The Washington Manual Flashcards
What’s the definition of hypertension?
The presence of blood pressure elevation to a level that places patients at an increased risk for end organ damage in several vascular beds including the retina, kidneys, brain, heart, and large conduit arteries
What is the definition of hypertensive crisis?
Hypertensive urgencies and emergencies
What is the definition of hypertensive urgency?
- Substantial increase in BP, usually with diastolic >120
- Features:
- optic disk edema
- progressive end-organ complications rather than damage
- severe perioperative HTN
What is the definition of hypertensive emergency?
- systolic BP >210, diastolic >130
- Presenting with:
- HA
- blurred vision
- focal neurologic sx and malignant HTN
What is malignant hypertension?
Elevated BP with papilledema
Having HTN increases risk for CVA by how much?
4x per the Framingham study
Having HTN increases your risk for CHF by how much?
6x per the Framingham study
What is the breakdown between primary and secondary hypertension?
90% vs 10%
What are causes of secondary HTN?
TRACKPADS
- Thyroid dx (hyper)
- Renovascular dx (renal artery stenosis)
- Aorta, coarction of
- Cushing syndrome
- Kidney disease, chronic
- Pheochromocytoma
- Aldosteronism (hyper)
- Drugs (OCPs, decongestants, NSAIDs, appetite suppressants, cyclosporins, exogenous thyroid hormone, recent alcohol consumption, caffeine, anabolic steroids, ma haung, illegal stimulants)
- Sleep apnea
How do you take an accurate BP?
Use correct size BP cuff (inflatable bladder encircles at least 80% of arm)
Take 2 readings, 2 mins apart, in each arm
What are indications to do a workup for secondary hypertension?
- Age at onset: younger than 30 or older than 60
- HTN thats difficult to control after therapy intiated
- Stable HTN that has become difficult to control
- Clinical occurence of HTN crisis
- Presence or s/sx of 2ndary cause such as hypokalemia or metabolic alkalosis not explained by diuretic therapy
What are your target areas in a PE of a hypertensive patient?
- Investigate for end organ damage or 2ndary cause of HTN by noting the presence of:
- Carotid bruits
- S3 or S4
- Cardiac murmurs
- neuro defects
- elevated JVP
- rales
- retinopathy
- unequal pulses
- enlarged/small kidneys
- cushingoid features
- abdominal bruits
Name two medications that can cause rebound HTN
Beta blockers
Alpha agonists
What is the workup for a patient with possible target organ damage?
- UA
- HCT
- plasma glucose
- BMP
- CBC
- Calcium
- Uric acid
- FLP
- EKG
- CXR
- Check (LVH)
What is the MOA of thiazide diuretics?
Blocks sodium reabsorption predominately in the distal convoluted tubule by inhibition of the thiazide-sensitive Na/Cl cotransporter
What is the mechanism of action of a loop diuretic?
Blocks sodium reabsorption in the thick ascending loop of Henle through inhibition of the Na/K/2Cl cotransporter
What are the most effective hypertensive agents in patients with renal insufficiency?
Loop diuretics with GFR <35
How do potassium sparing diuretics work?
- Competitively inhibiting the actions of aldosterone on the kidney (spironolactone and eplenerone)
- Inhibiting the epithelial Na+ channel in the distal nephron to inhibt the reabsorption of sodium and the secretion of potassium ions
Potassium sparing diuretics are often combined with what other agent, and why?
Thiazide diuretics because they are a weak diuretic on their own
What are side effects of thiazide diuretics?
- Weakness, muscle cramps, impotence
- Hypokalemia, hypomagnesemia, HL (increases LDL and TGs), hypercalcemia, hypergylcemia, hyponatremia, and rarely azotemia
- possible pancreatitis
- Limited when used in small doses (12.5-25mg)
What are side effects of loop diuretics?
- Hypomagnesemia, hypocalcemia, hypokalemia
- Irreversible ototoxicity
What are side effects of spironolactone and eplenerone?
What are side effects of triamterene?
Renal tubular damage and renal calculi
What is the MOA of beta blockers?
- Competitive inhibition of the effects of catecholemines at beta-adrenergic receptors, which decreases HR and CO
- Decreases plasma renin and cause a resetting of baroreceptors to accept lower level of BP
- Cause release of vasodilatory prostaglandins, decrease plasma volume, and may have CNS mediated anti-HTN effect
What are the two classes of beta blockers?
Cardioselective with beta-1 blocking effects
Non-cardioselective with beta-1 and beta-2 blocking effects
Which of the two classes can be given to pts with COPD, DM, or peripheral disease?
At low doses, the cardioselective agents
At higer doses, the medication loses its beta-1 selectivity and may cause unwanted effects in these patients
Which are the beta adrenergic antagotnists with ISA? What is their special feature?
- They cause less bradycardia
- Some beta blockers (eg oxprenolol, pindolol, penbutolol, and acebutolol) exhibit intrinsic sumpathomimetic activity (ISA)
- Agents are capable of exerting low-level agonist activity at the B-adenergenic receptor while simulatenously acting as a receptor site antagonist
- therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy
What are side effects of beta blockers?
- High degree AV block, HF, Raynauds phenomenon, impotence
- Lipophilic BB (propranolol) have higher incidence of CNS side effects including insomnia and depression
- Propranolol can also cause congestion
How can beta blockers affect an FLP?
Increased TGs and decreased HDL with non-selective BB
What are side effects of labetalol?
Hepatocellular damage
Postural HTN
Positive ANA
Lupus like syndrome
Tremors
Potential HoTN in setting of halothane anesthesia
Which beta blockers are more likely to cause reflex tachycardia?
Carvedilol and lebatalol due to initial vasodilatory effect
What can happen with abrupt withdrawal of a chronic beta blocker and why?
Chronic antagonism increases receptor density, so it can precipitate angina pectoris
What were the findings of the ALLHAT trial?
- Decreased cardiovascular and cerebrovascular morbidity and mortality with the use of thiazide diuretics thus this class of drug is favored as first line therapy unless there is a contradiction to their use or the characteristics of a patient’s profile (concomitant disease, age, race) mandate the institution of a different agent
- Calcium channel antagonists and ACE inhibitors have a low-side effect profile and have been shown to decrease BP to degrees similar to those observed with diuretics and B-adrenergic antagonists, resulting in reductions in morbidity and mortality similar to diuretics, making them reasonable initial agents
