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Renal Yr2 Exam 2 > HTN > Flashcards

HTN Flashcards

1
Q

HTN is more prevalent in:

A
  • Non Hispanic Black Populations

- Older Persons

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2
Q

JNC7 bases BP upon:

A

-The average of two or more properly measured readings at each of two or more visits after an initial screen

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3
Q

Normal BP

A

-Systolic: <80

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4
Q

Pre-HTN

A
  • Systolic: 120-139

- Diastolic: 80-89

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5
Q

Hypertension Stage 1

A
  • Systolic 140-159

- Diastolic: 90-99

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6
Q

Hypertension Stage 2

A
  • Systolic > or equal to 160

- Diastolic > or equal to 100

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7
Q

Isolated Systolic HTN

A

When BP is > or equal to 140/<90mmHg

-Wide pulse pressure present

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8
Q

Isolated Systolic HTN more common in individuals

A

Over age 60. Have diminished compliance of vasculature

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9
Q

Blood pressure increases with

A

Age

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10
Q

Non-reversible Risk Factors:

A
  • African-American descent

- Family history of HTN

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11
Q

Reversible Risk Factors

A
  • Pre-HTN
  • Obesity
  • Sedentary Lifestyle
  • High sodium diet
  • Excessive alcohol intake
  • Metabolic Syndrome
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12
Q

HTN major risk factor for:

A
  • CV disease
  • Chronic Kidney Disease
  • Dementia
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13
Q

HTN single most important risk factor for?

A

Stroke

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14
Q

MCC death in persons w/HTN is?

A

Coronary artery disease

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15
Q

Left Ventricular Hypertrophy

A

Strong predictor of sudden death and MI in persons with HTN

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16
Q

In HTN, microalbuminuria

A

Marker for Increased CV risk

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17
Q

Diagnosis: requires SEVERAL BP measurements

A

1) Use validated sphygmomanometer
2) Correct size cuff on BARE arm
3) Resting quiet for at least 5 minutes
4) Back supported
5) Feet on ground & uncrossed
6) No talking

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18
Q

Masked HTN definition:

A

Normal in office, but underlying HTN target organ injury

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19
Q

PseudoHTN

A

See in older persons, falsely increased systolic & diastolic pressure by cuff due to STIFF vascular tree caused by atherosclerosis

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20
Q

Ambulatory reading > office measurements

A

Classification of bp based on average of 2+ readings obtained more than 1 min. apart on 2 or more visits

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21
Q

Ambulatory BP Monitoring

A
  • Evaluates mean 24 hr B.P.
  • Difference b/w mean daytime and mean nighttime bp
  • Avg difference used to evaluate for noctural dipping.
  • > 10% is dipping (good thing)
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22
Q

Lack of nocturnal dipping causes

A

More strain on CV system

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23
Q

Non-dipping (bad) often seen in

A
  • African Americans
  • Chronic Kidney Disease
  • Sleep Disorders
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24
Q

Lack of nocturnal dipping associated with

A

Increased CV risk

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25
Q

As we grow older our arteries become stiffer and less compliant

A
  • Stiffening, get increased speed of reflected waves

- Faster the pulse wave velocity, the greater the end organ damage.

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26
Q

Measurement of central aortic pressure and pulse wave velocity are better correlated with end-organ damage

A

> than brachial BP

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27
Q

Most anti-HTNs cannot slow pulse wave velocity

A

Statins do improve vasculature compliance.

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28
Q

3 questions to ask when evaluating HTN

A

1) BP: Essential (primary) vs. Secondary
2) CV Risk factors
3) End organ damage

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29
Q

Who is more prone to pseudo HTN?

