Hypertension Flashcards

(63 cards)

1
Q

what defines hypertension?

A

average of two or more readings of either:

  • systolic BP > 130 mmHg
  • diastolic BP > 80 mmHg
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2
Q
  • what is this device and its purpose?
  • how should it be positioned for proper use?
A
  • sphygmomanometer
  • used to measure BP.
    • cuff should be placed around arm such that the white strip at the end of the non-velcrow side is aligned within the white arrow range on the velcrow side
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3
Q

describe the proper technique for determing blood pressure?

A
  • patient should be seated for at least 5 minutes
  • ideally, patient has not been smoking/had caffeine recently
  • patient should be in a quite comfortable room
  • take multiple measurements (esp. if a reading looks look it could be off)
    • also take measurements in each arm. certain conditions can cause big disparities in BP between arm
  • proper cuff use:
    • place cuff correctly (middle of upper arm)
    • ensure cuff size is correct
    • delate cuff slowly after BP is obtained (2 mmHg/second)
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4
Q

what blood pressures are considered normal, elevated, and define stage 1 and stage 2 hypertension?

A
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5
Q

what is isolated systolic hypertension?

A

normal diastolic blood pressure with elevated systolic blood pressure (SBP > 130)

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6
Q

what is isolated diastolic hypertension?

A

elevated diastolic blood pressure (>80) with a normal systolic blood pressure

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7
Q

what is white coat hypertension?

A

elevated BP due to stress of doctors to stress of doctors office?

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8
Q

what is “masked” hypertension?

A

a normal BP reading at the doctor’s office, but is elevated during the rest of daily life

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9
Q

how to obtain and interpret an accurate blood pressure reading if you suspect white coat/masked hypertension

A

obtain of the following:

1. ambulatory blood pressure

  • monitors patient’s BP throughout the day
  • HTN considered to be
    • an daytime (awake) BP average of > 130/80 mmHg
    • a 24 hr average of > 125/75 mmHg

2. home blood presure

  • patient keeps daily log of BPs
  • HTN considered by be
    • an average reading of > 130/80 mmHg
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10
Q

primary vs secondary hypertension

A
  • Primary hypertension
    • aka essential / idiopathic hypertension:
    • Hypertension for which no specific identifiable cause can be found
  • Secondary Hypertension:
    • Hypertension caused by another underlying medical problem.
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11
Q

what is hypertensive urgency?

how should we approach treatment

A
  • severe hypertension without symptoms
  • avoid rapid reduction in BP when treating. since patient has acclimated to this high blood pressure, rapid reduction could patient to have a hypotensive crisis/pass out
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12
Q

what is a hypertensive emergency?

how to approach treatment?

A
  • uncontrolled hypertension that is causing acute end-organ dysfunction
    • _​_is syptomatic
      • watch out for confusion, headaches, vision problems
  • it appropriate to treat this patient more rapidly than a pt with hypertensive urgency, since they are at high risk of sepsis/death
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13
Q

what is malignant hypertension?

A

Severe hypertension with retinal changes or papilledema

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14
Q

describe the relationship between changes in BP and risk of associated disease

A
  • As BP goes up, risk of hypertension associated disease goes up in a graded fashion from as low as 115/75.
    • for example: every 20mmHg increase in SBP / 10mmHg in DBP doubles risk of heart disease.
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15
Q

prevalence/relevant statistics pertaining the hypertension

A
  • Most common reason for outpatient doctor appointment
  • Most common reason for prescription medication use in the United States
  • Worldwide leading cause of death
  • Prevalence is increasing here in the US as population ages, and as obesity epidemic grows.
  • More than half of patients > 65 years old are hypertensive
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16
Q

HTN significantly increases the risk of scope of what disease?

A

 Stroke

 Peripheral arterial disease

 Kidney disease

 Congestive heart failure

 Coronary artery disease

 Atrial fibrillation

 Aortic dissection

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17
Q

what factors predispose hypertension?

A
  • Genetic predisposition
  • Excess weight
  • Lack of exercise
  • Increased Sodium intake
  • Increased alcohol consumption
  • Psychological stress
  • Decreased intake of potassium and calcium
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18
Q

review the effects of a1, a2, B1 and B2 stimulation

A

 α1- contracts vascular smooth muscle –> vasoconstriction.

 α2- negative feedback, inhibits more norepinephrine release (decreases vasoconstriction)

 β1- 1. Increases cardiac chronotropy and inotropy and 2. increases renin release.

 β2- EPI causes vascular smooth muscle relaxation –> vasodilation.

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19
Q

what is autonomic upregulation/downregulation?

what populations does it effect the most?

