Therapeutics I Exam I (HTN) Flashcards
Antihypertensives (431 cards)
1
Q
What is the pacemaker of the heart?
A
Sinoatrial node (SA)
2
Q
What is the blood pressure equation?
A
BP= Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
3
Q
What sensor in the body is the short-term regulator of blood pressure?
A
Baroreceptors
4
Q
What system in the body is the long-term regulator of blood pressure?
A
Kidneys with RAAS
5
Q
What is cardiac output?
A
This is the amount of blood pumped by each ventricle in one minute. Typical output is 5-6L/min for a normal person.
6
Q
What is systemic vascular resistance?
A
The resistance the heart has to pump against in the vasculature to get the blood out of the heart.
7
Q
What is the equation to calculate the cardiac output?
A
Cardiac output= Stroke volume x heart rate
8
Q
What is stroke volume?
A
This is the amount of blood pumped out of the heart in one heart beat. Typically the heart leaved 30-45% of the blood in the heart while the rest is pumped through the body.
9
Q
What are the 3 things that make up stroke volume?
A
Preload, afterload, and contractility
10
Q
What is preload?
A
Preload is the amount of stretch that the cardiac myocytes feel at the end of ventricular filling.
11
Q
What is afterload?
A
Afterload is the resistance the left ventricle must overcome to eject blood through the aorta.
12
Q
What is contractility?
A
Contractility is the force of contraction of the heart muscle.
13
Q
Based on the blood pressure and cardiac output equation, it would make sense that as HR increases so does BP. However, does this actually occur?
A
It can occur but mainly if the heart rate increases, the vasculature will dilate to bring back blood pressure homeostasis via the reflex arc.
14
Q
What is the equation for stroke volume?
A
Stroke volume = end diastolic volume - end systolic volume
15
Q
What is inotropy?
A
Inotropy is the change in force of contraction of the heart. If inotropy is +, then the force of contraction has increased and vice versa.
16
Q
What is chronotropy?
A
Chronotropy is the change in the heart rate. If chronotropy is +, then the heart rate has increased and vice versa.
17
Q
If inotropy is negative, then the force of contraction of the heart has ____________.
A
Decreased
18
Q
If inotropy is positive, then the force of contraction of the heart has ____________.
A
Increased
19
Q
If chronotropy is negative, then the heart rate has ____________.
A
Decreased
20
Q
If chronotropy is positive, then the heart rate has ____________.
A
Increased
21
Q
Baroreceptors are _____________ that relay information about blood pressure to the ___________ ___________.
A
Mechanoreceptors
Adrenal Medulla
22
Q
If baroreceptors detect a falling blood pressure, what are the steps that occur to bring the blood pressure back to normal?
A
- Baroreceptors sense low BP
- Baroreceptors signal adrenal medulla to secrete catecholamines
- This release triggers increases sympathetic activity via alpha and beta receptors
- Via beta-1, the heart rate and stroke volume increase which increase cardiac output to increase BP
- Via alpha-1, smooth muscle vasoconstriction which increases systemic vasculature resistance which increases BP
23
Q
Intrarenal baroreceptors activate _______ when they sense low BP or blood perfusion.
A
RAAS
24
Q
Kidneys are primarily responsible for long-term BP control by controlling _______ _________.
A
Blood volume
25
If there is decreased renal perfusion (decreased blood flow), there will be __________ reabsorption of sodium and water. This will allow the blood volume to increase and stabilize BP.
Increased
26
Pressure in the renal arterioles stimulates the production of __________.
Renin
27
What is vasopressin/ antidiuretic hormone?
This hormone is released from the posterior pituitary gland and aids in blood pressure control via regulation of water reabsorption. It tells the kidney to reabsorb water.
28
Blockade of the RAAS can have protective effects that aid in the prevention and treatment of what 4 issues?
1. Hypertension
2. MI
3. Heart Failure
4. Chronic Kidney Disease
29
What compound is the a part of the RAAS, is the sole substrate for renin, and mainly synthesized in the liver?
Angiotensinogen
30
What enzyme is made, stored, and secreted by juxtaglomerular cells in the kidneys?
Renin
31
What triggers the release of renin that activates the RAAS?
It can be triggered for release via baroreceptors in afferent arteriole sensing low pressure.
32
What is the function of renin in the RAAS?
Renin cleaves angiotensinogen to angiotensin I. This is the rate limiting step of the RAAS.
33
What is the rate-limiting step of the RAAS?
Angiotensinogen conversion to angiotensin I via renin.
34
What enzyme in the RAAS is the major determinant of angiotensin II production?
Renin
35
Does angiotensin I have any biological activity?
No. Angiotensin I is inactive.
36
What is the substrate for angiotensin converting enzyme (ACE) in the RAAS?
Angiotensin I
37
What enzyme facilitates the conversion of angiotensin I to angiotensin II?
ACE
38
Where does conversion of angiotensin I to angiotensin II via ACE occur?
Lungs
39
What is unique about the angiotensin-converting enzyme (ACE)?
It is a nonspecific enzyme that also inactivates bradykinin which is a proinflammatory mediator.
40
What is a possible effect of inhibiting the ACE enzymes via an ACE-inhibitor directly related to bradykinin?
If ACE is inhibited, it can no longer inactive bradykinin, a pro-inflammatory molecule that causes smooth muscle contraction. If this molecule is in high amounts, it can cause a cough.
41
Thinking about the different products of the RAAS, which one is the main potent vasoconstrictor?
Angiotensin II
42
Via what 2 ways does angiotensin II actually increase blood pressure?
1. It is a potent vasoconstrictor which increase systemic vascular resistance which increases BP
2. Triggers the reabsorption of Na and water directly through proximal tubule and indirectly by triggering aldosterone secretion
43
There are two angiotensin II receptors, which one has a higher affinity for angiotensin II?
Angiotensin II Type I Receptor (AT1R)
44
What type of molecule is aldosterone?
Aldosterone is a steroid hormone that is stimulated by angiotensin II with RAAS activation.
45
What are the two normal functions of aldosterone?
Aldosterone is triggered by angiotensin II. It works to increase blood pressure by increase Na+ and water retention and increasing K+ excretion.
46
What are the 4 main classes of drugs that inhibit the actions of angiotensin II in the RAAS system to work as antihypertensives?
1. Angiotensin-converting enzyme inhibitors (ACE-Is)
2. Angiotensin II Receptor Blockers (ARBs)
3. Direct Renin Inhibitors
4. Calcium channels blockers
47
What is the MOA of ACE-inhibitors?
They inhibit the conversion of angiotensin I to angiotensin II
48
What is the universal suffix for ACE-inhibitors?
-pril
49
How are ACE-inhibitors metabolized?
Several are prodrugs that must be activated via hepatic metabolism. This decreases their potency but increases their oral bioavailability.
50
Where are ACE-inhibitors excreted?
Kidneys
51
Are ACE-inhibitors renoprotective?
Yes! ACE-inhibitors protect the kidneys and can be used in chronic kidney disease.
52
What is the MOA of angiotensin II receptor blockers (ARBs)?
They selectivity and competitively bind the angiotensin II receptors (AT1R).
53
Can ACE-inhibitors and ARBs be used concurrently?
No. They are very similar and have similar efficacy and therefore should not be used together.
54
What is the universal suffix for ARBs?
-sartan
55
Where are ARBs excreted from?
Renal
56
What is the drug class called ARNIs?
