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Pathology I > Cell Injury And Death > Flashcards

Cell Injury And Death Flashcards

1
Q

Etiology

A

Cause of disease

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2
Q

Pathogenesis

A

Mechanism of development of disease

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3
Q

Molecular/morphological changes

A

Biochemical and structural alterations seen in disease

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4
Q

Clinical manifestations

A

Functional consequences of disease

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5
Q

Adaptation of a cell in response to stress is associated with adjustments in _______ and _______ of the cell.

A

Structure and function

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6
Q

When does cell unjustly occur?

A

when limits of adaptation are surpassed or when

undergo adaptation and/or injury function adaptive responses are not available.

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7
Q

What are the limitations of survival of an injured cell?

A

nature and

duration of the injury and concurrent exposure to other cell stressors.

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8
Q

Necrosis is characterized by:

A

structural changes that result from cell death

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9
Q

Is there inflammation associated with post-Mortem change (autolysis)?

A

No

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10
Q

What are the five morphologic patterns of adaptation for cells under stress?

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
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11
Q

Morphologic adaptation pattern that results in shrinkage of cells or organs due to loss of cell substance.

A

Atrophy

This is associated with reduced function of cell but not necessarily death

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12
Q

Postpartum involution of uterus and age-related changes of thymus are examples of what kind of cell adaptation?

A

Physiologic atrophy

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13
Q

What are causes of pathological atrophy?

A
  • disuse
  • hypoxia
  • pressure
  • denervation
  • endocrine deficiency
  • idiopathic
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14
Q

Osteoporosis is an example of what cell adaptation?

A

Pathological atrophy from disuse

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15
Q

tissue and organ atrophy associated with

diminished blood or oxygen supply

A

Pathological atrophy associated with hypoxia

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16
Q

neoplasms, aneurysms or other conditions that compress adjacent structures can cause what kind of cell adaptation?

A

Pathological atrophy due to pressure

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17
Q

atrophy of skeletal muscle following interruption of nerve supply is an example of what kind of cell adaptation?

A

Pathologic atrophy due to denervation

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18
Q

atrophy of target organs associated with hormone inadequacy can cause what kind of cell adaptation?

A

Pathologic atrophy due to endocrine deficiency

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19
Q

Cell adaptation seen in Alzheimer’s is an example of:

A

Idiopathic atrophy (unknown origin)

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20
Q

Cell adaptation resulting in enlargement of existing, non-dividing cells?

A

Hypertrophy

As seen in skeletal and cardiac muscle cells

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21
Q

If myocardial hypertrophy occurs with athletic conditioning, when does it become pathologic?

A

when caused by hypertension, valve lesions, etc.

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22
Q

Cell adaptation resulting in enlargement of tissue due to proliferation of cells capable of mitosis

A

Hyperplasia

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23
Q

What regulates proliferation as seen in hyperplasia?

A

growth factors, cytokines and growth inhibitors

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24
Q

Wound repair and tissue regeneration is an example of what kind of cell adaptation?

A

Hyperplasia

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25
Q

Compensatory responses, as in partial organ loss or physical stress is an example of what kind of cell adaptation?

A

Hyperplasia

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26
Q

Enlargement of a uterus during pregnancy or breasts during lactation, due to hormones are examples of what kind of cell adaptation?

A

Hyperplasia

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27
Q

Abnormal hormonal stimulation of growth factors on target cells due to chronic irritation or viruses can cause what kind of cell adaptation?

A

Pathologic hyperplasia

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28
Q

Cancer is an example of what cell adaptation?

A

Pathological hyperplasia after exposure of carcinogen

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29
Q

Cell adaptation where there is substitution of one type of “mature” cell with another “mature” cell type that may be better suited to cope with an altered environment

A

Metaplasia

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30
Q

Reprogramming of stem (reserve) cells of epithelium or of undifferentiated mesenchymal cells in connective tissue is an example of what kind of cell adaptation?

A

Metaplasia

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31
Q

What kind of cell adaptation occurs in Barrett’s esophagus?

