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Patho Phys Exam 1 > Cellular Injury > Flashcards

Cellular Injury Flashcards

1
Q

Adaptation to physiological stress and noxious stimuli is reversible or irreversible -

A

reversible

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2
Q

Hypertrophy

A

increase in cell size due to the synthesis of more cellular or cytosolic components (or increase in size of organelles)

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3
Q

Signal transduction pathway of stressors lead to

A

a stress (mechanical trigger)

Release of different GF or hormones (tropic factors) depending on the stressor

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4
Q

Physiologic hypertrophy

A

training athlete has a larger heart than a sedentary person which leads to a lower resting HR because the heart is larger, has more muscle, stronger, ejects more blood (a stronger heart with thicker walls)

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5
Q

Pathologic hypertrophy

A

chronic, uncontrolled hypertension causes heart to enlarge; must overcome increased pressure in arteries to eject blood which causes an increase in work demand or metabolic demand or excess endocrine stimulation

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6
Q

Pathologic hypertrophy can lead to what and why

A

progress to heart failure if BP is not reduced, heart can no longer adapt so this continued stress will lead to cell injury

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7
Q

Hyperplasia

A

increase in number of cells; cells must be able to divide and/or stem cells present

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8
Q

Physiologic hyperplasia

A

Pregnancy: hormonal hyperplasia (estrogen and progesterone leading to breast and uterus enlargement)

Remove part of liver: compensatory hyperplasia (increased growth factor leads to liver tissue regen)

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9
Q

Uterus enlargement is a result of

A

hyperplasia and hypertrophy

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10
Q

Pathologic Hyperplasia

A

Prostate: DHT –> BPH (enlarged prostate)

End of uterus cycle: estrogen, progesterone out of balance to inhibit sloughing –> endometrical hyperplasia

Gingival hyperplasia: drug induced by decreasing Ca channel blockers

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11
Q

Compensatory hyperplasia

A

Removing part of the liver and it growing back

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12
Q

Cause of gingival induced hyperplasia

A

drug induced- drug induced by decreasing Ca Channel blockers

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13
Q

Requirement for tissue to be able to develop hyperplasia

A

cells need to be able to divide

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14
Q

Atrophy (define)

A

loss of muscle mass, loss of cellular substance –> decreased cell size

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15
Q

Atrophy (cause)

A

loss of stimulation (nervous or hormonal), inadequate blood supply and inaqequate nutrients

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16
Q

loss of stimulation (nervous or hormonal), inadequate blood supply and inaqequate nutrients leads to what (3)

A

Reduced metabolic activity (reduced prt synthesis)

Stimulate prt degradation

Autophagy
During nutrient deprivation (or to clear misfolded
proteins), SER membrane encircles organelles to form
autophagic vacuole –> fuses with lysosome –> digest
cellular components

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17
Q

Why do cells atrophy

A

So they can control their internal environment and produce energy to survive –> fewer organelles means less ATP needed

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18
Q

Metaplasia

A

the conversion of one cell type to another

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19
Q

GERD (an example of what) and explain what happens

A

lining of esophagus (stratified squamous epithelium) becomes
same cell as lining of stomach (simple columnar epithelium with
mucus and bicarbonate producing cells)

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20
Q

GERD pro and con

A

Good in that it protects from acid better

Bad in that its worse protection from abrasion and can increase the risk of esophageal cancer

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21
Q

Relationship between metaplasia and cancer

A

normal cells can convert to cancerous ones- increases the risk for esophageal cancer

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22
Q

Mens Prostate cellular response

A

Prostate: DHT –> BPH (enlarged prostate)

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23
Q

Finasteride is a drug that inhibits the conversion of testosterone to dihydrotestosterone. What affect will it have on a person with benign prostatic hyperplasia (BPH) and how quickly will this happen?

A. Decrease the hyperplasia and cause
shrinkage of the prostate in a few hours B. Decrease the hyperplasia and cause
shrinkage of the prostate in a few months 
C. Increase the hyperplasia and cause
further prostate enlargement in a few
hours
D. Increase the hyperplasia and cause
further prostate enlargement in a few
months
A

Decrease the hyperplasia and cause

shrinkage of the prostate in a few months

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24
Q

Microscopic evaluation of a tissue obtained from a surgical procedure showed that multiple cells had an increased cell size due to an increase in the amount of cytoplasm, but nuclei remained uniform in size. Which of the following tissues and conditions is most likely to have resulted in this finding?

