodular collections of specialized macrophages (epithelioid cells and
multinucleated giant cells) usually surrounded by a rim of lymphocytes
Types:
1. Caseating granuloma (tubercle)
2. noncaseating granulomas
3. Gumma
4. Rounded or stellate granuloma
5. foreign body granulomas
Causes:
1. Tuberculosis (caseating granulomas).
2. Cat-scratch fever. (rounded or stellate granuloma)
3. Syphilis. (gumma)

4. Leprosy. (non caseating granulomas)

5. Fungal infections (e.g., coccidioidomycosis).
6. Parasitic infections (e.g., schistosomiasis).
7. Foreign bodies.
8. Beryllium.
9. Sarcoidosis
Q-14. Draw and label tuberculous granuloma.
ANS:
Q-15. List causes of chronic granulomatous inflammation.
ANS:
1. With persistent T-cell responses to certain microbes
Mycobacterium tuberculosis, Mycobacterium leprae T. pallidum, Cat-scratch disease
Gram-negative bacillus or fungi Blastomyces dermatitidis, Histoplasma capsulatum
2. immune- mediated inflammatory diseases
Crohn disease, which is one type of inflammatory bowel disease
3. Disease of unknown etiology sarcoidosis, and they develop in response to relatively
inert foreign bodies (e.g., suture or splinter), forming so-called foreign body granulomas.
Q-16. Enumerate four bacterial and one fungal granuloma along with causative agents of each
in a tubular form (granuloma on one side and causative agent in front of it)

ANS:
1. Caseating granulomas (Tuberculosis)  Mycobacterium tuberculosis
2. Stellate granuloma (Cat-scratch fever)  Bartonella henselae
3. Non caseating granulomas (Leprosy)  Mycobacterium leprae
4. Gumma (syphilis)  Treponema pallidum
5. Paranasal Aspergillus granuloma  Aspergillus flavus
6. Majocchi’s granuloma  deep cutaneous mycotic infection most commonly caused by
Trichophyton rubrum
Q-17. A young man presented in outdoor department with history of chronic fever, weight loss
and cervical Lymphadenopathy. The lymph node biopsy showed aggregates of epitheloid
cells.
a) What is the most likely diagnosis?
b) Name the parent cell of epitheloid cell.
c) What mediators induces granuloma formation.
ANS:
a) Tuberculosis
b) Macrophages
c) IFN-γ can also induce macrophages to fuse into large, multinucleate giant cells other
mediators involved are Interleukins 12, 13, 17, 4 and TGF β
Q-1. What is Gohn Focus?
1. A Ghon focus is a primary lesion usually subpleural, caused by mycobacterium bacilli

tuberculosis developed in the lung of a nonimmune host (usually a child).
2. It is a small area of granulomatous inflammation, only detectable by chest X-ray if it
calcifies
3. The classical location for primary infection is surrounding the lobar fissures, either in the
upper part of the lower lobe or lower part of the upper lobe.
4. If the Ghon focus also involves infection of adjacent lymphatics and hilar lymph nodes,
When a Ghon's complex undergoes fibrosis and calcification it is called a Ranke complex
Q-18. Tabulate differences between exudate and transudate
ANS:
An exudate is any fluid that filters from the circulatory system into lesions or areas of
inflammation
Its composition varies but generally includes water and the dissolved solutes of the blood,
some or all plasma proteins, white blood cells, platelets and RBC
Transudate
A fluid that passes through a membrane which filters out much of the protein and cellular
elements to yield a watery solution.
A transudate is due to increased pressure in the veins and capillaries pressure forcing fluid
through the vessel walls or low levels of protein the blood serum
The transudated fluid accumulates in tissues outside the blood vessels and can cause edema

Features Exudate Transudate

Causes Inflammation and increased Decreased colloid osmotic pressure
vascular permeability and increase hydrostatic pressure
Protein quantity in above 4gm/m3 Below

fluid
Fibrin High low
Specific gravity > 1.020 < 1.012
Appearance turbid due to protein Clear
Clotting on standing Yes no
Q-19. Enumerate the biological active cleavage products of complement system along with main
function of each one in tabular form. (Product on one side and its function in front of it)
ANS:
1. C5b-C9  membrane attack complex
2. C3a,C5a  anaphylotoxins stimulate the release of histamine
3. C5a  leukocyte chemotactic factor
4. C3b  opsonin
Q-20. Define healing by regeneration
ANS:
Healing by regeneration can occur only if the residual connective tissue framework is
structurally intact, as after partial surgical resection this is by proliferation of residual cells
and differentiation of tissue stem cells example are
1. In epithelia of the intestinal tract and skin, injured cells are rapidly replaced by
proliferation of residual cells and differentiation of tissue stem cells provided the
underlying basement membrane is intact.
2. Parenchymal organs with stable cell populations, but with the exception of the liver,
this is usually a limited process ie Pancreas, adrenal, thyroid, and lung.
The regenerative response of the liver that occurs after surgical removal of hepatic
tissue
The removal of tissue triggers a proliferative response of the remaining hepatocytes, and the
subsequent replication of hepatic non-parenchymal cells. This is initiated by
1. Cytokines (e.g., TNF, IL-6) that prepare the cells for replication by stimulating the
transition from G0 to G1 in the cell cycle.

2. HGF, TGF-α (produced by fibroblasts, endothelial cells, and liver nonparenchymal

cells) Progression through the cell cycle
Q-21. Enumerate the phases of cutaneous wound healing
ANS:
Cutaneous wound healing is a process that involves both epithelial regeneration and the
formation of connective tissue scar Depending on the nature and size of the wound, the
healing of skin wounds is said to occur by first or second intention.
Healing by First Intention
Within 24 hours,
1. Neutrophils are seen at the incision margin, migrating toward the fibrin clot.
2. Increased mitotic activity in Basal cells at the cut edge of the epidermis.
3. Within 24 to 48 hours, epithelial cells migrate and proliferate along the dermis
4. The cells meet in the midline beneath the surface scab
• By day 3,
1. Neutrophils are replaced by macrophages,
2. Granulation tissue progressively invades the incision space.
3. Vertically oriented Collagen fibers and do not bridge the incision.
4. Epithelial cell proliferation continues, yielding a thickened epidermal covering layer.
• By day 5,
1. Neovascularization reaches its peak as granulation tissue fills the incisional space.
2. Collagen fibrils become more abundant and begin to bridge the incision.
3. Surface keratinization occur as differentiation of surface cells and The epidermis
recovers its normal thickness
• 2 week,
nd
1. Continued collagen accumulation and fibroblast proliferation.

2. Diminishing of The leukocyte infiltrate, edema, and increased vascularity
3. Increased collagen deposition within the incisional scar and decrease vascular
channels.
• At the End of the first month,
1. The scar consists of a cellular connective tissue, largely devoid of inflammatory cells,
Covered by normal epidermis.
2. The dermal appendages destroyed in the line of the incision are permanently lost
Healing by second intention
1. A larger clot or scab rich in fibrin and fibronectin forms at the surface of the wound.
2. Inflammation is more intense because large tissue defects have a greater volume of
necrotic debris, exudate, and fibrin having a greater potential for secondary,
inflammation-mediated, injury.
3. Greater volume of granulation tissue to fill in the gaps and provide the underlying
framework for the regrowth of tissue epithelium. A greater volume of granulation
tissue generally results in a greater mass of scar tissue.

4. Wound contraction. Within 6 weeks, for example, large skin defects reduced their
size, largely by contraction. This process is due to the presence of myofibroblasts,
modified fibroblasts exhibiting features of contractile smooth muscle cells.
Q-22. Name the factors which delay in wound healing
ANS:
1. Nutrition  protein deficiency, vitamin C deficiency inhibit collagen synthesis and
retard healing.
2. Glucocorticoids (steroids)  retard scar formation because of inhibition of TGF-β
production
3. Mechanical variables  increased local pressure or torsion may cause wounds to
pull apart
4. Poor perfusion,  due to arteriosclerosis and diabetes or varicose veins also impairs
healing.
5. Infection:  prolongs inflammation increases the local tissue injury.
6. Foreign bodies  fragments of steel, glass, or even bone impede healing.
7. The type and extent of tissue injury  tissues composed of stable and labile cells,
complete restoration can occur. Injury to tissues composed of permanent cells must
inevitably result in scarring, as in healing of a myocardial infarct.
8. The location of the injury and the character of the tissue: For example,
inflammation arising in tissue spaces (e.g., pleural, peritoneal, or synovial cavities)
develops extensive exudates. Subsequent repair may occur by resolution “digestion of
the exudate, initiated by the proteolytic enzymes of leukocytes (fibrinolysis) and
resorption of the liquefied exudate by macrophages, in the absence of cellular
necrosis, normal tissue architecture is restored”. Organization occur in the setting of
larger accumulations, Granulation tissue grows into the exudate, and a fibrous scar
ultimately forms. Example organization of a fibrinous pericardial exudate.
9. Increase cell growth and ECM production for example, the accumulation of
exuberant amounts of collagen can give rise to prominent, raised scars known as
keloids.
Q-23. Briefly explain with the help of examples healing by Resolution, Regeneration,
Organization and Fibrosis
ANS:
 Resolution: digestion of the exudate, initiated by the proteolytic enzymes of

leukocytes (fibrinolysis) and resorption of the liquefied exudate by macrophages, in
the absence of cellular necrosis, normal tissue architecture is restored
Example: healing occur after inflammation in the lining of body cavities, such as the
meninges, pericardium, and pleura
 Regeneration: Healing by regeneration can occur only if the residual connective

tissue framework is structurally intact, as after partial surgical resection this is by
proliferation of residual cells and differentiation of tissue stem cells.

