Inflammation

Question 1

General description of necrosis?

Answer 1

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury.
Intracellular components extravaste.
Inflammatory process (unlike apoptosis)

Question 2

Places of coagulative necrosis?

Answer 2

Heart, liver, kidney

Question 3

Places of liquefactive necrosis?

Answer 3

Brain, bacterial abscess, pleural effusion

Question 4

Causes of caseous necrosis?

Answer 4

TB, systemic fungi

Question 5

Places of fatty necrosis?

Answer 5

Peripancreatic fat (saponification via lipase)

Question 6

Places of fibrinoid necrosis?

Answer 6

Blood vessels

Question 7

Places of gangrenous necrosis?

Answer 7

Limbs, GI tract

Question 8

Types of gangrenous necrosis?

Answer 8

Dry (ischemic coagulative); wet (w/ bacteria)

Question 9

Characteristics of reversible cell injury?

Answer 9

Decreased ATP synth
Cellular swelling (no ATP –>impaired Na/K pump)
Nuclear chromatin clumping
Decreased glycogen
Fatty change
Ribosomal detachment (decreased protein synth)

Question 10

Characteristics of irreversible cell injury?

Answer 10

Nuclear pyknosis, karyolysis, karyorrhexis
Ca influx-->caspase activation
Plasma mem damage
Lysosomal rupture
Mitochondrial permeability

Question 11

Describe red infarcts and where/when do they occur.

Answer 11

Hemorrhagic. Occur in loose tissues with collaterals (liver, lungs, intestine) or following reperfusion injury

Question 12

Pale infarcts: where/when do they occur.

Answer 12

Solid tissues w/ a single blood supply (heart, kidney, spleen)

Question 13

General description of apoptosis?

Answer 13

Programmed cell death requiring ATP. Can occur via intrinsic or extrinsic pathway, both of which work by activating cytosolic caspases–>cell breakdown.

Question 14

Does apoptosis involve inflammation?

Answer 14

NO

Question 15

What are the characteristics of apoptosis?

Answer 15

Cell shrinkage
Nuclear shrinkage (pyknosis)
Basophilia
Membrane blebbing
Nuclear fragmentation (karyorrhexis)
Formation of apoptotic bodies which are then phagocytosed

Question 16

What are situations in which the intrinsic pathway of apoptosis occurs?

Answer 16

Tissue remodeling in embryogenesis; when a GF if withdrawn from a proliferating cell population; following exposure to injurious stimuli

Question 17

How does the intrinsic path of apoptosis work? (general)

Answer 17

Changes in proportions of anti- and pro-apoptotic factors–>increased mitochondria permeability and cytochrome c release

Question 18

What’s the main pro-apoptotic factor in the intrinsic pathway? anti-apop?

Answer 18

Pro: Bax
Anti:Bcl-2

Question 19

What are the 2 general pathways of the extrinsic apoptosis path?

Answer 19

Ligand receptor interactions

Immune cell

Question 20

How do ligand receptor interactions–> extrinsic path of apoptosis?

Answer 20

FasL binds Fas (CD95), which activates caspases

Question 21

How do immune cells–> extrinsic path of apoptosis?

Answer 21

CTL release perforin and granzyme B–> holes in cell membrane

Question 22

General characteristics of hypovolemic/cardiogenic shock?

Answer 22

Low-output failure
Incr TPR
Low cardiac output
Cold, clammy patient (vasoconstriction)

Question 23

General characteristics of septic shock?

Answer 23

High-output failure
Decr TPR
Dilated arterioles, high venous return
Hot patient (vasodilation)

Question 24

Iron poisoning is one of the leading causes of fatality from toxicologic agents in kids. What’s its MOA?

Answer 24

Cell death due to peroxidation of membrane lipids

Question 25

What are the symptoms of acute iron poisoning?

Answer 25

Gastric bleeding

Question 26

What are the symptoms of chronic iron poisoning?

Answer 26

Metabolic acidosis, scarring leading to GI obstruction. Can cause death from necrotizing gastroenteritis.

Question 27

What are the 10 main granulomatous diseases?

Answer 27

1. Mycobacterium tb
2. Fungal infection
3. Treponema pallidum (syphilis)
4. M leprae (leprosy)
5. Bartonella henselae (cat scratch disease)
6. Sarcoidosis
7. Crohn’s disease
8. Granulomatosis w/ polyangiitis
9. Churg-Strauss syndrome
10. Beryllosis, silicosis

Question 28

Which drugs can, as a side effect, cause sequestering granulomas to breakdown–> disseminated disease?

Answer 28

Anti-TNF alpha drugs

Question 29

What’s the mechanism of granuloma formation?

Answer 29

TH1 cells secrete IFN gamma–> activating macrophages to secrete TNF alpha –>TNF alpha induces and maintains granuloma formation