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GBA Pathology > PATHOMA1 - Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

PATHOMA1 - Growth Adaptations, Cellular Injury, and Cell Death Flashcards

1
Q

What are the basic principles of growth adapdations?

A

An organ is in homeostasis with the physiologic stress placed on it. An increase, decrease, or change in stress on an organ can result in growth adaptations.

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2
Q

What leads to an increase in organ size?

A

An increase in stress

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3
Q

Hypertrophy occurs via what?

A

an increase in the size

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4
Q

Hyperplasia occurs via what?

A

an increase in the number of cells

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5
Q

What does hypertrophy involve?

A

gene activation, protein synthesis, and production of organelles.

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6
Q

What does Hyperplasia involve?

A

the production of new cells from stem cells.

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7
Q

Permanent tissues are… Do they undergo hypertrophy or hyperplasia?

A

cardiac muscle, skeletal muscle, and nerve, cannot make new cells and undergo hypertrophy only.

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8
Q

Pathologic hyperplasia leads to what?

A

(e.g., endometrial hyperplasia) can progress to dysplasia and,eventually cancer.

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9
Q

What is an exception to pathologic hyperplasia leading to cancer?

A

benign prostatic hyperplasia (BPH), which does notincrease the risk for prostate cancer,

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10
Q

What leads to a decrease in organ size?

A

A decrease in stress (e.g., decreased hormonal stimulation, disuse, or decreased nutrients/blood supply) (atrophy).

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11
Q

Atrophy occurs via?

A

a decrease in the size and number of cells

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12
Q

How does a decrease in cell number occur?

A

via apoptosis.

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13
Q

Decrease in cell size occurs via what?

A

ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components.

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14
Q

What happens in ubiquitin-proteosome degradation?

A

intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes.

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15
Q

What does autophagy of cellular components involve?

A

generation of autophagic vacuoles that fuse with lysosomes whose hydrolytic enzymes breakdown cellular components.

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16
Q

What happens in METAPLASIA?

A

change in stress on an organ leads to a change in cell type

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17
Q

Metaplasia most commonly involves?

A

change of one type of surface epithelium (squamous, columnar, or urothelial) to another

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18
Q

How do metaplastic cells handle the new stress?

A

they are better able to handle the new stress.

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19
Q

Esophagus is normally lined by what?

A

nonkeratinizing squamous epithelium (suited to handle friction of a food bolus)

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20
Q

Barrett esophagus

A

Acid reflux from the stomach causes metaplasia to nonciliated mucin-producing columnar cells (better able to handle the stress of acid

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21
Q

Metaplasia occurs via what?

A

programming of stem cells, which then produce the new cell type.

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22
Q

Is Metaplasia reversible?

A

with removal of the driving stressor.

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23
Q

Can metaplasia progress to cancer?

A

Under persistent stress, can progress to dysplasia and eventually result in cancer.

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24
Q

What is an exception to metaplasia leading to cancer?

A

apocrine metaplasia of breast, which carries no increased risk for cancer.

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25
Q

Vitamin A deficiency can result in what?

A

metaplasia,

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26
Q

Vitamin A is necessary for what?

A

differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye.

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27
Q

Keratomalacia

A

In vitamin A deficiency, the thin squamous lining of the conjunctiva undergoes metaplasia into stratified keratinizing squamous epithelium.

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28
Q

Myositis Ossificans

A

Mesenchymal (connective) tissues can undergo metaplasia. A classic example is myositis ossificans in which muscle tissue changes to bone during healing after trauma

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29
Q

DYSPLASIA is?

A

Disordered cellular growth

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30
Q

Dysplasia most often refers to?

A

proliferation of precancerous cells

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31
Q

Cervical intraepithelial neoplasia (CIN)

A

represents dysplasia and is a precursor to cervical cancer

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32
Q

Dysplasia often arises from?

A

longstanding pathologic hyperplasia (e.g., endometrial hyperplasia) or metaplasia (e.g., Barrett esophagus)

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33
Q

Is dysplasia is reversible?

A

yes, with alleviation of inciting stress.

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34
Q

In dysplasia what happens if stress persists?

A

dysplasia progresses to carcinoma irreversible)

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35
Q

What is aplasia?

A

it is failure of cell production during embryogenesis (e.g., unilateral renal agenesis)

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36
Q

What is hypoplasia?

