Cardiopulmonary 1: HTN Flashcards
(201 cards)
1
Q
benefit of olmesartan
A
can titrate very precisely - may be beneficial for petite patient
2
Q
endocrine adverse effect of spirinolactone
A
gynecomastia
3
Q
3 main AEs ACE inhibitors
A
angioedema
cough
teratogenicity
4
Q
ACC/AHA Guidelines: Normal BP
A
<120 / <80
5
Q
ACC/AHA Guidelines: Elevated BP
A
120 - 129 / <80
6
Q
ACC/AHA Guidelines: HTN stage 1
A
130 - 139 systolic OR 80 - 89 diastolic
7
Q
ACC/AHA Guidelines: HTN Stage 2
A
Systolic at least 140 OR diastolic at least 90
8
Q
ACC/AHA Guidelines: threshold to start treatment for a patient with clinical cardiovascular disease or a 10 year atherosclerotic cardiovascular disease (risk greater than 10%)
A
start treatment for a pressure greater than or equal to 130/80
9
Q
ACC/AHA Guidelines: threshold to start treatment for a patient with no clinical CVD and no 10 year atherosclerotic CVD (risk less than 10%)
A
start treatment at greater than or equal to 140/90
10
Q
ACC/AHA Guidelines: when should you consider two anti htn agents?
A
if patient, regardless of their risk, was greater than 20/10 mmHg over goa.
11
Q
ACC/AHA Guidelines: BP goal for ALL patients
A
< 130/80
12
Q
blood pressure goal when someone is hospitalized
A
generally will be a little more liberal. won’t intervene until over 150 systolic. do not want to risk organ perfusion.
13
Q
ACE inhibitor (definition)
A
angiotensin converting enzyme inhibitor
14
Q
ARB (definition)
A
angiotensin II receptor blocker
15
Q
DHP CCB (definition)
A
Dihydropyridine calcium channel blocker
16
Q
DHP CCBs are more geared towards
A
pressure control rather than rhythm control
17
Q
drug of choice categories for HTN in non-african american patients with no compelling indication (3)
A
thiazides
ACE-1/ARB
DHP CCB
18
Q
drug of choice categories for African-American patients with no compelling indication (2)
A
Thiazides
DHP CCB
19
Q
ACE inhibitors and ARBs in African American patients
A
inferior if given as mono-therapy for HTN
20
Q
drugs of choice categories for non African-American diabetic patients without CKD (3)
A
Thiazides
ACE-1/ARB
DHP CCB
21
Q
Drug of choice categories for African-American patients with diabetes but no CKD (2)
A
Thiazides
DHP CCB
22
Q
Drug of choice category for patient of any race who has CKD
A
ACE-1
23
Q
When a patient with HTN or diabetes starts approaching CKD, what will they be prescribed and why?
A
an ACE because they are renal protective and may slow down progression of CKD.
24
Q
Drug of choice for patient of any age and race who is s/p MI ?
What if HF is present ?
A
- Beta blocker + ACE-1
- Aldosterone antagonist if HF is present
25
What drug should be prescribed for a patient of any age/race who is s/p MI and also has a degree of HF present?
Aldosterone antagonist
26
Drug of choice for patient of any age/race who is being medicated for recurrent stroke prevention
Thiazide + ACE-1
27
Drugs of choice for patient with heart failure of any age/race (4)
*Beta Blocker + ACE-1*
Diuretics for fluid retention
Aldosterone antagonist
Hydralazine / ISO DN
28
Why thiazides + ACE-1 for patients at risk for recurrent stroke?
In setting of stroke, you may not want to have beta blocker because you don't want to slow down heart and risk perfusion.
29
What kind of diuretic is preferred in heart failure?
loop
30
Beta Blockers after MI
May benefit the heart by supporting it/giving it a slight break
31
african american patients and hydralazine/ISO DN
in the setting of HF, pts do better or at least do not do worse than patients just on ace inhibitors.
