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ILE I > ILE I Exam I HTN > Flashcards

ILE I Exam I HTN Flashcards

Miscellaneous facts I'm afraid of forgetting lol

1
Q

SOAP

A
  1. Subjective 2. Objective 3. Assessment 4. Plan
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2
Q

ADE

A

Can be allergies, ADRs, medication errors, overdoses

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3
Q

ADRs

A

Any injury or unpleasant side effect resulting from APPROPRIATE use of a medication

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4
Q

Hypotension

A

<90/<60

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5
Q

5 Steps for NT

A
  1. Biosynthesis
  2. Storage
  3. Release
  4. Receptor interaction
  5. Termination
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6
Q

Sympathetic NT

A

NE (some ACh)

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7
Q

Parasympathetic NT

A

ACh

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8
Q

Sympathetic effect on eyes

A

mydriasis

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9
Q

parasympathetic effect on eyes

A

mitosis

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10
Q

sympathetic effect on saliva

A

decreased production

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11
Q

sympathetic effect on SV and HR

A

increased

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12
Q

Parasympathetic effect on vasculature

A

None! :p

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13
Q

Sympathetic effect on vasculature

A

vasoconstrict

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14
Q

Sympathetic effect on liver

A

glycogen -> glucose

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15
Q

Parasympathetic effect on liver

A

bile production

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16
Q

Receptor found in lungs

A

B2

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17
Q

Receptor found in heart

A

B1

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18
Q

Parasympathetic nerve form

A

Long, short

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19
Q

Sympathetic nerve form

A

Short, long

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20
Q

mecamylamine and trimethaphan work at what point on the nerve?

A

Presynaptic

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21
Q

sweat glands have what innervation?

A

sympathetic (ACh -> M)

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22
Q

Blood vessels, cardiac tissue, SA/AV nodes, exocrine glands and eye muscles have what innervation?

A

Sympathetic (NE -> a, b)

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23
Q

SA/AV nodes, GI smooth muscle, bronchioles, eye muscles have what innervation?

A

parasympathetic (ACh -> M)

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24
Q

Tubocurare and succinylcholine work at what point in the nerve?

A

NMJ

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25
Q

Adrenergic receptor types

A

A1 (A1A, A1B, A1C), A2 (A2A, A2B, A2C), B (B1, B2, B3)

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26
Q

Which cells release renin?

A

JG cells (juxtaglomerular) (in kidney)

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27
Q

Which cells “wake up” JG cells?

A

Macula densa cells

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28
Q

With what do macula densa cells wake up JG cells?

A

prostaglandins (act locally)

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29
Q

What produces angiotensinogen

A

Liver cells

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30
Q

Angiotensinogen + renin

A

AT1

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31
Q

6 types of drug interactions

A
  1. Ion-ion
  2. Ion-Dipole
  3. Dipole-dipole
  4. Hydrophobic
  5. Pi
  6. pi-cation
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32
Q

Which receptor interactions are the strongest?

33
Q

Intrahepatic recycling

A

Drugs that are excreted from bile and reabsorbed by the portal vein

34
Q

Which electrolytes are lost when taking first-line anti-hypertensives?

A

Na, K, Mg, Cl,

35
Q

The excretion of which 2 substances decrease when taking first-line anti-hypertensives

A

Ca, Uric acid

36
Q

Which drugs mentioned in class are thiazides?

A

HCTZ, chlorthalidone

37
Q

how do thiazides work?

A

Sulfonamide (-SO2NH) donates proton and has a negative charge, which competes with Cl-

38
Q

DHP drug(s) mentioned in class

A

Amlodipine

39
Q

Non-DHP drug(s) mentioned in class

A

Verapamil and diltiazem

40
Q

DHP or non-DHP affects the heart as well as vasculature

41
Q

What is the reflex response experienced by patients taking CCB?

A

When taking DHP, carotid artery sense BP drop. NE released

42
Q

Reflex response is experienced when taking DHP or non-DHP?

43
Q

How do CCBs work?

