general pathology topic

2.  Most forms of disease state begin with cell injury
and consequently loss of cellular function.
 Cell injury is defined as- a variety of stresses a cell
encounters as a result of changes in its internal and
external environment.
 The cellular response to injury varies and
depends upon
 Type of cell and tissue invovled
 Extent of injury
 Type of injury

3.  Cell ProliferationCells are classified according to
their proliferative potentialinto
 a. Labile cells
 .b. Stable cells.
 c. Permanent cells.

4.  Labile cells:-
 These are continuously dividing cells which
pass directly from M to G1 phase of the cell
cycle.
 They are of short life span.-Examples are
epidermis of the skin, surface epithelium of
gastro-intestinal and genito-urinary system and
hemopoietic cells of the bone marrow.

5.  Stable cells: -
 Normally, these cells undergo few postnatal divisions
but are capable of division when activated or after
injury ( pass from Go to G1).
 They include hepatocytes, renal tubular cells,
glandular cells, and mesenchymal cells e.g smooth
muscle, osteoblasts, cartilage cells, endothelium and
connective tissue cells.
 Injury of these cells is followed by complete
regeneration if the supporting framework is
preserved.

6.  Permanent cells:
 These cells have left the cell cycle and CANNOT
undergo mitotic division in postnatal life.
 Permanent cells are found in the central nervous
system and heart.
 Once they are destroyed, they cannot regenerate.

8.  The cells which have the capacity to multiply
through out their life:
 A. Stable cells B.Permanent cells
 C.Labile cells D.None of the above
 Ans. ‘C’ [Ref. Harshmohan 3rd Ed Pg 135]

9.  In a 50-year-old woman found to be positive for hepatitis A
antibody, the serum aspartate aminotransferase (AST) level
was 275U/L and that of alanine aminotransferase (ALT) was
310U/L. A month later, these enzyme levels have returned to
normal. At the end of the month after infection, in which part
of the cell cycle are most of the hepatocytes going to be?
 a. G0 b. G1 c. S D. G2 e. M
 Ans. A
 Hepatocytes are quiescent (stable) cells that can re-enter the cell
cycle and proliferate in response to hepatic injury. The liver can
partially regenerate itself. Acute hepatitis results in hepatocyte
necrosi, marked by AST and ALT elevations.

10. 1. Cellular Adaptation- the cell may adapt to the
change and revert back to normal after the stress
removal
2. Sub Cellular changes- the residual effects may
persist in the cell as evidence of injury.
3. Intracellular accumulations- metabolites may
accumulate within the cell.
4. Reversible cell injury- injury may recover
5. Irriversible cell injury- the cell dies.

11.  Genetic cause
 Acquired causes

12.  Based on underlying agent:
 Hypoxia and ischaemia
 Physical agents
 Chemical agents and drugs
 Microbial agents
 Immunologic agents
 Nutritional derangement
 Psychological factors

13.  Deficiency of oxygen or hypoxia results in
failure to carry out cellular activities.
 Most common, causes of hypoxia are:
Reduced supply of blood to cells- ischaemia
Oxygen deprivation can result from other causes like-
anaemia, carbon monoxide poisoning,
cardiorespiration insufficiency and increase in
demand of tissues

14.  Mechanical trauma
 Thermal trauma
 Electricity
 Radiation rapid changes in atmospheric pressure

15.  Chemical poisons: cyanide, arsenic,mercury.
 Strong acid and alkalis
 Insecticides and pesticides
 High oxygen concentration
 Hypertonic glucose and salt
 Alcohol and narcotic drugs
 Theraputic drugs

16.  Infection caused by
 Bacteria
 Rickettsiae
 Viruses
 Fungi
 Protozoa
 Metazoa
 Parasites

17.  Immunity is a double edged sword :
Hypersensitivity reactions
Anaphylatic reactions
Autoimmune diseases

18.  Nutritional deficiency diseases :
deficiency of nutrients ( eg. Starvation), of protein
calorie ( eg. Marasmus, kwashiorkor)
Of minerals ( eg. Anaemia)
 Nutritional excess
Obesity
Atterosclerosis
Heart disease
Hypertension

19.  Mental stress
 Strain
 Anxiety
 Overwork
 Frustration

21. Reversible cell injury
Irreversible cell injury

22. HYPOXIA/ISCHAEMIA
↓ ATP
↓ Intercellular pH
(cytosol)
Damaged sodium
pump
(membrane)
↓ Protein
synthesis (RER)
Ultrastructural/Functional Changes
REVERSIBLE CELL INJURY

24.  2 essential features:
Inability of the cell to reverse mitochondrial
dysfunction
Disturbance in cell membrane function
 In addition: depletion of proteins, leakage of
lysosomal enzymes into cytoplasm, reduced
intracellular pH and further reduction in ATP.

