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MAD Exam 1 > Intro to Pathology > Flashcards

Intro to Pathology Flashcards

1
Q

general mechanisms of cell injury

A

-disruption of metabolism
-inflammatory processes
-infectious diseases
-diseases of immunity
-environmental injury
-neoplasia
-genetic disorders

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2
Q

adaptations as a cellular response are reversible, and include:

A

-atrophy
-hypertrophy
-hyperplasia
-metaplasia

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3
Q

hypertrophy

A

increased size of an organ/tissue caused by an increase in SIZE of cells

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4
Q

pathogenesis of hypertrophy

A

increased synthesis of cellular components → increase in cell SIZE

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5
Q

example of physiologic hypertrophy

A

uterus enlarging during pregnancy

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6
Q

example of pathologic hypertrophy

A

*left ventricular hypertrophy and cardiomyopathy
(clinical correlation: compromises cardiac function)

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7
Q

hyperplasia

A

increased size of an organ/tissue caused by an increased NUMBER of cells

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8
Q

pathogenesis of hyperplasia

A

increased mitotic activity/cell division → increased NUMBER of cells

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9
Q

example of physiologic hyperplasia

A

female breast exhibits hyperplasia during lactation for increased functional capacity

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10
Q

example 2 of physiologic hyperplasia

A

compensatory hyperplasia of the liver as a result of liver damage (increased mass following damage or loss)

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11
Q

examples of pathologic hyperplasia

A

-benign prostatic hyperplasia
-endometrial hyperplasia
-gynecomastia (breast growth in males)
-verruca plantaris (plantar warts)

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12
Q

dysplasia

A

disordered hyperplasia (can result from pathologic hyperplasia or metaplasia and can turn into neoplasia)

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13
Q

atrophy

A

decreased size of an organ/tissue caused by a decrease in mass of cells (size and/or number)

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14
Q

pathogenesis of atrophy

A
  1. reduction of cellular components
  2. loss of cells (apoptosis)
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15
Q

example of pathologic atrophy

A

alzheimers (results in loss of parenchyma)
cachexia (loss of adipose)
atrophic gastritis (antibodies attacking cells that make intrinsic factor - parietal cells)

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16
Q

metaplasia

A

replacement of one differentiated tissue by another (reprogramming of a cell to make a diff type of cell)

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17
Q

pathogenesis of metaplasia

A

*reprogrammed stem cells (persistent influences leading to metaplasia may induce neoplasia)
*usually due to exposure to an irritant (gastric acid, tobacco smoke, etc)

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18
Q

example of pathologic metaplasia

A

Barrett’s esophagus (making goblet cells in esophagus to protect from chronic acid reflux)

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19
Q

principles of cell injury

A
  1. injury depends on cause (duration, dose, type)
  2. injury depends on the cell’s specific response (cells respond differently to different things)
  3. injury results from functional abnormalities in one or more interconnected cellular components
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20
Q

top etiologies of cell injury

A
  1. oxygen deprivation (hypoxia or ischemia)
  2. chemicals
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21
Q

roles/functions of mitochondria in cell injury

A

decreased ATP production, high conductance channels, and leakage of cytochrome c into cytoplasm

22
Q

roles/functions of ATP depletion in cell injury

A
  1. reduced plasma membrane energy-dependent pumps (loss of Na+/K+ ATPase leads to cell swelling and ER dilation)
  2. altered cell metabolism (reliance on glycolysis and increased lactic acid)
  3. reduced protein synthesis
  4. unfolded protein responses
  5. mitochondrial membrane damage
23
Q

roles/functions of calcium in cell injury

A

*important mediator of cell injury (cell injury leads to influx of calcium)
*increased calcium in the cell causes enzymes to function, even when they shouldn’t be on

24
Q

roles/functions of free radicals in cell injury

A

molecules with unpaired electrons that, pathologically, disrupt macromolecules

25
Q

free radical generation physiologically

A

red-ox reactions and fenton reactions

26
Q

free radical generation pathologically

A

radiant energy, inflammatory oxidative bursts, enzymatic metabolism of exogenous chemicals/drugs, nitric oxide

27
Q

antioxidants

A

block initiation and scavenge free radicals
ex. vitamins E and A; ascorbic acid; glutathione

