Ant-HTN Pharmacotherapeutics Flashcards
1
Q
Define the following terms:
- Adrenergic
- Antagonist
- Agonist
- Afterload
- Preload
A
- Relating to nerve cells in which epinephrine (adrenaline) or norepinephrine (noradrenaline) acts as a neurotransmitter
- A drug that blocks or reduces the effect of a neurotransmitter.
- A drug that combines with the receptor to mimic or enhance the effect of a neurotransmitter.
- The tension or stress developed in the wall of the LVduring ejection (pressure the LV must overcome to eject blood)
- The initial stretching of the myocardium prior to contraction
2
Q
More definitions:
-End Diastolic Volume (EDV) “preload” (not really preload, but terms are used interchangeably)
- End Systolic Volume (ESV)
- End Diastolic Pressure (EDP)
- End Systolic Pressure (ESP)
A
- The volume of blood in the RV or LV at the end of diastole. An increase in EDV increases preload on the heart and (through the Frank-Starling mechanism) increases the amount of blood ejected from the ventricle during systole (SV)
- The volume of blood in the V at the end of contraction and the beginning of diastole. It is the lowest volume of blood in the V at any point during the cardiac cycle. The main factors that affect ESB are afterload and contractility of the heart
- The pressure in the ventricles at the end of diastole; an approximation of EDV (preload) or systole
- The pressure in the ventricles at the end of systole
3
Q
More definitions:
- Ionotropy
- Lusitropy
- Chronotropy
- Dromotrope
- Bathmotropy
- What are compelling indications?
A
-Contractility
-Relaxation
-Rate
-Conduction
-Excitability/irritability
(Positives agents increase, negative agents decrease)
-Things that compel the use of certain types of drugs to treat HTN due to comorbidities (e.g. someone with HTN and DM, the DM will dictate to some extent which drugs can be used to treat the HTN)
4
Q
- What are some potential factors that can effect BP and lead to HTN?
- What are the 5 lifestyle modifications recommended by the JNC 7 for reducing BP?
A
-Diet (Na, K, maybe Vit D), age, sedentary lifestyle, race, family history, tobacco use, stress, chronic conditions, obesity, alcohol
-Reducing sodium intake
Increasing exercise
Moderating alcohol consumption
Following DASH diet eating plan
Losing weight
5
Q
- What are the DHP CCBs?
- Which DHP CCB is IV only?
- What are the non-DHP CCBs?
A
-The -dipines!! Amlodipine Felodipine Nicardipine Nifedipine -Clevidipine (IV only) -Memorize these ones!!! Diltiazem Verapamil
6
Q
- DHP CCBs are selective for which tissue?
- When you think DHPs, what else should you think?
- Non-DHP CCBs are selective for which tissue?
A
- Arteriolar beds (vascular channels)
- Vasodilation!!
- AV node (cardiac channels)
7
Q
- What is the MOA of Dihydropyridine calcium channel blockers?
- What is the significance about the fact that DHPs do NOT work on VENOUS smooth muscle?
A
- Block calcium ion influx into VASCULAR smooth muscle; they are potent vasodilators
- There is no significant reduction in preload
8
Q
- What are the indications for DHP CCBs?
- What are the contraindications?
- What are the side effects of DHP CCbs?
- Why do they cause dizziness?
- Headache?
- Why are patients often taken off of DHPs?
- What is reflex tachycardia?
A
- HTN, Prinzmetal (vasospastic) angina, prevention of cerebral artery spasm after brain hemorrhage, Raynaud’s sydrome, migraine HA prophylaxis
- Pregnancy cat. C, conditions in which tachycardia is harmful (CAD, aortic stenosis, mitral stenosis
- Vasodilation-related symptoms: flushing, HA, dizziness, REFLEX TACHYCARDIA, peripheral edema
- Decrease BP leads to decreased cerebral perfusion which causes the dizziness
- Cerebral vasodilation
- Because of the peripheral edema
- The CV system compensates for decreased BP by increasing CO, primarily by increasing HR and contractility via SNS stimulation
9
Q
-What is the MOA of non-dihydropyridine calcium channel blockers?
A
- They block calcium influx into the myocardium with minimal vascular effects
- They are negative inotropes, dromotropes, and chronotropes
- By slowing down the conduction of electrical activity in the AV node, they decrease HR which leads to increased diastolic filling time and increased myocardial O2 supply which decreases the demand and workload of the heart
10
Q
- What are the indications for non-DHP CCBs?
- Contraindications?
- Side effects?
