what treatment would you use (2)? ≥ 60 BP goal: 150/90 non Black

thiazide diuretic ACE/ARB/CCB alone or in combo

Caution for ______(1 diuretic), esp with use of ACE + ARB tx, includes hormonal sx like gynecomastia irreg mentruation,menorrhagia, nipple tenderness AND hyperkalemia\ \ explain why?

1. K+ sparing (spironolactone\ \ \ ) 2. hyperK+ bc spironolactone is competitive antag of aldo

Name the pathology associated with drugs below 1. Clozapine → 2. methsergide → 3. MDMA, methsurgide, pergolide → 4. fenPhen, MDMA, cabargoline, methsurgide, pergolide→ 5. fenphen, bromocriptine, MDMA, cabargoline, methsurgide, pergolide →

1. acute effusive pericarditis 2. mitral stenosis 3. tricuspid reurg 4. mitral regurg 5. aortic regurg hint: 5HT2b assc path

Pharm Flashcards by Nneka I

what treatment would you use (2)?

≥ 60
BP goal: 150/90
non Black

thiazide diuretic
ACE/ARB/CCB alone or in combo

How well did you know this?

Not at all

Perfectly

how would you treat?

< 60 yo
BP goal: 140/90
black

thiazide vel CCB

How well did you know this?

Not at all

Perfectly

how would you treat

Diabetes w/o CKD
BP goal: < 140/90

thiazide diuretic vel CCB

How well did you know this?

Not at all

Perfectly

how would you treat?

all ages/races with CKD
± diabetes
BP goal: < 140/90

ACE ao ARB with another class

How well did you know this?

Not at all

Perfectly

criteria for stage I and II htn

bonus: idiopathic htn accounts for what % of pts

stage I = 140-159/90-99
Stage Il = >160/>100

bonus: idiopathic accts for 95% of pts (no known 2˚ cause)

How well did you know this?

Not at all

Perfectly

the more risks or the younger* the pt the more ______ you should tx.

*why younger?

aggressively

the younger the pt, the longer they have w dz

How well did you know this?

Not at all

Perfectly

afferent carotid sinus + aortic arch baroRs are monitored by ___ and ____ resp

IX (carotid) and X (aortic) resp

How well did you know this?

Not at all

Perfectly

efferent CNX + SNS fibers, and circulating catecholamines affect ___ (structure)

SA node

How well did you know this?

Not at all

Perfectly

competitively inh Na+K+CI- transporters in the PAT

loop diuretics

How well did you know this?

Not at all

Perfectly

inh Na/Cl exchange in distal ascending loop (TAL)

thiazide diurectics

How well did you know this?

Not at all

Perfectly

inh Na+ reabsorption in the distal tubule

K+ sparing diuretics

How well did you know this?

Not at all

Perfectly

SEs of _____ (2 diurectics) include

hypokalemia and hypomagnesium –> ± cardiac arryth
∆glucose tolerance
inc lipids + uric acid
voleume depletion
ED in men

loop and thiazide diuretics

How well did you know this?

Not at all

Perfectly

Caution for ______(1 diuretic), esp with use of ACE + ARB tx, includes hormonal sx like

gynecomastia
irreg mentruation,menorrhagia, nipple tenderness
AND hyperkalemia*

* explain why?

K+ sparing (spironolactone***)
hyperK+ bc spironolactone is competitive antag of aldo

How well did you know this?

Not at all

Perfectly

explain the bio efx of diuretics for htn

↓BP + CO –> ↑ Na and H2O clearance –> enhanced vol depletion –> overtime CO returns to normal

How well did you know this?

Not at all

Perfectly

explain the MOA of ACEi (2)

block endoth ACE conversion of AngI –> Ang II
↓ bradykinin breakdown –> (vasoD*)

How well did you know this?

Not at all

Perfectly

Explain the MOA of ARBs

comp binding for AngII (vasoC) to vasc endoth

How well did you know this?

