midterm 1 Flashcards
1
Q
10 rights
A
right drug, dose, time, route, pt, reason, documentation, refusal, education, evaluation
2
Q
chemical name
A
describes drug chemicals composition & molecular structure
3
Q
generic name
A
name given to drug approved by health canada
acetaminophen, ibuprofen
4
Q
trade name
A
commercial name given to drug by manufacturer; trademark with marketability (tylenol, advil)
5
Q
pharmaceutics
A
how various dosage forms/routes influence way body metabolizes drug & way drug effects body
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)
7
Q
what phases does pharmacokinetics include
A
absorption, distribution, metabolism, excretion, onset of action, half life, peak effect, duration of action
8
Q
absorption
A
movement of drug from site of admin into bloodstream for distribution (PO, SC, IV)
9
Q
metabolism
A
biological transformation of drug (liver most responsible)
9
Q
distribution
A
transport of drug in bloodstream to site of action
9
Q
excretion
A
eleminiation of drug from body (kidney primary way drug is eliminated) (lesser extent bowel & liver)
10
Q
onset of action
A
time it takes for drug to elicit therapeutic response
11
Q
peak effect
A
time needed for drug to reach its MAX therapeutic response
12
Q
duration of action
A
length of time that concentration is sufficicent to elicit therapeutic response
13
Q
toxicity
A
when peak blood level is too high & drug is poisonous
14
Q
half life
A
time it takes for 1/2 of drug to be removed from body
15
Q
why does half life matter
A
steady state
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
17
Q
pharmacodynamics
A
what drug does to body (cellular level)
18
Q
therapeutic effect
A
desired or intended effect of particular medication
19
Q
adverse effect
A
undesirable effect that are direct response to one or more drugs
20
Q
toxicity
A
producing adverse bodily effects due to poisonous qualities
21
Q
contraindication
A
any characteristic of pt that makes use of medication dangerous
22
Q
receptors
A
molecular structure within or on surface of cells where specific substances bind
23
agonist
drug that binds to receptors & stimulate activity at receptor site (stimulates response)
24
antagonist
drug that binds nad inhibits activity at receptor site
25
diabetes mellitus
disorder of carbohydrate metabolism that involves either deficiency of insulin, resistance of tissue (muscle, liver) to insulin, or both
26
organ involved in diabetes
pancreas
27
pancreas & aspects
digestive enzymes & hormones
islets of langerhan (alpha & beta cells)
28
is pancreas an exocrine or endocrine gland
exocrine because it secretes
29
islets of langerhan exocrine or endocrine
endocrine, alpha & beta cells secrete insulin
30
insulin causes high blood glucose t/f
T
31
glucagon causes low blood glucose t/f
T
32
beta cells do
secrete insulin
33
beta cell process
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
34
alpha cells do
glucagon
35
alpha cell process
glucagon goes into liver, releases glycogen, BG low --> alpha cells release glucagon to release glycogen to increase BG
36
blood glucose levels normal & diabetic
normal = 4-6
diabetic = 4-7
37
hemoglobin A1c
shows how much insulin as sit on hemoglobin molecules & should be < 7% (less thn)
38
patho of DM
destruction of beta cells in pancreas (insulin deficiency, autoimmune)
defective insulin receptors in tissues (glucose unable to be transported into cells)
39
cardinal signs of hyperglycemia
polyuria, polydipsia, polyphagia, weight loss, blurred vision, fatigue
40
type 1
abrupt onset, common in kids, autoimmune destruction of beta cells causing little/no insulin, ketosis
41
type 1 need exogenous insulin t/f
T
42
type 2
slower onset, exercise & diet management, oral hypoglycemic agent effective in controlling blood sugar, obese, adapted to hyperglycemia over long period of time
43
treatments for type 2
education, nutrition, physical activity, weight & lifestyle management, insulin & oral hypoglycemics
44
insulin is only hormone that
has capacity to lower blood sugar
