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pharm > midterm 1 > Flashcards

midterm 1 Flashcards

1
Q

10 rights

A

right drug, dose, time, route, pt, reason, documentation, refusal, education, evaluation

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2
Q

chemical name

A

describes drug chemicals composition & molecular structure

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3
Q

generic name

A

name given to drug approved by health canada

acetaminophen, ibuprofen

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4
Q

trade name

A

commercial name given to drug by manufacturer; trademark with marketability (tylenol, advil)

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5
Q

pharmaceutics

A

how various dosage forms/routes influence way body metabolizes drug & way drug effects body

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6
Q

pharmacokinetics

A

study of what the body does to drug (what happens to a drug from the time its put into body until it has left)

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7
Q

what phases does pharmacokinetics include

A

absorption, distribution, metabolism, excretion, onset of action, half life, peak effect, duration of action

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8
Q

absorption

A

movement of drug from site of admin into bloodstream for distribution (PO, SC, IV)

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9
Q

metabolism

A

biological transformation of drug (liver most responsible)

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9
Q

distribution

A

transport of drug in bloodstream to site of action

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9
Q

excretion

A

eleminiation of drug from body (kidney primary way drug is eliminated) (lesser extent bowel & liver)

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10
Q

onset of action

A

time it takes for drug to elicit therapeutic response

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11
Q

peak effect

A

time needed for drug to reach its MAX therapeutic response

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12
Q

duration of action

A

length of time that concentration is sufficicent to elicit therapeutic response

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13
Q

toxicity

A

when peak blood level is too high & drug is poisonous

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14
Q

half life

A

time it takes for 1/2 of drug to be removed from body

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15
Q

why does half life matter

A

steady state

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16
Q

steady state

A

amount of drug removed is equivalent to amount absorbed

once reached, consistent levels of drug in body that correlates with max therapeutic benefit

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17
Q

pharmacodynamics

A

what drug does to body (cellular level)

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18
Q

therapeutic effect

A

desired or intended effect of particular medication

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19
Q

adverse effect

A

undesirable effect that are direct response to one or more drugs

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20
Q

toxicity

A

producing adverse bodily effects due to poisonous qualities

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21
Q

contraindication

A

any characteristic of pt that makes use of medication dangerous

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22
Q

receptors

A

molecular structure within or on surface of cells where specific substances bind

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23
Q

agonist

A

drug that binds to receptors & stimulate activity at receptor site (stimulates response)

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24
Q

antagonist

A

drug that binds nad inhibits activity at receptor site

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25
Q

diabetes mellitus

A

disorder of carbohydrate metabolism that involves either deficiency of insulin, resistance of tissue (muscle, liver) to insulin, or both

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26
Q

organ involved in diabetes

A

pancreas

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27
Q

pancreas & aspects

A

digestive enzymes & hormones

islets of langerhan (alpha & beta cells)

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28
Q

is pancreas an exocrine or endocrine gland

A

exocrine because it secretes

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29
Q

islets of langerhan exocrine or endocrine

A

endocrine, alpha & beta cells secrete insulin

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30
Q

insulin causes high blood glucose t/f

A

T

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31
Q

glucagon causes low blood glucose t/f

A

T

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32
Q

beta cells do

A

secrete insulin

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33
Q

beta cell process

A

BG high, produce insulin, insulin goes into blood to increase transport of glucose into cells, storing in liver as glycogen & skeletal muscle to decrease BG

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34
Q

alpha cells do

A

glucagon

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35
Q

alpha cell process

A

glucagon goes into liver, releases glycogen, BG low –> alpha cells release glucagon to release glycogen to increase BG

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36
Q

blood glucose levels normal & diabetic

A

normal = 4-6
diabetic = 4-7

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37
Q

hemoglobin A1c

A

shows how much insulin as sit on hemoglobin molecules & should be < 7% (less thn)

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38
Q

patho of DM

A

destruction of beta cells in pancreas (insulin deficiency, autoimmune)

defective insulin receptors in tissues (glucose unable to be transported into cells)

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39
Q

cardinal signs of hyperglycemia

A

polyuria, polydipsia, polyphagia, weight loss, blurred vision, fatigue

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40
Q

type 1

A

abrupt onset, common in kids, autoimmune destruction of beta cells causing little/no insulin, ketosis