25.  Continued hypoxia leads to influx of large amount of
Calcium ions.
 Normal Ca ions – in ECF 10-3 M (millimoles)
Cytosole 10-7 M
 Leads to mitochondrial dysfunction
 Morphological mitochondrial changes:
 Vacuoles in mitochondria
 Deposition of amorphous Ca in mitochondrial matrix.

27.  The first step inhibited due to hypoxic injury is:
 a. Oxidative phosphorylation
 b. Glycogenesis
 c. Detachment of ribosomes from RER
 d. Cell shrinkage
 Ans. A The first point of attack of hypoxia id the cells
aerobic respiration, i.e. oxidative phosphorylation by
mitochondria ATP production is decreased → Na-K Pump
stops → more Na inside → cell becomes hyperosmolar →
water enters → swelling of cell → bleb formation → along
with this ribosomes also detach. This process is reversible if
O2 is supplied.

28.  Membranes in general and plasma membrane
 Mechanism:
Accelerated degradation of membrane phospholipids.
Cytoskeletal damage
Toxic oxygen radicals
Hydrolytic enzymes
Serum estimation of liberated intracellular enzymes

30. MEMBRANE DAMAGE
Nuclear changes
(Pyknosis, Karyolysis,
Karyorrhexis)
Cell Death
(myelin figures)
Serum enzyme
estimation ( SGOT,
LDH)
Libration of intacellular enzymes

33. See Ch. 1, p. 9,
Fig. 1-9

35.  The characteristic feature of hypoxic irreversible injury
is/are:
 a. Vacuolization of mitochondria
 b. Swelling of lysosomes
 c. Calcium densities
 d. All of the above
 Ans. D

36.  Cellular swelling and fatty change are example of:
 a. Reversible injury
 b. Irreversible injury
 c. Cellular swelling is reversible but fatty change is
irreversible
 d. None of the above
 Ans. A Fatty change is an indicator of reversible cell injury,
manifested by appearance of small or large lipid vacuoles in
cytoplasm and occurs with hypoxia. Basically seen in cells
involved in fat metabolism as in liver.


37.  Ischaemic reperfusion injury
 Radiolysis of water
 Chemical toxicity
 Hyperoxia (toxicity due to oxygen therapy)
 Cellular aging
 Killing of exogenous biologic agents
 Inflammatory damage
 Destruction of tumor cells
 Chemical carcinogenesis
 Atherosclerosis

39.  Generation of oxygen radicals begins within
mitochondrial inner membrane.
 When cytochrome oxidase catalyses of oxygen
(O2 ) to water (H2O)
 Intermediates between O2 and H2O are:
Superoxide oxygen O’2 : 1 electrone
Hydrogen peroxide H2O2 : 2 electrones
Hydroxyl radical OH- : 3 electrones

41. IONISING RADIATION
H2O
Radiolysis
OH-
Proliferating, cells
(eg. Epithelial cells)
Non-Proliferating cells
Eg. neuron
DNA Damage Lipid peroxidation
Inhibition of
DNA
replication
Cell
membrane
damage
Apoptosis Necrosis
CELL DEATH
Mechanisms
of cell injury
by ionising
radiation

42.  The histopathological manifestation of oxygen toxicity is
due to:
 a. Oxygenation of nucleic acid
 b. Oxygenation of cell organelles except (a)
 c. Free of oxygen redical
 d. Oxygenation of cell membrane
 Ans. C When patients are subjected to high oxygen
concentrations, the free oxygen radicals which are released
interact with cell organelles and autocatalytic reactions are
initiated resulting in mutation or cell death rather than in
oxygenation