A

it is a decrease in cell production during embryogenesis, resulting in a relatively small organ (e.g., streak ovary in Turner syndrome)

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37
Q

When does cellular injury occur?

A

when a stress exceeds the cells ability to adapt

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38
Q

The likelihood of injury depends on what?

A

the type of stress, its severity, and the type of cell affected.

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39
Q

What are highly susceptible to ischemic injury? As opposed to?

A

neurons whereas, skeletal muscle is relatively more resistant.

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40
Q

Slowly developing ischemia

A

eg: renal artery atherosclerosis, results in ATROPHY

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41
Q

acute ischemia

A

eg: renal artery embolus, results in INJURY

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42
Q

What are common causes of cellular injury?

A

inflammation, nutritional deficiency or excess, hypoxia, trauma, and genetic mutations.

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43
Q

What is HYPOXIA?

A

Low oxygen delivery to tissue; important cause of cellular injury

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44
Q

What is the final electron acceptor in the electron transport chain of oxidative phosphorylation?

A

Oxygen

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45
Q

Decreased oxygen results in what?

A

impairs oxidative phosphorylation, resulting in decreased ATP production

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46
Q

What does a lack of ATP leads to?

A

cellular injury

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47
Q

What are some causes of hypoxia?

A

include ischemia, hypoxemia, and decreased 02 - carrying capacity of blood.

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48
Q

Ischemia is?

A

decreased blood flow through an organ

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49
Q

Ischemia arises with?

A
  1. Decreased arterial perfusion (eg atherosclerosis) 2. Decreased venous drainage (eg Budd-Chiari syndrome) 3. Shock?generalized hypotension resulting in poor tissue perfusion
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50
Q

Hypoxemia is?

A

a low partial pressure of oxygen in the blood (Pao2< 60 mm Hg, SaO2<90%).

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51
Q

Hypoxemia arises with

A
  1. High altitude 2. Hypoventilation 3. Diffusion defect 4. V/Q mismatch
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52
Q

High altitude to hypoxemia, how?

A

Decreased barometric pressure results in decreased PaO2

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53
Q

Hypoventilation to hypoxemia, how?

A

Increased Paco, results in decreased PaO2

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54
Q

Diffusion defect to hypoxemia, how?

A

PAO2 not able to push as much O2 into the blood due to a thicker diffusion barrier (e.g., interstitial pulmonary fibrosis)

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55
Q

V/Q mismatch to hypoxemia, how?

A

Blood bypasses oxygenated lung (circulation problem, eg: right-to-left shunt), or oxygenated air cannot reach blood (ventilation problem, eg: atelectasis)

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56
Q

Decreased O2-carrying capacity arises with what?

A

hemoglobin (Hb) loss or dysfunction

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57
Q

What are some examples of Decreased O2-carrying capacity?

A
  1. Anemia 2. Carbon monoxide poisoning 3. Methemoglobinemia
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58
Q

Anemia leading to decreased O2 carrying capacity.

A

(decrease in RBC mass) PaO2 normal; SaO2 normal

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59
Q

Carbon monoxide poisoning

A

CO binds hemoglobin more avidly than oxygen

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60
Q

What is the PaO2 and SaO2 for carbon monoxide poisoning?

A

PaO2 normal; SaO2 decreased

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61
Q

Exposures for Carbon monoxide poisoning

A

include smoke from fires and exhaust from cars or gas heaters.

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62
Q

Classic finding for Carbon monoxide poisoning

A

cherry-red appearance of skin.

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63
Q

Early sign of exposure for Carbon monoxide poisoning

A

headache; significant exposure leads to coma and death.

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64
Q

What is Methemoglobinemia?

A

Iron in heme is oxidized to Fe3+ which cannot bind oxygen

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65
Q

PaO2 and SaO2 for Methemoglobinemia?

A

PaO2 normal; SaO2 decreased

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66
Q

Methemoglobinemia is Seen with?

A

oxidant stress (eg sulfa and nitrate drugs) or in newborns

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67
Q

Classic finding for Methemoglobinemia?

A

cyanosis with chocolate-colored blood.

68
Q

Treatment for Methemoglobinemia?

A

intravenous methylene blue, which helps reduce Fe3+ back to Fe2+ state.

69
Q

Hypoxia results in low ATP how?

A

impairs oxidative phosphorylation resulting in decreased ATP.