Not at all

Perfectly

ATP dep Extrusion Pump in gut and brain

P-glycoprotein

hint: beware if pt is on PGPi

How well did you know this?

Not at all

Perfectly

bupropion interferes with _____ CYP enz eliminatn of metropolol + bupropion metabs

CYP2D6

hint: sx temporal to buproprion tx

How well did you know this?

Not at all

Perfectly

inh of the delayed rectifier K+ current usually leads to?

what is the mechanism of the drugs listed below?

tosades de pointes (ventr dysrhythmia)

MOA: block cardiac repolz

How well did you know this?

Not at all

Perfectly

explain the MOA behind most drug induced valvular dz’s

involve 5HT2b rcp that modulate serotonin release

How well did you know this?

Not at all

Perfectly

Name the pathology associated with drugs below

Clozapine →
methsergide →
MDMA, methsurgide, pergolide →
fenPhen, MDMA, cabargoline, methsurgide, pergolide→
fenphen, bromocriptine, MDMA, cabargoline, methsurgide, pergolide →

acute effusive pericarditis
mitral stenosis
tricuspid reurg
mitral regurg
aortic regurg

hint: 5HT2b assc path

How well did you know this?

Not at all

Perfectly

why is there an ↑risk of MI with NSAIDs?

prothrombotic: COX1i → inh TXA2 –> ↓plt aggr’n
hint: also cause fluid rtn → heart failure

How well did you know this?

Not at all

Perfectly

↑O2 delivery to myocard tissue is deps on _____

coronary Artery vasoD

How well did you know this?

Not at all

Perfectly

what does MOAN/MONA stand for and what can it tx?

Morphine
O2
ASA
Nitroglycerin

tx for MI and angina

How well did you know this?

Not at all

Perfectly

Name the drug for MI/angina * irrev COX1 inh → blocks TXA2 and PG prodn →↓plt aggrn * ↓inflamm but ↑bleeding risk

Aspirin (ASA)

Name the drug for MI/angina * enz rxn w sulfhydryl grps → reduction * activates guanylyl cyclase → ↑cGMP→ ↓intracell Ca → sm muscle relaxn → VasoD * venous dilation →↓preload * relieves CA vasospasm\* (epicardial CA + collaterols)

Nitrates hint: reduced to NO

endothelial NO also inh what two functions?

antiinflamm efx 1. plt aggr'n 2. WBC-endoth interactions

std dosing for Nitrates (2)

1. 0.4 mg (sublingual/spray) 2. cont infusion/IV (titrate)

Contraindications for ___ include: * STEMI * systolic hypotension (\<90) * PDEi use\* * hypertophic CMP * aortic stenosis \*explain why?

nitrates \*bonus: PDEi block cGMP breakdown --\> uncontrolled vasoD + vol depletion?

Name the drug: * pain control * ↓SNS output → ↓O2 demand * vasoD efx → ↓preload

Morphine hint: req 2A recommendation

definitive tx for MI means

angioplasty balloon in cath lab

DOC for unstable\* angina

ASA

tx for angina, syncope and heart failure in aortic stenosis

slow nitroglyceride admin (3 doses)

tx plan for cocaine/chest pain w/ sympathomimetic sx? - 3

1. GABAagonist (benzo) THEN anti htn 2. nitroglyc for coronary vasospasm VIPI: **BBs contraindicated!!!**

Tx plan for preeclampsia? - 2 what should be given with special consult - 3

1. Magnesium sulfate 2. Hydralazine hint: **H**ydralazine, **l**abetalol, **m**ethyldopa, **n**ifedipine. **H**e **L**ikes **M**y **N**eonate _special conults:_ 1. thiazides, 2. CCBs 3. clonadine

Name the indications for the dx's below 1. Diabetes - 2 2. COPD -1 3. Aortic Dissection -1

1. ACE + ARBS 2. CCBs 3. BBs

Name the contraindications for the dx below 1. diabetes 2. COPD 3. aortic dissection 4. depression - 2

1. BBs 2. BBs 3. VasoD's alone 4. BBs + m-dopa

why should you moderatly dec BP in pts with chronic htn

rapid change --\> ischemia + stroke

dec vasc compliance + inc CO result in

widened pulse pressure hint: see egs of inc CO below

This drug can: * slows diabetic renal dz * protects htn pts w/ prev healthy kidneys * improves renal artery stenosis but what's the worst case scenario?

