Hypertension PPT Flashcards
1
Q
What are the types of hypertension called?
A
primary and secondary
2
Q
what is the difference between primary and secondary hypertension?
A
primary has no known cause while secondary is caused by something
3
Q
list the causes of secondary hypertension we discussed in class
(hint: 4)
A
OSA (overweight)
Renal impairment
Diet
Certain medications
4
Q
hypertension causes ________ ______
A
endothelial injury
5
Q
endothelial injury leads to what?
(hint: 2 things)
A
impaired synthesis
impaired release of nitric oxide
6
Q
hypertension promotes ________ _______
A
inflammatory mediators
7
Q
hypertension accelerates the development of what?
A
atherosclerosis
8
Q
hypertension is known as the “_______ _____ ______”
A
“silent killer disease”
9
Q
hypertension is ________ if it is not treated
A
progressive
10
Q
Hypertension causes increased cardiac _______ and ventricular __________
A
afterload;
hypertrophy
11
Q
if hypertension is left untreated it can lead to end-organ damage affecting which organs?
(hint: 5)
A
heart
brain
kidneys
arteries
eyes
12
Q
the cycle of death plays a role in both _________ and ____ ______
A
hypertension and heart failure
13
Q
error card
A
14
Q
sympathetic stimulation causes the adrenal medulla to secrete what into the blood?
A
both norepinephrine and epinephrine
15
Q
norepinephrine is a strong ____________ hormone
A
vasoconstrictor
16
Q
what does stimulation of the SNS during stress or exercise cause? why?
A
local constriction or veins and arterioles because of the release of norepinephrine from sympathetic nerve endings.
17
Q
Angiotensin II is a very strong ____________ from _____
A
vasoconstrictor; RAAS
18
Q
angiotensin II will increase _______ _____ _____ and therefore the ____ _____
A
peripheral vascular disease;
blood pressure
19
Q
histamine has a _________ effect on arterioles. this is a part of the _________ response
A
vasodilator;
inflammatory
20
Q
serotonin is released by ________ during ________ response
A
platelets;
inflammatory
21
Q
what does the release of serotonin cause?
A
causes vasoconstriction and can cause vascular spasm
22
Q
bradykinin causes intense ________ of arterioles, increased _______ ___________ and _________ of venules.
A
dilation;
capillary permeability;
constriction
23
Q
Kinins play special roles in regulating ____ _____ and _______ _______ in inflamed tissues.
A
blood flow;
capillary leakage
24
Q
where do kinins help regulate blood flow?
(hint: 3 places)
A
skin
salivary tract
GI tract
25
prostaglandins are made from ________ ____
arachidonic acid
26
when there is a tissue injury, there is release of ________ ____ from the cell membrane which initiates __________ synthesis
arachidonic acid;
prostaglandins
27
some prostaglandins cause __________ and others __________
vasoconstriction;
vasodilation
28
where does bradykinin come from?
globulin (kininogen) present in body fluids.
29
how do corticosteroids produce anti-inflammatory response?
by blocking release of arachidonic acid and preventing prostaglandin synthesis
30
when you ave HTN it is not only about the heart, but also what?
blood vessels
kidneys
vascular resistance
31
increased resistance = increased ?
blood pressure
32
what does first line treatment for hypertension begin with?
(hint: 3)
Non-pharmacologic interventions:
- diet
- exercise
- life-style management
33
what should patient education on lifestyle management include?
good sleep
smoking cessation
alcohol consumption
34
how can sleep impact BP?
too little or too much increases the inflammatory response which increases the BP
35
what are first line medications for hypertension?
(hint: 3)
Angiotensin-Converting Enzyme (ACE) Inhibitors
Angiotensin II Receptor Blockers (ARBS)
Thiazide Diuretics
36
are beta blockers first line treatment for hypertension?
no
37
what should be done if blood pressure goal is not met after the use of first-line medications?
(hint: 3 things)
can increase dose
add a second or third drug
Change to a different drug
38
what type of diuretic is used for HF vs HTN?
loop diuretic for HF and thiazide diuretic for HTN
39
pharmacologic management for hypertension works to alter what?
the body regulator mechanisms
40
is pharmacologic management for HTN a cure?
no, it is a bandaid
41
what must be taken into account when choosing a medication for hypertension?
the co-morbidities
42
why might pharmacologic management for hypertension require more than one medication?