70
Q

Low ATP disrupts what?

A

key cellular functions including 1. Na/K pump 2. Ca2+ pump 3. Aerobic glycolysis

71
Q

Disruption of Na/K pump results in what?

A

sodium and water buildup in the cell

72
Q

Disruption of Ca2+ pump results in what?

A

Ca2+ buildup in the cytosol of the cell

73
Q

Disruption of Aerobic glycolysis results in what?

A

switch to anaerobic glycolysis. Lactic acid buildup results in low pH, which denatures proteins and precipitates DMA.

74
Q

The hallmark of reversible injury is

A

cellular swelling.

75
Q

Cytosol swelling results in

A

loss or microvilli and membrane blebbing.

76
Q

Swelling of the rough endoplasmic reticulum (RER) results in

A

dissociation of ribosomes and decreased protein synthesis.

77
Q

The hallmark of irreversible injury is

A

membrane damage.

78
Q

Plasma membrane damage results in

A
  1. Cytosolic enzymes leaking into the serum {e.g cardiac troponin) 2. Additional calcium entering into the cell
79
Q

Mitochondrial membrane damage results in

A
  1. Loss of the electron transport chain (inner mitochondrial membrane) 2. Cytochrome c leaking into cytosol (activates apoptosis)
80
Q

Lysosome membrane damage results in

A

hydrolytic enzymes leaking into the cytosol, which in turn, are activated by the high intracellular calcium.

81
Q

The end result of irreversible injury is

A

cell death.

82
Q

The morphologic hallmark of cell death is

A

loss of the nucleus,

83
Q

loss of the nucleus occurs via

A

nuclear condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis)

84
Q

The two mechanisms of cell death are

A

necrosis and apoptosis.

85
Q

NECROSIS

A

A. Death of large groups of cells followed by acute inflammation B. Due to some underlying pathologic process; never physiologic C. Divided into several types based on gross features

86
Q

GROSS PATTERNS OF NECROSIS

A

A. Coagulative necrosis, B. liquefactive necrosis, C. Gangrenous necrosis D. Caseous necrosis E. Fat necrosis F. Fibrinoid necrosis

87
Q

What is Coagulative necrosis?

A

Necrotic tissue that remains firm, cell shape and organ structure are preserved by coagulation of proteins, but the nucleus disappears

88
Q

Coagulative necrosis is Characteristic of?

A

ischemic infarction of any organ except the brain

89
Q

Area of infarcted tissue for Coagulative necrosis?

A

It is often wedge-shaped (pointing to focus of vascular occlusion) and pale.

90
Q

What is Red infarction

A

arises if blood re-enters a loosely organized tissue (e.g. pulmonary or testicular infarction)

91
Q

What is Liquefactive necrosis?

A

Necrotic tissue that becomes liquefied; enzymatic lysis of cells and protein results in liquefaction.

92
Q

Liquefactive necrosis is Characteristic of?

A

Brain infarction, abscess, pancreatitis

93
Q

What type of necrosis for brain infarction?

A

Liquefactive necrosis - Proteolytic enzymes from microglial cells liquefy the brain.

94
Q

What type of necrosis for abscess?

A

Liquefactive necrosis - proteolytic enzymes from neutrophils liquefy tissue

95
Q

What type of necrosis for pancreatitis?

A

Liquefactive necrosis - Proteolytic enzymes from pancreas liquefy parenchyma.

96
Q

What is Gangrenous necrosis?

A

Coagulative necrosis that resembles mummified tissue (dry gangrene)

97
Q

Gangrenous necrosis is characteristic of?

A

ischemia of lower limb and GI tract

98
Q

What is wet gangrene?

A

superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene).

99
Q

What is Caseous necrosis?

A

Soft and friable necrotic tissue with cottage cheese-like appearance. It’s a combination of coagulative and liquefactive necrosis

100
Q

What is caseous necrosis characteristic of?

A

granulomatous inflammation due to tuberculous or fungal infection

101
Q

What is fat necrosis?

A

Necrotic adipose tissue with chalky-white appearance due to deposition of calcium

102
Q

What is fat necrosis characteristic of?

A

trauma to fat (eg. breast) and pancreatitis-mediated damage of peripancreatic fat

103
Q

Fat necrosis and saponification

A

Fatty acids released by trauma (eg to breast) or lipase (eg pancreatitis) join with calcium via a process called saponification which is an example of dystrophic calcification in which calcium deposits on dead tissues.