ACEi worst case scenario: failed dx of renal htn + ø f/u --\> **ARF/hyperK+ and sudden death**

* - Where loop diruectivs ct on acive Na/K/C transporters * - ROMK and NKCC2 activity segment?

Thick Ascending Limb LOH (TAL)

what common Rx combo is used (2)?

1. Thiazide + K sparing 2. Loop + K-sparing

Name the drug and SEs: ## Footnote MOA: Osmotic diuretic.tubular fluid osmolarity urine flow, intracranial/ intraocular pressure. use for: Drug overdose, elevated intracranial/intraocular pressure. SEs: Pulmonary edema, dehydration, hypo- or hypernatremia. Contraindicated in anuria, HF.

Mannitol

_MOA_: CAHi. Causes self-limited NaHCO3 diuresis and ↓ total body HCO3− stores. _use for_: Glaucoma, metabolic alkalosis, altitude sickness, pseudotumor cerebri. Alkalinizes urine\* Name that drug....

Acetazolomide

SEs include: * Proximal renal tubular acidosis\*, paresthesias, NH3 toxicity, sulfa allergy, hypokalemia. * Promotes calcium phosphate stone formation (insoluble at high pH). Name that drug....

Acetazolamide hint: “ACID”azolamide causes ACIDosis.

MOA: Inhibit NaCl reabsorption in early DCT diluting capacity of nephron.Ca2+ excretion. Use: Hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis. Name that drug (3)....

Thiazide diuretics * Hydrochlorothiazide, * chlorthalidone, * metolazone.

SEs include: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia. Sulfa allergy. Name that drug (3)....

Thiazide diuretics (Hyper **GLUC**) * Hydrochlorothiazide, * chlorthalidone, * metolazone.

\_\_\_\_\_\_\_\_ (2) are competitive aldosterone receptor **antag**onists in cortical CT. ______ (2) block Na+ channels in the cortical CT. what's the drug class?

* Spironolactone + eplerenone * Amiloride + Triamterene * Potassium-sparing diuretics (Ta**K**e a **SEAT**)

Use for: Hyperaldo, K+ depletion, HF, hepatic ascites, nephrogenic DI, antiandrogen. Adverse SEs: Hyperkalemia (± arrhythmias), endocrine sx (eg, gynecomastia, antiandrogen effects). drug class?

Potassium-sparing diuretics * Spironolactone, (for ascites, may cause endocrine sx) * Eplerenone, * Amiloride, (for nephro DI) * Triamterene.

MOA: Nonsulfa inh of NKCC in TAL Use: Diuresis in patients allergic to sulfa drugs. Name the drug (1) and class?

Ethacrynic acid (most ototoxic) class: Loop diuretics

MOA: * Sulfa NKCC inh of TAL * ↓ hypertonicity of medulla, preventing concentration of urine. * ↑ PGE release (vasodilatory effect on afferent arteriole) * Inh by NSAIDs. * Ca2+ excretion\*

_Loop Diuretics_ * Furosemide, * bumetanide, * torsemide hint: Loops Lose Ca2+\*

Use for: hypertension, hypercalcemia, edema (HF, cirrhosis, nephrotic syndrome, pulmonary edema), SEs include\*: Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), metabolic Alkalosis, Nephritis (interstitial), Gout.\* drug class and drugs (3)

_Loop Diuretics_ * Furosemide, * bumetanide, * torsemide hint: OHH DAANG!\* for SEs

