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MS2 Unit4 CardioResp > Pharm > Flashcards

Pharm Flashcards

1
Q

what treatment would you use (2)?

  • ≥ 60
  • BP goal: 150/90
  • non Black
A
  • thiazide diuretic
  • ACE/ARB/CCB alone or in combo
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2
Q

how would you treat?

  • < 60 yo
  • BP goal: 140/90
  • black
A

thiazide vel CCB

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3
Q

how would you treat

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

thiazide diuretic vel CCB

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4
Q

how would you treat?

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

ACE ao ARB with another class

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5
Q

criteria for stage I and II htn

bonus: idiopathic htn accounts for what % of pts

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

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

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6
Q

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

*why younger?

A

aggressively

the younger the pt, the longer they have w dz

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7
Q

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

A

IX (carotid) and X (aortic) resp

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8
Q

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

A

SA node

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9
Q

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

A

loop diuretics

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10
Q

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

A

thiazide diurectics

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11
Q

inh Na+ reabsorption in the distal tubule

A

K+ sparing diuretics

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12
Q

SEs of _____ (2 diurectics) include

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

loop and thiazide diuretics

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13
Q

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?

A
  1. K+ sparing (spironolactone***)
  2. hyperK+ bc spironolactone is competitive antag of aldo
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14
Q

explain the bio efx of diuretics for htn

A

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

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15
Q

explain the MOA of ACEi (2)

A
  • block endoth ACE conversion of AngI –> Ang II
  • ↓ bradykinin breakdown –> (vasoD*)
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16
Q

Explain the MOA of ARBs

A

comp binding for AngII (vasoC) to vasc endoth

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17
Q

ATP dep Extrusion Pump in gut and brain

A

P-glycoprotein

hint: beware if pt is on PGPi

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18
Q

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

A

CYP2D6

hint: sx temporal to buproprion tx

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19
Q

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

what is the mechanism of the drugs listed below?

A

tosades de pointes (ventr dysrhythmia)

MOA: block cardiac repolz

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20
Q

explain the MOA behind most drug induced valvular dz’s

A

involve 5HT2b rcp that modulate serotonin release

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21
Q

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 →
A
  1. acute effusive pericarditis
  2. mitral stenosis
  3. tricuspid reurg
  4. mitral regurg
  5. aortic regurg

hint: 5HT2b assc path

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22
Q

why is there an ↑risk of MI with NSAIDs?

A

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

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23
Q

↑O2 delivery to myocard tissue is deps on _____

A

coronary Artery vasoD

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24
Q

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

A
  • Morphine
  • O2
  • ASA
  • Nitroglycerin

tx for MI and angina

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25
Q

Name the drug for MI/angina

  • irrev COX1 inh → blocks TXA2 and PG prodn →↓plt aggrn
  • ↓inflamm but ↑bleeding risk
A

Aspirin (ASA)

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26
Q

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)
A

Nitrates

hint: reduced to NO

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27
Q

endothelial NO also inh what two functions?

A

antiinflamm efx

  1. plt aggr’n
  2. WBC-endoth interactions
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28
Q

std dosing for Nitrates (2)

A
  1. 0.4 mg (sublingual/spray)
  2. cont infusion/IV (titrate)
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29
Q

Contraindications for ___ include:

  • STEMI
  • systolic hypotension (<90)
  • PDEi use*
  • hypertophic CMP
  • aortic stenosis

*explain why?

A

nitrates

*bonus: PDEi block cGMP breakdown –> uncontrolled vasoD + vol depletion?

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30
Q

Name the drug:

  • pain control
  • ↓SNS output → ↓O2 demand
  • vasoD efx → ↓preload
A

Morphine

hint: req 2A recommendation

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31
Q

definitive tx for MI means

A

angioplasty balloon in cath lab

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32
Q

DOC for unstable* angina

A

ASA

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33
Q
A
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34
Q

tx for angina, syncope and heart failure in aortic stenosis

A

slow nitroglyceride admin (3 doses)

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35
Q

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

A
  1. GABAagonist (benzo) THEN anti htn
  2. nitroglyc for coronary vasospasm

VIPI: BBs contraindicated!!!

