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ABSN > PathoPharm Review - E4 > Flashcards

PathoPharm Review - E4 Flashcards

1
Q

Phases of drug action: pharmaceutic (1)

A

drug dissolves to be used and absorbed in blood and body (dissolution) all oral drugs and only occurs w/ oral drugs

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2
Q

Phases of drug action: pharmacokinetic (2)

A

drug moving through the body and what the body does to the drug (4 processes: absorption, distribution, metabolism, excretion)

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3
Q

Phases of drug action: pharmacodynamic

A

what the drug does to the body (MOA, intended effect, therapeutic action)

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4
Q

what drugs are 100% bioavailable

A

IV drugs

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5
Q

example of protein binding: warfarin/coumadin

A

this is a blood thinner that is 97-99% protein bound so if a pt has low albumin a person is at greater risk for bleeding due to higher effect of drug exerted

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6
Q

a drug uses CYP450 system as a substrates

A

the drug uses the system for metabolism (it initiates the drug)

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7
Q

if a drug uses CYP450 system as an inducer

A

the system increases the breakdown and elimination of the drug to lower the drugs therapeutic effect
“induce the drug out like a birth, lowering effect b/c drug is no longer in the body”

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8
Q

if a drug uses CYP450 system as an inhibitor

A

the system decreases the breakdown and elimination of the drug to increase the amount of drug in the body and increase the therapeutic effect risk for toxicity
“inhibits the uptake so the drug stays readily available in the bloodstream”

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9
Q

grapefruit is an example of “” in the CYP450 process

A

inhibitor

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10
Q

goal of steady state

A

when intake of a drug is equal to the amount of drug metabolized and excreted (the state when the BP meds will have BP always under control)
takes 4-5 half lives to get to steady state

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11
Q

agonist

A

a drug that has the ability to initiate a desired therapeutic effect by binding to a receptor

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12
Q

antagonist

A

a drug that produces its action not be stimulating receptors but by preventing/blocking/inhibiting other natural substances (ligands) from binding and causing a response

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13
Q

drug interactions that increase therapeutic effect: additive effects

A

2 drugs taken w/ similar MOA (they become stronger together)

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14
Q

drug interactions that increase therapeutic effect: synergism/potentiation

A

2 drugs w/ different MOA but result in a combined drug effect greater than that of either drug alone (still will become stronger together)

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15
Q

drug interactions that increase therapeutic effect: activation

A

activation of drug - metabolizing enzymes in the liver which decreases metabolism rate of the drug

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16
Q

drug interactions that increase therapeutic effect: displacement

A

displacement of one drug from plasma protein binding sties by a second drug which increases effect of displaced drug

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17
Q

what organization approves medications

A

food and drug administration

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18
Q

Controlled substances: schedule 1

A

not approved for medical use, there is no reason to ever prescribe it bc they have no therapeutic effects (ex: heroin, LSD)

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19
Q

Controlled substances: schedule 5

A

low potential for abuse, meds that contain small amounts of certain narcotics or stimulants, usually antitussives (cough suppressants w/ codeine, ephendrine containing meds)

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20
Q

what schedule are narcotics

A

schedule 2 -> no auto refills watch closely

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21
Q

what is the qualification for a drug to be classified as over the courter and then sold

A

“consumers must be able to diagnose own condition and monitor effectiveness easily” , meds are low risk for side effects & abuse (no medical background needed to understand med function

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22
Q

teratogens: category A

A

safe for fetus (ex: acetaminophen)

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23
Q

teratogens: category X

A

drugs that have known risk that cannot be outweighed by possible benefit, pt usually have to be on bc to take (ex: thalidomine, chemo, istretinoin/retin A aka accutane)

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24
Q

dysplasia

A

abnormal changes in size/shape/organization of mature cells (often associated w/ neoplastic growths aka cancer cells)

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25
Q

what cell adaptation is most associated with cancer

A

metaplasia (it can predispose to cancer)

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26
Q

what are the 5 signs of localized inflammation

A

redness, swelling, heat, pain, loss of function

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27
Q

IgG

A

most common, 75-80%, protects against bacterial and viral infections produced once an infection has been on going or resolved & can easily leave bloodstream and go into tissues
Ex: pervious infection or vaccine

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28
Q

IgM

A

10%, activates compliment for cytotoxic functions for early, recent infections, 1st to be produced and signal

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29
Q

IgA

A

secretory functions, protects against infections found in saliva, tears, GI/GU & breastmilk

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30
Q

IgD

A

trace amounts in serum, more on B cells, stimulates B cells to multiply and differentiate & secrete other immunoglobulins

31
Q

IgE

A

role in immunity against parasites and allergic reactions, signaling of mast cell degranulation

32
Q

passive immunity

A

-transfer of plasma containing antibodies from an immunized person to non immunized per
- mother to fetus (IgG cross placenta, IgA in BM so vaccinated mom can pass that)
-injection of antibodies not a vaccine, like actual plasma w/ the antibodies

33
Q

active immunity

A

-protected state due to body’s own immune response
-active infections
-vaccines

34
Q

who cannot receive a attenuated vaccine

A

people w/ weak immune systems (spec diseases: lung, heart, kidney or metabolic)