Examples
1. In epithelia of the intestinal tract and skin, injured cells are rapidly replaced by
proliferation of residual cells and differentiation of tissue stem cells provided the
underlying basement membrane is intact.
2. Parenchymal organs with stable cell populations, but with the exception of the
liver, this is usually a limited process i.e. Pancreas, adrenal, thyroid, and lung.
3. Liver: The regenerative response of the liver that occurs after surgical removal of
hepatic tissue. The removal of tissue triggers a proliferative response of the
remaining hepatocytes, and the subsequent replication of hepatic non-
parenchymal cells. This is initiated by
Cytokines (e.g., TNF, IL-6) that prepare the cells for replication by stimulating the
transition from G0 to G1 in the cell cycle and HGF, TGF-α
 Organization: Organization occur in the setting of larger accumulations in the lining
of body cavities, when exudates may not be completely removed Granulation
(fibroblasts and blood vessels) tissue grows into the exudate, and a fibrous scar
ultimately forms.
Example
Organization of a fibrinous pericardial exudate.
 Fibrosis: repair occurs by replacement of the no-regenerated cells with connective

tissue, leading to the formation of a scar, or by a combination of regeneration of some
cells and scar formation occur in those conditions if tissue injury is severe or chronic
and results in damage to parenchymal cells and epithelia as well as the connective
tissue, or if non dividing cells are injured,
1. angiogenesis formation of new blood vessels
2. Formation of granulation tissue, Migration and proliferation of fibroblasts and
deposition of connective tissue, which, together with abundant vessels and
interspersed leukocytes, has a pink, granular appearance.
3. Remodeling, Maturation and reorganization of the fibrous tissue to produce the
stable fibrous scar
Fibrosis in Parenchymal Organs: fibrosis is used to denote the excessive deposition
of collagen and other ECM components in a tissue in chronic diseases. Mechanisms of
fibrosis are the same as those of scar formation during tissue repair but fibrosis is
induced by Persistent stimulation of collagen synthesis by injurious stimuli such as
infections, immunologic reactions, chronic diseases and other types of tissue injury.
Examples The fibrosis seen in chronic diseases such as pulmonary fibrosis
Q-24. Following appendectomy, the surgeon applied neat surgical sutures to the incision line. Enlist
the steps of healing in this patient in chronological order.
ANS:
Healing will be by first intention
Already mentioned*

Neoplasia 29
Q-1. Define Neoplasia.
ANS:
Neoplasia is an abnormal new growth of tissue its cells are said to be transformed because
they continue to replicate, apparently unaware of the regulatory influences that control
normal cell growth
Q-2. What are the types of neoplasm? Give two examples of each.
ANS:
1. Benign tumor they are circumscribed and localized, amenable to local surgical
removal and do not transform into cancer. Uterine fibroids and melanocytic nevi (skin
moles).
2. Potentially-malignant neoplasms include carcinoma in situ. They are localized, do
not invade and destroy but in time, may transform into a cancer. Examples are Ductal
carcinoma in situ of the breast, Colon polyps transform into colon cancer if left
untreated.
3. Malignant neoplasms are commonly called cancer. They invade and destroy the
surrounding tissue, may form metastases and untreated or unresponsive to
treatment, will prove fatal. examples are Renal cell carcinoma, Hepatocellular
carcinoma
Q-3. Tabulate differences between benign and malignant tumor.
ANS:
Characteristics Benign Malignant
Differentiation/ Well differentiated; structure Some lack of differentiation with

anaplasia sometimes typical of tissue of anaplasia; structure often atypical
origin
Rate of growth Usually progressive and slow; Erratic and may be slow to rapid;
may come to a standstill or mitotic figures may be numerous
regress; mitotic figures rare and and abnormal
normal
Local invasion Usually cohesive expansile Locally invasive, infiltrating
welldemarcated masses that do surrounding tissue; sometimes
not invade or infiltrate may be seemingly cohesive and
surrounding normal tissues expansile
Metastasis Absent Frequently present; the larger and

more undifferentiated the primary,
the more likely are metastases

Neoplasia 30
Q-4. Give examples of benign and malignant tumor.
ANS:
1. Connective tissue and derivatives
a. Benign: Fibroma, Lipoma, Chondroma
b. Malignant: Fibrosarcoma, Liposarcoma, Chondrosarcoma
2. Epithelial lining of glands or ducts
a. Benign: Adenoma, Papilloma
b. Malignant: Adenocarcinoma, Papillary carcinomas
3. Respiratory passages
a. Benign: Bronchial adenoma
b. Malignant: Bronchogenic carcinoma
4. Renal epithelium
a. Benign: Renal tubular adenoma
b. Malignant: Renal cell carcinoma
5. Liver cells
a. Benign: Liver cell adenoma
b. Malignant: Hepatocellular carcinoma
Q-5. Briefly comment on the characteristic features of malignant neoplasms.
ANS:
Characteristics Malignant
Differentiation/ Some lack of differentiation with anaplasia; structure often

anaplasia atypical
Rate of growth Erratic and may be slow to rapid; mitotic figures may be
numerous and abnormal
Local invasion Locally invasive, infiltrating surrounding tissue, non-encapsulated

; sometimes may be seemingly cohesive and expansile,
Metastasis Frequently present; the larger and more undifferentiated the

primary, the more likely are metastases
Q-6. Give a brief description of Grading and Staging of cancer.
ANS:
A method to quantify the clinical aggressiveness and its apparent extent and spread of a given
neoplasm in the individual patient for making an accurate prognosis and for comparing end
results of various treatment protocols.
Grading: The grading of a cancer attempts to establish some estimate of the level of
malignancy based on
1. cytologic differentiation of tumor cells

Neoplasia 31
2. number of mitoses within the tumor.

The cancer may be classified as grade I, II, III, or IV, in order of increasing anaplasia. Criteria
for the individual grades vary with each form of neoplasia. Grade l is well differentiated and
when moving toward IV it is poorly differentiated.
Staging: Staging of cancers is based on
1. size of the primary (Tumor) lesion, T
2. extent of spread to regional lymph nodes, N
3. presence or absence of metastases. M
This assessment usually is based on clinical and radiographic examination (CT scan, MRI) and
in some cases surgical exploration.
Two methods of staging:
TNM system (T, primary tumor; N, regional lymph node involvement; M, metastases) In the
TNM system,
T0, T1, T2, T3, and T4 describe the increasing size of the primary lesion;
N0, N1, N2, and N3 indicate progressively advancing node involvement;
M0 and M1 reflect the absence and presence, respectively, of distant metastases
AJC (American Joint Committee) system. In the AJC method, the cancers are divided into
stages 0 to IV, incorporating the size of primary lesions and the presence of nodal spread and
of distant metastases.
Q-7. What are different effects of a tumor on the host
ANS:
A. Tumor Impingement on nearby structures
1. Pituitary adenoma on normal gland compression of normal tissue ----
Hypopitutrism
2. Pancreatic carcinoma on bile duct Produce fatal billiary tract obstruction
3. Renal artery leiomyoma ischemia & hypertention
4. Hormones production B cell tumor produce hyperinsulinism
5. Ulceration/bleeding colon, Gastric, and Renal cell carcinomas
B. Infection (often due to obstruction)
1. Pulmonary infections due to blocked bronchi (lung carcinoma)
2. Urinary infections due to blocked ureters (cervical carcinoma)
C. Rupture or Infarction
1. Ovarian, Hepatocellular, and Adrenal cortical carcinomas; Melanocarcinoma
metastases
D. Cancer Cachexia
1. Progressive weakness, loss of appetite, anemia and profound weight loss (>20 lbs.)
E. Paraneoplastic Syndromes
1. Endocrinopathies
2. Neuromyopathies
3. Osteochondral Disorders
4. Vascular Phenomena
5. Fever
6. Nephrotic Syndrome

Neoplasia 32
Q-8. What are the clinical aspects of the tumors?
ANS:
1. Location and impingement on adjacent structures
2. Development of paraneoplastic syndromes
3. Bleeding and infections when tumor ulcerates
4. Symptoms of rupture and infarction
5. Cachexia or wasting
Q-9. Define Metastasis describe its steps/Name the various methods of tumor spread with
examples/Enlist the pathways of metastasis with examples.
ANS:
Metastases are secondary implants of a tumor that are discontinuous with the primary tumor
and located in distant tissues, metastasis identifies a neoplasm as malignant
Malignant neoplasms disseminate by one of three pathways:
1. Seeding within body cavities
i) Cancers of the ovary, the neoplasms invade peritoneal cavity which often cover the
peritoneal surfaces and not invade the underlying tissues. Here is an instance of the
ability to re-implant elsewhere that seems to be separable from the capacity to
invade.
ii) Neoplasms of the central nervous system, such as a medulloblastoma or
ependymoma, may penetrate the cerebral ventricles and be carried by the
cerebrospinal fluid to reimplant on the meningeal surfaces, either within the brain or
in the spinal cord.
2. Lymphatic spread,
It is more typical in carcinomas, the pattern of lymph node involvement depends
principally on the site of the primary neoplasm and the natural pathways of local
lymphatic drainage.
i) Lung carcinomas metastasize first to the regional bronchial lymph nodes then to
the tracheobronchial and hilar nodes.
ii) Carcinoma of the breast (upper outer quadrant) spreads to the axillary nodes.
Medial breast lesions may drain to the nodes along the internal mammary artery
and then to supraclavicular and infraclavicular nodes.
iii) skip metastases when cancer cells seem to traverse the lymphatic channels within
the immediately proximate nodes to be trapped in subsequent lymph nodes,
iv) A “sentinel lymph node” is the first regional lymph node that receives lymph flow
from a primary tumor.
Enlargement of nodes involve in metastasis The necrotic products of the neoplasm and
tumor antigens often evoke immunologic responses in the nodes, such as hyperplasia of
the follicles (lymphadenitis) and proliferation of macrophages in the subcapsular sinuses
(sinus histiocytosis).
3. Hematogenous spread
Hematogenous spread is the favored pathway for sarcomas, but carcinomas use it as well.
As might be expected,

Neoplasia 33
Veins are penetrated more than arteries blood-borne cells follow the venous flow
draining the site of the neoplasm tumor cells often stopping in the first capillary bed they
encounter. Since all portal area drainage flows to the liver, and all caval blood flows to the
lungs, the liver and lungs are the most frequently involved secondary sites in
hematogenous dissemination
i) Carcinomas of the thyroid and prostate through the paravertebral plexus
vertebral metastases
ii) Renal cell carcinoma often invades the renal vein to grow in a snakelike fashion up
the inferior vena cava, sometimes reaching the right side of the heart.
iii) Hepatocellular carcinomas often penetrate portal and hepatic radicles to grow
within them into the main venous channels.
Sometime anatomic localization of a neoplasm and its venous drainage cannot wholly
explain the systemic distributions of metastases. For example,
i) prostatic carcinoma spreads to bone,
ii) bronchogenic carcinomas tend to involve the adrenals and the brain,
iii) neuroblastomas spread to the liver and bones.
Q-10. Simply name dysplastic conditions that are considered pre-malignant.
ANS:
1. Atypical endometrial hyperplasia   endometrial carcinoma
2. Barrette esophagus  adenocarcinoma of esophagus
3. Squamous metaplasia in bronchial epithelium squamous cell carcinoma
4. Colon polyps adenocarcinoma of colon
5. Cervical intraepithelial neoplasm  invasive cervical carcinoma
Q-11. What do you mean by oncogenic viruses?
ANS:
A. Oncogenic RNA Viruses
1. Retrovirus, the human T cell lymphotropic virus-1 (HTLV-1)
B. Oncogenic DNA viruses:
1. Human papilloma virus HPV,
2. Epstein-Barr virus (EBV),
3. Kaposi sarcoma herpes virus (KSHV, also called human herpesvirus-8 [HHV-8]),
4. Hepatitis B virus (HBV) and Hepatitis C virus (HCV)
Q-12. Name oncogenic viruses and bacterium that are associated with tumors.
ANS:
A. VIRUSES:
1. human T cell lymphotropic virus-1 (HTLV-1)  T cell leukemia/lymphoma.
2. Human papilloma virus HPV  benign squamous papillomas (warts) in humans