(hint: 3)
To avoid maxing out the dose
Minimize avoid side effects
Synergistic effect
43
medications for hypertension help with _______ management
symptom
44
what do medications for hypertension help to decrease?
helps to decrease BP and peripheral vascular resistance which will help decrease the pressure on the heart
45
what are the 4 ACE inhibitors we discussed in class?
Lisinopril
Enalapril
Ramipril
Captopril
46
what are the 3 ARB (Angiotensin II Receptor Blockers) we discussed in class?
Losartan
Irbesartan
Valsartan
47
what are the 2 thiazide diuretics we discussed in class?
Hydrochlorothiazide (HCTZ)
Chlorthalidone
48
what are the 4 beta blockers we discussed in class?
Metoprolol
Atenolol
Bisoprolol
Labetalol
49
what are the 4 calcium channel blockers we discussed in class?
Amlodipine
Felodipine
Diltiazem
Verapamil
50
what type of medication is rarely used for HTN but can be?
renin inhibitors
51
what renin inhibitor did we discuss in class?
Aliskiren (Tekturna)
52
what do thiazide diuretics inhibit?
inhibit reabsorption of sodium and chloride from the distal tubules in the kidneys
53
what do thiazide diuretics decrease?
(hint: 2)
decrease peripheral resistance
decrease preload
54
who are thiazide diuretic better for?
Better for sodium sensitive HTN as in African Americans and older adults
55
how is urination impacted in a pt with renal impairment?
they will not urinate as much as someone with normal renal function
56
thiazide diuretics are generally ___ ______
well tolerated
57
list the adverse effects of thiazide diuretics
(hint: 5)
Hypokalemia
Hyperglycemia
Can cause exacerbation of gout
Other electrolyte imbalances (i.e. Calcium)
Orthostasis
58
who should thiazide diuretics not be given to?
anyone with renal impairment
pts with a hx of gout
59
how can thiazide diuretics cause an exacerbation of gout?
it increases uric acid
60
why should you keep a close eye on diabetic pts who are on thiazide diuretics for hypertension?
thiazide diuretics can increase hyperglycemia
61
who are thiazide diuretics contraindicated in?
those allergic to sulfa drugs
avoid in renal failure
62
thiazide diuretics can increase the risk of ______ and ______ toxicity
digoxin;
lithium
63
Thiazide diuretics can cause decreased effect of ______ ______ medications
diabetes mellitus
64
lithium is a ______ medication
psych
65
what labs should be assessed in pts taking thiazide diuretics?
(hint: 2)
potassium
glucose
66
what vitals should be checked in pts taking thiazide diuretics?
BP
HR
67
what time of day should thiazide diuretics not be given and why?
do not want to give at night bc it encourages urination (they will be up all night)
68
what should be included in pt education for someone taking thiazide diuretic for hypertension?
(hint: 5)
minimize alcohol intake
stop smoking
AVOID NSAIDS
diet change
exercise
69
indications for Angiotensin-converting enzyme (ACE) Inhibitors?
(hint: 5)
Hypertension
Heart failure
Diabetes
Post myocardial infarction
Post percutaneous coronary intervention
70
ACE inhibitors are typically ____ agents
oral
71
which ACE inhibitor can be given both orally and IV?
enalapril
72
what do Angiotensin-converting enzyme (ACE) Inhibitors decrease?
decreases aldosterone production
decreases vasoconstriction
decreases preload
decreases afterload
73
what do Angiotensin-converting enzyme (ACE) Inhibitors inhibit?
angiotensin II production
74
Angiotensin-converting enzyme (ACE) Inhibitors interfere with what?
RAAS
75
Angiotensin-converting enzyme (ACE) Inhibitors keep the ________ effects of bradykinin
vasodilation
76
what do the names of Angiotensin-converting enzyme (ACE) Inhibitors end with?
"pril"
77
Step 1 of RAAS activation:
what causes the kidneys to activate the RAAS?
(hint: 3)
SNS stimulation
Hypotension
Decreased sodium delivery
78
Step 2 of RAAS activation:
the kidneys release _____
renin
79
Step 3 of RAAS activation:
renin converts __________ to __________
angiotensinogen to angiotensin I
80
Step 4 of RAAS activation:
__________ is converted to __________
angiotensin I is converted to angiotensin II
81
Step 5 of RAAS activation:
Angiotensin II triggers the _____ _____ to release ______ and the ______ to release ______
adrenal cortex to release aldosterone
pituitary to release ADH
82
Step 6 of RAAS activation:
The release of aldosterone and ADH causes what?
renal sodium & fluid retention
83
Step 7 of RAAS activation:
renal sodium and fluid retention causes what?
