PHARM II Block II Specific Trivia Flashcards
1
Q
What is the greater predictor of CVD in pts older than 50 y/o
SBP or DBP
A
SBP!
Sustained elevated BP is directly correlated: Myocardial Infarction Angina Heart Failure Kidney Failure Early death secondary to CV cause Retinopathy
2
Q
What is the differnce between essential and secondary HTN
A
Essential Hypertension: 90% (no identifiable cause) Possibly Genetic Can only be controlled not cured Contributed mostly by obesity
Secondary Hypertension:
Results from comorbid disease or is drug-induced
< 10% of individuals have this type
Removal of the offending agent or treatment of comorbid disease should be first step in management
Renal dysfunction from chronic kidney disease or renovascular disease is the most common secondary cause
3
Q
What is the Tx approach to secondary HTN
A
Removal of the offending agent or treatment of comorbid disease should be first step in management
4
Q
What is the most common cause of secondary HTN
A
Renal dysfunction from chronic kidney disease or renovascular disease is the most common secondary cause
5
Q
What is the definition of resistant HTN
A
American Heart Association (AHA) Definition: “When a patient is not at their blood pressure goal despite use of optimal doses of three anti-hypertensives from different classes, ideally including a diuretic”
6
Q
What is the cause of Isolated Systolic HTN
A
Results from pathophysiologic changes in the arterial vasculature consistent with aging (arteriosclerosis)
7
Q
What is the criteria for Isolated systolic HTN
A
SBP > 140 and DBP< 90
8
Q
Higher pulse pressures indicated increased risk of…
A
Arterial stiffness and CV risk
9
Q
List as many CV risk fxs
A
Age (≥55 years for men to 65 years for women)
Diabetes Mellitus
Dyslipidemia: elevated LDL, total cholesterol or triglycerides; low HDL
Albuminuria: protein in the urine
Family History of Premature CV disease
Obesity (BMI ≥ 30 kg/m2)
Physical Inactivity
Tobacco Use
10
Q
What is the formual fr BP
A
CO x Total peripheral resistance
11
Q
MAP calculation
A
(2DBP+SBP)/ 3
Examply 120/80
160+120=280/3=roughly 90
12
Q
What effect does NO have on peripheral resistance
A
Decreases peripheral resistance
13
Q
What effect does prostycyclins, Kinins, ANP all have on peripheral vasc resistance
A
All decrease resitance
14
Q
What effect do thomboxanes, enodthelin both have on perifpheral vasc resist.
A
Increase resistance via vasocon
15
Q
What is the most influential contributor to homeostatic regullation of BP
A
RAAS system
Sympathetic nervous system activity is regulated largely by negative feedback via the baroreceptor feedback mechanism
16
Q
What three mechanism stimulate the release of renin
A
Low BP, Low fluid volume in the glomerulus, or increased B1 sympathetic stim.
17
Q
What is the effect of Angiotesin II
A
Stimulates aldosterone, mild vasocon, and increases NaCL and H2O reabsorption
18
Q
What are the baroreceptors of the Renin aldo system
A
Juxtaglomeluar cells (these also secrete renin)
19
Q
What are the important actions of Angio II
A
Vascular smooth muscle (constricts)
Adrenal cortex (aldosterone synthesis and release)
Kidney (increase Na+ re-absorption)
Heart (increase rate)
Brain (increases anti-diuretic hormone release)
20
Q
What is the MOA of Thiazide and Thiazide like diuertics
A
Mechanism of Action: inhibit sodium and chloride reabsorption in the early distal convoluted tubule (DCT) resulting in water retention in the tubule
Loss of sodium increases urine volume
Lowers BP by increasing Na+ and water elimination
With continued use the volume returns to normal but reduced peripheral resistance (PR) still keeps BP lower
21
Q
What must pts have in order for thiazide/like medications to work
A
Functioning kidneys (CrCL>30 or SCR<2.5)
Excception when in reduce renal function metolazone works and is the DOC
22
Q
What is the best tolerated HTN tx class of drugs
A
Thiazide/ Like meds
23
Q
Diuretics are most effective when combined with…
A
ACEI or ARBs
24
Q
Combining thiazieds with what other mediations can reduce Hypokalemia
A
Potassium sparing agents
Combinations include
Triamterene/Hydrochlorothiazide (Maxzide and Dyazide)
Amiloride/Hydrochlorothiazide (Moduretic)
Spironolactone/Hydrochlorothiazide (Aldactazide)
25
What is the MOA for ACEI
Inhibits the Renin-Angiotensin-Aldosterone System (RAAS) by inhibiting the conversion of angiotensin I to angiotensin II
Reducing :
Vascular smooth muscle constriction
Aldosterone synthesis and release
Na+ re-absorption
Heart rate
Anti-Diuretic Hormone (ADH) release
Also increase the availability of the vasodilator bradykinin by inhibiting its breakdown
26
What effect doe ACEI have on bradykinin
increase the availability of the vasodilator bradykinin by inhibiting its breakdown
27
Do ACEI impact heartrate
NO!
Lowers blood pressure by reducing peripheral vascular resistance without increasing cardiac output, rate, or contractility
28
What is the role of bradykinin
Bradykinin is involved in the production of nitric oxide and prostaglandins (Ex: prostacyclin)
Nitric oxide and prostacyclin are vasodilators
29
What is the hypothosised reason for a cough and angioedema with ACEI Tx
Bradykinin and a related substance “substance P” are probably responsible for inducing a cough and angioedema
30
Are ACE effective in African american populations
Reduced effectiveness unless combined with a CCB or diuretics
31
What are the ADE of ACEI
```
Taste disturbance
HOTN
Hyper K+
Increased Cr and BUN
(Up to 20% increase is acceptable)
```
32
What is the only C/I to ACEI
Renal artery stenosis
Should also monitor K+, Cr, BUN and baseline and two weeks into Tx
33
When Rx an ACE what is the F/u and monitoring required
Monitoring: potassium, serum creatinine, and BUN at baseline and two weeks into therapy
34
Can ACEI be used in pregnancy
Nope preg CaT D
35
A pt on an ACEI gets pregnant, what do you do
DC the ACEI
36
What is the renal trifecta
Diuretics: reduce plasma volume and concentrate blood urine (increase SCr)
+
ACEI/ARB: blocks renal compensation and dilates efferent arteriole
+
NSAIDs: inhibits prostaglandins and bradykinin, producing vasoconstriction of the afferent renal arteriole
Result: drug induced acute kidney injury
37
What is the MOA of ARBs
Antagonize angiotensin II at the AT1 receptor
AT1 predominates in the vasculature
Prevents the vasoconstrictor effects of this receptor
Block aldosterone secretion, leading to decrease salt and water retention
AT2 produces arteriolar and venous dilation
38
What is the clinical use of ARBs
Reserve ARBs for patients that do not tolerate ACEIs
39
Should ACE and ARbs be used simultaneously
NO!
