inflammation drugs Flashcards

1
Q

what drugs treat inflammation

A
recombivant dna (IL-1 antagonists)
monoclonal Abs (infliximab)
antipyretics
NSAIDs
glucocorticoids
antihistamines
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2
Q

fever response

A

macrophages release PG2
hypothalamus increases set point
conservation of heat: vasoconstriction, less sweating
production of heat: shivering, muscle contractions

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3
Q

antipyretic drug types

A

acetaminophen

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4
Q

why do we need to decrease fever in children

A

febrile seizure occurs in children who have a prolonged fever of more than 38.5

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5
Q

what should we NOT treat fever with

A

NSAIDS like ASA because it can cause reyes syndrome in children and teens

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6
Q

why should we treat fever in adults

A

can have very adverse side effects (tissue wasting, delirium, coma, less mental activity, more E needed, more effect in older adults

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7
Q

reyes syndrome

A

caused by NSAIDS used to treat viral infections/fever
lethargy, confusion, brain damage
diarrhea, liver failure

mostly in children who cannot oxidize fatty acids

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8
Q

measures to take before we treat with acetaminophen

A

confirm fever
check renal and hepatic function
monitor fluids/electrolytes
discomfort, pain, malaise, other symptoms

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9
Q

acetaminophen interactions

A

alcohol– liver function problems

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10
Q

acetaminophen adult limit

A

4g/day (be careful that you’re not getting too much does from OTC meds)

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11
Q

acetaminophen side effects

A
can cause liver dysfunction when abused or taken with alcohol
inhibits warfarin (anticoagulant) so bleeding can occur
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12
Q

NSAID types

A

COX I and COX II inhibition: ibuprofen, naproxen, diclofenac, ASA
COX II inhibition only: celecoxib/celebrex

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13
Q

NSAID COX I inhibition

A

inhibits:
gastric mucous secretion
renal perfusion
platelet aggregation

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14
Q

NSAID COX II inhibition

A

alleviates:
fever
pain
inflammation

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15
Q

NSAID adverse effects

A

GI irritation– pain, bleeding ulcers, heartburn (so take with food/milk)
kidney perfusion problems (abuse leads to renal failure)

ASA can cause tinnitus/hearing damage in adults
increase action with oral coagulants
reyes syndrome in children when used to treat viruses/fever

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16
Q

NSAID purpose

A

inflammation, pain, fever
safe
OTC

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17
Q

NSAID interactions

A

alcohol can cause liver/renal impairment
don’t overdose with OTCs
oral anticoagulants increase effect

18
Q

endogenous cortisol

A

glucocorticoid
increases blood glucose via catabolism of glycogen, fatty acids, and protein
immune system suppression

(suppress histamine, PGs via cox II, phagocytes/lymphocytes)

19
Q

glucocorticoid types

A

hydrocortisone
prednisone

turn to cortisol in liver, then are metabolized

20
Q

glucocorticoid purpose

A
anti inflammatory for SEVERE (asthma, arthritis) or acute inflammation-- functions at HIGHER THAN NORMAL PHYSIOLOGICAL LEVELS ONLY
adrenal insufficiency (addison's disease-- must administer normal dose of mineralo/glucocorticoids)
21
Q

glucocorticoid use

A

short term (4-10d) due to adverse side effects
take in the morning
take at the same time every day
do not stop abruptly (adrenal crisis)
take with food to avoid gastric irritation (can also take anti-ulcer meds)
guard against infection
have some on hand in case you cannot reach the pharmacy
don’t take herbs (interactions)
monitor weight daily

22
Q

glucocorticoids pharmacokinetics

A

1/2 life = 3.5h

adrenal suppression lasts 30-36 h
-titrate dose

23
Q

adrenal crisis

A

caused when you abruptly stop taking glucocorticoids
since your body stopped producing endogenous cortisol, when you stop supplying it with EXOGENOUS cortisol, there will be extreme problems

shock, flu, seizures, HTN

24
Q

glucocorticoid adverse effects

A
cushings syndrome
delayed healing
higher risk of infection
hyperglycemia
electrolyte imbalance (mineralocorticoid effects)-- therefore check body weight for retention of H2O and Na+, K+ release
masks infection (no inflam response)-- immunosuppression
peptic ulcers (damages epithelia)
osteoporosis (inhibits osteoclasts)
fragile skin
easy bruises
mood changes (prednisone psychosis)
gastric upset and bleeding
25
cushings disease
due to increased amounts of cortisol ``` purple striae on stomach muscle atrophy (thin extremities) carry weight differently (moonface, buffalo hump, abdomen) bruising easily delayed healing more body and facial hair thinning hair ```
26
why do we use glucocorticoids
``` inflammation (severe--rheumatoid arthritis, COLD, lupus) adrenal insufficiency (addison's disease) ```
27
what else causes inflammation (other than injury)
histamine release in allergic reactions-- so we use antihistamines contact dermatitis, hay fever, etc.
28
histamine
released by mast cells, basophil cells, and platelets in the VASCULAR inflammatory response cause vasodilation, and can sometimes cause ANAPHYLAXIS (life threatening immune response)
29
histamine receptors
H1: smooth muscle (vasodilation, bronchoconstriction, itch, pain) H2: releases HCl in stomach
30
antihistamine types
1st generation: benadryl (diphenhydramine) | 2nd generation: claritin (loratidine), allegra (fexofenadine)
31
other names for antihistamines
antihistamenics | H1 receptor antagonists
32
antihistamine MOA
blocks histamine action at H1 receptors (smooth muscle response)
33
what are antihistamines for?
OTC | prevention and relief of symptoms
34
diphenhydramine (benadryl)
1st generation | in cold and allergy medication
35
benadryl adverse effects
drowsiness, dizziness, nervousness, dry mouth, nausea less common: restlessness, insomnia, palpitations additive effect caution of resp airway disease, glaucoma, urinary retention, peptic ulcers
36
benadryl in children
not in children younger than 6 years due to sedative effects
37
benadryl in older adults
do not use as it is a sedative and can cause dizziness and decreased BP
38
benadryl interaction
additive with other 1st gen antihistamines | additive with CNS suppressants
39
2nd generation antihistamine difference from 1st generation
non-drowsy and less antimuscurinic effects
40
antihistamine pharmacokinetics
50% 1st pass effect liver metabolism 1/2 life = 4-12 h