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Pathology > 1-Cell Responses to Bad Things > Flashcards

1-Cell Responses to Bad Things Flashcards

1
Q

Give me a definition of pathology.

A

the study of disease and the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease

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2
Q

What does general pathology study?

A

The study where CELLS and TISSUES react to abnormal stimuli, which are the cause of disease

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3
Q

What does Systemic pathology study?

A

Studies alterations in specialized ORGANS and tissues that are responsible for disorders

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4
Q

What are the 2 etiologies for disease?

A

Genetic or acquired

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5
Q

What is the pathogenesis of disease? (generally)

A

The sequence of events in the response of cells or tissues to a harmful agent

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6
Q

What does diagnostic pathology study?

A

morphological changes in tissues to identify the nature and progression of disease

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7
Q

What is adaptation?

A

The ability to adjust and come with change.

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8
Q

What happens if the cell stress exceedes adaptive capabilities?

A

Cell injury

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9
Q

Name 4 different cell adaptations to stress/injury

A

Hypertrophy (increase size), Hyperplasia (increase #), Atrophy (decrease size and fxn) and Metaplasia (change phenotype)

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10
Q

What types of injuries are reversible?

A

mild or transient, no damaging or long term effects. (like hypoxia)

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11
Q

What types of injuries are irreversible?

A

If it’s long and progressive, causing necrosis or apoptosis

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12
Q

What occurs during hypertrophy?

A

increase in SIZE of cells, not #’s.

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13
Q

What happens to an organ when it’s cells undergo hypertrophy?

A

It gets bigger and heavier, like cardiac or skeletal muscle in athletes.

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14
Q

What types of molecules signal a cell to undergo hypertrophy?

A

Growth factors and vasoactive agents

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15
Q

Which signaling pathway does a cell use for physiological hypertrophy?

A

P3K/Akt pathway

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16
Q

Which signaling pathway does a cell use for pathological hypertrophy?

A

G-proteins

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17
Q

What kind of drugs make the smooth ER selectively hypertrophic?

A

Barbituates

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18
Q

What occurs during hyperplasia?

A

Increase in the NUMBER of cells in an organ

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19
Q

What signals cells to undergo hyperplasia?

A

Growth factors

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20
Q

When do cells undergo physiological hormonal hyperplasia?

A

when the tissue needs an increase in functional capacity

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21
Q

What are some examples of hormonal hyperplasia?

A

proliferation of the glandular epithelium of the boob (puberty and pregnancy)

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22
Q

When do cells undergo physiological compensatory hyperplasia?

A

After damage. It increases the tissue mass.

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23
Q

What is the famous example of compensatory hyperplasia?

A

Liver resection causes partial re-growth of the liver by compensatory hyperplasia (look up myth of prometheus)

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24
Q

When does pathological hyperplasia occur?

A

When there is excess hormones or growth factors

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25
Q

What are some examples of pathological hyperplasia?

A

endometrial hyperplasia (menstration), benign prostatic hyperplasia (BPH)

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26
Q

What occurs during atrophy?

A

The organ/tissue is reduced in size from a decrease in cell size and number

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27
Q

What are some examples of physiological (normal) atrophy?

A

Embryonic structures (notocord), and uterus (postpartum)

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28
Q

What are some causes of pathological atrophy?

A

Decreased workload, denervation, low blood supply, and bad nutrition

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29
Q

What decreases in the cell to cause atrophy?

A

Protein synthesis

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30
Q

What happens in autophagy?

A

The cell eats its own components to survive.

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31
Q

What occurs in metaplasia?

A

It’s a reversible change, where 1 differentiated cell type is replaced with another cell type.

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32
Q

How does metaplasia and GERD relate?

A

When stomach acid irritates the esophagus for a long time, it undergoes metaplasia from squamous to columnar

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33
Q

How does metaplasia and smoking relate?

A

Chronic irritation of the respiratory tract causes metaplasia from columnar to squamous (thereby losing it’s cilia and ability to transport phlem cough cough)

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34
Q

What occurs in connective tissue metaplasia?