43.  Cell death is a state of irreversible injury
 In living body it may occur as:
Local or focal change (autolysis, necrosis and
apoptosis)
Changes that follow( gangrene and pathologic
calcification)
End of life ( somatic death)

44.  Disintegration of the cell by its own
hydrolytic enzymes liberated from lysosomes
 It is rapid in some tissues rich in hydrolytic
enzymes such as pancreas and gastric mucosa.
 Morphologically , autolysis is identified by :
 Homogeneous and eosinophilic cytoplasm
 Loss of cellular details
 Remains of cell as debris

45.  Defined as- focal death along
with degradation of tissue by
hydrolytic enzymes librated by
cells, accompanied by
inflammation.
 2 essential features:
 Cell digestion by lytic
enzymes
 Denaturation of proteins

46. Morphologic changes in necrosis:
 Cytoplasmic
 Homogenous and intensely eosinophilic
 Occasionally: vacuolation or dystrophic calcification
 Nuclear
 Pyknosis- condensation of nuclear chromatin
 Karyolysis – undergo dissolution
 Karyorrhexis- fragmentation into many clumps

47.  3) Disappearance of nuclear chromatin is called
as:
 A. Pyknosis
 B. Karyolysis
 C. Karyorhexis
 D. None
 Ans. (A) (Ref: Robbin’s –7th Ed/Pg 29, 30)
 pyknosis, characterized by nuclear shrinkage &
increased basophilia. Here. the DNA apparently
condenses into a solid, shrunken basophilia mass.

48.  The fading of cellular chromatin is
 a. Karyolysis b. Karyorrhexis
 c. Pyknosis d. Cytolysis
 Ans. A [Ref: Robbin’s 7th Ed Pg 29, 30]
 Nuclear changes assume one of the 3 patterns, all due to
the non-specific breakdown of the DNA.
 Karyolysis: the basophilia of the chromatin may fade,
presumably due to the DNAse activity.
 Pyknosis: it is characterized by the nuclear shrinkage
and increased basophilia; the DNA condenses into a solid
shrunken mass.

49.  Pyknosis is characterized by
 a. Nuclear basophilia b. Nuclear Shrinkage
c. Nucleus disintegration d. Nucleolus disintegration
 Ans. B

50.  A glassy homogenous, increased eosinophilia with moth
eaten appearance in a cell is indicated of:
 a. Reversible fatty change b. Reversible hypoxia
 c. Necrosis d. B and C
 Ans. C These are the characteristic features of a necrotic cell
which is coupled with nuclear changes – Pyknosis,
keryolysis, keryohyrrexia.

51.  Karyolysis leads to:
 a. Decreased eosinophilia
 b. Increased eosinophilia
 c. Decreased basophilia
 d. Increased basophilia

 Ans. C
 Due to karyolysis the basophila decreases but a necrotic
cell in initial stages is characterized by increased eosinophilia.
Increase in basophilia is typical of pyknosis

52.  5 types :
 Coagulative necrosis
 Liquefaction (colliquative) necrosis
 Caseous necrosis
 Fat necrosis
 Fibrinoid necrosis

53.  Most common type
 Caused by irreversible focal injury, mostly from
sudden cessation of blood flow (ischaemia)and
less often from bacterial and chemical agents
 Organs affected are: heart, kidney and spleen.

54.  Foci of coagulative necrosis:
 In early stages: pale, firm,
and slightly swollen.
 With progression: become
more yellowish, softer, and
shrunken.

55.  Hallmark of coagulative
necrosis: conversion of normal
cells into their ‘tombstones’ i.e.
outlines of the cells are retained
so that the cell type can still be
recognised but their cytoplasm
and nuclear details are lost.
 Necrosed cells are swollen and
appear more eosinophillic than
normal

56.  Microscopic changes are the result of:
 Denaturation of proteins
 Enzymatic digestion of the cell.
 Eventually, the necrosed focus is infiltrated by
inflammatory cells and
 The dead cells are phagocytosed leaving
granular debris and fragments of cells.

57.  Myocardial infarct is an example of:
 a. Coagulation necrosis b.Liquefactive necrosis
 c. Caseous necrosi
 d. Cell death nut not of necrosis
 Ans. A

58.  Hypoxic death leads to:
 a. Coagulation necrosis b.Liquefactive necrosis
 c. Caseous necrosis
 d. Cell death nut not of necrosis
 Ans. A

59.  Coagulation necrosis is seen in all cells (except in):
 a. Liver b. Heart c. Brain d. Lungs
 Ans. C
 The process of coagulative necrosis is
characteristic of hypoxic death of cells in all
tissues except the brain.