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36
Q

Tx plan for preeclampsia? - 2

what should be given with special consult - 3

A
  1. Magnesium sulfate
  2. Hydralazine

hint: Hydralazine, labetalol, methyldopa, nifedipine. He Likes My Neonate

special conults:

  1. thiazides,
  2. CCBs
  3. clonadine
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37
Q

Name the indications for the dx’s below

  1. Diabetes - 2
  2. COPD -1
  3. Aortic Dissection -1
A
  1. ACE + ARBS
  2. CCBs
  3. BBs
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38
Q

Name the contraindications for the dx below

  1. diabetes
  2. COPD
  3. aortic dissection
  4. depression - 2
A
  1. BBs
  2. BBs
  3. VasoD’s alone
  4. BBs + m-dopa
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39
Q

why should you moderatly dec BP in pts with chronic htn

A

rapid change –> ischemia + stroke

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40
Q

dec vasc compliance + inc CO result in

A

widened pulse pressure

hint: see egs of inc CO below

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41
Q

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?

A

ACEi

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

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42
Q
    • Where loop diruectivs ct on acive Na/K/C transporters
    • ROMK and NKCC2 activity

segment?

A

Thick Ascending Limb LOH (TAL)

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43
Q

what common Rx combo is used (2)?

A
  1. Thiazide + K sparing
  2. Loop + K-sparing
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44
Q

Name the drug and SEs:

MOA: Osmotic diuretic.tubular fluid osmolarity Žurine flow, intracranial/ intraocular pressure.

use for: Drug overdose, elevated intracranial/intraocular pressure.

SEs: Pulmonary edema, dehydration, hypo- or hypernatremia. Contraindicated in anuria, HF.

A

Mannitol

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45
Q

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….

A

Acetazolomide

46
Q

SEs include:

  • Proximal renal tubular acidosis*, paresthesias, NH3 toxicity, sulfa allergy, hypokalemia.
  • Promotes calcium phosphate stone formation (insoluble at high pH).

Name that drug….

A

Acetazolamide

hint: “ACID”azolamide causes ACIDosis.

47
Q

MOA: Inhibit NaCl reabsorption in early DCT Ždiluting capacity of nephron.Ca2+ excretion.

Use: Hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

Name that drug (3)….

A

Thiazide diuretics

  • Hydrochlorothiazide,
  • chlorthalidone,
  • metolazone.
48
Q

SEs include: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia. Sulfa allergy.

Name that drug (3)….

A

Thiazide diuretics (Hyper GLUC)

  • Hydrochlorothiazide,
  • chlorthalidone,
  • metolazone.
49
Q

________ (2) are competitive aldosterone receptor antagonists in cortical CT. ______ (2) block Na+ channels in the cortical CT.

what’s the drug class?

A
  • Spironolactone + eplerenone
  • Amiloride + Triamterene
  • Potassium-sparing diuretics (TaKe a SEAT)
50
Q

Use for: Hyperaldo, K+ depletion, HF, hepatic ascites, nephrogenic DI, antiandrogen.

Adverse SEs: Hyperkalemia (± arrhythmias), endocrine sx (eg, gynecomastia, antiandrogen effects).

drug class?

A

​Potassium-sparing diuretics

  • Spironolactone, (for ascites, may cause endocrine sx)
  • Eplerenone,
  • Amiloride, (for nephro DI)
  • Triamterene.
51
Q

MOA: Nonsulfa inh of NKCC in TAL

Use: Diuresis in patients allergic to sulfa drugs.

Name the drug (1) and class?

A

Ethacrynic acid (most ototoxic)

class: Loop diuretics

52
Q

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*
A

Loop Diuretics

  • Furosemide,
  • bumetanide,
  • torsemide

hint: Loops Lose Ca2+*

53
Q

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)

A

Loop Diuretics

  • Furosemide,
  • bumetanide,
  • torsemide

hint: OHH DAANG!* for SEs

54
Q

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

A

thalidomide

hint: thalidomide babies in the 1950s

55
Q

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

A

Lepromatous Hansen’s (M. Leprae)

56
Q

Prophylacitc dapsone for expsoure is usually tx for ____

A

Peds pts expsoed to M. Leprae

57
Q

Name the drug

  • MOA: Inhibits arabinosyl transferase enz (cell wall synth) in M leprae
  • SEs: Neuropathy + Optic neuritis
A

Ethambutol

58
Q

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

A

Catecholamines

histo:

  1. myocardial necrosis with contraction bands
  2. inflamm mø infiltrate
59
Q

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

A
  1. Brian lesion - pheochromocytoma
  2. stress - Takoktsubo Cadiomyopthay (octupus L ventricle)
  3. vasopressor agetns
  4. cocaine
60
Q

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

A

↑lipid peroxidation in myocyte membranes

hint: stop treatment!

