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Pathology > Lec1 Cell Injury > Flashcards

Lec1 Cell Injury Flashcards

1
Q

What is Adaptation? Is it irreversible or reversible? What are the 4 types?

A
  • cell avoids injury
  • reversible
  • can be pathological or physiological
  • 4 types
  • – hypertrophy
  • – hyperplasia
  • – atrophy
  • – metaplasia
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2
Q

What is Hypertrophy? What change in cells

A
  • type of adaptation
  • bigger cells
  • increase in cell size due to increase in number of cell organelles, structural proteins DNA
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3
Q

What is hyperplasia? What change in cells?

A
  • type of adaptation
  • increase in number of cells due to more cell division
  • can only occur in dividing cells [not skeletal or cardiac muscle]
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4
Q

What is atrophy? What changes in cells?

A
  • type of adaptation
  • decrease size and function of cell [and sometimes number]
  • apoptosis
  • may not be reversible
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5
Q

What is Metaplasia? What changes in cells?

A
  • type of adaptation
  • reprogramming of stem cells, replacement of one type of differentiated tissue by another type of differentiated tissue
  • no change in size or number of tissues
  • pretty much always pathologic
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6
Q

physiological causes of hypertrophy

A
  • high estrogen in pregnancy
  • uterus myometrial hypertrophy
  • breast in lactation
  • development
  • skeleal muscle
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7
Q

pathological causes of hypertrophy

A
  • hypertension –> left ventricular hypertrophy
  • kidney contractile nephritis –> kidney hypertrophy
  • increased nutrition [extra calories] –> hypertrophy of adipocytes
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8
Q

Physiological causes of hyperplasia

A
  • development
  • uterus in pregnancy - glandular hyperplasia
  • breast in lactation
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9
Q

pathological causes of hyperplasia

A
  • chronic blood loss –> erythroid hyperplasia

- obesity –> hyperplasia of adipocytes

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10
Q

Stresses that cause atrophy

A

physiologic
- menopause [withdraw hormones]

pathoglogic

  • immobilization [decreased functional demand]
  • starvation [decreased nutrients]

aging
[ex. myocardial atrophy]

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11
Q

How do functional demand, endocrine stimulation/withdrawl, and nutrition cause adaptations?

A

increase functional demand = hypertrophy + hyperplasia
endocrine stimulation = hypertophy + hyperplasia
increased nutrition = hypertrophy and hyperplasia

decrease functional demand = atrophy
endocrine withdrawl = atrophy
decreased nutrition = atrophy

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12
Q

Stresses that cause metaplasia

A

smoking: pseudostratified –> squamous in trachea

GI acid from stomach to esophagus

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13
Q

Types of intracellular storage material

A
  1. normal endogenous substance accumulates as by-product of normal metabolism
  2. normal endogenous substance accumulated at increased rate
  3. Normal or abnormal endogenous substance accumulates due to genetic defect in biochemical pathway [inborn error]
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14
Q

What is lipofuscin?

A
  • polymer of lipids
  • wear and tear pigment
  • seen in liver/heart in elderly
  • often in atrophic tissue
  • usually innocuous
  • shows up as brown pigment
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15
Q

What are two examples of normal intracellular materials produced at increased rate?

A

Triglycerides in liver in alcohol
= indication of reversible injury

Hemosiderin

  • in small amounts post-hemmorage is innocuous
  • in large amount in hereditary hemochromatosis may cause irreversible injury
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16
Q

What is hemosiderin? What disease associated with it?

A
  • in liver
  • in small amounts [post hemorrhage] is innocuous
  • in large amount [hereditary hemochromatosis] may cause irreversible injury
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17
Q

What are different mech by which genetic defect in biochemical pathway may cause increase in intracellular substance?

A
  1. failure of breakdown of normal or abnormal substance [storage disease] [often cause irreversible injury]
  2. Error in producing or packaging of normal or abnormal substance
  3. Exogenous material accumulates and can’t be metabolized
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18
Q

What type of disease is niemann-pick?

A
  • inborn storage disease

- failure in breakdown of sphingomyelin

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19
Q

What type of disease is hurler syndrome?

A
  • inborn storage disease

- failure in breakdown of mucopolysaccharides

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20
Q

What type of disease is hereditary tyrosinemia?

A
  • inborn storage disease

- failure in breakdown of precursor tyrosine metabolites

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21
Q

What is alpha-1-antitrypsin? What disease?