Neoplasia 34
3. Epstein-Barr virus (EBV)  Infectious mononucleosis, Burkitt lymphoma, B cell

lymphomas, Hodgkin lymphoma, nasopharyngeal carcinoma
4. Kaposi sarcoma herpes virus
5. Hepatitis B virus (HBV) and Hepatitis C virus (HCV) hepatocellular carcinoma
B. BACTERIA
1. Helicobacter pylori  Gastric adenocarcinoma and MALT lymphoma.
Q-13. Enumerate fundamental steps in carcinogenesis.
ANS:
Genetic lesions
1. Karyotypic Changes in Tumors
i) Balanced Translocations
ii) Deletions
iii) Gene Amplifications
iv) Aneuploidy
2. Over expression of MicroRNAs
3. Epigenetic Modifications
Hallmarks of cancer
1. Self-sufficiency in growth signals
2. Insensitivity to growth inhibitory signals
3. Evasion of cell death
4. Limitless replicative potential
5. Development of sustained angiogenesis
6. Ability to invade and metastasize
7. reprogramming of metabolic pathways
8. ability to evade the immune system.
Q-14. Enumerate the antitumor mechanism in the body.
ANS:
1. Tumor Suppressors genes
i) Retinoblastoma Gene  control G1 to S transition of the cell cycle
ii) T53 Gene  controls the expression and activity of genes involved in cell
cycle arrest, DNA repair, cellular senescence, and apoptosis, angiogenesis
inhibitor.
2. Tumor Antigens
i) Products of Mutated Oncogenes and Tumor Suppressor Genes
ii) Products of Other Mutated Genes
iii) Tumor Antigens Produced by Oncogenic Viruses
iv) Onco-fetal Antigens
v) Altered Cell Surface Glycolipids and Glycoproteins
vi) Cell Type–Specific Differentiation Antigens
3. Antitumor Effector Mechanisms
i) Cytotoxic T Lymphocytes
ii) Natural Killer Cells

Neoplasia 35
iii) Macrophages
iv) Humoral Mechanisms
Q-15. Enumerate the karyotype changes in the tumor.
ANS:
1. Balanced Translocations
2. Deletions
3. Gene Amplifications
4. Aneuploidy
Q-16. Enumerate different carcinogenic agents
ANS:
1. Chemicals
2. radiant energy,
3. microbial agents.
Q-17. How do cancers evade immune system?
ANS:
1. Selective outgrowth of antigen-negative variants
Loss or reduced expression of histocompatibility molecules. Tumor cells may fail to
express normal levels of human leukocyte antigen (HLA) class I, escaping attack by
CTLs. Such cells, however, may trigger NK cells.
2. Immunosuppression.
Many oncogenic agents (e.g., chemicals, ionizing radiation)
Tumors or tumor products also may be immunosuppressive.
For example,
i) TGFβ, secreted by tumor a potent immunosuppressant.
ii) The immune response induced by the tumor may inhibit tumor immunity.
iii) Recognition of tumor cells by T cell inhibitory receptor, CTLA-4, or activation
of regulatory T cells that suppress immune responses.
iv) Some tumors express FasL, which can engage Fas on immune cell surfaces and
induce apoptosis in immune cells
3. Antigen masking.
Many tumor cells produce glycocalyx molecules, such as sialic acid–containing
mucopolysaccharides, This thick coat may block access of immune cells to
antigen-presenting molecules, thereby preventing antigen recognition and cell killing.
4. Downregulation of co-stimulatory molecules.
Costimulatory molecules are required to initiate strong T cell responses. Many tumors
reduce expression of these costimulatory molecules.

Diseases of the Immune System 36
Q-1.
a) Define immunity.
b) Enumerate components of innate immunity. Summarize biological barriers in innate
c) immunity?
ANS:
Innate(native)immunity It is nonspecific and present from birth. Encompasses protective
factors present in an individual independent of antigenic stimulus, It is an initial, rapid
recognition system for detection of pathogens.
1) Skin and mucus membranes block entry of pathogens and secrete antimicrobial peptides
and enzymes.
2) Cationic peptides (defensins) are secreted by cells into phagocytic vacuoles and damage
bacterial membranes.
3) Cathelicidins are stored in secretory granules, which when activated make bacterial
membranes more permeable.
4) Lysozyme is released into lachrymal and saliva secretions.
Q-2. Give the main features of active acquired immunity and passive acquired immunity with
examples
ANS:
Active immunity is resistance induced after contact with foreign antigens (e.g.,
microorganisms). This contact may consist of clinical or subclinical infection,
immunization with live or killed infectious agents or their antigens, or exposure to microbial
products (e.g., toxins and toxoids). In all these instances, the host actively produces an
immune response consisting of antibodies and activated helper and cytotoxic T lymphocytes.
Main advantage is that resistance is long term but its major disadvantage is its slow onset
Passive immunity is resistance based on antibodies preformed in another host.
Administration of antibody against diphtheria, tetanus, botulism, etc., makes large amounts of
antitoxin immediately available to neutralize the toxins. Likewise, preformed antibodies to
certain viruses (e.g., rabies and hepatitis A and B viruses) can be injected during the
incubation period to limit viral multiplication.
Other forms of passive immunity are IgG passed from mother to foetus during pregnancy and
IgA passed from mother to new-born during breast feeding. The main advantage of passive
immunization is the prompt availability of large amounts of antibody; disadvantages are the
short life span of these antibodies and possible hypersensitivity reactions if globulins from
another species are used.

Q-3.
a) Define Hypersensitivity
b) Classify hypersensitivity.
c) Give pathophysiology of type I hypersensitivity.
d) Give three examples type I hypersensitivity.
e) List the mediators of type I hypersensitivity.
f) How is it possible to avoid hypersensitivity (Type I) in a person?
ANS:
a) HYPERSENSITIVITY:
Hypersensitivity is the term used when an immune response results in exaggerated or
inappropriate reactions harmful to the host
b) CLASSIFICATION:
1. Type 1 immediate (anaphylactic) Hypersensitivity
2. Type 2 Cytotoxic Hypersensitivity
3. Type 3 immune complex Hypersensitivity
4. Typ4 4 Delayed (cell mediated) Hypersensitivity
c) PATHOPHYSIOLOGY OF TYPE I HYPERSENSITIVITY.
1. Antigen (allergin) induce igE antibody that bind to mast cells and basophils
2. When exposed to the allergen again the allergen cross links the bound igE on those
cells this cause degranulation and release of mediators eg histamine
d) EXAMPLES TYPE I HYPERSENSITIVITY.
1. Asthma,
2. hay fever,
3. allergic rhinitis,
4. allergic conjunctives,
5. drug allergies i.e. penicillin,
e) MEDIATORS OF TYPE I HYPERSENSITIVITY
1. Histamine,
2. Slow-reacting substance of anaphylaxis (SRS-A)
3. Eosinophil chemotactic factor of anaphylaxis (ECF-A),
4. Serotonin,
5. Prostaglandins and thromboxane,
6. Platelet activating factor
f) HOW TO AVOID HYPERSENSITIVITY
1. Acute desensitization
Administration of very small amounts of antigen at 15-minute intervals.
Antigen–IgE complexes form on a small scale, and not enough mediator is released to
produce a major reaction. This permits the administration of a drug or foreign protein
to a hypersensitive person, but the hypersensitive state returns because IgE continues
to be made.
2. Chronic desensitization
Long-term weekly administration of the antigen to which the person is
hypersensitive. This stimulates the production of IgA and IgG-blocking antibodies,
which can prevent subsequent antigen from reaching IgE on mast cells, thus

preventing a reaction. It also induces regulatory T cells to produce IL-10, which

reduces the synthesis of IgE.
Q-4. Give the salient features of type II hypersensitivity
ANS:
Occurs when antibody directed at antigens of the cell membrane activates complement
This generates a membrane attack complex, which damages the cell membrane.
The antibody (IgG or IgM) attaches to the antigen via its Fab region and acts as a bridge to
complement via its Fc region.
Q-5. Give three examples of type II hypersensitivity
ANS:
1. Complement-mediated lysis as in haemolytic anaemias,
2. ABO transfusion reactions.
3. Rh incompatibility.
Q-6. Name the steps to avoid type II hypersensitivity
ANS:
1. Proper blood grouping.
2. Administration of anti RH anti bodies to Rh negative mother prior to birth of baby.
3. Avoid drugs causing haemolytic anaemias
Q-7. Give brief description of immune complex (Type III) reactions.
ANS:
Immune complex hypersensitivity occurs when antigen–antibody complexes induce an
inflammatory response in tissues. Wherever immune complexes are deposited, they activate the
complement system. Polymorphonuclear cells are attracted to the site, and inflammation and
tissue injury occur. Two typical type III hypersensitivity reactions are the Arthus reaction and
serum sickness Arthus reaction is the name given to the inflammation caused by the deposition
of immune complexes at a localized site. In contrast to the Arthus reaction, which is localized
inflammation, serum sickness is a systemic inflammatory response to the presence of immune
complexes deposited in many areas of the body.
1. Glomerulonephritis
2. Rheumatoid Arthritis
3. Systemic Lupus Erythematosus

Q-8. Give a brief account of type IV (delayed hypersensitivity).
ANS:
Delayed (cell-mediated) hypersensitivity. The macrophage ingests the antigen, processes it,
and presents an epitope on its surface in association with class II major histocompatibility
complex (MHC) protein. The helper T (Th-1) cell is activated and produces gamma interferon,
which activates macrophages. These two types of cells mediate delayed hypersensitivity.
TCR, T-cell receptor.
Delayed hypersensitivity is a function of T lymphocytes, not antibody. It can be transferred by
immunologically committed (sensitized) T cells, not by serum. The response is “delayed” (i.e.,
it starts hours [or days] after contact with the antigen and often lasts for days).
Examples
1. Contact Hypersensitivity
2. Tuberculin-Type
Hypersensitivity
3. Erythema Multiforme,
Stevens-Johnson Syndrome,
and Toxic Epidermal
Necrolysis
Q-9. Name the classes and subclasses of immunoglobulins.
ANS:
1. IgG
i) IgG1, IgG2, IgG3 and IgG4. (Based on differences of their heavy chains)
2. IgA

i) IgA1 and IgA2. (Based on differences of their heavy chains)