45
peak insulin is
most at risk for hypoglycemia (greatest amount of medication in system)
46
insulin types
rapid, short, intermediate, long
47
rapid acting onset
10-15min
48
rapid acting peak
60-90 mins
49
rapid acting duration
3.5-6 hr
50
rapid acting names of insulin
aspart (novorapid), lispro (humalog), glulisine (apidra)
51
rapid acting can be given SC but not IV
T
52
when can insulin be given
15min before meal
53
short acting onset
30 min
54
short acting peak
2-3hr
55
short acting duration
6.5hr
56
short acting insulin names
regular insulin (humulin regular, novolin, toronto)
57
short acting insulin is responding to
peak in blood glucose
58
short acting = what kind of infusion
IV bolus
59
intermediate acting onset
2-4hr
60
intermediate acting peak
4-10hr
61
intermediate acting duration
12-18hr
62
intermediate acting insulin names
isophane (humulin N, novolin NPH)
63
intermediate acting is basal insulin because
reacting to keep the BG at moderate level
64
goal of intermediate acting
steady state
65
long acting onset
2-4hr
66
long acting peak
none
67
long acting duration
20-24hr
68
long acting is basal because
provides a prolonged glucose control
69
long acting insulin names
glargine (lantus), determir (levemir)
70
which insulin is cloudy
intermediate
71
insulin preferred route of delivery
basal-bolus
72
unopened insulin vial kept in fridge, opened vial expires
30 days after opening
73
insulin side effects
hypoglycemia
weight gain
lipodystrophy
tachycardia, palpitations
headache, weakness, fatigue
74
hypoglycemia signs
dry mouth
blurred vision
anxious
perspiration
dizziness
diaphoretic
sleepiness
confusion
difficulty speaking
weak
75
treatment of hypoglycemia
see policy
assess LOC
diabetic protocol (glucose tablets 15g, glucagon SC)
76
if pt BG not < 4 but reports feeling lightheaded
give snack or juice
77
antagonist - insulin causes . . . & examples
hyperglycemia
epi, furosemide, niacin, thiazides, thyroid hormone, corticosteroids
78
protagonist - insulin causes . . . . & examples
hypoglycemia
alcohol, anabolic steroids, sulpha antibiotics
79
oral hypoglycemic agents (type 2) based on
premise that insulin still being produced
80
biguanide
metformin, 1st line treatment
81
action of biguanide
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
82
side effects of biguanide
abdominal bloating, anorexia, nausea, cramping, feeling full, flatulence, metallic taste, vit b12 reduction
83
biguanide does not...
stimulate insulin production = does not cause significant hypoglycemia
84
sulfonylureas is only used
in type 2
85
sulfonylureas must have
functioning beta cells because it stimulates insulin from beta cells
86
action of sulfonylureas
stimulates insulin secrete from beta cells
improves sensitivity to insulin in tissue
decreases production of glucagon
87
side effects of sulfonylureas
hypoglycemia, weight gain, gi symptoms, rashes
88
sulfonylureas may cause hypoglycemia t/f
T
89
thiazolidinediones is what type of drug
insulin-sensitizing drug
90
action of thiazolidinediones
regulates genes involved in glucose & lipid metabolism
decrease insulin resistance by enhancing sensitivity of insulin receptor
91
does thiazolidinediones cause hypoglycemia
NO
92
why thiazolidinediones controversial
cardiac risks
93
gliptins
pt that don't respond well to metformin & sulfonylureas
94
action of gliptins
delaying breakdown of incretin hormines --> results in increased insulin & lower glucagon secretion = hypoglycemia
95
glinides action
increase insulin secretion from pancreas with shorter duration of action & given with meal
96
glinides structurally different than sulfonylureas but similar mechanism of
action
97
a-glucosidase is a
inhibitor
98
example of a-glucosidase
acarbose (glucobay)
99
action of a-glucosidase
slows down digestion and absorption of glucose post meal
100
side effects of a-glucosidase
gi symptoms
101
does a-glucosidase cause hypoglycemia
NO
102
nursing assessment for diabetes
- assess knowledge & provide education
- type 1 or 2?
