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MOD1 > CH3 > Flashcards

CH3 Flashcards

1
Q

What are the “5 Rs” of inflammation?

A 
Recognition
Recruit
Remove
Regulate
Repair
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2
Q

Can hypoxia trigger inflammation?

A

Yes

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3
Q

What do these mean: rubor, tumor, calor, dolar

A

Redness, swelling, heat, pain

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4
Q

What R’s recognize microbes? Where are they located?

A

Toll-like R’s (TLRs)

Throughout the entire cell

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5
Q

What do cytosolic R’s detect?

A 
Uric acid (DNA breakdown)
ATP (mito dmg)
low K (plasma membrane injury)
Free-floating DNA (nuclear dmg)
Urate crystals (gout)
Amyloid deposits (Alzheimer)
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6
Q

What contributes to permeability?

A

Endothelial cell contraction (subsequent elimination of tight junctions), transcytosis

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7
Q

What are extensive burns so dangerous?

A

Induces inflammation (histamine, vascular permeability) that is so extensive, the fluid loss in the vascular system may be fatal

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8
Q

What is lymphangitis?

A

Lymphatic inflammation

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9
Q

What is lymphadenitis?

A

Lymph node inflammation

D/t hyperplasia of lymphoid follicles and increased lymphocyte and macro numbers

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10
Q

Red streaks near a skin wound is a sign of what?

A

Wound infection that has spread to nearby lymphatic channels

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11
Q

What chemokines play a role in chemotaxis of neutrophils? How do neutrophils move during chemotaxis?

A

C5a, N-formylmethionine, IL-8, LTB4

Filopodia extension

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12
Q

What R’s do phagocytes have to initiate phagocytosis?

A

Mannose R’s: a lectin that binds mannose on microbial cell walls
Scavenger R’s: microbes, LDL particles
Opsonin R’s: C3b, IgG antibodies, mannose-binding lectin

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13
Q

What are the initial extensions during the engulfment phase of phagocytosis?

A

Psuedopods (cytoplasmic extensions) –> phagosome –> fuse with lysosomes

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14
Q

What are the enzymes that defend against ROS?

A 
SOD (superoxide dismutase)
Catalase
Glutathione peroxidase
Ceruloplasmin (binds Cu)
Tranferrin (binds Fe)
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15
Q

What is NO a product of?

A

Arginine and nitric oxide synthase (NOS)

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16
Q

What is ONOO-?

A

Peroxynitrate, a highly reactive FR made of NO and superoxide (O2-)

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17
Q

What is the role of alpha-1-antitrypsin?

A

Protease inh (prevents excessive tissue breakdown)

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18
Q

What does lysozyme do?

A

Cleaves acid-N-acetylglucosamine bond found in glycopeptide bacterial coats

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19
Q

What is major basic protein?

A

Found in esinophils, primary defense vs parasites

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20
Q

Why is IL-17 important?

A

Stimulates inflammation, if absent infection risk rises substantially

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21
Q

What leads to the termination of inflammation?

A 
Inflammation subsides when the irritant is removed
Mediators have short half-lifes
Neutrophils live short lives 
Lipoxin, TGF-b, IL-10
Neural impulses inh TNF
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22
Q

Where are complement proteins synthesized?

A

Liver

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23
Q

What does histamine bind to?

A

H1 R’s

H1 R antagonist is what antihistamine drugs are!

24
Q

What are the different chemokine groups?

A

CXC (IL-8)
CC (MCP-1), monocytes, eosinophils, basophils, lymphs
C (lymphocyte specific)
CXXXC (fractalkine, monocytes and T cells)

