exam 3 pp meds

crystalloids

replace fluids and promote urine output

smaller so can exit plasma into interstitial spaces

colloids

moecules larger so stay in vascular space

expand plasma volume

more osmotic pressure (higher solute conc in blood = pull water out of cells into vascular space = more volume blood)

normal saline (crystalloid)

make them normal again —> resuscitation effort from hemorrhage and acidosis

ns 0.9 NaCl

hydration needs - hemorrhage metabolic acidosis

isotonic

no heart/renal failure, used in conjunction, resuscitation efforts

lactated ringers (crystalloid)

lactated losing blood and electrolyte balance from giving milk to baby, cant have renal liver or acidic

LR RL

blood loss, electrolyte imbalances

isotonic

not for ph<7.5 (acidic)

not for renal or liver failure/disease

0.45 normal saline

.45NS

hypernatremia, diabetic ketoacidosis

hypotonic

not for burns, trauma, liver disease

look at pumonary edema and electrolytes

D5.45NS (dextrose sodium chloride)

d double —> hypertonix then hypotonic

used with 20ml KCL 1L

hypertonic then hypotonic after dextrose is used

maintenance no resuc

monitor electrolytes, pulmonary overload

D5/D5Wc(electrolyte free water)

use: persistent hypoglycemia or reduction in serum osmolality to treat hypernatremia

not for resuscitation or maintenance fluid

no ICP

no diabetes

dextran 40 (colloid)

MOA: raise oncotic pressure of blood

fluid replacement

monitor vital signs, fluid overload, bleeding

no heart failure, aki

albumin (colloid)

raise volume

na outside

k inside

high na levels = cells dehydrated

SS: thirst, fatigue, weakness, muscle twitching, altered mental, less conscious

treat with: hypotonic (if hypovolemic) or diuretics (if hypervolemic)

nacl med

MOA: supplement for low

AE: hypernat and edema

consideration: monitor levels and fluid accum

kcl

k gives you iv site pain, no renal failure or postassium sparking direutic ace inhibitors, give upright bc esophagitis

moa: replace potassium

ae - gi irritation, hyperk, iv site pain

considerations - iv pump

no renal failure, potassium sparing diuretic, burn, adrenal insufficency, ace inhibitors

admin sitting upright bc esophag.

no crush

dilute liquid forms

respiratory

for all monitor: vital signs, respiratory function and rate

with long acting- restlessness/insomnia

SABA short acting beta adrenergic agonists (albuterol)

beta 2 - bronchodilation, chest pain, short so not for prophylaxis, tachy restlessness

MOA: beta 2 cause bronchodilation

AE: headache, nervous, restlessness tachy, chest pain

Considerations: not for asthma prophylaxis

caution HTN

LABA (-terol)

beta bronchodilation, stay in lab long so up hr and bp, eat snakcs during means DM/hyperthyroidism

MOA: not rescue, beta 2 bronchodilation

AE: anxiety, insomnia, tremors

Considerations: elevation BP HR monitor VS

gluocse monitor with DM

caution hyperthyroidism

anticholinergics (sama)

anti - usually against using bc hard so educate mdi, look skin color before, less cholinergic so dry and hoarse voice

MOA: block cholinergic receptors = bronchodilation

AE: cough, drying of mucosa, hoarseness, bitter

Considerations: education of MDI use

2-3min wait b4 puffs

skin color o2 lvls lung sounds

LAMA (-pium)

lama like candy, candy cause glaucoma, slowly, pupils dilate when see candy

MOA: inhbiit acetylcholine = bronchodilation

AE: dry mouth, hoarseness, pupil dilation, restelessness

considerations: sugarless candy for dry

effects take time

no glaucoma

budesonide

bud in to control inflammation, protein synthesis, leukocute and fibroblast migration, bud gets thrush and flushed so he cant breathe (FEV1) so educate him if hes preg

MOA: prevent or control inflammation —> control protein synthesis, leukocyte and fibroblast migration, capilarry permeability

AE: headache, candidas

Considerations: FEV1 monitor

educate admin

can use during preg

methylxanthines (-phylline)

xanthines phyllines phosphidesterase - bronchodilation and muscle relaxation, phil has insomnia tremors and seizures and interacts a lot with people bc he thinks everyone is safe margin

