Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Rapid Review Pathology > Chapter 2 - Cell Injury > Flashcards

Chapter 2 - Cell Injury Flashcards

0
Q

O2 diffusion

A

O2 in atmosphere → ↑PAO2 → ↑PaO2 → ↑SaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Define hypoxia.

A

Inadequate oxygenation of tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

O2 content equation

A

O2 content = (Hb g/dL × 1.34) × SaO2 + PaO2 × 0.003

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does hypoxia affect ATP synthesis?

A

Hypoxia: ↓ATP synthesis by oxidation phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the pulse oximeter read if there is a dyshemoglobinemia present?

A

Pulse oximeter: falsely ↑SaO2 in metHb and COHb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the co-oximeter read if there is a dyshemoglobinemia present?

A

Co-oximeter: accurately measures ↓SaO2 in metHb, COHb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical finding in hypoxia

A

Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define ischemia.

A

Ischemia: ↓arterial blood inflow and/or venous outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ischemia consequences

A

Ischemia consequences: atrophy, infarction, organ dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define hypoxemia.

A

Hypoxemia: ↓PaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define respiratory acidosis.

A

Respiratory acidosis: CO2 retention in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does ↑Alveolar PCO2 affect Alveolar PO2, PaO2 and SaO2?

A

↑Alveolar PCO2 = ↓Alveolar PO2 = ↓PaO2 = ↓SaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define ventilation defect.

A

Ventilation defect: lung perfused but not ventilated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give an example of a diffuse ventilation defect.

A

RDS: diffuse ventilation defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does a ventilation defect produce?

A

Ventilation defect: produces intrapulmonary shunting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a perfusion defect?

A

Perfusion defect: lung ventilated but not perfused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does a perfusion defect affect dead space?

A

Perfusion defect: ↑dead space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define diffusion defect.

A

Diffusion defect: ↓O2 diffusion thru alveolar-capillary interface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give two examples of diffusion defect.

A

Diffusion defect: interstitial fibrosis, pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define anemia.

A

Anemia: ↓Hb concentration; ↓O2 content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List four causes of anemia.

A

Anemia: ↓production Hb/RBCs; ↑destruction/sequestration RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does anemia affect PaO2, SaO2, and O2 content?

A

Anemia: normal Pao2/Sao2; ↓O2 content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define methemoglobinemia.

A

MetHb: heme Fe3+; cannot attach to O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is metHb reduced?

A

MetHb reduction: NADH electrons → cytochrome b5 → cytochrome b5 reductase → heme Fe2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List one cause of metHb.

A

MetHb: oxidant stresses (drugs, sepsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the pathogenesis of hypoxia in methemoglobinemia.

A

MetHb: heme Fe3+; normal PaO2, ↓SaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does methemoglobin affect the oxygen binding curve?

A

MetHb: shifts OBC to left; lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does oxygen administration affect cyanosis in methemoglobinemia?

A

MetHb: cyanosis is unresponsive to administration of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the treatment for methemoglobinemia and how does it work?

A

MetHb Rx: IV methylene blue; accelerates NADPH-methemoglobin reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the leading cause of death by poisoning?

A

Carbon monoxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

List three causes of CO poisoning.

A

↑CO: car exhaust, smoke inhalation, wood stoves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the pathogenesis of hypoxia in carbon monoxide poisoning.

A

CO: high affinity for heme groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the pathogenesis of hypoxia in CO poisoning.

A

COHb: inhibits cytochrome oxidase; left-shifted OBC; ↓SaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List two clinical findings in CO poisoning.

A

CO poisoning: headache, cherry-red discoloration (usually postmortem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List three lab findings in CO poisoning.

A

CO poisoning: normal PaO2, ↓SaO2, lactic acidosis (hypoxia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the treatment for CO poisoning?

A

Rx CO poisoning: 100% O2 via nonrebreather mask/endotracheal tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is 2,3-BPG and its role in the OBC?

A

2,3-BPG: glycolysis intermediate; stabilizes taut form Hb (↑release O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

List six causes of left-shifted OBC.

A

Left-shifted OBC: ↓2,3-BPG, CO, alkalosis, metHb, fetal Hb, hypothermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do COHb and MetHb affect SaO2, PaO2, and the OBC?