40
What are the pros and cons of ARBs over ACEI
ARBs benefits
-Low/No bradykinin associated cough
-Low/No angioedema issue
ARBs drawbacks
-Cost $$$ compared to ACEIs
-Not as much clinical data as ACEIs
Both ARBs and ACEIs
Category D in pregnancy
Caution with renal stenosis
41
What is the MOA of Aliskiren
Direct Renin Inhibitor (DRI)
Mechanism of Action:
- Inhibits renin
- Reduces angiotensin I and II and aldosterone
- Is not limited by angiotensin II production through non-ACE dependent pathways or indirect activations of AT2 receptors
42
CAn aliskiren be used in pregnancy
No
43
What are the ADE of aliskiren
Adverse Effects
- Diarrhea (at high doses)
- Cough and angioedema, but less than ACEIs
- Hyperkalemia
- Increased serum creatinine and BUN
- Hypotension in volume and/or salt depleted patients
- Hypersensitivity to sulfonamide component
44
What adrugs should be avoided in aliskirin Rx
Avoid combined use of ARBS or ACEI
Avoid NSAIDs (renal trifecta)
Avoid lithium
45
What is the MOA of A1 blocking agents
Mechanism of Action:
Selectively block α1 receptors and prevent vasoconstrictor actions of these receptors
Decrease peripheral vascular resistance and relax both arterial and venous smooth muscle on both arteries and veins (mainly arteries)
46
Should A1 blockers be used as mono tx fror HTN
No and its rarely the 1st step
47
What med class can be used in pts with BPH and HTN
Or have resistant HTN already on diuretic, BB, and ACEI
A1 blockers
48
Is prazosin acceptable to use in BPH
NO it is howeever indicated for PTSD
49
What are the ADE of A1 Blockers
```
Ortho HOTN
Tachy reflex
Edema-prazosin (may require a diuretic)
HA/Dizzy/wkness
Inhibition of ejaculation
```
50
What is the MAO of A2 agonist
Stimulate presynaptic α2 receptors in the CNS inhibits (via negative feedback) sympathetic outflow to the heart, kidneys, and peripheral vasculature causing peripheral vasodilation
Reduction of sympathetic outflow will result in a net decrease in blood pressure
51
A2 agonists are best used with what other drugs
best used in combination with agents that have different MOA (diuretics and ACEI) and not with adrenergic blockers
52
What are the ADE of A2 agonist
Drowsiness
Dry mouth
Edema/fluid retention
53
What are the ADE of clonidine
Its and A2 agonsit
So Dry mouth
Sedation
Constipation
Ortho HOTN
54
Can you abruptly wthdrwl clonidine?
NO!
Abrupt withdrawal of doses >1mg/day can result in life-threatening hypertensive crisis mediated by increased sympathetic nervous activity
Withdrawn gradually while other anti-hypertensive agents are being initiated
Symptoms: nervousness, tachycardia, headache, and sweating after omitting 1 or 2 doses
55
If a pt is taking clonidine and starts to get depressed
What should you do
Withdrwl clonidine
56
Is clonidine safe in geriatrics
No
57
What effect do Clonidine and TCAs have on eachother
```
Tricyclic antidepressants (TCAs) may block the antihypertensive effect of clonidine and potentiate anticholinergic effects
(Example: amitryptyline)
```
58
When methyldopa is used to treat HTN in a pregnant pt
How should it be dosed
TID or QID
59
What is the MOA of Bblockers
Mechanisms of Action: antagonize β receptors
Antagonizing β1 receptors in the heart causing decreased cardiac output (decrease rate and force of contraction)
Decrease sympathetic outflow from CNS and inhibit the release of renin secretion from the
Kidney
-Results in the reduction of angiotensin II and aldosterone causing reduced peripheral resistance and sodium and water retention
60
What are the clinical outcomes of using BB
reduce systolic BP by 10-20mm Hg and diastolic pressure by 10-15mm Hg
61
What are the plethora of uses for BB
HTN , Angina, Select arrythmias, CF, MI, Hyperthyroid, Migraine HA, Pheos, Gluacoma
62
Where are B1 and B2 receptors found
β1 receptors are primarily on the heart
β2 receptors
Primarily located at the bronchial tree, skeletal muscle blood vessels, kidney, and liver
-Not very important for the treatment of primary hypertension, but are of concern in asthma and diabetes
-Activated β2 receptors causes bronchial dilation and can increase blood glucose due to glycogenolysis
-β2 receptors antagonist restrict bronchioles and reduce glucose production ( which is a problem for asthma and lung pts)
63
What is the MOA of ISA BB
Partial BB agonsist
Option for patients who need a beta blocker but experience significant bradycardia from a non-ISA agent
-Avoid use post myocardial infarction
64
Can ISA BB be used in MI
NO
| Do not use acebutolol pindolol or penbutolol
APP
65
Which two BB have high lipid soluablilty and what does ADE does this cause
Propranolol and Bisprolol
Lipophilic agents enter the CNS better and may result in more cases of:
Drowsiness, mental confusion, nightmares, and depression
66
If you wanted to avoid CNS S/s of BB which two would you use and why
Atenolol and Nadolol
They have the lowest lipid soluability
67
What effect do BB have on glycemia
mask symptoms of hypoglycemia and reduce the ability to recover from hypoglycemia (sympathetic activation of beta receptors)
So avoid in DM
68
What effect do BB have on Asthma Pts
non-cardioselective β-blockers can make bronchoconstriction worse, and block the action of bronchodilators
So caution with proprnolol, nadolol, and timolol
(PNT)
69
Do BB effect erections
Yes may decrease libido or cause ED
70
What would happen if you rapidly withdrew BB
may induce angina, myocardial infarction, and even sudden death in patients with ischemic heart disease
71
Should BB and CCB be used together
may produce bradycardia if used with non-dihydropyridine calcium-channel blockers (Non-DHP CCB) such as verapamil or diltiazem
72
Can BB be used with NSAIDs
may impair the hypotensive effects of beta blockers by interference with the auto regulation of renal blood flow
73
Can BB be used with clonidine
Yes, but increased risk of clonidine withdrawal hypertensive crisis if stopped before beta blocker can be initiated (may have to taper for 1 week)
74
How long should clonidine be tappered with BB admin
1 week, if not it can cause HTN crisis
75
What is the MOA of mixed A1 and NSBB
In hypertension, decrease’s rate and strength of contraction of heart without reflex vasoconstriction (α1 antagonism)
In CHF, decreases afterload by inhibiting vasoconstriction (α1 antagonism) while decreasing SNS tone via β-blockade
76
What are the two mixed A1 and NSBB
Carvedilol and Labetolol
77
What are the 3 ISABB
Acebutolol, Pindolo, penbutolol
78
What are the 3 B1 selective BB
Atenolol, metropolol, bispropolol
79
What are the three NSBB
Propranolol
Nadolol
Timolol
80
What is the MOA of CCB
Block the inward movement (L-type calcium channel) of calcium ions through the L channels of arterial smooth muscle cells and cardiac cells of the coronary and systemic arterial vasculature
Arteriolar vasodilators that cause a decrease in smooth muscle tone and vascular resistance
81
What are the 2 types of CCB
Dihydropyridines (DHP):
-Minimal direct cardiac effect, may cause compensative tachycardia
End in “pine”; amlodipine, nicardipine, felodipine
Non-dihydropyridines (Non-DHP):
- More selective for myocardium
- Negative inotrope
82
What type of CCB are Preferred in patients with fast heart rates and even for rate control with atrial fibrillation who cannot tolerate a beta blockers
Non DHPs
- Verapamil
- Diltiazem
83
What is the least selective NONDHP CCB
Verapamil
Significant effects on both cardiac and vascular smooth muscle cells
84
What is the clinical use of Verapamil
Angina, supraventricular tachyarrhythmia, and prophylaxis for migraine!! And Cluster headaches!!