A

When tissues undergo trauma, cartilage, bone or adipose tissue can form in the tissues that do not contain these elements. Whaaaaaaaaaaaaaaaaaaaa

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35
Q

Does metaplasia change the phenotype of an already differentiated cell?

A

No. It reprograms the STEM cells to differentiate into a new cell type.

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36
Q

Why does hypoxia injure cells?

A

No oxphos –> no ATP –> bad things.

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37
Q

What are some morpholgical signs of reversible injury?

A

cell swelling, blebbing of membrane, detachment of ribosomes, and clumping of nuclear chromatin.

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38
Q

Why does cell swelling occur in reversible injury?

A

Loss of ATP production –> failure of Na/K ATPases on plasma membrane –> more Na in cell –> cell swells

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39
Q

When the injurious stimulus isn’t removed, and the cell injury becomes irreversible, what is the sequence of morphological events that occurs?

A

(BULG). Biochemical alterations –> Ultrastructural changes –> Light microscopy changes –> Gross morphological changes.

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40
Q

What is the first sign of cell injury?

A

Cell swelling

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41
Q

What part of the cell is injured for a cell to undergo necrosis?

A

Membrane.

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42
Q

What part of the cell is injured for a cell to undergo apoptosis?

A

DNA

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43
Q

Generally, what is the pathogenesis of necrosis?

A

membrane injured –> cell swells –> cell components leak out of cell –> inflammation of tissue

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44
Q

Is necrosis pathological, physiological, or both?

A

ALWAYS Pathological

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45
Q

What is the general pathogenesis of apoptosis?

A

DNA injured –> cell signals itself to die –> shrinks –> fragments into nucleosome-sized fragments –> cell membrane remains intact –> apoptotic bodies are eaten

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46
Q

Is apoptosis pathological, physiological, or both?

A

Both

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47
Q

Coagulative necrosis- cause

A

ischemia

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48
Q

Coagulative necrosis- clinical presentation

A

firm, eosinophilic, anucleate cells

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49
Q

Liquefactive necrosis- cause

A

focal bacterial infections

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50
Q

Liquefactive necrosis- clinical presentation

A

creamy yellow (pudding) discharge in CNS, hypoxic death of cells in CNS

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51
Q

What type of necrosis is gangrene?

A

Nothing specific- used in clinical practice to say it’s a combo of coagulative and liquefactive necrosis

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52
Q

Caseous necrosis- cause

A

TB infections

53
Q

Caseous necrosis- clinical presentation

A

“Cheese”-like consistency of tissue, form granulomas

54
Q

Why is the pattern of fat necrosis weird?

A

Because it’s not specific- just used clinically

55
Q

Fat necrosis- cause

A

release of pancreatic lipases into the pancreas and peritoneal cavity

56
Q

Fat necrosis- clinical presentation

A

Focal areas of fat destruction, usually asympomatic

57
Q

Fibrinoid necrosis- cause

A

complexes of antigens and antibodies deposit into the walls of arteries

58
Q

Fibrinoid necrosis- clinical presentation

A

bright pink fibrinoid on histological cross section

59
Q

What % of ATP depletion is needed before problems occur?

A

Only 5-10% depletion

60
Q

Why is ATP bad for Ca homeostasis?

A

Ca++ ATPase pump fails –> influx of Ca++

61
Q

What 3 things injure mitochondria?

A

Ca++, ROS, and low O2

62
Q

What is the function of the high-conductance pore when mitochondria are injured?

A

loss of mitochondrial membrane potential –> failure of oxphos –> NECROSIS

63
Q

What are the function of the caspases and cytochrome c on the mitochrondrial membrane?

A

they’re enzymes that can be bound when DNA is damaged –> these leak into the cytosol –> death by APOPTOSIS

64
Q

Is cytosolic free Calcium high or low in the cell?

A

Very very very low.

65
Q

Where is Ca++ stored?