25
What is IL-6 made by? IL-17?
Macrophage T-lymphocytes (it promotes neutrophil recruitment)
26
What are the complement inh?
C1 inh DAF: prevent C3 convertase formation CD59: prevents MAC formation
27
What are kinin mediators derived from? What's an example?
Kininogens via kallikrein proteases Bradykinin
28
What is the role of bradykinin? PAF? Which is associated with ADP?
Increases vascular permeability and vasodilation, pain inducer, similar to histamine Vasoconstrictor and bronchoconstrictor, at low conc does the opposite plus increasing vascular permeability PAF
29
What do Substance P and neurokinin A do?
Increase vascular permeability
30
What are the different kinds of inflammation patterns? What are their details?
Serous, fibrinous, purulent Serous: transudate, fluid not infected, low leuk presence, skin blisters Fibrinous: fibrin in extracellular space, exudate, can cause scarring, pericardium/meninges/pleura Purulent (suppurative): abcess, puss, bacerial infection with liquefactive necrosis, acute appendicitis
31
What's an abscess?
Localized collection of purulent inflammatory tissue caused by purulent/suppuratory inflammation deep in the tissue Caused by seeding of pyogenic bacteria (acute inflammation) Central mass is pus May develop a walled off area over time
32
What are ulcers?
Surace excavation of tissue caused by surface inflammation, often seen in diabetics
33
What do macrophages activate with their MHC complexes? What's then released to increase macro activity?
T lymphocytes IFN-y
34
What are the special differentiated macros?
``` Kupffer cells (liver) Sinus histocytes (spleen and lymph nodes) Microglial cells (brain) Alveolar (lungs) ```
35
What cytokines activate M1 macros? M2?
M1: IFN-y, microbes M2: IL-4/13
36
What are the different CD4+ T lymphocytes and what do they promote?
TH1: IFN-y --> macro activation TH2: IL-4/5/13, eosinophils for parasite defense and M2 activation TH17: IL-17 --> neutrophil recruitment
37
In what dx does a neutrophil exudate persist for many months?
Osteomyelitis
38
What are prominent in the response to chronic lung damage caused by smoking?
Neutrophils
39
What's the state where macros differentiate? What are the types? How do the macros differentiate?
Granulomatous inflammation, foreign body (no response)and immune (response) Epitheloid cells (abundant cytoplasm) or giant cells (fused macros, multinucleated)
40
What are the mediators of the acute phase response?
TNF, IL-1, IL-6, type 1 interferons
41
What are the acute phase proteins?
CRP (via IL-6), opsoinin Fibrinogen (via IL-6), binds RBC forming stacks Serum amyloid A (via TNF or IL-1), opsonin Hepcidin, sequesters Fe during & can cause anemia
42
Leukocytosis vs leukemoid reactions vs lymphocytosis vs leucopenia.
Leukocytosis: response to bacterial infection, elevated white count Leukemoid reaction: extreme wbc elevation and looks like leukemia, causes left shift with immature neutrophils Increase in lymphocyte # Decreased circulating WBCs
43
Acute phase response does what to: sweating, BP, P, appetite, affect, body temp.
Decreases d/t blood internalization, raises, raises, lowers, malaise, rigors and chills
44
What are the degrees of tissue regeneration?
Labile Stable Permanent
45
What primes liver cells to respond to GFs? What GFs does the liver then respond to? What's the response? What's the termination GF?
IL-6 HGF and TGH-a, increased metabolism and entrance into the cell cycle TGF-B
46
What are the steps of scar formation?
Angiogenesis Granulation Remodeling
47
What causes vasodilation during angiogenesis?
NO, NOT VEGF (though VEGF-A stimulates NO production)
48
What growth factor stimulates endothelial proliferation during angiogenesis? Structural maturation? What suppresses angiogenesis?
FGF-2 Ang 1 & 2 PDGF and TGF-B, these increase ECM protein synthesis
49
What protein cross-talks with VEGF during angiogenesis to mediate sprouting/branching/spacing?
Notch
50
What enzymes degrade the ECM for remodeling during tissue repair?
MMP (matrix metalloproteinases)
51
What do M2 macros produce that contributes to the granulation of tissue?
PDGF, FGF-2, TGF-B
52
What inhibit MMPs (matrix metalloproteinases)?
TGF-B and TIMPs
53
What are the major collagen providers in fibrosis of organ parenchyma? What cytokine activates them?
``` Myofibroblasts (most organs) Stellate cells (liver) ``` TGF-B
54
Define dihiscence.
Rupture of a wound
55
Where are contractures most likely to occur?
Palms, soles, anterior thorax

MOD1 (5 decks)

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