28
Q

enzymatic inactivation of ROS

A
  1. superoxide dismutase
  2. catalase
  3. glutathione peroxidase
29
Q

superoxide dismutase

A

*an antioxidant enzyme that catalyzes the conversion of superoxide to hydrogen peroxide
*converts superoxide anion and H+ into hydrogen peroxide and oxygen: 2O2*− + 2H+ → H2O2 + O2

30
Q

catalase

A

*an antioxidant enzyme that catalyzes the decomposition of hydrogen peroxide to water and oxygen
*converts hydrogen peroxide (H2O2) to oxygen and water: 2H2O2 → 2H2O + O2

31
Q

glutathione peroxidase

A

*an antioxidant enzyme that converts hydroxy radical and GSH to water and GSSG: 2GSH + H2O2 → GSSG + 2H2O

GSH is reduced glutathione
GSSG is glutathione disulfide

32
Q

oxidative stress

A

*an imbalance between the production of reactive oxygen species and the organism’s ability to neutralize them and repair damage done on cells

*when a free radical gets inside a particular system and damages those molecules

33
Q

oxidative stress on lipid membrane

A

-plasma and organelle membrane damage by hydroxyl radical
-lipid-free radical interaction yields autocatalytic processes

34
Q

oxidative stress and proteins

A

*induces conformational changes, leading to:
-altered enzyme activity and membrane potential
-protein-protein cross-links, fragmentation
-protein fragmentation

35
Q

oxidative stress and DNA

A

-thymine reactions result in single-strand DNA breaks
-aging and malignant transformation

36
Q

ischemia

A

reduced blood flow
-causes include thrombosis, shock, hypotension, etc

37
Q

hypoxia

A

reduced oxygen availability
-glycolysis can continue (causing lactic acid buildup)
-causes include pulmonary disease, anemia, carbon monoxide poisoning

38
Q

morphology of hypoxia cell injury

A

1) mitochondria first affected so decreased ATP production
2) leads to failed Na+/K+ ATPase and Ca2+ pump, causing cell to swell (hydropic change), plasma membrane changes, ER swelling, and mitochondrial swelling
3) failure of protein synthesis and disaggregation of ribosomes
4) increased glycolysis (pH change, more lactic acid) leads to clumped DNA

39
Q

lipid accumulations (steatosis)

A

fatty change of liver or heart muscle
-accumulated triglycerides within parenchymal cells (alcohol abuse, toxins, diabetes, obesity)
-may be reversible or progressive

40
Q

cholesterol accumulations in cells

A

-atherosclerosis
-inflammation and necrosis
-cholesterolosis
-xanthomas

41
Q

causes of protein accumulations

A

-protein reabsorption (renal disease or glomerulonephritis)
-excess synthesis
-protein folding defects

42
Q

protein folding defects

A
  1. defective intracellular transport
  2. ER stress induced by abnormally folded proteins
  3. aggregation of abnormal proteins
43
Q

glycogen accumulation

A

excessive intracellular stores
-abnormal glycogen metabolism (diabetes, glycogen storage diseases)

44
Q

pigment accumulation

A

colored substances accumulate within the cell (may be normal cellular constituent or abnormal)

45
Q

lipofuscin

A

intracytoplasmic brown pigment, results from protein degradation over time; seen in cells undergoing slow, regressive changes (liver, heart)

46
Q

bilirubin

A

derived from hemoglobin breakdown, gets processed in liver, normally excreted in urine
-excess could result from hemolytic disorders
-elevated bilirubin can cause jaundice
-can result from liver dysfunction or biliary obstruction

47
Q

hemosiderin

A

derived from hemoglobin breakdown (the iron part)
-golden, yellow-brown crystalline pigment
-appears in bruises or can cause hemosiderosis (systemic overload)

48
Q

exogenous pigment - carbon accumulation

A

accumulation usually due to inhalation
-can lead to anthracosis (black lung)
-tattoos also allow carbon accumulation that persists in macrophages

49
Q

senescence

A

progressive decline in cellular function/viability caused by accumulation of genetic mutations, progressively decreased replication, and defective protein homeostasis

50
Q

intrinsic clock and senescence

A

progressive declining proliferative and replicative activity
-telomeres ensure complete replication of chromosomal end
-telomerase adds telomeres (active in germ cells/stem cells, but NOT somatic cells)

51
Q

extrinsic clock

A

progressive accumulation of cellular and molecular damage (DNA damage, etc)

MAD Exam 1 (20 decks)

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