Inflammation Flashcards
212-217 (unfinished)
General description of necrosis?
Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury.
Intracellular components extravaste.
Inflammatory process (unlike apoptosis)
Places of coagulative necrosis?
Heart, liver, kidney
Places of liquefactive necrosis?
Brain, bacterial abscess, pleural effusion
Causes of caseous necrosis?
TB, systemic fungi
Places of fatty necrosis?
Peripancreatic fat (saponification via lipase)
Places of fibrinoid necrosis?
Blood vessels
Places of gangrenous necrosis?
Limbs, GI tract
Types of gangrenous necrosis?
Dry (ischemic coagulative); wet (w/ bacteria)
Characteristics of reversible cell injury?
Decreased ATP synth
Cellular swelling (no ATP –>impaired Na/K pump)
Nuclear chromatin clumping
Decreased glycogen
Fatty change
Ribosomal detachment (decreased protein synth)
Characteristics of irreversible cell injury?
Nuclear pyknosis, karyolysis, karyorrhexis Ca influx-->caspase activation Plasma mem damage Lysosomal rupture Mitochondrial permeability
Describe red infarcts and where/when do they occur.
Hemorrhagic. Occur in loose tissues with collaterals (liver, lungs, intestine) or following reperfusion injury
Pale infarcts: where/when do they occur.
Solid tissues w/ a single blood supply (heart, kidney, spleen)
General description of apoptosis?
Programmed cell death requiring ATP. Can occur via intrinsic or extrinsic pathway, both of which work by activating cytosolic caspases–>cell breakdown.
Does apoptosis involve inflammation?
NO
What are the characteristics of apoptosis?
Cell shrinkage Nuclear shrinkage (pyknosis) Basophilia Membrane blebbing Nuclear fragmentation (karyorrhexis) Formation of apoptotic bodies which are then phagocytosed
What are situations in which the intrinsic pathway of apoptosis occurs?
Tissue remodeling in embryogenesis; when a GF if withdrawn from a proliferating cell population; following exposure to injurious stimuli
How does the intrinsic path of apoptosis work? (general)
Changes in proportions of anti- and pro-apoptotic factors–>increased mitochondria permeability and cytochrome c release
What’s the main pro-apoptotic factor in the intrinsic pathway? anti-apop?
Pro: Bax
Anti:Bcl-2
What are the 2 general pathways of the extrinsic apoptosis path?
Ligand receptor interactions
Immune cell
How do ligand receptor interactions–> extrinsic path of apoptosis?
FasL binds Fas (CD95), which activates caspases
How do immune cells–> extrinsic path of apoptosis?
CTL release perforin and granzyme B–> holes in cell membrane
General characteristics of hypovolemic/cardiogenic shock?
Low-output failure
Incr TPR
Low cardiac output
Cold, clammy patient (vasoconstriction)
General characteristics of septic shock?
High-output failure
Decr TPR
Dilated arterioles, high venous return
Hot patient (vasodilation)
Iron poisoning is one of the leading causes of fatality from toxicologic agents in kids. What’s its MOA?
Cell death due to peroxidation of membrane lipids
What are the symptoms of acute iron poisoning?
Gastric bleeding
What are the symptoms of chronic iron poisoning?
Metabolic acidosis, scarring leading to GI obstruction. Can cause death from necrotizing gastroenteritis.
What are the 10 main granulomatous diseases?
- Mycobacterium tb
- Fungal infection
- Treponema pallidum (syphilis)
- M leprae (leprosy)
- Bartonella henselae (cat scratch disease)
- Sarcoidosis
- Crohn’s disease
- Granulomatosis w/ polyangiitis
- Churg-Strauss syndrome
- Beryllosis, silicosis
Which drugs can, as a side effect, cause sequestering granulomas to breakdown–> disseminated disease?
Anti-TNF alpha drugs
What’s the mechanism of granuloma formation?
TH1 cells secrete IFN gamma–> activating macrophages to secrete TNF alpha –>TNF alpha induces and maintains granuloma formation