MOA: inhibit phosphodiesterase = bronchodilation and smooth muscle relaxation

AE: insomnia, tremors, seizures

Considerations: narrow safe margin

IV PO-IV very slow

cyp450 interactions

glucocorticoids (asone)

asone - corticoids dont dilate, they reduce inflam and up beta 2 responsiveness, candida causes asone atone to change (dysphonia) so rinse mouth daily, monitor glucose and cataracts and growth

MOA: reduce inflam, increased responsiveness to beta 2, NOT DILATOR

AE:oropharyngeal candidasis, dysphonia (voice change)

Considerations: daily

rinse mouth after

glucose lvl monitor

cataract monitor

growth imapir in children

mast cell stabilizer (intal/cromolyn)

intal supressed by mast cells, reduces inflammation, bad intal causes cough bitterness hoarseness, makes you cry so clear your nose and keep on the low dose only, intal takes 2 weeks to arrive

MOA: supress inflammation, prevent mast cell release of histamine leukotrienes antigens NOT DILATORS

AE:mild cough, bitter, hoarseness

Considerations: low dose, clear nose

2 wk improvement time

leukotriene modifiers

leuk has chronic asthma and this reduces the inflammation, leuk has NVD and he is taking warfarain so he monitors prothrombin time and ratio, he also has hepatic impairment

MOA: reduce inflam of asthma, not for acute attach

AE: headache nausea diarrhea

Considerations: monitor prothrombin time and normalized ratio in warfarin pt

existing hepatic impairment caution (metab in hepatic)

targetted therapy/biologic

omali is an antagonist IGE, shooter so cv clot risk, depends on the levels and plans it every 2-4 weeks for 12 weeks

MOA: Omalizumab SQ, antagonist IgE

AE: type 3 hypersensitivities, CV clot riksk

Considerations: dosed dependent on ige lvls

2-4 wks

12 wk effects

anti hypertensive

all risk: hypotension, check vitals

Angiotensin-converting enzyme (ACE)

Angiotensin receptor blockers (ARB)

both angio —> hyper k chem panel, angioedema

Beta adrenergic receptor blockers

Calcium channel blockers (CCB)

Diuretics

Alpha 1 receptor blocker

alpha agonist

direct acting vasodilaters

ACE 1 RAAS inhibitory drugs (-pril)

ACE pril, inhibits ACE (angiotensin converting enzyme), monitor chem panel k, cough

MOA: inhibitor ACE, artery dilator, supress aldosterone

considerations: chem panel monitor (k)

new cough

ACE 1 enalapril

hypo

hyperkal

cough

allergic severe: angiodema

ARB - Angio II receptor blockers (-sartan)

arbys sartan burgers have less k and aldo more pee out, hyper k, eat make you cough, dont eat while preg

MOA: block angio 1 to 2, dilation arterioles and veins, less k and aldosterone secretion. more pee na water

AEL hypotension, hyperkal, cough

considerations: angioedema, chem panel, no preg

beta adrenergic blockers (-lol) (respiratory and heart)

lol your a beta 1 blocker, brady has low hr and contractibility so hes fatigued, take his apical pulse first, slow position changes, slow off, class 2 heart failure

MOA: down HR and contractability (block beta 1)

AE: fluid retention, bradycardia, fatgiue, insomnia, drowsiness, confusion

considerations: take apical pulsefirst

change position slowly

steady off

class II

calcium channel blockers (-pine)

pines have lots of calcium, piners are like miners that do vasodilation to mines, low oxy down there so dizzy, flushing, edema, and ginvial hyperplasia, check ecg, they have no grapefruit or alc down there

MOA: vasodilations on ARTERIES, down BP

AE: dizziness, headache, flushing, peripherial edema, ginvial hyperplasia

considerations: ECG

minor is dizzy flush headache

no grapefruit

no alc

calcium channel blocker: verapamil

vera likes calcium, vasodilation, aloe vera has extra coronary perfusion and less contraction, she has vertigo cause shes a lady that has heart block from breakup and edema, vertigo is ortho hypo risk

