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H&D > Wk 2 Path Lab > Flashcards

Wk 2 Path Lab Flashcards

1
Q

4 common causes of cellular injury

A
  1. inflammation
  2. nutritional deficiency or excess
  3. hypoxia
  4. trauma
  5. genetic mutation
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2
Q

3 causes of hypoxia

A
  1. ischemia
  2. hypoxemia
  3. decreased O2-carrying capacity of blood
    4.
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3
Q

What is the consequence of decreased oxygen?

A

Impaired oxidative phosphorylation -> decreased ATP production
Lack of ATP -> cellular injury

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4
Q

4 causes of hypoxemia

A
  1. high altitude
  2. hypoventilation
  3. diffusion defect
  4. V/Q mismastch
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5
Q

What is the hallmark of reversible injury?

A

cellular swelling

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6
Q

What does cellular swelling lead to?

A

loss of microvilli
membrane blebbing
swelling of RER

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7
Q

What is the hallmark of irreversible injury?

A

Cellular membrane damage

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8
Q

What 3 membranes can be damaged to -> irreversible damage?

A
  1. cell membrane
  2. mitochondrial membrane
  3. lysosome membrane
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9
Q

What 2 things does plasma membrane damage result in?

A
  1. cytosolic enzymes leaking into the serum (cardiac troponin)
  2. additional calcium entering the cell
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10
Q

What does mitochondrial membrane damage lead to?

A
  1. loss of electron transport chain (inner mito membrane)
  2. Cytochrome C leaking into cytosol (activates apoptosis)
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11
Q

What is the end result of irreversible injury?

A

cell death

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12
Q

What is the morphologic hallmark of cell death?

A

Loss of nucleus

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13
Q

How does loss of cell death occur?

A
  1. pyknosis (= nuclear condensation)
  2. karyorrhexis (=fragmentation)
  3. karyolysis (=dissolution)
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14
Q

What is necrosis?

A

= death of a large group of cells followed by acute inflammation
-divided into types based on gross features

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15
Q

6 types of necrosis

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. gangrenous necrosis
  4. caseous
  5. fat
  6. fibrinoid
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16
Q

6 types of necrosis

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. gangrenous necrosis
  4. caseous
  5. fat
  6. fibrinoid
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17
Q

What is coagulative necrosis?

A
  1. tissue remains firm
  2. cell shape and organ structure preserved
  3. nucleus disappears
  4. characteristic of ischemic infarction of any organ except the brain
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18
Q

Which one is necrosis and what is it of?

A

L is necrosis - no nuclei in glomerulus or tubules
-often pale and wedge-shaped, pointing toward area of occlusion

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19
Q

What is red infarction?

A
  1. blood has re-entered the tissue
  2. the tissue is loosely organized
20
Q

What is liquefactive necrosis?

A

= enzymatic lysis of cells and protein results in liquifaction

21
Q

Where/when is liquifaction necrosis found?

A
  1. brain infarction - proteolytic enzymes from microglial cells liquify the brain
  2. abscess - proteolytic enzymes from neutrophils liquify tissue
  3. pancreatitis - proteolytic enzymes from pancrease liquefy parenchyma
22
Q

What is gangrenous necrosis?

A

=coagulative necrosis that resembles mummified tissue

23
Q

When/where is gangrenous necrosis found?

A

ischemia of lower limb and GI tract
-if superimposed infection of dead tissues occurs, then liquifactive necrosis ensues (wet gangrene)

24
Q

What is caceous necrosis?

A

= soft and friable necrotic tissue
-“cottage cheese-like” appearance
-combination of coagulative and liquefactive necrosis

25
Q

Where/when is caseous necrosis found?

A

char of granulomatous inflammation due to TB or fungal infection

26
Q

What is fat necrosis?

A

=necrotic adipose tissue w/ chalky-white appearance due to deposition of calcium

27
Q

When and why does fat necrosis occur?

A

characteristic of trauma to fat and pancreatitis-mediated damage of peripancreatic fat
-fatty acids released by trauma or lipase join w/ calcium via saponification

28
Q

What is fibrinoid necrosis?