These are drugs that include an angiotensin II receptor blocker (ARB) and a Neprilysin inhibitor.
57
What is the MOA of ARNIs?
ARNIs induce vasodilation and natruiresis. These drugs inhibit neprilysin which blocks the breakdown of natriuretic peptides.
58
What condition are ARNIs indicated for?
Heart failure
59
What is the brand name for the one ARNI discussed in class?
Entresto. It contains valsartan and sacubitril.
60
What is the MOA of direct renin inhibitors (DRIs)?
They inhibit the conversion of angiotensinogen to angiotensin I by inhibiting renin.
61
What was the one discussed DRI?
Aliskiren (Tekturna)
62
T or F: DRIs are more effective than ACE-Is and ARBs?
False. DRIs are not more effective and were designed to reduce the dry cough seen as a side effect with ACE-inhibitors.
63
What were the 5 discussed ACE-inhibitors?
Ramipril (Altace)
Enalaprilat (Vasotec IV)
Benazepril (Lotensin)
Enalapril (Vasotec, Epaned)
Lisinopril (Prinivil, Zestril)
ACE-inhibitors are REBELs
64
What were the 4 discussed ARBs?
Losartan (Cozaar)
Olmesartan (Benicar)
Valsartan (Diovan)
Irbesartan (Avapro)
LOVI the ARBs
65
What is the brand name for the ACE-I called Ramipril?
Altace
66
What is the brand name for the ACE-I called Enalaprilat?
Vasotec IV (this drug is administered via IV)
67
What is the brand name for the ACE-I called Benazapril?
Lotensin
68
What is the brand name for the ACE-I called Enalapril?
Vasotec or Epaned
69
What is the brand name for the ACE-I called Lisinopril?
Prinivil or Zestril
70
What is the brand name for the ARB called Losartan?
Cozaar
71
What is the brand name for the ARB called Olmesartan?
Benicar
72
What is the brand name for the ARB called Valsartan?
Diovan
73
What is the brand name for the ARB called Irbesartan?
Avapro
74
What is the brand name for the DRI (direct renin inhibitor) named Aliskiren?
Tekturna
75
What is the brand name for the ARNI (ARBs + Neprilysin inhibitor) that has both sacubitril and valsartan?
Entresto
76
What artery supplies the nephron in the kidneys?
The afferent arteriole. This artery supplies blood to the glomerulus to be filtered.
77
What type of substances does the nephron normally filter?
The nephron typically filters small substances like water and electrolytes. If large substances like proteins, RBCs and more are being filtered then this indicates kidney dysfunction.
78
Where do loop diuretics work?
Thick ascending limb of Henle's loop
79
Where do thiazides work?
Distal convoluted tubule
80
Where do potassium sparing diuretics work?
Cortical collecting duct
81
________ constrict the afferent arteriole that supplies blood to the nephron.
NSAIDs
82
What is the definition of a diuretic?
Diuretics increase urine volume
83
What is the definition of a natriuretic?
Natriuretic increase renal sodium excretion
84
What is the one class of diuretics that is generally used for treating edema?
Loop diuretics
85
What is the one class of diuretics that is generally 1st line use for hypertension?
Thiazide diuretics
86
What is the one class of diuretics that is generally used to offset electrolyte loss?
Potassium sparing electrolytes
87
ACE-Inhibitors have a higher risk compared to ARBs for ________________.
Angioedema
88
What is the MOA for thiazide diuretics?
They inhibit the Na+/Cl- transporter in the distal convoluted tubule. It inhibits the reabsorption of NaCl into the tubule and keeps it in the lumen where water will follow and produce more urine. It also enhances calcium reabsorption.
89
What is unique about thiazide diuretics compared to the other diuretics?
Calcium levels increases which is not seen with the other diuretics.
90
How do thiazide diuretics act as antihypertensives long-term?
Long-term these medications should decrease systemic vascular resistance.
91
What are the two thiazide diuretics discussed in class?
Chlorthalidone (Hygroton) and Hydrochlorothiazide (Microzide)
92
Is chlorthalidone or hydrochlorothiazide a more potent thiazide diuretic?
Chlorthalidone (Hygroton) is the more potent thiazide diuretic.
93
Loop diuretics also diminish lumen-positive __________ from K+ recycling, increased Mg, and Ca2+ excretion.
Potential
94
All thiazide diuretics are __________ derivatives.
Sulfonamide
95
What is unique about thiazide diuretics and hypersensitivity?
Thiazide diuretics are sulfonamide derivatives and those with sulfonamide hypersensitivity can have reactions to these diuretics.
96
What is the MOA of loop diuretics?
Loop diuretics inhibit the Na+/K+/Cl- transporter in the thick ascending loop of Henle's loop. They work by reducing the reabsorption of NaCl and water will follow later on in the collecting duct.
97
Loop diuretics deplete _____________ more than the other diuretics.
Electrolytes
98
What are the two loop diuretics discussed?
Furosemide (Lasix) and Torsemide (Demadex)
99
Most loop diuretics are also _________ derivatives. However, ________ acid (Edecrin) is not derived from this and instead is derived from phenoxyacetic acids.
Sulfonamide
Ethacrynic acid
100
Is the loop diuretic furosemide (Lasix) or torsemide (Demadex) more potent?
Torsemide is more potent than furosemide but the most potent loop diuretic is Bumetanide (Bumex).
101
T or F: Aldosterone antagonist drugs are the same thing as potassium sparing diuretics.
True! However, not all potassium sparing diuretics are aldosterone antagonists.
102
What is the MOA of potassium sparing diuretics?
They inhibit the epithelial Na+ channels in the collecting ducts of the nephron. They inhibit influx on Na+ and water follows. Additionally, it stops the efflux of K+ which increases the conc. of it in the body.
103
What is the main purpose for using potassium sparing diuretics?
The main purpose of these diuretics is to offset the potassium loss from other diuretics.
104
What is the one potassium sparing diuretic we need to know?
Triamterene/ HCTZ (Maxzide)
105
What is the MOA of aldosterone antagonist?
Aldosterone antagonist bind mineralocorticoid receptors to competitively antagonize aldosterone stopping it from increasing blood pressure by increasing Na+ and water retention and increasing K+ excretion.
106
What is the main aldosterone antagonist?
Spironolactone (Aldactone)
107
What is unique about the aldosterone antagonist known as spironolactone?
It is a synthetic steroid that has a high selectivity for the mineralocorticoid receptor that aldosterone binds to.
108
___________ is a spironolactone analog that has a greater affinity for the mineralocorticoid receptor compared to spironolactone.
Eplerenone
109
What electrolyte stimulates the contraction of smooth muscle and cardiac myocytes in the heart?
Calcium
110
What is the effect of calcium channels blockers?
They block the entry of calcium into the cardiac myocytes and causes vascular smooth muscle relaxation to reduce blood pressure.
111
What are the two groups of calcium channel blockers?
Dihydropyridines and non-dihydropyridines
112
What is the universal ending for the calcium channel blocker group called dihydropyridines?
-dipine
113
Do DHPs or non-DPHs have greater effects on smooth vascular muscle relaxation compared to cardiac effects?
Dihydropyridines have greater effects on smooth vascular muscle compared to cardiac effects.
114
What enzyme in the liver metabolizes DPHs in the liver?
CYP3A4
115
DPHs (a type of calcium channel blocker) are major substrates for ___________ and are also ________ ___________ of that enzyme.