A

Columnar cell metaplasia of lower esophagus

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32
Q

Ossification of fibrous scars is an example of what cell adaptation?

A

Metaplasia

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33
Q

Atypical substitution of one type of “mature” cell with another “mature” cell type resulting in lack of cellular uniformity and increased mitosis resembling cancer

A

Dysplasia

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34
Q

Are dysplasic cell adaptations reversible?

A

Mild to moderate are, but if entire layer of epithelium is involved, it will likely lead to cancer

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35
Q

The HPV virus will cause what kind of cell adaptation in the uterine cervix?

A

Dysplasia

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36
Q

hypoxic injury due to decreased blood flow

A

Ischemia

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37
Q

Local causes of ischemia

A
  • arterial occlusion
  • venous obstruction
  • shunting of blood (steal syndrome)
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38
Q

Systemic causes if ischemia

A
  • congestive heart failure

- shock

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39
Q

Causes of reversible and irreversible cell injury:

A
  • ischemia
  • hypoxia
  • anoxia
  • aging
  • nutritional
  • endocrine
  • genetic
  • immune
  • infections
  • physical agents
  • chemical agents
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40
Q

decreased blood oxygen levels

A

Hypoxemia

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41
Q

What is the difference between hypoxic hypoxia and anemic hypoxia?

A

The decreased blood oxygen levels in hypoxic hypoxia is cause by decreased availability of oxygen while anemic hypoxia is due to deficiency in oxygen delivery associated with hemoglobin and/or iron

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42
Q

How does cyanide cause cell injury?

A

disrupts mitochondrial cytochrome oxidases effectively stopping oxidation and ATP production

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43
Q

What are some examples of physical agents that can cause cell injury?

A

mechanical trauma, temperature extremes, electrical injury, various forms of radiant energy, etc.

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44
Q

What is the mechanism of injury associated with a hypoxic injury?

A

Compromised oxidative phosphorylation and therefore decreased ATP synthesis. Without ATP to perform work, membrane permeability increases and cells/organelles swell

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45
Q

How can reperfusion of hypoxic tissue with blood cause additional injury to the cell?

A
  • more free radical formation with sudden onset of oxygen and oxidative phosphorylation
  • inflammation
  • calcium from reestablished blood flood enters and damages injured cells
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46
Q

Most calcium is sequestered in the mitochondria and endoplasmic reticulum of cells and maintained at very low levels. Reperfusion of hypoxic tissue can result in calcium entering injured cells, causing further damage by activating what?

A
  • phospholipases (degrading lipid membranes)
  • proteases (degrading enzymes and cell structures)
  • ATPases (inhibiting oxidative phosphorylation)
  • endonucleases (breaking peptide bonds)
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47
Q

Exposure to free radicals can cause cell injury. What are some ways that we can be exposed?

A
  • radiation
  • enzymatic metabolism
  • redox reactions
  • transition metals (iron, copper)
  • products of lipid oxidation
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48
Q

How are free radicals removed or degraded?

A

by spontaneous decay and/or action of enzymes.

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49
Q

What are common causes of alterations to membrane permeability after cell injury?

A
  • ATP depletion
  • activation of phospholipases
  • direct damage to the membrane
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50
Q

Irreversible damage to the mitochondria leads to:

A

Cell death

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51
Q

What is considered to be the indicator for severe cell injury and death?

A

Increased serum enzyme levels due to altered membrane homeostasis and permeability

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52
Q

Necrosis

A

Pattern of change as a cell dies after injury

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53
Q

self-digestion by enzymes derived from

lysosomes within the injured cell

A

Intrinsic (autolysis) denaturation

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54
Q

digestion of cell components by enzymes derived from inflammatory leukocytes

A

Extrinsic (heterolysis) denaturation

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55
Q

Characteristic features of necrosis include:

A
  • cell swelling
  • disruption of organelles
  • consumption of glycogen
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56
Q

What is considered the “hallmark” of cell death

A

Nuclear changes

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57
Q

Shrinking and increased basophilic staining of the nucleus on light microscopy

A

Pyknosis

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58
Q

fragmentation and breakdown of nuclei

A

Karyorrhexis

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59
Q

dissolution of nucleus

A

Karyolysis

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60
Q

What kind of necrosis is characterized by predominantly cytoplasmic proteins being denatured?