A

COHb and MetHb: ↓SaO2, normal PaO2, left-shifted OBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

List four causes of right-shifted OBC.

A

Right-shifted OBC: ↑2,3-BPG, fever, acidosis, high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does high altitude affect atmospheric pressure of O2 and percentage of atmospheric O2?

A

High altitude: ↓atmospheric pressure; normal % atmospheric O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the acid-base disturbance when at a high altitude?

How are 2,3-BPG levels and the OBC affected?

A

High altitude: hypoxemia/respiratory alkalosis; ↑2,3-BPG; right-shifted OBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name two electron donors in the oxidative pathway.

A

Oxidative pathway: transfer electrons from NADH, FADH2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does the phosphorylation pathway do?

A

Phosphorylation pathway: synthesis of ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do CO and CN affect the ETC?

A

CO and CN: inhibit cytochrome oxidase; ETC is shut down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

List two causes of CN poisoning.

A

CN poisoning: house fires (most common); excess nitroprusside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What two types of poisoning are seen in house fires?

A

CO + CN poisoning: house fires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the pathogenesis of hypoxia common to CO and CN poisoning?

A

CO + CN poisoning: shutdown of ETC prevents diffusion of O2 from blood to tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does the mixed venous O2 content compare to the arterial O2 content in CN poisoning?

A

CN poisoning: mixed venous O2 content similar to arterial O2 content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What enzyme is inhibited by CO and CN and what results?

A

CO and CN: inhibit cytochrome oxidase; lactic acidosis (hypoxia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe the treatment for CN poisoning?

A

Rx CN poisoning: based on high affinity of CN for metHb and cobalt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

List two uncouplers of oxidative phosphorylation.

A

Uncouplers: thermogenin (brown fat), dinitrophenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

The presence of dinitrophenol may result in what?

A

Dinitrophenol: danger of hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What does thermogenin do?

A

Thermogenin: stabilizes body temperature in newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

List two mitochondrial toxins. What do they do?

A

Mitochondrial toxins: alcohol, salicylates; act like “uncouplers”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

List two watershed areas in the body.

A

Watershed areas: cerebral arteries, mesenteric arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is a complication of global hypoxia?

A

Watershed infarction in brain: complication global hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where does ischemic colitis occur?

A

Ischemic colitis: splenic flexure at junction of superior/inferior mesenteric artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

ST-segment depression on ECG indicates what?

A

ST-segment depression ECG: subendocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

List two factors resulting in subendocardial ischemia.

A

Subendocardial ischemia: coronary artery atherosclerosis; cardiac hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

List two locations in the nephron that are susceptible to ischemia.

A

Nephron locations susceptible to hypoxia: proximal tubule in cortex; thick ascending limb medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which is the most adversely affected cell in tissue hypoxia?

A

Neurons: most adversely affected cell in tissue hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Which hepatocytes are most susceptible to hypoxia?

A

Zone III hepatocytes: most susceptible to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the primary source of ATP in hypoxia and what is the result?

A

Anaerobic glycolysis: primary ATP source in hypoxia; lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What does increased intracellular lactate do?

A

↑Intracellular lactate: acid pH denatures structural/enzymic proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What may lactic acidosis be a sign of?

A

Lactic acidosis: may be a sign of tissue hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What results from an impaired Na+/K+-ATPase?

A

Na+/K+-ATPase pump impaired (reversible): intracellular swelling (↑Na+ and H2O)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What results from an impaired Ca2+-ATPase pump?

A

Ca2+-ATPase pump impaired (irreversible): cannot pump Ca2+ out of cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are four lethal effects of increased cytosolic Ca2+?

A

↑Ca2+ in cytosol: activates phospholipase, protease, endonuclease, caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the effect of increased Ca2+ in mitochondria?

A

↑Ca2+ in mitochondria: ↑membrane permeability to cytochrome c → apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Define free radical?

A

FR: single unpaired electron in outer orbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What do free radicals do?

A

FRs: “steal” electrons from molecules, which become FRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do free radicals primarily target?

A

FRs: damage membranes and nucleic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe the relationship between free radical damage and age.

A

FR damage accumulates with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe two important roles of free radicals.

A

FRs important in microbial killing by leukocytes

FRs important in reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

List two transitional metals that generate hydroxyl free radicals.

