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adn semester 2 > Chapter 32 HTN > Flashcards

Chapter 32 HTN Flashcards

1
Q

the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vessels (peripheral vascular disease), kidneys (nephrosclerosis), and eyes (retinal damage)

A

most common complications of hypertension are target organ diseases occurring in

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2
Q

can also result from the high salt intake through mechanisms mediated by the renin-angiotensin-aldosterone system (RAAS).

A

Ventricular fibrosis

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3
Q

is a multifunctional cytokine with fibrogenic properties. Overproduction of TGF-β1 (in part mediated by angiotensin II) results in fibrosis and ventricular dysfunction.

A

Transforming growth factor-β1 (TGF-β1)

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4
Q

is a compensatory mechanism that strengthens cardiac contraction and increases CO

A

LVH ( left ventricular hypertrophy)

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5
Q

occurs when the heart’s compensatory mechanisms are overwhelmed and the heart can no longer pump enough blood to meet the body’s demands

A

HF

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6
Q

. However, increased contractility increases myocardial work and O2 demand. Progressive LVH, especially in the presence of CAD, is associated with the development of HF.

A

LVH is a compensatory mechanism that strengthens cardiac contraction and increases CO

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7
Q

Atherosclerosis is the

A

most common cause of cerebrovascular disease.

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8
Q

Hypertension is a

A

significant risk factor for cerebral atherosclerosis and stroke

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9
Q

Portions of the atherosclerotic plaque or the blood clot that forms with disruption of the plaque may break off and travel to cerebral vessels, producing a thromboembolism.

A

patient may have transient ischemic attacks or a stroke

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10
Q

is a physiologic process that keeps cerebral blood flow constant despite fluctuations in BP.

A

Autoregulation

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11
Q

may occur after a marked rise in BP if autoregulation does not decrease the cerebral blood flow.

A

Hypertensive encephalopathy

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12
Q

. When BP exceeds the body’s ability to autoregulate, the cerebral vessels suddenly dilate, capillary permeability increases, and

A

cerebral edema develops

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13
Q

Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels.

A

This leads to peripheral vascular disease (PVD), aortic aneurysm, and aortic dissection

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14
Q

(ischemic leg pain precipitated by activity and relieved by rest) is a classic symptom of PVD.

A

Intermittent claudication

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15
Q

Hypertension is one of the

A

leading causes of chronic kidney disease (CKD)

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16
Q

ischemia caused by the narrowing of the renal blood vessels. this leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of nephrons

A

Renal disease results from

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17
Q

albuminuria, proteinuria, microscopic hematuria, and high serum creatinine and blood urea nitrogen (BUN) levels.

A

Laboratory signs of renal disease are

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18
Q

Nocturia is an early symptom of renal disease

A

Nocturia

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19
Q

the severity and duration of hypertension.

A

appearance of the retina gives essential information about

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20
Q

the heart, brain, and kidneys.

A

Damage to the retinal vessels indicates related vessel damage in

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21
Q

blurring of vision, retinal hemorrhage, and vision loss.

A

Manifestations of severe retinal damage include

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22
Q

.the glomerular filtration rate

A

Creatinine clearance reflects

23
Q

renal insufficiency.

A

Decreases in creatinine clearance indicate

24
Q

hyperaldosteronism, a cause of secondary hypertension.

A

Measurement of serum electrolytes, especially potassium, is essential to detect

25
Q

Some patients have elevated BP readings in a clinical setting and normal readings when BP is measured elsewhere.

A

“white coat” hypertension.

26
Q

is one method for diagnosing white coat hypertension. It is a noninvasive, fully automated system that measures BP at preset intervals over a 12- to 24-hour period

A

Ambulatory BP monitoring (ABPM)

27
Q

in the early morning, decreases during the day, and is lowest at night.

A

BP is highest

28
Q

Some patients with hypertension do not show a typical nocturnal dip in BP. They are referred to as

A

“nondippers.”

29
Q

Patients at highest risk for CVD are “reverse dippers.” These patients have an increase in nighttime systolic BP.

A

“reverse dippers.”

30
Q

These are (1) manage blood pressure, (2) control cholesterol, (3) reduce blood sugar, (4) get active, (5) eat better, (6) lose weight, and (7) stop smoking.

A

The AHA’s “Life’s Simple 7” steps support ways to modify and improve health.