CYP3A4
Weak Inhibitors
116
What were the 3 dihydropyridines calcium channels blockers discussed in class?
Amlodipine (Norvasc)
Nifedipine LA (Adalat CC, Nifedical XL, Procardia XL)
Amlodipine/Benazepril (Lotrel)
117
Why is extended release nifedipine used and not immediate release?
IR nifedipine is variable and leads to a high concentration of that drug quickly while long-acting is more steady state.
118
Do DPHs or non-DPH calcium channel blockers have a greater cardiac effect than compared to coronary and peripheral vasodilation?
Non-dihydropyridines have a greater cardiac effect and induce negative inotropic and chronotropic effects resulting in reduced contractility and heart rate.
119
Non-DPHs are metabolized by what enzyme in the liver?
CYP3A4
120
Non-DPHs are metabolized by _________ enzyme in the liver and are __________ ________ of that enzyme. Additionally they are inhibitors of the __________________.
CYP3A4
Moderate inhibitors
P-glycoprotein
121
What is the main indication for the use of non-DPH calcium channel blockers?
Atrial fibrillation and tachycardia
122
Are beta-blockers 1st line treatment for hypertension?
No
123
Which beta receptor controls the heart and the kidneys?
Beta 1 (causes + inotropic and chronotropic effects in the heart and induces renin secretion when the sympathetic system is activated)
124
Which beta receptor controls the lung and pancreas?
Beta 2 (causes bronchial smooth muscle relaxation and increased secretions from the pancreas when the sympathetic system is activated)
125
Which alpha receptor controls vascular constriction?
Alpha 1 (activation of the sympathetic system activates alpha 1 to induce vasoconstriction)
126
What would be the main 4 effects of a cardiovascular focused beta blocker?
1. Negative inotropic effects (decreases contractility)
2. Negative chronotropic effects (decreases HR)
3. Decreases cardiac output
4. Slows conduction in the atria and AV node
127
What would be the main effect of a pulmonary focused beta blocker?
This would increase airway resistance as blocking beat 2 in the lungs inhibits the bronchial smooth muscle dilation.
128
What would be the main effect of a renal focused beta blocker?
The kidneys have beta 1 receptors in them. When blocked, the release of renin is inhibited.
129
What was the 1 nonselective beta blocker discussed during class?
Propranolol
130
What were the 2 cardioselective beta blockers discussed during class?
Atenolol (Tenormin
Metoprolol tartate (Lopressor)
Metoprolol succinate (Toprol XL)
131
Where was the 1 cardioselective and vasodilatory beta blocker discussed that inhibits beta 1 and can cause vasodilation through nitric oxide?
Nebivolol
132
What were the 2 discussed mixed acting alpha and beta blockers discussed during class?
Carvedilol (Coreg)
Carvedilol phosphate CR
Labetalol (Normodyne/Trandate)
133
Are beta-blocker drugs mostly lipophilic or lipophobic?
Beta-blockers are lipophilic meaning they readily cross the BBB. This can increase the risk for side effects like dizziness, drowsiness, depression, and other adverse CNS effects.
134
_________ is a major determinant of metoprolol clearance in the liver.
CYP2D6
135
What is the brand name for the drug atenolol?
Tenormin
136
What is the brand name for metoprolol tartate?
Lopressor
137
What is the brand name for metoprolol succiante?
Toprol XL
138
What is the brand name for propranolol?
Inderal
139
What is the brand name for carvedilol?
Coreg
140
What is the brand name for labetalol?
Normodyne and Trandate
141
What is the brand name for amlodipine?
Norvasc
142
What is the brand name for nifedipine?
Adalat CC, Nifedical XL, and Procardia XL
143
What are the two non-DHPs discussed in class?
Diltiazem (Cardizem CD, etc) and Verapamil (Calan, Veralan)
144
What are some of the different brand names for Diltiazem?
Cardizem CD, Cartia XT, Dilt-XR, Taztia XT, Tiadyit ER, and Tiazac
145
What are some of the different brand names for Verapamil?
Calan, Calan SR, and Verelan
146
Bradykinin is a _______________.
Vasodilator. Remember that using ACE-Is stops the inactivation of bradykinin leading to more vasodilation from that molecule.
147
What is Logp?
This is the log of the partition coefficient of a solute between octanol in water.
148
What does a + logp mean?
A + logp means that there is more drug in the octanol than the water meaning that drug is more lipophilic/hydrophobic.
149
What does a -logp mean?
A =logp means that there is more drug in water than in octanol meaning that the drug is more hydrophilic/lipophobic.
150
What group is attached to ACE inhibitors to make them more hydrophilic in order to be excreted from the body?
Glucuronic acid
151
What is an isostere?
This is when two molecules can have similar activity when substituted for one another.
152
Are direct vasodilators typically used with other medications?
Yes, they are typically used with beta-blockers and diuretics.
153
What is typically triggered if direct vasodilators are used as monotherapy?
The vasodilators will trigger the neurohumoral compensatory reflex to increase heart rate and increase renin secretion to bring blood pressure back to homeostasis.
154
What were the 4 direct vasodilators that were discussed in class?
1. Hydralazine
2. Minoxidil
3. Fenoldopam
4. Sodium Nitroprusside
155
T or F: Direct vasodilators causes vein and arterial dilation.
False. Direct vasodilators only cause arterial dilation and not vein dilation. This reduces the risk for orthostatic hypotension.
156
What is the MOA for the direct vasodilator hydralazine?
The MOA of unknown but it is thought that it inhibits calcium release from the sarcoplasmic reticulum preventing muscle contraction.
157
What is the MOA for Minoxidil?
Minodixil hyperpolarizes the smooth muscle membranes through opening of K+ channels.
158
What is the MOA for Fenoldopam?
It is a dopamine (D1) receptor agonist
159
What is the MOA for Sodium Nitroprusside?
This drug is activated in the blood vessels and converted to nitric oxide. NO activates guanylyl cyclase to synthesize cGMP which relaxes smooth muscle.
160
What is unique about the bioavailability of hydralazine?
It is largely variable due to the acetylator status of the patient. Slow acetylators are at higher risk for adverse effects.
161
What is the bioavailability of Minoxidil, Fenoldopam, and Sodium Nitroprusside?
These are 100% bioavailable. Minoxidil is taken orally and is 100% while Fenoldopam and Sodium Nitroprusside are IV.
162
What is the metabolic by-product produced from the metabolism of sodium nitroprusside in the blood vessels?
Cyanide
163
How are all the direct vasodilators eliminated from the body?
Renally
164
What are the 2 main indications for use for the direct vasodilator hydralazine?
Pregnancy induce hypertension/eclampsia and heart failure (used in combo with nitrates)
165
What are the two indications for the direct vasodilator minodixil?
Resistant hypertension and alopecia
166
What is the indication for the direct vasodilator fenoldopam?
Hypertensive emergency
167
What is the indication for the direct vasodilator sodium nitroprusside?
Hypertensive emergency
168
What are the general adverse effects of direct vasodilators in terms of causing vasodilation to reduce BP?
Headaches, flushing, nasal congestion, vertigo, nausea, and vomiting
169
What are the general adverse effects of direct vasodilators in terms of cardiac stimulation?
Tachycardia and palpitations (activated due to the SNS reflex)
170
Does Minoxidil or hydralazine induce greater fluid retention as an adverse effect?
Minoxidil
171
Hydralazine can increase the risk of __________ _________ generally with doses higher than _________ per day.