32
Four major classes of anti hypertensives (first lines)
Thiazides
CCBs
ACE-Is`
ARBs
33
If response is not effective enough on first line therapy, what should you do next?
increase dose (up to max dose) of that first line drug and reevaluate prior to adding a second agent.
34
disadvantage of adding second agent
unsure of where potential side effect may be coming from
35
what to consider before putting patient on a single tablet combination drug? (ie: an ACE/thiazide) Why?
try the patient on the two separate tablets first before putting them on a combo tablet. evaluate their response. it is easier to titrate individual agents separately. combo drug doses are fixed. once patient is solid for a month or two, then consider combo pill.
36
Advantages of combo drugs
less pill burden
37
disadvantage of combo drug
cannot titrate
38
once established that max dose of first line is not effective enough for pt's HTN, what is the appropriate next step?
start the pt on a second agent as an individual pill. do not start the pt on second agent as a combo pill.
39
later line alternatives "A" list (5)
| and why are they later line?
- alpha 1/beta blockers
- direct vasodilators
- central alpha2-adrenergic agonists
- beta-blockers
- loop diuretics
- too powerful as a first line treatment
40
example: direct vasodilator
| A list
hydralazine
41
example: beta-blocker
| A list
metoprolol
42
example: loop diuretic
| A list
furosemide
43
which beta blocker is recommended to pregnant women with htn?
labetalol
44
other use for labetalol, carvedilol, or hydralazine
hypertensive urgency
45
you'll more often see furosemide prescribed for
heart failure rather than htn
46
later-line alternatives "B" list (3) for htn
- aldosterone antagonists
- alpha-1 blocker
- vasodilating beta-blocker
47
example: aldosterone antagonist
| B list
spirinolactone
48
Example: vasodilating beta blocker
| B list
nebivolol
49
nebivolol FYI
not a popular medication
50
Mechanism of action: thiazide
inhibit active exchange of Na and Cl (in equal amounts) in the distal convoluted tubule (last step of tubule)
*most often used
51
mechanism of action: loop diuretics
inhibit exchange of Na/Cl/K on thick segment of ascending loop of henle (where a lot of concentration takes place)
*HF
52
mechanism of action: K sparing diuretics and main function
inhibits reabsorption of Na in distal convoluted tubule and collecting duct. The main function is antagonizing aldosterone (while sparing potassium). Allows you to pee out sodium and hold on to K.
53
you may often see K sparing diuretics prescribed with _____ and why?
thiazides, which waste a lot of K. adding a K sparing diuretic may help prevent hypokalemia.
54
aldosterone is released when body perceives
that you need fluid
55
what does it mean when it is said that K sparing diuretics antagonize aldosterone?
that they bind to receptor and prevent aldosterone from being released and retaining fluid. They allow your body to excrete the fluid instead.
56
Therapeutic indications of thiazides (2)
hypertension
| edema
57
3 thiazide drugs used for HTN
chlorothiazide
hydrochlorothiazide
chlorthalidone
58
which thiazide do you see in pediatric htn
chlorothiazide
59
which thiazide do you see more in adult htn?
hydrochlorothiazide
60
chlorthalidone vs hctz
old thiazide drug used for htn which has a longer duration of action
61
thiazide drug used for edema
metalozone
62
metolazone may be seen when a patient is already prescribed
a loop diuretic. it provides an extra push.
63
drug interactions involving thiazide involve
electrolytes
64
thiazide and digoxin
k wasting drug predisposes pt to hypokalemia, putting them at risk for digoxin toxicity. requires tighter monitoring.
65
thiazide and lithium
thiazide wastes sodium. lithium resembles sodium to the kidney. if you are wasting a lot of sodium, the lithium will be retained by the kidney and can accumulate, resulting in lithium toxicity.
requires tighter monitoring.
66
thiazide and electrolyte supplements
the electrolyte supplement may not be as effective
67
thiazide and ototoxicity
no risk, unlike other diuretics
68
thiazide and sulfonamide allergy
there is a sulfa-like compound in thiazide, proceed with caution. understand what the allergy actually is before proceeding.