- BG levels
- medication effects on BG
- signs hypo/hyperglycemia
103
describe basal bolus
basal (steady state)
bolus (post meal)
104
what is the rule for metformin & radiographic tests
held 8 hrs before, 48 hrs after procedure
associated with acute kidney disease, lactic acid
105
CO =
amount of blood ejected from left ventricle (4-8L/min)
106
SVR
force (resistance) left ventricle overcome to eject volume of blood (Afterload)
measurement of force of blood against walls of blood vessels
107
normal BP & HR
100/60 - 139/89
60-100
108
stage 1 hypertension
130-139 or 80-89
109
stage 2 hypertension
140 or higher,
or
90 or higher
110
6 categories of hypertensives
adrenergic
angiotensin - converting enzymes (ACE) inhibitors
angiotensin receptor blockers (ARBs)
calcium channel blockers (CCBs)
vasodilators
diuretics
111
what do all the hypertensive drugs have
vasodilator effects (decreasing PVR & BP) except diuretics
112
SNS stimulation
increase HR, force of contractions, vasoconstriction, release of renin from kidney = hypertension
113
PSN stimulation
conserves energy as slows HR, increases intestinal & gland activity, relaxes sphincter muscles in GI
114
adrenergic drugs
agonists (CAUSES ACTION) modify finction of SNS
OR
antagonist blocks/prevents action in ANS
115
alpha 2 adrenergic is a
agonist (causes action) acts by modifying SNS; stimulates alpha 2 adrenergics receptors to decrease SNS activity = vasodilation
116
is alpha 2 adrenergic central acting
YES
117
lack of norepinephrine production w/ alpha 2 adrenergic results in
reduced BP & renin
118
examples of alpha 2 adrenergic
clonidine & methyldopa
119
renin is
potent vasoconstrictor
120
why is alpha 2 adrenergic not first line treatment
adverse effects (orthostatic hypotension, fatigue, dizziness)
121
important thing about alpha 2 adrenergic drugs
not to stop abruptly ... severe rebound hypertension
122
rebound hypertension
sudden & dangerous rise in BP
123
alpha 1 blockers are a
antagonist (inhibits response)
124
examples alpha 1 blockers
doxazosin, prazosin (minipress), terazosin
125
action of alpha 1 blockers
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
When receptors block norepinephrine in alpha 1 blockers...
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
beta blockers
antagonists (inhibits response) - periphery
128
examples of beta blockers
metoprolol, propranolol, atenolol
129
action of beta blocker
block beta receptors to reduce HR, slow conduction, & decrease contractility = decreased peripheral vascular resistance & reduces renin
130
beta 1 receptors (ASK FOR CLARIFICATION)
131
alpha & beta blockers
acts in periphery at blood vessels to reduce HR & cause vasodilation
132
example of alpha & beta blocker
labetolol
133
alpha & beta blockers primarily used in TX of
heart failure (can be used in HTN & angina)
shown to slow progression of heart failure & decrease hospitalizations
134
can any category of adrenergic drugs be used alone or in combo with another hypertensive??
YES
135
adverse effects of adrenergic drugs
bradycardia, orthostatic hypotension, dizziness, drowsiness, dry mouth, depression, edema, sexual dysfunction
136
orthostatic hypotension
BP drop of > 20 systolic
OR
> 10 diastolic
within 3 mins of standing from lying or sitting
137
first dose syncope with alpha 1 blockers (terazosin, prazosin, doxazosin)
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
renin-angiotensin-aldosterone system regulates
BP & fluid balance
139
angiotensin I converted to
angiotensin II in lungs
140
angiotensin II is
potent vasoconstrictor, stimulates secretion of hormone aldosterone from adrenal cortexa
141
aldosterone causes tubules of kideneys to
increase reabsorption of Na, H2O & K+ into blood = increase volume of fluid, increasing BP
142
angiotensin converting enzyme (ACE) inihibitor
inhibits conversion of angiotensin 1 to 2 causing VASODILATION & inhibits aldosterone (water & Na diuresis) --> decreases systemic vascular resistance = lowering BP
143
ACE inhibitor helpful in pts with
hypertension & CHF
diabetic pt @ risk of renal disease = preserves kidney function but dilation
144
examples of ACE inhibitors
captopril, perindopril, ramipril, enalapril
145
angiotensin II receptor blockers
blocks binding of angiotensin II receptor sites - blocking vasoconstriction & secretion of aldosterone (interferes with aldosterone secretion & blocking angiotensin = blocking vasoconstriction)
146
angiotensin II receptor block similar to
ACE inhibitors but w/o cough!!!!