31
Q

to 2300 mg/day or less

A

sodium intake

32
Q

bread products, lunch meat and cured meats, pizza, soup, sandwiches, and poultry

A

“Salty Six.”

33
Q

is around 4200 mg/day in men and 3300 mg/day in women

A

Average sodium intake

34
Q

excess alcohol intake that results in cirrhosis is a frequent cause of secondary hypertension.

A

cirrhosis- alcohol then HTN

35
Q

and increases BP, especially in people with hypertension

A

Nicotine contained in tobacco causes vasoconstriction

36
Q

A wide variety of pathophysiologic responses can occur, including hypertension and tachycardia, inflammation, endothelial dysfunction, increased platelet aggregation, insulin resistance, and central obesity.12

A

activating the SNS and stress hormones.

37
Q

is orthostatic hypotension

A

common side effect of several of the antihypertensive drugs

38
Q

may occur with many antihypertensive drugs.

A

Sexual problems

39
Q

is the failure to reach goal BP in patients who are taking full doses of an appropriate 3-drug therapy regimen that includes a diuretic.

A

. Resistant hypertension

40
Q

of the renal nerves (known as renal denervation) may help lower BP and SNS activity in patients with resistant hypertension

A

Percutaneous catheter-based radiofrequency ablation

41
Q

Overactive renal nerves can be a

A

cause of resistant hypertension

42
Q

Some patients have elevated BP readings in a clinical setting and normal readings when BP is measured elsewhere. This phenomenon is referred to as

A

“white coat” hypertension.

43
Q

is one method for diagnosing white coat hypertension. It is a noninvasive, fully automated system that measures BP at preset intervals over a 12- to 24-hour period. The equipment is worn continuously for 24 hours, and results are reviewed by the provider.

A

Ambulatory BP monitoring (ABPM)

44
Q
  • Improper BP measurements (i.e., inappropriate BP cuff size)
  • Inadequate drug doses
  • Inappropriate drug therapy
  • Poor adherence to drug regimen (e.g., due to side effects, finances)
  • White coat syndrome
A

• Causes of pseudoresistant hypertension:

45
Q

Some people have a wide gap between the first Korotkoff sound and subsequent beats. This is called the

A

auscultatory gap.

46
Q

decrease of 20 mm Hg or more in SBP, a decrease of 10 mm Hg or more in DBP, and/or an increase in the HR of 20 beats/min.

A

Orthostatic hypotension

47
Q

(1) loss of elasticity in large arteries from atherosclerosis, (2) increased collagen content and stiffness of the myocardium, (3) increased peripheral vascular resistance, (4) decreased adrenergic receptor sensitivity, (5) blunting of baroreceptor reflexes, (6) decreased renal function(7) decreased renin response to sodium and water depletion.

A

age-related physical changes:

48
Q

is a term used to indicate either a hypertensive urgency or emergency

A

Hypertensive crisis

49
Q

have evidence of target organ disease. It most often requires hospitalization for immediate, controlled reduction of BP. Without prompt treatment, a hypertensive emergency can produce severe problems. These include encephalopathy, intracranial or subarachnoid hemorrhage, HF, MI, renal failure, dissecting aortic aneurysm, and retinopathy

A

Hypertensive emergencies

50
Q

has no clinical evidence of target organ disease. Hospitalization may not be needed to correct the BP. Hypertensive urgency is much more common than hypertensive emergency. It may be associated with chronic, stable complications such as stable angina, chronic HF, or prior MI or cerebrovascular accident with no threat of an acute event.

A

Hypertensive urgency

51
Q

occurs more often in patients with a history of hypertension who have not adhered to their medication regimens or who have been undermedicated. Rapidly increasing BP can cause shearing of the endothelial surface due to turbulent blood flow within the vessels leading to further vascular damage and the release of more vasoconstricting substances. A vicious cycle of BP elevation follows, leading to life-threatening damage to target organs

A

A hypertensive crisis

52
Q

often presents as hypertensive encephalopathy, a syndrome in which a sudden rise in BP is associated with a severe headache, nausea, vomiting, seizures, confusion, and coma. Th

A

A hypertensive emergency

53
Q

is the most effective IV drug to treat hypertensive emergencies

A

Sodium nitroprusside

adn semester 2 (19 decks)

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