60.  Coagulative necrosis is seen in:
 a. Brain b. Breast c. Liver d. All
 Ans. C

61.  Coagulative necrosis is typically seen with:
 a. Focal bacterial infections
 b. Hypoxic death
 c. Loss of tissue architecture
 d. All of the above

 Ans. B
 Coagulative necrosis is associated with hypoxic death and
maintenance of tissue architecture in all the cells of the body except
in brain where characteristically liquefaction necrosis is seen and
tissue architecture is lost. Caseous necrosis is typically seen in TB
where tissue architecture is partially lost.

62.  It occurs commonly due to ischaemic injury and
bacterial or fungal infections.
 It occurs due to degradation of tissue by the
action of powerful hydrolytic enzymes.
 Common eg. Infarct brain and abscess cavity.

63.  Liquefaction necrosis is commonly seen in
a. Brain b. Lung c. Liver d.
Spleen
 Ans. A

64.  Found in the centre of foci of tuberculous
infection.
 It is a combined feature of coagulative and
liquefactive necrosis.

65.  Foci of caseous necrosis, as the
name implies, resemble dry
cheese and are soft, granular and
yellowish.
 This appearence is partly
attributed to the histotoxic
effects of lipopolysaccharides
present in the capsule of the
tubercle bacilli, Mycobacterium
tuberculosis.

66.  The necrosed foci are
structureless, eosinophilic and
contain granular debris.
 The surrounding tissue shows
characteristic granulomatous
iflammatory reaction
consisting of epitheloid cells
with interspersed giant cells of
langhan’s or foreign body type
and peripherally lymphocytes.

67.  5) Caseation necrosis is suggestive of-
 A. Tuberculosis B. Sarcoidosis
C. Leprosy D. Mid line lethal
granuloma
 Ans. 'A'(Ref: Harsh Mohan, Ed. 2nd Pg-35)

68.  It is a special form of cell death occurring at two
anatomically different locations but
morphologically similar lesions.
 These are:
Following pancreatic necrosis
Traumatic fat necrosis commonly in breast

69.  Fat necrosis in either of the 2 instances results in
hydrolylsis of neutral fat present in adipose
cells into glycerol and free fatty acids.
 The damaged adipose cells assume cloudy
appearance when only free fatty remain
behind , after glycerol leaks out.
 The leaked out free fatty acids, complex with Ca
to form Ca soaps (sponification)

70.  Appears as yellowish-white and firm deposits.
 Ca soap imparts the necrosed foci firmer and
chalky white appearance.

71.  The necrosed fat cell
has a cloudy
appearance
 Surrounded by
inflammatory reaction.
 Formation of calcium
soaps is identified in the
tissue sections as
amorphous, granular
and basophilic material.

72.  It is characterized by the deposition of fibrin-
like material which has the staining properties of
fibrin.
 It is encountered in various examples of
immunologic tissue injury (eg. Autoimmune
diseases, arthus reaction), artioles in
hypertension, peptic ulcer etc.

74.  Identified by brightly
eosinophilic, hyaline-like
deposition in the vessel
wall or on the luminal
surface of a peptic ulcer
 Local haemorrhages may
occur due to rupture of
these blood vessels.

75.  Which of the following is correctly matched
 a. Caseating necrosis – Tuberculosis
 b.Caseation - yellow fever
 c. Fat necrosis – Pancreatitis d. Gumma – infarction
 Ans. A & C

76.  Hypoxic death leads to
 a. Liquef active necrosis b. Coagulative necrosis
 c. Caseous necrosis d. Fat necrosis
 Ans. B

77.  Apoptosis is a form of ‘coordinated and
internally programmed cell death’ which is of
significance in variety of physiologic pathologic
conditions.
 Apoptosis in Greek meaning ‘falling off’ or
‘dropping off’.

