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S2B5 MEDI > Hypertension > Flashcards

Hypertension Flashcards

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
Q

symptoms seen with hypertension?

A
  • HTN is usually asymptomatic
  • but if there are symptoms:
    • headache
    • impotence
    • fatigue
    • palpatations
    • dizziness
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26
Q

what exams/assessments to complete on a physical exam of a hypertensive patient?

A
  • body habitus
  • retinal exam
  • palpation of:
    • pulses
    • apical impulse (on heart apex)
    • thyroid
  • ascultation of
    • bruits (listen to arteries)
    • heart
  • measure blood pressure?
27
Q

what labs to obtain in itial workup of HTN?

A
  • serum level of
    • key electrolytes
      • sodium
      • potassium
      • calcium
    • glucose
    • fasting lipids
    • TSH
    • BUN/CR
    • albumin excretion
    • hemotocrit
  • electrocardiograpm
28
Q

what lifestyle interventions can be implemented to manage high blood pressure?

A
  • 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
Q

what does the rules/benefits of the DASH diet?

A
  • 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
Q

what hypertensive patients should be treated with lifestyle changes?

A

all patients with an elevated BP

31
Q

what patients should be medicated for HTN?

A
  • 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
Q

first line medications for HTN

A
  • “ACT”
    • ACE inhibitors/ARBs
    • thiazide diuretics
    • calcium channel blockers (long acting)
33
Q

beta blockers are the top choice anti-HTN meds for what populations?

A
  • ischemic heart disease
  • CHF with reduced ejection fraction
34
Q

drugs that inhibit Angiotesin II are the go-to anti-HTN drug for what patient populations? why?

(what are the anti-angiotensin II drugs)

A
  • 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
      1. increases “selectivity” of the glomular membrane (such that contents like albumin do not get filtred)
35
Q

what is the treatment standard for african american patients with hypertension?

A
  • 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
Q

what is the standard treatment for a pregnant patient with HTN?

A
  • 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
Q

thiazide diuretics MOA and adverse effects

A

MOA: inhibit Na+, Cl+ reabsorption from distal tubule

AES:

  • electrolytie imbalanes (eg, hypokalemia)
  • increase urinary frequency
38
Q

MOA and adverse effects of calcium channel blockers

A
  • 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
Q

what are the common adverse effects of ACEs/ARBs?

A

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
Q

common adverse effects of beta blockers

A
  • fatigue
  • bradycardia
  • bronchospasm (with B2 antagonists)
  • rebound hypertension with abrupt discontinuation
41
Q

what are the AEs of aldosterone antagonists and what drug (s) fall into this category?

A

spironolactone = prototypical aldosterone antagonists

AEs:

  • hyperkalemia (aldosterone promotes K+ secretion)
  • others: occur from aldsterone binding to progesterone/androgen receptors
    • gynocomastia
    • irregular menses
    • impotence
42
Q

direct vasodilators.

  • what drugs fall into this category?
  • AEs?
  • role in treating HTN?
A
  • 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
Q

what is the role of peripheral beta blockers in HTN and what side effect do they all share?

A
  • peripheral alpha blockers decrease peripheral resistance by directly blocking smooth muscle vasoconstriction
  • all can cause hypotension
44
Q

central alpha 2 blockers

what drugs fit into this category?

what is their role in treating HTN and what are their AEs?

A
  • drugs: methyldopa, clonidine
  • lower peripheral resistance by inhibiting NE release
    • good for patients with autonomic neuropathy
  • AEs
    • dry mouth
    • somnolence
    • rebound hypertension
45
Q

the standard dose of most anti-HTN medications reduce BP by what amount?

A

SBP by 8-10 mmHg

DBP by 4-7 mmHg

46
Q

discuss anti-HTN therapy in terms of

  • what goal blood pressure is
  • achieving greatest BP reduction
  • being cautious with treatment
A
  • 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
Q

hypertensive urgency

  • define
  • how are patients treated?
A
  • 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
Q

hypertensive emergency

  • define
  • how should these patients be treated
A
  • 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
Q

how to treat hypertension following an acute stroke?

A
  • 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
Q

what qualifies as resistant hypertension?

A

resistant hypertension = uncontrolled BP in a patient on three medications, one of which is a diuretic

51
Q

when to suspect secondary hypertension?

A
  • 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
Q

renal parenchymal disease

  • how to diagnose?
  • how to treat?
A
  • 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
Q
  • what is primary aldosteronism?
  • describe its presentation and how to diagnose it.
A
  • = 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
Q

what is renovascular hypertension?

when to suspect renovascular hypertension?

how to diagnose it?

A
  • 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
Q

how to treat/diagnose hypertensive patients with obstructive sleep apnea (OSA)?

A
  • diagnose OSA with a polysomnograph
  • HTN may be resistant until treated with a CPAP
56
Q

what drugs can induce hypertension?

A

 Oral contraceptive pills  NSAIDS
 Steroids
 Decongestants

 Appetite suppressants
 Monoamine Oxidase inhibitors  Tricyclic Antidepressants
 Erythropoietin
 Cyclosporine
 Clonidine withdrawl

57
Q

what is a phyeochromocytoma?

how to we diagnose and treat it?

A
  • 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
Q

hyperthyroid

  • presentation
  • relation
A
59
Q

what is cushing’s syndrome?

how does it effect blood pressure/describe its presentation

A
  • 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
Q

how do hypo and hyper - thyroidism effect blood prsesure and how else do they present? how do diagnose them

A
  • 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
Q

how does aortic coarctation effect BP and how does it present?

A
  • 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
Q

what is congenital adrenal hyperplasia and how does it present?

A
  • 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
Q

what is acromegaly?

A

an excess of growth hormone secretion by the pituitary gland

can cause hypertension

S2B5 MEDI (7 decks)

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