A

Block Ca2+ flow into vascular muscle/SA node, decreasing heart rate

44
Q

Adverse effects of CCBs

A

Hypotension, Constipation, Muscle weakness, Flushing, Swelling in the lower extremities, Gingival hyperplasia, Headache

45
Q

Bradykinin is produced when

A

ACE inhibitors block AT1->AT2

46
Q

which anti-hypertensive causes cough? why?

A

ACEI, ARBs,

bradykinin buildup

47
Q

Which 2 ACEI were mentioned in class?

A

Enalapril, captopril

48
Q

ACEI MOA

A

Block AT1 -> AT2, block bradykinin breakdown

49
Q

One of the 2 ACEI mentioned in class is a prodrug. Which one?

A

Enalapril (esters -> COOH)

50
Q

Taste disturbance is caused by which drug class?

51
Q

Swelling of lower extremities is caused by which drug class?

52
Q

What does AT2 do?

A

Produces aldosterone and causes vasoconstriction

53
Q

Why would you use an ARB over an ACEI?

A

ARBs cause less coughing (but still a problem)

54
Q

Does bradykinin breakdown occur when taking an ACEI? An ARB?

A

ACEI - no

ARB - yes!

55
Q

Angioedema occurs much less with (ACEI/ARB) than with (ACEI/ARB)

A

much less with ARBs

56
Q

Which drugs mentioned in class are ARBs?

A

-Valsartan (any -sartan)

57
Q

ARB MOA

A

ATII antagonist at ATI receptor

58
Q

Adverse effects of ARBs

A

Hypotension, Dizziness, Headache, Nausea and Vomiting (N/V), Cough, Increased K+ levels, Decreased GFR.

59
Q

OBRA purpose

A

Requires drug utilization reviews to lessen medication costs and errors

60
Q

OBRA introduced 3 requirements for pharmacists. What were they?

A
  1. Prospective DUR review
  2. Patient counseling
  3. Record keeping
61
Q

Beta blockers side effects

A

Bradycardia, Sedation, Fatigue, Shortness of Breath (SOB), Headache, Sleep Disturbances, Sexual Dysfunction

62
Q

BB MOA

A

Blocks B1 receptor in heart -> Decreased heart rate, Decreased central sympathetic outflow, Decreased Renin release

63
Q

Direct vasodilators MOA

A

open potassium channels resulting in hyperpolarization of vascular smooth muscle. Inside of cell becomes more negative as K leaves

64
Q

Side effects of direct vasodilators

A

hypotension, reflex response, hypertrichosis (minoxidil)

65
Q

Direct vasodilators presented in class

A

Minoxidil, hydralazine

66
Q

SA node is controlled by ___ which is controlled by ___ which has ___ receptors

A

SA node is controlled by vagal nerve, which is controlled by the vasomotor center, which has A2 receptors

67
Q

Centrally acting antihypertensives (CAA) MOA

A

Decrease sympathetic outflow, many are A2 antagonists

68
Q

CAAs adverse effects

A

Sedation, Bradycardia, Constipation, Dry mouth, Dizziness

69
Q

Decreased venous return does what to BP? Do CAAs cause a decrease in venous return?

A

decreased venous return = lower BP, yes

70
Q

CAAs mentioned in class

A

Clonidine, alpha-methyl-dopa, alpha-methyl-norepinephrine

71
Q

Loop diuretic MOA

A

The loop diuretics are the most powerful diuretics known due primarily to their site of action. Inhibition of the Na+/1K+/2Cl- symport results in a powerful diuretic effect resulting in the loss of these ions along with Ca+2 and Mg+2.

72
Q

Most powerful diuretic

A

Loop diuretic

73
Q

Adverse effects of loop diuretics

A

electrolyte imbalance

74
Q

Loop diuretics mentioned in class

75
Q

Loop diuretics vs thiazide diuretics; which causes loss of Ca?

76
Q

Aldosterone antagonist MOA

A

inhibit aldosterone mediated stimulation of ENaC and Na+/ATPase synthesis resulting in increased Na+ excretion and decreased K+ excretion.

77
Q

A1 antagonists

A

inhibit A1 receptors in vasculature, allowing them to vasodilator

78
Q

A1 antagonists

ILE I (18 decks)

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