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41
Q

type 1 need exogenous insulin t/f

A

T

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42
Q

type 2

A

slower onset, exercise & diet management, oral hypoglycemic agent effective in controlling blood sugar, obese, adapted to hyperglycemia over long period of time

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43
Q

treatments for type 2

A

education, nutrition, physical activity, weight & lifestyle management, insulin & oral hypoglycemics

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44
Q

insulin is only hormone that

A

has capacity to lower blood sugar

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45
Q

peak insulin is

A

most at risk for hypoglycemia (greatest amount of medication in system)

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46
Q

insulin types

A

rapid, short, intermediate, long

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47
Q

rapid acting onset

A

10-15min

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48
Q

rapid acting peak

A

60-90 mins

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49
Q

rapid acting duration

A

3.5-6 hr

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50
Q

rapid acting names of insulin

A

aspart (novorapid), lispro (humalog), glulisine (apidra)

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51
Q

rapid acting can be given SC but not IV

A

T

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52
Q

when can insulin be given

A

15min before meal

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53
Q

short acting onset

A

30 min

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54
Q

short acting peak

A

2-3hr

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55
Q

short acting duration

A

6.5hr

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56
Q

short acting insulin names

A

regular insulin (humulin regular, novolin, toronto)

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57
Q

short acting insulin is responding to

A

peak in blood glucose

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58
Q

short acting = what kind of infusion

A

IV bolus

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59
Q

intermediate acting onset

A

2-4hr

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60
Q

intermediate acting peak

A

4-10hr

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61
Q

intermediate acting duration

A

12-18hr

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62
Q

intermediate acting insulin names

A

isophane (humulin N, novolin NPH)

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63
Q

intermediate acting is basal insulin because

A

reacting to keep the BG at moderate level

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64
Q

goal of intermediate acting

A

steady state

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65
Q

long acting onset

A

2-4hr

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66
Q

long acting peak

A

none

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67
Q

long acting duration

A

20-24hr

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68
Q

long acting is basal because

A

provides a prolonged glucose control

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69
Q

long acting insulin names

A

glargine (lantus), determir (levemir)

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70
Q

which insulin is cloudy

A

intermediate

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71
Q

insulin preferred route of delivery

A

basal-bolus

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72
Q

unopened insulin vial kept in fridge, opened vial expires

A

30 days after opening

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73
Q

insulin side effects

A

hypoglycemia
weight gain
lipodystrophy
tachycardia, palpitations
headache, weakness, fatigue

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74
Q

hypoglycemia signs

A

dry mouth
blurred vision
anxious
perspiration
dizziness
diaphoretic
sleepiness
confusion
difficulty speaking
weak

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75
Q

treatment of hypoglycemia

A

see policy
assess LOC
diabetic protocol (glucose tablets 15g, glucagon SC)

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76
Q

if pt BG not < 4 but reports feeling lightheaded

A

give snack or juice

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77
Q

antagonist - insulin causes . . . & examples

A

hyperglycemia

epi, furosemide, niacin, thiazides, thyroid hormone, corticosteroids

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78
Q

protagonist - insulin causes . . . . & examples

A

hypoglycemia

alcohol, anabolic steroids, sulpha antibiotics

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79
Q

oral hypoglycemic agents (type 2) based on

A

premise that insulin still being produced

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80
Q

biguanide

A

metformin, 1st line treatment

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81
Q

action of biguanide

A
  1. decrease glucose production by liver
  2. decrease intestinal absorption of glucose
  3. improves insulin receptor sensitivity in liver, skeletal muscle, adipose –> increased glucose uptake by organs
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82
Q

side effects of biguanide

A

abdominal bloating, anorexia, nausea, cramping, feeling full, flatulence, metallic taste, vit b12 reduction

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83
Q

biguanide does not…

A

stimulate insulin production = does not cause significant hypoglycemia

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84
Q

sulfonylureas is only used

A

in type 2

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85
Q

sulfonylureas must have

A

functioning beta cells because it stimulates insulin from beta cells

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86
Q

action of sulfonylureas

A

stimulates insulin secrete from beta cells

improves sensitivity to insulin in tissue

decreases production of glucagon

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87
Q

side effects of sulfonylureas

A

hypoglycemia, weight gain, gi symptoms, rashes

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88
Q

sulfonylureas may cause hypoglycemia t/f

A

T

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89
Q

thiazolidinediones is what type of drug

A

insulin-sensitizing drug

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90
Q

action of thiazolidinediones

A

regulates genes involved in glucose & lipid metabolism

decrease insulin resistance by enhancing sensitivity of insulin receptor

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91
Q

does thiazolidinediones cause hypoglycemia

A

NO

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92
Q

why thiazolidinediones controversial

A

cardiac risks

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93
Q

gliptins

A

pt that don’t respond well to metformin & sulfonylureas

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94
Q

action of gliptins

A

delaying breakdown of incretin hormines –> results in increased insulin & lower glucagon secretion = hypoglycemia