increased blood volume
84
Angiotensin II causes cardiac & vascular _________ as well as systemic ___________
hypertrophy;
vasoconstriction
85
the release of angiotensin II causes thirst which can contribute to increased _____ _____
blood volume
86
list the adverse effects of ACE inhibitors
(hint: 5)
hyperkalemia
dizziness
cough
angioedema
hypotension
87
ACE inhibitors are generally well what?
well tolerated and absorbed
88
what is a very common side effect of ACE inhibitors?
cough
89
The cough from ACE inhibitors is related to ______, the activation of _________ pathway, and _________ production
kinins;
arachidonic;
prostaglandin
90
when does ACE cough typically begin?
within one to two weeks of initiation
91
when does ACE cough typically resolve?
within a few days of stopping medication
92
There is an increased incidence in the ACE cough in _______ ethnicity
chinese
93
Why does angioedema occur from ACE inhibitors?
because of elevated bradykinin causing vasodilation
94
when angioedema occurs, what is responsible for inactivating bradykinin?
Angiotensin II
95
What is the black box warning for ACE inhibitors?
They cause serious fetal abnormalities so not to given in pregnancy and given cautiously in childbearing women
96
because of the black box warning of ACE inhibitors, _________ is very important
contraception
97
How does angioedema present?
swelling of the face, hands and lips
98
Why is it especially important not to give ACE inhibitors during the third trimester of pregnancy?
they can dry up amniotic fluid
99
What must the nurse be aware of in pts who take ACE inhibitors?
renal function and potassium
100
What labs should be checked on a pt taking ACE inhibitors?
potassium
BUN
creatinine
101
what should the nurse be aware of when administering ACE inhibitors?
(hint: 3)
administration to childbearing women
when to give the med
when to hold the med
102
what drugs should not be taken with ACE inhibitors?
NSAIDs
103
how should ACE inhibitors be taken?
on an empty stomach
104
what vital sign should be closely monitored for a pt taking ACE inhibitors?
blood pressure
105
What should be included in pt education for someone taking ACE inhibitors?
report swelling of the lips, face, or difficulty breathing (sx of angioedema)
106
What are the indications for Angiotensin II Receptor Blockers (ARBS)?
(hint: 2)
Hypertension
when an ACEI can not be used
107
ARBS bind with __________ receptors in ______ _____ _____ and ______ ______ to stop __________ and __________ __________
angiotensin II;
vascular smooth muscle;
adrenal cortex;
vasoconstriction;
aldosterone production
108
ARBS block angiotensin II from binding at receptor sites where?
(hint: 5)
Brain
Kidneys
Heart
Periphery
Adrenal tissue
109
We know that ARBS are given when the pt cannot tolerate ACE inhibitors. How do they differ from ACEI?
They provide the same amount of protection without leading to ACE cough
110
True or False: ACE & ARB can be given together.
FALSE they should NOT be given together
111
What do the names of ARB drugs end in?
"sartan"
112
List the adverse effects of ARBS
(hint: 8)
Cough
Hyperkalemia
Headaches
Dizziness
Syncope
GI complaints
Xerostomia (Dry mouth)
Alopecia
113
Cough and hyperkalemia are adverse effects of both ACEI and ARBS. What is important to note here?
Cough and hyperkalemia occur LESS in ARBS as opposed to ACEI
114
what two adverse effects of ARBS that we previously mentioned are not common?
Xerostomia and alopecia
115
Why is there an increase in creatinine when taking ARBS?
due to possible decreased glomerular filtration rate
116
list the drug-drug interactions with ARBS
(hint: 3)
ACE inhibitors
Diltiazem
Oral anti-fungals
117
ARBS should be avoided during _______
pregnancy
118
what labs should be checked for a pt taking ARBS?
(hint: 2)
BUN
Creatinine
119
There are some drug interactions with ARBS related to what?
what happens?
cytochrome P450
Patient may be inducer or inhibitor, so may have to adjust dose
120
what should the nurse monitor when a pt is taking ARBS?
(hint: 2)
renal function
blood pressure
121
how can ARBS be given?
with or without foods
122
list the indications for calcium channel blockers
(hint: 6)
Hypertension
Angina
Rate Control in A fib
Supraventricular Tachycardia (SVT)
Raynaud Syndrome
Migraines
123
what calcium channel blocker is given for migraines?
verapamil
124
what are the two types of calcium channel blockers?
Dihydropyridine
Non-Dihydropyridine
125
what do calcium channel blockers decrease/slow?