MOA: vasodilation in heart and arterioles, coronary perfusion, LESS CONTRACTION

AE: flushing vertigo heart block edema to ankles

considerations: monitor edema

orthostatic hypotension

calcium channel blocker: Cdiltiazem

cdiltiazem calcium, dilf make heart block and liver fucked up, hypo in elderly

MOA: lower pressure, vasodilation of arteries

AE: heart block, liver enzymes

considerations: no liver impair

elderly = hypo

thiazide like diuretics (hydrochlorothiazide)

azides so up na excretion and pee out more water H K Na on the side (DCT), thad works in a lab value and cant hear

MOA: inhibit na reabsorption in DCT = excrete water na k H

AE: hypokalemia

considerations: lab values

hearing loss

alpha 1 adrenergic antagonist (doxazosin)

doxa boxa: if you box you are less sympathetic and have BENIGN PROSTATE HYPERTROPHY, prostate makes you drowsy n said, no other antihypertensives bc boxers need high blood pressure

MOA: block sympathetic receptors in arterioles = vasodilation

AE: dizzy headache somnolence (drowsy)

considerations: no NSAID

other antihypertensives will mean hypotension

alpha 2 agonist clonidine

clones up alpha 2, down sympath, dry mouth. brady, rebound, cns depression, clones do lots of drug drug interactions, clones mean renal function

MOA: less sympath nerve impulse = vasodilation

AE: NV constipation, dry mouth, bradycard, rebound hypertension if sudden stop, cns dep

considerations: no preg breastfeed

DD interaction

renal function lab

vasodilators hydralazine

hydra hydro massage palpitates muscles which relax them, hydra on chem panel, when you palpitation it rebounds htn with sudden stop, nsaid ortho hypo and no use with antihyper, hydra = fluid retention

MOA: vasodilation by relax arterial smooth muscle

AE: headache, palpitation, flushing, nausea

considerations: chem and electrolyte panel

fluid retention

rebound HTN anxierty with sudden stop

orthostatic hypo education

NSAID reduce effects

use with other antihyper. = severe hypotension

hyperlipidemia meds

all check LFT

VLDL - cholesterol and triglycerides

LDL - bad cholesterol, mostly cholesterol

HDL - good, protein mostly

statins

stat! remove HMG for her LDL, hmg has big muscles that leak and she does too many steroids so joint pain and heartburn, she eats and cant drink alc

MOA: inhibit HMG reductase, remove LDL

AE: muscle joint pain, heartburn, rhadomyolysis

Considerations: food for gi discomfort

new muscle pain reported

lft

no alc

bile acid - cholestyramine, colesevelam, colestipol (col)

col is like colon —> bile increase excretion of chol in stool, bloating constipation, absorption messed up, lft electro, no anticoag and take with food

MOA: binds with bile to increase excretion of cholesterol stool

AE: bloating and constipation

Considerations: 204 hr before or after meds

lft electrolytes

no anticoagulants

food

niacin

nia jax is VLDL and fatty acids, she has hot flashes flushing and is gassy, look at her lft and glucose levels, no gout

MOA: VLDL

AE: flushing, hot flash, nausea, gas, diarrhea

Considerations: LFT glucose

no gout

gemfibrozil

gemma removed triglycerides from recipe, replaced with dysPEPSIa, gemma was pregnant so she cramping, LFT, glucose, PT/INR, food, no liver gallbladder impairment, decrease dose with kidney

MOA: remove triglycerides from circulation

AE: dyspepsia, cramping

Considerations: lab values, PT/INR, glucose, LFT

food for gi distress

no pt with CKD, liver impairment, gallbladder

dose decrease with kidney

zetia

Z - zero absorption of cholestrol small intestine

E - elevation of LFT

T - 2-4 after before bile acid

I - intestinal issue - diarrhea

A - aching muscles, rhabdomyolysis

MOA: inhibit absorption of cholesterol in small intestine

AE: mild respiratory congestion, muscle weak

Considerations: 2 - 4 hour after bile acid

lipid

lft

ANGINA and MI PHARM

drugs reduce mycardial demands for 02

• slow hr, reduce preload, reduce contract, low BP

aspirin

ashley takes aspirin so her platelets wont stick and she bleeds. her stomach hurts bc she drank so she chews on aspirin