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95
Q

glinides action

A

increase insulin secretion from pancreas with shorter duration of action & given with meal

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96
Q

glinides structurally different than sulfonylureas but similar mechanism of

A

action

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97
Q

a-glucosidase is a

A

inhibitor

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98
Q

example of a-glucosidase

A

acarbose (glucobay)

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99
Q

action of a-glucosidase

A

slows down digestion and absorption of glucose post meal

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100
Q

side effects of a-glucosidase

A

gi symptoms

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101
Q

does a-glucosidase cause hypoglycemia

A

NO

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102
Q

nursing assessment for diabetes

A
  • assess knowledge & provide education
  • type 1 or 2?
  • BG levels
  • medication effects on BG
  • signs hypo/hyperglycemia
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103
Q

describe basal bolus

A

basal (steady state)

bolus (post meal)

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104
Q

what is the rule for metformin & radiographic tests

A

held 8 hrs before, 48 hrs after procedure

associated with acute kidney disease, lactic acid

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105
Q

CO =

A

amount of blood ejected from left ventricle (4-8L/min)

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106
Q

SVR

A

force (resistance) left ventricle overcome to eject volume of blood (Afterload)

measurement of force of blood against walls of blood vessels

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107
Q

normal BP & HR

A

100/60 - 139/89

60-100

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108
Q

stage 1 hypertension

A

130-139 or 80-89

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109
Q

stage 2 hypertension

A

140 or higher,

or

90 or higher

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110
Q

6 categories of hypertensives

A

adrenergic
angiotensin - converting enzymes (ACE) inhibitors
angiotensin receptor blockers (ARBs)
calcium channel blockers (CCBs)
vasodilators
diuretics

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111
Q

what do all the hypertensive drugs have

A

vasodilator effects (decreasing PVR & BP) except diuretics

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112
Q

SNS stimulation

A

increase HR, force of contractions, vasoconstriction, release of renin from kidney = hypertension

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113
Q

PSN stimulation

A

conserves energy as slows HR, increases intestinal & gland activity, relaxes sphincter muscles in GI

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114
Q

adrenergic drugs

A

agonists (CAUSES ACTION) modify finction of SNS

OR

antagonist blocks/prevents action in ANS

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115
Q

alpha 2 adrenergic is a

A

agonist (causes action) acts by modifying SNS; stimulates alpha 2 adrenergics receptors to decrease SNS activity = vasodilation

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116
Q

is alpha 2 adrenergic central acting

A

YES

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117
Q

lack of norepinephrine production w/ alpha 2 adrenergic results in

A

reduced BP & renin

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118
Q

examples of alpha 2 adrenergic

A

clonidine & methyldopa

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119
Q

renin is

A

potent vasoconstrictor

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120
Q

why is alpha 2 adrenergic not first line treatment

A

adverse effects (orthostatic hypotension, fatigue, dizziness)

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121
Q

important thing about alpha 2 adrenergic drugs

A

not to stop abruptly … severe rebound hypertension

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122
Q

rebound hypertension

A

sudden & dangerous rise in BP

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123
Q

alpha 1 blockers are a

A

antagonist (inhibits response)

124
Q

examples alpha 1 blockers

A

doxazosin, prazosin (minipress), terazosin

125
Q

action of alpha 1 blockers

A

modify function of SNS; block alpha 1 receptors to dilate arteries & veins

increase urine flow rates & decrease outflow obstruction

blocking of norepinephrine = dilation of arteries & veins

126
Q

When receptors block norepinephrine in alpha 1 blockers…

A

BP decreased by dilating arteries & veins (reduces peripheral vascular resistance & increased cardiac output, urine output increased by preventing smooth muslce contractions in neck & bladder

127
Q

beta blockers

A

antagonists (inhibits response) - periphery

128
Q

examples of beta blockers

A

metoprolol, propranolol, atenolol

129
Q

action of beta blocker

A

block beta receptors to reduce HR, slow conduction, & decrease contractility = decreased peripheral vascular resistance & reduces renin

130
Q

beta 1 receptors (ASK FOR CLARIFICATION)

A
131
Q

alpha & beta blockers

A

acts in periphery at blood vessels to reduce HR & cause vasodilation

132
Q

example of alpha & beta blocker

A

labetolol

133
Q

alpha & beta blockers primarily used in TX of

A

heart failure (can be used in HTN & angina)

shown to slow progression of heart failure & decrease hospitalizations

134
Q

can any category of adrenergic drugs be used alone or in combo with another hypertensive??

