Inflammation 2 Flashcards

1
Q

What are the main cytokine stimulators of fever? These are called PYROGENS!

A

IL-1

TNF-a

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2
Q

What are the main cytokines of the acute phase response?

A

IL-6, IL-1, TNF-a, INF-y, & TGF-B

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3
Q

Signs are subjective or objective?

A

Objective

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4
Q

Symptoms are subjective or objective?

A

Subjective

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5
Q

Patients can have as many diseases as they want is called the _______

A

Hickam’s dictum

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6
Q

Chronic inflammation consists of 3 components

A

1: active inflammation
2: tissue destruction
3: attempted repair

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7
Q

There are 4 causes of chronic inflamm.

A

1: prolonged infection
2: prolonged toxic exposure
3: autoimmune disease
4: unknown ischemic

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8
Q

What cells are the key players in chronic inflamm?

A

Macs

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9
Q

What cytokine activates macs?

A

IFN-gamma

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10
Q

Macs secrete lots of things. Name 4.

A

Neutrophil chemotactic factor
TGF-B
PDGF
FGF

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11
Q

Macs are drawn to inflammation sites by what chemical factors?

A

MCP-1, C5a, PDGF, TGF-a

Fibrinonectin & fibrinopeptide frags

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12
Q

T cells and macrophages are coupled in chronic inflammation. How?

A

Macs present Ag to Tcell and activate Tcells with IL-12.

Tcells in turn release IFN-y

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13
Q

What is a granuloma?

A

When 2 or more macs work together.

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14
Q

What are 5 examples of granulomatous diseases?

A

TB, Leprosy, Syphilis, Sarcoidosis, & cat-scratch disease

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15
Q

How are sarcoidosis and TB alike? Different?

A

Alike: both in lung and spread by lymph nodes.

Different: Sarcoidosis doesn’t have a rim of lymphocytes, but has tight naked granulomas

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16
Q

Lymphangitis is?

A

inflammation of the lymph channels

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17
Q

Lymphadenitis is?

A

Inflamed lymph node

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18
Q

Lymphadenopathy is?

A

enlarged lymph node

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19
Q

Chronic inflammation influences systemic responses. What is one aspect that is not like an acute inflammation response?

A

Chronic causes anemia.

Watch out for bleeding, which would throw off measurements.

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20
Q

What are the 4 primary systemic effects of inflammation, acute or chronic?

A

1: body temp
2: Heart rate
3: respiratory rate
4: White blood cell count

Think vitals or SIRS

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21
Q

What causes fever? On a gross level

A
Infection (By far most common/important)
Infarction
Tumors
Non-infection inflamm
hemorrhage
brain damage
drug Rxn
Heatstroke
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22
Q

What are the 2 most common causes of anemia?

A

1: Iron deficient
2: Chronic inflammation

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23
Q

In general, why are we anemic in chronic inflammation?

A

Microbes use our iron, thus, our phagocytic cells retain iron to hide it from the microbes. BUT the body doesn’t let hemoglobin levels to fall below 10 g/dl.

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24
Q

If hemoglobin is below 10 g/dl what is probably occurring?

A

Hemorrhage!

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25
Q

Physiologically, how do we become anemic?

A

INF, TNF-a, and lipopolysaccharide down regulate Ferroportin.

26
Q

What is ferroportin?

A

Only iron export protein in iron-transporting cells. If it’s down regulated, then this will lower iron levels released from cell.

27
Q

What does hepcidin do?

A

Inhibits Iron absorption in the gut and binds to ferroportin to chaperon it to destruction

28
Q

How do macs store iron?

A

create Ferritin

Store and retain Iron in macs

29
Q

What stimulates macs to create ferritin?

A

IL-1,6,10

TNF-a

30
Q

Why do corticosteroids have such a repertoire of side effects?

A

They block production of arachodonic acid (AA).

