Clinical aspects of HTN - Henry

Question 1

essential HTN**

Answer 1

-no identifiable cause
-most common cause of HTN*
-increased peripheral vascular resistance,
but normal CO**
-no cure, but there are treatments*
-usually asymptomatic, normal labs

-3 possible causes: genetic, low nephron number (premies), acquired renal failure

Question 2

secondary HTN**

Answer 2

• usually have something you can treat* (ex. take out tumor or treat renal stenosis)
• more resistant to therapy** (harder to control)

Question 3

RAAS

Answer 3

• contributes to high BP
• treat with ACEI, ARB, etc.
• renin released from juxtaglomerular cells in kidney

Question 4

endothelin

Answer 4

• from normal endothelium

- reduces levels of NO –> vasoconstriction –> high bp

Question 5

how to approach HTN

Answer 5

1. measure BP
2. evaluate CV risk (ex. lipid status for atherosclerosis, EKG for heart damage LVH, urine)
3. suspect and evaluate for secondary HTN

Question 6

orthostatic HTN

Answer 6

• fall in BP upon standing

- diabetic neuropathy is a cause

Question 7

organ damage from HTN*

Answer 7

1. heart
   -LVH, diastolic dysfunction, CHF, atherosclerosis, CAD
   -HFrEF, HFpEF* (most common)
2. peripheral arterial disease (PAD)
   -caused by atherosclerosis –> obstruction and decrease compliance (remodeling)
   -usually lower extremities
3. brain
   -high BP most modifiable risk factor for stroke (infarction)**
   -cognitive impairment
   (dementia)
   -malignant HTN –> cerebral edema, increased intracranial pressure
4. kidneys
   -leading cause of renal failure
   -expand volume –> increase BP
   -glomerular sclerosis with chronic HTN
   -good control of BP slows progression of renal disease (goal is BP 130/80 or less)***
5. eyes
   -vision loss due to retinal damage
   -early HTN –> cotton wool spots
   -late HTN –> copper wire changes
   -malignant HTN –> papilledema* of optic nerve

Question 8

slide 26

Answer 8

-target organ damage

Question 9

HTN emergency***

-malignant HTN

Answer 9

• major elevations in BP with acute target organ dysfunction
• ex. aortic dissection, eclampsia
• lower BP quickly

Question 10

what is the target goal of BP with target organ damage?**

Answer 10

-BP 130/80**

Question 11

secondary causes of HTN

Answer 11

1. metabolic syndrome
   - big player (60% cases)
   - insulin resistance/glucose intolerance (diabetes) –> dyslipidemia (atherosclerosis), hypertrophy of VSM (decrease compliance), + sympathetic response (vasoconstriction)
2. renovascular HTN (2 types)
   - stenosis of renal artery from atherosclerosis* (males) –> under perfusion –> + RAAS
   - fibromuscular dysplasia* (females) –> string of pearls on arteriogram from thickening of artery
   - flash pulmonary edema and unilateral small kidney**
3. renal parenchymal HTN
   - anything causing renal damage + RAAS
   - increased BUN, creatinine, proteinuria
4. primary aldosteronism
   - excess aldosterone excretion from adrenal cortex
   - will see hypokalemia*
   - adrenal tumor possible
   - plasma aldosterone to plasma renin ratio >20 for diagnosis
5. Cushing syndrome
   - excess cortisol secretion from adrenal gland
   - weight gain, abdominal stria, truncal obesity, buffalo hump, HTN, high glucose
6. pheochromocytoma
   - tumor from chromaffin tissue in adrenal medulla
   - secrete NE, Epi –> increase sympathetic –> increase BP
   - pounding headachee, palpitations, tremor, diaphoresis
   - caused by multiple adrenal neoplasia (type 2A, 2B), von hippel-lindau disease, neurofibromatosis*

Question 12

who is more at risk for HTN and CV disease and renal problems?

Answer 12

african americans

Question 13

pulse pressure***

Answer 13

-with increasing age, systolic bp rises while diastolic bp declines** –> WIDER pulse pressure