A

YES

135
Q

adverse effects of adrenergic drugs

A

bradycardia, orthostatic hypotension, dizziness, drowsiness, dry mouth, depression, edema, sexual dysfunction

136
Q

orthostatic hypotension

A

BP drop of > 20 systolic

OR

> 10 diastolic

within 3 mins of standing from lying or sitting

137
Q

first dose syncope with alpha 1 blockers (terazosin, prazosin, doxazosin)

A

sudden & severe fall in BP that can occur with changing from lying to standing position first time alpha blocker used or being resumed after months off

postural hypotension happen shortly after first dose absorbed into blood & result in fainting (syncope)

138
Q

renin-angiotensin-aldosterone system regulates

A

BP & fluid balance

139
Q

angiotensin I converted to

A

angiotensin II in lungs

140
Q

angiotensin II is

A

potent vasoconstrictor, stimulates secretion of hormone aldosterone from adrenal cortexa

141
Q

aldosterone causes tubules of kideneys to

A

increase reabsorption of Na, H2O & K+ into blood = increase volume of fluid, increasing BP

142
Q

angiotensin converting enzyme (ACE) inihibitor

A

inhibits conversion of angiotensin 1 to 2 causing VASODILATION & inhibits aldosterone (water & Na diuresis) –> decreases systemic vascular resistance = lowering BP

143
Q

ACE inhibitor helpful in pts with

A

hypertension & CHF

diabetic pt @ risk of renal disease = preserves kidney function but dilation

144
Q

examples of ACE inhibitors

A

captopril, perindopril, ramipril, enalapril

145
Q

angiotensin II receptor blockers

A

blocks binding of angiotensin II receptor sites - blocking vasoconstriction & secretion of aldosterone (interferes with aldosterone secretion & blocking angiotensin = blocking vasoconstriction)

146
Q

angiotensin II receptor block similar to

A

ACE inhibitors but w/o cough!!!!

147
Q

calcium channel blockers

A

interfere with influx of calcium ions into heart & vascular smooth muscles which lowers BP by reducing cardiac output & peripheral resistance

148
Q

CCB causing relaxation of smooth muscles causes….

A

relaxation of arteries causes dilation —> decreasing force (systemic vascular resistance) against what heart exert when delivering blood to body (afterload)

149
Q

examples of CCB

A

verapamil diltiazem decrease HR

150
Q

CCBs recommended for pts who

A

can’t tolerate diuretics & beta blockers, safe for diabetic, gout, COPD

151
Q

vasodilators

A

acts directly on arteriole (vascular) smooth musle to cause muscle relaxation, leading to vasodilation & drop in BP

act directly on vascular smooth muscle, NOT ON RECEPTORS

152
Q

EXAMPLES OF VASODILATORS

A

Nitroprusside has both venous & arterial effects WHEREAS hydralazine acts primarily through arteriolar vasodilation

153
Q

ACE inhibitor side effects

A

dizziness, headache, cough, hypotension, hyperkalemia

154
Q

why does ACE inhibitor cause hyperkalemia

A

inhibit aldosterone cause H2O & Na loss but K+ remains in blood

155
Q

normal K+ levels

A

3.5-5

156
Q

why is dry cough symptom of ACE inhib

A

accumulation of bradykinins in respiratory tract (reversible with stopping med)

157
Q

ARBs side effects

A

common upper resp infection, headache, dizziness, inability to sleep, dyspnea, back pain, hyperkalemia less common than ACE

158
Q

CCB side effects

A

STRONG MED

dizziness, lightheadedness, headache, hypotension, bradycardia

159
Q

vasodilator side effects

A

dizziness, headahce, tachycardia, HF

160
Q

diuretic action

A

Most diuretics help the kidneys remove salt and water through the urine. This lowers the amount of fluid flowing through the veins and arteries. As a result, blood pressure goes down