A
- Stable angina (in combo with BB), tachycardias, HTN (diltiazem)
- Hypotension, acute CHF/cardiomyopathy, heart blocks, sick sinus syndrome, Wolf-Parkinson-White syndrome
- Bradychardia/heart block (from SA and AV node suppression), HF and hypotension (from reduced contractility), constipation (especially with verapamil in the elderly)
11
Q
-What is Wolf-Parkinson-White syndrome?
A
In WPW, transport of electricity goes through an accessory pathway called the Bundle of Kent rather than through the AV node. It is not blocked by CCB, but the AV node is. So, the use of CCB promote conduction through the accessory pathway, and because it does not have a conduction delay (like the AV node), heart rates can reach very high rates
12
Q
- Which population are CCBs especially effective in?
- When are they preferred over BB and ACEI?
- Why should you use caution when combining non-DHPs with BB?
- What type of interaction deo CCBs have with simvastatin?
- Where are CCBs metabolized?
- How does grapefruit juice effect bioavailability?
- Which DHP CCB has a 40 hour half life which helps to mitigate the reflex tachy commonly seen with CCBs?
A
- Blacks
- In the elderly
- There is potential for depressing AV conduction and sinus node automaticity as well as contractility
- Combo can lead increase blood levels of simvastatin which increases the risk of rhabdomyolysis
- Liver, CYP450
- Increases it
- Amlodipine
13
Q
- What is the MOA of peripheral vasodilators?
- Indications?
- Contraindications?
- Side effects?
A
- They relax vascular smooth muscle, which decreases PVR and afterload which leads to peripheral vasodilation
- Resistant HTN! Single nucleotide polymorphisms (SNP)??, alopecia (hair loss)
- Conditions in which tachycardia is harmful (CAD, aortic/mitral stenosis)
- Hypotension; can stimulate reflex tachy, increase myocardial contractility, cause HA, palpitations and fluid retention if given alone (give with BBs); also Vasodilation-related symptoms: flushing, dizziness, HA, reflex tachycardia, peripheral edema
14
Q
- What are the three drugs we learned about that are peripheral vasodilators?
- What is a potential side effect specific to Hydralazine?
- Why should you use Minoxidil with a loop diuretic?
- What is the potential side effect specific to Sodium nitroprusside?
A
- Hydralazine, Minoxidil, Sodium notroprusside
- Immunologic effect (lupus-like syndrome), GI disturbances
- Because it can cause marked fluid retention and pericardial effusion which can lead to tamponade (BLACK BOX WARNING) Also can cause hirsutism
- Cyanide poisoning
15
Q
- What is the suffix used with Angiotensin Converting Enzyme Inhibitors (ACE-I)?
- What are a few of these drugs?
- What is their MOA?
- How are they cardio protective?
- How are they renal protective?
A
- (-pril)
- Lisinopril, enalapril, captopril, ramipril, benazepril etc…
- Inhibition of RAAS decreases the amount of angiotensin II (strong vasoconstrictor) in the blood, and increases the amount of bradykinin (potent vasodilator)
- Slow progression of LVH after an MI, reduce incidence of a 2nd MI, reduce CV complications in patients with risk factors
- Reduce intraglomerular pressure through relaxation of the efferent ateriole and overall reduction in BP
16
Q
- What are the indications for -prils?
- Contraindications?
A
- HTN, post MI CAD, CHF (drug of choice for combined CHF and HTN, and HF if EF <45 even without HTN), DM (with or without HTN due to real protection
- Pregnancy D (black box: teratogenic during 2nd and 3rd trimesters), acute renal dysfunction, bilateral renal stenosis (ok in unilateral)
17
Q
-What kinds of side effets do -prils have?
A
-Dry “annoying” cough from increased bradykinin occurs in 5-20% of patients is not dose related and occurs more in women than men; hypotension, hyperkalemia, acute renal failure, angioedema
18
Q
- What is angioedema?
- How high must the dose be in order for this to occur?
A
- Angioedema is associated with a deficiency of C1 esterase, the enzyme that cleaves bradykinin. Bradykinin is a potent vasodilator that increases permeability and allows the accumulation of fluid within the interstitial space. ACE is one of the main ways that bradykinin is degraded. When ACE is inhibited, bradykinin can’t be broken down and ends up with a run-away amount and subsequent swelling.
- Dose does not matter, and it occurs within one week of beginning therapy
19
Q
- ACE inhibitors are increasingly used as the DOC for which type of HTN?
- Which population are these meds more effective in?
- Which populations are these less effective in?
- What are the benefits of combining an ACE and an ARB?
- Why must you consider renal dosing in patients with renal impairment?
A
- Mild to moderat
- Younger white patients
- Blacks, elderly and patients with predominantly systolic HTN
- There are none
- Most -prils are cleared by the kidneys