85
What is the clinical use of diltiazem
supraventricular tachyarrhythmia (decrease rate in atrial flutter and atrial fibrillation)
86
What is the major diff between NONDHP and DHP CCB
DHPs mostly vasodilate
NonDHPS decease HR, AV node conduction and contractility and also vasodilate
87
CCB are most effective in what pt population
BLACK PEOPLE
88
Should CCB be used in HF
Caution!
Amlodipine touted as safe in patients with hypertension and advanced heart failure
Studies have shown a 38% increased risk of heart failure with amlodipine vs. diuretic
89
A pt has HTN and Asthma
What drug is best
CCB not BB
90
A pt has HTN and DM
Use what drug
CCB not BB ( they mask glycemia)
91
A pt has HTN and angina
Use what drug
CCB
92
A pt has HTN and PVD
Use what drug class
CCB
93
What is the drug class that can treat Isolated sys HTN
CCB
94
What is dihyropyridines with CCB
Watch for ankle edema, flushing, dizziness, headache, and fatigue
Nifedipine: gingival enlargement
Avoid high dose short-acting CCBs because of increased risk of MI due to excessive vasodilation and marked reflex tachycardia (Nifidipine)
95
You just started a pt on verapamil and now they cany poop, is this normal
Yes Verapamil causes constipation
96
What medications should be avoided when RX CCB
Digoxin with Verapamil or Diltiazem
May increase digoxin (anti arrhythmic agent) level by 20-70%
Beta blockers with Verapamil or Diltiazem produce additive negative inotropic effects (bradycardia)
Only Dihydropyridine CCBs can be safely combined with beta blockers
(So dont use verapamil or diltizem with BB)
97
What is the MOA of hydralazine and minoxadil
Direct Arterial Vasodilators
Mechanism of Action: directly relaxes arteries and arterioles in smooth muscle and decreases peripheral vascular resistance and arterial blood pressure
98
What are the clinical uses of hydralazine
Reserves for severe HTN in refractory HTN +3 meds
Or used in HTN emergency to rapidly drop the BP
Can be used safely in pregnant pts
Also used in combo with isosorbide dinitrate to treat HTN and HF in black pts
99
A pregnant black pt started a recent HTN med but cant remember the name
Today she presetns with a headache, TachyHR, Nausea, diaphories, palpations, and angina, you notice a butterfly like rash on her face that spares the corners of her mouth
What is the medication she most likely started on
Hydralazine
100
What is the clinical use of minoxidil
Used when maximal doses of hydralazine are not effective or in patients with renal failure and severe hypertension who do not respond well to hydralazine
Greater reflex sympathetic stimulation and sodium and water retention
Also can be used topically for male pattern baldness
101
You recently started a pt on hydralazine for refractory HTN
Today they present with Renal failure and severe HTN
What drug should be used now
Minoxadil
102
What are the ADE of minoxidil
TachyHR, palpations, angina, sweating, and edema,
Same as hydralazine
ALSO MAJOR HAIR GROWTH
103
What are the 1st line agents to pharm tx of HTN
First-line agents include thiazide/thiazide-like diuretics, CCBs, and ACE inhibitors or ARBs
104
When mono tx vs 2 drug tx be used for htn
Single antihypertensive drug is reasonable in adults with stage 1 hypertension and BP goal <130/80 mm Hg with dosage titration and sequential addition of other agents to achieve the BP target
2 first-line agents of different classes is recommended in adults with stage 2 hypertension
105
In black adults with hypertension but without HF or CKD, including those with DM, initial antihypertensive treatment should include…
Thyazid diuertic or CCB
106
A pt presents with an elevated BP of 190/130 with LOC, possible aortic dissection, with pulm edema
Think
HTN crisis
| Admit, TX emergently
107
What are the S/s of HTN crisis
```
Stroke
Loss of consciousness
Memory loss
Crushing chest pain/ Heart attack
Damage to the eyes and kidneys
Aortic dissection
Angina (unstable chest pain)
Pulmonary edema
Eclampsia
```
108
What is the MOA of nitro
Forms free radical NO
Venous dilation more than arterial dialtion
Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure), may modestly reduce afterload
Dilates coronary arteries and improves collateral flow to ischemic regions
109
What are the 3 clin uses of nitro
Acute decomp HF ( WARM AND WET or COLD and DRY- inotrope alt)
HTN emergency ( Ideal choice for pts with ischemic HDz, MI, HTN s/p bypass, pulm edema)
Considered the preferred agent for preload reduction in patients with pulmonary congestion
110
What is Considered the preferred agent for preload reduction in patients with pulmonary congestion
Nitro
111
Why must nitro be stored in glass bottles
PVC tubing and bags may absorb nitroglycerin
Use glass bottles and special non-PVC tubing to administer IV nitroglycerin when possible (pre-mixed bottles)
112
You are in the ED treating a warm and wet HF pt, your collegue just administered nitro
What are the ADE of nitro tx
Severe HA, Vomitting, ICP, and methemoglobinemia
113
What is the MOA of sodium nitroprusside
mixed arterial–venous vasodilator, acts on smooth muscle increasing synthesis of nitric oxide to produce a balanced vasodilating action
Effectsd afterload more
114
What is considered DOC for most cases of hypertensive emergency
Sodium nitroprusside
115
Your in the ED treating a warm and wet HF pt
Your collegue just administered sodium nitroprusside
labs come back and the pt has poor renal function
What ADE is this pt at risk of
Cyanide poisoning
Combines with hemoglobin to produce cyanide and cyanmethemoglobin
Cyanide hepatically metabolized and thiocyanate renally excreted
116
What are the ADE of sodium nitroprusside
HOTN, Cyanide toxic, ICP
117
What is the MOA of Fenoldopam
Direct Dopamine Agonist
D1 agonist that bind with moderate affinity to α2 receptors
Rapid acting vasodilator
Decreases peripheral vascular resistance and BP secondary to increased renal blood flow, and natriuresis/diuresis
6 times more potent as dopamine in producing renal vasodilation
118
What is the clin use of fenoldopam
treatment in hospital, short-term (up to 48hrs) management of severe hypertension when rapid, but quickly reversible, emergency reduction of blood pressure is clinically indicated (HTN CRISIS)
119
A pt presents with HTN crisis, and you promptyl drop the BP with fenoldopam
What are the ADE you know must be aware of
Headache/flushing/dizziness
N/V
Reflex tachycardia
Hypokalemia
120
What is special about nicardipine
It can be in tablets and IV ( Iv dose not require a loading dose)
useful in patients acute with intracerebral hemorrhage/acute ischemic stroke, hypertensive encephalopathy, preeclampsia or eclampsia, acute renal failure, sympathetic crisis, and perioperative hypertension
121
What is special about enalaprilat
ACEI that can be used IV
Only ACEI available in IV formulation
Advantageous in patients who are in need of prolonged BP control
Titration difficult and hypotension can potentially develop in some patients
