Hypertension Flashcards

1
Q

Normal BP

A

less than 120

and

Less than 80

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2
Q

Elevated BP

A

120 - 129

and

Less than 80

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3
Q

Stage 1 Hypertension

High Blood Pressure

A

130 - 139

or

80 - 89

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4
Q

Stage 2 hypertension

High blood pressure

A

140 or higher

or

90 or higher

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5
Q

Hypertensive Crisis

Consult your doctor immediately

A

Higher than 180

and/or

Higher than 120

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6
Q

What is primary (or essential) hypertension

A

Primary (or essential) hypertension (90-95%): unclear etiology but multifactorial (genetic and environmental factors)

Recall that secondary hypertension (5-10%) is hypertension contributing to another disease or medications

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7
Q

What are the complications of hypertension

A

Left ventricular hypertrophy

Heart failure

ischemic stroke

Intracerebral hemorrhage

Ischemic heart disease

Chronic kidney disease and end-stage renal disease (bad for kidneys)

Risk of CVD doubles with every 20 mmHg increase, starting at 115 mmHg

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8
Q

Treatment of hypertension

A

address secondary cause, if present

lifestyle modification

Pharmacological therapy

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9
Q

What are first-line hypertension drugs?

What are different drug classes associated with hypertension drugs?

A
  • roughly equivalent BP lowering efficacy
  • Consider: cost, side effects, other health conditions, occasionally ethnicity
  • Drug classes
    • Thiazide diuretic
    • Angiotensin-converting enzyme inhibitor (ACEI)
    • Angiotensin II receptor blocker (ARB)
    • Long-acting calcium channel blocker (most often dihydropyridines (DHP))
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10
Q

Understand the physiological mechanisms that can be targeted for the treatment of hypertension

A

Lifestyle Modifications

Weight reduction

Adopt DASH eating plan

Dietary sodium reduction

Physical activity

Moderation of alcohol consumption

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11
Q

Antihypertensives

A

Reduce sympathetic tone/stimulation

Beta-blockers (propranolol), alpha blockers (prazosin), alpha two agonist (clonidine)

  • Antihypertensives; reduce plasma volume: diuretics
    • gets rid of more fluid and therefore decrease blood volume
  • Relax arterial smooth muscle, cause vasodilation (smooth muscle tone)
    • Renin-angiotensin inhibitors
    • Ca2+ channel blockers
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12
Q

What does Short term MAP regulation look like?

A

Depends on increases in CO and TPR through baroreceptor reflexes and SNS activation

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13
Q

What does Long-term MAP regulation look like?

A

vasoconstriction due to angiotensin II, increased fluid volume due to aldosterone and vasopressin

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14
Q

MAP =

A

CO x TRP

Beta-blockers = decrease in force and rate of cardiac contraction = decrease CO

Diuretics, angiotensin inhibitors, beta receptor blockers = Decrease blood volume = decrease CO

Peripherally acting sympatholytics, Ca channel blockers, direct vasodilators, angiotensin inhibitors = relax vascular smooth muscle = decrease TPR

Centrally acting sympatholytics, Beta receptor blockers -> decreased sympathetic outflow = decrease CO and TPR

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15
Q

Diuretics (“water pills”)

A
  • Often a first choice for treatment of mild/moderate hypertension
  • Low-cost but effective drugs: treatment of hypertension associated with reduced morbidity and mortality
  • Act on various segments of the nephron to produce an increase in renal sodium excretion leading to an increase in urine volume
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16
Q

What are the initial and delayed effects of diuretics (“water pills”)

A

Initial effects: reduction in blood volume resulting in decreased blood pressure due to decreases in cardiac output (stroke volume)

Delayed effects: after 6-8 weeks, blood volume and cardiac output are restored back to normal, but peripheral resistance declines

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17
Q

What are mediators in secretion and reabsorption?