161
Q

nursing assessment

A

CAD risk –> ace inhib = dry cough, no cardioselective beta 2 blockers –> bronchial constriction –> worsening asthma

TAKE BP & HR PRIOR TO ADMIN (APICAL 1MIN)

POSTURAL HYPOTENSION

162
Q

WHEN WOULD YOU HOLD BETA BLOCKER

A

SYSTOLIC < 90

OR

HR = < 60

163
Q

interventions

A
  • educate about monitor BP & HR, adhering to med
  • changing positions slowly to avoid postural hypo
  • educate on foods containing potassium (at risk for high potassium)
164
Q

heart failure

A

inability to pump blood in sufficient amount from ventricles to meet metabolic needs (impaired ejection fraction)

165
Q

left HF

A

left ventricle not pumping blood efficiently

pulmonary edema, dyspnea, cough

166
Q

right HF

A

right ventricle not pumping blood efficiently

pedal edema, jugular venous distention, ascites, liver congestion

occurs because of L HF

167
Q

ejection fraction …

A

decreases, blood accumulates in R & L ventricles causing pressure to build up in vessels

pressure from L ventricle = pulmonary edema

R pressure in ventricle = venous congestion peripheral edema

168
Q

heart failure medication

A

ACE inhib
ARB
beta blockers
cardiac glycosides
diuretics
omega 3

169
Q

cardiac glycoside example

A

digoxin

170
Q

mechanism of cardiac glycoside

A

increases intracellular calcium levels = increases contractility & cardiac output (increases renal perfusion), suppression of SA - AV node conduction (decrease HR)

171
Q

digoxin toxicity

A

narrow therapeutic window = blood work done to determine levels

green/yellow halo, anorexia, bradycardia, confusion

172
Q

adverse effects digoxin

A

cardiac dysrhythmias (bradycardia, tachycardia), headache, confusion, visual disturbances, flickering lights, N & V

173
Q

loading dose

A

larger initial dose to achieve therapeutic effect faster

174
Q

nursing assessment for cardiac glycosides

A

apical 1 min (hold < 60 or > 120)

weight changes (1kg or more in 24hr or 2.3kg in week)

bloodwork

intake/output balances

175
Q

diuretics

A

accelerate rate of urine formation by removing water & sodium from body

176
Q

uses for diuretics

A

heart disease (HF, HTN) = edema, hypertension

renal disease

177
Q

GFR

A

rate at which blood flows into and out of the glomerulus & filtering occurs

used to gauge how well kidney functioning

178
Q

thiazide effective TX for

A

HF & HTN

179
Q

symptoms of hypokalemia

A

muscle cramps, irregular HR, muscle weakness

180
Q

major effects of thiazide stem from

A

electrolyte disturbances –> precipitating hypokalemia & metabolic changes (hyperlipidemia, hyperglycemia, hyperuricemia)

181
Q

common dysrhythmias

A

supraventricular, ventricular

182
Q

antidysrhythmics adverse effects

A

all can cause dysrhythmias

hypersensitivity reactions

N & V

dizziness

headache

prolongation of QT

183
Q

drug interactions with dysrhythmias

A

warfarin sodium

grapefruit juice

184
Q

why does grapefruit juice interact with dysrhythmics

A

interfere with metabolism which increases amount of drug in blood

185
Q

nursing assessment dysrhythmics

A

measure BP, apical, input/output, cardiac rhythm

measure serum potassium levels prior

186
Q

nursing elevation of dysrhythmics

A

monitor therapeutic response: decreased BP in HTN, decreased edema & fatigue, reg HR

187
Q

angina pectoris

A

supply of oxygen & nutrients in blood is insufficient to meet demands of heart (heart muscle “aches”)

188
Q

ischemia

A

poor blood supply to organ

189
Q

ischemic heart disease

A

poor blood supply to heart muscle

atherosclerosis

coronary artery disease

190
Q

MI

A

necrosis cardiac tissue

191
Q

hypoxia

A

low oxygen reaching tissue

192
Q

hypoxemia

A

low oxygen in blood

193
Q

drugs for angina

A

nitrates & nitrites

beta blockers

calcium channel blockers

194
Q

nitrates action

A

cause vasodilation because of relaxation of smooth muscle

potent dilating effect on coronary artery

195
Q

result of nitrates

A

oxygen to ischemic myocardial tissue

196
Q

nitrate types

A

nitroglycerin (rapid & long)

isosorbide dinitrate (rapid & long)

isosorbide mononitrate (long)