35
Q

what are the live vaccines

A

MMR
flu mist
varicella

36
Q

what are the two ways RAAS affects BP

A

1) Na & H2O retention (fluid volume)
2) Vasoconstrictor & H2O retention (tighter/smaller passage)
how much volume is on board in blood vessels to keep normal BP

37
Q

HTN crisis: urgency

A

-no S/s of end stage organ damage
-BP >180/120
-treat w/ oral agents & gradually reduce
-causes: anxiety, pain, abrupt withdrawal

38
Q

HTN crisis: emergency

A

-uncontrolled BP that leads to end organ damage
-BP: >180/120
-S/s: headache, blurred vision, stroke, brain hem, chest pain, acute coronary syndrome, heart dysry
-aggressively lower BP in mins to hours w/ IV meds (labetalol)

39
Q

MOA for all diuretics

A

-increased urinary output
-decreased circulating volume
-decreased arterial resistance

40
Q

what is the first line management of HTN

A

hydrochlorothiazide -> works on distal tubules

41
Q

what does loop diuretics cause

A

profound diuresis (so used for HTN & fluid overload)

42
Q

what pts should not take propranolol & carvedilol

A

pt’s with lung disease, asthma or COPD bc it is non selective and will block beta 2

43
Q

when do we hold beta blockers

A

HR is less than 60 or systolic BP is less than 100

44
Q

what is the biggest complaint from pts to switch from an ace inhibitor

A

dry, nonproductive persistent cough

45
Q

adverse reactions of statins

A

myopathy (muscle weakness) -> rhabdomyolysis (breakdown of muscle fibers & leads to AK failure)

46
Q

what statins need to be taken at night

A

simvastatin and rosuvastatin bc chol is highest at night and these drugs have short half lives

47
Q

what is the gold standard for hyperlipidemia treatment

A

statins w/ diet & exercise

48
Q

metformin MOA

A

lowers BG by decreasing production of glucose in the liver & enhances glucose uptake & utilization by muscle
(met for my muscles, min glucose in liver)

49
Q

metformin nursing considerations

A

-must be held 48 hrs before IV contrast
-do not use in pts w/ elevated ALT levels

50
Q

gabapentin & pregablin indication

A

to complement opioid effects and used specifically neuropathic pain

51
Q

gabapentin & pregablin nursing considerations

A

can only be partially reversed with naloxone
(the pent up tin man is only partially human)

52
Q

what NSAID has no anti inflammatory property

A

acetaminophen

53
Q

NSAID MOA

A

anti prostaglandins by blocking key enzyme COX which is crucial for the production of prostaglandins

54
Q

adult acetaminophen dosage

A

4g/24 hr

55
Q

phenytoin causes what special side effects

A

gingival hyperplasia teeth -> dentist

56
Q

gold standard for rapid mgt of seizures

A

if needed (usually stop on their own) IV push benzodiazepines

57
Q

metabolic syndrome

A

WC: >40, >35
TAGs: >150 or meds
HDL: <40 (M), <50 (W) or meds
BP: >130 or >85 or meds
FBG: >110 or meds
BMI: >30

58
Q

a delta

A

myelinated; pain is sharp, cutting, pinched & localized

59
Q

c fibers

A

nonmyelinated; pain is dull, burning, achy & poorly localized

60
Q

heparin antidote

A

protamine sulfate (SE: hypotension)

61
Q

LMWH nursing considerations

A

do not give w/ heparin
BBW: potential spinal hematoma if pt has epidural catheter

62
Q

warfarin MOA

A

vitamin K inhibitor -> prevents the synthesis of factors VII, IX, X & prothrombin

63
Q

warfarin antidote

A

vitamin K

64
Q

apixaban & rivaroxaban antidote

A

andexxa

65
Q

aspirin MOA

A

blocks prostaglandin synthesis through the COX enzyme pathways (+blocks platelet aggregation)

66
Q

aspirin antidote

A

desmopressin (DDAVP)

67
Q

clopidogrel & ticagrelor nursing considerations

A

BBW (clopid): pt w/ certain genetic abnormalities, who may have higher rate of CV events due to reduced conversion to its active metabolite
BBW (tica): increased bleeding risk w/ aspirin doses over 100mg (so can give w/ baby aspirin)

68
Q

clopidogrel & ticagrelor antidote

A

DDAVP or platelet transfusion

69
Q

long term side effects corticosteroid use

A

-clouded eyes
-high BS
-increased risk of infections
-thinning bones
-suppressed adrenal gland hormone production
-thin skin, bruising, slow wound healing

70
Q

lactulose use

A

liver disease & hepatic encephalopathy
digested in large intestine creating a hyper-osmotic environment which draws water into the colon + reduces blood ammonia levels

71
Q

polyethylene glycol use

A

given before diagnostic surgical bowel procedures bowel prep for col

72
Q

anticholinergic effects

A

“hot as a hare”
“dry as a bone”
“blind as a bat”
“red as a beet”
“mad as a hatter”

73
Q

lam & pam MOA

A

enhance inhibitory effects of GABA in CNS (increasing GABAs relaxing effect, we inhibit anxiety w/ gaba)

74
Q

benzo antidote

A

flumazenil

ABSN (145 decks)

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