Lupus Syndrome
200mg/day
172
Minoxidil can increase the risk for _________ and _________.
Hirsutism and Hypertrichosis
173
What is the black box warning for Minoxidil?
Cardiac effects
174
Sodium Nitroprusside can increase the risk of _________ toxicity.
Cyanide
175
What are the symptoms of cyanide toxicity that can be seen with sodium nitroprusside use?
Metabolic acidosis, tinnitus, and confusion
176
When on sodium nitroprusside, thiocyanate levels should be monitored if the infusion is greater than _____ days, or at a dose greater than _______ mcg/kg/day, or if _________ dysfunction is present.
3
3
Renal
177
Where are the alpha-1 receptors located?
Vascular smooth muscle.
178
What does the activation of the SNS do to vascular smooth msucle where alpha-1 receptors are located?
Release of NE to activate alpha-1 receptors causes vasoconstriction of peripheral vessels which increase peripheral resistance and causes an increase in blood pressure.
179
Where are alpha-2 receptors located?
These are located in the CNS and they are the presynaptic autoreceptors.
180
What does activation of alpha-2 receptors in the CNS do?
It inhibits the release of NE which allows for vasodilation and reduced BP.
181
What were to two non-selective alpha blockers discussed?
Phenoxybenzamine and Phentolamine
182
What were the 3 non-selective alpha-1 blockers discussed?
Terazosin, Doxazosin, and Prazosin
183
What were the 3 selective alpha-1A blockers discussed?
Silodosin, Alfuzosin, and Tamsulosin
184
What was the 1 alpha-2 blocker discussed?
Yohimbine
185
What is the main indication for use for all alpha blockers?
Benign prostatic hyperplasia (BPH).
It can be used for essential hypertension but typically only used here if all other options have failed)
186
Alfuzosin bioavailability increases or decreases when taken with food?
Increases with food
187
Where are alpha blockers metabolized?
Hepatically
188
Where are alpha blockers eliminated from?
Urine and feces (Tamsulosin is urine only)
189
Does Tamsulosin (Flomax) bioavailability increase or decrease with food?
Decreases with food
190
What are the 4 main adverse effects of alpha blockers?
Fatigue, fluid retention, dizziness, and headache
191
What is a warning when starting out on an alpha blocker?
1st dose effect of orthostatic hypotension which can be offset by taking medication at night.
192
What were the 3 central acting alpha-2 agonist drug discussed?
Clonidine, Guanfacine, and Guanabenz
193
What is the MOA of the centrally acting alpha-2 agonist drugs?
Drugs like clonidine, Guanfacine, and Guanabenz stimulate presynaptic autoreceptors which leads to suppressed sympathetic outflow from the CNS.
194
What was the one centrally acting sympatholytic drug that is an analog of DOPA that was discussed in class?
Methyldopa
195
What is the MOA of Methyldopa?
Methyldopa is an analog of DOPA. When in the neuron, it is converted to alpha-methylnorepinephrine and replace the NE that is stored in the vesicles. When released into the synapse, it stimulates alpha-2 receptors which suppresses symapthetic outflow to the body.
196
What is the onset of action for Methydopa?
3-6 hours
197
What is the onset of Clonidine with tablets and the patch?
Tablets is 0.5-1 hr while the patch is 2-3 days.
198
Where is methyldopa metabolized?
Hepatically and intestinally
199
Where are all the CNS acting alpha-2 agonists metabolized?
Hepatically
200
Where are all the centrally acting sympatholytic drugs eliminated?
Urine
201
What are the 4 major indications for the use of the centrally acting alpha-2 agonist drug called Clonidine?
1. Essential hypertension
2. Hypertension in pregnancy
3. Vasomotor symptoms associated with menopause
4. Opioid withdrawl
202
What is the main indication for use for the centrally acting alpha-2 agonist drug called Guanfacine?
ADHD
203
What are the 2 indications for use for the centrally acting DOPA analog drug called Methyldopa?
1. Essential hypertension
2. Hypertension in pregnancy
204
What are the general adverse effects associated with centrally acting sympatholytic drugs like the alpha-2 agonists?
Sedation, dry mouth, sleep disturbances, nightmares, restlessness, depression, bradycardia, abdominal pain, nausea, and constipation
205
Which centrally acting alpha-2 agonist has the greatest risk of rebound hypertension when discontinued?
Clonidine
206
What can happen if a person abruptly discontinues the use of centrally acting sympatholytic drugs like alpha-2 agonists?
Withdrawal symptoms can occur and tapering should be used when discontinuing this medication.
207
What are the unique adverse effects associated with Methyldopa use?
Sedation, Parkinsonian signs, decreased libido, gynecomastia in males, hepatotoxicity, and hemolytic blood disorders.
208
What is the MOA for organic nitrates?
Organic nitrates produce nitric oxide in smooth muscle resulting in a potent vasodilator effect.
209
What were the 3 organic nitrates discussed?
Nitroglycerin, Isosorbide mononitrate, and isosorbide dinitrate
210
Out of the 3 organic nitrates, which has the highest bioavailabilty?
Isosorbide mononitrate with 100%. Nitroglycerin and isosorbide dinitrate are very variable.
211
Where are the organic nitrates metabolized?
Hepatically (nitroglycerin is also metabolized in RBC vascular walls).
212
How are all the organic nitrates eliminated?
Renally
213
What are the 3 indications for the use of the organic nitrate, Nitroglycerin?
1. Angina
2. Acute Coronary Syndrome
3. Hypertensive Emergency
214
What are the two indicatios for both isosorbide mononitrate and dinitrate?
Angina and heart failure
215
What are the common adverse effects seen with organic nitrates?
Orthostatic hypotension, dizziness, lightheadedness, tachycardia, palpitations, and headaches (more with nitroglycerin)
(THOLDS P)
216
What are the 2 contraindications for use with organic nitrates?
1. Current phosphodiesterase inhibitor use (Sildenafil/ Vardenafil)
2. Right ventricular infarction
217
T or F: Tolerance does not develop with organic nitrate use.
False. Typically pseudotolerance develops with rapid continuous exposure due to the neurohumoral counter-regulation with 24 hours. Real tolerance occurs in 72 hours.
218
How can tolerance be combated with organic nitrate use?
To prevent tolerance with organic nitrate use, a nitrate-free interval for 8-12 hours is given at night.
219
A patient taking aspirin, clopidogrel, atorvastatin, metoprolol, heparin, and nitroglycerin develops a headache at night. Which of the medications is likely causing the headache?
Nitroglycerin
220
A patient is admitted due to uncontrolled hypertension. She was started on hydralazine along with her home medications including lisinopril, furosemide, nifedipine, hydrochlorothiazide, metformin, and atorvastatin. The PCP notices that the patient is experiencing reflex tachycardia following the addition of the hydralazine. What medication can be changed or added to counter this action?
Add a beta blocker like metoprolol 25mg BID
221
A PCP approaches with regarding the initiation of a clonidine patch in a patient with uncontrolled HTN with noncompliance. The PCP is unfamiliar about the specifics. What is an important characteristic to mention?
The onset ranges from 2-3 days
222
T or F: For the metabolism of ACE-inhibitors like Enalapril or Ramipril, many are ester-containing prodrugs that require hepatic metabolism in order to be active.
True
223
Where are ACE-Is excreted from?
Kidneys mainly
224
Out of the 5 ACE-Is that we need to know, which ones are prodrugs?
