HTN 2 Flashcards

1
Q

What is MOA of ACE-I?

A

stops conversion of angiotensin I into angiotensin II

  • vasodilators
  • prevents LV remodeling
  • reduces mortality
  • blocks aldosterone and decreases Na and water retention
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2
Q

What is MOA of ARB?

A

blocks AT1 receptor

  • vasodilator
  • same as ACE but no cough
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3
Q

What are ADE of ACE/ARB (3)?

A

hyperkalemia
hypotension
angioedema and cough (ACE-I)

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4
Q

T/F you can combine ACE and ARB

A

False

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5
Q

What patient population benefits from ACE and ARBS?

A

white young men

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6
Q

contraindications for ACE/ARB?

A
  • pregnancy
  • CKD
  • cough
  • hyperkalemia
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7
Q

Drug interactions with ACE-I and ARBS?

A

NSAIDS

-PDE5/viagra

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8
Q

What should be monitored in ACE and ARBS?

A
  • serum creatinine

- K

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9
Q

What is MOA for Aliskiren?

A
  • blocks renin

- stops RAAS system

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10
Q

When should you not use Aliskiren?

A
  • when CrCL is less than 60

- pregnancy

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11
Q

T/F Aliskiren works synergistically with ACE and ARBs?

A

TRUE

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12
Q

T/F Aliskiren is first line treatment for HTN

A

False

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13
Q

What is MOA of beta blockers?

A

blocks beta 1 and beta 2 receptors to slow HR down?

-stops renin release

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14
Q

Name one non-selective B1 and B2 blocker?

A

Propranolol

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15
Q

Name 1 selective B1 blocker?

A

Metoprolol

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16
Q

Name alpha 1 and beta 1 blocker (3)?

A

Carvedilol and Nebivolol and Labetalol

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17
Q

T/F Labetalol is safe in pregnancy

A

TRUE

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18
Q

ADE with Beta blockers (3)

A
  • bradycardia
  • AV node blocks
  • bronchospasm
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19
Q

T/F Metoprolol and propranolol undergo extensive first pass effect?

A

TRUE

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20
Q

What should you monitor in beta blockers (4)?

A
  • HR
  • BS in diabetes
  • CHF
  • edema
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21
Q

Drug interactions with Beta Blockers (4)?

A
  • NSAIDS
  • CCB
  • digoxin
  • cardiac depressants
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22
Q

What are the clinical uses of beta blockers (5)?

A
  • angina
  • post MI
  • HF
  • HTN
  • antiarrhythmics (propranolol is used to treat atrial arrhythmias
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23
Q

T/F Carvedilol is the go to treatment for HF?

A

TRUE

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24
Q

T/F Propranolol is used to treat migraines because it is lipophilic

A

TRUE

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25
Q

What is the mechanism of Prazosin and Doxazosin?

A

Alpha 1 blocker

-block NE and EPI from binding to alpha 1 receptor to prevent vasoconstriction

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26
Q

What are drug interactions of Prazosin and Doxazosin? (3)

A

decrease efficacy of dabigatran(anti-coagulant)

  • linagliptin/ DM med
  • vincristine cancer med)
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27
Q

what are the clinical uses if Alpha 1 blockers? (2)

A
  • BPH

- PTSD/reduces bad dreams

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28
Q

T/F Alpha 1 blockers induce the first dose phenomenon

A

-TRUE

29
Q

What is MOA for clonidine and methyldopa?

A
  • they are central alpha 2 agonist
  • they bind alpha 2 receptors to decrease cAMP via G proteins
  • decrease cAMP decrease intracellular Ca
  • no release of NE
  • decrease sympathetic outflow and increases vagal tone
30
Q

What are ADE in alpha 2 agonists (3)?

A

anticholinergic effects

  • rebound HTN
  • hepatitis/hemolytic anemia
31
Q

What is the clinical use of methyldopa/clonidine?

A
  • 1t line TX for HTN in pregnancy and peds
32
Q

T/F Diuretic should be given with alpha 2 agonist

A

TRUE

33
Q

What are the drug interactions with alpha 2 agonists (4)?

A
  • MOA
  • PDE5
  • lithium
  • tricyclic antidepressants
34
Q

What should you monitor when using C2AA?

A

LFTS

35
Q

T/F C2AA are 2nd or 3rdd line treatments in non pregnant people?