\_\_\_\_ (drug) was used to treat Erythema NodosumLeprosum (ENL), and caused fetal limb defects.

thalidomide hint: thalidomide babies in the 1950s

dapsone + rifampin + clofazimine for 2 yrs (sterile lesions) is treatment for \_\_\_\_

Lepromatous Hansen's (M. Leprae)

Prophylacitc dapsone for expsoure is usually tx for \_\_\_\_

Peds pts expsoed to M. Leprae

Name the drug * MOA: Inhibits arabinosyl transferase enz (cell wall synth) in M leprae * SEs: Neuropathy + Optic neuritis

Ethambutol

Ca+ overload leads to toxic _____ levels --\> ↑ HR --\> focal microvasc vasoC. Describe histopath (2)

Catecholamines histo: 1. myocardial necrosis with contraction bands 2. inflamm mø infiltrate

4 mechanisms of intense ANS stimulation in catecholamine assc myocardial dz?

1. Brian lesion - pheochromocytoma 2. stress - Takoktsubo Cadiomyopthay (octupus L ventricle) 3. vasopressor agetns 4. cocaine

Anthracyclines, doxorubicin, and daunorubicine cause **dilated** cardiomyopthay + heart failure. Why?

↑lipid peroxidation in myocyte membranes hint: stop treatment!

phenothiazines, chloroquine, lithium and cocaine cause cardiomypathy. How? (3)

* myofiber swelling * cytoplasmic vacuolizn * fatty replacement hint: stop treatment!

statin + resin combo reduces lipid lowering agents by \_\_\_\_ while statin + ezetimibe reduces lipid lowering agents by \_\_\_\_

statin + resin: 50% tatin + ezetimibe: 60%

statin + fibrates is bad due to risk of \_\_\_\_

myositis (body muscle inflamm)

\_\_\_% chol in LDL and \_\_\_% chol in HDL. which one is good/bad for you?

70% chol in LDL - BAD 20% chol in HDL - GOOD! hint: ↓ LDL/HDL ratio

Name the drug class and drugs within: (2) binds endopeptidase that targets LDLR degradn --\> ↓ LDL degradn + ↑LDL blood removal

PCSK9i: * alirocumab * evolucumab

Name the drug: * inh dietary/biliary chol abso at GI brush border --\> ↓chol delivery to liver * synegistic with statins (18% KDK reduction as monotx) * 1 daily pill * rare SEs: LFTs, diarrhea

Ezetimibe

Name the drug class: * 1st line, best tolerated * blocks convers of HMG-CoA --\> mevalonate (chol precursor * rare SEs: hepatotox myopthay (w/niacin vel fibrates)

HMG-CRi (statins)

Benefits of statins include (2)

* counteract osteoporosis * ↓ CAD rel-death by 20% (C-reactive prot assc)

\_\_\_\_ (2 statins) can be administered 1x day; why are older statins taken in the evening?

* atorvastain (lipitor) + rosuvastatin (crestor) * shorter half life --\> taken in evening

Name the drug class and drugs (3): * bind gut bile acids (via anion exchange) for stool secretion * SEs: ↑5% in TGs + ↓fat sol abs of drugs/vits (contra in coumarin tx)

Bile Acid Resins: * Cholestyrine * colestipol * colesevelam hint: forces liver to make more bile acids

Name the drug class and drugs (3): * Upregulate LPL--\> TG clearance * Activates PPAR-𝛂 to induce HDL synthesis * SEs: Myopathy (w/ statins), chol gallstones (via chol 7α-hydroxylase inh)

Fibrates: GBF * Gemfibrozil, * bezafibrate, * fenofibrate

Name the drug: * inh lipolysis (hormone-sensitive lipase) in fat * ↓ hepatic VLDL synthesis * serious SEs: Hepatotox, Hyperglycemia, Hyperuricemia * not so serious SEs: flushing, pruritis, dyspepsia, rash