Benazepril (Lotensin), Enalapril (Vasotec, Epaned), and Ramipril (Altace)
225
Which ACE-i is only available in an IV formulation?
Enalaprilat (Vasotec IV)
226
How are ARBs excreted?
Renally
227
Out of the ARBs we need to know, which one is a prodrug?
Olmesartan
228
T or F: Most ARBs are dosed 1x per day while Losartan is dosed 4x per day.
False. Losartan has a shorter half-life compared to the others but can be dosed 2x per day, not 4.
229
________ arteriole returns filtered blood from the glomerulus to the kidney and back to general circulation.
Efferent
230
_______ _______ is the blood filtering component of the nephron. It consists of the glomerulus and Bowman's capsule.
Renal Corpuscle
231
______% of Americans have high blood pressure. The prevalence of high blood pressure increases with _______ and is higher in patients who are ________.
46%
Age
Black
232
T or F: Early life stressors can increase the risk for cardiovascular disease.
True!
233
What is circadian dipping and how is it related to black people and the treatment of their hypertension?
Circadian dipping is when the blood pressure dips to its lowest point during sleep. Black people have less dipping which increases the risk for cardiovascular disease.
234
T or F: Essential/Primary HTN can be cured but cannot be controlled.
False. Essential HTN can be controlled but not cured.
235
T or F: Secondary HTN is caused by medications or comorbid diseases and can be cured and/or managed.
True
236
What are the 6 general risk factors for primary hypertension?
1. Genetics
2. Obesity
3. Excess sodium intake
4. Low Potassium intake
5. Lack of physical activity
6. Excess alcohol intake
237
What are some prescription medications that can cause secondary hypertension?
Amphetamines, oral contraceptives, NSAIDs, and systemic corticosteroids
238
What are some OTC medications that can cause secondary hypertension?
Caffeine, decongestants (mostly alpha agonists so this makes sense), and NSAIDs.
239
T or F: Kidney disease can contribute to secondary hypertension.
True
240
What is Obstructive Sleep Apnea?
This is a condition in which the body is not able to properly breathe during sleep leading to decreased oxygen levels increasing oxidative stress.
241
What are the current and new treatments for obstructive sleep apnea?
Weight loss, CPAP machine, surgery, and/or oral appliances. The new drug approved for this is called Zepbound (Tirzepatide).
242
Hypertension is associated with an increased risk for ____________________.
Cardiovascular disease (CVD)
243
For each _______ mmHg systolic increase or ____ mmHg diastolic increase, the risk for CVD doubles.
20
10
244
What are the 8 end-stage damages that can occur due to uncontrolled hypertension?
1. Cardiovascular disease
2. Angina
3. MI
4. Heart failure
5. Stroke
6. Kidney disease
7. Peripheral arterial disease
8. Abdominal aortic aneursym
245
What is the leading cause of death in the world?
Cardiovascular diseases
246
What are some modifiable risk factors for CVD?
Smoking, diabetes, dyslipidemia, obesity, low fitness, and poor diet
247
What are some fixed risk factors for CVD?
Male sex, CKD, family history of CVD, increased age, low socioeconomic status, obstructive sleep apnea, and stress
248
Most individuals with hypertension do not have any symptoms. However, some people do. What is the most common symptom that people experience with hypertension?
Headache
249
T or F: ACC/AHA guidelines suggest a repeat evaluation every 6 months is reasonable for patients with a normal blood pressure to be rechecked.
False. It is every 1 year.
250
If a hypertension diagnosis is made, several tests should be done to facilitate _________ _____ _____ __________.
CVD risk factor profiling. This allows us to establish a baseline for medication use, screen for possible secondary causes of HTN, and evaluate end-organ damage.
251
How did the 2017 guideline change the recommendation for the diagnosis of hypertension?
Hypertension used to be defined as 140/90 but now it is 130/80.
252
What was the SPRINT trial?
This was the landmark trial that led to the change in the diagnostic criteria for hypertension (now 130/80). The study showed that the incidence of CVD was decreased when a lower blood pressure was treated with medication.
253
In order to make a proper HTN diagnosis, an average of ____ to _____ measurements need to be obtained on ____ to _____ seperate occasions.
2 to 3
2 to 3
254
What is considered a normal blood pressure?
Less than 120 systolic and less than 80 diastolic
255
What is considered an elevated blood pressure?
Between 120-129 systolic and less than 80 diastolic
256
What is considered Stage 1 Hypertension?
Between 130-139 systolic or between 80-89 diastolic.
257
What is considered Stage 2 Hypertension?
140 or greater systolic or 90 or great diastolic
258
What is the definition of orthostatic hypotension in terms of mmHg decrease?
Decrease of greater than 20 mmHg systolic OR decrease of greater than 10 mmHg diastolic
259
For treating hypertension, the goal is to reduce ________ and ________ related to target-organ damage.
Morbidity and Mortality
260
What is the primary purpose of HTN therapy?
Reducing the risk for CVD or events.
261
T or F: A sustained 12 mmHg reduction in systolic blood pressure over 10 years will prevent 3 deaths in every 11 patients treated.
False. It will prevent 1 death in every 11 patients treated.
262
What is the treatment goal for blood pressure for ALL patients?
Less than 130/80 mmHg
For those 65 and older we just say less than 130 systolic because diastolic will typically follow
263
What is an average BP of 136/78 mmHg classified as?
Stage 1 HTN
264
What is an average BP of 124/68 mmHg classified as?
Elevated
265
What is an average BP of 156/88 mmHg classified as?
Stage II HTN
266
What is an average BP of 138/96 mmHg classified as?
Stage II HTN
267
In terms of interpreting guidelines for medication use, what does COR and LOE mean?
COR means class of recommendation going from Class I (strong) to class III (strong harm) and measures the strength of the recommendation. LOE means level of evidence going from Level A and level C-EO and measures the quality of the recommendation based on clinical studies.
268
What are some non pharmacological treatments for hypertension?
1. Lose weight- 1 kg lost is 1mmHg decrease. Aim for IBW
2. Health Diet- DASH diet
3. Decrease sodium- less than 1,500mg per day or reduce by 1,000mg per day
4. Increase exercise- 90-150 min/week of aerobic exercise
5. Increase dietary potassium intake- 3,500-5,000mg from diet
6. Limit alcohol
269
Someone presents with an elevated BP (120-129/80). What is the next step?
Counsel on nonpharmacological therapies. Reassess BP in 3-6 months.
270
Someone presents with stage I HTN (130-139/80-89), what is the next step?
Assess clinical ASCVD past medical history or estimate the 10 year CVD risk.
271
If someone presents with stage I HTN and it was found they have a 10-year CVD risk of 18.3%, what is the next step?
Counsel on nonpharmacological therapies and start a blood pressure medication. Reassess in 1 month.
272
What causes cardiovascular diseases of artherosclerotic origin?
Atherosclerosis causes the arteries to narrow, weaken, and be less flexible. Basically, fatty buildup lines the artery walls which results in plaque. It can rupture and cause clots or the body can clot the plaque so it does not break open.
273
When it comes to initiating therapy for HTN, what rule do you want to follow?
Start slow and titrate up accordingly.
274
What are the 6 clinical definitions of atheroscleotic cardiovascular disease (ASCVD)?
