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Pathology Test 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is necrosis?

A

Death of cells, tissue, or organs

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2
Q

What is ischemia?

A

Reversible injury due to inadequate blood supply (REVERSIBLE!)

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3
Q

What is infarction?

A

Irreversible necrosis

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4
Q

Definitions of etiology & morphology?

A 
etiology = cause
Morphology = visible manifestation
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5
Q

What does reserve capacity have to do with adaption?

A

Most vital organs hace a large reserve capacity to survive (don’t need it all to live, but do to maximize survival).

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6
Q

What is the danger of reserve capacity?

A

Common disease uses up reserve capacity silently until it is too late to fix.

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7
Q

Artherosclerosis

A

Narrowing of the lumen of blood vessels.

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8
Q

Pulmonary Emphysema

A

irreversible enlargement of airspaces due to destruction of the alveolar walls.

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9
Q

Dyspnea

A

SOB

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10
Q

Injury is defined as

A

reversible pathophysiologic and morphologic response to stress and noxious stimulus (exceeding capacity of cell/tissue/organ to adapt, but not enough to be lethal)

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11
Q

Reactive Oxygen Species (ROS) examples

A

superoxide, OH, radicals, and ONOO-

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12
Q

Amylase function

A

digests CHO

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13
Q

What secretes amylase?

A

pancreas (to duodenum) & salivary glands (to saliva)

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14
Q

Lipase is supposed to be release by what into what?

A

Pancreas secretes into duodenum

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15
Q

Lipase is not normally found in the

A

retroperitoneal peri-pancreatic fat

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16
Q

Pancreatitis causes

A

lipase to leak out into the retroperitoneal peri-pancreatic fat

Amylase & lipase to leak into blood stream

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17
Q

Creatine phosphokinase (CPK) AKA

A

Creatine kinase

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18
Q

Creatine Kinase concentrated in which organs?

A

Muscle: MM
Brain: BB
Heart: MB

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19
Q

Myocardial infarction releases what into blood stream?

A

Troponin

MB Creatine Kinase

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20
Q

What is the gold standard serum test for myocardial infarction?

A

Troponin

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21
Q

What do troponins do?

A

regulate calcium mediated contraction of all muscle.

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22
Q

Alanine Aminotransferase (ALT) formula

A

glutamate + pyruvate ⇌ α-ketoglutarate + alanine

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23
Q

Which is more specific for liver injury? ALT or AST?

A

ALT (even though there is much more AST in the liver and other organs)

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24
Q

Aspartate Aminotransferase (AST) formula

A

Aspartate (Asp) + α-ketoglutarate ↔ oxaloacetate + glutamate (Glu)

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25
Q

AST located where?

A

Liver, muscle, and other organs (general)

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26
Q

Alkaline Phosphate (alk phos) is released by liver when?

A

BIliary obstruction or hepatic space occupying lesion (general for abnormality).

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27
Q

Gamma-glutamyl-transferase (GGT) does what?

A

outer cell membrane enzyme that transports amino acids into cells

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28
Q

When is GGT released?

A

Toxic liver injuries

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29
Q

Lactate dehydrogenase converts what to what?

A

Lactate to pyruvate (removes 2 hydrogens)

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30
Q

When is LDH released?

A

Injury to RBC, liver, muscle, and other organs

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31
Q

What is coagulative necrosis?

A

morphologic, irreversible injury to a cell caused by ischemia (except brain!)

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32
Q

What is the maximum period of time the brain, heart, and liver can experience ischemia without major damage?

A

Brain: 3 minutes
Heart: 20 minutes
Liver: 2 hours

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33
Q

Ischemia not relieved in time leads to

A

infarction and irreversible necrosis

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34
Q

Coagulative necrosis features

A

eosinophilic cytoplasm (pink)
Nucleus is pyknosis, karyorrhexis, karyolysis
acute inflammatory response

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35
Q

Pyknosis

A

condensation, shrinkage, and hyperbasophilia of dead cell nucleus.

Apoptosis or necrosis

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36
Q

Karyorrhexis

A

fragmentation of dead nucleus

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37
Q

karyolysis

A

fading away of dead nucleus

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38
Q

Liquefactive necrosis

A

conversion of solid tissue to liquid

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39
Q

Causes of liquefactive necrosis

A

severe infection, toxicity, or ischemia in brain (exception)

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40
Q

What is an abscess?

