Hypertension Flashcards

1
Q

what is blood pressure

A

*measure of adequacy of circulation
*balance between: blood volume ejected by LV & peripheral resistance to blood flow
*adequate BP is vital to perfusion of body tissues

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2
Q

complications of elevated BP

A

*intracranial hemorrhage
*stroke
*vascular disease
*kidney damage
*hypertensive heart disease
*retinopathy

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3
Q

complications of low BP

A

*shock
*kidney failure
*anoxic encephalopathy
*lactic acidosis

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4
Q

BP measurement technique: in-office

A

*2 readings, 5 minutes apart, sitting in chair
*confirm elevated readings in the contralateral arm

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5
Q

BP measurement technique: ambulatory BP monitoring

A

*indicated for evaluation of “white-coat” HTN
*absence of 10-20% BP decrease during sleep may indicate increased CVD risk

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6
Q

BP measurement technique: self-measurement

A

*provides information on response to therapy
*may help improve adherence to therapy and evaluate “white coat” HTN

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7
Q

changes in systolic & diastolic BP with age

A

*systolic BP continues to rise throughout life
*diastolic BP starts to decrease around age 50
*this phenomenon is due to stiffening of blood vessels

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8
Q

cardiovascular disease risk based on BP

A

*each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range, starting from 115/75 mmHg
*the BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors

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9
Q

ACC/AHA blood pressure classifications

A

*normal: SBP < 120 mmHg AND DPB < 80
*elevated: SBP 120-129 OR DBP <80
*stage 1 HTN: SBP 130-139 OR DBP 80-89
*stage 2 HTN: SBP 140+ OR DBP 90+

note: whichever value is the higher stage is what HTN you have

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10
Q

epidemiology of HTN

A

*CVA & SVD are the most common causes of death and disability in developed countries
*HTN is a key modifiable risk factor
*HTN affects nearly 50% of adult population in the world
*primary HTN accounts for 90% of cases

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11
Q

causes of primary HTN

A

*multifactorial: obesity, insulin resistnace, age, sodium retention, sympathetic activation, etc

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12
Q

target organ damage resulting from long-standing HTN

A

1) heart:
-left ventricular hypertrophy
-angina or myocardial infarction
-heart failure

2) brain: stroke or TIA
3) chronic kidney disease
4) peripheral arterial disease
5) retinopathy
6) aortic aneurysms and dissections

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13
Q

pathophysiology of LV hypertrophy as a result of long-standing HTN

A

*according to law of Laplace (wall stress law), INCREASING THE THICKNESS OF THE LV WALL actually DECREASES the wall stress
*hence, an increase in wall thickness in response to increased pressure maintains/decreases wall stress

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14
Q

heart failure and HTN

A

*people in heart failure are extremely sensitive to small changes in blood pressure (compared to people without heart failure)
*therefore, we need to maintain their BP even lower than normal because it does not take much afterload to compromise their stroke volume

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15
Q

HTN complication: higher wall thickness:lumen ration in the arteries

A

*law of Laplace applies to arteries too (increasing the wall thickness helps to decrease the wall stress)
*therefore, arteries and arterioles become hyperplastic/hypertrophied, which can lead to more complications down the line

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16
Q

HTN and retinopathy

A

*long-standing HTN can cause retinopathy, characterized by:
-cotton wool spots
-AV nicking
-thin arteries
-papilledema

17
Q

identifiable causes of secondary HTN

A

*sleep apnea
*drug-induced or related causes
*chronic kidney disease
*primary aldosteronism
*renovascular disease
*chronic steroid therapy & Cushing’s syndrome
*pheochromocytoma
*coarctation of the aorta
*thyroid or parathyroid disease
*renal channelopathy

18
Q

pheochromocytoma - overview

A

*rare cause of secondary HTN
*tumor containing chromaffin cells which secrete catecholamines (esp. EPINEPHRINE)
*young-middle aged with female predominance