A
  • Elderly
  • Chronically ill
  • These groups are also prone to orthostatic hypotension.
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30
Q

Meds that can elevate BP:

A
  • Oral contraceptives
  • Corticosteroids
  • Monoamine oxidase inhibitors
  • NSAIDs
  • Sympathomimetic preparations for cold or diet
  • Cocaine
  • Alcohol
  • Serotonin
  • Glycyrrhizinic acid (true licorice) in chewing tobacco
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31
Q

Physical Exam:

A
  • Measurement of vital signs
  • BMI
  • Cardiopulm exam
  • Auscultation of major blood vessels to identify bruits
  • Fundoscopic examination
  • Neuro
  • Evaluate extremities for edema and circulatory abnormalities.
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32
Q

Labs:

A
  • CBC
  • Lipid and biochem profiles
  • Urinalysis
  • Electrocardiogram
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33
Q

Wait to measure renin and aldosterone until:

A
  • See pt w/HYPOkalemia or resistant HTN

- Increased plasma aldo:renin ratio: suggests dietary Na+ excess HTN.

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34
Q

Clinical marker for LVH:

A
  • S4 gallop
  • Apical lift ECG
  • ECHO
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35
Q

Clinical marker for angina, prior MI, prior revascularization

A

History

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36
Q

Clinical marker for heart failure:

A

-History, lung RALES, S3 gallop, Chest x-ray, Echo

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37
Q

Marker for Stroke, TIA, Leukoariosis (white matter changes on imaging)

A

History and brain imaging

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38
Q

Marker Chronic Kidney Disease

A

eGFR, Creatinine, U/A, microalbumin

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39
Q

Marker Peripheral Artery Disease

A

-Claudication, bruits, diminished pulses

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40
Q

Marker Retinopathy

A

-Fundoscopic evaluation, general and focal narrowing, AV nicking, Copper wiring, cottom wool spots, microaneurysms, Frame and blot hemorrhages

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41
Q

Essential HTN

A

90% of patients with htn evaluated in the primary care setting

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42
Q

Classic Features of Essential HTN

A
  • Onset in fourth or fifth decade of life
  • A positive family hx for HTN
  • Initial BP low categorized as stage 1 HTN
  • And easily controlled with 1 or 2 medications
  • No target organ damage
  • Normal results of routine lab studies
  • BP that does not increase from an established level of control over a short period of time
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43
Q

Things that make you think secondary forms of HTN:

A
  • Age of onset, before 30, over 50
  • BP >180/110 mmHg at diagnosis, significant target organ damage
  • Poor response to an appropriate 3 drug regimen
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44
Q

Lifestyle modifications are appropriate to lower bp in patients with

A

Pre-HTN

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45
Q

Lifestyle modifications + drug treatment

A

Stage 1 or greater HTN

46
Q

Weight Reduction, maintaining normal body weight

A

5-20 mmHg reduction/10 kg weight loss

47
Q

Adapting DASH eating plan

A

8-14 mmHg reduction

48
Q

Dietary sodium reduction, no more than 1500 mg/day

A

2-8 mmHg

49
Q

Physical Activity, 30 minutes/day

A

4-9 mmHg

50
Q

Moderation of alcohol consumption

A

2-4 mmHg

51
Q

Goal of treatment of HTN:

A

Reduce CV mortality and morbidity by lowering BP

52
Q

Goal in general population of anti-HTN treatment

A

Lower BP below 140/90 mmHg

53
Q

Linear, progressive increase risk of ischemic heart disease and stroke in patients with bp higher than

A

115/75 mmHg

54
Q

Most anti-HTN agents reduce blood pressure by 10-15% and ALL classes of anti-HTN drugs

A

Reduce CV morbidity and mortality vs. placebo

55
Q

Treatment of systolic heart failure and proteinuria in kidney disease

A

ACE Inhibitors and ARBs

56
Q

Salt sensitive HTN

A

Diuretics, may be good in:

  • Elderly
  • Low GFR
57
Q

Coronary artery disease and migraine headaches

A

Beta-blockers

58
Q

Clinical trials have shown that achieving appropriate blood pressure targets is MORE important in reducing morbidity and mortality than

A

The choice of Anti-HTN therapy

59
Q

Use these drugs to help lower BP in patients who are likely to be sodium sensitive:

  • Older patients
  • Black
  • Lower pre-txt plasma renin activity
A

Calcium channel blockers

Diuretics

60
Q

Use for younger, white, and higher pre-txt plasma renin activity

A

ACE-Inhibitors or

Beta-blockers

61
Q

Lifestyle modification and drug treatment are indicated for all patients with

A

Stage I HTN or greater

62
Q

Patient with stage II HTN often require treatment with

A

more than one agent

63
Q

Resistant HTN

A

Patients whose BP remains above goal on maximum doses of 3 meds one of which is a diuretic.