A. Bronchial epithelium with chronic irritation
B. Liver following partial resection
C. Ovary following menopause
D. Skeletal muscle in the lower limb of a
quadriplegic
E. Uterine smooth muscle in pregnancy

A

Uterine smooth muscle in pregnancy

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25
Q

Denervation of skeletal muscle or dramatically reduced use of skeletal muscle or bone?

A

hypertrophy

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26
Q

Chronic irritation, such as with acid reflux into the esophagus, or smoking’s effect on the trachea/bronchial epithelium?

A

metplasia

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27
Q

Lose hormones following menopause

A

atrophy

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28
Q

Cell injury by Hypoxia can be caused by what (3 thing)

A

Ischemia (reduced blood flow)

Reduced O2 carrying capacity (anemia with decreased iron and hemoglobin, CO poisoning)

Respiratory failure (reduced oxygenation in the blood)

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29
Q

Events following reversible cell injury

A

Biochemical cell changes leading to decreased cell function –> ultrastructural changes (damaged organelles or cytoskeleton) –> light microscopic changes –> gross morphological changes

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30
Q

Cell swelling (hydropic change or vacuolar degeneration) reversible injury microscopic changes

A
  1. loss of microvilli
  2. cell swells –> ER Swells –> can pinch off and form vacuokes (distended, pinched off segments of ER)
  3. “Blebs”
  4. Darker pink stain=increased protein coagulation
  5. increased weight –> increased turgor (more firm)
  6. increased pallor (more pale) b/c compression of capillaries and decreased blood flow
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31
Q

Is cell swelling reversible or not?

A

yeah, as are its effects

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32
Q

Necrosis, reversible or not?

A

No

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33
Q

Necrosis (irreversible) biological changes

A

Sequential development of biochemical and morphological changes

Biological changes and cell death –> ultrastructural changes –>
light microscopic changes and gross morphological changes
that are MUCH more prevalent

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34
Q

Cell appearance of necrosis

A

leakage of cell content, cell fragmentation more
prevalent than whole cells, cytoplasm “moth eaten” from digested organelles, loss of or odd looking nuclei, increased eosinophilia in
cytoplasm

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35
Q

Nuclei in necrosis

A

Pyknosis: Irreversible condensation DNA chromatin –> solid,
shrunken, dark mass

  1. Karyorrhexis: nucleases are released –> pyknotic nucleus
    fragments
  2. Karyolysis: DNase activation–> chromatin dissolution
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36
Q

Nuclei in necrosis

A

Pyknosis: Irreversible condensation DNA chromatin –> solid,
shrunken, dark mass

  1. Karyorrhexis: nucleases are released –> pyknotic nucleus
    fragments
  2. Karyolysis: DNase activation–> chromatin dissolution
    (do not see nucleus)
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37
Q

How does the body respond to necrosis

A

by inflammation due to the release of cellular contents

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38
Q

Pyknosis:

A

Irreversible condensation DNA chromatin –> solid,

shrunken, dark mass

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39
Q

Karyorrhexis:

A

nucleases are released –> pyknotic nucleus

fragments (nuclei are broken up)

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40
Q

Karyolysis:

A

DNase activation–> chromatin dissolution (do not see nucleus)

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41
Q

Feature of coagulative necrosis

A

in a solid organ (cells stay intact)

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42
Q

Characteristics of coagulative necrosis and what causes each (2)

A

PALE-loss of blood so caused by ischemia

Wedge shaped: blood supply to this area is lost (ischemia)

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43
Q

infarct

A

area of ischemic necrosis, can be caused by a clot

44
Q

Mechanism of coagulative necrosis/infarct

A

firm tissue when not degraded –> ischemia –> proteins and enzymes are denatured –> enzymes (proteases) renedered inactive –> longer for tissue to degrade

45
Q

Liquefactive necrosis

A

an abscess: accumulation of pus in an enclosed space in a tissue (pus: exudate formed at the site of inflammation during infection-dead leuko and neutros)

46
Q

Mechanism of liquefactive necrosis formation

A

Bacterial or fungal infection recruits inflammatory cells –> release proteolytic enzymes that destroy (or liquefy)
the surrounding tissue

47
Q

what causes liquefactive necrosis formation in the brain

A

Ischemia, not an infection since the brain has a lot of fat from myelin sheath!!