A

mitochondria and ER

66
Q

Increased Ca++ activates which enzymes?

A

(PEA’s). Phospholipases, Endonucleases, ATPases

67
Q

Which 2 metals causes ROS formation?

A

Cu and Fe

68
Q

What do ROS’s do to lipids in membranes?

A

It peroxidizes them, attacking the double bonds.

69
Q

What is the effects of ROS’s on proteins?

A

They oxidize proteins, changing the morphology.

70
Q

What is the effects of ROS’s on DNA?

A

ROS’s can cause single and double strand breaks as well cross linking of the strands.

71
Q

If a tissue is hypoxic, what energy-producing pathway can still occur?

A

Anaerobic glycolysis

72
Q

What is hypoxia?

A

When there is a reduced O2 availability from various causes

73
Q

Which is worse: hypoxia or ischemia? Why?

A

Ischemia. It’s worse because O2 and nutrients are decreased, therefore over time even glycolysis can’t occur.

74
Q

What is ischemia-reperfusion injury?

A

Reperfused tissues may lose more cells at the end of ischemia.

75
Q

What is the mechanism behing ischemia-reperfusion injury?

A

Either from cell antioxidant defense mechanisms are down and/or Ca may enter reperfused cells.

76
Q

What is the most affected organ by adverse reactions of drugs?

A

The liver. Most of drug metabolism happens there.

77
Q

What is direct chemical cell injury?

A

Where chemicals bind directly to critical molecular components on cells.

78
Q

What is indirect chemical cell injury?

A

Chemicals are converted to a reactive toxic metabolite and then can cause membrane damage by making ROS’s

79
Q

Does apoptosis elicit an inflammatory reaction in the cell?

A

No. The apoptotic bodies are rapidly eaten b4 cell contents leak out.

80
Q

Why is apoptosis a normal physiological process?

A

It maintains homeostasis by regulating cell populations and harmful cell populations.

81
Q

In apoptosis, do cells grow or shrink?

A

Shrink

82
Q

What is the most characteristic feature of apoptosis?

A

Chromatin condensation.

83
Q

What eats apoptotic bodies?

A

Macrophages

84
Q

The intrinsic pathway of apoptosis is a result of what dysfunction?

A

increased mitochondrial permeability

85
Q

The intrinsic pathway of apoptosis leads to the activation of what initiating caspase?

A

Caspase 9

86
Q

The extrinsic pathway of apoptosis is a result of what dysfunction?

A

Binding of plasma membrane death receptors (TNF’s)

87
Q

The extrinsic pathway of apoptosis leads to the activation of what initiating caspases?

A

Caspase 8 and 10

88
Q

The extrinsic and intrinsic apoptotic pathways lead to the activation of what 2 executing caspases?

A

Caspase 3 and 6

89
Q

Apoptosis is triggered mainly by DNA damage, but what other 2 mechanisms can trigger apoptosis?

A

growth factor deprivation and protein misfolding.

90
Q

How can there be intracellular accumulations if a substance’s rate of metabolism is altered?

A

If the production is normal but the rate of metabolism to remove it is inadequate, then it can accumulate in cells.

91
Q

How can a substance accumulate in cells if the transport is altered?

A

Defects in protein folding and transport can accumulate the substance, and is part of a lot of degenerative disorders in the CNS

92
Q

How can a substance accumulate in cells if a substances enzymes are altered?

A

If the enzymes are altered, the metabolism is altered for the substance and can cause storage disorders.

93
Q

What happens if a cell can’t metabolize or transport a substance?

A

It accumulates, like carbon particles.

94
Q

What is steatosis?

A

Abnormal accumulations of triglycerides in parenchymal cells (liver, heart, muscle, kidney)

95
Q

What types of things cause steatosis?

A

toxins, protein malnutrition, diabeeeetus, obesity, alcoholism and anoxia

96
Q

What is the main mechanism behind triglyceride accumulations in the liver?

A

Either there is WAYYY to much coming in or it’s export mechanism is defective.