64
Q

10% cases HTN due to secondary htn

A

Consider in pts who have clinical features inconsistent with essential HTN.
Common secondary causes: drugs, increasing obesity, obstructive sleep apnea

65
Q

Renal vascular htn

A

1-3% general HTN population
10% patients with resistant htn
30% pts in htn crisis

66
Q

Renal artery stenosis does NOT make a diagnosis of

A

Renal vascular htn

67
Q

70% or more luminal narrowing

A

Increases renin production from ischemic kidney

68
Q

Not all abdominal bruits are from renal artery

A

Diastolic component to bruit= renal artery lesion

69
Q

Unilateral disease

A

-nonischemic kidney increased perfusion, higher Na+ excretion and suppression of renin release

70
Q

Bilateral disease

A

-Increases in renin cause ECV expansion and volume dependent htn.

71
Q

Pulse pressure is a good assessment of

A

End organ damage

72
Q

Fibromuscular dysplasia

A

Most common cause of renovascular htn in younger women, esp childbearing age. Medial subtype most common. “String of beads” on angiography.

  • Balloon angioplasty is the treatment of choice
  • Stents reserve only if angioplasty fails
73
Q

Renal revascularization only improves htn in patients with

A

Anatomic lesion that is hemodynamically significant to activate the renin-angiotensin system.

74
Q

BOLD MRI

A

Bilateral renal artery stenosis present, ACE inhibitors and ARBS can make acute renal failure worse.

75
Q

Gold standard for identifying renal artery stenosis

A

-Renal angiography

76
Q

Top causes of secondary HTN

A 
#1: Primary hyperaldosteronism
#2: Renal parenchymal disease
77
Q

HTN is the 2nd most common cause of

A

End stage renal disease.

78
Q

3 mechanisms involved in HTN of renal disease

A

1) volume expansion b/c can’t get rid of salt and water
2) over secretion renin
3) Decreased production renal vasodilators

79
Q

Primary aldosteronism

A
  • Overproduction of aldosterone by adrenal glands
  • HTN, hypokalemia with renal wasting of potassium and metabolic ALKALOSIS.
  • Suppressed plasma renin activity
  • Increased aldosterone levels
80
Q

When to suspect primary aldosteronism:

A

Person with spontaneous hypokalemia, marked hypokalemia precipitated by usual dose of diuretics, resistant HTN, hypertension and adrenal mass, or hypokalemia despite use of ACE inhibitors or ARBs.

81
Q

Almost half of patients with primary aldosteronism have

A

Normal potassium levels

82
Q

Plasma aldosterone: renin ratio

A

Screening test for primary aldosteronism
urine aldosterone excretion 12 mcg/24 hours (33.2nmol/day) or higher after correction of hypokalemia and adherence to HIGH sodium diet for 3 days.

83
Q

Adrenal imaging

A
  • Aldosterone producing adenoma (Conn syndrome)

- Primary unilateral adrenal hyperplasia

84
Q

Can use spironolactone for treatment of

A

Primary aldosteronism

85
Q

Sometimes obese pts or with resistant htn can see dramatic decrease in bp when started on

A

Aldosterone antagonist

86
Q

Pheochromocytoma

A

Tumors of chromaffin cells, derived from neural crest.