A
  • chronically hypertensive patients tend to have increased sypathetic tone, which leads to a down-regulation (decreased number of) of adrenergic receptors
    • this especially effects hypertensive patients who are overweight or have obstructive sleep apnea
  • conversely, patients with with a chronic blockage of adrenergic receptors (taking alpha or beta blockers) experience sympathetic upregulation (_increased in numbe_r of adrenergic receptors)
    • thus, when these patients discontinue, for example, their beta - blockers, they have severe rebound hypertension
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20
Q

what leads to “rebound hypertension”

A

blockade cessation (rapid discontinuation of alpha or beta blockers)

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21
Q

what is the effect of increased serum sodium on peripheral vascular resistance?

A
  • Increased sodium=increased water, so intravascular volume expands.
  • Increased intravascular volume initially leads to hypertension by increasing cardiac output.
  • Subsequently, peripheral vascular resistance goes up (in kidney and brain) to maintain constant rate of blood flow.
    • _​_P=QR
      • flow = Q = P/R
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22
Q

renin

  • is secreted from what part of the body?
  • in response to what stimuli?
A
  • Secreted by the renal afferent arteriole in response to
    • Decreased NaCl transport in distal tubule of loop of Henle
    • Decreased stretch / pressure
    • Increased sympathetics
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23
Q

what are the adverse effects of Ang II and aldosterone?

A
  • cause vascular remodeling & growth –> athersclerosis
    • athersclerosis will decrease vessel:
      • diameter –> increasing vessel resistance
      • compliance: compliance = V/P, and a decreased compliance means a greater increase P per incease in V. so the vessel is less able to accomdate volume changes
        • together these defects increase afterload against the heart, increasing systolic pressure and widening pulse pressure
  • cardiac hypertrophy and fibrosis
  • nephrosclerosis
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24
Q

risk factors for hypertension?