3. IgM
4. IgE
5. IgD
Q-10. Enumerate the Physiochemical characteristics and biological functions of

Immunoglobulin M
ANS:
1. IgM is the main immunoglobulin produced early in the primary response.
2. It is present as a monomer on the surface of virtually all B cells, where it functions as
an antigen-binding receptor.
3. In serum, it is a pentamer composed of five H2L2 units plus one molecule of J (joining)
chain IgM has a μ heavy chain.
4. Because the pentamer has 10 antigen-binding sites, it is the most efficient
immunoglobulin in agglutination, complement fixation (activation), and other
antibody reactions and is important in defense against bacteria and viruses.
5. It can be produced by the fetus in certain infections.
6. It has the highest avidity of the immunoglobulins; its interaction with antigen can
involve all 10 of its binding sites.
Q-11. Give the physicochemical characteristics and biological functions of IgG.
ANS:
1. Each IgG molecule consists of two L chains and two H chains linked by disulfide bonds
(molecular formula H2L2).
2. Because it has two identical antigen-binding sites, it is said to be divalent.
3. There are four subclasses, IgG1–IgG4, based on antigenic differences in the H chains
and on the number and location of disulfide bonds.
4. IgG1 makes up most (65%) of the total IgG. IgG2 antibody is directed against
polysaccharide antigens and is an important host defense against encapsulated
bacteria.
5. IgG is the predominant antibody in the secondary response and constitutes an
important defense against bacteria and viruses.
6. IgG is the only antibody to cross the placenta; only its Fc portion binds to receptors on
the surface of placental cells. It is therefore the most abundant immunoglobulin in
newborns.
7. IgG is one of the two immunoglobulins that can activate complement
8. IgG is the immunoglobulin that opsonizes. It can opsonize (i.e., enhance phagocytosis)
because there are receptors for the γH chain on the surface of phagocytes.
9. There are four subclasses of IgG. Subclasses IgG1 and IgG3 are more effective
opsonizers than are IgG2 and IgG4.

Q-12. What is autoimmunity?
ANS:
A disorder of the body’s defence mechanism in which an immune is generated against
components or products of its own tissues, treating them as a foreign materiel and attacking
them.
Q-13. Define and enlist the autoimmune diseases.
ANS:
One o fa number of otherwise unrelated disorders caused by inflammation and destruction of
tissues by the body’s own immune response.
These disorders include
1. acquired hemolytic anemia,
2. pernicious anemia,
3. rheumatic fever,
4. rheumatoid arthritis,
5. glomerulonephritis,
6. systemic lupus erythematous,
7. myasthenia gravis.
Q-14. What is the mechanism of autoimmune diseases?
ANS:
A. Molecular Mimicry
Various bacteria and viruses are implicated as the source of cross-reacting antigens that
trigger the activation of auto reactive T cells or B cells.
For example, Reiter’s syndrome occurs following infections with Shigella or Chlamydia, and
GuillainBarré syndrome occurs following infections with Campylobacter.
The concept of molecular mimicry is used to explain these phenomena (i.e., the
environmental trigger resembles [mimics] a component of the body sufficiently that an
immune attack is directed against the cross-reacting body component). One of the best
characterized examples of molecular mimicry is the relationship between the M protein of S.
pyogenes and the myosin of cardiac muscle. Antibodies against certain M proteins cross-react
with cardiac myosin, leading to rheumatic fever.
B. Alteration of Normal Proteins
Drugs can bind to normal proteins and make them immunogenic. Procainamide induced
systemic lupus erythematosus is an example of this mechanism.
C. Release of Sequestered Antigens
Certain tissues (e.g., sperm, central nervous system, and the lens and uveal tract of the eye)
are sequestered so that their antigens are not exposed to the immune system.

These are known as immunologically privileged sites. When such antigens enter the
circulation accidentally (e.g., after damage), they elicit both humoral and cellular responses,
producing aspermatogenesis, encephalitis, or endophthalmitis, respectively.
Sperm, in particular, must be in a sequestered, immunologically privileged site, because they
develop after immunologic maturity has been reached and yet are normally not subject to
immune attack.
Intracellular antigens, such as DNA, histones, and mitochondrial enzymes, are normally
sequestered from the immune system. However, bacterial or viral infection may damage cells
and cause the release of these sequestered antigens, which then elicit an immune response.
Once autoantibodies are formed, subsequent release of sequestered antigens results in the
formation of immune complexes and the symptoms of the autoimmune disease.
In addition to infection, radiation and chemicals can also damage cells and release
sequestered intracellular components. For example, sunlight is known to exacerbate the skin
rash in patients with systemic lupus erythematosus.
It is thought that ultraviolet (UV) radiation damages cells, which releases the normally
sequestered DNA and histones that are the major antigens in this disease.
D. Epitope Spreading
Epitope spreading is the term used to describe the new exposure of sequestered autoantigens
as a result of damage to cells caused by viral infection. These newly exposed autoantigens
stimulate auto reactive T cells, and autoimmune disease results. In an animal model, a
multiple sclerosis–like disease was caused by infection with an encephalomyelitis virus. Note
that the self-reactive T cells were directed against cellular antigens rather than the antigens
of the virus.
E. Failure of Regulatory T Cells
Regulatory T cells (TR) suppress the pro inflammatory effects of other T cells. TR cells are
characterized as CD4 positive, CD25 positive, and FoxP3 positive. An important function of
TR cells is to produce IL-10, which inhibits pro inflammatory Th-1 cells. Patients with a
mutation in the FoxP3 gene have an increase in autoimmune diseases, such as systemic lupus
erythematosus, because they have lost the function of their regulatory T cells.
Q-15. Enumerate the features of T-lymphocytes, their types and functions.
ANS:
Features of T cells:
1. T cells constitute 65% to 80% of the recirculating pool of small lymphocytes.
2. Within lymph nodes, they are located in the inner, subcortical region, not in the
germinal centers.
3. The life span of T cells is long: months or years.
4. They can be stimulated to divide when exposed to certain mitogens
5. Most human T cells have receptors for sheep erythrocytes on their surface and can
form “rosettes” with them for differentiation.
6. Types of T cells are present following effector functions.
CD-4

1. TH-1 Cells functions is to activate macrophages to kill intracellular microbes

2. TH-2 Cells functions is to stimulate development of TH-2 cells, enhances calls
switching to IgE
3. Th-17 Cells function is to recruits neutrophils to site of infection. Protect against
spread bacteria infections
CD-8
They mediate cytotoxic response destroy virus infected cells tumor cells and has role
in graft rejection.
Regulatory functions of T cells are the following:
1. Antibody production
2. Cell mediated immunity
3. Suppression of certain immune responses
Q-16. Give four differences between T-lymphocytes and B-lymphocytes
ANS:
Q-17. How does a primary immune response differ from secondary immune response in terms
of prior sensitization, onset, magnitude, duration and type of antibody?
ANS:
Features Primary immune Response Secondary immune Response

prior sensitization No prior sensitization Prior sensitization
onset Delayed Rapid
magnitude Lesser Greater
duration Small Large
type of antibody IgM IgG

Q-18. A one-year-old male boy remained alright for the first 6 – 9 months after birth. He then
started having recurrent bacterial infections causing otitis media and pneumonia.
a) Which immune cells are likely to be deficient in him?
b) How will you classify primary immunodeficiency disorders?
ANS:
a) B cells and the disease is X-linked Agammaglobinulinemia (Bruton Disease)
b) Classification:
A. B- Cell Deficiency
1. X-linked Agammaglobinulinemia (Bruton Disease)
2. Selective immunoglobulin deficiency
B. T- Cell Deficiency
1. Thymic Aplasia (Di-Georges Syndrome)
2. Chronic Muco-cutaneous Candidiasis
3. Hyper-IgM syndrome
4. Interleukin – 12 Receptor Deficiency
C. Combined B & T Deficiency
1. Severe Combined Immunodeficiency disease (SCID)
2. Wiskott – Aldrich Syndrome
3. Ataxia Telangiectasia
D. Complement
1. Hereditary angioedema
2. Recurrent infections
3. Autoimmune disease
E. Phagocytes
1. Chronic Granulatmous disease
2. Chediak Higashi Syndrome
Q-19. Name complement proteins. Give a sketch of different pathways of complement

activation.
ANS:
1. C3b -- Opsonin
2. C5a -- Chemotactic
3. C3a & C5a – Anaphylatoxin
4. C5 – C9 – Membrane attack complex


Clinical Bacteriology 46
Q-1.
a) Enumerate the organisms causing food poisoning?
b) How they cause symptoms
c) How will you diagnose a case of food poisoning?
ANS:
a) ORGANISMS CAUSING FOOD POISONING
1. Staphylococcus Aureus
2. Bacillus Cereus
3. Clostridium species
4. E.Coli
5. Salmonellae
b) PATHOGENESIS:
The pathogenesis of diarrhea in food poisoning is classified broadly into either non-
inflammatory or inflammatory types.
i) Non-inflammatory diarrhea is caused by the action of enterotoxins on the secretory

mechanisms of the mucosa of the small intestine, without invasion.
This leads to large volume watery stools in the absence of blood, pus, or severe abdominal
pain. Occasionally, profound dehydration may result.
The enterotoxins may be either preformed before ingestion or produced in the gut after
ingestion.
ii) Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to
invasion and destruction. The colon or the distal small bowel commonly is involved.
The diarrhea usually is bloody; mucoid and leukocytes are present.
Patients are usually febrile and may appear toxic. Dehydration is less likely than with non-
inflammatory diarrhea because of smaller stool volumes
c) LABORATORY DIAGNOSE
1. CBC with differential
2. Serum electrolyte assessment
3. BUN and creatinine levels
4. Stool Gram staining and Loeffler methylene blue staining for WBCs: To help
differentiate invasive disease from noninvasive disease
5. Microscopic examination of the stool: To detect any ova and parasites
6. Bacterial culture and sensitivity for enteric pathogens (eg, Salmonella, Shigella,
Campylobacter organisms): Mandatory when a stool sample shows positive results for
WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days
7. Blood culture in febrile patients
8. C difficile assay: To help rule out antibiotic-associated diarrhea in patients receiving
antibiotics or in those with a history of recent antibiotic use
Q-2.
a) Give a brief description of the pathogenic determinants of Neisseria meningitides
b) How will you diagnose meningococcal meningitis in the laboratory?
ANS:
a) PATHOGENIC DETERMINANTS OF NEISSERIA MENINGITIDES (MENINGOCOCCI)

Meningococci have three important virulence factors:

