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Pathology 1 > Ch 1 - Disease At Cell Level > Flashcards

Ch 1 - Disease At Cell Level Flashcards

0
Q

What is atrophy?

A

Wasting of tissues, organs, or entire body as from death and reabsorption of cells
Lessened function

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0
Q

Necrosis vs apoptosis: nuclear changes?

A

Necrosis = pyknosis ->karyorrhexis -> karyolysis Apoptosis = nucleosome size fragments

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1
Q

What is hypertrophy?

A

Increase in SIZE of cells

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2
Q

What is hyperplasia?

A

Increase in NUMBER of cells (excluding tumor formation)

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2
Q

Necrosis vs apoptosis: Plasma membrane?

A

Necrosis = Disrupted Apoptosis = Intact/altered

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3
Q

What is hypoplasia?

A

Incomplete development of organ or tissue

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3
Q

Necrosis vs apoptosis: Cell contents?

A

Necrosis = Enzymatically digested Apoptosis = Intact

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4
Q

What is metaplasia?

A

Reversible replacement of one differentiated cell type with another mature differentiated cell type

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4
Q

Necrosis vs apoptosis: Adjacent inflammation?

A

Necrosis = Frequent Apoptosis = NO

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5
Q

What is Barrett’s esophagus?

A

Example of metaplasia - squamous mucosa grows into esophagus

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5
Q

Necrosis vs apoptosis: Physiological or pathological?

A

Necrosis = Pathologic ONLY Apoptosis = Often physiological (can be pathologic)

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6
Q

What is anaplasia?

A

Change in structure of cells and change in their orientation to each other

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6
Q

Seven causes of cell injury?

A
  1. O2 deprivation 2. Physical agents 3. Chemical agents/drugs 4. Infectious agents 5. Immunilogic reactions 6. Genetic derangements 7. Nutritional imbalances
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7
Q

What is aplasia?

A

Defective development or congenital absence of organ or tissue

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7
Q

5 biochemical mechanisms of cell injury?

A
  1. ATP depletion 2. Mitochondrial damage 3. High intracellular Ca2+ 4. O2 deprivation and O2-derived free radicals 5. Defects in membrane permeability
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8
Q

What is dysplasia?

A

Abnormal tissue growth with loss of cell orientation, shape, and size

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8
Q

Hypoxia vs ischemia?

A

Hypoxia = inadequate oxygenation Ischemia = loss of blood supply

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9
Q

Which cellular pathology is pre-cancerous?

A

Dysplasia

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9
Q

What is MPT?

A

Mitochondrial Permeability Transition (leakage of cytochrome C into the cytosol)

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10
Q

What happens when the limits of adaptive responses are exceeded?

A

Cell injury

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10
Q

What is the outcome of decreased ATP due to cell injury?

A

Increased glycolysis -> Decreased glycogen, decreased pH => clumping of nuclear chromatin

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11
Q

What are the two types of cell injury?

A

Reversible and irreversible

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11
Q

Why does decreased ATP cause decreased pH?

A

Use anaerobic respiration, produces LACTIC ACID

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12
Q

Cell swelling reversible vs irreversible injury?

A 
Reversible = generalized cell swelling
Irreversible = increased swelling
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12
Q

What causes free radical formation in the ER?

A

P-450 oxidases, B5 oxidases

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13
Q

Which type of cell injury has blebs?

A

Reversible

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13
Q

What causes free radical formation in the mitochondria?

A

P-450 oxidases, B5 oxidases, respiratory chain oxidation

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14
Q

Which type of cell injury has swelling of the ER?

A

Both

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14
Q

What causes free radical formation in the plasma membrane?

A

NADPH oxidase

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15
Q

Which type of cell injury has ribosome detachment from ER?

A

Reversible

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15
Q

What causes free radical formation in the cytosol?

A

Xanthine oxidase, transition metals (Cu, Fe)

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16
Q

What happens to the mitochondria in reversible cell injury?

A

Swelling

Decreased oxidative phosphorylation => decreased ATP synthesis

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16
Q

What causes free radical formation in the peroxisomes?

A

Multiple oxidases

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17
Q

What happens to the mitochondria in irreversible cell injury?

A

Swollen with amorphous densities (vacuolization)

Ca2+ influx due to membrane permeability

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17
Q

What causes free radical formation in the lysosomes?

A

Myeloperoxidases, NO synthase

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18
Q

What happens to nuclear chromatin in reversible cell injury?

A

Clumping

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18
Q

What are the 4 oxygen derived free radicals?

A

Hydrogen Peroxide, superoxide, hydroxyl radical, nitric oxide

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19
Q

What happens to nucleus in irreversible injury?

A

Condensation (pyknosis) -> fragmentation (karyorrhexis) -> nucleus dissolution (karyolysis)

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19
Q

How do free radicals cause cell injury?

A

Peroxidation of membrane lipids, DNA fragmentation, and/or protein cross-linking and fragmentation

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20
Q

Which type of cellular injury causes lysosome swelling and rupture?

A

Irreversible

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20
Q

How is superoxide neutralized?