Avoid in patients with decompensated HF or acute MI, pregnancy, or bilat renal art stenosis
122
What is special about esmolol
Ultra short acting B1 selective BB
Useful in conditions related to severe tachycardia, and increased cardiac output, and severe post-op hypertension
Avoid in patients with decompensated heart failure,
123
What is special about labetolol
Mechanism of action: selective α1 and non-selective beta blocker
Used for both urgency (PO) and emergency (IV)
Does NOT cause reflex tachycardia (no increase in myocardial O2 demand) so it is preferred in coronary artery disease, acute dissection, end stage renal disease, acute intracerebral hemorrhage/acute ischemic stroke or MI
Does not reduce cerebral blood flow
124
Can enalaprilat cause angioedema
Yes
125
What is diuresis
C ondition that causes urine to be excreted, usually associated with large volumes
126
What is uremia
an accumulation of nitrogenous waste products in the blood due to impaired renal filtration
127
What is tubular secretion
process in which the nephrons produce and release substances (ions, acids, and bases) that facilitate sodium ion reabsorption and maintain acid-base balance
128
How much fluid is filtered at the glomerulas dialy
180L
129
What is a NML GFR
About 130mls/mil
130
What is the best overall index of kidney fx
GFR
131
What is widely used to estimate GFR
CrCl
132
What is the cockcroft-gault equation
CrCl= (140-age) x wt (kg) (O.85 for females)
All divided by (Scrx72)
133
What is the most accurate way to find a CrCl
24 hr urine
134
What is a NML CrCl
90-140
135
ADH works were
Collecting ducts
136
Where is the majority of sodium absorbed in the Nephron
In the PCT
137
Is the descending loop of henle permiable to sodium
No
138
Is the thick ascending loop of henle permeable to water
No
139
Where do loop directs have thier greatest effect
The thick ascending loop of henle
140
How do loop diruertics work on the loop of henle
Loop diuretics inhibit the co-transporter; which reduces the lumen-positive potential, causing an increase in urinary excretion of divalent cations in addition to NaCl
Loop diuretics are the most efficacious of all diuretic classes
141
Is the DCT permeable to water
Relatively impermeable to water
142
Where is calcium reabsobped in the nephron
In the DCT
143
What part of the nephron do thiazides work at
The DCT
144
Where do Sodium Channel blockers and aldosterone agonist work in the nephron
Collecting Duct
145
What are the clin used of Diuretics
Edema (e.g., secondary CHF, etc.) (i.e., primarily thiazides and loops)
Hypertension (i.e., primarily thiazides)
Acute renal failure
Hypercalcemia (i.e., loops)
Hypercalciuria (with renal stone
formation) (i.e., thiazides)
Glaucoma (i.e., Carbonic Anhydrous Inhibitors)
Mountain sickness (i.e., acetazolamide)
Acute brain injuries (i.e., mannitol)
146
What is the MOA of Carbonic Anhydrous Inhibitors
Mechanism of Action: increases sodium and water excretion by inhibiting the enzyme carbonic anhydrase in the proximal convoluted tubular cells
Results in increased Na+ excretion because H+ is no longer being excreted to combine with HCO3-
Loss of HCO3- causes hyperchloremic metabolic acidosis and decreased efficacy after several days therapy
147
After several days o acetazolamide Tx was is the pt at an increased Rsk of
Hypercholremic Metabolic acidosis
148
What are the clin uses of Acetazolamide
Tx open angle glaucoma (decreases production of aqueous humor)
Or mountain sickness
It works by decreasing the amount of CSF and pH of the CSF where carbonic acid is responsible for secreting bicarbonate
Creates a mild acidosis resulting in hyperventilation
(Prophylaxis)
Can also be used for absene SZR
149
Where is acetazolamide absorbed
absorbed well orally, not metabolized in the body, but excreted totally by the proximal convoluted tubules (PCT)
150
Your on a sumit in south america, and you treated your companions with acetazolamide for 5 days prior to accent to reduce SOB, pulm edema, cerebral edema..
One of your hikers has a sulfa allergy, and another has poor kindey function,
What are the ADE of acetazola,ide Tx
CNS: drowsiness, anorexia, headache, depression
Allergic rash (sulfonamide derivative)
Hypokalemia
Hyperchloremic Metabolic Acidosis
Kidney Stones: Ca2+ less soluble in an alkaline environment; risk increases 10 fold
151
Can a pt in liver failure take acetazolamide
No, should be avoided in pts with cirrhosis
152
Can a pt with COPD take acetazolmide
Should be used with caution
153
What is the MOA of mannitol
Osmotically active agent (largely confined to the extracellular space) that is filtered by the glomerulus but not reabsorbed causes water to be retained in these segments (PCT) and promotes a water diuresis
Increases urinary output secondary to increased plasma volume delivered to the kidneys resulting from a hypertonic plasma that draws fluid out of the tissues and promotes water diuresis (osmotic gradient that attracts water)
154
What are the two clin uses of mannitol
Tx of the oliguric phase of acute renal failure
And ICP
Also can be used to maintain urine flow in toxic states
(MUST BE GIVEN IV)
155
should pts in CHF get mannitol
No, it increases vascular fluid and can worsen the condition
156
What are the C/I for mannitol
active intracranial bleeding, pulmonary edema, or chronic edema due to cardio insufficiency
157
What is the loop diuretic that is safe to use in pts with sulfa allergies
Ethacrynic acid
158
What is the MOA of Loop diuretics
increases urinary output by selectively blocking the reabsorption of Na+ and Cl- (i.e., Na+/K+/2Cl- co-transporter) in the ascending loop of Henle
159
What does it mean to be a “high-cieling: diuertic like furosemide
Effacacy increases with dose
160
What is teh DOC in reducing extra volume in HF
Loop diuretcs
161
What is the drug class of diuretics that can treat
Acute renal failure
Hyperkaleia
Acute hypre Ca2+
Or an Anion overdose (bromide, fluoride, iodide)
Loop diuretic
162
What are the ADE of loop diuertics
THink all electrolytes will be down
Hypo K, Hypo Ca2+, Acute hypovolemia,
Can cause ototoxicity/ deafness (can be perminint)
Hyperurecemia
Ethacrynic acid and furosemide compete with uric acid for the renal secretory systems (blocking the system can cause or exacerbate gout)
163
What is the only 2 contra/ind for loop diuertics
Hypersensitivity to Sulfonamide: except Ethacrynic acid
Anuric patients or patients with severe electrolyte disturbances
164
Should loop diuretics be used with NSAIDs
No, they work opposite of eachother
165
What effect do aminoglycoside ABX have on the nephron
Nephrotoxic, avoid in use with loop diuretics
166
Which two loop diuretics are most likely to cause hyperurecimaia
Both furosemide and ethacrynic acid are more likely to cause hyperuricemia; compete with uric acid for secretion
167
What are the clin uses for Thiazide/like diuretics
HTN, HF(edema reduction), Hypercalcemia (useful in tx kidney stones)
DI
168
What diuretic can be used to treat….DI!!!?