A
  • Increasing age
  • Overweight
  • Excess EtOH
  • Excess Na
  • Dyslipidemia
  • Vitamin D deficiency
  • African American race
  • Physical inactivity
  • Depression
  • Impatient personality type
  • Parents with hypertension
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25
symptoms seen with hypertension?
* HTN is usually asymptomatic * but if there are symptoms: * headache * impotence * fatigue * palpatations * dizziness
26
what exams/assessments to complete on a physical exam of a hypertensive patient?
* body habitus * retinal exam * palpation of: * pulses * apical impulse (on heart apex) * thyroid * ascultation of * bruits (listen to arteries) * heart * measure blood pressure?
27
what labs to obtain in itial workup of HTN?
* serum level of * key electrolytes * sodium * potassium * calcium * glucose * fasting lipids * TSH * BUN/CR * albumin excretion * hemotocrit * electrocardiograpm
28
what lifestyle interventions can be implemented to manage high blood pressure?
* weight loss * increse physical activity * diet changes: * _decrease_ dietary sodium * _supplement_ potassium and calcium * replace vitamin D (to increase Ca++ absoprtion) * limit alcohol intake * limit NSAIDS
29
what does the rules/benefits of the DASH diet?
* increased fruits, vegetables, whole grains and low fat dairy * decreased red meat, sugar and extra fats * benefits of treatment: * 30-40% reduction in stroke * 20-25% reduction in CHF/MI
30
what hypertensive patients should be treated with lifestyle changes?
all patients with an elevated BP
31
what patients should be medicated for HTN?
* patients with **stage 1 HTN** (SBP of 130-139, DBP of 80-80) **+ any of the following** * ASCVD risk \> 10% * cardiovascular disease * diabetes * chronicc kidney disease * ALL patients with stage 2 HTN (SBP\>140, DPB\>90)
32
first line medications for HTN
* "ACT" * ACE inhibitors/ARBs * thiazide diuretics * calcium channel blockers (long acting)
33
beta blockers are the top choice anti-HTN meds for what populations?
* ischemic heart disease * CHF with reduced ejection fraction
34
drugs that inhibit Angiotesin II are the go-to anti-HTN drug for what patient populations? why? (what are the anti-angiotensin II drugs)
* this includes ACE inhibitors and ARBs (AT1 receptor blockers) * best in patients with: * chronic kidney disease * diabetes with albuminuria * this is because Ang II inhibition relieves glomerular damage & innapropriate filtration of blood contents by * 1. inhibiting vasoconstriction of the efferent arteriole, relieving the glomerulus of high hydrostatic pressure * 2. increases "selectivity" of the glomular membrane (such that contents like albumin do not get filtred)
35
what is the treatment standard for african american patients with hypertension?
* for AA patients WITHOUT ischemic heart disease or chronic kidney disease: * initial treatment with a Ca++ channel blocker or thiazide (or both at the same time)
36
what is the standard treatment for a pregnant patient with HTN?
* meds to give: * methyldopa (a2 blocker) * labetolol (a1 and non-selective B blocker) * nifedipine (a dihydropiridine Ca++ channel blocker) * do NOT give ACEs or ARBS!!
37
thiazide diuretics MOA and adverse effects
MOA: inhibit Na+, Cl+ reabsorption from distal tubule AES: * electrolytie imbalanes (eg, hypokalemia) * increase urinary frequency
38
MOA and adverse effects of calcium channel blockers
* MOA: block L-type voltage gated Ca++ channels in **cardiac muscle** and **vascular smooth muscle** , which * decreases CO (by lowering heart rate and contraction force) * decreases vasoconstriction * this lowers BP --\> reduces HTN * adverse effects * flushing * headaches * edema (strongest AEs seen in DHP Ca+ calcium blockers, the **-dipines**)
39
what are the common adverse effects of ACEs/ARBs?
both ACEs and ARBs: * renal insufficiency: * _efferent arteriole dilation_ from ang II inhibition (*especially* in the context of a stenotic renal artery, which is a contraindication for ACE inhibitors/ARBs) can drop hydrostatic pressure in the glomerulus to the point where _filtration is insufficient_ for proper kidney function * hyperkalemia * Ang II stimulates the production of _aldosterone_, a significant contributer to K+ secretion (aldosterone promotes Na+ absorption in the _collecting tubules_, which is paired to K+ exchange). blocking Ang II and thus aldsterone can cause K+ retention --\> hyperkalemia ACE inhibitors specifically: * _persistent cough_ and _angioedema_ * in addition to blocking ACE enzyme, ACE inhibitors block degredation of bradykinin, which then accumulates. bradykinin is a pro-inflammatory, vasodilating mediator that can cause edema and a persistent cough
40
common adverse effects of beta blockers
* fatigue * bradycardia * bronchospasm (with B2 antagonists) * _rebound hypertension_ with abrupt discontinuation
41
what are the AEs of aldosterone antagonists and what drug (s) fall into this category?
spironolactone = prototypical aldosterone antagonists AEs: * hyperkalemia (aldosterone promotes K+ secretion) * others: occur from aldsterone binding to progesterone/androgen receptors * gynocomastia * irregular menses * impotence
42
_direct vasodilators_. * what drugs fall into this category? * AEs? * role in treating HTN?
* work by decreasing peripheral resistance. * _are not the first line of treatment_ for HTN * drugs = **hydralazine, minoxidil** * side effects of both: * excessive vasodilation, fluid retention, hypotension, reflex tachycardia * hydralazine adverse effects: _lupus like syndrome_ * minoxidil adverse effects: * _hypertrichosis_ (stimulates hair growth) * _pericardial effusion_
43
what is the role of peripheral beta blockers in HTN and what side effect do they all share?
* peripheral alpha blockers decrease peripheral resistance by _directly blocking_ smooth muscle vasoconstriction * all can cause hypotension
44
central alpha 2 blockers what drugs fit into this category? what is their role in treating HTN and what are their AEs?
* drugs: methyldopa, clonidine * lower peripheral resistance by inhibiting NE release * good for patients with **autonomic neuropathy** * AEs * dry mouth * somnolence * rebound hypertension
45
the standard dose of most anti-HTN medications reduce BP by what amount?