61
Q

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

A
  • myofiber swelling
  • cytoplasmic vacuolizn
  • fatty replacement

hint: stop treatment!

62
Q

statin + resin combo reduces lipid lowering agents by ____

while statin + ezetimibe reduces lipid lowering agents by ____

A

statin + resin: 50%

tatin + ezetimibe: 60%

63
Q

statin + fibrates is bad due to risk of ____

A

myositis (body muscle inflamm)

64
Q

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

A

70% chol in LDL - BAD

20% chol in HDL - GOOD!

hint: ↓ LDL/HDL ratio

65
Q

Name the drug class and drugs within: (2)

binds endopeptidase that targets LDLR degradn –> ↓ LDL degradn + ↑LDL blood removal

A

PCSK9i:

  • alirocumab
  • evolucumab
66
Q

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
67
Q

Name the drug class:

  • 1st line, best tolerated
  • blocks convers of HMG-CoA –> mevalonate (chol precursor
  • rare SEs: hepatotox myopthay (w/niacin vel fibrates)
A

HMG-CRi (statins)

68
Q

Benefits of statins include (2)

A
  • counteract osteoporosis
  • ↓ CAD rel-death by 20% (C-reactive prot assc)
69
Q

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

A
  • atorvastain (lipitor) + rosuvastatin (crestor)
  • shorter half life –> taken in evening
70
Q

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)
A

Bile Acid Resins:

  • Cholestyrine
  • colestipol
  • colesevelam

hint: forces liver to make more bile acids

71
Q

Name the drug class and drugs (3):

  • Upregulate LPLŽ–> TG clearance
  • Activates PPAR-𝛂 to induce HDL synthesis
  • SEs: Myopathy (w/ statins), chol gallstones (via chol 7α-hydroxylase inh)
A

Fibrates: GBF

  • Gemfibrozil,
  • bezafibrate,
  • fenofibrate
72
Q

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
A

Nicotinic Acid (Niacin (vit B3))

hint: affects a lipid parameters

74
Q

when is drug tx consider for lowering lipids?

A

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

75
Q

name the drugs (2)?

  • anti IL5 Ab
  • for asthma w/ high serum eosionphils
A
  1. Mepolizumab
  2. Reslizumab

hint: MR = My Rash

76
Q

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
A

omalizumab

77
Q

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
A

LTi (antiLTs)

  1. Zafirlukast
  2. montelukast

hint: NSAIDS ↓ COX1/2 –> ↑LTs –> ↑asthma sx

78
Q

____ (rx) rapid onset, selective 5-LOXi that ↓LT prodn. Can adjunct with steroids.

Bonus: Whats a common SE?

A

Zileuton

bonus: Liver tox

79
Q

3 delivery devices for asthma/COPD tx ?

A
  • Metered Dose (MDI)
  • Dry Powder (DPI)
  • Soft Mist (SMI)
80
Q

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?
A
  1. Cromolyn
  2. Nedocromil

drug relieved by β2 agonist

hint: cant use for COPD, alt only for mild/persistent asthma

81
Q

___% of rx is inhaled –> lungs

___% is swalows –> GI abs –> first pass metabs (liver)

A

10-20% inhaled

80-90% swallowed

84
Q

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

A
  1. Inhaled short aciting β2 agonists (SABA)
  2. inhaled long acting β2 agonists (LABA)
  3. inhaled anticholinergics (anti-M rcp)
  4. PDE inh’s
85
Q

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

A
  1. Inhaled CCsSs
  2. AntiLTs
  3. Cromones
  4. Anti-Abs (IgE vs IL5)
87
Q
  • prodrug activated by esterase
  • ↓systemic abs + systemic SEs
A

Ciclesonide

89
Q

Name the drug class:

  • ↓inflamm (PGs. LTs. ILs) –> ↓BHR
  • inhibits late response
  • ± cause oropharyngeal candidiasis (how would you prevent*)
  • SEs: edema, htn, metabolic changes
A

Inhaled glucoCCs

*prevent candidiasis w spacers and gargling

90
Q

CCSs reserved for severe, asthma acute attack (2)

A

CCSs reserved for severe, acute attack (2) - PI

  1. Prednisone
  2. IV steroids
93
Q

Name the drug

  • selective PDE4i –> blocks neutrophil migration
  • approved for COPD
  • anti inflamm action –> 2˚ lung function improvement
A

Roflumilast

94
Q

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

A
  • Tezacaftor
  • Ivacaftor

hint: IT Crowd; ↑CFTR activity

95
Q

____ is a corrector that ↑CFTR qty in CF pts

96
Q

Name the drug class and drugs (3)

  • weak bronchoD
  • nonselective PDEi (3,4,5,)
  • anti-inf, ↓diaphragm fatige
  • adenosine rcp antag –> ↓apop
A

Methylxanthines

  1. theophylline
  2. theobromine
  3. caffeine
97
Q

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

A

CYP450 metabs

98
Q

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

A

theophyline (methylxanthines); narrow therap window

hint:

  • anti-inf: 5-10 mg/L
  • bronchoD: 10-20 mg/L (minor SEs)
  • > 40 mg/L major SEs
99
Q

describe the methylxanthine dose range for

  1. NVD, anorexia, headache, insomnia, GERD
  2. cardiac arrythmia, seizure
A
  1. 15-20 mg/L: NVD, anorexia, headache, insomnia, GERD
  2. >40 mg/L: cardiac arrythmia, seizure
100
Q

Methylxanthines can restore ____sensitivity at a low dose; while glucosteroids can restore ____ sensitivity at a low dose

A
  • CCS;
  • β rcp (dt to β2 agonist overuse)
101
Q

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

A
  1. ↑histone DEacetylation –> ↓inflamm genes
  2. ↓NF-𝜿B transx (cytokine prodn)
102
Q

use this methylxanthine for bronchispams or status asthmaticus

A

Aminophylline IV

105
Q

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
A

Cystic Fibrosis (CF)

106
Q

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

A
  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
107
Q

a CYP inducer would show ______ effects, while a CYP inh would show _____effects

A

slow, accumulated; rapid

108
Q

How would you tx Fume Fever (3)?

A
  1. supportive
  2. NSAIDs (fever + chills)
  3. suggest appropo PPE
109
Q

Supportive care for beta-agonist toxidrome (3)?

A
  • electrolyte replacement
  • IV fluids
  • BEnzos (GABAergic)
110
Q

list by shortest to longest duration of effect…whats the assc toxidrome?

  • terbutaline (SQ)
  • Albuterol
  • Clenbuterol
A

Albuterol >Terbutaline > CLenbuterol

111
Q

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
A

Beta agonists (sympathomimetic tox)

hint: wt loss supplements

112
Q

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

A

Physostigmine; TCA

hint: stop, watch HR, have atropine

113
Q

Name the drug?

  • Carbamate acetylcholinesterase inh
  • blocks ACh breakdsown
  • Crosses BBB (delirium tx)
  • good for antichol poisoning
A

physostigmine

114
Q

Treatment for Antichol toxidrome (3)?

A
  • supportive care
  • benzos
  • physostigmine
115
Q

Methylxanthine tox mgt include (4)?

bonus: why wouldnt you use phenytoin?

A
  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

116
Q

What’s the drug?

  • structural analogies of adenosine (prolonged seizures)
  • act as 𝛂1,2 anatags
  • ↑ endo catechols
  • PDE inh
  • β rcp agonists
A

Methylxanthines (T,C)

theophylline

Caffeine

118
Q

3 major enzymes with Theophylline metabs?

A

CYPs:

  1. 3A
  2. 1A2
  3. 2E1
119
Q

intranasal CCS for allergies (1)

A

fluticasone

120
Q

surface acting CCSs for asthma (2)

A
  1. budesonide
  2. flunisolide
121
Q

Explain the mechanism behind ASA for Kwasaki

A

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

MS2 Unit4 CardioResp (4 decks)

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