197
Q

side effects of nitroglycerin

A

headaches, reflex tachycardia, postural hypotension, tolerance

198
Q

reflex tachycardia

A

BP decreases, heart beats faster in attempt to raise it

can happen in response to decrease in blood volume

199
Q

nitrates contraindications

A

viagra = MASSIVE hypotension & paradoxical bradycardia & increase in angina

200
Q

nursing interventions for nitrates

A

BP HR prior; teaching that alcohol consumption & spending time in hot baths & hot tubs will result in vasodilation, hypotension, fainting

teach pt to change position slowly to avoid postural hypotension

teaching about patches

201
Q

antipsychotic uses

A

alleviate psychosis:

schizophrenia, delusional disorders, bipolar, depression etc

202
Q

mechanisms of antipsychotics

A

reduce acute symptoms

prevents exacerbation of symptoms

supports ongoing maintenance

short/long term

203
Q

positive symptoms of psychosis

A

hallucinations, delusions, thought disorders

204
Q

are all antipsychotics used to treat positive symptoms?

A

YES

205
Q

negative symptoms of psychosis

A

blunted/flat affect, emotional/social withdraw, impaired concentration/cognition

206
Q

do 2nd & 3rd generation antipsychotics treat both positive and negative symptoms

A

YES

207
Q

4 key dopamine neurotransmitter pathways

A
  • mesolimbic pathway
  • mesocortical pathway
  • nigrostriatal pathway
  • tuberoinfundibular pathway
208
Q

mesolimbic pathway

A

mediates positive symptoms

209
Q

mesocortical pathway

A

mediates negative (& some +) symptoms

210
Q

nigrostriatal pathway

A

regulates posture & voluntary movements

211
Q

tuberoinfundibular pathway

A

regulates prolactin

212
Q

how antipsychotics work

A

preventing actions (antagonist)

preventing dopamine from moving from 1 neuron to next

213
Q

what do antipsychotics do in brain

A

block the actions of neurotransmitters (antagonistic)

214
Q

how many classes of antipsychotics

A

3

215
Q

1st gen antipsychotic

A

typical/conventional

antagonist (treat + symptoms)

216
Q

1st gen antipsychotics cause what kind of side effects & why

A

EPS (td) becuase of dopamine block (increase s/s)

217
Q

dopamine receptor antagonist examples

A
  • loxapine
  • haloperidol (haldol)
  • flupenthixol (long acting)
  • trifluoperazine
  • methotrimeprazine (nozinan)
  • chlorpromazine (largectil)
218
Q

2nd gen antipsychotics

A

atypical/novel

created to produce less s/s

219
Q

serotonin-dopamine antagonists are which gen

A

2nd

220
Q

examples of serotonin-dopamine antagonists

A

clozapine (clozaril)
risperidone (risperdal)
olanzapine (zyprexa)
quetiapine (seroquel)

221
Q

3rd gen antipsychotic

A

partial dopamine antagonist

less eps, more anticholingeric

stimulate or blokc, depending on levels

222
Q

dopamine system stabilizer is what kind gen of antipsychotic

A

3rd gen

223
Q

examples of dopamine system stabilizer

A

aripiprzaole (abilify)
brexpiprazole (rexulti)
caiprazine (vraylar)

224
Q

acetylcholine

A

main neurotransmitter in parasympathetic nervous system (rest & digest)

bradycardia, hypersalivation, increased urination, N & V

225
Q

antipsychotic causes too much acetylcholine which

A

causes EPS

226
Q

antiparkinsonism treatment for EPS causes

A

anticholinergic symptoms (dry mouth, tachycardia)

227
Q

anticholinergic side effects

A

blurred vision
dry mouth
urinary retention
psychomotor agitation
tachycardia
dizziness
decreased BP

228
Q

extrapyramidal symptoms

A

dystonia
akinesia
akathisia
parkinsonism
tardive dyskinesia

229
Q

atypical antipsychotic side effects

A

metabolic syndrome, agranulocytosis, neuroleptic malignant syndrome

230
Q

metabolic syndrome

A

increase BP

high blood sugar (insulin resistance)

excessive fat around waist

high triglyceride, high LDL (bad cholesterol)

low levels of good cholesterol (HDL)