A

Coagulation necrosis

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61
Q

Where is coagulation necrosis commonly seen?

A

most “solid” organs (heart, kidney, muscle, adrenal, etc.).

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62
Q

In what type of necrosis is the cell outline and the basic tissue architecture preserved for a time before being removed? (Sometimes referred to as “fried egg whites” appearance)

A

Coagulation

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63
Q

bacterial abscesses and infarcts of soft tissues lead to what type of necrosis?

A

Liquefaction necrosis

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64
Q

In what type of necrosis is tissue rapidly destroyed by autolysis mechanisms and debris removed? (Often a fluid filled cavity forms at site of destruction)

A

Liquefaction necrosis

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65
Q

Type of necrosis where damaged tissue becomes “cheesy” in appearance

A

Caseous necrosis

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66
Q

What are common causes of caseous necrosis?

A

TB

Leprosy

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67
Q

Caseous necrosis is considered to be a combination of what types of necrosis?

A

Coagulation and liquefaction

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68
Q

What characterized fat necrosis?

A

Saponification caused by hydrolysis of lipid deposits in adipose tissue combining with calcium to form soaps which appear as chalky white deposits

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69
Q

Enzymatic fat necrosis is characteristic of:

A

Acute pancreatitis

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70
Q

inflammation and the formation of dense fibrous tissue deposits in subcutaneous adipose tissue (especially breast)

A

Traumatic fat necrosis

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71
Q

Type of necrosis where vascular or perivascular tissues are injured and blood vessels become more permeable to plasma proteins producing characteristic deposits

A

Fibrinoid necrosis

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72
Q

What are some causes of fibrinoid necrosis?

A
  • malignant HTN
  • vasculitis
  • immune complex disease
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73
Q

Type of necrosis characterized by chronic, nodular and potentially deforming fibrotic scars

A

Gummatous necrosis

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74
Q

When does gummatous necrosis occur?

A

During tertiary stage of syphillis

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75
Q

coagulation necrosis that is modified by bacterial activity

A

Gangrene

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76
Q

Where is gangrene most common?

A

in an extremity that has lost its blood supply

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77
Q

Type of gangrene where coagulation predominates and affected tissues dry out before significant bacterial infections are established

A

Dry gangrene (mummification)

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78
Q

What causes dry gangrene?

A

Frostbite

Infarctions

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79
Q

Type of gangrene where liquefaction predominates and affected tissues become soft

A

Wet (moist) gangrene

80
Q

Wet (moist) gangrene can be caused by:

A
  • arterial occlusion with deep infarcts of an extremity
  • intestinal infarcts
  • acute appendicitis
  • cholecystitis
81
Q

Type of gangrene that occurs in deep, blood-deprived wounds (aerobic conditions) contaminated with anaerobic bacteria that produce gas

A

Gas (infectious) gangrene

82
Q

Gas (infectious) gangrene is caused by:

A
  • compound fracture

- contamination of surgical site or other deep wound

83
Q

Programmed cell death is called

A

Apoptosis

84
Q

How is programmed cell death different from cell death due to injury?

A

Cell membranes do not rupture and no inflammation

85
Q

What are the steps of apoptosis?

A
  • Chromatin condenses
  • This aggregation leads to karyorrhexis of nucleus
  • cell continue to shrink into apoptosis bodies
  • these are consumed by phagocytes
86
Q

Apoptosis is a regulated process to eliminate cells that are no longer required. What can cause it?

