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gen path- exam 1 > Cell injury/death/adaptation > Flashcards

Cell injury/death/adaptation Flashcards

1
Q

what is the difference between etiology and pathogenesis?

A

Etiology- ORIGIN of disease, WHY a disease occurs

Pathogenesis- DEVELOPMENT of disease, HOW a disease occurs

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2
Q

cerebral infarction, myocardial infarction and Renal atrophy are all forms of _____ injury

A

hypoxic

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3
Q

what are the (4) cellular targets for injury?

A

1) cell membranes
2) mitochondria
3) cell proteins
4) DNA

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4
Q

T/F: clinical signs and symptoms are usually closely timed to the molecular/biochemical changes following injury

A

FALSE

clinical signs are usually several steps removed

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5
Q

What are the effects of Hypoxia-ischemia on the cell membrane?

A

impairs Na+ pump: Na+ and Ca++ influx, K+ efflux

cell swells as water floods cell

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6
Q

What are the end effects of Hypoxia-ischemia on cellular metabolism?

A

1) decreased glycogen stores

2) increased lipid deposition

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7
Q

Generation of reactive oxygen species is associated with what?

A

1) inflammation
2) oxygen toxicity
3) chemical/drugs
4) radiation (UV, X-ray)
5) Aging

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8
Q

how do ROS (reactive Ox) damage cellular components?

A
  • lipid peroxidation
  • protein fragmentation
  • single strand DNA breaks
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9
Q

ROS cause _____-_____ DNA breaks

A

single-strand

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10
Q

How are reactive oxygen species controlled by cells?

A

1) enzymes
2) antioxidants (vitamins, glutathione)
3) serum proteins (bind/reduce iron and copper)

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11
Q

_____ (an ion) activates many enzymes inside the cell, and its concentration within the cell is highly controlled

A

calcium (Ca2+)

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12
Q

the degree of cell injury is determined by what factors?

A

A) physiologic state of the cell
B) intensity of insult
C) duration of insult
D) # of exposures to insult

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13
Q

what are the signaling mechanisms for cellular apoptosis?

A

1) intrinsic program
2) “death signals”
3) removal of a trophic signals – e.g. hormones
4) ROS, radiation, and toxins
5) effect of cytotoxic T cells

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14
Q

Fas-ligand binding to Fas receptor is a form of _____ signals

A

death signals

trigger apoptosis

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15
Q

the ____ gene family serve as on and off switches that regulate the membrane permeability of the mitochondria

A

Bcl-2 gene family

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16
Q

Bcl-2 and bcl-x gene products ______ apoptosis

A

inhibit

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17
Q

when does cell death occur?

A

Cell death occurs when the insult overcomes compensation mechanisms

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18
Q

apoptosis signaling pathways converge on an autocatalytic proteolytic cascade of ________

A

caspases

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19
Q

high cytoplasmic levels of Ca2+ will activate which digressive enzymes?

A

a. phospholipases
b. proteases
c. endonucleases
d. ATPase

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20
Q

Cell injury may result in what 4 effects?

A

a. Reversible cell injury
b. Cellular adaptations associated with changes in cell number, size or differentiation
c. Cellular adaptations associated with abnormal accumulations
d. Cell death – necrosis or apoptosis

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21
Q

what are the common causes of reversible cell damage?

A

a. Toxins
b. Infectious agents
c. Hypoxia
d. Thermal injury

22
Q

what are the 2 morphological types of reversible cell injury?

A

hydropic change and fatty change

23
Q

what are the morphological types of necrosis?

A

Coagulative
Liquefactive
Caseous
Enzymatic (fat)

24
Q

what are the characteristics of coagulative necrosis?

A

1) cytoplasmic proteins are coagulated

2) The nucleus is lost, but the pink outline of the cell is still present

25
Q

what are the characteristics of liquefactive necrosis?

A

A) The tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response.

B) associated with focal bacterial or fungal infections

26
Q

what is Caseous Necrosis?