A

localized liquefactive necrosis

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41
Q

Caseous Necrosis is what type of necrosis and looks like this?

A

Coagulative necrosis

Cheese

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42
Q

Gangrene is progressed?

A

Ischemia –> necrosis (specifically coagulative)

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43
Q

Fat Necrosis results from

A

Pancreatic lipase melting fat which reacts with calcium to form chalky white saponifications (soap)

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44
Q

What are features of apoptosis? (4)

A

1: cell shrinkage
2: hypereosinophilia
3: chromatin condensation and karyorrhexis
4: phagocytosis by macrophages

45
Q

Apoptosis has which feature about it?

A

Halo

46
Q

2 differences between Apoptosis and Necrosis?

A

Necrosis has an inflammatory response.

Apoptosis keeps its cell membrane intact.

47
Q

What are the 5 electrolytes involved with adaptation?

A

Potassium, Sodium, Bicarb, Cl, Calcium

48
Q

Why is Potassium the most important?

A

Abnormal levels impair the heart’s electrical signaling for synchronized contraction.

49
Q

Hypokalemia signs and symptoms

A

Muscle contraction interference (weakness and myalgias: muscle aches) in leg first.

Digestion shutdown (low peristalsis)

Tachycardia (irritable) and SOB

50
Q

Hyperkalemia signs and symptoms

A

Confusion and nerve malfunction (tingling and loss of reflex)

Bradycardia

Muscle weakness and myalgias

51
Q

Which is more likely to cause fatal cardiac arrhythmia? Hypo- or hyper- kalemia?

A

Hypokalemia

52
Q

Sodium’s role in the body?

A

Maintain tonicity of the bodily fluids (osmolality)

53
Q

Hyponatremia of blood and fluids causes the cell to do what?

S&S?

A

Water enters the cell (because Na content outside the cell is less)

If brain swells due to hyponatremia, leading to HA, confusion, malaise, coma, seizure, and death

54
Q

Severe Hypernatremia causes?

A

Depression of respiratory center in brain

55
Q

Bicarbonate influences?

A

Body pH blood buffer

CO2 + H2O H2CO3 HCO3- + H

56
Q

If low bicarb, what results?

A

Acidosis: too much acid or too little buffer.

Renal failure limits acid elimination or lactic acid build up.

57
Q

Respiratory failure would cause?

A

Acidosis in form of carbonic acid.

58
Q

What 2 things cause alkalosis?

A

Hyperventilation (opposite as resp failure)

Vomiting (leaves too much bicard around)

59
Q

Which enzyme passes the kidney tubules and is excreted?

A

Amylase.

If renal failure, increased serum amylase levels

60
Q

90% of acute pancreatitis cases have elevated lipase and amylase. What is the sensitivity for these combined tests?

A

90%

61
Q

Sense and Specif example:

40% of patients with elevated lipase do not have acute pancreatitis. What is the specificity of elevated lipase for acute pancreatitis?

A

60%

62
Q

What is the di Ritis ratio? Normal

A

AST over ALT

1.15 (15% higher)

63
Q

Acute hepatic injury leads to which di Ritis ratio? Chronic?

A

Acute: under 1
Chronic: over 1

64
Q

Bilirubin is

A

breakdown of heme excreted in urine and bile. Biliary function can be influenced by obstruction.

65
Q

Hyperbilirubinemia and a di Ritis of less than 1.5 indicates

A

biliary ductal obstruction outside the liver

66
Q

Hyperbilirubinemia and a di Ritis of over 1.5 indicates

A

biliary ductal obstruction inside the liver

67
Q

Alcohol causes which di Ritis ratio?

A

2-9 (but can be other diseases)

68
Q

Gamm-glutamyltransferase (GGT) has the function of? Which organ has the most GGT?

A

GGT transports amino acids into the cell. All cells have GGT, the liver has the most.