A

=necrotic damage to blood vessel wall

29
Q

When/where and why does fibrinoid necrosis occur?

A

leaking of proteins (ie fibrin) into vessel wall -> microscopic pink staining

-characteristic of malignant hypertension and vasculitis

30
Q

What are 3 normal occurrences of apoptosis?

A
  1. endometrial shedding during menstrual cycle
  2. removal of cells during embryogenesis (b/w fingers and toes)
  3. CD8+ T cell-mediated killing of virally infected cells
30
Q

What are 3 normal occurrences of apoptosis?

A
  1. endometrial shedding during menstrual cycle
  2. removal of cells during embryogenesis (b/w fingers and toes)
  3. CD8+ T cell-mediated killing of virally infected cells
31
Q

What are the morphological changes that occur w/ apoptosis?

A
  1. dying cell shrinks, leading cytoplasm to condense and become more eosinophilic (pink)
  2. nucleus condenses and fragments in organized manner
  3. apoptotic bodies fall from the cell and are removed by macrophages (not followed by inflammation)
32
Q

What mediates apoptosis?

A

Capases (enzymes) activate proteases to breakdown cytoskeletion and endonucleases to breakdown DNA

33
Q

How are caspases activated?
3 pathways

A
  1. intrinsic mitochondrial pathway
  2. extrinsic receptor-ligand pathway
  3. cytotoxic CD8+ T cell-mediated pathway
34
Q

How are caspases activated?
3 pathways

A
  1. intrinsic mitochondrial pathway
  2. extrinsic receptor-ligand pathway
  3. cytotoxic CD8+ T cell-mediated pathway
35
Q

What is the intrinsic mito pathway?

A
  1. cellular injury, DNA damage or decreased hormonal stimulation -> inactivation of Bcl2
  2. Lack of Bcl2 allows cytochrome C to leak from the inner mito matrix into the cytoplasm, activates caspases
36
Q

What is the intrinsic mito pathway?

A
  1. cellular injury, DNA damage or decreased hormonal stimulation -> inactivation of Bcl2
  2. Lack of Bcl2 allows cytochrome C to leak from the inner mito matrix into the cytoplasm, activates caspases
37
Q

What is the extrinsic receptor-ligand pathway?

A
  1. FAS ligand binds FAS death receptor (CD95) on the target cell, activating caspases
  2. TNF binds TNF receptor on target cell, activating caspases
38
Q

What is the cytotoxic CD8+ T cell-mediated pathway?

A
  1. perforins secreted by CD8+ T cell create pores in membrane of target cell
  2. Granzyme from CD8+ T cell enters pores and activates caspases
  3. CD8+ T-cell killing of virally infected cells is an example
39
Q

What characterizes acute inflammation?

A
  1. presence of edema and neutrophils in tissue
  2. innate immunity activation
40
Q

What characterizes acute inflammation?

A
  1. presence of edema and neutrophils in tissue
  2. innate immunity activation
41
Q

5 mediators of acute inflammation

A
  1. TLRs
  2. Arachidonic acid metabolites
  3. Mast cells
  4. Complement
  5. Hageman Factor (Factor XII)
42
Q

What are TLRs?

A

Toll-like receptors that recognize PAMPs
ex. CD14 present on macrophages that recognizes LPS of GN bacteria
-> activates transcription factor NF-kB -> immune response genes activated -> mediators generated
-also on lymphocytes, so have role in mediating chronic inflammation

43
Q

What is arachidonic acid

A

-released from phospholipid cell membrane by phospholipase A2
-acted on by cycooxygenase (produces prostaglandins - mediate vasodilation and vascular permeability) or 5-lipooxygenase (produces leukotrienes that attract neutrophils)

44
Q

Where are mast cells?

A

Throughout CT

45
Q

What activates mast cells?

A
  1. tissue trauma
  2. complement proteins C3a and C5a
  3. cross-linking of cell surface IgE by antigen
46
Q

What activates mast cells?

A
  1. tissue trauma
  2. complement proteins C3a and C5a
  3. cross-linking of cell surface IgE by antigen

H&D (23 decks)

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