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Pathophysiology I > week 1 - cellular adaption, injury & death > Flashcards

week 1 - cellular adaption, injury & death Flashcards

1
Q

What is the most abundant cation in ECF

A

Na+

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2
Q

What is the most abundant cation in ICF

A

K+

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3
Q

What is the main function of nucleus

A

contains DNA

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4
Q

What is the main function of ribosomes

A

protein synthesis

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5
Q

What is the main function of lysosome

A

contain enzymes. recycling system

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6
Q

What is the main function of ER (Endoplasmic Reticulum) / golgi apparatus

A

protein synthesis and delivery

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7
Q

What is the main function of mitochondria

A

ATP generation

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8
Q

Protein receptors in cell membranes

A

allow cell signaling, transport in/out of the cell

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9
Q

What is the technical term for cell shrinkage?

A

crynation

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10
Q

What is the technical term for bursting of a cell?

A

lysis

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11
Q

Explain the difference between homeostasis and compensation

A

Homeostasis:
- dynamic steady state within normal range
- part of normal physiology
- ex. blood sugar

Compensation:
- makes up for a defect by moving some parameters outside normal range
- beneficial in short term, detrimental long term
- e.g. enlarged heart left ventricle

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12
Q

What types of cells (from which organs) tend to undergo mitosis (cell division)? and what types do not once differentiated?

A

Undergo mitosis: skin, liver, blood
Not undergo mitosis: muscle

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13
Q

List 5 cellular adaptations

A

atrophy
hyperatrophy
hyperplasia
metaplasia
dysplasia

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14
Q

Define atrophy

A

Decreased cell size due to loss of cellular components, mainly due to disuse.

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15
Q

What is the primary substance in muscle cell that atrophy?

A

proteins; myosin and actin

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16
Q

What cause atrophy? (list 8)

A

Disuse
Denervation (remove/block nerve)
ischemia
nutrient starvation
interruption of endocrine signals
persistent cell injury from chronic infection
inflammation
aging

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17
Q

Define hypertrophy, and give example(s)

A

Increased cell size due to the increased demand of the body part.
e.g. weight lifting (micro scar –> increase cell size as repair)
e.g. heart left ventricle (push out more blood)

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18
Q

What are pros and cons of hypertrophy of the heart (left ventricle)?

A

Pros: heart pushes more blood out to the body system

Cons:
- larger muscle requires more blood for the heart itself. (coronary issue - can’t provide enough blood to the enlarged heart with higher demand)
- enlarged muscle narrows the chamber of LV –> leads to heart failure

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19
Q

What is atherosclerosis?

A

A condition in which there is an obstruction within the arteries due to presence of plaque.
Because of that, blood flow is restcricted to the organs and body tissues.

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20
Q

Define hyperplasia, and give example(s)

A

Increase in cell number
A response to stress or hormonal stimulation to increase functional capacity.
To meet increased demands

e.g. callus on foot / hand (protection of skin)
e.g. blood: increase of RBC at a higher altitude
e.g. liver: increase metabolism
regeneration after surgery

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21
Q

Define metaplasia, and give example(s)

A

Replacement of cell type to one that withstand better to the altered environment
(harsh environment, physical stressors, chronic injury/inflammation)

e.g. Barrett Esophagus
e.g. loss of mucociliary elevator due to smoking

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22
Q

Is metaplasia cancer?

A

NO. But the irritant inducing metaplasia could cause malignant change if continued overtime.

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23
Q

Explain Barrett Esophagus

A

Metaplasia
In Gastric Esophageal Reflux Disease, columnar epithelium is replaced with squamous epithelium to stand acid

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24
Q

In esophagus and airways, what is the common type of cellular adaptation?

A

metaplasia

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25
Q

What type of cellular adaptation happen in bronchi after chronic stress/damage (e.g. smoking)?

Explain how the cellular adaptation occurs.

A

metaplasia

Ciliated epithelium is replaced with stratified squamous due to the damage to celia by smoke.
This cause the loss of mucociliary elevator –> chronic cough

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26
Q

Define dysplasia, and give example(s)

A

Disordered growth of cells, respond to stressors.

e.g. cervical dysplasia due to chronic infection –> risk to cervical cancer
e.g. dysplasia in colon due to toxins from stool that cause injury –> polyps –> risk to cancer

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27
Q

What type of cellular adaptation is common in squamous epithelium?

A

dysplasia

28
Q

Is dysplasia cancer?

A

No. But it is associated with increased cancer risk (screening for cancer needed).

29
Q

What is the benefit of dysplasia?

A

There’s no positive benefit.

30
Q

Explain the difference between hypoxia and ischemia

A

Hypoxia: low oxygen
Ischemia: Loss of blood supply

31
Q

How cell injury / death happens in extreme cold weather?