Thiazides have the ability to reduce polyuria and produce hyperosmolar urine (can substitute for antidiuretic hormone)
169
What is the hypothosis on how thiazides work
The most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion
170
What are the 5 main actions of thiazide/ like meds
```
Increase NA and Cl- excretion
Loss of K+
Loss of Mg+
Decreased urinary calcium exceretion
Reduced PVR
```
171
As a class, thiazides become inefective at what GFR
Less than 30 mlls/min
Except for metolazone which remains effective all the way to 10-20 mls.min
172
What is the only thiazide available for IV admin
Chlorothiazide
173
What effect do thiazides have on lipids
5-10% increase in LDL
174
When starting a pt on thiazdes, how often should you check thier K+
Q 2-4 wks then q6-12 months
If K falls below 3.5 , add a potassium supplemtn or a potassium sparing combo
175
How do thiazides effect diabetes pts
Impairs release of insulin and tissue uptake of glucose
Diabetes patients may have difficulty maintaining appropriate blood sugar levels
176
Can pts with a sulfa d/o take thiazides
No
They should take a loop diurttic- etharcynic acid
177
Can thiazides be used with ACEI
No may cause severe HOTN
178
Can thiazides be used with digoxin
No, can causes hypokalemia
179
Can pts on lithium take thiazides
No, may cause toxiciity
180
Can pts taking NSAID take thaizides
No, it may blunt the diuretic effect
Remember NSAIDs decrease flow to the glomerulus
181
What are the two thiazide and the three thiazide like meds
Thiazide:
HTCZ and chlorothiazide
Like:
Chlothalidone
Indapamide
Metolazone
182
What is the MOA of Eplerenone and Spironolactone
Aldosterone antagonist
Increases urinary output by blocking the effects of aldosterone in the collecting duct leading to Na+ loss and K+ retention
183
What is the MOA of Amiloride and triamterene
Na+ channel inhibitor
Increases urinary output by excreting Na+ and retaining K+ in the collecting duct; does not work on aldosterone
184
What effect does aldosterone have on the heart
contributes to cardiac hypertrophy and myocardial fibrosis
185
You have a pt that presents with ascitis, what diuretic is indicated for this pt
K+sparing
186
Spironolactone is used off label to treat what GYN condition
Polycystic ovarian syndrome
187
What is the DOC (diuretic) for hepatic cirrhosis
Spirinolactone
188
How are K sparing diuretcs used in Resistant HTN
in combination with a thiazide or loop diuretic (HCTZ or furosemide)
189
How are K+ sparing diuretics used in HF
aldosterone antagonists prevents the remodeling that occurs as compensation for the progressive failure of the heart
(Spirinolactone, epelerone)
190
How are potassium sparing diuretics used in secondary hyperaldosteronism
spironolactone, more effective in patients with hepatic cirrhosis and nephrotic syndrome
191
What effect does spirnolactone have on adrogens
Blocks androgen receptors and inhibits steroid synthesis at high doses
Can be used for polycystic ovary syndrome
192
What are the ADE of sprinolactone
Hyper K and gynocomastio in males
Can use epleronone instead for the males
193
What are the contra/ind for K+ sparing diuretics
Actic PUD or pregnancy
194
What is the DOC for lithioum induce DI
Triamterene
195
What effect does K have on glucose and what is its relevance to K+ sparing diuretics
K+ is needed to move glucose across the cell; when K+ levels fall, less glucose moves across the cell and more glucose remains in the plasma
Can cause hyper glycemia
196
Using K+_ sparing diuertics cause gout and how
Yes
Can lead to hyperuracemia and a gout flare
Due to secondary competition for uric acid secretion within the organic acid secretory system (i.e., diuretic secreted and uric acid is retained)
197
What area of the heart has the fastest phase 4 depolarization
Sinoatrial node
Also has a higher resting potential
198
What is phase 0 of the action potential of the heart
rapid depolarization due to influx of sodium ions, generates an action potential (cell depolarizes and begins to contract)
199
What is phase 1 of the action potential
early rapid repolarization due to potassium moving out of cell (contraction is in process)
200
What is phase 2 of an action potential
plateau phase mainly due to the inward movement of calcium ions into the muscle cell and function in myocardial contraction
201
What is phase 3 of an action potential
repolarization, potassium ions move out of cell
202
What is phase 4 of an action potential
potassium flows out and sodium seeps into the cell (membrane potential has returned to its resting level and is ready for the next action potential)
203
What is the difference between absolute and relative refractory period
Absolute refractory period is the interval during which a second action potential absolutely cannot be initiated, NO matter how large a stimulus is applied
Relative refractory period is the interval immediately following the absolute refractory period, during which initiation of a second action potential is inhibited but not impossible
204
What is re-entry phenomenon/ heartblocks
1st degree heart block:
Electrical impulse travel through AV node too slowly, but impulse reaches ventricles
Results in PR prolongation
2nd degree heart block:
Electrical impulses travel slowly through the AV node and occasionally get blocked, causing the ventricles to beat out of sequence
3rd degree heart block:
Electric impulses do not reach the ventricles from the atria, so the ventricles create their own impulse, which causes the ventricles to beat out of sequence with the atria
Can be a life-threatening condition
205
Excessive prolongation of the QTi leads to increased risk of…
Torsades de pointes
206
What is the most common cause of QTi prolongation
Drug-induced
207
When the QTi is greater than 500 miliseconds what is the pt at risk of
Torsasdes
208
Is aflutter a rentry problem
Yes
209
Waht are common causes of PSVT
digitalis toxicity, caffeine intake, anxiety, alcohol, Wolff-Parkinson-White syndrome
210
Is antiarrhymic thearpy alwasy beneficial
CAST trial proved that continued treatment with encainide and flecainide resulted in a 2-3 fold increase in death and challenged the assumption that antiarrhythmic therapy is always beneficial
211
What is the most common system of antiarrhythmic classification
Vaughn-Williams Classification
212
What is a class IA drug
Na+ channel blocker that:
Lengthen the refractory period
Decrease automaticity in sodium-dependent conduction tissue
Decrease conduction velocity
213
What is a class IB drug
Fast Na+ channel blocker
Weak sodium channel blockers
Shortens phase 3 repolarization in ventricular muscle fibers decreases refractory period
Possess local anesthetic activity
214
What is a class IC channel blocker
Potent Na channel Blocker
Slows the conduction velocity while having little effect on the refractory period
Useful in both supraventricular and ventricular arrhythmias but are not often used for ventricular arrhythmias due to proarrhythmia risk
215
