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Adult Clinical Medicine > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the definition of essential hypertension

A

-Systolic Blood pressure (BP) 140 mm Hg or higher
OR
-Diastolic BP 90 mm Hg or greater
-Elevated BP are consistent over time in patient’s usual state of health
-No evident secondary cause.

*Thus, Essential hypertension = Primary hypertension

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2
Q

Why do we call primary hypertension “essential hypertension”

A
  1. Systolic blood pressure (SBP) rises with age due to arterial stiffening (True)
  2. Historical Misconception : aged blood vessels “require” higher blood pressures for organ perfusion
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3
Q

What is the relationship between BP and mortality

A

“J-point” or “U-shaped” curve of mortality and BP
*high mortality w/ high pressures and very low pressures

Mortality greater for SBP over 139 vs. 100-119 mm Hg

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4
Q

Describe the pathophysiology of essential BP

A
  1. ↑ Cardiac Output (CO) and/or ↑ Peripheral Vascular Resistance (PVR)
  2. CO = Stroke Volume (SV) x Heart Rate (HR)
  3. PVR determined by systemic and local factors that either dilate or constrict arteries.
  4. Increased SV due to increased extra-cellular volume, generally from higher sodium levels
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5
Q

What can cause increased PVR?

A
  1. ↑ by SNS vasoconstriction
  2. ↑ by higher Angiotensin II (from ↑RAAS) and/or lower kallikrein-kinin levels
  3. Impaired endothelial-dependent local vasodilation (impaired local NO production or impaired NO-dependent signaling)
  4. Mediating factors: Metabolic stress of overweight/obesity – ↑insulin resistance
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6
Q

How do you make sure it’s hypertension

A
  1. recheck BP after patient seated calmly for 10 minutes (resting)
  2. Elevated BP over 2-3 visits over ≥ 2 weeks
  3. Make sure it’s “primary HTN” - rule out secondary causes,)
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7
Q

Risk stratification for HTN

A
  1. other CV risks: hyperlipidemia, smoking, DM2, known vascular dz
  2. assess for BP related end organ damage
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8
Q

What is the goal sodium intake daily

A

less than 1500-2000mg daily

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9
Q

What PE is important to do for HTN

A
  1. funduscopic
  2. cardiopulmonary
  3. pulses of 4 extremities
  4. neurologic examination
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10
Q

What is the appropriate measurement technique to take BP

A
  1. Patient seated 10 or more minutes
  2. Back supported and feet are on floor
  3. Arm supported at 90-degree angle
  4. Appropriate size cuff (use markings on cuff)
  5. Measure BP in both arms - highest BP guides treatment
  6. Record BP to closest even number
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11
Q

How do confirm the dx of HTN

A

2+ readings 140/90 or higher, spaced at least 2 weeks apart

  • In anxious patients, consider home BP cuff or ambulatory BP monitor to rule out White Coat HTN (~13%)
  • Rule out secondary causes of HTN
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12
Q

Secondary causes of HTN

A
  1. Heavy EtOH use (even mild withdrawal causes SNS activation)
  2. Most antidepressants are BP-neutral but venlafaxine will ↑BP
  3. Hypo and hyperthyroidism
  4. renovascular disease
  5. Primary renal disease
  6. OCPs
  7. NSAIDS
  8. Stimulants (cocaine, meth)
  9. PCC
  10. primary aldosteronism
  11. Cushing’s
  12. Sleep apnea**
  13. Coarctation of the aorta
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13
Q

When people are on 3 meds for HTN and its still not well controlled, you should think ____

A

secondary HTN

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14
Q

Clues to secondary HTN

A
  1. thin, health before age 30
  2. Obese with snoring and daytime somnolence? (OSA)
  3. Onset of HTN before puberty?– congenital
  4. Recently started on NSAIDs OR birth control containing estrogen OR venlafaxine OR taking steroids;
  5. Social hx for heavy EtOH use/SNS activating substances?
  6. Fatigue, unintentional weight gain, cold intolerance, constipation?
  7. Fhx of secondary cause
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15
Q

What are the 5 P’s of pheochromocytoma?

A
  1. palpitations
  2. perspiration
  3. pallor
  4. pounding HA
  5. increased BP
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16
Q

Screening for sleep apnea

A
  1. feel refreshed in the morning?
  2. Fall asleep easily
  3. snore?
  4. wake themselves up sometimes
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17
Q

What are Cushing features

A
  1. cushingoid facies,
  2. buffalo hump,
  3. increased supraclavicular fat pad,
  4. central obesity,
  5. purple stria
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18
Q

Assessing for target organ damage

A
  1. Neurological: HA, transient sx (blindness, weakness)
    * R/O prior CVA w/ CN, strength, sensation, and cerebellar testing
  2. CV: CP, DOE, claudication, decreased pulses, S4- LVH
  3. Opthalmology” cotton-wool spots, AV nicking
  4. Pulm: rales (CHF)
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19
Q