A

Superoxide dismutase (SOD)

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21
Q

Which type of cell injury has low intracellular pH?

A

Both

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21
Q

How is hydrogen peroxide neutralized?

A

Catalase

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22
Q

What would you see under light microscopy with reversible cell injury?

A

Fatty change (steatosis)

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22
Q

How is hydroxyl radical neutralized?

A

Converted to H2O2 (2GSH –> GSSG using glutathione peroxidase)

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23
Q

What would you see under light microscopy with irreversible cell injury?

A

Calcification

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23
Q

What is used for free radical neutralization in membranes?

A

Vit. E + A, beta-carotene

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24
Q

Is nuclear clumping the same as nuclear condensation?

A

NO

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24
Q

What is used for free radical neutralization in mitochondria?

A

SOD, glutathione peroxidase

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25
Q

What are blebs?

A

Outpouchings of plasma membrane

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25
Q

What is used for free radical neutralization in Peroxisomes?

A

Catalase

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26
Q

What is the ultimate result of cell injury?

A

Cell death

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26
Q

What is used for free radical neutralization in the cytosol?

A

SOD, Vit. C, glutathione peroxidase, Ferritin, Cerucoplasmin, Quercitin

27
Q

What is necrosis?

A

Cell death

27
Q

How is free radical injury initiated?

A

radiation exposure, metabolism of drugs, redox reaction, nitric oxide, transition metals, leukocyte oxidative burst

28
Q

What is apoptosis?

A

Programmed cell death

28
Q

How is free radical degradation produced?

A

enzymes, spontaneous decay, antioxidants

29
Q

What enzyme do you check for in serum for MI?

A

Serum CK-MB

29
Q

What is a major cause of injury after thrombolytic therapy?

A

Reperfusion after anoxia

30
Q

Necrosis vs apoptosis: cell size?

A

Necrosis=enlarged

Apoptosis = reduced

30
Q

What are the 2 categories of toxins?

A

Direct and indirect

31
Q

What are the subcellular responses to injury?

A

Induction (hypertrophy) of smooth ER, lysosomal catabolism, mitochondrial alterations, cytoskeletal abnormalities

32
Q

What is the function of P-450 oxidases?

A

Neutralize toxins in liver (but produce free radicals)

33
Q

What are the mitochondrial alterations with cellular hypertrophy?

A

Increased number (due to increased cellular processes)

34
Q

What are the mitochondrial alterations with cellular atrophy?

A

Decreased number

35
Q

What are the mitochondrial alterations with nutrient deficiency or EtOH liver disease?

A

Increased size (megamitochondria)

36
Q

What is impaired (cytoskeleton) with cell injury?

A

Intracellular organelle/molecular transport, basic cell architecture/shape/polarity, signals to nucleus, tissue integrity/mechanical strength, cellular mobility, phagocytosis (SCAFFOLD/STRUCTURAL IMPAIRMENTS)

37
Q

What are the roles of heat shock proteins (HSPs)?

A
  1. Protein folding 2. Disaggregation of protein-protein complexes 3. Protein transport to cell organelles (CHAPERONES)
38
Q

Where does coagulative necrosis occur?

A

Heart, liver, kidney

39
Q

What is coagulative necrosis the result of?

A

Protein denaturation

40
Q

What is coag. Necrosis characteristic of?

A

Hypoxic death

41
Q

Is cell outline preserved in coag. Necrosis?

42
Q

Where does liquefactive necrosis occur?

43
Q

What is liq. Necrosis a result of ?

A

Enzymatic digestion

44
Q

What is liq. Necrosis characteristic of ?

A

bacterial infection, or hypoxic death w/in CNS (stroke)

45
Q

Is the basic architecture of cells preserved in liq. Necrosis?

A

NO - obliterated

46
Q

Where does gangrenous necrosis occur?

A

limbs, GI tract

47
Q

What is gangrenous necrosis?

A

Loss of blood supply & coag. Necrosis

48
Q

What causes wet gangrene?

A

Coag. Necrosis plus liquefactive action of bacterial infection and attracted leukocytes

49
Q

What is caseous necrosis characteristic of?

A

Tuberculosis

50
Q

What is caseous necrosis?

A

a distinct form of coag. Necrosis

51
Q

Is tissue architecture preserved with caseous necrosis?

A

NO - obliterated

52
Q

What is seen microscopically with caseous necrosis?

A

amorphous granular debris of fragmented coag. Cell, enclosed w/in distinctive inflammatory border

53
Q

Where does fat necrosis occur?

54
Q

What is fat necrosis?

A

Focal area of fat destruction (usually due to lipase release from pancreas)

55
Q

What happens when fat necrosis combines with Ca2+?

A

Create grossly visible chalky areas

56
Q

What is seen microscopically with fat necrosis?

A

Foci of shadowy outlines of fat cells w/ basophilic Ca2+ deposits, surrounded by inflammatory reaction

57
Q

Where does fibrinoid necrosis occur?

A

Blood vessels

58
Q

When does apoptosis occur?

A

embryogenesis, hormone induction (menstruation), immune cell-mediated death, injurious stimuli, regulation of cell pop. And tumor suppression, atrophy

59
Q

What needs to be activated to initiate apoptosis?