104
Q

dystrophic calcification

A

the necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate

105
Q

Dystrophic calcification vs metastatic calcification

A

high serum calcium or phosphate levels lead to calcium deposition in normal tissues (eg. hyperparathyroidism leading to nephrocalcinosis)

106
Q

Fibrinoid necrosis

A

Necrotic damage to blood vessel wall, Leaking of proteins (including fibrin) into vessel wall results in bright pink staining of the wall microscopically

107
Q

What is fibrinoid necrosis characteristic of?

A

malignant hypertension and vasculitis

108
Q

What is apoptosis?

A

Energy (ATP)-dependent, genetically programmed cell death involving single cells or small groups of cells.

109
Q

Examples of apoptosis include

A
  1. Endometrial shedding during menstrual cycle 2. Removal of cells during embryogenesis 3. CD8+ T cell-mediated killing of virally infected cells
110
Q

Morphology of apoptosis

A
  1. Dying cell shrinks, leading cytoplasm to become more eosinophilic (pink) 2. Nucleus condenses (pyknosis) and fragments (karyorrhexis).
111
Q

Apoptotic bodies

A

fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation

112
Q

Apoptosis is mediated by

A

caspases that activate proteases and endonucleases

113
Q

Proteases

A

break down the cytoskeleton.

114
Q

Endonucleases

A

break down DNA,

115
Q

How are caspases activated?

A
  1. Intrinsic mitochondrial pathway 2. Extrinsic receptor-ligand pathway 3. Cytotoxic CD8+ Tcell-mediated pathway
116
Q

What is the main molecule in the intrinsic mitochondrial pathway?

A

Bcl2

117
Q

What happens to Bcl2 in the intrinsic mitochondrial pathway?

A

Cellular injury, DNA damage, or loss of hormonal stimulation leads to inactivation of Bcl2

118
Q

In the intrinsic mitochondrial pathway lack of Bcl 2 results in what?

A

allows cytochrome c to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases.

119
Q

What is the extrinsic receptor-ligand pathway?

A

FAS ligand binds to (CD95) FAS death receptor and TNF binds TNF receptor (both activate caspases)

120
Q

What is an example of FAS ligand binding to FAS death receptor (CD95) on the target cell activating caspases

A

negative selection of thymocytes in thymus

121
Q

Cytotoxic CD8+ T cell-mediated pathway releases what?

A

perforins and granzyme ex CD8+ T-cell killing of virally infected cells is an example.

122
Q

Perforins

A

secreted by CD8+ T cell create pores in membrane of target cell

123
Q

Granzyme

A

secreted from CD8+ T cell enters pores and activates caspases

124
Q

Free radicals are what?

A

chemical species with an unpaired electron in their outer orbit.

125
Q

When does physiologic generation of free radicals occur?

A

it occurs during oxidative phosphorylation

126
Q

How are free radicals generated physiologically?

A

Cytochrome c oxidase (complex IV) transfers electrons to oxygen. Partial reduction of O2 yields superoxide (O2.) hydrogen peroxide (H202), and hydroxyl radicals (OH.)

127
Q

Pathologic generation of free radicals arises with?

A

Ionizing radiation, inflammation, metals, drugs and chemicals

128
Q

Ionizing radiation and Pathologic generation of free radicals

A

water hydrolyzed to hydroxyl free radical

129
Q

Inflammation and Pathologic generation of free radicals

A

NADPH oxidase generates superoxide ions during oxygen dependent killing by neutrophils.

130
Q

Metals and Pathologic generation of free radicals

A

(e.g., copper and iron) Fe generates hydroxyl free radicals (Fenton reaction).

131
Q

Drugs and chemicals and Pathologic generation of free radicals

A

P450 system of liver metabolizes drugs (e.g acetaminophen), generating free radicals.

132
Q

Free radicals cause

A

cellular injury via peroxidation of lipids and oxidation of DNA and proteins; DNA damage is implicated in aging and oncogenesis.

133
Q

Elimination of free radicals occurs via what?

