Wk 2 Path Lab

Question 1

4 common causes of cellular injury

Answer 1

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

Question 2

3 causes of hypoxia

Answer 2

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

Question 3

What is the consequence of decreased oxygen?

Answer 3

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

Question 4

4 causes of hypoxemia

Answer 4

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

Question 5

What is the hallmark of reversible injury?

Answer 5

cellular swelling

Question 6

What does cellular swelling lead to?

Answer 6

loss of microvilli
membrane blebbing
swelling of RER

Question 7

What is the hallmark of irreversible injury?

Answer 7

Cellular membrane damage

Question 8

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

Answer 8

1. cell membrane
2. mitochondrial membrane
3. lysosome membrane

Question 9

What 2 things does plasma membrane damage result in?

Answer 9

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

Question 10

What does mitochondrial membrane damage lead to?

Answer 10

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

Question 11

What is the end result of irreversible injury?

Answer 11

cell death

Question 12

What is the morphologic hallmark of cell death?

Answer 12

Loss of nucleus

Question 13

How does loss of cell death occur?

Answer 13

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

Question 14

What is necrosis?

Answer 14

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

Question 15

6 types of necrosis

Answer 15

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

Question 16

6 types of necrosis

Answer 16

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

Question 17

What is coagulative necrosis?

Answer 17

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

Question 18

Which one is necrosis and what is it of?

Answer 18

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

Question 19

What is red infarction?

Answer 19

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

Question 20

What is liquefactive necrosis?

Answer 20

= enzymatic lysis of cells and protein results in liquifaction

Question 21

Where/when is liquifaction necrosis found?

Answer 21

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

Question 22

What is gangrenous necrosis?

Answer 22

=coagulative necrosis that resembles mummified tissue

Question 23

When/where is gangrenous necrosis found?

Answer 23

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

Question 24

What is caceous necrosis?

Answer 24

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

Question 25

Where/when is caseous necrosis found?

Answer 25

char of granulomatous inflammation due to TB or fungal infection

Question 26

What is fat necrosis?

Answer 26

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

Question 27

When and why does fat necrosis occur?

Answer 27

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

Question 28

What is fibrinoid necrosis?

Answer 28

=necrotic damage to blood vessel wall

Question 29

When/where and why does fibrinoid necrosis occur?

Answer 29

leaking of proteins (ie fibrin) into vessel wall -> microscopic pink staining -characteristic of malignant hypertension and vasculitis

Question 30

What are 3 normal occurrences of apoptosis?

Answer 30

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

Question 30

What are 3 normal occurrences of apoptosis?

Answer 30

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

Question 31

What are the morphological changes that occur w/ apoptosis?

Answer 31

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)

Question 32

What mediates apoptosis?

Answer 32

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

Question 33

How are caspases activated? 3 pathways

Answer 33

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

Question 34

How are caspases activated? 3 pathways

Answer 34

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

Question 35

What is the intrinsic mito pathway?

Answer 35

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

Question 36

What is the intrinsic mito pathway?

Answer 36

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

Question 37

What is the extrinsic receptor-ligand pathway?

Answer 37

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

Question 38

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

Answer 38

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

Question 39

What characterizes acute inflammation?

Answer 39

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

Question 40

What characterizes acute inflammation?

Answer 40

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

Question 41

5 mediators of acute inflammation

Answer 41

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

Question 42

What are TLRs?

Answer 42

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

Question 43

What is arachidonic acid

Answer 43

-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)

Question 44

Where are mast cells?

Answer 44

Throughout CT

Question 45

What activates mast cells?

Answer 45

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

Question 46

What activates mast cells?

Answer 46

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