A

Iron, copper: transitional metals that generate hydroxyl FRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the most destructive free radical?

A

Hydroxyl FR: most destructive FR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What produces superoxide free radicals?

A

Superoxide FRs: oxidase reactions; exposure to high O2 concentration
Superoxide FRs: NADPH oxidase in phagocyte cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

List two sources of nitric oxide free radical gas.

A

Nitric oxide FR gas: macrophages/endothelial cells; cigarettes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe the importance of oxidized LDL.

A

Oxidized LDL: FR important in atherogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe the enzymatic reaction performed by SOD.

A

SOD: neutralizes superoxide FRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What does glutathione peroxidase do?

A

Glutathione peroxidase: neutralizes H2O2, hydroxyl, NAPQ1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does catalase do?

A

Catalase: neutralizes H2O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What does vitamin E do?

A

Vitamin E: prevents FR injury of cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the best neutralizer of hydroxyl free radicals?

A

Vitamin C: best neutralizer of hydroxyl FRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What vitamin is reduced in smokers?

A

Smokers: ↓vitamin C levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What results from acetaminophen poisoning?

A

Acetaminophen poisoning: diffuse chemical hepatitis due to NAPQ1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Alcohol induces the synthesis of which cytochrome P450 isozyme resulting in what?

A

Alcohol: induces synthesis CYP2E1 isoenzyme
Alcohol: ↑CYP2E1 synthesis; ↑metabolism of alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the treatment for acetaminophen poisoning and what does it do?

A

N-Acetylcysteine: Rx acetaminophen poisoning; provides cysteine for GSH synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What may result from use of acetaminophen and NSAIDs?

A

Acetaminophen + NSAIDs: FR injury of kidneys; renal papillary necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is carbon tetrachloride and how does it become a free radical?

A

CCL4: solvent in dry cleaning; cytochrome P450 converts it into FR

91
Q

List three factors involved in reperfusion injury.

A

Reperfusion injury: superoxide FRs + ↑cytosolic Ca2+ + neutrophils

92
Q

Retinopathy of prematurity may result in the setting of RDS due to what?

A

Retinopathy prematurity in RDS: ↑superoxide FRs from O2 therapy

93
Q

How does iron overload affect free radical production?

A

Iron overload: ↑OH· FRs via Fenton reaction

94
Q

How does excess copper affect free radical production?

A

Excess copper: ↑OH· FRs via Fenton reaction; hepatotoxic/neurotoxic

95
Q

Salicylates and alcohol affect which cellular organelle resulting in what?

A

Salicylates, alcohol damage mitochondria; megamitochondria in hepatocytes

96
Q

Phenobarbital increases the synthesis of which cytochrome P450 isozyme resulting in what?

A

Phenobarbital: ↑CYP2B2 synthesis; converts drug to inactive metabolite

97
Q

Phenytoin increases the synthesis of which cytochrome P450 isozyme resulting in what?

A

Phenytoin: ↑CYP3A4 synthesis in cytochrome P450 system; ↑metabolism of phenytoin

98
Q

List two effects of SER hyperplasia.

A

SER hyperplasia: ↑drug metabolism; ↓drug effectiveness

99
Q

List two SER inhibitors.

A

SER inhibitors: proton/histamine H2-receptor blockers; histamine receptor blockers

100
Q

List two effects of SER inhibition.

A

SER inhibition: ↓drug metabolism; drug toxicity

101
Q

Where are hydrolytic enzymes that are synthesized in the RER transported? Once there, what happens to these enzymes?

A

Hydrolytic enzymes undergo posttranslational modification in Golgi apparatus

102
Q

Describe the posttranslational modification of hydrolytic enzymes.

A

Phosphotransferase attaches P to mannose residues on enzymes → mannose 6-P

103
Q

Describe what occurs following posttranslational modification of lysosomal enzymes.

A

Mannose 6-P on lysosomal enzyme attaches to receptors on Golgi membrane

104
Q

Describe what occurs after vesicles containing receptor-bound lysosomal enzymes pinch off the Golgi apparatus.

A

Vesicles pinch off Golgi membrane → deliver enzymes to lysosomes; some vesicles return to Golgi

105
Q

What does the phagolysosome contain?

A

Phagolysosome: contains lysosomal enzymes

106
Q

What is inclusion-(I) cell disease and which enzyme is affected?