1. Acute Coronary Syndrome
2. Stable or Unstable Angina
3. Stroke or Transient Ischemic Attack
4. History of MI
5. Coronary or other Arterial Revascularization
6. Periphereal Arterial Disease of Artherosclerotic Origin
275
In stage 1 HTN, starting with just 1 medication is good unless there are compelling indications that say otherwise. What are those two indications?
Heart failure and Post MI
276
If someone is diagnosed with stage II hypertension, how do you know if you start 1 or 2 medications?
Any compelling indication that signifies more than 1 medication or a BP that is 20/10 mmHg greater than goal. Anything above 150/90 will likely need 2 medications to start.
277
T or F: Most patients will require multiple agents for BP control.
True
278
What was the Hygia Chronotherapy trial?
This trial looked at the proper time to dose antihypertensive medications (am vs pm). It was found that PM dosing improved BP control and reduced CVD events. However, other studies have said otherwise.
279
T or F: If a person is diagnosed with HTN and it is not under control, they should follow-up and be monitored every month.
True
280
What are the 4 classes of antihypertensives that are the 1st line therapies?
A. Thiazide Diuretics
B. Angiotensin Converting Enzyme Inhibitors (ACE-is)
C. Angiotensin II Receptor Blockers (ARBs)
D. Calcium Channel Blockers
281
When starting older adults (65 and older) on antihypertensive medication, what are some things to keep in mind?
Consider their other conditions, cognition, and adverse effects. Have caution with drugs that cause orthostatic hypotension or syncope. When the medication is started make sure to start a low dose and titrate up slowly.
282
______ or ________ are preferred without the presence of compelling indication for black people.
Thiazide diuretics
CCB
283
What is preeclampsia?
This is a dangerous form of hypertension during or after pregnancy that poses significant risk to the mother and the fetus.
284
What is the BP for gestational hypertension?
BP of 140 or greater/90 mmHg that occurs after 20 weeks of pregnancy.
285
What are the 3 antihypertensive medications that are safe to use during pregnancy?
Methyldopa, Nifedipine, and Labetalol (may use hydralazine)
286
What antihypertensive drugs should absolutely not be used during pregnancy?
ACE inhibitors, ARBs, DRIs, and Aldosterone Antagonist
287
What is heart failure with reduced ejection fraction?
This is when the left ventricle of the heart cannot pump blood effectively to the body. 40% or less of the blood within the left ventricle is pumped out.
288
What two medications must someone with HTN and heart failure with reduced ejection fraction be treated with?
ACEi/ARBs/or ARNIs + Beta-blocker (bisoprolol, carvedilol, or metoprolol succinate)
289
What class of drugs should absolutely be avoided in those with HTN and heart failure with reduced ejection fraction?
Non-DHP CCBs like Diltiazem and Verapamil
290
For someone that has HTN and is post MI, what two medications must be used?
ACEi/ARBs + cardioselective beta blocker (atenolol, metoprolol)
291
What is the definition of chronic kidney disease?
This is a GFR less than 60 mL/min for at least 3 months.
292
What is considered macroalbuminuria?
This is a condition where there is an abnormally high level of albumin in the urine, which can indicate kidney damage. This is an albuminuria score of 300 or greater.
293
At patient with CKD stage 3 and hypertension presents to the clinic with HTN. What medication should they be on?
ACEi or ARBs
294
A patient with CKD stage 2 and an albuminuria score of 420 mg/g presents to the clinic with HTN. What medication should they be on?
ACEi or ARBs
295
A patient with a CKD score of stage 1 with GFR of 105 mL/min and an albuminuria score of 26 mg/g appears to the clinic with HTN. What medication should they be on.
As this patient does not have CKD and has normal levels of albumin in their urine. This means we can start them on any 1st line antihypertensive medication. It does not have to be an ACEi or an ARB specifically.
296
What is the definition of resistant hypertension?
BP greater than 130/80 with 3 prescription antihypertensive medications at optimal doses.
OR
BP at the goal of 130/80 but 4 or more antihypertensives medications are needed.
297
A diabetic patient comes into the clinic with HTN. What medication is appropriate for them?
Any first line medication works unless they have an albuminuria score greater than 300 which tells us to give an ACEi or ARB
298
What medications should be given for HTN in secondary stroke prevention?
Thiazide diuretic or ACEi/ARB or a combination of both.
299
T or F: Compelling indications should be the primary consideration when choosing which pharmacotherapy to select.
True!
300
Patient presents with an average BP of 136/82 and a 10yr ASCVD risk of 7%. What stage is this and are medications needed?
This is stage I HTN and no medication would be recommended at this point. Nonpharmacological therapies should be counselled on.
301
Patient presents with an average BP of 132/76 and is post-MI. What stage is this and are medications needed?
This is stage I HTN and medication is needed as this patient has clinical ASCVD. As the post-MI is a compelling indication, this patient needs an ACEi/ARB paired with a cardioselective beta-blocker.
302
Patient presents with an average BP of 158/96. What stage is this and are medications needed?
This is stage II HTN and medication is needed. They are above the 20/10 2 medication indication meaning they need to start two antihypertensive medications. It could be a thiazide with an ACEi/ARBs or CCB.
303
Patient presents with an average BP of 142/86 and CKD stage 3. What stage is this and are medications needed?
This is stage II HTN and a compelling indication with the CKD stage 3. This patient needs an ACEi/ARB. Since the patient is not above the 20/10 2 medication mark, they can stay on this and reassessment can be completed.
304
Patient presents with average BP of 136/70, diabetes mellitus, and an albuminuria score of 334 mg/g. What stage is this and are medications needed?
This is stage I HTN and the patient has a compelling indication of DM and albuminuria score greater than 300. We could always calculate 10 year ASCVD score to help. I would recommend an ACEi/ARB.
305
What was the ALLHAT trial?
This trial compared the 1st line antihypertensives agents to see which was more effective. It showed no significant differences between the medications which is why there are 4 classes of 1st line antihypertensive medications.
306
T or F: Between the two thiazide diuretics, hydrochlorothiazide is 1.5x as potent as chlorthalidone.
False. Chlorthalidone is 1.5x more potent than hydrochlorothiazide.
307
What is the dosing for chlorthalidone (Hygroton)?
12.5-25 mg daily
308
What is the dosing for hydrochlorothiazide (Microzide)?
12.5-25 mg daily
309
What is the maximum dose for chlorthalidone (Hygroton)?
25 mg daily
310
What is the maximum dose for hydrochlorothiazide (Microzide)?
50 mg daily (25mg is preferred)
311
When should thiazide diuretics be dosed?
They should be dosed in the morning to avoid nocturnal diuresis.
312
T or F: Thiazide diuretics are the preferred first line treatment for secondary stroke prevention.
True
313
What are the 5 most common adverse effects associated with thiazide diuretics?
Increased urination, hyponatremia, hypomagnesemia, hypokalemia, and HYPERcalcemia.
314
What is the one contraindication for the use of thiazide diuretics?
Anuria (unable to produce urine)
315
What are the 4 main drug interactions with thiazide diuretics?
1. Antidiabetic agents
2. Lithium
3. NSAIDs
4. SSRIs
316
T or F: Sulfonamide hypersensitivity do not need to be cautioned or monitored when using thiazide diuretics.
False! This is a precaution as these drugs are derivatives of sulfonamides.
317
What is the brand name for the ACE-inhibitor that has both lisinopril and hydrochlorothiazide in it?
Zestoretic and Prinzide
318
What is the dosing for Ramipril (Altace)?
2.5 mg daily
319
What is the maximum dose for Ramipril (Altace)?