147
calcium channel blockers
interfere with influx of calcium ions into heart & vascular smooth muscles which lowers BP by reducing cardiac output & peripheral resistance
148
CCB causing relaxation of smooth muscles causes....
relaxation of arteries causes dilation ---> decreasing force (systemic vascular resistance) against what heart exert when delivering blood to body (afterload)
149
examples of CCB
verapamil diltiazem decrease HR
150
CCBs recommended for pts who
can't tolerate diuretics & beta blockers, safe for diabetic, gout, COPD
151
vasodilators
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
EXAMPLES OF VASODILATORS
Nitroprusside has both venous & arterial effects WHEREAS hydralazine acts primarily through arteriolar vasodilation
153
ACE inhibitor side effects
dizziness, headache, cough, hypotension, hyperkalemia
154
why does ACE inhibitor cause hyperkalemia
inhibit aldosterone cause H2O & Na loss but K+ remains in blood
155
normal K+ levels
3.5-5
156
why is dry cough symptom of ACE inhib
accumulation of bradykinins in respiratory tract (reversible with stopping med)
157
ARBs side effects
common upper resp infection, headache, dizziness, inability to sleep, dyspnea, back pain, hyperkalemia less common than ACE
158
CCB side effects
STRONG MED
dizziness, lightheadedness, headache, hypotension, bradycardia
159
vasodilator side effects
dizziness, headahce, tachycardia, HF
160
diuretic action
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
nursing assessment
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
WHEN WOULD YOU HOLD BETA BLOCKER
SYSTOLIC < 90
OR
HR = < 60
163
interventions
- 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
heart failure
inability to pump blood in sufficient amount from ventricles to meet metabolic needs (impaired ejection fraction)
165
left HF
left ventricle not pumping blood efficiently
pulmonary edema, dyspnea, cough
166
right HF
right ventricle not pumping blood efficiently
pedal edema, jugular venous distention, ascites, liver congestion
occurs because of L HF
167
ejection fraction ...
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
heart failure medication
ACE inhib
ARB
beta blockers
cardiac glycosides
diuretics
omega 3
169
cardiac glycoside example
digoxin
170
mechanism of cardiac glycoside
increases intracellular calcium levels = increases contractility & cardiac output (increases renal perfusion), suppression of SA - AV node conduction (decrease HR)
171
digoxin toxicity
narrow therapeutic window = blood work done to determine levels
green/yellow halo, anorexia, bradycardia, confusion
172
adverse effects digoxin
cardiac dysrhythmias (bradycardia, tachycardia), headache, confusion, visual disturbances, flickering lights, N & V
173
loading dose
larger initial dose to achieve therapeutic effect faster
174
nursing assessment for cardiac glycosides
apical 1 min (hold < 60 or > 120)
weight changes (1kg or more in 24hr or 2.3kg in week)
bloodwork
intake/output balances
175
diuretics
accelerate rate of urine formation by removing water & sodium from body
176
uses for diuretics
heart disease (HF, HTN) = edema, hypertension
renal disease
177
GFR
rate at which blood flows into and out of the glomerulus & filtering occurs
used to gauge how well kidney functioning
178
thiazide effective TX for
HF & HTN
179
symptoms of hypokalemia
muscle cramps, irregular HR, muscle weakness
180
major effects of thiazide stem from
electrolyte disturbances --> precipitating hypokalemia & metabolic changes (hyperlipidemia, hyperglycemia, hyperuricemia)
181
common dysrhythmias
supraventricular, ventricular
182
antidysrhythmics adverse effects
all can cause dysrhythmias
hypersensitivity reactions
N & V
dizziness
headache
prolongation of QT
183
drug interactions with dysrhythmias
warfarin sodium
grapefruit juice
184
why does grapefruit juice interact with dysrhythmics
interfere with metabolism which increases amount of drug in blood
185
nursing assessment dysrhythmics
measure BP, apical, input/output, cardiac rhythm
measure serum potassium levels prior
186
nursing elevation of dysrhythmics
monitor therapeutic response: decreased BP in HTN, decreased edema & fatigue, reg HR
187
angina pectoris
supply of oxygen & nutrients in blood is insufficient to meet demands of heart (heart muscle "aches")