231
Q

most common medication that causes metabolic syndrome

A

olanzapine

232
Q

agranulocytosis

A

blood disorder characterized by decrease in WBC

symptoms susually develop in 1-6 mon

WBC done qweekly X 6 mons & then q2weeks then qmonthly

233
Q

symptoms of agranulocytosis

A

fever

sore throat

any sign of infection

fatigue

flu like symptoms

234
Q

neuroleptic malignant syndrome

A

medical emergency!!!!!

gen occurs 3-9 days after starting therapy

235
Q

symptoms of neuroleptic malignant syndrome (NMS)

A

high fever

increase HR

fluctuating BP

diaphoresis

change in LOC

tremors

muscle rigidity

236
Q

most common medication hthat causes agranulocytosis

A

clozapine

237
Q

nursing process for antipsychotics

A
  • medication adherence
  • VS
  • LOC
  • blood work: WBC, CK, lipids, triglycerides
  • clozapine related myocarditis
  • discourage smoking
  • weight management
238
Q

extrapyramidal symptoms include

A

dystonia
akathisia
akinesia
parkinsonism
rabbit syndrome
pisa syndrome
tardive dyskinesia

239
Q

acute dystonic reaction

A
  • severe involuntary muscle spasms
  • difficulty swallowing
  • stiff neck
  • thick tongue
  • extreme facial grimacing
240
Q

oculogyric crisis

A

dystonic movement characterized by upward deviation of eyeball

241
Q

akathisia

A
  • need for movement
  • restlessness/pacing
  • “my nerves are jumping”
  • nervous energy
242
Q

akinesia

A

immobility, weakness

complaints of fatigue

lack of muscle movement

243
Q

parkinsonism

A

resting tremor

shuffling gait

mask-like face

drooling

244
Q

tardive dyskinesia of face & head

A
  • backward-forward tongue circuling
  • chewing or sideways movements of jaw
  • facial grimacing
  • increased blinking
245
Q

tardive dyskinesia neck & trunk

A

difficulty swallowing

hip rocking

irregular twisting, turning of shoulders

246
Q

tardive dyskinesia limbs

A

irregular jerky movements

peculiar awkward gait

pill rolling

247
Q

abnormal involuntary movement scale (AIMS)

A

early detection of TD & ongoign assessment of TD

rating scale for 7 parts of body

248
Q

7 body parts in AIMS

A

face, lips, jaw, tongue, upper extremities, lower extremities, trunk

249
Q

rabbit syndrome

A

fast rhythmic movement of lips

250
Q

pisa syndrome

A

leaning to one side

251
Q

too much dopamine in brain causes symptoms

A

schizophrenia/psychosis

252
Q

1st gen antipsychotic meds block

A

dopamine thus reducing positive symptoms

253
Q

2ns gen blocks or partial blocks…

A

dopamine & serotonin receptor thus reducing positive & negatiev symptoms

254
Q

3rd gen partial blocks

A

dopamine ruding positive & negative symptoms

255
Q

what is main neurotransmitter responsible for EPS

A

imbalance between dopamine & acetylcholine

256
Q

anticholinergic antiparkinsonism agents

A

benztropine, procyclidine

dystonia, parkinsonism

257
Q

antihistamineric antiparkinsonian agents

A

diphenhydramine (benadryl)

dystonia

anticholinergic effects

258
Q

beta blocker antiparkinsonian agents

A

propanolol

akathesia

259
Q

benzodiazepine antiparkinsonian agent

A

clonazepam (rivotril), diazepam (valium), lorazepam (ativan)

akathesia, akinesia

260
Q
A
261
Q

example of loop diuretic

A

furosemide (lasix)

262
Q

pharmacodynamics of loop diuretics

A

inhibits transcription of na, k & cl in loop of henle = decreased fluid plasma volume & cardiac output (potent diuretic)

263
Q

side effects of loop diuretics

A

hypokalemia (increases urinary k+ loss), < na, ca (bone loss), dehydration, dizziness, urinary frequency

264
Q

nursing process loop diuretic

A

BP & HR prior

signs of dehydration

signs low K+

265
Q

what is loop diuretic used for

A

HTN HF

266
Q

thiazide diuretic example

A

hydrochlorothiazide (1st line TX HTN)

