Hypertension

Question 1

Hypertension

Answer 1

Etio:

90% unknown etio (primary HTN)

Sys-HTN in elderly – central arterial loss of elasticity

10% secondary to sleep apnea, drug induced, kidney, thyroid etc. Lifestyle (obesity, alcohol, Na+, phy inactivity)

Question 2

Renin–Angiotensin–Aldosterone system (RAAS)

Answer 2

Reduced renal blood flow >> renin release

angiotensinogen ———-> angiotensin I by renin

angiotensin I —————> angiotensin II by ACE

angiotensin II >>> increase secretion of aldosterone

• Angiotensin II = vasoconstrictor*
• Aldosterone = Na+ conservation*

Question 3

Adverse outcome related to HTN

Answer 3

MI 50%

Stroke 33%

Renal failure 15%

Clinical complications: renal failure, stroke, coronary insufficiency, MI, CHF, dementia, encephalopathy, blindness

Question 4

Systolic vs Diastolic

Answer 4

s-BP peak of ventricular contraction

d-BP resting resistance

Diastolic more ipt risk factor before age 50

Systolic more ipt after age 50.

sBP rises thru life, dBP levels/falls after age 50

Isolated dHTN in younger adults (likely benign).

Isolated sHTN in older adults (CV risk)

Question 5

Symptoms of HTN

Answer 5

Early

H/A, tinnitus, dizziness, retina narrowed arterioles with sclerosis.

Advanced

Eye (retinal vessel hemorrhage, exudate, papilledema).

Brain (hypertensive encephalopathy: HA, N/V, convulsion, coma).

Heart (CHF, enlarged left ventricle).

Kidney (hematuria, proteinuria, renal failure)

Question 6

Medical treatment

Answer 6

Pre-HTN lifestyle modification.

HTN: goal below 140/90 (130/80 if DM or kidney dz)

Severe uncontrolled HTN 180/110 – urgent or immediate tx/hospitalization.

Hypertensive emergencies (Evidence of impending/progressive target organ dysfunc – HTN encephalopathy, stroke, acute MI, left ventricular failure with pulmonary edema, unstable angina pectoris) – immediate BP reduction in 1 hour, ICU admission. Non-emerg: H/A, SOB, nosebleeds, severe anxiety.

Question 7

Pharmacology

Answer 7

Diuretics: help kidneys eliminate sodium

α-, B-Adrenergic receptor Blockers: block NE and EPI binding, relax BV and reduce speed of contractions

Angiotensin Converting Enzyme (ACE) inhibitors: Block ACE conversion of angiotensin I to angiontensin II (raises BP by triggering sodium and water retention)

Angiotensin Receptor Blockers (ARBs): blocks angiontensin II from receptors

Calcium Channel Blockers: Slows movement of calcium into smooth muscle cells of heart and blood vessels. Weakens contractions by slowing nerve impulses to heart

Direct Vasodilators: act quickly and are used for emergencies (can cause fluid retention and tachycardia)

Question 8

Dental management

Answer 8

• Monitor BP
• Dental Tx: Defer tx if higher than 180/110
• Chair position: orthostatic hypotension
• ABX: avoid calrithromycin/ertyrhomycin if pt on calcium channel blockers (amlodipine) —> exag’d low BP
• NSAIDs – if > 2 weeks, may decrease efficacy of anti-hypertensive drugs
• EPI:
  
  • <180/110 two carp 1:100K epi safe.
  • >180/110 med consult for EPI.
  • Avoid levonordefrin.
  • Potential B-blocker interaction with EPI (unlikely) may result in vasoconstriction (2 carp ok).
  • No EPI if malignant hyperthermia (inhalation general anesthetics)
• Stress reduction: triazolam, nitrous
• Bleeding: excessive possible but unlikely
• Greater risk if can’t meet a 4-MET demand (metabolic equiv: 1 flight of stairs w/o chest pain, SOB or fatigue)

Question 9

Endodontic Literature

Answer 9

Vickers, Baumgartner 2002: Ferric sulphate and Racellet pellets no effect on BP / pulse