188
ischemia
poor blood supply to organ
189
ischemic heart disease
poor blood supply to heart muscle
atherosclerosis
coronary artery disease
190
MI
necrosis cardiac tissue
191
hypoxia
low oxygen reaching tissue
192
hypoxemia
low oxygen in blood
193
drugs for angina
nitrates & nitrites
beta blockers
calcium channel blockers
194
nitrates action
cause vasodilation because of relaxation of smooth muscle
potent dilating effect on coronary artery
195
result of nitrates
oxygen to ischemic myocardial tissue
196
nitrate types
nitroglycerin (rapid & long)
isosorbide dinitrate (rapid & long)
isosorbide mononitrate (long)
197
side effects of nitroglycerin
headaches, reflex tachycardia, postural hypotension, tolerance
198
reflex tachycardia
BP decreases, heart beats faster in attempt to raise it
can happen in response to decrease in blood volume
199
nitrates contraindications
viagra = MASSIVE hypotension & paradoxical bradycardia & increase in angina
200
nursing interventions for nitrates
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
antipsychotic uses
alleviate psychosis:
schizophrenia, delusional disorders, bipolar, depression etc
202
mechanisms of antipsychotics
reduce acute symptoms
prevents exacerbation of symptoms
supports ongoing maintenance
short/long term
203
positive symptoms of psychosis
hallucinations, delusions, thought disorders
204
are all antipsychotics used to treat positive symptoms?
YES
205
negative symptoms of psychosis
blunted/flat affect, emotional/social withdraw, impaired concentration/cognition
206
do 2nd & 3rd generation antipsychotics treat both positive and negative symptoms
YES
207
4 key dopamine neurotransmitter pathways
- mesolimbic pathway
- mesocortical pathway
- nigrostriatal pathway
- tuberoinfundibular pathway
208
mesolimbic pathway
mediates positive symptoms
209
mesocortical pathway
mediates negative (& some +) symptoms
210
nigrostriatal pathway
regulates posture & voluntary movements
211
tuberoinfundibular pathway
regulates prolactin
212
how antipsychotics work
preventing actions (antagonist)
preventing dopamine from moving from 1 neuron to next
213
what do antipsychotics do in brain
block the actions of neurotransmitters (antagonistic)
214
how many classes of antipsychotics
3
215
1st gen antipsychotic
typical/conventional
antagonist (treat + symptoms)
216
1st gen antipsychotics cause what kind of side effects & why
EPS (td) becuase of dopamine block (increase s/s)
217
dopamine receptor antagonist examples
- loxapine
- haloperidol (haldol)
- flupenthixol (long acting)
- trifluoperazine
- methotrimeprazine (nozinan)
- chlorpromazine (largectil)
218
2nd gen antipsychotics
atypical/novel
created to produce less s/s
219
serotonin-dopamine antagonists are which gen
2nd
220
examples of serotonin-dopamine antagonists
clozapine (clozaril)
risperidone (risperdal)
olanzapine (zyprexa)
quetiapine (seroquel)
221
3rd gen antipsychotic
partial dopamine antagonist
less eps, more anticholingeric
stimulate or blokc, depending on levels
222
dopamine system stabilizer is what kind gen of antipsychotic
3rd gen
223
examples of dopamine system stabilizer
aripiprzaole (abilify)
brexpiprazole (rexulti)
caiprazine (vraylar)
224
acetylcholine
main neurotransmitter in parasympathetic nervous system (rest & digest)
bradycardia, hypersalivation, increased urination, N & V
225
antipsychotic causes too much acetylcholine which
causes EPS
226
antiparkinsonism treatment for EPS causes
anticholinergic symptoms (dry mouth, tachycardia)
227
anticholinergic side effects
blurred vision
dry mouth
urinary retention
psychomotor agitation
tachycardia
dizziness
decreased BP
228
extrapyramidal symptoms
dystonia
akinesia
akathisia
parkinsonism
tardive dyskinesia
229
atypical antipsychotic side effects
metabolic syndrome, agranulocytosis, neuroleptic malignant syndrome
230
metabolic syndrome
increase BP
high blood sugar (insulin resistance)
excessive fat around waist
high triglyceride, high LDL (bad cholesterol)
low levels of good cholesterol (HDL)
231
most common medication that causes metabolic syndrome
olanzapine
232
agranulocytosis
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
symptoms of agranulocytosis
fever
sore throat
any sign of infection
fatigue
flu like symptoms
234
neuroleptic malignant syndrome
medical emergency!!!!!