A

vasoconstriction –> increase blood viscosity –> eventual vasodilation (may feel hot) –> swelling, peripheral nerve damage

32
Q

Explain carbon monoxide (CO) toxicity

A

CO binds to hemoglobin and interferes with oxygen delivery by RBC (–> hypoxia)

33
Q

What happens to an injured cell? List 5 pathways.

A
  1. Intracellular accumulations (reversible / irreversible)
  2. Reversible cell swelling
  3. Irreversible cell injury - pathologic calcification
  4. Irreversible cell death by necrosis
  5. Irreversible cell death by apoptosis
34
Q

What is intracellular accumulations?
Is it reversible or irreversible?

A

Accumulation of normal cell substance (e.g. lipids, carbohydrates, glycogen, protein) in injured cell.
Increases injury.

Irreversible - in case of genetic disorder
Reversible - if not genetic disorder

35
Q

Give 2 examples of reversible intracellular accumulations

A

Abnormal triglycerides in cell (steatosis)

  1. Fatty liver with alcohol abuse. Alcohol interferes with lipid metabolism in hepatocytes.
  2. Fatty liver from NAFLD (non alcoholic fatty liver disease). High adipose in liver (even in children) often due to sedentary lifestyle and improper diet.
36
Q

Give 2 examples of irreversible intracellular accumulations

A

Inborn errors of metabolism

  1. Tay Sachs disease. A genetic disorder, fat accumulation in neurons. That results in the destruction of nerve cells in the brain and spinal cord.
  2. Excessive glycogen storage in liver (inborn error metabolism or diabetes mellitus). Renal tubule cells reabsorb glucose and accumulate glycogen.
37
Q

Give 2 examples of irreversible intracellular accumulations

A

Inborn errors of metabolism

  1. Tay Sachs disease. A genetic disorder, fat accumulation in neurons. That results in the destruction of nerve cells in the brain and spinal cord.
  2. Excessive glycogen storage in liver (inborn error metabolism or diabetes mellitus). Renal tubule cells reabsorb glucose and accumulate glycogen.
38
Q

Explain what happens in reversible cell swelling. How is the condition reversible?

A

Ischemia (hypoxia) –> lack of O2 –> low production of ATP
–> Na+/K+ cell pump (ATPase) fails due to lack of ATP –> Na+ increase in ICF (through Na+ diffusion channel) –>
Na+ pulls H2O (osmosis) –> cell swelling = hydropic / reversible injury

It can be reversed once blood / O2 is restored in the cell –> ATP production is back –> functional ATPase –> Na+ out of cell –> water follows

39
Q

How excessive glycogen accumulation in hepatocytes happens?

A

Excessive glycogen storage happens due to either inborn error metabolism or diabetes mellitus; renal tubule cells reabsorb glucose and accumulate glycogen.
It is a irreversible intracellular accumulations.

40
Q

Explain pathologic calcification

A

Irreversible cell injury.
Ca++ salts precipitate in or out of cells. Causes decrease of ATP, membrane damage, DNA damage.

Once cell is damaged, Ca++ can enter the cell.

e.g. Ca++ precipitate in kidney tubules with hypercalcemia

41
Q

Explain how necrosis happens in a cell

A

Ischemia / hypoxia –> lack of O2 –>
loss of electrochemical gradients (low ATP –> Na+/K+ pump fail –> Na+ increase in cell)
–> continued swelling –> disruption of permeability barrier of plasma membrane

   --> influx Ca++ ions to cells --> mitochondrial dysfunction 
   --> degradation of plasma membrane & chromatin

   --> lysosomal enzyme released 
   --> cell membrane rupture

   (Ca++ and lysosomal enzyme both contribute to the 
   membrane rupture)

–> cell contents out - to interstitial fluid and to blood

42
Q

What type of enzyme is released when disruption of permeability barrier of plasma membrane happens?

A

lysosomal enzymes

43
Q

How to identify where necrotic tissue exists?

A

Blood test, markers of cell-specific content

44
Q

Identify which organ(s) / system(s) following markers of necrosis would come from?

  • troponin
  • CPK-MB (creatine phophokinase)
  • ALT (alanine transaminase)
  • serum amylase or lipase
A
  • cardiac (specific)
  • cardiac, also from severe skeletal injury, lung injury, renal failure
  • liver damage
  • pancreatic cell necrosis
45
Q

List 4 types of necrotic tissue

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Fat necrosis
  4. Caseous necrosis
46
Q

Describe coagulative necrosis.
Where are the common sites?

A

Most common.
Solid, tissue architecture present.
Denatured proteins.

Common sites: heart, kidney, connective tissue

47
Q

Describe liquefactive necrosis.
Where are the common sites?