A

I-cell disease: defect in posttranslational modification lysosomal enzymes; deficient phosphotransferase

107
Q

What is lysosomal storage disease?

A

Lysosomal storage disease: ↓lysosomal enzymes; accumulation of complex substrates

108
Q

What is Chediak-Higashi Syndrome?

A

CHS: giant lysosomal granules (fusion defect); defect in formation of phagolysosomes

109
Q

What is the cytoskeleton composed of?

A

Cytoskeleton: microtubules, actin filaments, intermediate filaments

110
Q

Which two chemotherapeutic agents inhibit the synthesis of tubulin? What phase of the cell cycle is affected?

A

G2 phase defects: etoposide, bleomycin

111
Q

Name three compounds that cause mitotic spindle defects.

A

Mitotic spindle defects: vinca alkaloids, colchicine, paclitaxel

112
Q

What is ubiquitin?

A

Ubiquitin: marker for damaged intermediate filaments

113
Q

What are Mallory and Lewy bodies?

A

Mallory and Lewy bodies: ubiquinated keratin/neurofilament intermediate filaments, respectively

114
Q

What is the most common cause of fatty change in the liver?

A

Alcohol: most common cause of fatty change

115
Q

What is packaged in the VLDL fraction?

A

VLDL: liver-synthesized TGs

116
Q

What is the carbohydrate substrate for TG synthesis?

A

G3-P: carbohydrate substrate for TG synthesis

117
Q

What are the two functions of apoB-100?

A

ApoB-100: helps form VLDL and secrete VLDL from liver into blood

118
Q

How does kwashiorkor affect TG synthesis?

A

Kwashiorkor: ↑CHO → ↑DHAP → ↑G3-P → ↑TG synthesis

119
Q

How does alcohol affect TG synthesis?

A

Alcohol: ↑NADH → ↑conversion DHAP to G-3P → ↑synthesis TG

120
Q

How does alcohol affect FA synthesis in the liver?

A

Alcohol: ↑acetyl CoA → ↑synthesis FAs in liver

121
Q

List three effects alcohol has on FA.

A

Alcohol: ↑FAs → ↑synthesis, ↑mobilization from adipose; ↓β-oxidation FAs in mitochondria

122
Q

In kwashiorkor, how is apoB-100 affected and what results?

A

Kwashiorkor: ↓protein intake → ↓apoB-100 → ↓packaging/secretion of VLDL

123
Q

How does fatty liver affect TG and VLDL?

A

Fatty liver: ↑synthesis TG; ↓packaging/secretion VLDL

124
Q

What is ferritin?

A

Ferritin: soluble iron-binding protein in macrophages

125
Q

Where is ferritin synthesized?

A

Ferritin: synthesized in macrophages and hepatocytes

126
Q

What is a decrease in serum ferritin an indicator of?

A

Serum ferritin: ↓in iron deficiency anemia

127
Q

What is hemosiderin? What stains hemosiderin positive?

A

Hemosiderin: ferritin degradation product; Prussian blue positive

128
Q

What is dystrophic calcification?

A

Dystrophic calcification: calcification of necrotic (damaged) tissue

129
Q

What is the relationship between dystrophic calcification and serum calcium and phosphate levels?

A

Dystrophic calcification: serum calcium and phosphate are normal

130
Q

What is metastatic calcification?

A

Metastatic calcification: calcification of normal tissue

131
Q

What is the relationship between metastatic calcification and serum calcium and phosphate levels?

A

Metastatic calcification: ↑serum calcium and/or phosphate

132
Q

What is nephrocalcinosis and what does it produce?

A

Nephrocalcinosis: metastatic calcification of collecting ducts; produces diabetes insipidus

133
Q

What is atrophy?

A

Atrophy: ↓size/weight of tissue or organ

134
Q

List four causes of atrophy.

A

Atrophy: ↓hormone stimulation, ↓innervation, ↓blood flow, ↓nutrients

135
Q

What does increased luminal pressure result in? Which two organs may be affected?

A

Atrophy: ↑luminal pressure → compression atrophy (pancreas, kidney)

136
Q

What occurs during autophagy?

A

Autophagy: vacuoles with organelles fuse with lysosomes; enzyme degradation of organelles

137
Q

What is brown atrophy?