1. A polysaccharide capsule that enables the organism to resist phagocytosis by
polymorphonuclear leukocytes (PMNs).
2. Endotoxin, which causes fever, shock and other patho-physiological changes (in purified
form, endotoxin can reproduce many of the clinical manifestations of meningococcemia).
3. An immunoglobulin (IgA) protease that helps the bacteria attach to the membranes of the
upper respiratory tract by cleaving secretory IgA.
b) LABORATORY DIAGNOSIS
1. smears and culture of the blood and spinal fluid samples.
2. A presumptive diagnosis of the meningococcal meningitis can be made if gram-
negative cocci are seen in the smear of spinal fluid.
3. The organism grows best on chocolate agar.
4. Identification of Neisseria can be made if oxidase-positive colonies of gram-negative
diplococcic are found.
5. The differentiation between N.Meningitidis and N.Gonorrhoeae is made on the basis
of sugar fermentation: Meningococci ferment maltose, whereas gonococci do not
(both organisms ferment glucose).
6. Immunofluorescence can also be used to identify these species.
7. However, a procedure that can assist in the rapid diagnosis of meningococcal
meningitis is the latex agglutination test, which detects capsular polysaccharide in the
spinal fluid.
i) Quelling Reaction
ii) Latex Agglutination
Q-3.
a) Enumerate the important features of pathogenesis by Strep. Pyogenes (Group A
Streptococci)
b) what is the criteria of classification of Streptococci? Name the species of Streptococci in
each group
ANS:
a) PATHOGENESIS BY STREP. PYOGENES (GROUP A STREPTOCOCCI)
Group A streptococci produce three important inflammations- related enzymes:
1. Hyaluronidase degrades hyaluronic acid, which is the ground substance of the
subcutaneous tissue. Hyaluronidase is known as spreading factor because it facilitates
the rapid spread of S. Pyogenes in skin infections (Cellulitis).
2. Streptokinase (Fibrinolysin) activates plasminogen to form plasmin, which dissolves
fibrin clots, thrombi, and emboli. It can be used to lyse thrombi in the coronary arteries
of the heart attack patients.
3. DNAse (Streptodornase) degrades DNA in exudates or necrotic tissue. Antibody to
DNAse B develops during pyoderma; this can be used for diagnostic purposes.
Streptokinase- Streptodornase mixtures applied as a skin test gives a positive reaction
in most adults, indicating normal cell-mediated immunity.
1. Erythrogenic toxin - scarlet fever

2. Streptolysin O - B hemolysis (ASO titers)
3. Streptolysin S - B hemolysis (ASO titers)
4. Pyogenic Exotoxin A - TSST
5. Exotoxin B - Necrotizing fasciitis

6. (M Protien) - Acute Rh. Fever – Glomerulonephritis

Lesion caused by these bacteria may be
1. Pyogenic
i) Local—pharyngitis
ii) Disseminated—sepsis
2. Toxigenic—scarlet fever, toxic shock
3. Immune mediated—rheumatic fever, acute glomerulonephritis
b) CRITERIA OF CLASSIFICATION OF STREPTOCOCCI
 On the basis of hemolysis:
1. β hemolytic
i) S. pyogenes
ii) S. Agalactiae
2. α hemolytic
i) S. pneumonae
ii) S. Viridans
3. α or non-hemolytic
i) E. Faecalis
ii) S. bovis
 Lansfeild classification
1. Group A
i) S. Pyogenes
2. Group B
i) S. Agalactiae
3. Group D
i) E. Faecalis
ii) S. bovis
Q-4. Classification of Streptococci on the basis of hemolysis
ANS:
CLASSIFICATION IS ON THE BASIS OF HEMOLYSIS:
1. β hemolytic
i) S. pyogenes
ii) S. Agalactiae
2. α hemolytic
i) S. pneumonae
ii) S. Viridans
3. α or non-hemolytic
i) E. Faecalis
ii) S. bovis
Q-5.
a) How would you classify Mycobacteria?
b) Briefly discuss lab diagnosis of pulmonary tuberculosis
ANS:
a) CLASSIFICATION OF MYCOBACTERIA
A. Typical
1. M. Tuberculosis

2. M, Bovis
3. M.Leprae
B. Atypical
i) Group 1 (photochromogenes)
1. M.kansasi
2. M.Marinum
ii) Group 2(Schotochromogenes)
M.scrofulceam
iii) Group 3 (non-chromogens)
M.Avuimintracilluar
iv) Group 4(rapidly growing)
M.fortiutumchelonai complex
b) LAB DIAGNOSIS OF PULMONARY TUBERCULOSIS
1. Treat sputum sample with NAOH human cells mucus and other bacteria.
2. Acid fast staining of sputum/ziehl Nelson /Flouresence microscopy
3. Culture on Lowenstein Jensen agar 8 weeks,
4. Production of CO2 in 2 weeks in liquid BACTEC medium
5. T.B produces niacin and catalase.
6. Nucleic acid amplification test
7. PPD skin test (tuberculin) false positive in BCG vaccinated individual
8. IGRA (interferon Gamma Release assay )
9. Lung biopsy from apex lung showing caseous necrosis invade granuloma
Q-6.
a) Enlist the pyogenic bacteria?
b) Name the laboratory tests used for the isolation of Staph. Aureus?
ANS:
a) PYOGENIC BACTERIA
1. S.pyogenes
2. S,Agalactiae
3. E.Faecalis
4. S. Bovis
5. S.Pneumoniae(encapsulated pyogenes)
6. Viridans
7. S. Aureus
8. S.Epidermidis
9. S,Saprophyticus
b) LABORATORY TESTS USED FOR THE ISOLATION OF STAPH. AUREUS
1. Smears from staphylococcal lesions reveal gram positive cocci in grape like clusters.
2. Cultures of S. Aureus typically yield golden yellow colonies that are usually B-hemolytic.
3. S. Aureus is coagulase positive Mannitol salt agar is a commonly used screening device
for S. aureus . Cultures of coagulase negative staphylococci typically yields white
colonies that are non hemolytic.
4. The two coagulase negative staphylococci are distinguished by their reaction to the
antibiotic novobiocin. s.epidermidis is sensitive whereas S. saprophyticus is resistant.
5. Laboratory findings that support a diagnosis of toxic shock syndrome include the
isolation of a TSST producing strain of S. Aureus and development of antibodies to the
toxin during convalescence, although the latter is not useful for diagnosis during the
acute disease.

Staphylococcus
Coagulase
Positive Negative
Staphylococcus Novobiocin
Aureus
Sensitive Resistant
Staphylococcus Staphylococcus
Epidermidis Saprophyticus
Q-7. Name the enzymes and toxins released by Staph aureus?
ANS:
ENZYMES AND TOXINS RELEASED BY STAPH AUREUS
1. Enterotoxin
2. Toxic shock syndrome toxin
3. Ex foliatin
4. Alpha toxin
5. PV leucocidin
Enzymes includes:
1. Coagulase
2. Fibrinolysin
3. Hyaluronidase
4. proteases
5. Nucleases
6. Lipases
Q-8.
a) Name the Clostridium species of medical importance?
b) How will you diagnose a case of tetanus in laboratory?
ANS:
a) CLOSTRIDIUM SPECIES
1. Clostridium tetani
2. Clostridium perfringens
3. Clostridium botulinum
4. Clostridium defficile
b) LABORATORY DIAGNOSE
1. Clostridium Tetani are anaerobic, Spore forming gram positive rods.
2. There is no microbiologic or serologic diagnosis.
3. Organisms are rarely isolated from the wound site.
4. Tetani produces terminal spore (i.e. a spore at the end of the rod).
5. This gives the organism the characteristic appearance of a “tennis racket”.

Q-9. Name the tests used for the diagnosis of secondary Syphilis in the lab?
ANS:
TESTS USED FOR DIAGNOSIS:
1. Venereal disease research laboratory (VDRL) test. The VDRL test checks blood or spinal
fluid.
2. Rapid plasma reagin (RPR) test. The RPR test also finds syphilis antibodies.
3. Rapid immunochromatographic test.
4. Enzyme immunoassay (EIA) test.
5. Fluorescent treponemal antibody absorption (FTA-ABS) test.
6. Treponema pallidum particle agglutination assay (TPPA). This test is not done on spinal
fluid.
7. Darkfield microscopy. This test uses a special microscope to look for the bacteria in a
sample of fluid or tissue from an open sore. This test is used mainly to diagnose syphilis
in an early stage.
8. Microhemagglutination assay (MHA-TP). The MHA-TP is used to confirm a syphilis
infection after another test shows positive results for syphilis.
Q-10. Enumerate the etiological agents of urinary tract infection(UTI)?
ANS:
AGENTS CAUSES UTI
A. Bacterial causes
1. E.coli
2. Klebsiella
3. Proteus
4. Morganella
5. Pseudomonas aeruginosa
6. Achromaobacter
7. Staphylococcus saprophyticus
8. Enterococcus faecalis
9. Enterobacterclocae
B. Viral
1. Adenovirus
2. CMV
C. Fungi
1. Candida albicans
Q-11. Define Rheumatic fever? How will you diagnose this in the lab?
ANS:
Rheumatic fever: Rheumatic fever (RF) is a systemic, post streptococcal (group A β-
hemolytic), non-suppurative inflammatory disease, principally affecting the heart, joints,
central nervous system, skin and subcutaneous tissues.

LAB diagnosis:
A. Major criteria: (JONES)
1. Carditis
2. Polyarthritis
3. Chorea (Sydenham’s chorea)
4. Erythema marginatum
5. Subcutaneous nodules
B. Minor criteria:
1. Fever
2. Arthralgia
3. Previous history of RF
4. Laboratory findings of elevated ESR, raised C-reactive protein, and leukocytosis
5. ECG finding of prolonged PR interval.
C. Laboratory diagnosis:
1. Positive throat culture for group A streptococcus,
2. Titer of Antistreptolysin O and S,
3. Titer of Anti-streptokinase,
4. Titer of Anti-strepto hyaluronidase
5. Titer of anti DNAase B).
Q-12. A 39 year old woman with a history of urinary tract infection comes to the emergency
room with burning urination along with frequency and urgency. She says her urine smells
like ammonia?
a) Name the genus of the organism causing urinary tract infection.
b) Briefly describe the pathogenesis of this organism.
c) Name the two important species of this genus.
ANS:
a) GENUS OF THE ORGANISM
Proteus
b) PATHOGENESIS OF THIS ORGANISM
1. The organisms are present in the human colon as well as in soil and water.
2. Their tendency to cause urinary tract infections is probably due to their presence in the
colon and to colonization of the urethra, especially in women.
3. The vigorous motility of proteus organisms may contribute to their ability to invade the
urinary tract.
4. Production of the enzyme urease is an important feature of the pathogenesis of urinary
tract infections by this group.
5. Urease hydrolyzes the urea in urine to form ammonia, which raises the PH, producing an
alkaline urine.
6. This encourages the formation of stones called struvite composed of magnesium
ammonium phosphate.
7. Stones in the urinary tract obstruct urine flow, damage urinary epithelium, and serve as a
nidus for recurrent infection by trapping bacteria within the stone.
8. Because alkaline urine also favors growth of the organisms and more extensive renal
damage, treatment involves keeping the urine at a low PH.
c) TWO IMPORTANT SPECIES OF THIS GENUS
1. Proteus morganii is now morganellamorganii.
2. proteus rettgeri is now providenciarettgeri