97
Q

Why does alcoholism cause fatty accumulations in the liver?

A

Because it causes a reduced breakdown and an increased synthesis of fats in the liver.

98
Q

What is the histological appearance of fatty accumulations?

A

Clear vacuoles

99
Q

What types of staining could you use to identify fatty accumulations on a histological specimen?

A

Sudan IV or Oil Red-O (shows up orange-red)

100
Q

What is the gross examination of a liver with fatty accumulations?

A

Yellow, heavy, greasy (like a McDonalds hamburger patty)

101
Q

Atherosclerotic plaques are an accumulation of what substance?

A

Cholesterol

102
Q

What is the histological appearance of atherosclerotic plaques?

A

Foamy

103
Q

What are Xanthomas?

A

clusters of foamy cells in the subepithelial connective tissue, showing up as yellow wart-type things on the skin

104
Q

An accumulation of what substance in macrophages causes xanthomas?

A

Cholesterol

105
Q

What is cholesterolosis?

A

focal accumulations of cholesterol-laden macrophages in the gallbladder

106
Q

Neimann-Pick disease is a defect in what cellular organelle?

A

Lysosomes

107
Q

Neimann-Pick disease involves accumulations of what substance?

A

Cholesterol

108
Q

What is the histological appearance of intracellular protein accumulations?

A

Rounded, eosinophilic droplets, vacuoles or aggregates in the cytoplasm.

109
Q

Protein accumulations are best seen in which organ?

A

Kidney (renal tubules)

110
Q

If there is a defect in the protein α1-antitrypsin, what clinical manifestation might occur?

A

Emphysema

111
Q

Accumulations of the cytoskeletal proteins keratin intermediate filaments in the liver is indicative of what chronic condition?

A

Alcoholism

112
Q

Accumulations of the cytoskeletal proteins cause neurofibrillary tangles in the CNS, which is indicative of what chronic condition?

A

Alzheimers

113
Q

What is the histological appearance of hyaline accumulations?

A

homogenous, glassy, pink

114
Q

What is the histological appearance of glycogen accumulations?

A

Clear vacuoles in the cytoplasm

115
Q

Tattoing causes pigment accumulation in what dermal cells?

A

Macrophages

116
Q

What endogenous pigment is the “wear-and-tear” pigment, and is the tell tale sign of ROS injury?

A

Lipofuscin

117
Q

What is the histological appearance of lipofuscin?

A

Yellow-brown, finely granular, often perinuclear

118
Q

How is melanin synthesized in melanocytes?

A

Tyrosine —-Tyrosinase—> DHPhe

119
Q

Hemosiderin serves to store which substance?

A

Fe

120
Q

What is the histological appearance of hemosiderin?

A

Yellow-to-brown, granular

121
Q

What 3 conditions can cause hemosiderin accumulations?

A

(Basically anything that increases Fe). 1. eating more Fe, 2. hemolytic anemia, 3. repeated blood transfusions

122
Q

What is the histological appearance of Fe pigments?

A

coarse, blue granular pigments in the cytoplasm (under Prussian blue histological stain)

123
Q

When does dystrophic calcification occur?

A

When tissues are dying. Remember dy- for dy-

124
Q

In distrophic calcification, are serum levels of Ca increased, decreased, or normal?

A

Normal. There is no problem with Ca metabolism, just that local tissues are necrosing.

125
Q

When does metastatic calcification occur?

A

When there is an issue with Ca metabolism, and there is Ca deposition in otherwise normal tissues.

126
Q

In metastatic calcification, are serum levels of Ca increased, decreased, or normal?

A

Increased

127
Q

Increased secretion of what hormone can cause metastatic calcification?

A

PTH

128
Q

What is the morphological appearance of calcium salt accumulations?

A

basophilic, amorphous granular, clumped, either extra- or intracellular

129
Q

What 2 effects lead to cellular aging?

A

Genetic abnormalities and/or cellular damage.

Pathology (4 decks)

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