A
  • diminished growth factors or hormones

- activated genetic mechanisms that identify abnormal cells

87
Q

Examples of apoptosis

A
  • Involution of hormone-dependent tissues (e.g.
    endometrium, post-lactating breast)
  • tissue remodeling
  • destruction of neutrophils and eosinophils
88
Q

It has been reported that cyclic overload of tendons
activates stress-activated protein kinases in tendon fibroblasts causing some of these cells to ________. Consequently, collagen synthesis and repair responses are diminished which lead to weakening of the collagenous matrix and increased risk for tearing.

A

undergo apoptosis

89
Q

ATP is depleted in muscle causing actin-myosin bonds to lock up in what post-Mortem change

A

Rigor mortis

90
Q

What is algor mortis

A

Cooling of body core temperature

91
Q

The post-Mortem change where the color of skin changes due to pooling of blood causing staining with hemoglobin derivatives

A

Livor mortis

92
Q

A group of disorders characterized by alterations of organelles and the cytoskeleton

A

Subcellular alterations

93
Q

a type of subcellular alteration where damaged cell components are taken up by autophagosomes and lipid products accumulate in residual bodies

A

Autophagocytosis

94
Q

What is lipofuscin?

A

The lipid accumulations in residual bodies during autophagocytosis that is common during aging and chronic degenerative disease

95
Q

A type of subcellular alteration where there is expansion of the smooth endoplasmic reticulum (SER) of hepatocytes

A

Induction

96
Q

prolonged exposure to chemicals and
drugs metabolized by the P-450 centered mixed function oxidase of the SER will cause what kind of subcellular alteration? Why?

A

Induction (expansion), because it increases the capacity of the liver to metabolize a variety of agents including barbiturates, steroids, certain carcinogens, alcohol, CCl4, bilirubin, and bile acids.

97
Q

Abnormalities of the cytoskeleton affect functions that include:

A

phagocytosis, locomotion, movement of organelles and ciliary activity

98
Q

hereditary spherocytosis, Kartagener’s syndrome and leukocyte defects all have abnormalities of what?

A

Cytoskeleton

99
Q

Substances that cannot otherwise be mobilized or excreted from the cell are stores in ________ or other sytoplasmic structures.

A

Lysozyme

100
Q

What are common causes of storage disorders?

A
  • metabolism inadequate to remove
  • abnormal endogenous (internal origin) substances
  • congenital enzyme abnormality
  • abnormal exogenous (external origin) substance
101
Q

Accumulation of lipids in parenchymal cells of organs associated with lipid metabolism.

A

Fatty metamorphosis (steatosis, fatty “change”)

102
Q

Fatty metamorphosis is common in where?

A

Liver due to alcohol abuse, diabetes, obesity

103
Q

Fatty metamorphosis is less common where?

A

Heart, muscle and kidney

104
Q

Lipid accumulation in hepatocytes can be caused by:

A
  • obesity
  • alcohol abuse
  • diabetes
  • kwashiorkor (protein deficiency due to malnourishment)
  • toxic injury
  • liver infection
105
Q

What are the gross changes associated with fatty liver?

A
  • enlargement, softening and yellowing of liver

- blunting of liver margins

106
Q

What are the pathogenic mechanisms of fatty change in the liver?

A
  • hyperlipidemia
  • excess FA synthesis
  • impaired FA oxidation
  • excess esterification of FA to TG
  • apoprotein insufficiency
  • failure to secrete lipoproteins
107
Q

What is adiposity?

A

Stromal infiltration of fat

108
Q

What are common locations of adiposity?

A
  • lymph nodes
  • pancreas
  • right ventricle and atria
109
Q

Chronic hypoxia (anemia) to the heart causes fatty deposits in what kind of pattern?

A

Triggered effect - alternating yellow (fat) and red (muscle) bands of tissue

110
Q

Profound hypoxia and myocardial infections (such as diphtheria) cause what kind of pattern of fat deposits?

A

Uniform

111
Q

Clusters of lipid-containing macrophages- common in dermis and tendons and associated with hyperlipidemia.