(hint: 4)
decrease cardiac workload
decrease myocardial O2 consumption
decrease contractility
slows AV conduction
126
what do calcium channel blockers inhibit?
Inhibits the movement of calcium across the membranes of the myocardial/arterial muscle cells
127
what do calcium channel blockers alter and block?
Alter action potential and block muscle cell contractions
128
what effect do calcium channel blockers have on arteries?
they relax and dilate arteries
129
What happens when calcium channel blockers cause vasodilation to coronary and peripheral arteries?
this leads to a decrease in BP which leads to more blood getting into the heart
130
how do calcium channel blockers decrease myocardial O2 consumption?
myocardial O2 consumption is increased when the workload is increased because it needs more O2 to keep up with the demand
since calcium channel blockers decrease the workload, there is less demand for O2
131
what do the name of Dihydropyridine CCBs end in?
"pine"
132
Dihydropyridine CCBs are more _______ ________
vascular selective
133
Dihydropyridine CCBs have more of a direct effect on __________ and less ________ of _____
vasodilation;
reduction of calcium
134
what do Dihydropyridine CCBs have no effect on?
AV contraction
kidneys
135
why might Dihydropyridine CCBs increase HR?
due to vasodilation
136
list the three Dihydropyridine CCBs we discussed in class
(hint: 3)
Amlodipine
Felodipine
Nifedipine
137
list the side effects of Dihydropyridine CCBs
(hint: 7)
Peripheral/pedal edema
Headache
Flushing
Lightheadedness
dizziness
increased HR
GI side effects
138
what is the common symptom of Dihydropyridine CCBs?
peripheral edema
139
What should you definitely keep an eye on when a pt is taking Dihydropyridine CCBs and why?
blood pressure because they decrease it
140
For people taking CCBs, what drink can they NOT have and why? which CCB is this especially important in?
grapefruit juice bc it increases risk for hypotension and other side effects
especially important when taking Non-Dihydropyridine diltiazem
141
what are the indications for Non-Dihydropyridine CCBs?
(hint: 3)
Hypertension
Angina
Arrhythmias (i.e. A fib or SVT)
142
Non-Dihydropyridine CCBs have a ______ inotropic effect. what does this mean?
negative
it means they decrease the force of contraction
143
what do Non-Dihydropyridine CCBs slow?
slows AV conduction
slows the rate of the SA node
144
Calcium channel blockers affect the calcium channels of ______ _____ ______
vascular smooth muscle
145
what are the two Non-Dihydropyridine CCBs we discussed in class? how can they both be given?
verapamil
diltiazem
both can be given IV
146
list the adverse effects of Non-Dihydropyridine CCBs
(hint: 3)
Bradycardia
Decreased cardiac output
GI side effects (constipation)
147
Non-Dihydropyridine CCBs should not be used in those with what?
heart block
148
With calcium channel blockers, you need to monitor blood pressure as well as _____ _____. why?
heart rate
bc some people can really brady down (into HR of 30)
149
which adverse effect of Non-Dihydropyridine CCBs is not too much of an issue?
GI side effects
150
when administering calcium channel blockers, the nurse must be aware of ________ issues
conduction
151
all calcium channel blockers should be avoided in those with what?
heart failure
152
what should ALWAYS be checked on a pt taking a calcium channel blocker? When would the doctor need to be called?
apical HR;
call doctor if <60 bpm
153
What 5 types of medications should the nurse be checking for orthostasis?
ACE inhibitors
Thiazide diuretics
Calcium channel blockers
Beta blockers
Alpha blockers
154
what three types of drugs MUST the nurse check apical HR?
Calcium channel blockers
Beta blockers
Digoxin
155
what lab monitoring is done when a pt is on calcium channel blockers?
there is no lab monitoring for CCBs
156
what does grapefruit juice inhibit? what does this mean and what does it cause?
inhibits CYP3A medications
this means that the juice interferes with the enzyme CYP3A in the liver, which is responsible for metabolizing many medications.
this causes increase of medication levels in the blood increasing risk of adverse effects and events
157
when grapefruit juice inhibits CYP3A, it decreases the metabolism of what type of medications?
(hint: 3)
oral antifungals
calcium channel blockers (esp Diltiazem)
Statins
158
For people taking calcium channel blockers there is an increased risk of possible constipation. what should be included in pt education?
increase fiber in diet
159
Are beta blockers considered first line treatment for hypertension?
no
160
list the indications for beta blockers
(hint: 9)
Hypertension (but not first line)
All patients after myocardial infarction
All patients after percutaneous coronary intervention
HR reduction in atrial fibrillation
Palpitations
Heart failure
Migraines
Performance Anxiety
Hyperthyroidism
161
why are beta blockers indicated for all pts after a myocardial infarction?
to decrease the risk of sudden death after MI
162
What do beta blockers decrease?