What are cotton wool spots

A

infarction of nerve fiber layer of the retina

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20
Q

Labs to rule out secondary causes of HTN

A
  1. Electrolytes (including sodium, potassium, calcium)
    - Excludes hyperaldosteronism, hyperparathyroidism as secondary causes
  2. Creatinine (rule out renal disease)
  3. Thyroid Stimulating Hormone (rule out hypothyroid)
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21
Q

Labs/tests to risk-stratify for HTN

A
  1. Lipid Panel (to further define 10yr CV risk profile)
  2. fasting glucose of HbgA1c (look for DM)
  3. EKG (assess for left ventricular hypertrophy as sign of cardiac damage from long-standing hypertension)
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22
Q

Counseling for life style modifications for HTN BEFORE starting meds

A
  1. Weight maintenance/loss: ↓10kg = ↓BP 5-20 mm Hg (only if BMI over/= 25)
  2. 30 minutes exercise/day: ↓BP 4-9 mm Hg
  3. Sodium <2400 mg/day: ↓BP 2-8 mm Hg (some are salt sensitive, ie. AA)
  4. Restrict EtOH: ↓BP 2-4 mm Hg (2 drinks/day for males, 1 drink/day for females)
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23
Q

Counseling after initiating medication for BP

A
  1. same as before starting meds

2. medication adherence

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24
Q

Eighth Joint National Committee on Hypertension (JNC8) Recommendations Goal BP:

A
  1. Adults 60 years or older and NO CKD: less than 150/90
  2. Adults 60 years or older and + CKD: less than 140/90
  3. Adults less than 60 years: less than 140/90
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25
Q

Compelling indications for classes of antihypertensive medications

A
  1. CKD: ACEI or ARB–> especially with proteinuria
  2. black/AA: diuretic or CCB
  3. all other race/ethnicity: diuretic or ACEI/ARBs or CCB
26
Q

1st line agents for HTN

A
  1. Thiazide-type diuretic
  2. ACEI/ARB
    Calcium-channel Blocker (CCB)
27
Q

2nd line agents for HTN

A
  1. BB
  2. aldosterone antagonist diuretic (spironoloatone)
  3. others
28
Q

Mechanism of action- decrease total body salt and water (decreased blood volume)

A

thiazide and loop diuretics

29
Q

side effects of thiazide and loop diuretics

A
  1. Dehydration (MUCH more common with loop diuretics (e.g., furosemide) at higher doses, elderly can be sensitive to thiazides as well)
  2. Hypokalemia (monitor for this)
  3. Worsens insulin resistance in DM/metabolic syndrome
  4. Contra-indicated in pregnancy as increased extracellular volume needed to support fetus
  5. Increases uric acid and may cause gout attacks
30
Q

Mechanism of Action

Competes with Aldosterone at distal renal tubule, conserves potassium while causing excretion of sodium/water

A

aldosterone antagonist

31
Q

side effects of aldosterone antagonists

A
  1. Hyperkalemia (monitor electrolytes after initiation, contra-indicated if baseline non-hemolyzed potassium over 5.0-5.3 mg/dl)
  2. Dehydration (less profound than loop diuretics)
32
Q

Beneficial effects of aldosterone antagonists

A

Uric Acid neutral, unique amongst diuretic class

33
Q

Mechanism of Action
Inhibits activation of Renin-Angiotensin-Aldosterone system, leads to decreased salt/water retention by kidney and decreased peripheral vascular resistance

A

ACEI

34
Q

Side effects of ACEI

A
  1. Hyperkalemia (monitor electrolytes after initiation, contra-indicated if baseline non-hemolyzed potassium over5.0-5.3 mg/dl)
  2. Cough (up to 10% of patients)
  3. Urticaria/Angioedema (1/3000)
  4. Contra-indicated in pregnancy (birth defects)
35
Q

benefits of ACEI

A

Beneficial Effect: Up to 25% decreased incidence of DM in HTNive individuals

36
Q

Mechanism of Action: Inhibits RAAS one step later than ACE-I (inhibits Angiotensin II binding to receptor and secretion of Aldosterone)

A

RAAS

37
Q

Side effects of ARBs

A
  1. Hyperkalemia (same risks as ACE-I)

2. Angioedema- case reports of this in pts who had angioedema with ACE-I, but much rarer to occur than with ACE-I

38
Q

benefits of ARBs

A

Decreased Insulin resistance (LIFE/ICARUS study), similar 25% decrease in DM in at-risk subjects to ACE-Is

39
Q

MOA for dihydropyridine and non-DHP (CCBs)

A

Dihydropyridine (DHP): Vasodilate peripheral blood vessels and decrease vascular resistance

Non-DHP: Predominantly lower heart rate, have lesser peripheral dilation properties