20 mg daily
320
What is the dosing for Enalapril (Vasotec/Epaned)?
5-10 mg daily
321
What is the maximum dose for Enalapril (Vasotec/Epaned)?
40 mg daily
322
What is the dosing for Benazepril (Lotensin)?
10 mg daily
323
What is the maximum dose for Benazepril (Lotensin)?
40 mg daily
324
What is the dosing for lisinopril (Prinivil/Zestril)?
5-10 mg daily
325
What is the maximum dose for lisinopril (Prinivil/Zestril)?
40 mg daily
326
What is the dosing for Lisinopril/HCTZ (Zestoretic/Prinzide)?
10/12.5 mg daily
327
What is the maximum dose for Lisinopril/HCTZ (Zestoretic/Prinzide)?
80/50 mg daily (40mg preferred)
328
What are the common adverse effects associated with ACE-inhibitors AND ARBs?
Hyperkalemia, increased serum creatinine levels that are transient and should return in 1 month, dry cough (not with ARBs) and angioedema due to increased bradykinin (less with ARBs), and acute hypotension in older population.
329
What is the black box warning associated with ACE-inhibitors and ARBs?
Avoid during pregnancy and be cautious with those of child bearing age.
330
How are ACEis and ARBs actually renoprotective?
ACEi/ARBs block the effects of angiotensin II from causing efferent arteriole constriction and induce vasodilation to decrease glomerular pressure.
331
Under normal conditions, does the afferent arteriole or the efferent arteriole that supplies the nephron have a larger diamater?
The afferent arterioles have a larger diameters compared to the efferent arteriole which allows more blood to enter the glomerulus. This increased blood flow increases the glomerulus filtration rate (GFR). The efferent arterioles are smaller to regulate the resistance to blow leaving the glomerulus. Angiotensin II acts on the efferent arteriole causing vasoconstriction and increased glomerular pressure.
332
What are the 3 contraindications for ACE-inhibitor use?
History of ACE-i induced angioedema, history of hereditary angioedema, and bilateral renal artery stenosis.
333
T or F: A person presenting with hyperkalemia does not need to be monitored when put on an ACE-inhibitor.
False. Persons with hyperkalemia need to be precautioned and monitored as this is an adverse effect of using ACE-is. Additionally those with CKD need to be monitored as well.
334
What are the main drug interactions with ACE-inhibitors and ARBs ?
ARBs, ACEis, DRis, and ARNIs can NEVER be used together!!!!
Lithium
NSAIDs
Drugs causing hyperkalemia like K+ sparing diuretics, aldosterone antagonist, trimethoprim, SGLT-2 inhibitors, and heparin.
335
What is the triple threat of medications?
NSAIDs- constrict afferent
ACEis/ARBs- dilate efferent
Thiazides- lower blood volume
With the 3 together, they will disrupt the kidney's ability to maintain hemodynamics. It will reduce GFR and could cause potential acute kidney injury.
336
What is the brand name for Losartan/HCTZ?
Hyzaar
337
What is dosing for Losartan (Cozaar)?
25-50 mg daily
338
What is the maximum dosing for Losartan (Cozaar)?
100 mg daily
339
What is dosing for Olmesartan (Benicar)?
20 mg daily
340
What is the maximum dose for Olmesartan (Benicar)?
40 mg daily
341
What is the dosing for Valsartan (Diovan)?
80-160 mg daily
342
What is the maximum dosing for Valsartan (Diovan)?
320mg daily
343
What is the dosing for Irbesartan (Avapro)?
150 mg daily
344
What is the maximum dose for Irbesartan (Avapro)?
300 mg daily
345
What is the dose for Losartan/HCTZ (Hyzaar)?
50/12.5 mg daily
346
What is the maximum dose for Losartan/HCTZ (Hyzaar)?
100/25 mg daily
347
What is the 1 contraindication for the use of ARBs?
Bilateral Renal Artery Stenosis
348
Is angioedema a contraindication for ARBs use?
No. It is a precaution that needs to be monitored, but avoid in those who have had angioedema with ARBs before.
349
What was the ONTARGET trial?
This trial showed that ARBs and ACEi have similar efficacy in high risk patients while putting both together leads to greater risk of acute kidney injury.
350
What is the brand name for the Dihydropyridine CCB amlodipine- benazepril?
Lotrel
351
What is the dosing for amlodipine (Norvasc)?
2.5-5 mg daily
352
What is the maximum dose for amlodipine (Norvasc)?
10 mg daily
353
What is the dosing for Nifedipine LA (Adalat CC, Nifedical XL, Procardia XL)?
30-60 mg daily
354
What is the maximum dose for Nifedipine LA(Adalat CC, Nifedical XL, Procardia XL)?
90 mg daily
355
What is the dosing for Amlodipine-Benazepril (Lotrel)?
2.5/ 10 mg daily
356
What is the maximum dosing for Amlodipine-Benazepril (Lotrel)?
10/40 mg daily
357
T or F: Short acting dihydropyridines should be avoided for the treatment of hypertension.
True! Use long acting dihydropyridines.
358
T or F: Non-DPHs are more potent peripheral vasodilators compared to DPHs.
False. DHPs are more potent peripheral vasodilators compared to non-DHPs.
359
What are the 6 common adverse effects associated with DPH CCBs like amlodipine and nifedipine?
Dose-related peripheral/pedal edema
Reflex Tachycardia
Dizziness
Headache
Flushing
Gingival hyperplasia
360
What are the precautions for the use for DHP CCBs like amlodipine (Norvasc) and nifedipine?
GERD as CCBs can relax the lower esophageal sphincter.
361
What are the 1 main drug interaction with amlodipine?
The major one is HMG-CoA Reductase Inhibitors. Avoid together or use simvastatin doses less than 20mg. It also is a major substrate and weak inhibitor of CYP3A4.
362
What is the major drug interaction for the non-DHPs CCBs like diltiazem or verapamil?
HMG-CoA Reductase Inhibitors like simvastatin. If used together, do not exceed 10 mg per day of simvastatin.
363
T or F: Nondihydropyridines are AB rated meaning they are interchangeable on a mg-per-mg basis.
False. These drugs are not interchangeable on a mg-per-mg basis,
364
What is the brand name for the 12 hour formulation of the non-DHP CCB diltiazem?
Cardizem SR
365
What are the brand names for the 24 formulation of diltiazem?
Cardizem CD, Cartia XT, Dilt XR, Taztia XT, Tiadylt ER, and Tiazac.
366
What is the brand name for immediate release verapamil?
Calan
367
What is the brand name for extended release verapamil?
Verelan and Calan SR
368
What is the brand name for the delayed onset/chronotherapeutic verapamil?
Verelan PM
369
What are the adverse effects associated with Non-DHP CCB like diltiazem and verapamil?
Bradycardia, constipation, and adverse effects associated with DPHs but at a lesser extent.
370
What is the dosing for furosemide (Lasix)?
20-80 mg daily in 1 to 2 divided doses
371
What is the max dose for furosemide (Lasix)?
Up to 160 mg per day
372
What is the dosing for Torsemide (Demadex)?
5-10 mg daily
373
What is the maximum dose for Torsemide (Demadex)?
Up to 200 mg daily
374
What are the two contraindications for use of non-DPH CCBs like Diltiazem and Verapamil?
Acute MI and Heart Block
375
T or F: If a patient does not have edema or symptomatic heart failure, it is inappropriate to use loop diuretics like furosemide or torsemide.