A
  • alpha-1 antitrypsin is protease inhibitor of neutrophil elastase
  • alpha 1 antitrypsin deficiency: mutation in AA causes slow folding of protein, partially folded precursor stuck in ER of hepatocytes
  • – causes irreversible cell [ER] injury and death
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22
Q

What are the pathophysiological effects of alpha-1-antitrypsin deficiency?

A
  • hepatic injury due to entrapment abnormal a1AT in ER causes hepatic scarring [fibrosis and cirrhosis]
  • deficiency a1AT in rest of body causes pulmonary emphysema
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23
Q

What are four neurodegenerative diseases associated with abnormal protein folding

A
  • alzheimers
  • parkinsons
  • huntingtons
  • prion disease
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24
Q

Effect of carbon dust accumulation

A
  • can’t be metabolized so accumulates
  • often innocuous
  • in large amounts can cause pulmonary fibrosis
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25
Q

What is pneumoconiosis?

A

A non-neoplastic disorder of lungs due to toxic inhalants

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26
Q

Reversible cell injury

A
  • hydropic change

- swelling of organelles

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27
Q

How can you tell hydropic change? What causes it?

A
  • swollen, clear cytoplasm

- due to influx of sodium and water into damaged cell

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28
Q

Types of Irreversible cell injury

A
  • damage to mitochondrial aerobic respiration
  • damage to integrity of plasma membrane
  • fragmented organelles
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29
Q

2 Causes of irreversible cell injury

A
  • ischemia

- free radicals

30
Q

What is Ischemia?

A

decreased blood flow leads to hypoxia and hypoglycemia

- causes irreversible cell injury

31
Q

What effect do free radicals have on cells [adaptation, reversible or irreversible cell injury]

A

chemical species with single unpaired electron in outer orbital
- cause irreversible cell injury

32
Q

Effect of intracellular calcification

A
  • due to cellular injury which allows influx Ca ions
  • impairs mitochondrial oxidative phosphorylation
  • – less ATP
  • activates intracellular enzymes to facilitate cell death
33
Q

Two types of calcification in tissues [different from intracellular]

A
  • dystrophic calcification

- metastatic calcification

34
Q

Dystrophic calcification

A
  • tissue calcification in injured tissue
  • normal serum Ca
  • normal Ca metabolism
35
Q

Which type of tissue calcification occurs in injured tissues?

A

dystrophic calcification

36
Q

4 Examples of dystrophic calcification

A
  • heart valves [old, abnormal, injured]
  • atherosclerotic blood vessels
  • areas of necrosis
  • neoplasms
37
Q

What is basis for diagnostic mammography?

A

dystrophic calcification

38
Q

Metastatic calcification

A
  • occurs in normal tissues
  • Excess Ca salts accumulate
  • increased serum Ca due to derangement in Ca metabolism
  • – ex. hyperparathyroidism, destruction bone, Vit D intoxication, chronic renal failure
39
Q

Which type of calcification has abnormal serum Ca level?

A

Metastatic calcification

40
Q

4 common sites of metastatic calcifiction

A
  • stomach [mucosa]
  • kidneys [tubules]
  • lungs [alveolar septa]
  • blood vessels
41
Q

Necrosis

A
  • morphologic changes that follow cell death in living tissue
  • degradative proteins cause enzymatic digestion and/or denaturation
  • characterized by pyknosis/karyorrhexis/karolysis
  • stimulates acute inflammation
  • bigger cells, occurs in multiple cells
  • disrupted plasma membrane
  • uncontrolled mech, from infection, membrane injury, ATP depletion, ischemia
42
Q

5 Types of Necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • fat
  • fibrinoid
43
Q

What is coagulative necrosis? Architecture? Mech? Cells? Location?

A
  • Cause: ISCHEMIA OR HYPOXIA
  • architecture preserved
  • in heart [after MI] or kidney
  • big neutrophils [PMN]
  • mech: denaturation of proteins
44
Q

What is pyknosis?

A

small nuclei, sign of necrosis

45
Q

What is karyorrhexis?

A

nuclei broken up into small pieces, sign of necrosis

46
Q

What is karyolysis?

A

lack of nuclei, sign of necrosis

47
Q

What is liquefactive necrosis? Architecture? Mech? Cells? Location?

A
  • Cause: Bacterial, fungal infection
  • causes abscess in lung/liver
  • increased PMNs [neutrophils]
  • architecture obliterated because of complete enzymatic digestion
  • in lung, liver, or brain
48
Q

What is caseous necrosis? Architecture? Mech? Cells? Location?