267
Q

pharmacodynamics thiazide diuretic

A

inhibits Na, K, Cl reabsorption in distal convoluted tubules = decreased fluid plasma volume & cardiac output

268
Q

side effects thiazide

A

hypokalemia (increases urinary K loss) < Na, dehydration, dizziness, urinary frequency, erectile

269
Q

nursing process thiazide

A

BP HR

signs of dehydration & low K

270
Q

potassium sparing diuretic example

A

spironolactone

271
Q

potassium sparing diuretic example

A

spironolactone

272
Q

potassium sparing pharmacodynamics

A

interferes w Na-K exchange in collecting ducts & distal convoluted tubules; blocks aldosterone receptors - blocks reabsorption of Na & H2O

273
Q

side effect K+ sparing

A

hyperkalemia (prevents K loss), dizziness, <Na, dehydration, urinary frequency

274
Q

dysrhymthics examples

A

propafenone, sotalol, flecainide (1st TX a fib)

275
Q

pharmacodynamics dysrhythmics

A

blocks sodium channels; little effect on adp or repolarizing

276
Q

side effects dysrhythmics

A

dizziness, visual disturbances, dyspnea

277
Q

dysrhythmics can be used

A

dysrhythmias, HF

278
Q

what drugs for HTN

A

adrenergic, ACE, ARB, CCB, vasodilators, loop diuretic, thiazide, potassium sparing

279
Q

what drug for HF

A

adrenergic, ACE, ARB, cardiac glycosides, loop, thiazide, potassium sparing, dysrhythmics, nitrates

280
Q

drugs for dysrhythmics

A

adrenergic, CCB, cardiac glycoside, dysrhythmics

281
Q

drug for angina

A

adrenergic, CCB, nitrates

282
Q

adrenergic examples

A

beta blockers: propranolol, atenolol, metprolol

clonidine

terazosin

283
Q

off label uses of clonidine

A

migraine, cramps, withdrawal

284
Q

pharmacodynamics adrenergic

A

modify SNS;

mimics norepinephrine & epi

reduced SNS stimulation = vasodilation

285
Q

side effects adrenergic

A

ortho hypo, 1st dose syncope, bradycardia, dizziness, drowsiness, sexual dysfunction

286
Q

nursing process adrenergic

A

BP APICAL

hold BP < 90 or HR < 60

287
Q

adrenergic uses

A

HTN HF angina dysrhythmia

288
Q

ACE example

A

“pril”

ramipril, captopril, enalapril

289
Q

ACE pharm dyna

A

interferes conversion angiotensin 1 to 2 causing vasodilation & inhibits aldosterone

290
Q

side effects ACE

A

hypo, dizziness, fatigue, dry cough

291
Q

ACE used for

A

HTN HF

292
Q

ARB example

A

“tan”

losartan, valsartan, candesartan

293
Q

ARB pharmdy

A

interferes angiotensin 2 causing vasodilation & inhibits aldosterone

294
Q

side effects ARB

A

hypo, dizziness, upper resp infection

295
Q

nursing process ARB

A

BP HR

given to pt who develop cough with ACE

296
Q

ARB used for

A

HTN HF

297
Q

CCB ex

A

verapamil, amlodipine, diltiazem

298
Q

CCB pharmdy

A

smooth muscle relax = slowing influx of calcium into heart & vascular smooth muscle = < conductivity, > vasodilation

299
Q

CCB side effects

A

hypo, bradycardia (suppression av-sv node conduction d/t calcium), light headedness

300
Q

uses CCB

A

HTN angina dysrhythmias

301
Q

vasodilators ex

A

hydralazine (nitroprusside = htn emergencies)

302
Q

pharmdy vasodilators

A

relaxation of arterial & venous smooth muscle = vasodilation

303
Q

side effects vasodilators

A

hypo, reflex tachy, dizziness

304
Q

vasodilators used for

A

hypertension

305
Q

cardiac glycosides ex

A

digoxin

306
Q

pharmdy digoxin

A

increases calcium levels in heart = increase contractility & output & renal perfusion, suppresses AV/SA node conduction = decrease HR

307
Q

side effects cardio glycosides

A

hypo, bradycardia, toxicity: yellow halo, anorexia, N&V, diarrhea

308
Q

nursing process cardiac glycosides

A

BP APICAL

< 60 or > 120 = toxicity

309
Q

cardiac glycoside used for

A

HF dysrhythmics

310
Q
A

pharm (4 decks)

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