True. Loop diuretics are not first line for HTN. They are used when their is fluid accumulation.
376
What are the main adverse effects associated with loop diuretics?
Hypokalemia, hypomagnesemia, hyponatremia, hypocalcemia, hypovolemia, dehydration, and sometimes ototoxicity.
377
What are the 5 main drug interactions with loop diuretics?
Antidiabetic agents, lithium, NSAIDs, SSRIs, and volume depleting agents like SLGT-2 Inhibitors
378
Which diuretic class has the weak diuretic properties and is only used in combination with other diuretics?
K+ sparing diuretics.
379
What is the one K+ sparing diuretic we need to know?
Triamterene/HCTZ
380
What is the brand name for the K+ sparing diuretic called Triamterene/HCTZ?
Maxzide
381
What is the dosing for Triamterene/ HCTZ (Maxzide)?
25-37.5 mg daily
382
What is the maximum dose for Triamterene/ HCTZ (Maxzide)?
50-75 mg daily
383
What is the main contraindication and boxed warning for K+ sparing diuretics?
Hyperkalemia greater than 5.5 mEq/L
384
What is the dosing for the aldosterone antagonist called spironolactone (Aldactone)?
12.5-25 mg daily
385
What is the max dose for spironolactone (Aldactone)?
100 mg daily (50mg is preferred)
386
Spironolactone is a steroid. It has anti-_________ properties that produce side effects of gynecomastia in males and menstrual irregularities in females.
Androgen
387
What is the doseing for atenolol (Tenormin)?
25 mg daily or BID
388
What is the maximum dose for atenolol (Tenormin)?
100 mg daily
389
What is the dosing for metoprolol tartrate (Lopressor)?
50 mg BID WF
390
What is the maximum dose for metoprolol tartrate (Lopressor)?
100-200 mg daily
391
What is the dosing for metoprolol succinate (Toprol-XL)?
25-100 mg daily
392
What is the maximum dose for metoprolol succinate (Toprol-XL)?
50-200 mg daily (past 100mg of any metoprolol starts to affect beta 2 receptors as well)
393
What type of drug is propranolol?
This is a non-selective beta blocker that acts on beta 1, 2, and 3
394
What is the dosing for propranolol (Inderal) and propranolol LA (Inderal LA)?
80 mg daily (or BID for Inderal)
395
What is the maximum dose for propranolol (Inderal) and propranolol LA (Inderal LA)?
160 mg daily
396
What type of drugs are carvedilol and labetalol?
These are mixed acting a1 and b1+b2 blockers.
397
What is the dosing for Carvedilol (Coreg)?
6.25 mg BID
398
What is the max dose for Carvedilol (Coreg)?
25 mg BID
399
What is the dosing for Carvedilol phosphate (Coreg CR)?
20 mg daily
400
What is the maximum dose for Carvedilol phosphate (Coreg CR)?
80 mg daily
401
What is the dosing for labetalol (Normodyne/Trandate)?
100 mg BID
402
What is the maximum dose for labetalol (Normodyne/Trandate)?
800 mg daily divided into 2 doses
403
What is the box warning associated with beta blockers?
These drugs must be tapered off to avoid tachycardia and rebound hypertension.
404
T or F: Diabetes is not a precaution when it comes to beta blockers.
False. Beta blockers could cause hypoglycemia
405
What is a huge adverse effect of the non-DHP CCB called Verapamil (Verelan/ Calan)?
Constipation!!!!!
406
When pressure within the arteries rises, the blood flow to organs __________.
Increases
407
When resistance within the arteries rises, the blood flow to organs __________.
Decreases
408
T or F: Very small changes in the radius of an artery can lead to drastic changes to blood pressure.
True
409
What is the flow equation?
Flow= pressure/resistance
410
T or F: High acute resistance increases blood flow to organs.
False. High acute resistance decreases blood flow to organs.
411
In acute severe hypertensive emergencies there is _________ resistance which leads to low blood flow and low perfusion of tissues allowing for rapid end organ damage.
Increased
412
In terms of blood pressure, how is a hypertensive crisis defined?
There is really no formal definition for hypertensive crisis in terms of blood pressure. In 2018, it was said that a SBP greater than 180 or a DBP greater than 120 could be categorized as an emergency.
413
What is the definition of hypertensive urgency?
This is a very high blood pressure without evidence of end-organ damage
414
What is the definition of a hypertensive emergency?
This is a very high blood pressure with evidence of end-organ damage.
415
What are some common causes of a hypertensive crisis?
Surgery, preeclampsia, pheochromocytoma, therapy non-adherence, intoxicants like cocaine and amphetamines, or it may be idiopathic.
416
What is classified as a high and interventional blood pressure for postoperative patients?
SBP greater than 190 or DBP greater than 100 on two consecutive readings.
417
What is classified as a high and interventional blood pressure for patients with preeclampsia?
SBP greater than or equal to 169 or DBP greater than 109 on two consecutive readings.
418
End-organ damage occurs when the diastolic blood pressure is at _______ mmHg.
130
419
What are examples of end-organ damage that is caused by a hypertensive emergency?
Hypertensive encephalopathy
Hemorrhagic stroke/CVA
Cerebral edema
Acute coronary syndrome
Acute heart failure
Aortic dissection
Pulmonary edema
Acute Renal Failure
Glonerulonephritis
420
What is the goal for care in a situation of hypertensive urgency?
Control blood pressure to prevent end-organ damage.
421
How should blood pressure be decreased in a situation of hypertensive urgency?
A gradual controlled decrease in BP over 24--48 hours that should be manageable with oral agents.
422
What is the goal for care in a situation of hypertensive emergency?
Control blood pressure to stop end-organ damage.
423
How should blood pressure be decreased in a situation of hypertensive emergency?
Decrease SBP by 25% of the maximum then to 160/110-100 in the next 2-6 hours. A normal blood pressure should be achieved 24 to 48 hours. It will likely require IV agents and ICU admission.
424
How should blood pressure be decreased in a situation of hypertensive emergency specifically for aortic dissection and eclampsia?
Decrease by 25% in the first 15 minutes and then get SBP less than 120-140 in the first hour.
425
If aortic dissection, it is okay to target both pulse pressure and heart rate?
Yes. We try to decrease the heart rate and blood pressure to reduce the twist seen in the aorta.
426
What is the gold standard medication used in hypertensive crisis?
Nitroprusside as the onset is 5 seconds and the duration is 1-2 minutes. It is a potent arterial dilator. Need to monitor the cyanide toxicity with this drug.
427
Why is labetalol a good choice during an aortic dissection?
Labetalol is a mixed acting beta blocker that acts on alpha1 and beta 1 and 2. It produces vasodilation and decrease heart rate giving more time for life saving measures.
428
What is the MOA of esmolol?
This is a selective beta-1 blocker. It is not great for emergency hypertension but it is good for aortic dissections. It decreases the heart rate but have no effect on vasodilation
429
What is the MOA of the drug Nicardipine?
This is an L-1 calcium channel blocker that causes arterial and venous dilation. It is used in cerebral hemorrhage.
430
Where does nitroglycerin act?
It is mainly a potent venous dilator meaning it has little effect on systemic vascular resisitance and is therefore not great for typical arterial hypertension.
431
What is the drug Clevidipine?
This is an IV CCB that reduces BP when oral is not feasible or desired. Onset it 2-4 minutes with duration being 15 minutes.