19
Q

pheochromocytoma - clinical features

A

*intermittent HTN, palpitations, sweating, anxiety “spells”
*may be provoked by triggers such as tyramine-containing foods (beer, cheese, wine), pain, trauma, drugs (clonidine, TCA, opiates)

20
Q

pheochromocytoma - screening

A

*best detected during or immediately after episodes
*3 options, looking for excess breakdown products of epinephrine:
1) plasma free metanephrine
2) 24h urine metanephrine
3) 24h urine VMA

21
Q

pheochromocytoma - diagnosis

A

*imaging for localization of tumor:
-MIBG scintigraphy
-CT
-MRI

22
Q

pheochromocytoma - treatment

A

*surgical removal of tumor:
-anesthesia must avoid certain triggers
*caution with beta blockers!!! (can cause unopposed alpha stimulation → Pheo crisis)
*must start BP control with alpha blockers (phenoxybenzamine) and then start beta blocker once the irreversible alpha blocker is on board

23
Q

pheochromocytoma “pheo crisis” with beta blockers

A

*Pheo crisis: beta blockers can cause unopposed alpha stimulation:
-by blocking the beta receptors, all the catecholamines (epi and NE) will go to alpha-1 receptors → significant vasoconstriction

24
Q

medication timeline for preparing a pheochromocytoma patient for surgery

A
  1. epinephrine from the tumor → BP to increase
  2. give phenoxybenzamine first (an irreversible alpha blocker) → BP goes LOWER THAN ORIGINAL BASELINE b/c the catecholamines are going to beta 2, causing vasodilation
  3. give non-selective beta blocker
25
Q

coarctation of the aorta

A

*defined by location of coarctation relative to ligamentum arteriosum (preductal. ductal, or postductal)
*must be considered in young pts with HTN, particularly if they have lower BP or weak pulses noted in the legs (> 20mmHg DIFFERENCE, with ARMS > LEGS)
*high association with BICUSPID AORTIC VALVE
*if symptomatic, angioplasty vs. surgery
*even with repair, have a lower than expected life expectancy
*collateral blood supply typically forms to maintain perfusion of the abdomen

26
Q

characteristic CXR finding of aortic coarctation

A

*rib-notching on ribs on CXR
*this is evidence of collateralization of blood flow through the intercostal arteries to help supply blood beyond the coarctation
*the bone adapts to having a large vessel running by it

27
Q

behaviors associated with HTN risk

A

*excessive alcohol
*sodium consumption
*obesity/dietary excess
*lack of aerobic exercise

28
Q

lifestyle modifications to manage HTN

A

*weight reduction
*DASH eating plan
*dietary sodium reduction
*physical activity
*moderation of alcohol consumption

29
Q

HTN tx based on ACC/AHA BP classifications

A

*normal: encourage lifestyle modifications, no meds
*elevated: encourage lifestyle modifications, no meds
*stage 1 HTN: emphasize lifestyle modifications, START 1 MEDICATION
*stage 2 HTN: emphasize lifestyle modifications, START 2 MEDICATIONS

30
Q

first-line antihypertensive drug therapies

A

*thiazide diuretics
*calcium channel blockers
*ACE inhibitors
*angiotensin receptor blockers (ARB)

31
Q

compelling indications for individual antihypertensive drug classes in HEART FAILURE patients

A

*ACE inhibitors or angiotensin receptor blockers (ARB)
*beta blockers
*aldosterone antagonist (ALDO ANT)

32
Q

compelling indications for individual antihypertensive drug classes in POST-MYOCARDIAL INFARCTION PATIENTS

A

*beta blockers
*ACE inhibitors or angiotensin receptor blockers (ARB)
*aldosterone antagonist (ALDO ANT)

33
Q

compelling indications for individual antihypertensive drug classes for DIABETES PATIENTS

A

*ACE inhibitors or angiotensin receptor blockers (ARB)

34
Q

compelling indications for individual antihypertensive drug classes for CHRONIC KIDNEY DISEASE patients

A

*ACE inhibitors or angiotensin receptor blockers (ARB)