Renal Htn

Front 1

Kidney actions when BP falls...

Back 1

-Angiotensinogen (renin) --> Ang I (ACE) --> Ang II --> vasoconstriction --> BP rises

Front 2

Kidney actions when BP falls...

Back 2

-Angiotensinogen (renin) --> Ang I (ACE) --> Ang II --> vasoconstriction --> BP rises

Front 3

definitions

Back 3

-slide 2

Front 4

Target organ damage

Back 4

1. Heart: LV hypertrophy, ischemic heart dz. CHF
2 Kidney: 2nd most common cause of ESRD
3. CVA: most common cause of stroke
4. peripheral arterial disease
5. retinopathy

Front 5

the increase in risk from BP begins as the BP rise above..

Back 5

110/75

Front 6

definitions

Back 6

-slide 2

Front 7

Kidney actions when BP falls...

Back 7

-Angiotensinogen (renin) --> Ang I (ACE) --> Ang II --> vasoconstriction --> BP rises

Front 8

Target organ damage

Back 8

1. Heart: LV hypertrophy, ischemic heart dz. CHF
2 Kidney: 2nd most common cause of ESRD
3. CVA: most common cause of stroke
4. peripheral arterial disease
5. retinopathy

Front 9

Causes of resistant HTN: Vol overload and pseudotolerance

Back 9

1. excess Na intake
2. vol retention from kidney disease
3. inadequate diuretic therapy

Front 10

the increase in risk from BP begins as the BP rise above..

Back 10

110/75

Front 11

Causes of resistant HTN: Drug- induced or other causes

Back 11

1. nonadherence
2. inadequate doses
3. NSAIDs
4. cocaine, amphetamines
5. Sympathomimetics
6. OCs
7. adrenal steroids
8. cyclosporine
9. erythropoietin

Front 12

definitions

Back 12

-slide 2

Front 13

Target organ damage

Back 13

1. Heart: LV hypertrophy, ischemic heart dz. CHF
2 Kidney: 2nd most common cause of ESRD
3. CVA: most common cause of stroke
4. peripheral arterial disease
5. retinopathy

Front 14

Causes of resistant HTN: Vol overload and pseudotolerance

Back 14

1. excess Na intake
2. vol retention from kidney disease
3. inadequate diuretic therapy

Front 15

patho of essential HTN

Back 15

-increase sympathetic neural activity, with enhanced beta adrenergic responsiveness
-inc angiotensin II activity and mineralcorticoid excess
-Hypertension is about twice as common in subjects who have one or two hypertensive parents and multiple epidemiologic studies suggest that genetic factors account for approximately 30 percent of the variation in blood pressure in various populations .
-Reduced adult nephron mass predisposes to hypertension, which may be related to genetic factors, intrauterine developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), and post-natal environment (eg, malnutrition, infections).

Front 16

the increase in risk from BP begins as the BP rise above..

Back 16

110/75

Front 17

Causes of resistant HTN: Drug- induced or other causes

Back 17

1. nonadherence
2. inadequate doses
3. NSAIDs
4. cocaine, amphetamines
5. Sympathomimetics
6. OCs
7. adrenal steroids
8. cyclosporine
9. erythropoietin

Front 18

Malignant HTN

Back 18

-marked HTN with retinal hemorrhages, exudate, or papilledema
-assoc with diastolic P >120 (can occur at diastolic P as low as 100)

Front 19

HTN urgency

Back 19

-sever HTN
-diastolic >120
-asymptomatic pts
-no evidence of end organ damage

Front 20

Causes of resistant HTN: Vol overload and pseudotolerance

Back 20

1. excess Na intake
2. vol retention from kidney disease
3. inadequate diuretic therapy

Front 21

patho of essential HTN

Back 21

-increase sympathetic neural activity, with enhanced beta adrenergic responsiveness
-inc angiotensin II activity and mineralcorticoid excess
-Hypertension is about twice as common in subjects who have one or two hypertensive parents and multiple epidemiologic studies suggest that genetic factors account for approximately 30 percent of the variation in blood pressure in various populations .
-Reduced adult nephron mass predisposes to hypertension, which may be related to genetic factors, intrauterine developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), and post-natal environment (eg, malnutrition, infections).

Front 22

Causes of resistant HTN: Drug- induced or other causes

Back 22

1. nonadherence
2. inadequate doses
3. NSAIDs
4. cocaine, amphetamines
5. Sympathomimetics
6. OCs
7. adrenal steroids
8. cyclosporine
9. erythropoietin

Front 23

Malignant HTN

Back 23

-marked HTN with retinal hemorrhages, exudate, or papilledema
-assoc with diastolic P >120 (can occur at diastolic P as low as 100)

Front 24

identifiable causes/risk factors for HTN

Back 24

1. primary renal dz
2. more common and severe in blacks
3. if persons parents have HTN, person is at a higher risk
4. sodium intake
5. may be more common in persons with certain personality traits, such as hostile attitudes, impatient
6. obesity
7. dyslipidemia (independent of obseity)
8. sleep apnea
9. meds
10. chronic alcohol intake and alcohol abuse

Front 25

patho of essential HTN

Back 25

-increase sympathetic neural activity, with enhanced beta adrenergic responsiveness
-inc angiotensin II activity and mineralcorticoid excess
-Hypertension is about twice as common in subjects who have one or two hypertensive parents and multiple epidemiologic studies suggest that genetic factors account for approximately 30 percent of the variation in blood pressure in various populations .
-Reduced adult nephron mass predisposes to hypertension, which may be related to genetic factors, intrauterine developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), and post-natal environment (eg, malnutrition, infections).