Within the kidney tubules

A

Tubular epithelial cells

Luminal membrane facing tubule lumen

Basolateral membrane near capillaries

Tight junctions

Membranes on both sides contain channels and transporters that move solutes

Reabsorption is regulated by transporters, not through the cells because the tight junctions block

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18
Q

Explain sodium Reabsorption

A

Two Steps

  1. Diffuses from lumen into epithelial cells
  2. Actively transported out of cell on basolateral side

Specific channels and transporters on luminal side differ in different regions of the tubules, but pattern remains the same

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19
Q

Furosemide

A

(Lasix)

Loop diuretics

Ethacrynic acid (edecrin)

Block Na/K/2CL cotransporter (NKCC2) in ascending limb of loop of henle

Na continues through the lumen of the nephron and reaches the collecting duct. More water is retained in the lumen due to the osmotic effect of Na+

Most common uses: edema; short-term management of severe hypertension

Highest efficacy of the diuretics

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20
Q

What is the highest efficacy of the diuretics

A

Furosemide

Loop diuretic

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21
Q

What are the major side effects of furosemide?

A

Hypokalemia (low potassium)

  • K+ reabsorption decreased in loop
  • K+ secretion in collecting duct is increased due to higher level of Na+ in the lumen
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22
Q

hydrochlorothiazide

A

Thiazide diuretics

Hydrochlorothiazide, chlorthalidone

Block Na/Cl cotransporter (NCC) in distal tubule

Major use: long-term outpatient management of hypertension

Efficacy to cause diuresis is lower than loop diuretics

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23
Q

What are the adverse effects of Thiazide diuretics (hydrochlorothiazide, chlorthalidone)?

A

Adverse effects: similar to loop diuretics, can cause hypokalemia due to higher levels of sodium in the collecting duct

Chlorthalidone is more efficacious and longer acting than* *hctz* but also carries *greater* *risk of hypokalemia

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24
Q

Diuresis caused by loop diuretics is _____________ that caused by thiazides

A

Diuresis caused by loop diuretics is greater than that caused by thiazides

Higher effect for loop diuretics vs. thiazide

  • Max NaCl loop diuretics of the total amount 20-25% can be trapped in loop
  • Thiazide max about 5

Loop of Henle has higher effect on the NaCl reabsorption

25
Q

Potassium-sparing diuretics

A
  • Work on principal cells of the cortical collecting duct
  • Same region that is sensitive to aldosterone
    • Sodium channels that is just a sodium channel that pumps in and out, in addition, there is a potassium only channel
    • For loop diuretics. they cause hypokalemia because of the K loss
26
Q

What are the 2 mechanisms of Potassium-sparing diuretics

A

2 possible mechanisms

  1. Block collecting duct Na+ channels amiloride, triamterene
  2. Block aldosterone receptor spironolactone, eplerenone
    • The antagonist of the mineralocorticoid receptor and therefore opposite/blocking aldosterone
27
Q

What drug block collecting duct Na+ channels?

in potassium-sparing diuretics

A

amiloride, triamterene

28
Q

What drug blocks aldosterone receptors in potassium-sparing diuretics?

A

Spironolactone, eplerenone

29
Q

What are the side effects unique to spironolactone?

A

anti-androgen effects including gynecomastia, impotence

30
Q

Why are they called potassium-sparing?

A

Blocks Na reabsorption and therefore gets rid of less K

  • In the collecting ducts, Na+ and K+ move in opposite directions
  • Less Na+ reabsorbed = less K+ excreted
  • K+ is “spared” ie maintained in the body
31
Q

What are the major uses for potassium-sparing drugs?

A

Major uses: relatively weak as individual agents, however they:

  • Can be useful in treating some cases of resistant hypertension
  • Can offset hypokalemia caused by loop diuretics and thiazides
32
Q

What are the adverse effects of potassium-sparing drugs?

A

Can lead to hyperkalemia - elevated K+

33
Q

Diuretic adverse effects applying to multiple classes

What are the two classes all diuretics belong to?

A
  • All diuretics
    • Electrolyte imbalances - due to Ca imbalance
    • Dehydration
34
Q

What category does Thiazides and loop diuretics belong to?

A

Thiazides and loop diuretics (except ethacrynic acid) are sulfonamides;

Potential for allergic cross-reactivity with sulfonamide antibiotics

35
Q

Which drug would cause the largest amount of diuresis?