MOA: less platelet aggregation

AE: bleeding, epigastic distress

Considerations: LFT

no bleeding disorder, etoh

ACS - chew and swallow

nitrates

nitrate nos, relax and vasodilate, too much vasodilate is hypotension and flushing rash, iv cont monitor and sublingual hold if bp less than 90/60, gloves and take 3-5 min after first, less preload

MOA: smooth muscle relax with vasodilation

AE: hypotension, dizzy, flushing, rash

Considerations: iv cont monitoring

sublingual check bp, less than 90/60 hold

gloves

angina - take then 3-5 min take again

diltiazem - calcium channel blocker

MOA: inhibit calcium = relax muscle

reduce cardiac workload

for angina

heart failure medications

preload and afterload affected

ace inhibitors -pril and ARBs do the same (sartan)

reduce afterload, up excretion of na h20

lower peripherial resistance and blood volume

up cardiac output

entresto

entresto - neprilysin —> natriuresis, hyperkalemia, angioedema, trest that no pregnant, HFrEF

MOA:inhibit neprilysin = vasodilation and natriuresis

AE: hypotension, kyperkalemia, angioedema

Considerations: no preg

serum creatinine

HFrEF good

reduce preload and afterload

SGLT (-flozin)

SGLT flozin - during flozin, you pee more (loop diuretic) and you have natriuresis (less blood volume), your losing weight while standing, cant floss when preg so no 2nd 3rd, fungal if you dont floss

more loop diuretic and natriuresis = less blood volume, SGT weight loss, 2nd 3rd trimester, DD, glucose renal

MOA: up natriuresis with loop diuretic = less blood volume

AE: hypotension, fungal infection, weight loss

Considerations: no 2nd 3rd trimester

DD

glucose and renal function

spironolactone

MOA: less aldosterone = more na h20 excretion

AE: hyperkalemia, vomitting, libido

Considerations: no k foods, serum lab draws

beta blockers

slow heart rate

reduce BP

up squeeze of heart

reduce workload

digoxin

dig = forceful contractions to diggin in me, scratch with fingers = digit toxicity, scratch neutropenia, fingers touch apical for 1.8 minutes, dig for higher stage

MOA: forceful contraction, slower hr

AE: neutropenia, dysrhythmias, digitalis toxicity

Considerations: apical pulse 1 min

serum digoxin (hold if higher than 1,8)
geriatric caution

higher stage HF

diuretics (loop, -mides)

MOA: less reabsorption of nacl = pee out

AE: hypokalemia, hypotension

Considerations: serum electrolytes

geriatric caution

isordil

isor DILD: relaxed muscles and vasodilated them, its so good syncope, monitor hr and bp before and after, hurts so contact, slow position changes, no phosphodiesterase inhibitors

MOA: smooth muscle relaxer, vasodilation vein arteries

AE: hypotension, syncope

Considerations: vitals, bp hr pre post admin

contact if chest pain persists

slow position change

no phospdiesterase inhibitors

milrinone IV

mil millions blocked phosphodiesterase and let in calcium (contraction) so no other inotrophic agents, dysrhythmia and hypos, monitor cardiac and if new vent dysrthythmia

MOA: block phosphodiesterase, up calcium for contraction

AE: hypokalemia, tension, dysrhythmias

Considerations: electrolytes

cardiac monitoring

hold if new ventricular dys

caution other inotropic agents

hypernatremia

ICF —> ECF

bounding pulse, coma, confusion, hemorrhage, twitching, hyperreflexia, up bp

hyponatremia

ECF —> ICF

cellular swelling

dilutional - edema, ascites, weight gain, JVD

hypovolemia, hypotension, tachycardia, less reflexes

hyperkalemia

k into the ECF

cramping, neuromuscular irritability, weakness, tone loss

hypokalemia

k ecf into cells

excitability decreases, weakness, loss of tone, dysrhythmia, glucose intolerance

hypercalcemia

hyperparathyroidism, vitamin d

nonspecific symptoms, renal impairment, bone pain

hypocalcemia

less pTH or vit d

increased excitability, tingling/spasms, chevostek and trousseau

magnesium

both - excitability

hypo - alcohol, urinary loss

hyper - renal insufficiency, adrenal insufficiency