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SMUSPG-PHY1 > Inflammation > Flashcards

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
Q

why is inflammation so clinically relevant

A

causes pain

usually prescribed NSAIDs or narcotics

26
Q

What is the mechanism of action of NSAIDS/steroids

A

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
Q

Why is PRN dosing not useful in reducing pain

A

NSAIDs effect in 20-30 min

need 7-10 days to get anti-inflammatory effect, you

28
Q

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?

A

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
Q

What is the role of inflammation in renal patients and autoimmune pts?

A

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
Q

What is self-limited, local swelling of skin or soft tissue?

A

Angioedema
Occurs alone or as urticaria.

D/T breakdown of vascular wall-> spilling of fluid on hands, face, and lips

31
Q

What cause the loss of vascular integrity in angioedema

A

mast cell histamine
bradykinin mediated

TX- antihistamine and steroids -shut down inflam response

32
Q

What is difference with allergic reaction ?

A

widespread
IgE mediated -release of histamine and IgE Ab response

TX- anaphylaxi- EPI-PEN

33
Q

What is the treatment for urticaria

A

leukotriene inhibitors,
antihistamines
topical steroids, rarely systemic steroids

34
Q

What was the point of the scrotal swelling patient anecdote

A

angioedema due to his genetic deposition to Lisinopril
Switch ACE inhibitor
AA- genetic link poor outcome

35
Q

What are the steps of the immune response in Eczema and psoriasis

A

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
Q

What presents higher numbers in psoriasis patients even without plaques?

A

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

SMUSPG-PHY1 (15 decks)

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