A

Dissolution of dead cells occurs very quickly, a liquefactive area of lysosomal enzymes and dissolved tissue may result and form an abscess (pus) or cyst.

Common sites:
- area high in degradative enzymes (e.g. gut enzymes)
- area with less connective tissues (e.g. brain)
- areas with bacterial infection

48
Q

Describe fat necrosis
Where are the common sites?
How does it look like?

A

Death of adipose tissue

Common site: *pancreas, breast
*Due to trauma or pancreatitis, pancreatic lipase is released and breaks down fat

Appearance: chalky white deposits

49
Q

Describe caseous necrosis. How does it look like?

A

Specifically lung cell damaged by tuberculosis.

Appearance: white, soft, and fragile, resembling clumpy cheese

50
Q

Describe gangrene (2 types)

What is the factor to alter the types?

A

large area of necrotic tissue.
Either dry (coagulative) or wet (liquefactive from bacteria infection)

Dry or wet is influenced by the environment

51
Q

Define apoptosis

A

Programmed cell death. Normal process to eliminate unwanted or damaged cells.
Often arise from injury.

Energy dependent (need energy to happen).
Can’t stop it once starts

52
Q

How is apoptosis a part of developmental process?

A

During fetal development, excess cells disappear through apoptosis.

e.g. webbing between fingers.
e.g. excess neurons in brain

53
Q

How is apoptosis triggered / not triggered? (explain 3 patterns)

A
  1. Appropriately
    Any damaged or unwanted cells (including cancer cells = cells with genetic error)
  2. Inappropriately
    Body turn on apoptosis by error
  3. Suppressed inappropriately
    Some mechanisms of cancer evades the system - suppress apoptosis and cancer cells grow and multiply.
54
Q

Explain steps of how apoptosis happen.

A
  1. Cell injury –> receptor is detached from basement membrane –> cell signaling (e.g. TNFa) to death receptor.
  2. Caspase enzyme (in cell) gets activated.
    Dismantle / compartmentalize cell into membrane-bound packages .
  3. Phagocytic cells clean up the packages. (no leakage of cell contents to interstitial space)
    Lysosome in phagocytes break it down and recycle.

** NO INFLAMMATION **

55
Q

Compare similarities and differences between necrosis and apoptosis

A

Necrosis
- cell damage (usually happens to group of cells)
- swelling (including organelles)
- (cell can be repaired if the damage is not severe - not going to necrosis)
- cell membrane blebs
- cell membrane break down
- cell contents leak out to interstitial space
- cause INFLAMMATION

Apoptosis
- cell damage (single cell)
- Once a cell gets into apoptosis process, there’s no repair / go back
- cell membrane blebs
- cell signaling & caspase enzyme
- cell contents get compartmentalized and phagocytes breaks it down & recycle
- NO INFLAMMATION

56
Q

What is the significant enzyme in apoptosis process?

A

caspape enzyme

57
Q

Which process cause inflammation? Necrosis or Apoptosis?

A

Necrosis

58
Q

Explain the process of cell aging

A

Each time DNA replicated with cell division, telomeres (tips of chromosomes) do not get copied all the way.
Telomeres get shorten.
Once it reaches to a critical short length, cell division halts = senescence (aging) starts.

59
Q

Give an example how a cancer cell can affect telomeres.

A

Cancer cell rebuild chromosome tips (telomeres longer), allows cell divisions to continue

60
Q

Define
Algor motis

A

Postmortem reduction of body temperature

61
Q

Define
Poikilothemia

A

Body temperature same as environment after death

62
Q

Define
Livor mortis

A

Purple discoloration of dependent areas of skin due to blood pooling after death

63
Q

Define
Rigor mortis

A

Stiff muscle after death, typically after 6 hours of death.

64
Q

Postmortem autolysis

A

Dissolution of cells due to bacterial action & enzyme after death (body decomposition)

65
Q

Define infarction

A

obstruction of blood supply to tissue, causing local death of the tissue

66
Q

What is the effect and concern of long term use of corticosteroids?

A

Corticosteroids mimic the effects of hormones, such as cortisol. That increases the hormonal activities in the body and suppress the immune system, thus reduce inflammation.

Long term use of corticosteroids may cause adrenal glands to stop producing own hormone, cortisol. That is a concern of reduced immune system activities in the body.

After stopping corticosteroid use, it may take some time for the body to start making cortisol at a normal rate.

67
Q

A runner trains at a higher altitude (Denver, CO). What can happen to the person’s body (especially blood) to adapt to the decreased oxygen with elevation?

A

Lower O2 available –> body increases blood production (RBC) –> high RBC
–> higher viscosity of plasma –> increased risk of coagulation & clotting

Pathophysiology I (4 decks)

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