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FMS Week 10 > Pharmacotherapy of inflammation > Flashcards

Pharmacotherapy of inflammation Flashcards

1
Q

H3 v(down arrow) cAMP

A

presynaptic autoreceptors

brain

myenteric plexus

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2
Q

Cox 1 vs 2

A
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3
Q

HPA axis and cortisol

A
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4
Q

Abatacept mechanism of action

A

blocking the costimulatory signal required for T cell activation

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5
Q
A

NSAID use

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6
Q

NSAID toxicities

A
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7
Q

What organ systems affected by histamine receptors

A

Cardiovascualr

pulmonary

nervous system

GI

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8
Q

Cox 2 derived PGs are involved in renal function; inhibition of COX-2…

A

reduced water and salt excretion byt the kidney, leading to peripheral edema, HTN, and exacerbation of pre-existing HTN

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9
Q

Rituxumab

A

inhibitor of B cell function

approved for pts that fail to respond to anti-TNF-a therapy

Approved for tx of nonhodgekins lymphoma

chimeric mab against CD20 antigen found on the surface of normal and malignant B lymphocytes. IgG1 and k immunoglobulin

2-1000mg IV infusions separated by 2 weeks

admin of glucocorticoid recommended prior to infusion to reduce incedence severity of infusion reaction

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10
Q

NSAID USE AND GI COMPLICATIONS

A

incidence of dyspepsia id >40% often amenable to tx with H2 receptor antagonist or a PPI

incedence of complicated or symptomatic ulcer is 2-5%. may be life treatening

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11
Q

How is the GI system affected by histamine receptors

A

increawse in acid secretion H2

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12
Q

PGE2

A

involved in all processes leading to the classical signs of inflammation: redness, swelling, and pain

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13
Q
A

glucocorticoid effects on the immune cells

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14
Q

ASA has been found to lower rates of what CA

A

colorectal cancer

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15
Q

NSAID side effects

asprin allergy

A

angioedema

anaphylazis

resp symptoms

skin rxns

increased leukotrienes

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16
Q

Abatacept

A

inhibitor of t cell activation

fusion protein of the extracellular domain of the CTLA4 molecule and the Fc doman of human IgG1

approved for pts who do not respond well to methotrexate and for pts who do not respond or cannot tolerate TNA antagonists

30 minute infusion given at 2 and 4 weeks after 1st infusion, every 4 weeks thereafter. Fixed dose. 10mg/kg

MOA: blocing the costimulatory molecule required for T cell activation B7 (CD80/86)

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17
Q

PGF2-alpha

A

high levels have been reported in patients suffereing from RA, OA,reactive arthritis, and psoriatic arthritis

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18
Q

PGI2

A

is rapidly produced following tissue injury and is an important mediator the the edema and pain associated with acute inflammation. It is the most abundant prostanoid in synovial fluid in human arthritic knee joints

AKA prostacycline

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19
Q

Autoimmune diseases being successfully treated with anti-TNA therapy

A

RA

crohns

ankylosing spondylitis

juvenile RA

psoriac arthritis

psoriasis

sarcoidosis

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20
Q

PGD2

A

produced by antigen presenting DCs and TH2 cells, suggesting a role in antigen-specific immune system responses

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21
Q

H2 (histamine receptor 2)

^ cAMP

A

gastric mucosa

blood vessels/ smooth muscle cells

mast cells

cardiac muscle cells

brain

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22
Q

H4 v(down arrow) cAMP

A

Eosinophils

Neutrophils

CD4 T cells

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23
Q

NSAID side effects

Reye’s syndome

A

varicella infection of influenza virus

liver damage and encephalopathy

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24
Q

Fexofenadine (allegra)

A

2nd/3rd generation H1 receptor competative antagonist

long duration (12-24 hours)

Little to no anticholinergic, and alpha-adrenergic, and anti-serotonergic actions

less sedation than 1st generation H1 blackers

not useful for N or motion sickeness

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25
Q

Zafirlukast and Montelukast

A

Leukotriene pathway inhibitor

LTD4 receptor antagonist

inhibits CYP3A4 and CYP2C9 -> increased warfarin t1/2

orally active

for mild to moderate asthma

considered an alternative to low dose inhaled corticosteroid

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26
Q

Cortisol

A

Cortisol is the primary glucocorticoid in hiumans

glucocorticoids exert a wide range of physioklogic effects, including regulation of immune fn, growth, and carbohydrate, fat, and protein metabolism

cortisol is synthesized from cholesterol

the secretion of cortisol follows a circadian rhythm ans is controlled by pulses of ACTH tht peak in the early morning and after meals