A

TRUE-due to side effects

36
Q

What is MOA of Reserpine?

A
  • peripheral adrenergic antagonist

- blocks reuptake of NE into its storage vesicles to decrease vascular resistance and CO

37
Q

What are ADE of Reserpine?

A
  • sedation
  • depression
  • increase parasympathetic NS- congestion, diarrhea, increased gastric secretion
38
Q

when should you adjust dose of Reserpine?

A

when CrCl is < 10

39
Q

T/F Reserpine causes increased Na and H20 retention and must be given with a diuretic?

A

TRUE

40
Q

What is MOA of CCB’s?

A

they block L type calcium channels and thus induce peripheral and coronary artery vasodilation

41
Q

Where on the heart do CCB’s work?

A

SA node: decrease HR and O2 demand
ventricular myocardium: decreases O2 demand and contractility
-coronary arteries: increase vasodilation and O2 supply

42
Q

When is CCB’s considered 1st line treatment?

A

-in blacks who do not have HF or CKD

43
Q

where do DHP work? Name 2?

A
  • they work on blood vessels

- Amlodipine and Nifedipine

44
Q

Name 2 Non-DHP and where do they work?

A
  • in heart

- Veramipil and Diltiazem

45
Q

What are the clinical uses of Non-DHP (4)?

A
  • SVT
  • angina
  • HTN
  • rate control in a-fib
46
Q

What are the clinical uses of DHP (5)?

A
  • Amlodipine in HF
  • angina
  • Raynaud’s syndrome
  • Nifedipine used in premature labor
  • stroke and CHD prevention
47
Q

What are ADE with DHP (4)?

A
  • reflex tachycardia
  • gingival hyperplasia
  • peripheral edema
  • flushing
48
Q

What are ADE with non-DHP?

A

Verapimil-constipation

49
Q

T/F You should you Nifedipine in emergent/urgent HTN?

A

False-don’t use Nifedipine

50
Q

What should you monitor in when using CCB’s (4)?

A
  • EKG
  • HR
  • BP
  • LFT’s
51
Q

What are the drug interactions with CCB’s (5)?

A

reduces metabolism of:

  • cyclosporin
  • theophylline
  • simvastatin
  • tacrolimus
  • digoxin
  • CP40 system
52
Q

T/F Grapefruit juice inhibits metabolism of Nifedipine

A

TRUE

53
Q

What is MOA of Hydralazine/Minoxidil?

A
  • Direct Arterial Vasodilator
  • direct smooth muscle relaxers
  • arterial dilators
  • increases NO production in endothelium
54
Q

T/F Hydralazine isosorbide dinitrate is used in blacks to tx HF?

A

TRUE

55
Q

T/F Hydralazine can cause lupus like syndrome in women?

A

TRUE

56
Q

What should you monitor when using direct arterial vasodilators?

A

Renal function

57
Q

What are ADE for Hydralazine/Minoxidil (2)?

A
  • reflex tachycardia

- angina with CAD patients

58
Q

T/F Hydralazine decrease after load and increases CO

A

TRUE

59
Q

What medication can you give to prevent reflex tachycardia?

A

BB or clonidine

60
Q

What are other uses for DAV?

A
  • hypertrichosis

- minoxidil is used to treat male pattern baldness

61
Q

What is MOA for desmopressin/vasopressin?

A
  • ADH agonists
  • they bind V2 receptor in collecting tubule and increases cAMP
  • this signals increased aquaporins into luminal cell to increase H20 re-absorption
62
Q

What are the clinical uses of ADH agonist?

A
  • pituitary diabetes insipidus

- bed wetters

63
Q

What are ADE with ADH agonists?

A

-dilutional hyponatermia

64
Q

T/F ADH agonist increase urine concentration and reduce its volume

A

TRUE

65
Q

What is MOA of ADH antagonists?

A
  • Demeclocycline blocks cAMP

- block V1 and V2 receptors (Conivaptan and Tolvaptan)

66
Q

T/F Demeclocycline is a tetracycline derivative

A

TRUE

67
Q

What are ADE for ADH antagonists?

A
  • demeclocycline: bone and teeth abnormalities

- conivaptan: demyelination

68
Q

What are the clinical uses of ADH antagonists?

A

-SIADH (too much water)/Conivaptan