gen occurs 3-9 days after starting therapy
235
symptoms of neuroleptic malignant syndrome (NMS)
high fever
increase HR
fluctuating BP
diaphoresis
change in LOC
tremors
muscle rigidity
236
most common medication hthat causes agranulocytosis
clozapine
237
nursing process for antipsychotics
- medication adherence
- VS
- LOC
- blood work: WBC, CK, lipids, triglycerides
- clozapine related myocarditis
- discourage smoking
- weight management
238
extrapyramidal symptoms include
dystonia
akathisia
akinesia
parkinsonism
rabbit syndrome
pisa syndrome
tardive dyskinesia
239
acute dystonic reaction
- severe involuntary muscle spasms
- difficulty swallowing
- stiff neck
- thick tongue
- extreme facial grimacing
240
oculogyric crisis
dystonic movement characterized by upward deviation of eyeball
241
akathisia
- need for movement
- restlessness/pacing
- "my nerves are jumping"
- nervous energy
242
akinesia
immobility, weakness
complaints of fatigue
lack of muscle movement
243
parkinsonism
resting tremor
shuffling gait
mask-like face
drooling
244
tardive dyskinesia of face & head
- backward-forward tongue circuling
- chewing or sideways movements of jaw
- facial grimacing
- increased blinking
245
tardive dyskinesia neck & trunk
difficulty swallowing
hip rocking
irregular twisting, turning of shoulders
246
tardive dyskinesia limbs
irregular jerky movements
peculiar awkward gait
pill rolling
247
abnormal involuntary movement scale (AIMS)
early detection of TD & ongoign assessment of TD
rating scale for 7 parts of body
248
7 body parts in AIMS
face, lips, jaw, tongue, upper extremities, lower extremities, trunk
249
rabbit syndrome
fast rhythmic movement of lips
250
pisa syndrome
leaning to one side
251
too much dopamine in brain causes symptoms
schizophrenia/psychosis
252
1st gen antipsychotic meds block
dopamine thus reducing positive symptoms
253
2ns gen blocks or partial blocks...