What is a class II drug
BB
Block catecholamines at the beta receptor in the heart to decrease conduction velocity
Lengthen the refractory period
Decrease automaticity
216
What is a Class III drug
K+ blocker
Prolongs phase 3 (refractory period in ventricular and supraventricular tissue)
217
What is a class IV drug
Ca2+ blocker
Inhibits action potential in SA and AV nodes to prolong the refractory period
Slow conduction
Decrease automaticity
218
What are three Class Ia drugs
Disopyramide
Quinidine
Procanamide
All increase the QRS and QT,
Used to tx atrial and vent arrythmias
219
What are two Ib drugs
Lidocaine and Mexiletine
Both decrease the Qt interval
Used to treat Vent arrythmias
220
What are 2 class Ic drugs
Flecainide and propafenone
Both increase the QRs
Used to treat atrial and vent arrythmias
221
What are 4 class II drugs a
Propranolol
metroprolol
Atenolol
Esmolol
Both decrease HR and Increase PR
Used to treat Tachyarrhythmias caused by sympathetic activity, Supraventricular and Ventricular Arrthymias
222
What are 5 Class III drugs
```
Amioderone
Sotalol
Ibutilide
Dofetilide
Droedarone
```
All increase QT interval
Used to treat Atrail and Vent Arrythmias
223
Waht are 2 class IV drugs
Verapamil and diltiazem
Both decrease HR and increase PR
Used to treat: Atrial Arrthymias (atrial flutter/fibrillation), reentrant Supraventricular Tachycardia
224
What is the MOA of class I agents
Na channel blockers
Blocks voltage sensitive Na channels
Used for ryhtynm control
225
What effect do class Ia have on the refractory preiod
Decrease Phase 0 upstroke velocity and prolong repolarization
226
What effect do class Ib have on the refractory period
Prolong phase0 mildly and SHORTENS the repolarizatrion period
227
What effect does class Ic drugs have on the refractory period
Markedly delays phase0 , with minimal effect of the repolarization period
228
What are the ADE of quinidine
N/V/D, Cinchonism ( flushed sweaty skin with ringing of the ears), HOTN, Syncope, and skeletal muscle wkness especially MG pts
229
What is cinchonism
An ADE of quinidine
Ninchina is tha alkoloid of quinie
S/s: Flushed, sweaty skin, ringing in the ears
Anticholinergic Properties: blurred vision, tinnitus, headache, disorientation, and psychosis/hallucinations
High doses cause arrhythmias and ventricular tachycardia, which can be fatal
230
When Rx quinidine for a pt with Myasthenia Gravis, what should the provider be aware of
Quinidne can deprress all muscle funciton and can exacterbate MG
231
What is the most requently used Class IA agent
Procanamide
Used to treat SVT and Vent arrythmias
232
If procanimide is given to quickly, what happenes
HOTN
233
What is the active metabolite of procanimide that prolongs the duration of the action potential
NAPA (N-acetylprocanamide)
NAPA is secreted by the kidneys so procanaide needs renal dosing adjuctment
234
What are the ADE of procanamide
QT interval prolongations, and Syncope
Longer term can produce a lupus type rash/ syndrome
Arthralgia/ arthritis
And serum increases of antinuclear antibodies
235
Disopyramide crosses multiple classes, it is both a Class Ia and also..
Class III ( K+ blocker)
236
What is the role of disopyramide
ventricular arrhythmias that are refractory or intolerant to quinidine or procainamide
237
What is the class and clin use for Lidocaine
Class IB
Use: Terminate Ventricular Tachycardia with a pulse
Prevent ventricular fibrillation after cardioversion
An alternative agent in pulseless VT /VF if amiodarone is not available
238
Can you safely admin lidocaine to a pt with CHF or hepatic Dz ?
Yes, however the doseage must be adjucted
HF: Lidocaine’s volume of distribution and total body clearance may both be decreased
239
What is the least cardio toxic medication of the sodium channel blockers
Lidocaine
240
Can a pt in 3* HB get lidocaine
NO!
241
What is the relationship between lidocaine and amioderone
Amiodarone can increase lidocaine levels
242
What is the orally active form of lidocaine
Mexiletine
Used for Tx of Vent arrythmias with a previous MI
Also can be used off label to treat DM neuropathy
243
A pt who has an otherwise nml heart + SVT what is the lass of medications for clin use
Class Ic
These drugs can not be used in pts with HEART FAILURE OR post MI
(Flecaindie and propfenone)
244
Can flecaindie be used in HF
Specific to Flecainide: possesses negative inotropic effects and can exacerbate heart failure
245
What is the clin use of flecainde and what is the pill in pocket approach
Maintenance of sinus rhythm of atrial fib and flutter in patients without structural heart disease
“Pill in Pocket Approach”_ take a pill and use it when you feel S/s
246
Flecainide had death that was greater than placebo?
Yes, use pill in pocket approach, this med can be dangerous
247
What is the MOA of propafenone
Mechanism of Actions: Potent Na+ Channel Blocker
| Possess weak beta-blocking properties
248
What is the clin use of Class Ic meds
Indicated in patients without structural heart disease for supraventricular arrhythmias; rhythm control of atrial fibrillation or flutter and etc.
“Pill in Pocket Approach”
249
What effect do BB have on refractory periods
Diminish phase 4 depoloarizaation
| Prolong AV node conduction
250
What is the DOC in Afib / A Flutter
BB
251
Post MI patients should be started on β-blocker unless contraindicated to suppress….
PVCs
252
Due to its short Half life what B1 selective BB is used intraoperatively for blood pressure, heart rate control, and other acute arrhythmias requiring a beta blocker
Esmolol
253
What is the MOA of class III meds
Mechanism of Action: K+ Channel Blockers
Prolongs phase 3 (refractory period in ventricular and supraventricular tissue)
Electrophysiological Effects:
- Prolong duration of action potential and effective refractory period
- Interfere with the outward K+ currents or slow inward Na+ currents
- No significant effect on conduction velocity
- All class III agents have the potential to induce arrhythmias
254
Can Class III meds induce arrhythmias
Yes, all class III agents can
255
What is the MOA of amiodernone
Contains iodine and is related structurally to thyroxine
Has class I, II, III, IV actions but its main action is prolongation of the action potential and refractory period by blocking potassium channels
Possess both α-blocking activity, anti-angina, and vasodilatory effects
256
What is the DOC for pulseless VT/ Vfib ( cardiac arrest)
Amioderone
257
What is the prefered agent in pts with LVDF (HF)
Amioderone
258
What are the C/I to amioderone
Remember it contains iodine and is structurally similar to thyroxine… so
Iodine hypersensitivity
Hyperthyroidism
Third-degree heart block
259
What are the ADE of Amioderone
50% of pts stopped meds due to severeity of ADE
CNS effects: heartblock, HOTN, tremors, ataxia, neuropathy
Pulm Fibrosis
( CXR and Pulm fx tests are required at baseline and q 6-12 months)
Liver toxicity
(Monitor at baseline and q 6 months of tx)
Hypo/hyperthyroid
(Same monitor)
BLUE GRAY SKIN!