Nicotinic Acid (Niacin (vit B3)) hint: affects a lipid parameters

when is drug tx consider for lowering lipids?

no change with diet and wt reduction for 3-6 months

name the drugs (2)? * anti IL5 Ab * for asthma w/ high serum eosionphils

1. Mepolizumab 2. Reslizumab hint: MR = **M**y **R**ash

Name the drug: * Anti IgE monoclonal Ab * subQ admin every 204 wks * for severe asthma + poorly controlled oral CCSs * ↓need for inahlled CCS and ↓asthma exacerbations

omalizumab

name the class and 2 drugs responsible for: * DOC for ASA or antigen induced asthma * prophx for excerised induced asthma * slow onset LTD4 rcp antagonists

LTi (antiLTs) 1. Zafirlukast 2. montelukast hint: NSAIDS ↓ COX1/2 --\> ↑LTs --\> ↑asthma sx

\_\_\_\_ (rx) rapid onset, selective 5-LOXi that ↓LT prodn. Can adjunct with steroids. Bonus: Whats a common SE?

Zileuton bonus: Liver tox

3 delivery devices for asthma/COPD tx ?

* Metered Dose (MDI) * Dry Powder (DPI) * Soft Mist (SMI)

Name the drug (2): * ∆delayed Cl- channel --\> blocked mast cell degranulation --\> ↓histamine, PAF, LTC4 * prophylactic use: ↓BHR (allergens\*) * min SEs: thoart irritation + cough * what is the drug(s) relieved by?

1. Cromolyn 2. Nedocromil drug relieved by β2 agonist hint: cant use for COPD, alt only for mild/persistent asthma

\_\_\_% of rx is inhaled --\> lungs \_\_\_% is swalows --\> GI abs --\> first pass metabs (liver)

10-20% inhaled 80-90% swallowed

Current Bronchodilator Tx's for asthma + COPD (4)

1. Inhaled short aciting β2 agonists (SABA) 2. inhaled long acting β2 agonists (LABA) 3. inhaled anticholinergics (anti-M rcp) 4. PDE inh's

Current anti-inflamm agents for COPD + asthma (4)

1. Inhaled CCsSs 2. AntiLTs 3. Cromones 4. Anti-Abs (IgE vs IL5)

* prodrug activated by esterase * ↓systemic abs + systemic SEs

Ciclesonide

Name the drug class: * ↓inflamm (PGs. LTs. ILs) --\> ↓BHR * inhibits late response * ± cause oropharyngeal candidiasis (how would you prevent\*) * SEs: edema, htn, metabolic changes

Inhaled glucoCCs \*prevent candidiasis w spacers and gargling

CCSs reserved for severe, asthma acute attack (2)

CCSs reserved for severe, acute attack (2) - PI 1. Prednisone 2. IV steroids

Name the drug * selective PDE4i --\> blocks neutrophil migration * approved for COPD * anti inflamm action --\> 2˚ lung function improvement

Roflumilast

\_\_\_\_\_\_ (2 rx) are expensive potentatiors for CF pts w/ G551D mutation

* Tezacaftor * Ivacaftor hint: **IT C**rowd; ↑CFTR activity

\_\_\_\_ is a corrector that ↑CFTR qty in CF pts

VX-809

Name the drug class and drugs (3) * weak bronchoD * nonselective PDEi (3,4,5,) * anti-inf, ↓diaphragm fatige * adenosine rcp antag --\> ↓apop

Methylxanthines 1. theophylline 2. theobromine 3. caffeine

dt ____ metabolism; theophylline and methylxanthines can ↑toxicity with erythromycin, cimetidine, and fluoroquinolones

