Inflammation Flashcards

1
Q

Is inflammation acquired or innate?

A
born with it, 
not adaptable, 
same response, 
no memory, 
non-specific
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2
Q

What is the function of inflammation

A

Protects host - btwn lag of exposure to onset of adaptive immune responses

result in pain, loss of function and limiting, it can happen abnormally
NOT PATHOlogical- NORMAL response

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3
Q

What factors drive inflammation?

A

chemokines and cytokines-
immune cells-pathogen that induces an inflammatory response, target for meds

1] Vasoactive amines, 
2] Plasma protein systems, 
3] Eicosinoids derived from arachidonic acid (released from phospholipds with cell damage 
4] Platelet-Activating Factor, 
 6] Phagocyte products,
 7] Nitric oxide
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4
Q

What molecules are part of the vasoactive amines?

A

1] Histamine from mast cells and platelets,
2] Serotonin from platelets,
3] B cells in blood can also release histamine

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5
Q

Describe how seasonal allergies can be treated with an anti-histamine

A

runny nose, itchy, mucosal edema -allergen exposure,

histamine released by mast cells,
anti-histamines block the histamines from binding to its receptors

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6
Q

What molecules are part of the plasma proteins?

A

1] kinin molecules,
2] complement molecules,
3] clotting/fibrinolysis system

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7
Q

What molecules are part of Eicosinoids derived from Arachidonic acid family

A

1] Prostaglandins,

2] Leukotrienes

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8
Q

Which molecule is a target of NSAIDs?

A

prostaglandins, to limit inflammation

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9
Q

What drug is used to inhibit leukotrienes?

A

Montelukast (Singulair)

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10
Q

What molecules are part of the cytokines

A

1] IL-1,6, 8, 2

2] Tumor necrosis factor

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11
Q

What molecules are part of the phagocytic products family?

A

1] cationic proteins,
2] neutral proteases,
3] oxygen-derived free radicals

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12
Q

What is a potent vasodilator?

A

Nitric oxide
promotes inflammation,
few second T1/2

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13
Q

What are the functions of the signals released by CD4 T cells?

A

1] Macrophage and NK cell activation,
2] Promotion of antibody production,
3] Proinflammatory,
4] Suppression of effector cell function

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14
Q

What are the signals released by CD8 T cells?

A
Proinflammatory-Enhanced tissue regeneration
1] Cytotoxins,
 2] Perforin, 
3] Granzymes, 
4] Granulysin
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15
Q

What are the signals released by neutrophils?

A
Proinflammatory
1] Lysozymes, 
2] Collagenase, 
3] Cathespin, 4
] Elastase, 
5] NETs
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16
Q

How do B cells release histamine?

A

Promotes the complement cascade

17
Q

What are the step in inflammation?

A

1] Immediate vasoconstriction (denies blood flow) and blanching – only lasts a short timeseconds to minutes
Skin white

2].Acute vascular response – increased permeability and vasodilation (hyperemia)

3] Acute cellular response – movement of white/red cells into injured area,

4] f chronic cellular response if sufficient damage – led by macrophages, and then

5] ultimately resolution

Fingernail scratch- white at first when it blanches then it will become a red welt (vasodilation)

18
Q

Why is increased permeability and vasodilation important during inflammation?

A

vessels become more permeable leak fluid->

fluid big component of inflammatory process

19
Q

What are the 4 classical hallmark of inflammation??

A

1] Rubor, -red
2] Tumor- inc. size
3] Calor- warm
4] Dolar- pain pressure

***5] Loss of function, example joints become less flexi when inflamed

20
Q

What are acute phase reactants?

A

proteins whose serum concentrations rise or fall by 25% or more in inflammatory states

change in homeostatic mechanisms in response to pathology –

so used as markers to test for inflammation
Non-specific, EXCEPT for temporal arteritis, which will have elevated ESR

21
Q

What is the first identified APR

A

C-reactive protein-sign inflammation is happening OnLY
Assessing risk in cardivascular patients

1] Binds damaged cells, nuclear proteins, pathogens,
2] Activates complement pathway, and proinflammatory cytokines

no known values,

22
Q

What measures the change in viscosity of blood created by enhanced APR protein?

A

Estimated Sedimentation Rate,
thicken of blood, increases viscosity
Cells settle to bottom of vertical tube LONG RATE= HIGH RATE/INc ESR , takes longer to settle

inflammation = viscosity of the blood increases due to the amount of products produced

23
Q

How useful is ESR?

A

Less w/in isolation,
HELPFUL when CRP elevated

HIgh in obesity d/t IL-6 from adipose tissue

24
Q

Describe the ESR in anemic patients

A

absence of red cells reduces viscosity (low red count) and sed RATE rises

25
why is inflammation so clinically relevant
causes pain | usually prescribed NSAIDs or narcotics
26
What is the mechanism of action of NSAIDS/steroids
inhibit cyclo-oxygenase, Prostaglandin (archadionic acid) synthase, reducing inflammation, COX-1 and COX-2- **SE cardiac events SE- inhibits prostaglandins that produce mucous membranes GI
27
Why is PRN dosing not useful in reducing pain
NSAIDs effect in 20-30 min | need 7-10 days to get anti-inflammatory effect, you
28
Why do some people with high cholesterol and atherosclerosis, never have a heart attack and others have a heart attack when their cholesterol is not high?
If a plaque is stable= little risk of a heart attack. MI happen when the plaque ruptures. Cholesterol don’t affect the plaque because the cholesterol is already in the plaque Inflammation can soften the plaque= ruptures causing an embolism.
29
What is the role of inflammation in renal patients and autoimmune pts?
CKD don't clear pro-inflammatory molecules= INC inflam Assessment of APRs are useful in diagnosis/ monitoring rhuematoid arthritis, lupus, and giant cell arteritis
30
What is self-limited, local swelling of skin or soft tissue?
Angioedema Occurs alone or as urticaria. D/T breakdown of vascular wall-> spilling of fluid on hands, face, and lips
31
What cause the loss of vascular integrity in angioedema
mast cell histamine bradykinin mediated TX- antihistamine and steroids -shut down inflam response
32
What is difference with allergic reaction ?
widespread IgE mediated -release of histamine and IgE Ab response TX- anaphylaxi- EPI-PEN
33
What is the treatment for urticaria
leukotriene inhibitors, antihistamines topical steroids, rarely systemic steroids
34
What was the point of the scrotal swelling patient anecdote
angioedema due to his genetic deposition to Lisinopril Switch ACE inhibitor AA- genetic link poor outcome
35
What are the steps of the immune response in Eczema and psoriasis
Eczema pruritic autoimmune epidermal spongiosis-edema of the epidermis Risk factor and Immune 1] Skin breakdown= INC allergen penetration, 2] ABN immune response 3] Altered flora 4] Acute cytokines production draw in T-cells, immune cells
36
What presents higher numbers in psoriasis patients even without plaques?
dendritic cells in skin, macrophages, neutrophils= genetic antigens activates these cells. Native skin cells- release proinflammatory cytokines recruit more immune cells breakdown of skin products- which cause release of more inflammatory mediators POSITIVE FEEDBACK High turn over TX- topic steroids, methotaxate