48
Q

Does liquefactive necrosis formation in the brain scar?

A

No- the dead tissue is removed –> cavity or cystic space forms because neuronal tissue cannot be regenerated

49
Q

Gangrenous necrosis:

A

caused by ischemia, when multiple tissue layers

(limbs and toes) die from insufficient blood

50
Q

Causes of Gang green

A 
poor	circulation	(ex:	diabetes),	trauma	or	physical	
injury
51
Q

Dry Gang green

A

Frostbite, reduced blood flow (so actually coagulative necrosis not liquefactive)

52
Q

reduced blood flow causes _____ necrosis

A

coagulative

53
Q

Symptoms of dry gangrene

A

numbness or pain, tissue turns brown to

purple or black, tissue dries up and often falls off

54
Q

Wet Gangene

A

MOSTLY LIMBS

Reduced blood flow plus a bacterial infection

55
Q

wet gangrene symptoms

A

MOSTLY LIMBS

painful, swelling and blisters with pus, foul-
smelling discharge, tissue turns red then black

56
Q

Which gangrene is more dangerous-dry or wet

A

wet because infections can become systemic and lead to fever and sepsis

57
Q

Caseous necrosis

cause and body response

A

caused by TB-body tries to wall off and kill with macrophages –> necrotic cells are not completely digested, covered in inflammation –> cells appear cheese like (nasty af)

58
Q

Fat Necrosis (most common cause)

A

from acute pancreatitis-LIPASE driven

59
Q

How fat necrosis forms

A

from acute pancreatitis-LIPASE driven

Lipase leaks out of the damaged cells –> triglycerides in the fat of the mesentery around the pancreas broken down by escaped lipase –> becomes fatty acid

60
Q

Soap (what is it)

A

Fatty acids+Ca (saponification); see white, chalky deposits from soap

61
Q

Trauma to a tooth can cause inflammation and damage to the pulp that leads to a zone of necrosis from both tissue destruction and aerobic and anaerobic bacteria. This will most likely be:
A. Caseous necrosis B. Coagulative necrosis C. Fat necrosis D. Liquefactive necrosis E. Wet gangrene

A

Liquefactive necrosis

62
Q

A 34-year-old male had a high fever for the past 2 days. Physical exam reveals a heart murmur (an abnormal heart sound). Echocardiography shows destruction of the aortic valve by large, irregular vegetations (‘infected’ blood clots on the valve). Staphylococcus aureus is cultured from his blood. He develops abdominal pain. Abdominal CT shows a wedge-shaped 1.5 x 3 cm splenic lesion with the base on the capsule of the spleen. The splenic lesion is most likely the result of which of the following abnormalities?
A. Abscess formation B. Coagulative necrosis C. Fat necrosis D. Liquefactive necrosis E. Metaplasia

A

B. Coagulative necrosis

63
Q

A 40-year-old female has a sudden onset of severe abdominal pain. On physical examination she has diffuse tenderness in all abdominal quadrants, with marked guarding and muscular rigidity. She has laboratory findings that include an elevation of blood amylase and lipase. An abdominal CT scan reveals peritoneal fluid collections and enlargement of the pancreas. Which of the following will most likely accompany these findings?

A. Coagulative necrosis B. Dry gangrene C. Fat necrosis D. Liquefactive necrosis E. Ulcer

A

C. Fat necrosis

64
Q

Wedge/traingle shaped lesion? Pale? Solid?

A

coagulative necrosis

65
Q

Black/green tissue

A

Gangrenous

Trauma or physical injury (i.e. frost bite) or poor blood circulation (i.e. diabetes) to extremities

66
Q

Abscess filled with pus

A

Liquefactive Brain

caused by infarct or microbial
infection

67
Q

Cheese-like

A

Caseous

caused by TB and fungal infections

68
Q

Chalky white deposits (saponification)

A

Fat

caused by Action of lipases

69
Q

Apoptosis

A

irreversible cell injury/death

70
Q

two main signaling pathways which lead to apoptosis

A

Mitochondrial pathway: growth factor withdrawal, DNA damage, protein misfolding

  1. Death receptor pathway: activate death receptors (Fas or TNF
    receptor)
71
Q

two main signaling pathways which lead to apoptosis

What do they have in common?