78.  Shrinking of cell : with dense cytoplasm and almost
normal organelles.
 Convolution of cell membrane with formation of membrane-
bound near-spherical bodies called apoptotic bodies
containing compacted organelles.
 Chromatin condensation around the periphery of nucleus
 No acute inflammation.
 Phagocytosis of apoptotic bodies by macrophages

79.  Initiators of apoptosis
1. Absence of stimuli eg. Hormone, growth
factors, cytokines.
2. Activators of programmed cell death. Eg.
TNF receptors.
3. Intracellular stimuli eg. Heat, radiation,
hypoxia etc.
 Regulators of apoptosis.eg. bcl-2, p53,
caspases, bax etc.

80.  Progammed cell death.
1. Fas receptor activation- leads to activation of
caspase and subsequent proteolysis.
2. Ceramide generation- hydrolysis of plasma
membrane ceramide is generated which further
leads to mitochondrial injury.
3. DNA damage-
 produced by various agents such as ionising radiation,
chemotherapeutic agents, activated oxygen species lead to
apoptosis
 DNA damage affects nuclear protein p53 which induces the
synthesis of cell death protein bax.

81.  Phagocytosis
 The dead apoptotic cells and their fragments
possess cell surfacereceptors which facilitate
their identification by adjucent phagocytes.

82. Initiators of apoptosis
(transmembrane, intracellar)
Regulators of apoptosis
(bcl-2, others)
Programmed cell death
Fas receptor activation
(cytotoxic T cells)
DNA damage
(radiation,
chemotherapy,
free radicals
Caspases
ceramide
P53
Bax
Mitochondrial injury
DNA damage
APOPTOSIS
PHAGOCYTOSIS
MECHANISM
OF
APOPTOSIS

84. 1. Development of embryo
2. Physiologic involution of cells in hormone-
dependent tissues eg. Endometrial shedding.
3. Normal cell destruction followed by
replacement proliferation eg. Intestinal
epithelium

85. 1. Cell death in tumor
2. Cell death by cytotoxic T cells.
3. Cell death in viral infections
4. Pathologic atrophy of organ and tissues on
withdrawal of stimuli eg. Atrophy of kidney or
salivary glandon obstruction of ureter or ducts
respectively.
5. Cell death in response to injurious agents involved
in causation of necrosis eg. radiation., hypoxia and
mild thermal injury
6. Pgrogressive depletion of CD4+ T cells in AIDS

86.  Apoptosis is suggestive of:
A. Liquefaction degeneration. B. Coagulation
necrosis. C. Neoangiogenesis. D.
Epithelial dysplasia.
Ans. B (Ref: Rubin 3rd / 13, 14; Anderson 10th)

87.  Cytoplasmic cytochrome C is associated with:
 A. Glycolysis B. Apoptosis
 C. Drug metabolization D. All
 Ans. (B) (Ref: Robbin ‘s-7th Ed/Pg 29, 30)

88.  'Physiologic programmed cell death' is termed
as
 a. Apoptosis b. Lysis c. Autolysis
d. Autopsy
 Ans. A

89.  Apoptosis is a pathological process associated with:
 a. Cellular hyperplasia b. Cellular dysplasia
c. Cellular death d. Cellular hypertrophy
 Ans. C

90.  About apoptosis, true statement is:
 a. Injury due to hypoxia
 b. Inflammatory reaction is present
 c. Councilman bodies is a type of apoptosis
 d. All of these
 Ans. C

91.  Gene inhibiting apoptosis is:
 a. bcl2 b. P53 c.Ras d. N-myc
 Ans. A

94.  Gangrene is a potentially life-threatening condition
caused by a critically insufficient blood supply
(necrosis).
 This may occur after an injury or infection, or in
people suffering from any chronic health problem
affecting blood circulation.
 The primary cause of gangrene is reduced blood
supply to the affected tissues, which results
in cell death.
 Diabetes and long-term smoking increase the risk of
suffering from gangrene.

95.  Dry
 Wet
 Gas
 In either type of gangrene, coagulation necrosis
undergo liquefaction by the action of putrefactive
bacteria.

96.  Dry gangrene is a form of coagulative
necrosis that develops in ischemic tissue, where the blood
supply is inadequate to keep tissue viable.
 Dry gangrene is often due to peripheral artery disease, but can
be due to acute limb ischemia.
 The limited oxygen in the ischemic limb
limits putrefaction and bacteria fail to survive.
 The affected part is dry, shrunken and dark reddish-black.
 The line of separation usually brings about complete
separation, with eventual falling off of the gangrenous tissue if
it is not removed surgically, a process called autoamputation.