A
  • cause: TB
  • in lung [or lymph node]
  • architecture obliterated
  • get walled off area of whatever it is you can’t digest
  • causes granuloma
  • get macrophages, chronic inflammation
49
Q

What is fat necrosis? Architecture? Mech? Cells? Location?

A
  • cause: release of digestive enzymes, commonly follows acute pancreatitis
  • preserved architecture
  • chronic inflammatory cells present
  • mech: autodigestion by lipase
50
Q

What is fibrinoid necrosis? Architecture? Mech? Cells? Location?

A
  • cause: injury to blood vessel in setting of immune-mediated injury or hypertenstion
  • in blood vessel
  • preserved architecture
  • fibrin and PMNs [neutrophils] present
  • mech: immune-mediated or hypertension
51
Q

What type of cell death involves inflammation? why?

A

Necrosis

- because it involves breakdown of cell peripheral membranes

52
Q

Mech of apoptosis? Cause? Inflammation?

A
  • internal mechanism of programmed cell death via protease and endonuclease cascade
  • no inflammation
  • phagocytosis
  • cell membrane intact
  • small eosinophlic cell, fragmented apoptotic bodies
  • physiologic: normal develop., immune regulation
  • pathologic: virus, transplant rejection, ER stress
  • due to transplant rejection, ER cell death,
53
Q

Intrinsic pathways of apoptosis

A
  • cell injury by growth factor withdrawl, DNA damage, or protein misfolding
  • causes mitochondria release pro-apoptotic bodies [cytochrome C] –> caspases
54
Q

Extrinsic pathway of apoptosis

A
  • receptory ligated interaction activates capsases
55
Q

Telomerase function

A

Over time telomeres shorten leading to senescence, telomerase prevents shortening and leads to indefinite replication

56
Q

Hutchinson-gilford progeria

A
  • de novo autosomal dominant
  • abnormal intranuclear protein lamin A [progerin]
  • normal lamin A protects integrity of nucleus
57
Q

Werner syndrome

A
  • autosomal recessive causes dysfunctional DNA helicase
  • normal DNA helicase unwinds DNA during replication
  • abnormal causes accumulated DNA damage
58
Q

Genomic instability

A

idea that lifetime of somatic gene mutations [DNA damage] leads to senescence

59
Q

Superoxide dismutase [SOD]

A
  • SOD converts O2 –> H2O2, decreases ROS

- knockout of anti-SOD age-1 gene increases lifespan

60
Q

Environmental factors related to aging

A
  • reactive oxygen species

- diet

61
Q

How does reactive oxygen species [ROS] relate to aging?

A
  • over times ROS damage accumulates
  • causes cell breakdown, death
  • genomic DNA particularly susceptible
  • treat: antioxidants [vit A/D, beta carotene]
62
Q

How does quantity of diet effect aging?

A

caloric restriction [CR]: decreased intake increases lifespan
— lower metabolic rate –> decreased generation of ROS

nutrient abundance promotes:
– insulin/IGF pathway
– mTOR pathway [regulates cell growth, facilitates replicative senescence]
thus caloric restriction might inhibit these paths

63
Q

Red wine and aging

A
  • contains resveratrol that activates sirtruin [anti-aging protein
  • sirtruin may be molecular bases of effectiveness of caloric restriction
  • extends life span in mice and high fat, high cal diet
64
Q

What is advanced glycation end products [AGE]?

A
  • source: endogenous in DM, sausage, burger, cookies, occurs in browning meat
  • related to arthritis, atherosclerosis
  • increases ROS, upregulates inflammation
65
Q

What does sudan IV stain for?

A

Fat

66
Q

What does PAS stain for?

A

carbohydrates, glycogen

67
Q

Gangrenous necrosis

A
  • type of caogulative necrosis superimposed with liquifactive necrosis
  • usually due to diabetes get necrosis of limbs
68
Q

What does oil red O stain for?

A

triglycerides

69
Q

Etiologies of hepatic steatosis

A
  • starvation
  • obesity
  • diabetes mellitus
  • alcohol
70
Q

What is etiology of a myocardial infarction?

A
  • infarct = discrete area of coagulative necrosis secondary to occlusion of artery supplying or obstruction of venous outflow from area
71
Q

What is significance of elevated troponin-I or creatine kinase?

A
  • elevation indicates cell membrane breakdown and necrosis

- sign of MI

Pathology (15 decks)

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