40
Q

Side effects of CCBs

A
  1. edema
  2. bradycardia (non-DHP)
  3. CHF exacerbation (non-DHP)
41
Q

Mechanism of Action
Lowers heart rate (remember CO = HR x SV)
Decreases peripheral vascular resistance mediated by SNS

A

BB

42
Q

Side effects of BB

A
  1. CONTRA-INDICATED in asthma ( bronchoconstriction)
  2. Bradycardia (proportional to dose)
  3. CHF exacerbation (use encouraged in STABLE CHF patients, but with caution advised for low dose initiation and slow up-titration)
  4. Masks signs/symptoms of hypoglycemia in diabetes
  5. Increased insulin resistance in 1st-generation, neutral in 2nd-gen (metoprolol), decreased insulin resistance in 3rd-gen (carvedilol) per GEMINI study)\
43
Q

What BP meds are used in pregnancy

A

1st-line: Methyldopa (long track record)
2nd-line: Labetalol

Additional options:

  • Extended release nifedipine (safety well-documented in 3rd trimester)
  • Hydralazine (Rare fetal thrombocytopenia reported with hydralazine)
44
Q

When would you likely start 2 BP meds in combo

A

if SBP is over 160mmHg

*hard to differentiate if pt has side effect

45
Q

Flow chart of HTN management

A
  1. Determine BP goal for age/CKD status
  2. Tx w/ lifestyle interventions
  3. if BP still above goal, start BP rxn
  4. If BP remains above goal despite lifestyle interventions and starting BP rx: Reinforce lifestyle and adherence, Up-titrate or add rx
  5. Reassess/repeat

*can take about 2 weeks to see a difference in BP after med change

46
Q

CKD is defined as

A

GFR less than 60 ml/min/1.73 m2 OR

Microalbuminuria (over 30 mg albumin/g of creatinine)

47
Q

If there are no compelling indications, what anti-hypertensive medication should be first-line?

A

JNC-8 states thiazide diuretic or ACE-inhibitor or ARB or CCB

48
Q

___ superior in reducing CV events/death by 2.2%

A

ACE-I + CCB

49
Q

__ class of HTN is superior to ___ for stroke;
and
___ superior to __ for CHF

A

Diuretic
ACE-I

Diuretic
CCB

50
Q

CCB-ACE-I combinations may be slightly more beneficial than diuretics/ACE-I combinations in certain populations including

A

older white pts at high risk for CAD w/ normal creatinine clearance

51
Q

Studies have shown __ conditions may show benefit from looser control, but some show __ conditions are better with tighter control

A

looser: DM (150/90

Tighter: better stroke outcomes and equivalent mortality

52
Q

What is a hypertensive urgency

A

Blood pressure 180/120 or higher WITHOUT end-organ damage

*Often requires emergent evaluation for studies to rule out end-organ damage

53
Q

Tx of hypertensive urgency

A
  1. oral medications to lower BP to less than 160/100 over 3-6 hours
  2. Recommendation for initiating 1 medication with close follow-up to add a second – choose appropriate class of medication for patient in long-term with preference for diuretic class
54
Q

What is hypertensive emergency

A 
Elevated BP (180/120 mm Hg or over) AND end-organ damage
**End-organ damage
55
Q

Neuro signs of end organ damage from HTN

A
  1. reversible encephalopathy,
  2. hemorrhagic stroke,
  3. retinal exudates/hemorrhages- Retinal exudates due to ischemic changes, hemorrhages due to leaks of affected vessels.
  4. papilledema
56
Q

CV signs of end organ damage from HTN

A
  1. Unstable angina/MI,
  2. heart failure with pulmonary edema,
  3. aortic dissection
57
Q

renal damage signs of end organ damage from HTN

A
  1. proteinuria,
  2. hematuria,
  3. acute renal failure
58
Q

Evaluation of Hypertensive emergency (malignancy)

A
  1. Question for sx of emergency
  2. Exam including funduscopy, neurologic exam, and full cardiopulmonary exam including pulses and jugular venous pressure (JVP) assessment
  3. Data: UA, renal fxn, creatinine, EKG, neuro imaging ONLY required if +sx or abnormal exam

*Triage patient to Emergency Department if +sx or exam findings concerning for end-organ damage

59
Q

Therapy for hypertensive emergency

A
  1. Performed in E.D./ICU
  2. IV medications used to lower DBP by MAX of 25% in 2-6 hours
    * Can get hypoperfusion of the brain if you lower it too quickly
  3. Goal DBP 100-105 mm Hg within minutes to 2 hours
60
Q

What meds are commonly used to lower BP In a hypertensive emergency

A
  1. Nitroprusside (arterial/venodilator, limited by thiocyanate toxicity, especially in those with impaired renal function)
  2. Labetalol (alpha and beta-blocker)
  3. Fenoldopam (peripheral dopamine-1 agonist causes vasodilation, improves renal perfusion)
  4. Hydralazine (peripheral vasodilator)

*Used IV

Adult Clinical Medicine (26 decks)

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