A

Brown atrophy: ↑lipofuscin in cells (undigested lipid)

138
Q

List two mechanisms of atrophy.

A

Atrophy: cell shrinkage (loss of cytosol/organelles); apoptosis

139
Q

What is hypertrophy?

A

Hypertrophy: ↑cell size

140
Q

What does cardiac muscle hypertrophy occur in response to?

A

Cardiac muscle hypertrophy: ↑preload (↑volume in ventricle) or ↑afterload (↑resistance ventricle must contract against)

141
Q

What occurs to the remaining kidney postnephrectomy?

A

Remaining kidney postnephrectomy: undergoes compensatory hypertrophy

142
Q

Why does CMV hypertrophy of the cell occur?

A

CMV hypertrophy of cell: due to ↑iron uptake causing ↑cell growth

143
Q

What is hyperplasia?

A

Hyperplasia: ↑number of cells

144
Q

Give an example of hyperplasia due to increased hormone stimulation.

A

↑Hormone stimulation: estrogen → endometrial hyperplasia

145
Q

Give an example of hyperplasia due to increased hormone sensitivity.

A

↑Hormone sensitivity: DHT → prostate hyperplasia

146
Q

Give three examples of chronic irritation resulting in hyperplasia.

A

Chronic irritation: skin thickening (scratching), bronchial mucous gland hyperplasia (smokers), regenerative nodules in cirrhosis (alcohol excess)

147
Q

List an example of chemical imbalance resulting in hyperplasia.

A

Chemical imbalance: ↓serum Ca2+ → parathyroid gland hyperplasia

148
Q

How does iodine deficiency affect the thyroid?

A

Iodine deficiency → goiter (hyperplasia/hypertrophy)

149
Q

Give an example of hyperplasia resulting from stimulating antibodies.

A

Hyperplasia stimulating antibodies: Graves disease

150
Q

Give an example of hyperplasia resulting from a viral infection.

A

Hyperplasia: HPV → epidermal hyperplasia (common wart)

151
Q

What must be true for hyperplasia to occur?

A

Hyperplasia only occurs if cells can enter the cell cycle

152
Q

What do labile cells do? Give an example of labile cells.

A

Labile cells: continuously divide; e.g., stem cells in bone marrow

153
Q

What are stable cells? Give two examples of stable cells.

A

Stable cells: resting cells in G0 phase cell cycle; e.g., hepatocytes, smooth muscle cells

154
Q

Permanent cells cannot do what? Give three examples of permanent cells.

A

Permanent cells: cannot divide; e.g., neurons, skeletal/cardiac muscle

155
Q

There is the risk of what in hyperplasia? Give two examples.

A

Cancer risk in hyperplasia: endometrial hyperplasia, regenerative nodules in cirrhosis

156
Q

What is metaplasia?

A

Metaplasia: one adult cell type replaces another

157
Q

Give an example of squamous to glandular epithelium.

A

Squamous to glandular epithelium: acid reflux distal esophagus (Barrett esophagus)

158
Q

Give an example of glandular to other glandular epithelium.

A

Glandular to other glandular epithelium: atrophic gastritis due to Helicobacter pylori

159
Q

Give two examples of glandular to squamous epithelium.

A

Glandular to squamous epithelium: bronchus in smoker; endocervix

160
Q

Give an example of transitional to squamous epithelium.

A

Transitional to squamous epithelium: Schistosoma haematobium infection of urinary bladder

161
Q

What is mesenchymal metaplasia?

A

Mesenchymal metaplasia: bone developing in area of muscle trauma

162
Q

What is the mechanism of metaplasia?

A

Mechanism: reprogramming stem cells to utilize progeny cells with different gene expression

163
Q

List three examples of stimuli for reprogramming in metaplasia.

A

Stimuli for reprogramming: hormones (estrogen), vitamins (retinoic acid), chemicals (cigarette smoke)

164
Q

There is the risk of developing what in the setting of metaplasia and hyperplasia? The risk greater in metaplasia or hyperplasia?

A

Metaplasia and hyperplasia: risk for developing dysplasia; metaplasia > hyperplasia

165
Q

What is dysplasia?

A

Dysplasia: disordered cell growth

166
Q

List two risk factors for developing dysplasia.