69
thiazide use in anuric renal failure
if you have an impaired GFR (<10ml/min) or CrCl (<30), thiazide will not be effective.
70
normal creatinine clearance is usually
> 100ml/min
71
Adverse effects of thiazides:
| what will it decrease? (5)
Mainly sodium, potassium, chloride
| also phosphorus and magnesium
72
adverse effects of thiazides:
| what will it increase?
calcium, uric acid
| potentially glucose and lipids
73
adverse effect of thiazide, unrelated to electrolytes
photosensitivity and propensity to burn
74
Most powerful diuretics are
loop diuretics
75
aside from HF, what are two other indication for loop diuretics re: edema?
hepatic cirrhosis and renal disease (CrCl <30ml/min)
76
if a patient has a CrCl < 30 mL/min, which diuretic would be appropriate?
Loop diuretic
77
4 Examples of loop diuretics
Lasix
Bumetanide
Ethacrynic acid
Torsemide
78
Most potent loop diuretic
bumetanide (bumex)
79
How many doses per day may you need of lasix?
2-3
80
If patient has a true sulfa allergy, which loop diuretic is safest? and what are two downsides of this drug?
ethacrynic acid
- PO is extremely expensive
- ototoxic
81
Torsemide tends to be used when
lasix is in shortage
82
Duration of onset for lasix
~6 hours
| Lasix "lasts six"
83
what time should you avoid giving lasix?
bedtime
84
Which lytes are decreased in loop diuretic use? (5)
sodium, potassium, chloride, magnesium, calcium
85
What rate should loops be given IV and why?
No faster than 10mg/min, ototoxicity
86
Which metabolic alterations might you see in loop diuretic
increased glucose, uric acid, lipids
87
ototoxicity risk increases with
higher doses of loop diuretics
88
furosemide IV to oral conversions
1:2
89
Bumex IV to PO conversion
1:1
90
Bumex potency to lasix IV
1mg bumex: 40mg lasix
91
Which loop diuretic is most useful in refractory response to diuretics?
bumetanide
92
Loop diuretic drug interaction: digoxin
hypokalemia -> dig toxicity
93
loop diuretic drug interaction -> lithium
Na wasting, kidney retains lithium as it resembles Na. -> lithium toxicity
94
Loop diuretic drug interactions with other ototoxic drugs
ototoxicity - watch with k sparing diuretics
95
loop diuretics and sulfa allergy
proceed with caution
96
K sparing diuretic mech of action
block aldosterone in the distal convoluted tubule and collecting duct
97
K sparing diuretics are typically
used in combo with other agents as they have a modest diuretic effect
98
most common k sparing diuretic
spirinolactone
99
mechanism of action of triamterene and amiloride
acts on sodium-potassium exchange in the distal nephron
100
the diuretic effect of triamterene and amiloride is
modest. acts quicker than spirinolactone
101
caution with dyazide (triamterene/hctz)
order frequent bmps. this comvo drug can, over a long period of time, cause hyperkalemia.
102
best diuretic group in the setting of htn
Thiazides
103
long term implication with K sparing diuretic
watch for hyperkalemia
104
what is a possible explanation for ACE inhibitor induced cough?
degradation of bradykinin
105
ACE inhibitor mechanism of action
blocks conversion of angiotensin I to angiotensin II, halting vasoconstriction
106
in cases when renal afferent arteriolar pressure is increased, what is an intervention?
ACE inhibitors act as a renal protectant, lowering afferent and efferent pressure. * does not help in already low afferent pressures
107
ace inhibitors as a renal protectant in already low afferent pressures
does not help
108
best diuretic group in HF
loop diuretic
109
ACE inhibitors vs ARBs
they are not used together. Similar but not the same. people on ARBs probably did not benefit from ACEs.
