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

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

Flashcards in Week 1 - Lecture 2b - Cellular Adaptation and Response to Stress, Injury and Death Deck (46):
1

name three causes of cell stress and injury

deficiency
intoxication
trauma

2

Define deficiency

lack of substance necessary to the cell

- variety of specific chemicals
- energy supply

3

What can cause deficiency

nutritional deficiency
genetic disease
infection

4

Define intoxication

the presence of a substance that interferes with cell function

5

Origin intoxications

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

6

examples of external biological intoxication

produced by agents of infection
- bacteria, fungi

7

examples of external non-biological intoxication

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)

8

endogenous intoxication

genetic defect
abnormal accumulation

9

Define trauma

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

10

Mechanisms of cell injury

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

11

define hypoxia

cellular deprivation of oxygen
oxygen supply via blood is compromised

12

hypoxic injury

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)

2. result of other conditions
-poor oxygen levels (anemia)
-imparied oxygenation (lung disease)
Toxic agents (CO, H2S, cyanide)

13

define anoxia

complete lack of oxygen in blood (absolute deprivation

14

8 steps for an ischemic injury

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

15

Re-perfusion injuries

'secondary injury'
-re-perfusion of the tissue leads to further damage
-membrane pumps are still impaired

16

Free radicals and reactive oxygen species (ROS)

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

17

Impaired calcium homeostasis

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

18

Cellular adaptation and response to stress and injury

1. cells have a variety of mechanisms to cope with stress
2. they can live through unfavourable conditions

19

5 processes of adaptation

atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia

20

What is atrophy

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

loss of function associated with atrophic cell and tissue changes

spinal muscular atrophy
-degeneration of motor neurone of the spinal cord
-genetic condition
-resulting in weakness of voluntary muscles

22

Hypertrophy definition

increase in cell size

23

hypertrophy cause

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

What is hyperplasia

increase in number of cells

25

what causes hyperplasia

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

26

hyperplastic adaptation

uterus responds to increased hormone levels during menstrual cycle

27

Adaptation to hormonal signals

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

What is metaplasia

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

example of metaplasia

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

What is dysplasia

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

Dysplasia aetiology

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

Example of dysplasia

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

Cellular death is caused how

if the stressor is too great
or the stressor is too long

34

what are the two types of cellular death

apoptosis
necrosis

35

What is apoptosis

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

What are the reasons for apoptosis

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

examples of when apoptosis is used wrong

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

Apoptosis cycle

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

What is necrosis

disorderly process associated with inflammation
always pathological, related to cell injury

40

11 steps of necrosis

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

5 types of necrosis

coagulative
liquefactive
caseous
fat
gangrenous

42

coagulative necrosis

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

43

liquefactive necrosis

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

caseous necrosis

tuberculosis pulmonary infection
combination of coagulative and liquefactive necrosis

45

Fat necrosis

adipose tissue
action of lipases : triglycerides > free fatty acids

46

gangrenous necrosis

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