AA is a precursor to inflammatory mediators and inhibitors

31
Q

Why are NSAIDS better than corticosteroids?

A

They only block the production of prostaglandins. (block Cycloxygenase) Steroids block all Arachidonic acid byproducts.

32
Q

What enzyme does NSAIDS block?

A

cycloxygenase therefore inhibiting prostaglandins

33
Q

What do prostaglandins do?

A

Mediate pain ,fever, and signs and symptoms of inflammation.

34
Q

Why do NSAIDS cause gastric bleeds?

A

NSAIDS shutdown prostaglandins. There are prostaglandin mediated gastric muscoal protections.

35
Q

What do prostaglandins breakdown into?

What determines which by product produced?

A

Prostacyclin
Thromboxanes

Location in body

36
Q

Cyclooxygenase can be found in what 2 places in the body?

A

Endothelial cells

Platelets

37
Q

Where in the body is prostacyclin made from prostaglandin? Function?

A

Endothelial cells

Vasodilator and decreased clotting (platelet aggregation)

38
Q

Where in the body are thromboxanes made from prostaglandin?

A

Platelets

Vasoconstrictor and increased clotting (platelet aggregation)

39
Q

What is the difference between NSAIDS and Aspirin?

A

NSAIDs are reversible while Aspirin is irreversible.

40
Q

How does Aspirin work?

A

Increases endothelial prostagland/prostacyclin production which vasodilates and decreases clotting aggregation.

At the same time it zaps platelets, which inhibits production of thromboxane resulting in net increase of vasodilation and decreased clotting aggregation.

41
Q

What is serous inflammation?

A

Transudate.

42
Q

Pursuant inflammation is what? Contains? Aka

A

Pussy. Has neutrophils and also called suppurative.

43
Q

What does fibrinous inflammation look like? And how does it become fibrinous?

A

Shagged and tan

Increased fibrinogen in the blood with inflammation. (acute protein)

44
Q

Ulcerative goes through which layer of Epi?

A

Mucosal muscle. Otherwise it’s just an erosion.

45
Q

What causes the liver to produce acute reactive proteins?

A

IL-6

46
Q

Inflammation causes what 3 cytokines?

A

TNFa and IL1

IL6

47
Q

What are the acute phase proteins?

A

Fibrinogen
Amyloid A
Coreactive protein
C1 and C3

48
Q

What protein is shunted while acute phase going on?

A

Albumin. Which causes swelling!

49
Q

What is released by the Hypothalamus to regulate fever?

A

Pge2.

50
Q

The body will limit export, increase import iron to fight bacteria. However, the blood Hb level will not fall below

A

10

51
Q

When a Mac get inf or TNFa, how does it fight with iron strategy?

A

Ferroportin is decreased to lower export of iron.

52
Q

If a Mac gets IL6, how will it react to iron?

A

Hepcirin is increased, which binds and degrades ferroportin.

53
Q

What are the two steps involved to lower free iron by decreasing export?

A

Macs downreg ferroportin.

Hepcirin breaks ferroportin down as well.

54
Q

What happens to Macs when they hit INF and LPS?

A

Increase bivalent transporters which scavenge free iron.

55
Q

What does IL10 do to macs?

A

Increases their transferrin receptors, increases scavenging of free iron.

56
Q

Activated macs will eat what to lower iron?

A

RBC.

57
Q

What is LAD 1 deficiency?

A

Long umbilical cord.

Defective integrin

58
Q

What’s LAD2 deficiency?

A

No sialyly Lewis ligand. Therefore no ligand for p and e selectin

59
Q

What is chronic granulomatous disease?

A

No NADPH oxidase therefore no oxidative burst for phagocytes

60
Q

Myeloperoxidase deficiency will influence which cell?

A

Neutrophils

61
Q

Chediak higoshi deficiency results from what lacking?

A

Phagosome and lysosomes fusion.

62
Q

What are some acquired deficiencies?

A

Diabetes mellitus!