A

Both pathways –> executioner caspase (Caspase 3) –> cleave proteins
–> degrade DNA, nuclear matrix, cytoskeleton –> DNA and nuclear fragmentation

72
Q

Physiological apoptosis: (examples)

A

Embryogenesis: eliminate webbing between fingers

ii. Loss of hormones – cells involved in lactation after weaning

iii. Loss of growth factors – immune cells at the end of an immune
response

73
Q

Pathological Apoptosis does what

A

eliminate potentially harmful cells

74
Q

Patho apoptosis examples

A

Radiation, drugs, hypoxia/reoxygenation –> irreparable DNA damage

ii. Gene mutations, free radicals –> many misfolded proteins

75
Q

Features of apoptotic cells

5

A

i. Shrunken cell and nucleus ii. Fragmented DNA
iii. Condensed nuclear chromatin (dark stain) iv. Cytoplasmic bleb (damage to cytoskeleton)
v. Apoptotic body = bleb broken off
1. Phosphatidylserine (PS) flips from the inner to the outer leaflet
of the plasma membrane, macrophage recognizes the PS and
phagocytizes it

76
Q

Apoptosis vs necrosis

A

apoptosis DOES NOT cause inflammation

77
Q

apoptosis does not cause inflammation because

A

Does not cause inflammation because apoptotic bodies are phagocytized
before cytoplasmic contents leak out!

78
Q

Fatty changes (other pattern of reversible injury) –

A

steatosis of triglycerides in an

intracellular accumulation

79
Q

Fatty changes (cause of)

A

-Caused by an imbalance in fatty acid utilization, triglyceride synthesis, and
triglyceride mobilization –> increased triglycerides –> fatty changes

b. Becomes enlarged, pale/yellow, soft and greasy
c. Lipid vacuoles are present

80
Q

Hypoxia and/or ischemia causes cell injury via causing a decrease in what

A

ATP- you need oxygen and mitochondria to make ATP

81
Q

ATP is made two ways (2)

A

glycolysis (anoxic)

Aerobic respiration

82
Q

need what to run the Na-K-ATPase

A

ATP

83
Q

Lots or little Na in the celll?

K?

A

Na lots outside

lots of K inside

84
Q

Na-K-ATPase not working bc no ATP will result in what…

A

Gain in lots of Na+ in the cell (much more Na+) than K

then the cell is saturated with solution and swells with water; the ER also dilates –> ribosomes detach –> no protein synthesis

85
Q

How does a lack of ATP lead to reduced protein synthesis

A

Gain in lots of Na+ in the cell (much more Na+) than K

then the cell is saturated with solution and swells with water; the ER also dilates –> ribosomes detach –> no protein synthesis

86
Q

Na-K-ATPase not working bc no ATP reversible?

A

Yes!

87
Q

Hypoxia with its resultant decrease in ATP production causes an increase in anaerobic glycolysis. What affect does this have on intracellular pH?

A. Intracellular pH decreases (more acidic) B. Intracellular pH increases (more alkaline)

A

A. Intracellular pH decreases (more acidic)

88
Q

How do glycogen stores affect the extent or degree of cell injury?

A

Cells with more glycogen stores (liver and skeletal muscle) can go longer hypoxic

89
Q

How does ATP depletion affect intracellular Ca++ levels?

A

Intracellular Ca++ rises, also Ca++ channel membranes will be activated causing a further rise…

Many enzymes are activated by Ca++ such as ATPase which will deplete more ATP and protease, so this is bad.

90
Q

How does ATP depletion cause the reversible morphological changes such as cell swelling, ER dilation (vacuoles), blebbing and loss of microvilli?

A

A rise in Ca++ will cause the cytoplasm to detach and cause blebbing

91
Q

How does ATP depletion contribute to necrosis?

A

Short duration lack of ATP will likely be short…..

As membranes (plasma, ER, etc.) are damaged contents begin to leak out… The cell will eventually break open/fragment or fragment DNA-at this point it is dead

92
Q

How does ATP depletion contribute to necrosis? Or - How does it cause irreversible changes, such as DNA fragmentation and membrane damage?

A

Rise in intracellular Ca++ which will activate phospholipase which will cleave phospholipids on the plasma membrane and lysosomal membrane (cleave things), proteases, and endonucleases

93
Q

What are reactive oxygen species (ROS)?