Front 26

HTN urgency

Back 26

-sever HTN
-diastolic >120
-asymptomatic pts
-no evidence of end organ damage

Front 27

identifiable causes/risk factors for HTN

Back 27

1. primary renal dz
2. more common and severe in blacks
3. if persons parents have HTN, person is at a higher risk
4. sodium intake
5. may be more common in persons with certain personality traits, such as hostile attitudes, impatient
6. obesity
7. dyslipidemia (independent of obseity)
8. sleep apnea
9. meds
10. chronic alcohol intake and alcohol abuse

Front 28

Malignant HTN

Back 28

-marked HTN with retinal hemorrhages, exudate, or papilledema
-assoc with diastolic P >120 (can occur at diastolic P as low as 100)

Front 29

HTN urgency

Back 29

-sever HTN
-diastolic >120
-asymptomatic pts
-no evidence of end organ damage

Front 30

identifiable causes/risk factors for HTN

Back 30

1. primary renal dz
2. more common and severe in blacks
3. if persons parents have HTN, person is at a higher risk
4. sodium intake
5. may be more common in persons with certain personality traits, such as hostile attitudes, impatient
6. obesity
7. dyslipidemia (independent of obseity)
8. sleep apnea
9. meds
10. chronic alcohol intake and alcohol abuse

Front 31

secondary HTN

Back 31

1. pheochromocytoma
2. primary hyperaldosteronism
3. renovascular dz
4. cushings
5. endocrine: hypo/hyperthyroidism, hyperparathyroidsim
6. coarctation of the aorta

Front 32

diagnosis and screening

Back 32

-screening every 2 yrs with nml BP and yearly for preHTN
-In the absence of end-organ damage, the diagnosis of mild hypertension should not be made until the blood pressure has been measured on at least three to six visits, spaced over a period of weeks to months.

Front 33

white coat HTN

Back 33

-20 to 25 % of patients with mild office hypertension (diastolic pressure 90 to 104 mmHg) have "white-coat" or isolated office hypertension in that their blood pressure is repeatedly normal when measured at home, at work, or by ambulatory blood pressure monitoring

Front 34

w/u of HRN

Back 34

-History: meds, alcohol, smoking, FH, sx, extent og organ damage
-PE: The main goals on the physical examination are to evaluate for signs of end-organ damage (such as retinopathy) and for evidence of a cause of secondary hypertension.

Front 35

Labs

Back 35

1. Hct
2. UA
3. chemistries
4. fasting lipids
5. EKG

Front 36

when to suspect secondary HTN

Back 36

1. age- too young or old
2. no FH
3. BP poorly responding to tx
4. sudden onset
5. episodic HTN
6. buit- abdominal, back
7. decreased femoral pulses
8. abd mass
9. flash pulmonary edema
10. INCR Cr, BUN,EDEMA – intrinsic renal disease
11. truncal obseity
12. HYPOKALEMIA, HYPERCALCEMIA

Front 37

chronic kidney disease

Back 37

-CKD form any cause can lead to HTN
-HTN exacerbates progression of CKD- ateriosclerosis
-mechanism of CKD leading to HTN is initially RAA activation, later prominent sodium retention

Front 38

primary hyperaldosteronism

Back 38

-10-20% of pts with resistant HTN
-The presence of primary mineralocorticoid excess, primarily aldosterone, should be suspected in any patient with the triad of hypertension, unexplained hypokalemia, and metabolic alkalosis
->50% of pts with proven primary hyperaldosteronism are normokalemic at pres

Front 39

primary hyperaldosteronism dx and tx

Back 39

Dx: serum aldo to renin ratio (>20 is sig), 24 hr urine also level, CT with adrenal adenoma
Tx: Spironolactone, Resection of adrenal adenoma

Front 40

Renal artery stenosis

Back 40

-2-5% of all HTN
-common cause of resistant HTN
-common in older vasculopathys, rarely in young women
-Clues: flash pum edema, resistant HTN, worse renal funtion with ACE if bilat disease, bruit, hypokalemia

Front 41

renal artery stenosis dx and tx

Back 41

Dx: duplex US, MRA, captopril scan, angiography (gold standard!)
Tx: angioplasty, med mgmt, surgery

Front 42

Pheochromocytoma

Back 42

-<.2% of HTN pts
-Triad: HA, sweating, tachycardia
-50% of pts have paroxysmal HTN, rest appear to have essential HTN
-Dx: symptomatic pts, adrenal mass, FH
-Labs: urinary and plasma fractionated metanephrines and catecholamines
-Rx: alpha and beta blocker, surgery

Front 43

Obstructive sleep apnea

Back 43

-common among pt with resistant HTN who are referred for sleep studies
-the severity of sleep apnea correlates with the severity of HTN and both the incidence and severity of apnea

Front 44

lifestyle modifications to manage HTN

Back 44

1. wt loss
2. DASH eating plan
3. sodium reduction
4. exercise
5. moderation of alcohol consumption