Q-13. How will you classify staphylococci?
ANS:
Staphylococcus
Coagulase
Positive Negative
Staphylococcus Novobiocin
Aureus
Sensitive Resistant
Staphylococcus Staphylococcus
Epidermidis Saprophyticus
Q-14.
a) Name the organisms causing meningitis.
b) Define MRSA? What is the mechanism of resistance by this species of bacteria?
ANS:
a) ORGANISMS CAUSING MENINGITIS.
1. Neisseria meningitides
2. H.influenza
3. St.pmeumonia
4. Treponemapallidum
5. Borreliaburgdorferi
6. Leptospira
7. Chryseobacterium
8. Arenaviruses
9. Enterovirusese
b) MRSA AND ITS MECHANISM OF RESISTANCE:
MRSA stands for Methicillin Resistant S. aureus
1. A defining characteristic of MRSA is its ability to grow in the presence of penicillin-like
antibiotics, which normally prevent bacterial growth by inhibiting synthesis of cell wall
material.
2. This is due to a resistance gene, mecA, which stops β-lactam antibiotics from inactivating
the enzymes (transpeptidases) critical for cell wall synthesis.
3. mecA encodes penicillin-binding protein 2a (PBP2a), which differs from other penicillin-
binding proteins as its active site does not bind methicillin or other β-lactam antibiotics.
4. As such, PBP2a can continue to catalyze the transpeptidation reaction required for
peptidoglycan cross-linking, enabling cell wall synthesis in the presence of antibiotics.
5. As a consequence of the inability of PBP2a to interact with β-lactam moieties, acquisition
of mecA confers resistance to all β-lactam antibiotics in addition to methicillin.

Q-15. How do you classify Streptococci on the basis of Hemolysis and Lancefield groups?
ANS:
On the basis of Hemolysis
Streptococci
Hemolysis
β hemolytic α Hemolytic ϒ Hemolytic

(Complete hemolysis) (Partial hemolysis) (No hemolysis)
Bacitracin Optochin Growth on 6.5% NACL
Sensitive Resistant Sensitive Resistant Growth No Growth
Str. Str. Str. Str. E. Str.

Pyogenes Agalactiae Pneumonae Viridans Faecalis Bovis
Lancefield classification
1. Group A
i) S. Pyogenes
2. Group B (hydrolyse Hippurate)
i) S. Agalactiae
3. Group D (Hydrolyse Esculin in the presence of bile)
i) E. Faecalis (penicillin G resistant)
ii) S. bovis (Penicillin G sensitive)
Q-16. Give a brief account on serological diagnosis of syphilis?
ANS:
SEROLOGICAL DIAGNOSIS OF SYPHILIS:
1. Venereal disease research laboratory (VDRL) test. The VDRL test checks blood or spinal
fluid.
2. Rapid plasma reagin (RPR) test. The RPR test also finds syphilis antibodies.
3. Rapid immunochromatographic test.
4. Enzyme immunoassay (EIA) test.
5. Fluorescent treponemal antibody absorption (FTA-ABS) test.
6. Treponema pallidum particle agglutination assay (TPPA). This test is not done on spinal
fluid.

7. Darkfield microscopy. This test uses a special microscope to look for the bacteria in a
sample of fluid or tissue from an open sore. This test is used mainly to diagnose syphilis
in an early stage.
ANS:
Q-17.
a) Name the causative agent of Diphtheria
b) what are the complications of diphtheria?
c) How will you diagnose diphtheria in the laboratory? (Write only steps and no details A.
Name the causative agent of Diphtheria?
a) CAUSATIVE AGENT OF DIPHTHERIA

Corynebacterium diptheriae
b) COMPLICATIONS OF DIPHTHERIA
There are three prominent complications:
1. Extension of the membranes into the larynx and trachea, causing airway obstruction.
2. Myocarditis accompanied by arrhythmias and circulatory collapse.
3. Nerve weakness or paralysis, especially of the cranial nerves paralysis of the muscles
of the soft palate and pharynx can lead to regurgitation of fluids through the nose.
Peripheral neuritis affecting the muscles of the extremities also occurs.
c) LABORATORY DIAGNOSIS OF DIPHTHERIA:
1. Laboratory diagnosis involves both isolating the organism and demonstrating toxin
production.
2. Smeats of the throat swab should be stained with both Gram stain and methylene
blue.
3. Although the diagnosis of diphtheria cannot be made by examination of the smear,
4. The methylene blue stain is excellent for revealing the typical metachromatic
granules.
5. A throat swab should be cultured on Loefflers medium, a tellurite plate, and a blood
agar plate.
6. The tellurite late contains a telluruim salt that is reduced to elemental tellurium
within the organism.
7. The typical gray black color of tellurium in the colony is telltale diagnostic criterion,
8. If C. diphtheriae is recovered from the cultures, either animal inoculation or an
antibody based gel diffusion precipitin test is perfomed to document toxin production.
9. A PCR assay for the presence of the toxin gene in the organism isolated from the
patient can also be used.
ANS:
Q-18. Gram stained smear of urethral discharge of a 22-year-old sexually active male presented
with acute urethritis, showed gram negative intracellular diplococcic.
a) what is presumptive diagnosis and causative organism?
b) Enumerate the lesions caused by these organisms.
a) PRESUMPTIVE DIAGNOSIS AND CAUSATIVE ORGANISM

Gonorroeae and neisseria gonorroeae
b) LESIONS CAUSED BY THESE ORGANISM
 Gonorrhea in men is characterized primarily by
1. Urethritis accompanied by dysuria and a purulent discharge.
2. Epididymitis can occur.
 In women, infection is located primarily in the endocervix, causing
1. Purulent vaginal discharge

2. intermenstual bleeding(cervivitis).
3. Ascending infection of the uterine tubes (salpingitis, PID), which can result in sterility
or ectopic pregnancy as a result of scarring of the tubes.
 Infection that spreads to the joints and other areas of your body.
 Neonatal—ophthalmia neonatorum
1. Pharyngitis
2. Proctitis
3. Conjunctivitis
4. Arthritis
5. skin sores
Q-19.
a) what is mode of transmission and causative organism of cholera
b) Enumerate steps of pathogenesis of cholera
ANS:
a) MODE OF TRANSMISSION AND CAUSATIVE ORGANISM OF CHOLERA
V. cholera is transmitted by faecal contamination of water and food, primarily from human
sources. And Vibrio cholera.
b) PATHOGENESIS OF CHOLERA
1. The pathogenesis of cholera is dependent on colonization of the small intestine by the
organism and secretion of enterotoxin.
2. For colonization to occur, large numbers of bacteria must be ingested because the
organism is particularly sensitive to stomach acid. Persons with little or no stomach
acid, such as those taking antacids or those who have had gastrectomy, are much
more susceptible.
3. Adherence to the cells of the brush border of the gut,
4. Secretion of the bacterial enzyme mucinase, which dissolves the protective
glycoprotein coating over the intestinal cells.
5. After adhering, the organism multiplies and secretes an enterotoxin called choleragen
(cholera toxin).
6. This exotoxin can reproduce the symptoms of cholera even in the absence of the
Vibrio organisms.
7. choleragen consist of an A (active) subunit and a B (binding) subunit.
8. The B subunit, which is a pentamer composed of five identical proteins, binds to a
ganglioside receptor on the surface of the enterocyte.
9. The A subunit is inserted into the cytosol. Where it catalyzes the addition of ADP-
ribose to the Gs protein (Gs is the stimulatory protein).
10. This locks the Gs protein in the “on” position, which causes the persistent stimulation
of adenylate cyclase. The resulting overproduction of cyclic AMP
11. Cyclic AMP activates cyclic AMP dependent protein kinase, an enzyme that
phosphorylates ion transporter in the cell membrane, and blocks the absorption of
sodium and chloride by the microvilli and promotes the secretion of chloride and
water by the crypt cells.
12. The watery efflux enters the lumen of the gut, resulting in a massive watery diarrhea
that contains neither neutrophils nor red blood cells because the bacteria doesn’t
invade the intestinal mucosa.

13. Morbidity and death are due to dehydration and electrolyte imbalance.
Q-20.
a) Enumerate medically important Streptococci
b) Write down two characteristics of each Streptococcus
ANS:
a) MEDICALLY IMPORTANT STREPTOCOCCI
1. S.Pyogenes
2. S. Agalactiae
3. E. Faecalis
4. S.Bovis
5. S.Pneumoniae
6. Viridans Group
b) TWO CHARACTERISTICS OF EACH STREPTOCOCCUS
1. S.Pyogenes—Beta hemolytic and Bacitracin Sensitive
2. S. Agalactiae—Beta hemolytic and Bacitracin Resistant, hydrolyse hippurate
3. E. Faecalis—gamma hemolytic No growth on 6.5% NacL
4. S.Bovis—gamma Hemolytic and Growth on 6.5% NacL
5. S.Pneumoniae—alpha hemolytic, optochin sensitive and bile soluble
6. Viridans Group—alpha hemolytic optochin resistant and bile non soluble
Q-21.
a) Name different sexually transmitted infections causing agents?
b) How will you diagnose case of gonorrhea in male in the laboratory?
ANS:
a) SEXUALLY TRANSMITTED INFECTIONS CAUSING AGENTS
1. Trephonema Pallidum  syphilis
2. Neisseria Gonorrhoea Gonorrhoea
3. Chlamydia trachomatis  urethritis
4. HIV AIDS
5. HPV genital warts
6. HBV  Hepatitis
b) LABORATORY DIAGNOSE OF GONORRHEA
1. Specimens from mucosal sites, such as the urethra are cultured on Thayer Martin
medium.
2. Which is a chocolate agar containing antibiotics (vancomycin, Colistin, trimethoprim, and
nystatin) to suppress the normal flora.
3. The finding of an oxidase positive colony composed of gram negative diplococci is
sufficient to identify the isolate as a member of the genus Neisseria.
4. Specific identification of the gonococcus can be made either by its fermentation of glucose
(but not maltose or by fluorescent antibody staining).
5. Note that specimens from sterile sites, such as blood or joint fluid, can be cultured on
chocolate agar without antibiotics because there is no competing normal flora.