Optic neurtitis (monitor for visual impairments)
260
IS dronedarone more or less effective than amiodernone
What makes it differnt
Less effective
Derivative of amiodarone: does not posses the iodine moieties that are responsible for thyroid dysfunction like amiodarone
Maintain sinus rhythm in atrial fibrillation/flutter in patients with a history of paroxysmal or persistent atrial fibrillation
261
What is the mechanism of action of SOTALOL, dont get tricked thinking its just a BB )
Mechanism of Action: K+ Channel Blockers
Prolongs cardiac action potential
Increases the duration of the refractory period
Potent non selective beta blocker activity (Class II action)
50% beta blocking properties and K+ blocking properties (Class III)
Not classified as a beta blocker
262
What is the DOC for SVT and Vent arrhythmia is pediatric age groups
Sotalol
263
What is the black box warning for sotalol
Black Box Warning: patient initiated or reinitiated on sotalol should be placed for a minimum of 3 days (on their maintenance dose) in a facility that can provide cardiac resuscitation and continuous ECG monitoring
264
What is the clin use of Ibutilide
Rapid conversion of afib to NSR
Careful! It can cause torsades
265
If you give ibutilide, how long must you monitor the pt for torsades
Patients require continuous ECG monitoring for 4 hours post infusion or until QTc returns to baseline
266
What is the clinuse of Class III drug Dofetilide
Indicated for the conversion of atrial fibrillation/atrial flutter and maintenance of normal sinus rhythm in patients whose arrhythmia is of greater than one week duration and who have been converted to normal sinus rhythm
Reserved for patients in whom atrial fibrillation/atrial flutter is highly symptomatic
So essential you would use ibutilide in the acute phase and then dofetilide in the long term managment
267
You just succesfully converted a pt out of afib with ibutilide.. to maintain this pts therapy what drug should you use
Dofetilide,
268
What is the black box warning of dofetilide
Black Boxed Warning: hospitalization mandatory for initiation, obtain QTc 2-3 hours after each of the 1st five doses
Restricted to prescribers who have completed a specific manufacturer's training session
269
Can dofetilide be Rx outpt?
NO, requires hospitilization
270
A pt with poor renal function (CrCl) is given dofetilide, what ADE are they now at risk for
Dofetilide is excreted renally, so an accumulation of dofetilide can increase the QTi and lead to torsades
271
Where do CCB have thier action in on refractory periods
Phase 0
272
What is the MOA of Digoxin
Cardiac glycoside (inotrpe)
Inhibts the NA/+ pump
273
What are the clin effects of Digoxin
Inotrope and slows SA and AV node through vagus stim.
Slows HR and Av conduction
274
What is the clinical benifit of digoxin
Positive inotropic effects, increases the force of myocardial contraction and does not cause increase oxygen consumption
275
A pt has Afib, what drug can be used to prevent RVR
Digoxin
276
Should digoxin be used in HF pts
No
277
What electroyltes interact with digoxin
K+ and Ca2+
Hypokalemic results in increased digoxin binding and thereby enhances its therapeutic and toxic effects
Decreased K+ may cause an increased incidence of arrhythmias, which can lead to ventricular fibrillation and sudden death
Hyperkalemia reduces the effects of digoxin
Increase K+ reduces the enzyme-inhibiting actions of digoxin
Hypercalcemia enhances digitalis induced increases in intracellular calcium, which can lead to calcium overload and increased susceptibility to digitalis induced arrhythmias
278
A pt presents with halos around thier visual fields, what med did they prolly just take
Digoxin
279
What is the antidote to digoxin OD
Digoxin Immun fab
In patients not suffering from arrhythmias or electrolyte imbalances, discontinue digoxin for 2-3 days and restart if therapy is beneficial
280
What must be done when giving digoxin
MONITOR MONITOR MONITOR
281
What is the MOA of adenosine
Causes a slowing of the heart rate and AV conduction, which usually terminates the episode of tachycardia
Naturally occuring nucleotide in the body
Increase K and Ca2+ influx
Decreases conduction velocity, prolongs the refractory period and produces automaticity in the AV node
282
What is the Doc in Regular PSVT
Adenosine
283
What is the definition of paroxysmal AFib
spontaneous self-termination within 7 days of onset
284
What defines persistnet Afib
Lasting 7> days
285
What is longstanding persistnet Afib
Lasting more than 12 months
286
What are the Tx options for a pt with Afib and no structural HDz
If they are in an expiernce hospoital: ablation
```
If not or med tx is perferred:
Class IC ( Flecainide and Propfenone)
Dofetilide (Class III)
Dronedarone (Class III)
Sotolol (Class III)
```
If those dont work, you can either go straight to ablation or try amioderone 1st
If amio is unsuccefull, then abaltion
287
Can pts with Afib and structural Hdz get class Ic tx
No
288
What BB can be used in a pt with stable HF and needs vent rate control
Carvedilol, metoprolol, and bisoprolol
289
Should BB be used in pts with WPW
No
290
Can CCB be used in WPW
No
291
What two types of drugs can be used to control vent rate
BB Class II
And Non DHP CCBs Class IV
292
Is digoxin ever used a mono tx
No
Best Effective if additional HR control is needed when a patient is receiving a B-blocker, diltiazem, or verapamil
293
Can digoxin be given to a pt with WPW
No
294
What is the CHA2 DS2 VASc score
A rubric to asses if pts need anitcoag in afib
CHF (1)
HTN (1)
AGE (2) (>75)
DM (1)
Stroke (2)
```
Vasc Dz (1)
Age (1) (65-74)
Sex cat( 1)
```
Is score is greater than 2= anticoag tx
If score is 0-1 = consider asprinin
295
What is considered the first line Tx for stable pts with Afib by the AHA
Elecctircal cardioversion
296
Prior to coardioverting Afib, what must you do
Before converting MUST ensure absence of atrial thrombi!