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27
Q

Chronic NSAID use linked to an increased risk of…

A

MI

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28
Q

Histidine ——> histamine

enzynme

A

histidine decarboxylase

29
Q

Factors to conside (preexisting) when giving NSAIDs

A

stomach ulcer or bleeding

heart dz, inclduding MI or stroke

kidney dz/ HTN

co-administered meds/ supplements

30
Q

chronic use of glucocorticoids is associated with…

A

high risk for adverse affects

31
Q

Leukotriene pathways of arachadonic acid breakdown

A
32
Q

Arachadonic acid and COX pathway

A
33
Q

How is the nervous system affected by histamine receptors

A

stimulant of nerve endings H1

34
Q

Laratadine (claratin)

A

2nd/3rd generation H1 receptor competative antagonist

long duration (12-24 hours)

Little to no anticholinergic, and alpha-adrenergic, and anti-serotonergic actions

less sedation than 1st generation H1 blackers

not useful for N or motion sickeness

35
Q

Prednisone

A

glucocorticoid

short to medium acting

antiinflammatory 4x as much as cortisol

has high affinity for CBG and albumin

70-80 % protein bound

36
Q

3 cell types affected by intradermal weal and flare response

A

1) dilation of vasculature in the microcirculation causing reddening
2) increased permeability pf capillary of venular endothelium causes edematous wheal (a smooth, slightly elevated patch)
3) stimulation of sensory nerve endings causes a red, irregular flare surrounding the wheal; may be accompanied by itching sensation

37
Q

Apremilast

A

PDE-4 inhibitor

indicated for moderate to severe plaque psoriasis

increases intracellular cAMP, decreased TNAa production

Most common adverse affect N and D in first year of tx, nasopharyngitis, URI

Metabolized by CYP3A4 with subsequent glucuronidation and non-CYP mediated hydrolysis

excretion: 58% urine, 39% feces, severe renal impairment

associated with increased risk depression

38
Q

Side effects of high dose or prolonged glucocorticoid therapy

A
39
Q

Mechanism of histamine induced edema

A

contraction of endothelial cells happens along vasculature

40
Q

Classic mechanism of glucocorticoid action

A

you have your glucocorticoid

comes and binds to receptor which has a head shock protein component that dissociates

GR and GCS go to nucleaus and upregulate and downregulate certain genes

41
Q

Untoward effects of anti TNA therapy

A

TNFa is an important component of stress responses

TNA a is important for host defense mechanisms

pts on anti TNF therapy display increased incidence of infection, lupus, exacerbatiob of dymyelinating dz, and heart failure

may or may not be associated with increased risk of lymphoma

42
Q

H1 (histamine receptor 1)

^ IP3/DAG

A

blood vessels

endothelial cells

sensory nerve endings

GI smooth muscle cells

broncial smooth muscle

brain

MAIN one that the drugs target. Think of inflammation when you think of this

43
Q

How is the pulmonary system affected by histamine receptors

A

bronchoconstriction H1

44
Q

How is the cardiovascular system affected by histamine receptors

A

vasodilation of arterioles and precapillary sphincters via H1 (some H2)

Increase vascular permeability H1 (hives) also edema

Increase heart rate (direct effect and reflex tachycardia)

45
Q
A
46
Q

Cetrizine (zyrtec)

A

2nd/3rd generation H1 receptor competative antagonist

long duration (12-24 hours)

Little to no anticholinergic, and alpha-adrenergic, and anti-serotonergic actions

less sedation than 1st generation H1 blackers

not useful for N or motion sickeness

47
Q

Mechanism of histamine induced vasofilaiton

A

GC is guanylyl cyclase

influx of calcium happens

48
Q

Tofacitinib

A

JAK inhibitor

Blocks JAK 1 and 3 and to a lesser degree 2

approved for moderate to severe RA for pts that do not respond well to methotrexate

Side effects: inflammation of nasal passages and upper pharynx, URI, Increased risk TB and lymphoma, HA

Metabolized by CYP3A4

49
Q

diphenhydramine

A

1st generation H1 receptor competative antagonist

short duration (3-6 hours)

anticholinergic

anti a-adrenergic, anti serotonergic effeccts (penetration into CNS)

cause sedation

antiemetic, anti motion sickness

50
Q

Asprin (Acetylsalicylic acid)