A

Xanthoma

112
Q

Intimal plaques consisting of lipid deposits (chiefly

cholesterol and its esters) in large-medium arteries

A

Atherosclerosis

113
Q

Atherosclerosis causes luminal narrowing and promotes ______.

A

Thrombosis

114
Q

What is associated with cherry red spots of the macula and neurological deterioration and eventual death of infants?

A

Tay Sachs disease, a lysosomal storage disease

115
Q

What lysosomal storage disease is associated with a deficiency in hexosaminidase A with causes accumulation of ganglioside (the brain is affected since gangliosides are metabolized in nerve tissue)?

A

Tay Sachs disease

116
Q

What lysosomal storage disease is associated with a deficiency in sphingomyelinase casusing sphingomyelin and cholesterol to accumulate in macrophages and in neurons?

A

Niemann - Pick disease

117
Q

What is associated with cherry red spots of the macula, hepatospelnomegaly and infant death?

A

Niemann-pick disease

118
Q

What lysosomal storage disease is associated with a deficiency in glucocerebrosidase and causes accumulation of glucocerebroside
(typically in macrophages)?

A

Gaucher’s disease

119
Q

Synthesis of excessive quantities of immunoglobulins (Ig) by
plasma cells may give rise to large proteinaceous deposits known as Russell bodies that accumulate in the endoplasmic reticulum in what condition?

A

Multiple myeloma (plasma cell neoplasms)

120
Q

What condition is characterized by swelling, homogenous appearance, and increased fragility of affected segments of skeletal muscle due to hyaline accumulation?

A

“Zenker’s hyaline degeneration” (a segmental necrosis of skeletal muscle)

121
Q

Accumulated cytoplasmic fibrils (intermediate filaments) and ubiquitin in injured hepatocytes, often associated with alcohol abuse

A

Mallory bodies

122
Q

Lewy bodies are associated with what neurodegenerative disease?

A

Parkinson’s

123
Q

Neurofibrillary tangles are associated with what neurodegenerative diseases?

A

Alzheimer’s and Huntington’s

124
Q

CDJ and mad cow disease are associated with accumulation of what?

A

Abnormally folded prion proteins

125
Q

α1 antitrypsin deficiency, cystic fibrosis, familial hypercholesterolemia are all associated with what?

A

Defective transport and secretion of critical proteins (enzymes, receptors, etc.)

126
Q

Crooke’s hyaline are accumulated intermediate filaments in pituitary basophils in what disease?

A

Cushing’s

127
Q

What are the proteins that participate in activities of normal cells, including protein folding, disaggregation and intracellular transport? May minimize lethal injury during ischemia and reperfusion.

A

Chaperonins

128
Q

What proteins have a role in refolding denatured proteins or they may participate in the removal or sequestration of damaged components in certain cells undergoing chronic stress?

A

Ubiquitin

129
Q

A meshwork of fibrils comprised of peptides arranged in a beta-pleated sheet pattern that are deposited in organs and tissues?

A

Amyloid

130
Q

Amyloid light chain is associated with what amyloidosis?

A

Multiple myeloma

131
Q

Amyloid associated protein is associated with what kinds of amyloidoses?

A
  • Chronic inflammatory conditions such as RA, Crohn’s

- Infectious conditions such as TB, leprosy, osteomyelitis, etc.

132
Q

What condition consists of deposits of a modified prealbumin (transthyretin) in peripheral nerves?

A

Familial amyloid polyneuropathy

133
Q

Cardiac amyloid are associated with what kind of symptoms?

A

Irregular heartbeat, ventricular dysfunction and cardiomegaly

134
Q

Beta2-microglobulin amyloidosis what cause what?

A

Chronic renal failure needing long term dialysis

135
Q

Amyloid deposits in the pancreatic islets will result in?

A

Type 2 diabetes

136
Q

What is the treatment for amyloidosis?

A

amyloidosis is incurable but procedures that decrease the proteins that make up amyloid and control underlying contributing diseases may be useful. Conservative therapies might employ anti- inflammatory agents, dietary choices and supplements.