97.  Wet, or infected, gangrene is characterized by thriving
bacteria and has a poor prognosis (compared to dry gangrene)
due to septicemia resulting from the free communication
between infected fluid and circulatory fluid.
 The tissue is infected by saprogenic microorganisms
eg.Clostridium perfringens or Bacillus fusiformis , which
cause tissue to swell and emit a fetid smell.
 Wet gangrene usually develops rapidly due to blockage of
venous (mainly) and/or arterial blood flow.

98.  The affected part is saturated
with stagnant blood, which
promotes the rapid growth of
bacteria.
 The toxic products formed by
bacteria are absorbed, causing
systemic manifestation
of septicemia and finally death.
 The affected part is edematous,
soft, putrid, rotten and dark

99.  Gas gangrene is a bacterial
infection that produces gas within tissues.
 It can be caused by Clostridium, most
commonly alpha toxin producing Clostridium
perfringens, or various non-clostridial species.
 Infection spreads rapidly as the gases produced by
bacteria expand and infiltrate healthy tissue in the
vicinity.
 Because of its ability to quickly spread to
surrounding tissues, gas gangrene should be treated
as a medical emergency.

100.  Gas gangrene is caused by bacterial exotoxin-
producing clostridial species, which are mostly
found in soil.
 These environmental bacteria may enter the muscle
through a wound and subsequently proliferate in
necrotic tissue and secrete powerful toxins.
 These toxins destroy nearby tissue, generating gas at
the same time.
 A gas composition of 5.9% hydrogen, 3.4% carbon
dioxide, 74.5% nitrogen, and 16.1% oxygen was
reported in one clinical case.
 Progression to toxemia and shock is often very rapid.

101.  Gangrene is the death of a part accompanied
by
 a. Suppuration b. Putrefaction
 c. Calcification d. Coagulation
 Ans. B [Ref. Harshmohan 3rd Ed Pg 40]
 Gangrene is a form of necrosis of tissue with
superadded putrefaction.

102.  Gangrene is defined as:
 a. Necrosis of body parts
 b. Coagulative necrosis of body parts
 c. Necrosis with putrefaction
 d. All are true
 Ans. C

103.  Metastatic calcification is
deposition of calcium salts in
otherwise normal tissue,
because of elevated serum
levels of calcium.
 Occur because of deranged
metabolism as well as increased
absorption or decreased
excretion of calcium and related
minerals, as seen in
hyperparathyroidism.

104.  Dystrophic calcification is caused
by abnormalities or degeneration
of tissues resulting in mineral
deposition, though blood levels of
calcium remain normal.
 Metastatic calcification is often
found in many tissues throughout
a person or animal, whereas
dystrophic calcification is
localized.

105.  Dystrophic calcification are calcifications seen
in
a. Skin layers b.Salivary glands
 c . Normal tissues d. Dead tissue
 Ans. D [Ref. Harshmohan 3rd Ed Pg 42]
 Dystrophic calcification occurs in dead and degenerated
tissues. Calcium metabolism and serum calcium level are
normal. Commonly occurs in different types of necrosis,
infarcts, thrombi, hematomas etc.

106.  Metastatic calcifications are seen in
 a. Hypoparathyroidism b.Vitamin D deficiency
 c.Hypercalcemia d.All the above
 Ans. C

107.  Necrotic cells and tissue attract:
 a. Polyostotic calcification
 b. Dystrophic calcification
 c. Anatropic calcification
 d. None of the above
 Ans. B
 If necrotic cells and cellular debris are not promptly destroyed
and reabsorbed, they tend to attract calcium salts and become
mineralized. This is known as dystrophic calcification (Other
modes of calcification are not defined modes of calcification).

108.  Dystrophic calcification is commonly seen in:
 a. Hyperparathyroidism b.Vitamin D deficiency
 c. Atheromatous plaque d. Lungs
 Ans. C

109.  Metastatic calcification occurs in all except:
 a. Kidney b.Atheroma
 c. Fundus of stomach d.Wall of IVC
 Ans. B