A

Free radical (unpaired electron in its outer orbit) containing Oxygen therefore ROS will steal electrons –> chain rxn

Produced by macrophages and mitochondria

94
Q

What are antioxidants?

A

Vitamin C and E is-they will get rid of ROS

95
Q

What are some main causes of an increase in ROS or oxidative stress?

A

Oxidative stress is how ROS will damage things..

an infection needing macrophages will increase ROS

Chemical and radiation exposure

Protective mechanisms break down like with reperfusion
injury

96
Q

Define reperfusion therapy and what role does oxidative stress play in reperfusion injury?

A

Reperfusion (opening up a vessel to flood tissue that has no blood) will cause lots of ROS

Ex: myocytes experience ischemia, if no reperfusion
(blood supply not restored, tissue will die. If reperfusion occurs, tissue recovers but generates free
radicals

97
Q

How do reactive oxygen species (ROS) contribute to cell injury (necrosis or apoptosis)?

A
  1. Lipid peroxidation à damage membranes
  2. Cross-link or fragment proteins à degrade proteins and
    enzymes
  3. DNA damage à single strand breaks and mutations
98
Q

What is the association between periodontal disease and oxidative stress?

A

Seems to be a correlation, no hard proof. There are antioxidant toothpastes

99
Q

What are the main causes of mitochondrial damage ?

A

Hypoxia, radiation, and chemicals

100
Q

Explain how mitochondrial damage causes ATP depletion, ROS generation, and apoptosis.

A

No oxidative phosphorylation –> ATP depletion

OR Abnormal oxidative phosphorylation –> increases ROS

101
Q

Describe the cellular changes that are specifically associated with necrosis and how this causes some of the morphological changes associated with irreversible injury.

–What contributes to lysosomal membrane and plasma membrane damage? What is the consequence of this?

A

lysosomal membrane is damaged–> lysosomal enzymes ROS leak out –> –> necrosis

If most important membranes damaged, leads to cell necrosis!

  1. Mitochondrial membrane –> decreased ATP
  2. Lysosomal membrane –> leakage of enzymes –> digest the cell
  3. Plasma membrane –> influx of fluid and ions, loss of cell
    contents
102
Q

Lysosomal enzymes are pH dependent (i.e. activate at low pH). In a normal cell, the pH of a lysosome is about 4.8, whereas cytosolic pH is about 7.2. Which of the following most likely enables lysosomal enzymes to work in the cytosol of an injured cell?

A. Increased anaerobic glycolysis
 B. Increased intracellular Ca++
 C. Mitochondrial uncoupling 
D. Prolonged ATP depletion
 E. Reduced activity of the Na-K ATPase
A

A. Increased anaerobic glycolysis

this will produce more lactic acid..

103
Q

An abnormally large, prolonged increase in intracellular Ca++ will most likely contribute to necrosis by:

A. Activating endonucleases which fragment
DNA

B. Activating caspases which leads to
irreversible condensation of chromatin and
pyknosis

C. Activating proteases causing cytoskeletal
detachment from the plasma membrane

D. Activating water channels which causes
water influx and cell swelling

E. Recruiting inflammatory cells that release
proteolytic enzymes to kill the cell

A

A. Activating endonucleases which fragment

DNA

104
Q

A patient is admitted with severe substernal chest pain of 4 hours duration caused by a totally occlusive clot in a coronary artery. Lab tests reveal increased blood levels of creatine kinase (an important enzyme in cells such as cardiac muscle cells). This is most likely due to:

A. Cellular acidosis 
B. Cytoskeletal detachment and blebbing
C. Damage to plasma membranes 
D. Endoplasmic reticulum swelling
 E. Karyorrhexis
A

C. Damage to plasma membrane

The rest are reversible

105
Q

Explain how alcoholism and hypoxia can contribute to fatty changes in the liver and/or heart?

A

Imbalance in fatty acid utilization, triglyceride synthesis, and triglyceride mobilization
–> Increased triglycerides –>
Fatty changes

106
Q

Alcoholism and hypoxia can contribute to fatty changes in the liver and/or heart….

What are the morphological features – microscopic and gross level?

A

In the liver you get big empty lipid droplets within the hepatocytes

Liver at the gross level it is enlarged, pale yellow, soft and greasy

Patho Phys Exam 1 (14 decks)

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