69
Q

Serum GGT will increase when

A

Acute viral hepatitis
Tylenol overdose
Alcohol
Extrahepatic biliary obstruction

70
Q

When are GGT levels higher than AST/ALT? (2)

A

Cholestasis (back up of bile) extrahepatic biliary obstruction

Alcoholic liver disease

71
Q

Alkaline Phosphatase serum is from primarily the

A

bone and liver

72
Q

Increased Alk Phos is primarily indicative of

A

Biliary Obstruction (especially extra- b/c hepatocytes produce more Alk Phos)

73
Q

Malignant tumors in the liver cause production of more Alk Phos or GGT?

A

ALP

74
Q

What is a primary cause of lactic buildup?

A

Ischemia and hypoxia (anaerobic metabolism)

75
Q

LDH builds up in

A

everything basically

76
Q

What is the difference between autolysis and necrosis?

A

Autolysis is the gradual fading of cells (die of old age)

Necrosis recruits acute inflammatory response while autolysis doesn’t.

77
Q

What are the 4 factors that determine ischemia is reversible or not?

A

1: Vulnerability of tissue
2: Rate of development
3: alternative blood supply
4: blood oxygenation

78
Q

Cerebral infarctions are which kind of necrosis?

A

Liquefactive

79
Q

During an M.I., what is elevated?

A

CPK MB, Troponin, AST, LDH

80
Q

Compare and contrast CPK MB and Troponin serum levels associated with M.I.?

A

Both start around 3 hours and peak at 24 hrs. But Troponin normalizes at 10 days while CPK MB levels out at 3 days.

81
Q

Treatment for Gangrene?

A

Cut it off.

82
Q

Treatment for Caseous Necrosis?

A

Looks like cheese, but caused by fungi and bacteria. Antifungals and anti-TB drugs

83
Q

Treatment for Liquefactive Necrosis?

A

Abscess: drain it.

84
Q

What is hypertrophy? Where’s it occur?

A

Increase in the size of cells.

Typically found in places in low capacity to proliferate (uterus-hormone, heart, muscle-mechanical)

85
Q

What is hyperplasia?

A

Increase in the amount of cells.

Prostate. Liver. Boobs.

86
Q

What is atrophy?

A

Decrease in size. Move it or lose it.

87
Q

Describe a kidney undergoing atrophy?

A

Ischemic. Decreases function. (denervation, decreased endocrine, aging, lower perfusion)

88
Q

What is metaplasia?

A

Cells change type.

89
Q

Is metaplasia reversible?

A

Always.

90
Q

Is metaplasia ever physiologic?

A

Never. Always pathological

91
Q

What is the progression of metaplasia?

A

Metaplasia becomes dysplasia which becomes neoplastic.

92
Q

What is Barrots esophagus?

A

Metaplasia from columnar to squamous.

93
Q

Smoking changes the epithelium in the respiratory tract from what to what?

A

Pseudo columnar to squamous

94
Q

HPV changes the uterus epithelium. What to what?

A

Columnar to squamous.

95
Q

Where does metaplasia start?

A

At the basement membrane.

96
Q

Is dysplasia pre-neoplastic?

A

Basically always.

97
Q

There are three brown pigments. Go.

A

Iron compounds
Lipfuschin
Melanin.

98
Q

What are the iron compounds that stain brown?

A

Ferritin

Hemosidderin.

99
Q

Prussian blue stain is to detect which pigment?

A

Iron.

100
Q

What is the wear and tear figment?

A

Lipofuchsin.

101
Q

Melanin is used to do what?

A

Absorb uv rays and acts as a free radical reservoir.

102
Q

What are the black pigments?

A

Typically are carbon.

103
Q

How are we exposed to black pigment and what happens if it spreads?

A

Pulmonary is the main way to get carbon.

“anthracosis” is the term for spreading to lung nodes and distant tissue. It’s ok if nothing reacts with it.

104
Q

Calcification is typically dystrophic or metaplastic?

A

Dystrophic

105
Q

Dystrophic calcification. Describe

A

Localized and related to some tissue injury

106
Q

What types of lipids can accumulate?

A

Triglycerides

Cholesterol.

107
Q

What is steatosis?

A

Deposits of fat (liver perhaps)

108
Q

Kwashiorkor malnutrition is what kind of diet? Why steatosis?

A

High carb, low protein diet

Can’t export the fats from the liver.

Pathology Test 1 (7 decks)

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