dopamine & serotonin receptor thus reducing positive & negatiev symptoms
254
3rd gen partial blocks
dopamine ruding positive & negative symptoms
255
what is main neurotransmitter responsible for EPS
imbalance between dopamine & acetylcholine
256
anticholinergic antiparkinsonism agents
benztropine, procyclidine
dystonia, parkinsonism
257
antihistamineric antiparkinsonian agents
diphenhydramine (benadryl)
dystonia
anticholinergic effects
258
beta blocker antiparkinsonian agents
propanolol
akathesia
259
benzodiazepine antiparkinsonian agent
clonazepam (rivotril), diazepam (valium), lorazepam (ativan)
akathesia, akinesia
260
261
example of loop diuretic
furosemide (lasix)
262
pharmacodynamics of loop diuretics
inhibits transcription of na, k & cl in loop of henle = decreased fluid plasma volume & cardiac output (potent diuretic)
263
side effects of loop diuretics
hypokalemia (increases urinary k+ loss), < na, ca (bone loss), dehydration, dizziness, urinary frequency
264
nursing process loop diuretic
BP & HR prior
signs of dehydration
signs low K+
265
what is loop diuretic used for
HTN HF
266
thiazide diuretic example
hydrochlorothiazide (1st line TX HTN)
267
pharmacodynamics thiazide diuretic
inhibits Na, K, Cl reabsorption in distal convoluted tubules = decreased fluid plasma volume & cardiac output
268
side effects thiazide
hypokalemia (increases urinary K loss) < Na, dehydration, dizziness, urinary frequency, erectile
269
nursing process thiazide
BP HR
signs of dehydration & low K
270
potassium sparing diuretic example
spironolactone
271
potassium sparing diuretic example
spironolactone
272
potassium sparing pharmacodynamics
interferes w Na-K exchange in collecting ducts & distal convoluted tubules; blocks aldosterone receptors - blocks reabsorption of Na & H2O
273
side effect K+ sparing
hyperkalemia (prevents K loss), dizziness,
274
dysrhymthics examples
propafenone, sotalol, flecainide (1st TX a fib)
275
pharmacodynamics dysrhythmics
blocks sodium channels; little effect on adp or repolarizing
276
side effects dysrhythmics
dizziness, visual disturbances, dyspnea
277
dysrhythmics can be used
dysrhythmias, HF
278
what drugs for HTN
adrenergic, ACE, ARB, CCB, vasodilators, loop diuretic, thiazide, potassium sparing
279
what drug for HF
adrenergic, ACE, ARB, cardiac glycosides, loop, thiazide, potassium sparing, dysrhythmics, nitrates
280
drugs for dysrhythmics
adrenergic, CCB, cardiac glycoside, dysrhythmics
281
drug for angina
adrenergic, CCB, nitrates
282
adrenergic examples
beta blockers: propranolol, atenolol, metprolol
clonidine
terazosin
283
off label uses of clonidine
migraine, cramps, withdrawal
284
pharmacodynamics adrenergic
modify SNS;
mimics norepinephrine & epi
reduced SNS stimulation = vasodilation
285
side effects adrenergic
ortho hypo, 1st dose syncope, bradycardia, dizziness, drowsiness, sexual dysfunction
286
nursing process adrenergic
BP APICAL
hold BP < 90 or HR < 60
287
adrenergic uses
HTN HF angina dysrhythmia
288
ACE example
“pril”
ramipril, captopril, enalapril
289
ACE pharm dyna
interferes conversion angiotensin 1 to 2 causing vasodilation & inhibits aldosterone
290
side effects ACE
hypo, dizziness, fatigue, dry cough
291
ACE used for
HTN HF
292
ARB example
“tan”
losartan, valsartan, candesartan
293
ARB pharmdy
interferes angiotensin 2 causing vasodilation & inhibits aldosterone
294
side effects ARB
hypo, dizziness, upper resp infection
295
nursing process ARB
BP HR
given to pt who develop cough with ACE
296
ARB used for
HTN HF
297
CCB ex
verapamil, amlodipine, diltiazem
298
CCB pharmdy
smooth muscle relax = slowing influx of calcium into heart & vascular smooth muscle = < conductivity, > vasodilation
299
CCB side effects
hypo, bradycardia (suppression av-sv node conduction d/t calcium), light headedness
300
uses CCB
HTN angina dysrhythmias
301
vasodilators ex
hydralazine (nitroprusside = htn emergencies)
302
pharmdy vasodilators
relaxation of arterial & venous smooth muscle = vasodilation
303
side effects vasodilators
hypo, reflex tachy, dizziness
304
vasodilators used for
hypertension
305
cardiac glycosides ex
digoxin
306
pharmdy digoxin
increases calcium levels in heart = increase contractility & output & renal perfusion, suppresses AV/SA node conduction = decrease HR
307
side effects cardio glycosides
hypo, bradycardia, toxicity: yellow halo, anorexia, N&V, diarrhea
308
nursing process cardiac glycosides
BP APICAL
< 60 or > 120 = toxicity
309
cardiac glycoside used for
HF dysrhythmics
310
