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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
Q

What is IL-6 made by? IL-17?

A

Macrophage

T-lymphocytes (it promotes neutrophil recruitment)

26
Q

What are the complement inh?

A

C1 inh
DAF: prevent C3 convertase formation
CD59: prevents MAC formation

27
Q

What are kinin mediators derived from? What’s an example?

A

Kininogens via kallikrein proteases

Bradykinin

28
Q

What is the role of bradykinin? PAF? Which is associated with ADP?

A

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
Q

What do Substance P and neurokinin A do?

A

Increase vascular permeability

30
Q

What are the different kinds of inflammation patterns? What are their details?

A

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
Q

What’s an abscess?

A

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
Q

What are ulcers?

A

Surace excavation of tissue caused by surface inflammation, often seen in diabetics

33
Q

What do macrophages activate with their MHC complexes? What’s then released to increase macro activity?

A

T lymphocytes

IFN-y

34
Q

What are the special differentiated macros?

A 
Kupffer cells (liver)
Sinus histocytes (spleen and lymph nodes)
Microglial cells (brain)
Alveolar (lungs)
35
Q

What cytokines activate M1 macros? M2?

A

M1: IFN-y, microbes
M2: IL-4/13

36
Q

What are the different CD4+ T lymphocytes and what do they promote?

A

TH1: IFN-y –> macro activation
TH2: IL-4/5/13, eosinophils for parasite defense and M2 activation
TH17: IL-17 –> neutrophil recruitment

37
Q

In what dx does a neutrophil exudate persist for many months?

A

Osteomyelitis

38
Q

What are prominent in the response to chronic lung damage caused by smoking?

A

Neutrophils

39
Q

What’s the state where macros differentiate? What are the types? How do the macros differentiate?

A

Granulomatous inflammation, foreign body (no response)and immune (response)

Epitheloid cells (abundant cytoplasm) or giant cells (fused macros, multinucleated)

40
Q

What are the mediators of the acute phase response?

A

TNF, IL-1, IL-6, type 1 interferons

41
Q

What are the acute phase proteins?

A

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
Q

Leukocytosis vs leukemoid reactions vs lymphocytosis vs leucopenia.

A

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
Q

Acute phase response does what to: sweating, BP, P, appetite, affect, body temp.

A

Decreases d/t blood internalization, raises, raises, lowers, malaise, rigors and chills

44
Q

What are the degrees of tissue regeneration?

A

Labile
Stable
Permanent

45
Q

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?

A

IL-6

HGF and TGH-a, increased metabolism and entrance into the cell cycle

TGF-B

46
Q

What are the steps of scar formation?

A

Angiogenesis
Granulation
Remodeling

47
Q

What causes vasodilation during angiogenesis?

A

NO, NOT VEGF (though VEGF-A stimulates NO production)

48
Q

What growth factor stimulates endothelial proliferation during angiogenesis? Structural maturation? What suppresses angiogenesis?

A

FGF-2

Ang 1 & 2

PDGF and TGF-B, these increase ECM protein synthesis

49
Q

What protein cross-talks with VEGF during angiogenesis to mediate sprouting/branching/spacing?

A

Notch

50
Q

What enzymes degrade the ECM for remodeling during tissue repair?

A

MMP (matrix metalloproteinases)

51
Q

What do M2 macros produce that contributes to the granulation of tissue?

A

PDGF, FGF-2, TGF-B

52
Q

What inhibit MMPs (matrix metalloproteinases)?

A

TGF-B and TIMPs

53
Q

What are the major collagen providers in fibrosis of organ parenchyma? What cytokine activates them?

A 
Myofibroblasts (most organs)
Stellate cells (liver)

TGF-B

54
Q

Define dihiscence.

A

Rupture of a wound

55
Q

Where are contractures most likely to occur?

A

Palms, soles, anterior thorax

MOD1 (5 decks)

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