A

Execution caspases

60
Q

What do execution caspases do?

A

Activate endonucleases and induce catabolism of cytoskeleton

61
Q

What do endonucleases do?

A

DNA fragmentation

62
Q

What do catabolism of cytoskeleton and DNA fragmentation lead to in apoptotic pathways?

A

Formation of cytoplasmic bud

63
Q

What does the cytoplasmic bud become in apoptosis?

A

Apoptotic body

64
Q

What happens to apoptotic bodies?

A

Phagocytosed by macrophages

65
Q

What allows for cytochrome c to leak into cytosol in intrinsic apoptosis pathway?

66
Q

What does cytochrome C do in the cytosol in intrinsic apoptosis p/way?

A

Activates caspases

67
Q

How is extrinsic apoptosis pathway initiated?

A

Fas Ligand brings several Fas “death domains” in proximity -> Fas-associated death domain -> autocatalytic caspase activation

68
Q

What are 4 general mechanisms for intracellular accumulations?

A
  1. Abnormal metabolism (eg fatty change in liver) 2. Mutations causing alterations in protein folding and transport => defective molecules accumulate 3. Enzyme deficiencies = unable to break down compounds => accumulation in LYSOSOMES 4. inability to degrade phagocytosed particles
69
Q

Where does intracellular accumulation of lipids usually occur?

A

Usually liver, also heart, muscles, kidney

70
Q

What is steatosis?

A

abnormal TG accumulation in parenchymal cells

71
Q

What is steatosis commonly caused by?

A

EtOH abuse, toxins, protein malnutrition, DM, obesity, anorexia

72
Q

What is alcohol dehydrogenase used for?

A

Interconversion between alcohols and aldehydes/ketones

73
Q

What is the appearance of cholesterol accumulation microscopically?

A

“Foamy” appearance due to phagocytes

74
Q

Examples of cholesterol accumulations?

A

Atherosclerosis, xanthomas, inflammation, cholesterolosis, Niemann-Pick disease type C

75
Q

What are reabsorption droplets?

A

protein accumulations in proximal renal tubules (kidney disease w/ protein loss)

76
Q

What are Russell bodies?

A

protein accumulations in distended ER with large eosinophilic inclusions

77
Q

What is amyloidosis?

A

aggregation of abnormal proteins

78
Q

Examples of diseases involving protein accumulation?

A

Alzheimers, Huntington’s, Parkinson’s, maybe DM2

79
Q

What supplement is used to “clean up clutter” in the brain in protein accumulation diseases?

A

Glutathione

80
Q

What is “hyaline change” in regards to intracellular accumulations?

A

Variety of alteration - NOT a specific pattern of accumulation

81
Q

Microscopic appearance of hyaline change?

A

homogenous, glassy, pink appearance

82
Q

Intracellular examples of hyaline change?

A

reabsorption droplets, Russell bodies, Mallory alcoholic hyalin

83
Q

Extracellular examples of hyaline change?

A

collagenous/fibrous tissue (old scars), arterial wall hyalinization (HBP or DM2)

84
Q

What is the appearance of glycogen accumulation?

A

Clear vacuoles w/in cytoplasm

85
Q

What are the causes of glycogen accumulation (2)?

A

Glucose metabolism disorders (DM), Genetic disorders (glycogen storage diseases)

86
Q

What are 2 examples of exogenous pigment accumulations?

A

Carbon (coal), tattooing

87
Q

What are 3 examples of endogenous pigment accumulation?

A

Lipofuscin (lipid peroxidation), melanin (eg. Alkaptonuria), Hemosiderin (hemoglobin derived: stored/eaten)

88
Q

What is anthracosis?

A

Coal worker’s pneumoconiosis (exogenous pigment accumulation)

89
Q

What are the 2 types of pathologic calcification?

A

Dystrophic and metastatic

90
Q

Where is calcium deposited in dystrophic calc.?

A

Locally in DYING tissue

91
Q

What is the serum calcium level with dystrophic calc.?

92
Q

Is there calcium metabolism pathology with dystrophic calc.?

93
Q

Examples of dystrophic calcification?

A

atherosclerosis of arteries, damaged heart valves

94
Q

Where is calcium deposited in metastatic calcification?

A

In NORMAL tissue

95
Q

What is serum calcium level with metastatic calc.?

96
Q

What is metastatic calcification usually due to?

A

Secondary hypercalcemia

97
Q

What are the 4 principle causes of metastatic calc.?

A
  1. increased PTH 2. Bone destruction (multiple myeloma, Paget disease) 3. Vit. D related (toxicity, sarcoidosis) 4. Renal failure (PO4 retention)
98
Q

What does metastatic calc. principally affect?

A

Interstitial tissues of vasculature, kidneys, lungs, gastric mucosa

99
Q

What is multiple myeloma?

A

Widespread lucencies in bone

100
Q

What is distinctive to mult. Myeloma on x-rays?

A

Lucent, elliptical, subcortical shadows, especially in long bones = endosteal scalloping

Pathology 1 (6 decks)

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