A

weak acid

analgesic (anti pain)

Antipyretic

anti-platelet

anti inflammatory

rapidly absorbed from the stomach and intestine in unionized form due to it being acidic

IRRIVERSIBLY inhibits prostaglandin biosynthesis by ACETYLATING the enxyme CYCLOOXYGENASE (COX)

51
Q

How does ASA irriversibly inhibit prostaglandin biosynthesis

A

Acytelating COX

52
Q

chloropheniramine

A

1st generation H1 receptor competative antagonist

short duration (3-6 hours)

anticholinergic

anti a-adrenergic, anti serotonergic effeccts (penetration into CNS)

cause sedation

antiemetic, anti motion sickness

53
Q

Retuximan MOA

A
54
Q

Histamine storage sites

A

blood basophils and tissue mast cells

gastric mucosal cells

neurotransmitter vessicles

55
Q

Nabumetone

A

NSAID

Shows some selectivity for COX2 (in vitro)

56
Q

Indomethacin

A

NSAID

associated with increase risk of CV event (mostly MI)

side effects : hypersensativity, GI, slight renal toxicity

depression. HA- similar to seratonin in structure

57
Q

Tofacitinib MOA

A

Jak inhibitor

ultimately blocks transcription

58
Q

Anakinra

A

cytokine blocker

inhibitor of IL-1

recombinant, nonglycosylated synthetic form of the human IL-1 receptor antagonist (IL-1Ra), an endogenous regularot of IL 1 action

59
Q

Celecoxib

A

Cox 2 selective inhibitor

has not been shown to be any better than NSAIDS for upper GI (stomach) complications but has been shown to be associated with a significantly reddulced incidence of small bowel inflammatino and mucosal breaks than NSAIDS

It is a sulfonamide

t1/2 6-12 hours

Metabolized by CYP2c9

Inhibits CYP26( metabolism of metoprolol, SSRI, tricyclic antidepressants)

Significan 1st pass metabolism

RA and OA but not general pain

60
Q

Acetaminophen

A

weak base

analgesic and antipyretic

NOT ANTI INFLAMMATORY

No anti platelet effefcts

Severe HEPATOTOXICITY with oversidage caused by reactive quinone metabolites. Normally these metabolites are rapidly inactivated by conjugation with glutathione. With high toic levels of the drug, hepatic glutathione becomes depleted. The drug N-acetylcysteine is used to prevent hepatotoxicity

61
Q

Uses of H2 receptor antagonists

A

(H2 in the gut)

May be useful for reducing NSAID induced dyspepsia

Gastric and pepti ulcers ( most peptic ulcers due to h pylori. NSAID induced are usually gastric) there is no evidence that H2 antagonists prevent drug induced ulcers and their complications

esophageal reflux

few side effects

infrequent GI irritation

cimetidine is a potent inhibitor of P450 metabolism

62
Q

Use of COX-2 inhibitors in pts with ASA induced asthma

A

5-20% of pts with chron asthma are hypersensative to ASA. Likely due to cox 1 inhibition, leading to lipoxygenase pathway activation and production of cysteinyl leukotrienes -> bronchospasm and nasal obstruction

Some ppl have been ok with COX2 inhibitors but there is still a warning label on med

63
Q

Infliximab

A

cytokine blocker

inhibitor of TNF-a

chimeric mAb (human contant, mouse variable)

given IV

increased risk for TB

64
Q

Functions of histamine

A

mediator of immediate allergic and inflammatory reactions

role in gastric acid secretion

neurotransmitter and neuromodulator

chemotactic factor for neutrophils, eosinophils, basophils, monocytes, and lymphocytes

65
Q

Zileuton

A

Leukotriene pathway inhibitor

Inhibits 5-lipoxygenase

inhibits CYP3A4 can influence metabolism of terfenadine, warfarin, and theophulline

orally active

for mild to moderate asthma

considered an alternative to low dose inhaled corticosteroid

66
Q

2 areas of inhibition for leukotriene pathway of arachadonic acid

A
67
Q

NSAID side effects

Inhibition of COX-1

A

stomach irritation

prolonged bleed time

renal toxicity

CNS effects

68
Q

entanercept

A

cytokine blocker

inhibitor of TNF-a

Human TNF receptor linked to the Fc portion of human IgG1

Basically sponge for TNF-a. Like a decoy recep.

Given 2x/ week

FMS Week 10 (4 decks)

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