-Trans Esophageal Echocardiogram (TEE) guided to visualize the atria
or
3 or more weeks of anticoagulation prior to cardioversion
With 4 weeks anticoagulation required after cardioversion regardless of method
297
Regardless of method, what must all pts who are cardioverted from Afib be put on
Anticoag
298
Class IC drugs can use the pill and the pocket approach to Afib tx with out structural heart disease… what are the class IC drugs
Flecaindie and propafenone
299
How is amioderone used in pts after cardioverision of Afib
Initiated outpt after pts have rciveed cardiovert +anti coag
300
What is the drug that can be used to treat Afib in a pt with WPW
Amio
301
How do Epi and NE effect HF
Contributes to vent remoddeling and ypertrophy
302
What effect does Angio II have on HF
Stimulated vent hypertropyy and remodelling
303
What is the effect of BNP
Increases in response to stress and stretch of the ventricles
Hemodynamically causes vasodilation of arteries, veins, and coronary arteries
Neuro-hormonally decreases aldosterone, endothelin, and norepinephrine
Renally increases diuresis and naturesis
304
What are the good vs bad effects of Bradykinins and ACE
Good” effects:
ACE inhibitors cause increase in bradykinin levels causing
Decreased peripheral vascular resistance
Decreased blood pressure
Bradykinin is involved in the production of nitric oxide and prostaglandins (Ex: prostacyclin)
Nitric oxide and prostacyclin are vasodilators
“Bad” effect:
Bradykinin and a related substance “substance P” are probably responsible for inducing a cough and angioedema
ACE inhibitors increase bradykinin and increase substance P
Note: ARBs do not affect bradykinin levels
305
An elevated BNP is a sign of…
HF
306
What are the ACEI that have been approved for HF tx
Captopril (50mg)
Enalapril (10mg)
Lisinopril (40mg)
(CEL)
Perindopril
Ramipril
Trandolapril
307
What are the ARBs that have been approved
Candastartan (32 mg/day)
Losartan (150 mg./day)
Valsartan (160 mg/day)
(CLV)
308
What is the MOA of sacubactril
Sacubitril: neprilysin Inhibitor
Inhibits neprilysin, which increase levels of peptides that are normally degraded by neprilysin
More of these peptides (natriuretic peptides, bradykinin, adrenomedullin) means more vasodilation and sodium loss plus less cardiac and vascular hypertrophy and remodeling
309
A pt has a HFref
You start them on metoprolol, and lisinopril, furosemide, they have a K+ less than 5.0 and a CrCl greater than 30. So you start them on spirinolactone
You are considering wether to switch this pt to an ARNI, what C/I should be considered for initiaion of Rx
Contraindications:
Patients with a history of angioedema with a previous ACEI or ARB, concomitant use of an ACEI, and use with aliskiren in patients with diabetes.
Adverse Effects: hypotension, hyperkalemia, cough, dizziness, and renal failure
310
A pt with HfrRF is taking aliskiren for DM, can you safely give this pt an ARNI
NO!
311
If you use an ARNI with spirnoloactone what must you monitor
The K+ levels, can cause Hyper K
312
Can you use ARNI and NSaid
Think of renal trifecta
NSAIDS+ ACE/ARB/ARNI may laed to increase risk of renal impairment
313
How should pts with currnet or recent history of fluid retention be started on BB. ( think of a pt with HFreF
With a diuertic
314
What are the BB approved for use in HF
Bisprolol (10mg/day)
Carvedilol (25mg/ BID)
or (80mg/day CR)
Metoprolol (200mg/day)
315
When should you use Loop diuretics vs Thiazide./ like diuretics in HF
Loop Diuretics: best when fluid overload is excessive, needs to be done quickly, or when the kidney is impaired, GFR below 25 to 30mL/min
Thiazide and Thiazide-like Diuretics: may be used in mild fluid overload/regular management for hypertension
316
What is the cieling effect of furosemide
120-200 mg
317
What is the added benifit of K+ sparing diuretics in HF
Inhibit cardiac re-modeling = slows ventricular hypertrophy
318
What is the MOA of Nesiritide
Human B-type natriuretic peptide (hBNP): neurohormone secreted from the ventricles in response to symptomatic CHF
Causing:
Arterial and venous dilation
Enhanced Na+ excretion
Suppression of the Renin-Angiotensin-Aldosterone System (RAAS) and the sympathetic nervous system
319
What are the ADE of nesiritide
HOTN and azotemia
320
Digoxin, dopamine, dobutaine, and milrinone are all examples of what kind of drug
Inotrope
321
When is dopamiine used in the Tx of acute DHF
Generally avoided in the treatment of ADHF, except where the patient has significant systemic hypotension or cardiogenic shock in the face of elevated ventricular filling pressures
322
What is the MOA of dobuatmine
Selective β1 receptor agonist with a small amount of α1 and β2
Clin use; ADHF (cold and dry)
Can be use alt in Cold and wet
323
A pt is unresponsive to or has ADE to dopamine in shrot term severe HF whould be switched to waht drug
Dobutamine
324
What is the MOA of milinone
Inhibits phosphodiesterase III (PDE3), enzyme responsible for breakdown of cAMP to AMP in the heart and vascular smooth muscle
Positive inotrope, arterial vasodilation and venous vasodilation
Increase in stroke volume = increase CO, with little change in HR
Decrease in SVR
No direct adrenergic effect (useful when patients are using beta blockers)
325
What is the clin use of milrinone
Clinical Use: Acute Decompensated Heart Failure (ADHF)
Primarily cold and dry ADHF
Alternative/adjunct to diuretics in cold and wet ADHF
326
What is the recommended salt restritcion in pts with Staged A-D HF
Limit salt to 1500mg/day for stages A and B and consider less than 3 g/day for stages C and D
327
What is the NML PCWP and the CHF Optimal PCWP
NML 8-12 mmHg
Optimal CHF: less than 18 mmHg
328
What is a cariac index
| And what is a NML vs CHF optimal value
CI = CO/BSA; the volume of blood pumped by the heart (L/min) divided by the body surface area (m2)
CI is determined by two factors:
HR and SV; CO = HR X SV
Normal: 2.8-3.6
CHF optimal: >2.2
329
What are the S.s of a wet HF pts
```
D yspnea on exertion or rest
Orthopnea, paroxysmal nocturnal dyspnea
Peripheral edema
Rales
Early satiety, nausea/vomiting
Ascites
Hepatomegaly, splenomegaly
Jugular venous distention
Hepatojugular reflex
```
330
What are the S/s of a cold HF pt
```
Fatigue
Altered mental status or sleepiness
Cold extremities
Worsening renal function
Narrow pulse pressure
Hypotension
Hyponatremia
```
331
What are the two inotropes used for Cold and dry ADHF
Dobutaqmine and milrinone
332
What is the recommendation of use of steroids in HFreF
use at the lowest dose for the shortest length of time possible
Can cause fluid retention
333
Can yiou use metformin, pioglitazone or saxagliptin in HF pts
No
334
What is the DOC for intermittent claudication (muscle pain), for peripheral vascular disease
Cilostazol
335
CAn you use Cilostazol in HF pts
No
Phosphodiesterase inhibitors have decreased survival rates in patients with class III-IV heart failure
336
Can prazosin cause edema
Its an A1 blocker and yes
337
Your hiking and eceryone in your party gets kidney stones, Potassium probles, a rash on the face, met acidodis, and headache.. what drug did you use that caused this
Acetazolamide