137
Q

What glycogen storage disorder is caused by a deficiency of glucose-6-phosphatase?

A

Von Gierke’s disease

138
Q

How do children with von Gierke’s disease present?

A

Enlarged liver with a protruding abdomen and failure to thrive

139
Q

What glycogen storage disorder is caused by a defect in alpha1-glucosidase (a lysosomal enzyme) that affects the striated muscle?

A

Pompe’s disease

140
Q

In persistent hyperglycemia (severe diabetes mellitus), it is
common to see glycogen deposits where?

A

adjacent to the nuclei of hepatocytes, ß-cells, renal tubular cells and myocardial cells

141
Q

Tumors of melanocytes?

A

Pigmented nevi or moles

142
Q

The principal pigment of skin consisting largely of

tyrosine derivatives, that is synthesized in melanocytes by tyrosinase-dependent pathways. =

A

Melanin

143
Q

Congenital lack of melanin in variable patterns that affect skin, hair, and in some, the eyes

A

Albinism

144
Q

Acquired patchy areas of skin depigmentation

A

Vitiligo

145
Q

Condition with increased ACTH due to primary

insufficiency of the adrenal cortex that causes hyperpigmentation of the skin

A

Addison’s disease

146
Q

Melanin in the urine indicates what?

A

Extensive malignant melanoma

147
Q

tissue discoloration secondary to accumulated homogentisic acid.

A

Ochronosis

148
Q

Increased homogentistic acid in urine, giving it a black color?

A

Alkaptonuria

149
Q

The stainable form of iron is a complex of protein and ferric ions called?

A

Hemosiderin

Ferrous iron in heme groups (hemoglobin, myoglobin, cytochromes) does not stain. Neither does ferritin

150
Q

iron accumulates in macrophages with little effect on parenchymal cells

A

Hemosiderosis

151
Q

Iron accumulation that eventually causes parenchymal (organ) damage

A

Hemochromatosis

152
Q

The type of hemochromatosis that is associated with congenital gene defects that regulate intestinal absorption of iron; consequently iron is absorbed excessively.

A

Primary hemochromatosis

153
Q

Type of hemochromatosis that results from chronic hemolytic disorders and/or multiple transfusions?

A

Secondary hemochromatosis

154
Q

What is the classic “triad” manifestations of hemochromatosis?

A
  • cirrhosis
  • pancreatic fibrosis
  • bronzed skin
155
Q

tissue discoloration due to bilirubin excess

A

Jaundice

156
Q

brown-colored undigestible lipid derivatives that accumulate during aging or during atrophy/chronic injury (AKA aging or wear and tear pigment)

A

Lipofuscin

157
Q

Ingestion of lead produces a lead-sulfide line where?

A

Gingival margin

158
Q

What effects are most concerning with lead pigment deposits?

A

Can cause issues with CNS development

159
Q

What is the most common exogenous pigmentation?

A

Carbon, which is picked up by and stored by macrophages

160
Q

excess deposits of copper that affects the liver, basal ganglia and eyes (Kayser-Fleischer ring) is called what?

A

Wilson’s disease

161
Q

Two main patterns of tissue calcification?

A
  • amorphous calcium salts

- organized bone (pathologic ossification)

162
Q

The pathogenesis of tissue calcification involves two steps?

A
  • initiation/nucleation: critical step where deposits for crystallized nuclei
  • growth/accretion: the deposition of calcium continues one initiated
163
Q

What type of calcification occurs locally in diseased, injured or necrotic tissue where serum calcium and phosphorus levels are normal.

A

Dystrophic calcification

164
Q

Within cells, ________ are usually the first to calcify

A

mitochondria

165
Q

When calcium salts are complexed with coagulation factors. Include hematomas, blood clots (“phleboliths”), atherosclerotic plaques and valvular lesions, old scars, TB lesions, necrotic tissues, etc.

A

Extracellular calcification

166
Q

What often calcifies during menopause?