A

Risk factors: endometrial hyperplasia; Barrett esophagus

167
Q

List one risk factor for developing dysplasia related to infection.

A

Risk factor: HPV -> squamous dysplasia cervix

168
Q

List one risk factor for developing dysplasia related to chemicals.

A

Risk factor: cigarette smoke -> squamous dysplasia bronchus

169
Q

Name the type of dysplasia related to UV light.

A

Risk factor: UV light -> squamous dysplasia

170
Q

List one risk factor of dysplasia related to chronic skin irritation.

A

Risk factor: chronic skim irritation (3rd degree burn) -> squamous dysplasia

171
Q

What may dysplasia progress to?

A

Dysplasia may progress to cancer.

172
Q

How does dysplasia affect cell proliferation and mitotic activity?

A

Dysplasia: disorderly proliferation of cells;↑mitotic activity

173
Q

What three types of epithelium may be affected by dysplasia?

A

Dysplasia: may involve squamous, glandular, transitional epithelium

174
Q

What is necrosis?

A

Necrosis: death of groups of cells + inflammation

175
Q

What is coagulation necrosis?

A

Coagulation necrosis: preservation of structural outlines

176
Q

List three causes of coagulation necrosis due to denaturation of enzymes and structural proteins.

A

Coagulation necrosis: ↑intracellular lactic acid; ionizing radiation; heavy metals

177
Q

Name one microscopic feature of coagulation necrosis.

A

Coagulation necrosis: indistinct cell outlines in dead tissue

178
Q

What is an infarction?

A

Infarction: gross manifestation of coagulation necrosis

179
Q

Name two types of infarction.

A

Infarctions: pale and hemorrhagic types

180
Q

Pale infarctions are seen in what type of tissue? List three organs that may be affected by a pale infarction.

A

Pale infarctions: dense tissue; heart, kidney, spleen

181
Q

Hemorrhagic infarctions occur in what type of tissue? List three organs that may be affected by a hemorrhagic infarction.

A

Hemorrhagic infarctions: loose tissue; lung, bowel, testicle

182
Q

What type of necrosis is present in the setting of dry gangrene?

A

Dry gangrene: predominantly coagulation necrosis

183
Q

What is likely if a thrombus overlies an atherosclerotic plaque in a coronary artery?

A

Infarction likely if thrombus overlies atherosclerotic plaque in coronary artery

184
Q

Name two scenarios in which an infarction is less likely.

A

Infarction less likely: dual blood supply (lungs), collateral circulation (arcade system in superior/inferior mesenteric arteries)

185
Q

In what two scenarios are infarctions more likely?

A

Infarctions more likely: preexisting disease in tissue; end arteries

186
Q

Describe the mechanism by which liquefactive necrosis occurs.

A

Liquefactive necrosis: lysosomal enzyme destruction tissue by neutrophils

187
Q

What type of necrosis occurs in the setting of cerebral infarction?

A

Cerebral infarction: liquefactive not coagulative necrosis (exception to the rule)

188
Q

What type of necrosis occurs in a bacterial abscess?

A

Bacterial abscess: liquefactive necrosis

189
Q

Wet gangrene is predominantly what type of necrosis?

A

Wet gangrene: predominantly liquefactive necrosis

190
Q

Caseous necrosis is a variant of what type of necrosis?

A

Caseous necrosis: variant of coagulation necrosis

191
Q

What is responsible for the cheesy appearance of granulomas?

A

Lipid from cell wall Mycobacterium/systemic fungi → cheesy appearance in granulomas

192
Q

What is the most common cause of caseous necrosis?

A

Tuberculosis: most common cause of caseous necrosis

193
Q

Gummatous necrosis is what type of necrosis and is associated with what type of disease?

A

Gummatous necrosis: type of coagulation necrosis; associated with spirochetal disease (e.g., syphilis)

194
Q

What are the two most common sites for gummas?

A

Gummas: skin, bone most common sites

195
Q

Acute pancreatitis is associated with what type of necrosis?

A

Enzymatic fat necrosis: acute pancreatitis

196
Q

What occurs during saponification? What commonly occurs in areas of saponification?

A

Saponification: calcium combined with fatty acids; dystrophic calcification

197
Q

Trauma of fat tissue is related to what type of necrosis? Is this type of necrosis enzyme-mediated?

