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Medical Pathophysiology > Week 1 - Lecture 2b - Cellular Adaptation and Response to Stress, Injury and Death > Flashcards

Week 1 - Lecture 2b - Cellular Adaptation and Response to Stress, Injury and Death Flashcards

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USMLE® Step 1 flashcards
1
Q

name three causes of cell stress and injury

A

deficiency
intoxication
trauma

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2
Q

Define deficiency

A

lack of substance necessary to the cell

  • variety of specific chemicals
  • energy supply
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3
Q

What can cause deficiency

A

nutritional deficiency
genetic disease
infection

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4
Q

Define intoxication

A

the presence of a substance that interferes with cell function

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5
Q

Origin intoxications

A

outside the cell - external : exogenous : biological or non-biological
Inside of the cell - internal : endogenous : biological

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6
Q

examples of external biological intoxication

A

produced by agents of infection

- bacteria, fungi

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7
Q

examples of external non-biological intoxication

A

injurious chemicals

  • inhalation, swallowing
  • need to achieve a dose high enough to cause injury
    • therapeutic drugs - effective at prescribed level. can be fatal at high doses (barbiturates)
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8
Q

endogenous intoxication

A

genetic defect

abnormal accumulation

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9
Q

Define trauma

A

physical injury or damage resulting in loss of the cell’s structural integrity

some cases instant loss as a result of great damage
some cases physical damage arises gradually

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10
Q

Mechanisms of cell injury

A 
direct (for example thermal injury)
indirect : 3 major mechanisms
- hypoxic cell injury 
-free radical injury 
- impaired calcium homeostasis
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11
Q

define hypoxia

A

cellular deprivation of oxygen

oxygen supply via blood is compromised

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12
Q

hypoxic injury

A

1 : result of ischemia : interruption of blood supply;to tissue

  • rapid interruption is severe, metabolic needs are high
  • angina pectoris, stroke, cerebral ischemia, transient ischemic attack (TIA)
  1. result of other conditions
    -poor oxygen levels (anemia)
    -imparied oxygenation (lung disease)
    Toxic agents (CO, H2S, cyanide)
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13
Q

define anoxia

A

complete lack of oxygen in blood (absolute deprivation

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14
Q

8 steps for an ischemic injury

A
  1. blood flow compromised
  2. cell switch to anaerobic metabolism to maintain ATP level
  3. By-product is lactic acid (LA)
  4. Accumulating LA disrupts mitochondria
  5. decreasing ATP production results in dysfunction of membrane pumps
  6. Excessive sodium influx (Na/K ATP pump failed)
  7. Increased osmotic pressure (sodium is followed by water)
  8. Cell swell, waste products continue to accumulate
    - 1. if hypoxia ceased : cell will not die
    - 2. if not : cell dies
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15
Q

Re-perfusion injuries

A

‘secondary injury’

  • re-perfusion of the tissue leads to further damage
  • membrane pumps are still impaired
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16
Q

Free radicals and reactive oxygen species (ROS)

A

electrically uncharged atom or group of atoms having an unpaired electron that cause damage via :
:lipid peroxidation

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17
Q

Impaired calcium homeostasis

A

Ca2+ is an important second messenger and cytosolic signal for many cell responses

Intracellular Ca2+ concentration is low
– some Ca2+ is stored

Calcium activates enzymes in the cell

if Ca2+ homeostasis impaired

  • intracellular Ca2+ increases
  • mitochondria damaged, reduced ATP production
  • intracellular destructive enzymes are activated
  • cell membrane and cytoskeleton destroyed
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18
Q

Cellular adaptation and response to stress and injury

A
  1. cells have a variety of mechanisms to cope with stress

2. they can live through unfavourable conditions

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19
Q

5 processes of adaptation

A 
atrophy
hypertrophy 
hyperplasia
metaplasia
dysplasia
20
Q

What is atrophy

A

decrease in the size of a cell

due to

  • decrease in functional demand (muscular atrophy due to immobilised in cast)
  • decrease oxygen supply
  • removal of signals (neural : poliomyelitis / growth hormone: involution [decreased size, tissue and organ])
  • nutritional deprivation
  • ageing
21
Q

loss of function associated with atrophic cell and tissue changes

A

spinal muscular atrophy

  • degeneration of motor neurone of the spinal cord
  • genetic condition
  • resulting in weakness of voluntary muscles
22
Q

Hypertrophy definition

A

increase in cell size

23
Q

hypertrophy cause

A

increase in trophic (growth) signals
- signals increase > sex hormones
-increased sex hormones > hypertrophied reproductive cells during puberty
-during pregnancy hypertrophied breast cells > breast milk
Increase in demand
- strength building exercise

24
Q

What is hyperplasia

A

increase in number of cells

25
Q

what causes hyperplasia

A

increase in trophic (growth) signals
increase in demand
- some of the same conditions as for hypertrophy
-often appear together