A

Uterine fibroids

167
Q

What is a lithopedion?

A

A calcified fetus

168
Q

What kind of calcification occurs in normal tissues in association with hypercalcemia?

A

Metastatic calcification

169
Q

Where do metastatic calcification predictably occur?

A

pulmonary alveoli, gastric

hypercalcemia. mucosa (near parietal cells), small blood vessels and basement membranes of certain renal tubules.

170
Q

What can cause hypercalcemia?

A
  • Increased secretion of parathyroid hormone (tumor)
  • Destruction of bone tissue (multiple myeloma/metastasis)
  • Increased bony remodeling (Paget’s disease)
  • Increased Vitamin-D
  • Renal failure
171
Q

a condition marked by deposition of calcium salts in the skin

A

Calcinosis cutis

172
Q

A condition marked by deposition of calcium deposits in connective tissue

A

Calcinosis interstitialis

173
Q

Intraparenchymal cell triglycerides are deposited in hepatocytes in what condition?

A

Fatty metamorphosis of liver

174
Q

Intraparenchymal cell triglycerides are deposited in myocardia in what condition?

A

“Thrush breast”

175
Q

Focal deposits of lipid- containing macrophages in subcutaneous tissues, etc.

A

Xanthoma

176
Q

Cholesterol and other lipid deposits in intima of arteries?

A

Atherosclerosis

177
Q

Deposits of sphingomyelin in neurons and systemic macrophages occurs in what condition?

A

Niemann-Pick disease

178
Q

Gangliosides deposit in neurons in what condition?

A

Tay Sachs

179
Q

Ig is found in plasma cells form______.

A

Russell bodies

180
Q

Protein inclusions formed in pituitary basophils are called ______ and are seen in what disease?

A

Crooke’s hyaline

Cushing’s disease

181
Q

Protein inclusions in injured hepatocytes are called _______.

A

Mallory bodies

182
Q

Deposits of complex insoluble protein materials that appear under a number of circumstances

A

Amyloidosis

183
Q

Accumulated glycogen deposits in liver and kidney

A

Von Gierke’s disease

184
Q

Accumulations of glycogen in

myocardium (lethal at early age)

A

Pompe’s disease

185
Q

Hyperglycemia with glycogen deposits in hepatocytes and renal tubular epithelium

A

Diabetes mellitus

186
Q

Diffuse deposits of melanin in skin and mucous membranes can be secondary to what conditions?

A
  • Addison’s
  • pregnancy
  • functional basophilic adenoma of pituitary
187
Q

Focal aggregates of pigmented melanocytes

A

Pigmented nevi

188
Q

Ochronosis (tissue discoloration) cartilage deposits, discoloration of urine cause by deposits of homogentisic acid is called what?

A

Alkaptonuria

189
Q

Accumulation of lipofuscin in cells of several tissues including heart, liver and brain are associated with ______

A

Ageing, chronic injury (“wear and tear”, “brown atrophy”)

190
Q

Iron deposits in systemic macrophages

A

Hemosiderosis

191
Q

Iron deposits in liver, pancreas and skin, joints and heart, etc.

A

Hemochromatosis (“bronze diabetes”)- severe iron storage disorder

192
Q

Bilirubin accumulates in blood and tissue fluids, skin, sclera, etc.

A

Jaundice

193
Q

Discolored lead deposits at gingival line, organ and neurological damage

A

Plumbism (exposure to lead)

194
Q

Copper deposits in liver, basal ganglia and eye

A

Wilson’s disease

195
Q

Somatic (fibroblasts) cells undergo a predetermined number of divisions (doublings) and this number is species specific. How many doublings of fibroblasts is normal for human adults?

A

50 doublings

196
Q

Limitations in doubling capacity of a cell is known as:

A

Hayflick phenomenon

197
Q

The Hayflick phenomenon implies that biological organisms are programmed to “wear out”. What are the proposed mechanisms of this:

A
  • loss of chromosome telomeres

- “clock genes”

Pathology I (10 decks)

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