A

Traumatic fat necrosis: related to trauma of fat tissue; not enzyme-mediated

198
Q

What mediates fibrinoid necrosis?

A

Fibrinoid necrosis: necrosis of immune-mediated disease

199
Q

What is apoptosis?

A

Apoptosis: programmed cell death

200
Q

List four examples of normal destruction of cells during embryogenesis.

A

Embryogenesis: MIS → apoptosis müllerian structures male Embryogenesis: lost tissue between fingers/toes; shaping inner ear; cardiac morphogenesis

201
Q

How does a drop in estrogen and progesterone affect endometrial tissue?

A

Drop in estrogen/progesterone → menses

202
Q

How does a decrease in stimulating hormones affect the target tissue?

A

↓Stimulating hormones → atrophy of target tissue

203
Q

What occurs to the thymus with increasing age?

A

Normal involution of thymus

204
Q

Cytotoxic CD8 T cells target which two cell types resulting in what?

A

death tumor cells/virus infected cells by cytotoxic CD8 T cells

205
Q

Corticosteroids destroys what two cell types? What is its role in acute inflammation?

A

Corticosteroid destroys B/T cells; removes acute inflammatory cells in acute inflammation

206
Q

List three things that damage DNA resulting in apoptosis.

A

DNA damaged by radiation/FRs/toxins

207
Q

Apoptosis is associated with the removal with what type of proteins?

A

misfolded proteins removed

208
Q

Defects in apoptosis can lead to what two types of diseases?

A

Defects in apoptosis → cancer, autoimmune disease

209
Q

What does the extrinsic pathway of apoptosis require?

A

Extrinsic pathway of apoptosis: requires TNF-α

210
Q

What does TNF-alpha activate?

A

TNFR1 is a death receptor activated by TNF-α

211
Q

What is the main source of TNF-alpha? What other cell types produce TNF-alpha?

A

TNF-α: produced by macrophages (main source); endothelial and cardiac cells, and neurons

212
Q

What does TNFR1 binding with TNF-alpha activate?

A

TNFR1 binding with TNF-α activates initiator caspases 8 and 10

213
Q

What do initiator caspases activate?

A

Caspases: initiator caspases activate effector caspases (proteases, endonucleases)

214
Q

Which is the most important of the two pathways of apoptosis?

A

Intrinsic pathway of apoptosis: most important of the two pathways

215
Q

Name the genes and gene types of the BCL gene family.

A

BCL gene family: antiapoptotic genes (BCL-2 gene) and antiapoptotic genes (BAX, BAK genes)

216
Q

What type of gene is BCL-2 and what does it do?

A

BCL-2 gene: antiapoptosis gene; protein maintains mitochondrial membrane integrity to prevent leakage of cytochrome c

217
Q

What does BAK/BAX activation result in?

A

BAX/BAK activation: mitochondrial channels in membrane leak cytochrome c into cytosol

218
Q

Once leaked into the cytosol, what does cytochrome c do?

A

Cytochrome c → activates caspases in cytosol → apoptosis

219
Q

Once activated, what is the role of effector caspases?

A

Proteases destroy cytoarchitecture, endonucleases destroy nucleus

220
Q

In apoptosis, what do cytoplasmic buds contain?

A

Cytoplasmic buds contain nuclear/mitochondrial/other organelle fragments

221
Q

What do cytoplasmic buds do and become?

A

Cytoplasmic buds separate from membrane → apoptotic bodies

222
Q

What happens to apoptotic bodies?

A

Apoptotic bodies phagocytosed by neighboring cells/macrophages

223
Q

Describe three microscopic features of apoptosis?

A

Apoptosis: deeply eosinophilic cytoplasm; pyknotic nucleus; minimal inflammation

224
Q

What is pyroptosis?

A

Pyroptosis: proinflammatory cell death using caspase-1

225
Q

In pyroptosis, what three cell types and what three microbial pathogens may be destroyed?

A

Pyroptosis: monocyte/macrophage/dendritic cell destruction Salmonella, Shigella, Legionella

226
Q

Pyroptosis has been implicated in the pathogenesis of what five diseases?

A

Pyroptosis: MI, neurodegenerative disease, IBD, cerebral ischemia, endotoxic shock

Rapid Review Pathology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions