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FPP > (2) Cell Injury and Adaption > Flashcards

(2) Cell Injury and Adaption Flashcards

1
Q

4 Cellular Responses to Injury

A
  1. alter physiology/non-lethal stimulus
    ie. Increased demand, GF, less nutrients, chronic irritation
    → Hyperplasia/hypertrophy/atrophy/metaplasia
  2. Reduced O2, chemical injury, microbial infection
    ie. Acute/transient and progressive/severe
    →Acute reversible injury like swelling or fatty change
    →Irreversible like necorsis/apoptosis
  3. Metabolic change/genetic/aquired change/chonic
    -→intracellular accumulations, calcifications
  4. Cumulative sub-lethal injury overtime
    → cellular aging
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2
Q

Labile cells and examples

A

continously dividing

→hematopoetic cells or surface epi (chemo would affect these)

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3
Q

Stable tissues

A

quiescent; divide, but not often
→ in response to injury
→ the parenchyma of solid organs
→ endothelial cells, fibroblasts, sm msl cells

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4
Q

Permanent Tissues

A

non-proliferative

→ neurons and cardiac muscle cells

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5
Q

↑SIZE of cells; increase size organ

A

HYPERtrophy

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6
Q
  • more proteins/organelles
  • d/t tropic(GFs) or mechanical triggers
  • occurs in cells w/ limited capacity to divide
A

Hypertrophy

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7
Q

Physiologic Hypertrophy:

A

d/t increased fnx demand or hormonal stimulation. Like wt lifting or preg uterus

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8
Q

CC: Patho hypertrophy =

A

heart mscl in HTN
*thick lf ventricle and increased mass; in response to increased work load in HTN
See also w/ aortic vavle stenosis
*myofibers enlarge; increase filaments. Initially no change but leads to heart fail
In microscope: see enlarged nuclie and myofiber width

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9
Q

↑# of cells

*cells capable of division(labile and stable)

A

HYPERplasia:

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10
Q

Physiologic hyperplasia:

A

female boobs puberty/preg

  • Compensatory hyperplasia of liver after partial resection
  • CT response to wound healing
  • preg uterus both hypertrophy/hyperplasia
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11
Q

CC: Patho hyperplasia

A

Excessive stimulation by GF or hormones
-Endometrial hyperplasia; reversible and cells respond normally to regulatory mech. Puts you at increased risk for cancer
Microscope: increased # and crowding of glands with cells closely packed liking glands. Glands should be round

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12
Q

Benign Prostatic Hyperplasia

A

men >50
*nodules in prostate/perurethral = obstruction
cause=?
d/t androgen induced relesase of GF→ increased proliferation of stromal cells, decreased death of epithelial cells
*no increased risk of cancer

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13
Q

BPH pathogenesis:

A

androgen induced released of GF–> increased proli of stromal cells, decreated death of epithelial cells

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14
Q

↓size of a cell d/t loss of substance

  • severe leads to decreased organ size
  • decreased protein synth + increased degredation
  • decreased function but not death
A

Atrophy:

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15
Q

Causes of Atrophy

  1. Physiologic:
  2. Pathologic:
A
  1. loss of hormonal simulation (endometrium, menopaus)

2. decreased functional demand/loss of innervation/inadequte nutrition

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16
Q

cell type replaced by other adult cell type more able to handle stress
-Adaptive process to chronic stress+/or persisten cell injury

A

Metaplasia:

17
Q
  • cells become reprogrammed but is reversible

- can increase risk cancer

A

metaplasia

18
Q

Epithelial metaplasia in smoker: pathophysiology

A

Ciliated columnar epi→ squam epi (trachea of smokers)

*stimulus causing change may predispose to devo of malignant neoplasm

19
Q

Barrett Esophagus pathogenesis

A

sq epithelium at distal eso→ glandular epithelum like in stomach (protect reflux acid)
***predisposes devo of glandular carcinoma = adenocarcinoma

20
Q

Barretts Esophagus predisposes you to what type of cancer?

A

adenocarcinoma

21
Q

Causes of Squamos metaplasia at endocervix

A
  • columnar→ squamos at endocervix

- increase risk of HPV infection

22
Q

bone formation in soft tissue (msl/CT)at sites of injury

A

Mesenchymal metaplasia:

23
Q

inadequate oxygenation of blood (lung disease or lack of O2 in ambient air)
-reduced O2 carry capacity of blood (anemia, cyanide)

A

Hypoxia

24
Q

lack of blood to site (coronary art diseae/stroke/ heart attack)

A

Ischemia:

25
Q

Causes of Cell death

A
  1. O2 deprevation: hypoxia and ischemia
  2. Physical agents: trauma/temp extremes/ radiation
  3. Chemical agents
  4. Infections agents: virus/fungi/bacteria/parasites
  5. Immunologic rxns: autoimmune/hypersentivity
  6. Genetic derangements
  7. NUTRITION imbalance or aging
26
Q
  • can’t reverse mitochondiral dysfnx (lack of oxidative phosphorlyation and ATP generations)
  • mess up membrane fnx
  • have apoptosis and necrosis
A

Irreversible Cell Death

27
Q

Hallmark of irreverisble cell death

A

mitochondiral dyxfnx; lack of oxidative phosphorylation and ATP generations

28
Q

swelling/ pyknosis, karyorjexis, karyolysis/ enZ may leak out of cell/ disrupted pl membrane/often adjacent inflammation/always pathologic

A

Necrosis:

29
Q

shrinkage/framementation to nucleosomes/ intact plasma membrane/ contents are intact and released as apoptotic bodies/ no inflammaiton/ often physiologic, sometimes pathologic

A

Apoptosis:

30
Q

Two examples of Reversible Cell Change

A

Fatty change and vacuole change (hydopic change)

31
Q

lipid vacuoles in cytoplasm dt toxi or hypoxic injury. In cells dependent on fat metabolism
CC: fatty liver secondary to alcohol

A

Fatty Change: Reversible

32
Q
  • d/t failure of mmb pump to maintain homeostasis = mmb blebs~ failure of Na/K pump
  • see vacuoles in cells corresponding to distended ER
A

*Cell swelling: hydorpic change or vacuolar degen

33
Q

Cause steatosis:

A

alcohol, obesity, malnutrition, anoxia, diabetes

34
Q

What happens in steatosis

A

-hepatocytes are injured → intracell accumulation of triGs, liver gets big, elevated liver enZ from leaky hepatos
Clincal manifestations depend on cause/severity; can be reverible if cause removed. If mild, no effect on cell fnx but sever we see fucked cell fnx, cell death, cirrhosis

35
Q

What does a liver cell with steatosis look like under microscope

A

Microscopy: intracell accumulation of fat = liposome, will push aside nucleus

FPP (2 decks)

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