A

furosemide

36
Q

Renin-angiotensin related drugs result in what?

A

Aldosterone is released from the adrenal gland as a result of the:

Renin-Angiotensin Systems

SNS stimulation causes renin release from the kidney

Leads to angiotensin and aldosterone production

(vasoconstriction, Na and H2O retention = increase BP)

37
Q

Drugs targeting the renin-angiotensin system are what? what do they specifically target?

A

Drugs targeting the renin-angiotensin system

  1. Direct renin inhibitor: aliskiren (not used much)
  2. ACE inhibitors: lisinopril
    • prevent angiotensin II
  3. Angiotensin receptor blockers: losartan
    • newer drug

NOTE: drugs affecting the RAS have been observed to be less effecting in black patients

38
Q

Which drug is a direct renin inhibitor?

A

aliskiren

Targets the renin-angiotensin system

39
Q

Which drug is an ACE inhibitor?

A

Lisinopril

Prevents angiotensin II

Renin-angiotensin system target

40
Q

Which drug is an angiotensin receptor blocker?

A

losartan

Targets renin-angiotensin system

41
Q

What are the ACE inhibitor-specific effects?

A
  • Another function of ACE is to break down bradykinin
    • Bradykinin = inflammatory mediator that causes BV to dilate/increase permeability/edema
  • Increased levels of bradykinin lead to dry cough as side effect in up to 20% of patients
  • Less common but more serious: angioedema
    • Swelling of tongue and aroudn eyes
42
Q

What do calcium channel blockers do?

A

Calcium Channel Blockers

  • Lower BP by relaxing vascular smooth muscle
    • decrease amount of Ca that can enter the cell and therefore decrease the smooth muscle contraction
43
Q

Amlodipine

A

Dihydropyridines

Calcium channel blockers

Fairly selective for blood vessels - Ca channels in blood vessels

44
Q

Verapamil

A

Non-Dihydropyridines

Also blocks cardiac calcium channels (in addition to vascular affects)

Decreases rate, contractility, oxygen demand

Useful if hypertension accompanied by angina or certain types of arrhythmias

45
Q

Explain the mechanism for smooth muscle contraction

A

Arteriole smooth muscle contraction

Muscle contraction requires Ca2+ influx and/or release from the sarcoplasmic reticulum

46
Q

What SBP requires immediate medical attention?

A

Systolic BP > 180 mmHg

Elevated BP (less than 180) not a contraindication for most dental work but patient should follow up with physician

47
Q

What are the uses of epinephrine

A
  • Local anesthetic plus EPI can be used with caution and in modest amounts for patients. Potential interaction with beta blocker (unopposed alpha)
  • Epi-impregnated retraction cord contraindicated in patients with hypertension or CVD
48
Q

Postural hypotension possible in patients on antihypertensives

  • what population is it most prevalent?
  • When to be careful?
A

Postural hypotension

More prevalent in elderly

Be careful when standing up from chair

49
Q

What drug can reduce effect of antihypertensive drugs (after ~5 days)?

A

Treatment of pain with NSAIDs can reduce effect of antihypertensive drugs (after ~5 days)

50
Q

Which of these statement are true regarding drugs that affect the renin-angiotensin pathway?

  1. All of them are enzyme inhibitors
  2. Their ability to lower BP is roughly equivalent
  3. They all carry the same side effect profile
A
  1. Their ability to lower BP is roughly equivalent
51
Q

Loop diuretic drug

A

furosemide

52
Q

hydrochlorothiazide

A

thiazides

53
Q

Na channel blockers?

A

Amiloride

potassium sparing

54
Q

Spironolactone

A

aldosterone antagonists

Potassium sparing

55
Q

aliskiren

A

renin inhibitor

56
Q

lisinopril

A

ACE inhibitor

57
Q

Losartan

A

ARB

Renin-angiotensin related

58
Q

Dihydropyridine

A

amlodipine

Calcium channel blockers

59
Q

Non-dihydropyridine

A

verapamil

calcium channel blockers