SBP by 8-10 mmHg DBP by 4-7 mmHg
46
discuss anti-HTN therapy in terms of * what goal blood pressure is * achieving greatest BP reduction * being cautious with treatment
* goal blood pressure is \< 130/80 mmHg * _adding a second agent_ generally results in a greater reduction of blood pressure than doubling dose a current medication\* * reasses status after treatment each month until goal is met * be cautios rapidly reducing BP in elderly patients (monitor their diastolic BP)
47
hypertensive urgency * define * how are patients treated?
* severe elevation in BP that does NOT present with severe symptoms _or_ acute end organ damage * these patients are often _treated outpatient_ (not hospitalized) with oral medications * these patients need NOT be treated with a precitipitous drop in BP (rapid drop in BP) as they are asymptomatic/low risk. this is unnecessary/could be dangerous
48
hypertensive emergency * define * how should these patients be treated
* hypertensive emergency = severely elevated BP with acute symptoms/acute end organ damage * these patietns are **admitted to the ICU** * **​**given BP lowering conversations **_via IV_** * BP can be lowered precepitiously (rapidly) - _by 25% in the first 2-6 hrs_ and then lower to normal over days - months
49
how to treat hypertension following an _acute stroke_?
* do NOT aggressively treat BP in the days following a stroke * this is because the patients *may actually need a higher arterial pressure* to maintain cerebral blood flow ischemic tissue * if thrombolytics are needed: treat to \<185/110 * if no thrombolytics are needed: treat to lower by 15% first day after stroke if BP \> 220/110
50
what qualifies as resistant hypertension?
resistant hypertension = uncontrolled BP in a patient on three medications, one of which is a diuretic
51
when to suspect secondary hypertension?
* Severe (malignant) hypertension * Resistant hypertension\* * Hypertension _before age 30_ (without other risk factors) * Hypertension with _hypokalemia and metabolic alkalosis_ * Diastolic hypertension after age 65 * Suddenly uncontrolled hypertension with previous good control
52
renal parenchymal disease * how to diagnose? * how to treat?
* proteinurea \> 1000mg/day is diagnostic of renal parynchemal disease * indicates rental parynchymal disease as the cause of HTN * treated the same way, by controlling HTN
53
* what is primary aldosteronism? * describe its presentation and how to diagnose it.
* = excess aldosterone production by the adrenal glands * **presents with:** hypokalemia, hypertension, and alkalolsis * _hypokalemia_ - excess aldosterone drives K+ secretion. * _hypertension_ - excess aldosterone drives Na+ reabsorption --\> HTN * _metabolic alkalosis_ ​ * the body tries to correct the hypokalemic state by pulling K+ into the blood in exchange for H+ secretion. plasma [H+] drops, leading to metabolic alkalosis * **diagnosis:** * **​**check the **aldosterone to renin ratio:** * **​**an _elevated ratio_ indicates that renin production is normal, and the excess aldsterone is _at the level of the adrenal glands._ * follow up a + test result with _imaging_ to see if _there is a mass_ in the adrenal glands causing in appropriate secretion **​**
54
what is renovascular hypertension? when to suspect renovascular hypertension? how to diagnose it?
* HTN cause by _atherosclerosis_ or _fibromuscular dysplasia_ of the renal arteries * suspect in patients with an * adominal bruit "swishing sound" * a recent decrease in renal function * a _significant decrease_ in renal function _when starting an ACE inhibitor:_ * ACE inhibitors vasodilate the efferent arteriole, lowering the glomerular hydrostatic pressure/GFR. in a patient with stenotic renal arteries, this will *severely* limit filtration * (remember ACEs/ARBs are contraindicated in pts with renal stosis) * diagnose with: **renal artery ultrasound or angiography**
55
how to treat/diagnose hypertensive patients with obstructive sleep apnea (OSA)?
* diagnose OSA with a polysomnograph * HTN may be resistant until treated with a _CPAP_
56
what drugs can induce hypertension?
 Oral contraceptive pills  NSAIDS  Steroids  Decongestants  Appetite suppressants  Monoamine Oxidase inhibitors  Tricyclic Antidepressants  Erythropoietin  Cyclosporine  Clonidine withdrawl
57
what is a phyeochromocytoma? how to we diagnose and treat it?
* a pheochromocytoma is a catecholamine secreting tumor in the adrenal gland * it causes paraoxysmal hypertension - "spells"- espisodic, volatile hpyertension * include flushing, headache, nausea * diagnose by: measuring urine fractional metanephrins * treat with excision
58
hyperthyroid * presentation * relation
59
what is cushing's syndrome? how does it effect blood pressure/describe its presentation
* cushing's syndrome is an endocrine disorder characterized by excess secretion of cortisol (hypercortisolism) * causes * hyperblood pressure * central obesity * rapid weight gain * abdominal striations - a greater than 1 cm, are very dark red * facial plethora * easy bruising * proximal myopathy * diagnose with: * give 1 mg of dexamethasone of 1 mg at 11 pm * then draw blood for cortisol at 8 am the next morning
60
how do hypo and hyper - thyroidism effect blood prsesure and how else do they present? how do diagnose them
* both hyper and hypothyroidism can cause hypertension * hyperthyroidism: also causes * tremor * _weight loss_ * sweating * hypothyroidism - also causes * _weight gain_ * cold intolerance * constipation labs: get TSH and free L4 levels for both, add on T3 is you suspect hypethyroidism
61
how does aortic coarctation effect BP and how does it present?
* aortic stenosis that is distal to the branching of neck vessels * tends to present at ages under 30 * you'll see HIGH bp in upper extremities and LOW bp in lower etremities
62
what is congenital adrenal hyperplasia and how does it present?
* congenital adrenal hyperplasia causes an excess of mineralcorticoids in the blood, leading to hypertension * renin and aldosterone are normal * estrogen and adrogens are DECREASED * patient is _hypokalemic_
63
what is acromegaly?
an excess of growth hormone secretion by the pituitary gland can cause hypertension