26
Q

hyperplastic adaptation

A

uterus responds to increased hormone levels during menstrual cycle

27
Q

Adaptation to hormonal signals

A

dynamic process
one cell or tissue can undergo series of adaptation response
- ductal tissue of the breast
A: puberty - hyperplastic changes
B: pregnancy - hypertrophic change : to support production and delivery of milk
C: menopause - atrophic changes

28
Q

What is metaplasia

A

changing of one cell type to another
cells are fully differentiated
cells adapt to chronic or persistent stressor
if stimulus removed, cells revert back to their original type
most common type : epithelial tissue

29
Q

example of metaplasia

A

squamous metaplasia in bronchial tubes

etiology

  • stressor : cigarette smoke
  • Ciliated columnar cells turn to squamous epithelium
  • when stressor is removed cells often return to normal
  • if stressor persist: cell may develop changes that lead to pathologic changes
30
Q

What is dysplasia

A

Change in cell size, shape, uniformity, arrangement and structure
- response to chronic and persistent stressor
-likely to resolve after stressor is removed
Cells are not cancerous, but can progress to cancer

31
Q

Dysplasia aetiology

A

abnormal differentiation
- DNA may be reproduced with mutations
-these mutations are repeated as cells divide and proliferate
Larger changes to chromosomes may be evident

A: normal cells, large squamous cells with small nuclei
B: mild dysplasia, increased nucleus size, darkened colour
C: severe dysplasia, markedly enlarged nucleus with abnormal chromatin

32
Q

Example of dysplasia

A

bronchopulmonary dysplasia
bronchial and alveolar tissue of the lungs
-become thickened
-reducing ability to take air into lungs and oxygenate tissue
-reducing ability to excrete waste products and CO2

Etiology : multifactorial

  • immature lung tissue is susceptible damage
  • premature infants require mechanical ventilation to treat respiratory distress syndrome
  • -over distend airways and airspaces in infant
  • -stressor prompt cellular alterations
  • -chronic, irreversible tissue change
33
Q

Cellular death is caused how

A

if the stressor is too great

or the stressor is too long

34
Q

what are the two types of cellular death

A

apoptosis

necrosis

35
Q

What is apoptosis

A

adaptive response : involves a reduction in cell numbers by a process of self destruction
programmed cellular death prompted by highly-controlled signals
cell death does not result in release of intracellular fluids to surrounding microenvironment

36
Q

What are the reasons for apoptosis

A

development of limbs
day to day removal of unrequited cells (eg. immune system, uterus during the menstrual cycle)
damaged genetic material, maturation
cells undergo apoptosis to prevent transformation into a cancer cell

can be physiological or pathological

37
Q

examples of when apoptosis is used wrong

A

webbing hands into digits during the 7th week doesn’t occur

most cancers, Parkinson’s, alzeimer’s - does not take place in presence of correct stimuli

38
Q

Apoptosis cycle

A

activation of internal signals (eg. severe genetic damage) or external signals (eg. immune cells)

activate a cascade of intracellular reactions

cell shrinks, membrane blebs

DNA and nucleus fragments

whole cell fragments into apoptotic bodies

and phagocytosed

39
Q

What is necrosis

A

disorderly process associated with inflammation

always pathological, related to cell injury

40
Q

11 steps of necrosis

A
  1. poor ATP production
  2. dysfunction of membrane
  3. excessive sodium ion influx
  4. cause strong osmotic pressure
  5. draws water into cell
  6. calcium ions are released from cytoplasmic stores
  7. intracellular enzymes are activated
  8. these enzymes impair mitochondria and damage membrane
  9. Blebs (blisters) are formed
  10. Toxic chemicals accumulate
  11. eventually cell membrane rupture and inflammation follows
41
Q

5 types of necrosis

A 
coagulative
liquefactive 
caseous 
fat
gangrenous
42
Q

coagulative necrosis

A

kidneys, heart, adrenal glands
caused by hypoxia
protein denaturation
- albumin change from transparent state

43
Q

liquefactive necrosis

A

irreversible ischaemic injury to nerve cells in the brain

brain cells have high levels of digestive enzymes, and the brain has small amounts of connective tissue

44
Q

caseous necrosis

A

tuberculosis pulmonary infection

combination of coagulative and liquefactive necrosis

45
Q

Fat necrosis

A

adipose tissue

action of lipases : triglycerides > free fatty acids

46
Q

gangrenous necrosis

A

death of tissue from severe hypoxic injury

  • common due to blockage of arteries
  • bacterial infraction

dry gangrene
-skin dries, shrinks, becomes brown, black

wet gangrene

  • usually in internal organs
  • neurophils (main WBC) invade the site
  • liquefactive necrosis
  • site cold, swollen, black
  • if it becomes systemic: death can ensue

Medical Pathophysiology (30 decks)

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