110
degradation of bradykinin
The enzyme ACE (angiotensin converting enzyme) is the enzyme converting angio I to angio II. ACE is in the lungs. Bradykinin is usually released in response to ACE. When that conversion isn't able to happen, bradykinin (inflammatory mediator) has nowhere to really go and cannot be broken down. This causes a cough (or the very serious adverse effect - angioedemia)
111
ACE inhibitor which you'll most likely see dry cough
enalapril
112
how to fix ACE inhibitor dry cough?
by giving an ARB
113
renal afferent arteriole
bringing blood to the kidney
114
renal efferent arteriole
brings blood away from kidney
115
as creatinine goes up,
creatinine clearance goes down
116
when we start someone on an ace inhibitor, you're going to see
a bump in creatinine by about .2
117
if a patient recently started on an ace inhibitor has a bump in creatinine of about .5 or more
dc the ace inhibitor
118
indications for ace inhibitors (3)
htn, hf, post mi
119
ace inhibitors and heart rate
causes no change in heart rate
120
preload
force of blood coming into heart
121
afterload
what is ejected to the vessels and periphery
122
in the setting of heart failure, we want to see what in preload and afterload?
reduction.
123
potassium in ace inhibitors
because they decrease Na, K is retained
124
what population is at highest risk for angioedema in ace inhibitors?
african american women
125
drugs that ace inhibitors have interactions with (3)
K supplements
diuretics
asa
126
ace inhibitors and k supplements
decreased excretion of K
127
ace inhibitors and diuretics
hypotension - monitor
128
ace inhibitors and asa interaction
kidney function
129
3 contraindications for ace inhibitors
- renal artery stenosis
- pregnancy
- previous angioedema
130
renal artery stenosis and ace inhibitors
if the artery isn't able to dilate and contract, they won't be able as effective
131
pregnancy and ace inhibitors
category x teratogenicity
132
ace inhibitors and previous angioedema
do not administer.
133
when can ace inhibitor induced angioedema happen?
any time. first or hundredth dose.
| also can be if patient is under more stress or taking med at unusual time.
134
suffix for ace inhibitors
-pril
135
Angiotensin II Receptor antagonists (ARBs) mechanism of action
block angiotensin II receptors on cell membranes
136
suffix for ARBs
-artan
137
therapeutic indications for ARBs
hypertension, chf
138
ARBs are often seen in patients who
have failed ACE inhibitors
139
adverse effects of ARBs (4)
| and how they compare to ACEs
- teratogenicity
- cough (< ace)
- hyperkalemia (< ace)
- angioedema (< ace)
140
contraindication for ARBs
renal artery stenosis
141
drugs which ARBs interact with
- k sparing diuretics
- k supplements
- nsaids * renal damage
142
ACEs and ARBs: summary
ACEs stop the conversion of angio I to angio II, decreases aldosterone and vasocon, cant breakdown bradykinin (cough)
ARBs let that conversion happen, but they block the receptors. less cough, less hyperkalemia, less renal insufficiency.
drug interactions are very similar.
143
Calcium Channel Blockers mechanism of action
block inward movement of calcium into muscle by binding to calcium channels in the heart and SM of the coronary and peripheral vasculature.
144
2 subgroups of CCBs
non-dihydropyridines
| dihydropyridines
145
non-dihydropyridines are
CCBs used primarily for conduction disorders
146
dihydropyridines are
CCBs used for dilator properties (in htn and hf)
147
indications for CCBs (4)
hypertension
angina
arrhythmias
heart failure
148
examples of 2 non-dihydropyridine CCBs
diltiazem
| verapamil
149
examples of dihydropyridines end in
-pine
150
why has verapamil lost popularity
a lot of side effects, especially constipation
151
digoxin and verapamil
synergistic in a bad way - slows heart too much and can lead to heart block
152
verapamil and beta blockers drug interaction
bradycardia
153
if a patient in hf or heart block absolutely needs a CCB
give them a dihydropyridine, not a non.