A

a. Associated with M. tuberculosis infection.
b. The tissue has a white and “cheesy” appearance on gross examination.
c. the body “walls off” the area with granulocytes

27
Q

where is Fat Necrosis commonly found? what are its characteristics?

A

A) found in necrosis of breast or pancreatic tissue

B) adipose has a chalky white-yelllow color

C) dead cells look like “soap bubbles”

28
Q

Morphologic features of apoptosis include:

A

1) cell shrinkage
2) Chromatin condensation

29
Q

how does the morphology of necrosis and apoptosis differ?

A

Necrosis- Multiple cells, Cell swelling, Cell lysis

Apoptosis- Single cell, Cell shrinkage, Chromatin Condensation, Apoptotic bodies

30
Q

while inflammation is seen in forms of _______, it is not seen in ________

A

seen in necrosis, not seen in apoptosis

31
Q

Chronic cell injury leads to cell ________

A

adaptations

32
Q

how do cells change in response to chronic injury?

A

a. Alterations in cell size
b. Alterations in cell number
c. Alterations in cell differentiation
d. Intracellular accumulations

33
Q

what is atrophy? hypertrophy?

A

Atrophy - a decrease in cell size and function

Hypertrophy - an increase in cell size and is associated with an increase in functional capacity.

34
Q

what are the 2 etiologies of hypertrophy?

A

1) response to trophic signals (hormones)

2) response to increased functional demand (AKA muscle growth)

35
Q

what is hyperplasia? what are its general characteristics?

A

Hyperplasia - an increase in the number of cells in a tissue or organ

1) may involve the proliferation of epithelial and/or stromal cells
2) proliferation is stimulated by trophic factors
3) increase the risk for subsequent neoplasia’s

36
Q

what are some causes (etiologies) of cellular atrophy?

A 
A) decreased workload
B) loss of innervation
C) chronic ischemia (reduced bloodflow) 
D) starvation
E) lack of trophic factors
37
Q

what are the common etiological factors for hypertrophy?

A

A) increased functional demand
B) increased or imbalanced nutrition
C) increased hormonal stimulation

38
Q

Traumatic Keratosis is an example of what form of cell response?

A

Hyperplasia due to chronic irritation

39
Q

what is metaplasia?

A

Metaplasia - one adult cell type is replaced by another ADULT cell type in response to chronic stress.

40
Q

Acid reflux, and smoking, can both cause a _______ of epithelial tissues

A

metaplasia

41
Q

what is Steatosis?

A

Fatty liver

  • caused by triglyceride accumulation (intracellular accumulation)
42
Q

what is a Xanthoma?

A

cholesterol accumulation in the epithelium

  • common in elderly
43
Q

what are the histological characteristics of xanthomas?

A

foamy looking macrophages filled with cholesterol

44
Q

Cholesterol build-up in vessels can cause what 2 conditions?

A

Atherosclerosis

cholesterol thrombus

45
Q

alpha-1 anti-trypsin deficiency, Mallory bodies, and Alzheimers disease are all associated with an accumulation of what?

A

protein

46
Q

what is an example of a disease caused by carbohydrate accumulation?

A

glycogen storage disease

47
Q

what are 2 examples of conditions caused by exogenous carbon pigmentation

A

1) Anthracosis (asymptomatic… anthricite coal dust)

2) Pneumoconiosis (symptomatic- restriction. from coal)

48
Q

Melanotic-macules are caused by what?

A

accumulation of ENDOGENOUS pigments (melanin)

49
Q

what are the characteristics of a Hemosiderin? what causes them?

A

1) A yellow-brown pigment represents aggregates of ferritin micelles.
2) Its accumulation arises from excess iron locally due to hemorrhage and can lead to hemosiderosis.

50
Q

what causes Bilirubin to accumulate in the liver?

A

Accumulates in hepatocytes and bile ducts due to hemolysis, obstructed bile flow, and/or hepatocellular disease.

gen path- exam 1 (10 decks)

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