Q-22. A young boy presented with continuous fever for the last 5 days. The TLC count is
4800/cmm Blood culture showed growth of NLF with TSI revealing alkaline slant, Acidic
butt and H2S on interface.
a) What is your diagnosis?
b) Name the laboratory investigation for this disease?
c) Enumerate complications of the disease?
ANS:
a) TYPHOID FEVER
b) LAB INVESTIGATION:
1. In enterocolitis, the organism is most easily isolated from a stool sample.
2. In the enteric fevers, a blood culture is the procedure most likely to reveal the
organism during the first 2 weeks of illness.
3. Bone marrow cultures are often positive.
4. Stool cultures may also be positive especially in chronic carriers in whom the
organism is secreted in the bile into the intestinal tract.
5. Salmonellae form non lactose fermenting colonies on MacConkeys or EMB agar.
6. On TSI agar, an alkaline slant and an acid butt, frequently with both gas and H2S
(black color in the butt), are produced.
7. S. typhi is the major exception; it does not form gas and produces only a small amount
of H2S.
8. If the organism is urease negative (proteus organisms, which can produce a similar
reaction on TSI agar, are urease positive),
9. the Salmonella isolate can be identified and grouped by the slide agglutination test
into serogroup A, B, C, D or E based on its O antigen.
10. Definitive serotyping of the O, H, And Vi antigens is performed by special public health
laboratories for epidemiologic purposes,
11. Salmonellosis is a notifiable disesase, and an investigation to determine its sourve
should be under taken. Im certain cases of enteric fever and sepsis, when the
organism is difficult to recover, the diagnosis can be made serologically by detecting a
rise in antibody titre in the patient serum (widal test).
c) COMPLICATIONS:
1. Entero-colitis
2. Typhoid fever
3. Septicaemia and Osteomylitis, pneumonia, meningitis
4. Intestinal perforation
Q-23. A male child presents with fever and joint pains. On examination, he had cardiac murmur.
His lab reports show raised serum ASO titers. He had the history of sore throat about two
weeks back.
a) What is the clinical condition and causative agent?
b) What is the pathogenesis of the above condition?
c) Enlist the other six conditions caused by these bacteria
ANS:
a) CLINICAL CONDITION AND CAUSATIVE AGENT
Rheumatic fever caused by Streptococcus pyogenes.
b) PATHOGENESIS OF THE ABOVE CONDITION

1. A susceptible host, on being encountered with group A Streptococcus infection, usually

pharyngitis, mounts an autoimmune reaction by formation of autoantibodies against
bacteria.
2. Streptococcal epitopes present on the bacterial cell wall, cell membrane and the
streptococcal M protein, are immunologically identical to human molecules on myosin,
keratin, actin, laminin, vimentin and N-acetylglucosamine.
3. The autoantibodies cause damage to human tissues due to cross-reactivity between
epitopes in the components of bacteria and the host. Injury is caused by
 Type II antibody-mediated hypersensitivity reaction
 activation of complement and Fc receptor
 CD4+ T cytokine-mediated inflammatory responses.
4. Molecular mimicry and cross-reactivity between streptococcal M protein in particular and
the human molecules forms the basis of autoimmune damage to human target tissues in
RHD cardiac muscle and valves
c) SIX CONDITIONS CAUSED BY THESE BACTERIA

1. Toxic shock syndrome
2. Scarlet fever
3. Pharyngitis,
4. Impetigo,
5. Cellulitis
6. Sepsis
7. Acute glomerulonephritis
ANS:
Q-24.
a) Enumerate the bacterial causes of diarrhea.
b) Briefly describe the lab diagnosis of Salmonella Typhi.
c) Name the preventive measures for this disease.
a) BACTERIAL CAUSES OF DIARRHEA

1. E.coli
2. Salmonella Typhi
3. Shigella
4. Vibrio cholera
5. Campylobacter
6. Bacillus cereus
b) LAB DIAGNOSIS OF SALMONELLA TYPHI
1. In enterocolitis, the organism is most easily isolated from a stool sample.
2. In the enteric fevers, a blood culture is the procedure most likely to reveal the
organism during the first 2 weeks of illness.
3. Bone marrow cultures are often positive.
4. Stool cultures may also be positive especially in chronic carriers in whom the
organism is secreted in the bile into the intestinal tract.
5. Salmonellae form non lactose fermenting colonies on MacConkeys or EMB agar.
6. On TSI agar, an alkaline slant and an acid butt, frequently with both gas and H2S
(black color in the butt), are produced.
7. S. typhi is the major exception; it does not form gas and produces only a small amount
of H2S.
8. If the organism is urease negative (proteus organisms, which can produce a similar
reaction on TSI agar, are urease positive),

9. the Salmonella isolate can be identified and grouped by the slide agglutination test
into serogroup A, B, C, D or E based on its O antigen.
10. Definitive serotyping of the O, H, And Vi antigens is performed by special public health
laboratories for epidemiologic purposes,
11. Salmonellosis is a notifiable disesase, and an investigation to determine its sourve
should be under taken. Im certain cases of enteric fever and sepsis, when the
organism is difficult to recover, the diagnosis can be made serologically by detecting a
rise in antibody titre in the patient serum (widal test).
c) PREVENTIVE MEASURES FOR THIS DISEASE
1. Salmonella infections are prevented mainly by public health and personal hygiene
measures.
2. Proper sewage treatment, a chlorinated water supply that is monitored for
contamination by coliform bacteria, cultures of stool samples from food handlers to
detect carriers,
3. handwashing prior to food handling, pasteurization of milk, and proper cooking of
poultry , eggs and meat are all important .
4. Two vaccines are available, but they confer limited (50%-80%) protection against S.
typhi. One contains the Vi capsular polysaccharide of S. typhi (given intramuscularly),
the other contains a live, attenuated strain of S.typhi (given orally).
5. The two vaccines are equally effective. The vaccine is recommended for those who
will travel or reside in high risk areas and for those whose occupation brings them in
contact with the organism.
6. A new conjugate vaccine against typhoid fever containing the capsular polysaccharide
(Vi) antigen coupled to a carrier protein is safe and immunogenic in young children.
Q-25. Gram positive rod with metachromatic granules and “clubs shaped appearance” bacteria
were isolated from patient with a pseudomembranous lesion in throat.
a) What is clinical condition and causative organism?
b) Describe the mechanism of action of the main virulence factor involved in this condition
c) Name other three gram positive rods and the disease caused by them
ANS:
a) DIPHTHERIA
Coryne bacterium diphtherae
b) PATHOGENESIS
Exotoxin produced by this bacteria have two components
1. Binding domain (B domain)
2. Active domain (A domain)
Binding domain mediate binding of toxin to Glycoprotein of cell
Active domain cleave nicotinaminde form NAD and transfer the remaining ADP ribose to
Elongation factor 2 and inhibit protein synthesis
c) OTHER GRAM POSITIVE RODS
1. Bacillus anthrax—causes anthrax
2. Clostridium tateni—causes tetanus
3. Listeria monocytogene—causes meningitis and sepsis

General Bacteriology 61
Q-1. Define Sterilization, disinfection and antiseptics?
ANS:
Sterilization is the killing or removal of all microorganisms, including bacterial spores,
which are highly resistant.
Disinfection in the killing of many, but not all, microorganisms. For adequate disinfection,
pathogens must be killed, but some organisms and bacterial spores may survive.
Antiseptics are chemicals used to kill microorganisms in the surface of skin and mucous
membranes.
Q-2. Enumerate various methods of sterilization.
ANS:
A. Chemical agents
1. Disruption of the lipid containing cell membrane
i) Alcohol
ii) Phenols
iii) Detergents
2. Modification of proteins
i) Chlorine
ii) Iodine
iii) Heavy metals (mercury and silver)
iv) Hydrogen peroxide
v) Formaldehyde and Glutaraldehyde
vi) Ethylene oxide
3. Modification of DNA
i) Crystal violet (gentian violet)
ii) Malachite green
B. Physical agents
1. Heat
i) Moist heat sterilization, usually autoclaving (steam, at a pressure of 15lb/in 2.
Reaches a temperature of 121 degree c and is held at that temperature for 15 to 20
minutes)
ii) Dry heat or incineration (180 for 2 hours)
iii) Pasteurization (62 for 30 minutes followed by rapid cooling or “flash” pasteurization
at 72 for 15 seconds is often used)
2. Radiation
i) Ultraviolet light
ii) X rays
3. Filtration
Q-3. Give physical methods of sterilization with examples.
ANS:
Physical methods of sterilization
1. Heat

i) Moist heat sterilization, usually autoclaving (steam, at a pressure of 15lb/in 2.

Reaches a temperature of 121 degree c and is held at that temperature for 15 to 20
minutes)
ii) Dry heat or incineration (180 for 2 hours)
iii) Pasteurization (62 for 30 minutes followed by rapid cooling or “flash” pasteurization
at 72 for 15 seconds is often used)
2. Radiation
i) Ultraviolet light
ii) X rays
3. Filtration
Q-4. Describe principle of autoclaving? What are uses of autoclave? How you will evaluate
performance of autoclave?
ANS:
Autoclaving steam. At a pressure of 15 lb/in 2. reaches a temperature of 121 and is held at
that temperature for 15 to 20 minutes.
Autoclave uses
Autoclave kills microorganisms. including endospores, it also kills even the highly heat
resistant spores of Clostridium botulinum.
performance of autoclave evaluation:
1. Physical: pressure and temperature recording devices,
2. Chemical: indicators that change colour after being exposed to specific temperatures,
such as
temperature sensitive tape. The colour change upon exposure to the given
temperature,
3. Biological: Bacillus stearothermophilus spores are used, due to its resistance to heat,
for the testing that measures the biological performance of the autoclave process.
Q-5. What is optimal temperature, pressure and time for autoclaving?
ANS:
121 c .15lb/in 2. 15 to 20 minutes.
Q-6. Define vaccine and vaccination. Give the examples of important either through active
immunity or passive immunity?
ANS:
Vaccines are those substances which induce immunization either through active immunity
or passive immunity.
Vaccination:
Vaccination is the administration of antigenic material (a vaccine) to stimulate an individual's
immune system to develop adaptive immunity to a pathogen
Examples:
1. Bacterial capsular polysaccharides.