CYP450 metabs

SEs of ____ , an anti-inflamm bronchoD, are predisposition to nausea, diarrhea, **tachy cardia, arrythmia, and CNS excitation** dt \_\_\_\_\_\_

theophyline (methylxanthines); narrow therap window hint: * anti-inf: 5-10 mg/L * bronchoD: 10-20 mg/L (minor SEs) * \> 40 mg/L major SEs

describe the methylxanthine dose range for 1. NVD, anorexia, headache, insomnia, GERD 2. cardiac arrythmia, seizure

1. **15-20 mg/L:** NVD, anorexia, headache, insomnia, GERD 2. **\>40 mg/L:** cardiac arrythmia, seizure

Methylxanthines can restore \_\_\_\_sensitivity at a low dose; while glucosteroids can restore ____ sensitivity at a low dose

* CCS; * β rcp (dt to β2 agonist overuse)

Explain the process behind methylxanthine anti-inflamm effects (2)

1. ↑histone DEacetylation --\> ↓inflamm genes 2. ↓NF-𝜿B transx (cytokine prodn)

use this methylxanthine for bronchispams or status asthmaticus

Aminophylline IV

6 drugs currently available for _____ tx include: 1. pulmozyme 2. TOBI (aminoglycoside) 3. Azithromycin 4. hypertonic saline (7%)\* 5. high dose ibuprofen 6. Cayston 7. Kaydeco

Cystic Fibrosis (CF)

3 drugs after the discovery of CFTR mutation and CF gene; and their tx effect?

1. **_DNase_** - clearance of crosslinked DNA from dead cell accm in mucus plug --\> easier lung clearance w/o systemic abs 2. **_TOBI_** - poor bioavailbaility --\> directly delivery to lung ONLY 3. **_Ivacaftor_** - correct protein folding + inc CFTR activity

a CYP inducer would show ______ effects, while a CYP inh would show \_\_\_\_\_effects

slow, accumulated; rapid

How would you tx Fume Fever (3)?

1. supportive 2. NSAIDs (fever + chills) 3. suggest appropo PPE

Supportive care for beta-agonist toxidrome (3)?

* electrolyte replacement * IV fluids * BEnzos (GABAergic)

list by shortest to longest duration of effect...whats the assc toxidrome? * terbutaline (SQ) * Albuterol * Clenbuterol

Albuterol \>Terbutaline \> CLenbuterol

Clinical effects of ____ (rx) include: 1. Tachycardia + Low BP + diapharesis\* 2. agitation + tremor\* + palpitations 3. hypokalemia 4. AGMA (anion gap metab acidosis) ± lactic acidose 5. hyperglycemia

Beta agonists (sympathomimetic tox) hint: wt loss supplements

rapid admin of ____ can cause seizures. Combined with \_\_\_\_, it can cause asystole

Physostigmine; TCA hint: stop, watch HR, have atropine

Name the drug? * Carbamate acetylcholinesterase inh * blocks ACh breakdsown * Crosses BBB (delirium tx) * good for antichol poisoning

physostigmine

Treatment for Antichol toxidrome (3)?

* supportive care * benzos * physostigmine

Methylxanthine tox mgt include (4)? bonus: why wouldnt you use phenytoin?

1. ↓serum theo w/ activate charcoal 2. ↓serum tox w/ hemodialysis 3. β anatgs for ↓BP (refractory hypotension) 4. tx seizures with benzos, barbs, propofol bonus: uses GABAergic AEDs for these seizures; phenytoin is Ca channel mediated

What's the drug? * structural analogies of adenosine (prolonged seizures) * act as 𝛂1,2 anatags * ↑ endo catechols * PDE inh * β rcp agonists

Methylxanthines (T,C) theophylline Caffeine

3 major enzymes with Theophylline metabs?

CYPs: 1. 3A 2. 1A2 3. 2E1

intranasal CCS for allergies (1)

fluticasone

surface acting CCSs for asthma (2)

1. budesonide 2. flunisolide

Explain the mechanism behind ASA for Kwasaki

ASA inh plt COX →inh ↑TXA2 --\> ø thrombosis (and MI)

Pharm Flashcards

(111 cards)