154
diltiazem vs verapamil
just alike except without constipation
155
therapeutic effects of dihydropyridine CCBs
vasodilation on smooth muscle
156
dihydropyridine CCBs are very helpful in the setting of
hypertension and prinzmetal's (and variant) angina
157
types of angina CCBs treat
not activity induced. angina that is induced by overactive calcium channels.
158
indications for dihydropyridine CCBs
htn and heart failure
159
dihydropyridine CCB for hf
amlodipine
160
if a patient is on 10 mg of a dihydropyridine CCB and has slight ankle edema,
decrease dose to 5mg.
161
why can we use dihydro ccbs in heart failure?
bc they dont effect contractility as much, like non dihydros do.
162
beta-adrenergic blocker mechanism of action
competitively inhibit beta-adrenergic agonist receptors
163
two different types of beta adrenergic blockers
cardio selective
| cardio non selective
164
cardio non selective beta adrenergic receptors may be used in (3)
ascites
portal htn
alcohol withdrawal
165
nonselective BB agents block which receptors?
beta 1 and beta 2
166
nonselective BB agents are effective in causing
bronchoconstriction
167
beta blocker suffix
-olol
168
selective BB act on which receptor at normal doses?
beta-1
169
selective vs non selective BBs and glucose metabolism
selective - minimal effect
| nonselective - may effect
170
examples of selective BBs (2)
atenolol
| metoprolol
171
indications for beta blockers (4)
htn
angina
hf
mi
172
BBs, selective or non selective, should not be used in which condition? and when would it be ok to use?
decompensated HF
| until pt is euvolemic again
173
beta blockers like propanolol and labetolol CAN cause vasoconstriction. When would you want to avoid these?
in patients with COPD or asthma
174
true or false: propranolol is almost never used for cardiac reasons
true
175
non selective BBs and the BBB
they cross the BBB.
176
drug interactions: BBs
concurrent bp meds
| oral hypoglycemics
177
beta blockers and oral hypoglycemics - explain
they can mask hypoglycemia because the symptoms of hypoglycemia are adrenergically driven
178
Alpha/Beta-Adrenergic Blockers mechanism of action
they block beta-1, beta-2, and alpha-1 receptors in the same preparation.
179
if you have alpha-1 blockade:
BP is decreased
180
if you have alpha-2 stimulation (like in an alpha2 agonist):
BP is decreased.
181
alpha/beta-adrenergic blocker and lipid/carb metabolism
no effect
182
Alpha-1 adrenergic blockers mechanism of action and effect
Competitively block alpha-1 receptors, causing relaxation of arterial and venous smooth muscle. Decrease peripheral vascular resistance.
183
alpha-1 adrenergic blockers are very good at decreasing bp but
are so effective that it may be dangerous.
184
suffix for alpha-1 adrenergic blockers
-azosin
185
patient education for alpha-1 adrenergic blockers
high likelihood of first dose postural hypotension/syncope. Stay upright for 30 min after taking med.
186
centrally acting agent: alpha-2 agonist
| example
clonidine
187
therapeutic indication of clonidine, a centrally acting alpha-2 agonist
hypertension
| pain management
188
clonidine for pain management
alpha2 activity can also be analgesic (IV)
189
clonidine patient education
do not stop taking med abruptly
190
caution for elderly patients and clonidine
cholinergic effects
191
PTSD and clonidine
sometimes indicated for relaxation in the setting of PTSD
192
HTN urgency intervention when out of other options
clonidine
193
alpha-2 agonist: methyldopa indication
useful in htn when pregnant
194
pregnancy category: methyldopa
B
195
methyldopa is
alpha 2 agonist
196
management of the patient on methyldopa
monitor CBC
197
Vasodilators: hydralazine
2 therapeutic effects, 1 AE
decreases peripheral vascular resistance
increases cardiac output
provides reflex tachycardia*
198
indications of hydralazine in the htn pt
HTN
| HTN crisis
199
antihypertensive combination products typically contain
a diuretic
200
HTN urgency
systolic > 180, can be treated c po meds, no end organ damage
201
htn emergency
systolic > 200, end organ damage has taken place. need IV meds.