(hint: 4)
Decrease HR
Decrease BP
Decrease muscle contraction
Decrease renin release
163
what do beta blockers increase?
blood flow to the kidneys
164
what do beta blockers block/decrease?
SNS responses
165
Beta blockers work by blocking the __________ ________ in the heart and blood vessels that are normally activated by _________ and __________
beta-adrenergic receptors;
epinephrine and norepinephrine
166
What are the special uses for the beta blocker metoprolol?
(hint: 2)
heart failure
post myocardial infarction
167
What are the special uses for the beta blocker propranolol?
(hint: 2)
social anxiety
headaches
168
when should caution be used with beta blockers?
(hint: 3)
in those with chronic lung disease
in those with brady arrhythmias
in those with diabetes
169
why must caution be used in pts taking beta blockers who have chronic lung disease?
they may increase risk of asthma attacks
170
why might beta blockers increase the risk of asthma attacks ?
bc they block beta 2 receptors in the lungs and cause airways to constrict
171
Beta blockers may mask ___________ ________
hypoglycemia episodes
172
When a pt is taking beta blockers, keep an eye on _____ _____. this is especially important in ______ pts
blood sugar;
diabetic
173
what is important to note about NPO status and beta blockers?
make sure pt is given medication even when NPO
174
the nurse must assess for ____ _____ when a pt is taking beta blockers
side effects
175
for beta blockers, there are no major what?
lab concerns
176
What do selective beta blockers block?
beta 1 receptors
177
what do non-selective beta blockers block?
both beta 1 and beta 2 receptors
178
list the selective beta blockers we discussed in class
(hint: 4)
Metoprolol
Atenolol
Esmolol
Bisoprolol
179
list the non-selective beta blockers we discussed in class
(hint: 4)
Propranolol
Carvedilol
Nadolol
Sotalol
180
what is the BIGGEST selective beta blocker?
metoprolol
181
who are non-selective beta blockers contraindicated in?
(hint: 3)
pts with asthma, bronchospasm, and/or heart failure
182
What is important to note about cardio-selective beta blockers?
less likely to have symptoms but higher doses can cause lung symptoms
183
what are the two types of metoprolol?
succinate and tartrate
184
Which types of metoprolol are short-acting vs long-acting?
tartrate is short-acting
succinate is long-acting
185
when is succinate metoprolol dosed?
usually dosed daily
186
when is succinate metoprolol used?
(hint: 2)
in the tx of heart failure and hypertension
187
when is tartrate metoprolol used?
(hint: 2)
post myocardial infarction & for rate control in arrhythmias
188
how can tartrate metoprolol be given?
intravenously
189
can short-acting and long-acting metoprolol be used interchangeably? why or why not?
NO, they are not to be used interchangeably
they work differently; you need to know what kind the pt is on
190
what do alpha blockers inhibit? block?
alpha synapse at the alpha adrenergic receptors
Blocks SNS
191
what do alpha blockers prevent?
feedback of norepinephrine
192
What is important to note about the indication for alpha blockers?
(hint: 3)
they are not really used in BP control
they are considered 3rd-4th line treatment
not seen often anymore
193
Where are alpha 1 adrenoceptors located?
smooth muscle cell membrane
194
what do alpha 1 adrenoceptors promote?
contraction of the smooth muscle of peripheral blood vessels, bladder neck, prostate capsule, and prostate fibromuscular stroma
195
where are beta 1 adrenoceptors located?
cardiac muscle cell membrane
196
what do beta 1 adrenoceptors stimulate?
heart rate & myocardial contractility
197
alpha blockers block alpha receptors but can also block ____ _______
beta receptors
198
what is important to note about the first dose effect of alpha blockers?
very first time you give alpha blocker you need to keep an extremely close eye on the patient as they can drop BP too much
199
Alpha blockers have significant ______ ______
adverse effects
200
list the side effects of alpha blockers
(hint: 6)
orthostatic hypotension
tachycardia
vertigo
sexual dysfunction
syncope
dizziness
201
who should alpha blockers be avoided in and why?
older adults due to increased sedation/confusion
202
what are the two examples of alpha blockers we discussed in class?
doxazosin (Cardura)
prazosin (Minipress)