Streptococcus pneumonia, Neisseria meningitides, Haemophilus influenza. Vaccine for

Typhoid contains the capsular polysaccharide of Salmonella typhi.
2. Toxiods, Coynebacterium diphtheria vaccine contains the toxoid (formaldehyde
treated exotoxin),Clostridium tetani, Bordetella pertussis.
3. Whole bacteria
Killed ( Vibrio cholera vaccine , Rickettsia rickettsiae against typhus )live. Attenuated
(Mycobacterium bovis for TB, live, attenuated S. typhi. The vaccine against tularemia
contains live, attenuated Francisellarularensis).
4. purified proteins isolated from bacteria (B.pertussis acellular vaccine , Bacillus
anthracis vaccine a vaccine against anthrax)
5. Antitoxins (immunoglobulins) Tetanus. Botulinum. Diphtheria
Q-7. Tabulate differences between Exotoxin and Endotoxins?
ANS:
Q-8. Tabulate major differences between gram positive and gram negative cell wall.
ANS:
Gram positive Gram negative
Have thick and multilayer peptidoglycan Have thin single layer peptidoglycan
No outer membrane in between capsule Have outer membrane in between
Have teichoic acid Have no teichoic acid
Have no periplasmic space Have periplasmic space
Have no lipopolysaccharide Have lipopolysaccharide (endotoxin)
Give purple stain on gram staining Give pink stain on gram staining

Q-9. Name any four components of a bacterial cell?
ANS:
Components of bacterial cell wall:
1. Peptidoglycan layer
2. Outer membrane
3. Periplasmic space
4. Techoic acid
5. Capsule
6. Pilus
7. Flagellum
Q-10. What is the importance of Bacterial capsule? Name 3 capsulated microorganisms.
ANS:
The capsule is a well-defined structure of polysaccharide surrounding a bacterial cell and is
external to the cell wall. The one exception to the polysaccharide structure is the poly D
glutamic acid capsule of Bacillus anthraces. The capsule is considered a virulence factor
because it enhances the ability of bacteria to cause disease (e.g. prevents phagocytosis). The
capsule can protect cells from engulfment by eukaryotic cells, such as macrophages.
Q-11. What are the requirements for the growth of organism in the lab?
ANS:
1. Culture medias
i) Blood agar
ii) Chocolate gar
iii) Chocolate factor x and v
2. Temperature
3. Oxygen for aerobic organism growth
4. pH
5. salt concentration and nutrients
Q-12. Draw and label a bacterial growth curve.

Q-13. Enlist the chemicals used in gram staining procedure.
ANS:
1. Crystal violet to stain
2. Iodine used as mordant
3. Acetone to wash out the dye
4. Safranin to stain decolourised gram negative bacteria
Q-25. Define vaccination? Only name four commonly used vaccines.
ANS:
 Vaccination:
Vaccination is the administration of antigenic material (a vaccine) to stimulate an individual's
immune system to develop adaptive immunity to a pathogen
 Commonly used vaccines:
1. Polio vaccine—for Polio
2. Hib—for Hemophilus influenza
3. DTaP – for Diphtheria and pertussis (whooping cough)
4. MMR—for measles Mumps and Rubella
5. BCG—for Tuberculosis
6. Pneumococcal—for pneumonia

Parasitology 66
Q-1.
a) Enumerate the intestinal nematodes
b) Enlist the complications of Ascaris lumbricoides
ANS:
a) INTESTINAL NEMATODES
1. enterobius
2. tricuris
3. ascaris
4. anchylostoma necator
5. strongyloides
6. trichinella
b) COMPLICATIONS
1. The major damage occurs during larval migration
2. The principal sites of tissue reaction are the lungs,
3. inflammation with an eosinophilic exudate occurs in response to larval antigens.
4. adults may contribute to malnutrition, especially in children in developing countries.
5. Ascaris pneumonia with fever, cough, and eosinophilia can occur with a heavy larval
burden.
6. Abdominal pain and even obstruction can result from the presence of adult worms in the
intestine.
Q-2.
a) Which worms are named Hookworms?
b) What are the manifestations of pathogenic (clinical features) of hook worm disease and
laboratory diagnosis?
ANS:
a) HOOKWORMS
1. Ancylostoma duodenale
2. Necator americanus
b) CLINICAL FEATURES AND LABORATORY DIAGNOSIS
1. loss of blood at the site of attachment in the small intestine.
2. Blood is consumed by the worm and oozes from the site in response to an anticoagulant
made by the worm.
3. Weakness and pallor accompany the microcytic anemia
4. These symptoms occur in patients having malnutrition.
5. “Ground itch,” a pruritic papule or vesicle, can occur at the site of entry of the larvae into
the skin.
6. Pneumonia with eosinophilia can be seen during larval migration through the lungs.
Lab Diagnosis
1. microscopically by observing the eggs in the stools
2. Occult blood in the stools is frequent.
3. Eosinophilia is typical
Q-3. Name the parasites causing anemia.

Parasitology 67
1. Ancylostoma duodenale (microsytic anemia)

2. Necator americanus (microsytic anemia)
3. Plasmodium
4. Leishmania
5. babesia
6. diphyllobothrium latum (megaloblastic anemia )
Q-4.
a) Enumerate intestinal tissue nematodes
b) Give the pathogenesis of Hydatid
ANS:
a) INTESTINAL TISSUE NEMATODES. (NEMATODES)
1. Necator (hookworms)
2. Enterobius (pinworms)
3. Mosquitoborne: Wuchereria and Brugia
4. Ascaris and Ancylostoma
5. Trichuris,Trichinella, and Toxocara
6. Onchocerca (river blindness)
7. Dracunculus
8. Eye worm (Loa loa)
9. Strongyloides (threadworm)
b) PATHOGENESIS OF HYDATID CYST.
1. Cestode Echinococcus granulosus (dog tapeworm) eggs in food contaminated with dog
feces ingested by humans and hatch hexacanth larvae in the gut
2. migrate in the blood to various organs, especially the liver and brain.
3. Larvae form large, unilocular hydatid cysts containing many protoscoleces and daughter
cysts
4. hydatid cyst a space-occupying lesion. Also, if cyst ruptures, antigens in fluid can cause
anaphylaxis.
Q-5.
a) Enumerate the various forms of Leishmaniasis
b) What is the etiology and pathogenesis of visceral Leishmaniasis
ANS:
a) FORMS OF LEISHMANIASIS.
1. Leishmania donovani kala azar, visceral leishmaniasis
2. Leishmania tropica, cutaneous leishmaniasis
3. Leishmania mexicana, cutaneous leishmaniasis
4. Leishmania braziliensis mucocutaneous leishmaniasis
b) PATHOGENESIS OF VISCERAL LEISHMANIASIS?
1. Blood and tissue protozoan Leishmania donovani
2. Transmitted by sandflies (Phlebotomus or Lutzomyia).
3. Animal reservoir chiefly dogs, small carnivores, and rodents
4. When female sand-fly bites a human, promastigotes enter blood macrophages and form
amastigotes.
5. Amastigotes kill reticuloendothelial cells, especially in liver, spleen (splenomegaly), and
bone marrow and lead to anemia leukopenia and thrombocytopenia (bleeding)

Parasitology 68
Q-6.
a) Enumerate the hemoparasites
b) How plasmodium falciparum causes malignant tertian malaria and give its complications
c) Its vector and incubation period
d) How malaria is routinely diagnosed in the laboratory?
ANS:
a) HEMOPARASITES.
1. Plasmodium
2. Toxoplasma
3. Pneumocystis
4. Trypanosome
5. Leishmania
b) COMPLICATION
1. Because it recurs every third day and more severe than the other malarial spices
2. Complications are
3. Abrupt onset of fever 41 degree C and chills headache myalgia arthralgia
4. Nausea vomiting and abdominal pain patient feel well between febrile episodes
5. Splenomegaly hepatomegaly and anemia is common
6. Untreated falciparum malaria cause brain (cerebral malaria) and kidney damage ( black
water fever)
c) ITS VECTOR AND INCUBATION PERIOD
 female anopheles mosquito and 2 weeks
d) DIAGNOSIS:
1. thick blood smear for presence of organism and thin smear for specie identification
2. ring shape trophozoits are seen in rbc
3. gametocyte of p. falciparum are crecent shape (banana shape) other are spherical shape
4. PCRand ELISA

3rd Year Pathology

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3rd Year Pathology

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GENERAL

SALMAN KHAN | REHMAN MEDICAL COLLEGE

CELL INJURY, CELL DEATH, AND ADAPTATIONS 2

HEMODYNAMIC DISORDERS, THROMBOEMBOLISM, AND SHOCK 12

INFLAMMATION AND REPAIR 19

DISEASE OF IMMUNE SYSTEM 36

Q-1. Questions regarding necrosis.

KMU Past Papers Solved SEQs

f) MORPHOLOGY OF EACH TYPE OF NECROSIS.

KMU Past Papers Solved SEQs

Q-2. Questions regarding cell injury

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

3) An additional factor enhancing TG synthesis in alcohol excess is increased

a) FEATURES OF NECROSIS AND APOPTOSIS:

KMU Past Papers Solved SEQs

The Mitochondrial (Intrinsic) Pathway of Apoptosis

Extrinsic (cell death receptor initiated) pathway:

KMU Past Papers Solved SEQs

f) MORPHOLOGIC FEATURES OF APOPTOTIC CELL

KMU Past Papers Solved SEQs

2. Nuclear chromatin is condensed under the nuclear membrane i.e. pyknosis,

b) DIFFERENCES BETWEEN METASTATIC AND DYSTROPHIC CALCIFICATION.

c) CAUSES OF METASTATIC CALCIFICATION.

1. Increased secretion of parathyroid hormone, due to either primary parathyroid tumors or

Q-7. What are pigments? classify it and give examples.

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

6. Counter regulatory mechanisms, such as release of t-PA (tissue plasminogen activator,

B. Reduced Plasma Osmotic Pressure (Hypoproteinemia)

KMU Past Papers Solved SEQs

c) PATHOGENESIS OF CARDIAC EDEMA

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

KMU Past Papers Solved SEQs

Q-1. Define inflammation

Q-3. Tabulate differences between the two types of inflammation.

Acute inflammation Chronic inflammation

Rapid onset short duration Prolong duration

Q-4. Enumerate the causes of chronic inflammation

KMU Past Papers Solved SEQs

4. Mild forms of chronic inflammation in neurodegenerative disorders such as Alzheimer

Q-5. Enlist the causes of acute inflammation

Q-6. Enumerate different causes of inflammation giving an example in each case

Q-7. Name the localized cardinal signs of acute inflammation

Q-8. Name the systemic signs of acute inflammation

KMU Past Papers Solved SEQs

Q-9. Name the sequels of acute inflammation

Q-10. Enumerate types of acute inflammation on the basis of morphology of exudate.

Q-11. Enumerate the cell derived mediators of inflammation

KMU Past Papers Solved SEQs

Q-12. What is the role of macrophages in chronic inflammation?

KMU Past Papers Solved SEQs

4. Leprosy. (non caseating granulomas)

Q-14. Draw and label tuberculous granuloma.

Q-15. List causes of chronic granulomatous inflammation.

KMU Past Papers Solved SEQs

1. A Ghon focus is a primary lesion usually subpleural, caused by mycobacterium bacilli

Q-18. Tabulate differences between exudate and transudate

KMU Past Papers Solved SEQs