A

Antioxidants, Enzymes, Metal carrier proteins

134
Q

Elimination of free radicals via Antioxidants

A

glutathione and vitamins A , C, and E

135
Q

Elimination of free radicals via Enzymes

A

SOD, glutathione peroxidase, catalase

136
Q

Superoxide dismutase

A

(in mitochondria) superoxide (O2.?>H202)

137
Q

Glutathione peroxidase

A

(in mitochondria) GSH + free radical GSSH and H202

138
Q

Catalase

A

(in peroxisomes) H2O2 ?> O2 and H202

139
Q

Elimination of free radicals via Metal carrier proteins

A

transferrin and ceruloplasmin

140
Q

Free Radical Injury

A

Carbon tetrachloride (CCl4) and Reperfusion Injury

141
Q

Carbon tetrachloride - What is it used for?

A

Organic solvent used in the dry cleaning industry

142
Q

How is CCl4 metabolized?

A

Converted to CC14 free radicals by P450 system of hepatocytes

143
Q

CCl4 results in what?

A

cell injury with swelling of RER, ribosomes detach, impairing protein synthesis. Decreased apolipoproteins lead to fatty change in the liver

144
Q

Reperfusion injury

A

Return of blood to ischemic tissue results in production of O2-derived free radicals, which further damage tissue. Leads to a continued rise in cardiac enzymes (troponin) after reperfusion of infarcted myocardial tissue

145
Q

What is an amyloid?

A

It is a misfolded protein that deposits in the extracellular space, thereby damaging tissues.

146
Q

What are the shared features of amyloid proteins?

A

beta-pleated sheet configuration, Congo red staining and apple-green birefringence when viewed microscopically under polarized light Deposition can be systemic or localized,

147
Q

What is primary amyloidosis?

A

It is systemic deposition of AL amyloid, which is derived from immunoglobulin light chain

148
Q

What is primary amyloidosis associated with?

A

plasma cell dyscrasias (e.g multiple myeloma)

149
Q

Secondary amyloidosis is?

A

systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein (SAA).

150
Q

What is SAA?

A

It is an acute phase reactant that is increased in chronic inflammatory states, malignancy, and Familial Mediterranean Fever (FMF).

151
Q

What is FMF due to?

A

a dysfunction of neutrophils (autosomal recessive) and occurs in persons of Mediterranean origin.

152
Q

What does FMF present with?

A

episodes of fever and acute serosal inflammation

153
Q

FMF can mimic what?

A

appendicitis, arthritis, or myocardial infarction

154
Q

How does FMF result in AA amyloid deposition in tissues?

A

High SAA during attacks deposits as AA amyloid in tissues

155
Q

What is the most common organ involved in systemic amyloidosis?

A

kidney

156
Q

What are the clinical findings of systemic amyloidosis?

A

Nephrotic syndrome, Restrictive cardiomyopathy or arrhythmia, Tongue enlargement, malabsorption, and hepatosplenomegaly

157
Q

Diagnosis of systemic amyloidosis requires what?

A

tissue biopsy, Abdominal fat pad and rectum are easily accessible biopsy targets.

158
Q

Damaged organs of systemic amyloidosis must be…

A

transplanted. Amyloid cannot be removed.

159
Q

What is localized amyloidosis?

A

Amyloid deposition that is usually localized to a single organ

160
Q

What is senile cardiac amyloidosis?

A

Non-mutated serum transthyretin deposits in the heart. Usually asymptomatic; present in 25% of individuals > 80 years of age

161
Q

Familial amyloid cardiomyopathy

A

Mutated serum transthyretin deposits in the heart leading to restrictive cardiomyopathy, 5% of African Americans carry the mutated gene.

162
Q

Non-insulin-dependent diabetes mellitus (type II)

A

Anylin (derived from insulin) deposits in the islets of the pancreas,

163
Q

Alzheimer disease

A

amyloid beta (derived from J-amyloid precursor protein) deposits in the brain forming amyloid plaques

164
Q

Gene for J-APP is present on…

A

chromosome 21.

165
Q

Downs syndrome and Alzheimers?

A

Most individuals with Down syndrome (trisomy 21) develop Alzheimer disease by the age of 40 (early-onset).

166
Q

Dialysis-associated amyloidosis

A

B-microglobulin deposits in joints,

167
Q

Medullary carcinoma of the thyroid

A

Calcitonin (produced by tumor cells) deposits within the tumor (‘tumor cells in an amyloid background’).

GBA Pathology (20 decks)

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