  • Cause paroxysmal or sustained htn
  • excess production of catecholamines
  • Diaphoresis, headache, and anxiety frequently associated symtpoms
87
Q

Complications of pheochromocytoma

A
  • MI, stroke, cardiovascular collapse

- Can have germ-line mutations

88
Q

Familial pheochromocytoma occurs in

A
  • multiple endocrine neoplasia type II
  • von Hippel-Lindau disease
  • Neurofibromatosis
  • Familial paraganglioma
89
Q

Diagnosis pheo

A
  • Confirm excess catecholamine production supported by imaging studies
  • Fractionated catecholamines and metanephrines can be measured in the serum or via a 24-hour urine collection
  • MRI
  • CT scanning can localize
90
Q

Treatment of choice for pheochromocytoma

A

Surgical resection

-10-14 days before surgery give alpha blocker phenoxybenzamine , then beta-blockers started

91
Q

**Do NOT use Beta blockers without alpha blockage b/c

A

-Can lead to unopposed alpha stimulation and an increase in BP

92
Q

Catecholamines can induce vasoconstriction and pressure naturesis can cause decrease in plasma volume

A

-We can institute high sodium diet and avoid diuretics.

93
Q

HTN patient with impaired fasting glucose

A

Cushing syndrome

94
Q

Hypothyroidism

A
  • associated with diastolic htn
  • state of decreased cardiac output and contractility
  • Tissue perfusion maintained by increase in peripheral vasc. resistance mediated by increased activity of the sympathetic nervous system
95
Q

Hyperthyroidism

A
  • Associated with systolic HTN

- Wide pulse pressure due to increased CO and decreased peripheral vasc. resistance

96
Q

Hyperparathyroidism

A

-Hypercalcemia may increase BP directly by increasing peripheral vascular resistance and indirectly by increasing vascular sensitivity to catecholamines

97
Q

Acromegaly

A

-Can develop HTN due to Na+ retaining effects of GH.

98
Q

Coarctation of aorta

A
  • Constriction of vessel, detected in childhood
  • More common males
  • Assoc. with bicuspid aortic valve
  • Classic feature: increased BP in upper extremities and low BP in lower extremitie
99
Q

Symptoms of coarctation of aorta

A

Headache, cold feet, and claudication (pain by too little blood flow during exercise)
-Clinical signs: elevated bp in arms, murmurs in front and back of chest and delay in femoral pulse when radial and femoral pulses palpated.

100
Q

**NOTCHED ribs

A

Coarctation! Do surgical repair or balloon angioplasty

101
Q

Obstructive Sleep apnea

A
  • Upper body obesity
  • Overweight pts that snore loudly
  • Complains: morning headaches, daytime sleepiness
  • Sleep study**
  • Increased sympathetic nervous system
  • Treatment: continuous POSITIVE pressure, lower BP 3-5 mmHg.
  • Encourage to lose weight
102
Q

HTN emergency:

A
  • Need to hospitalize
  • Parenteral therapy!!!
  • HTN encephalopathy, aortic dissection, unstable angina, MI, eclampsia, pulmonary edema, and acute renal failure
  • Fibrinoid necrosis vascular lesion of malignant HTN
103
Q

HTN urgency

A
  • Severe HTN without evidence acute organ injury but occurring in setting in which it is important to decrease bp.
  • Oral therapy
104
Q

Common causes HTN urgency

A
  • Neglected essential HTN
  • Discontinuation of anti-htn therapy
  • Renovascular disease
  • Scleroderma
  • Stroke
105
Q

Sodium nitroprusside

A
  • DOC htn emergency
  • Don’t use in pts with kidney disease
  • Raises intracranial pressure in animals
  • Nitroprusside: worry about cyanide and thiocynate toxicity
106
Q

Labetalol

A

A combo of alpha and beta blocker

can use orally & IV

107
Q

Nicardipine and clevidipine

A

Ca2+ channel blockers

108
Q

Fenoldapam

A

IV dopamine agonist

Preserves renal perfusion and is good for patients with Increased creatinines

109
Q

Nitroglycerin

A

Good for pts w/acute congestive heart failure or coronary ischemia

110
Q

Esmolol

A

DOC for Aortic dissection!

Renal Yr2 Exam 2 (5 decks)

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