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Renal Exam > Pathophysiology of HTN > Flashcards

Pathophysiology of HTN Flashcards

1
Q

key steps for proper BP measurements

A
  1. properly prepare the pt
    -rest quietly for ~5 min
    -pt should be relaxed, sitting, both feet on floor, remove clothing under the cuff, no recent caffeine or smoking
  2. use proper technique for BP measurements
    -BP cuff size should be appropriate
    -use an upper arm measurement, around the level of the heart/right atrium
  3. take the proper measurements needed for dx and tx of elevated BP/HTN
  4. properly document BP readings & average multiple readings
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2
Q

normal blood pressure

A

SBP < 120 AND DBP < 80

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3
Q

elevated blood pressure

A

SBP 120-129 AND DBP < 80

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4
Q

stage 1 HTN

A

SBP 130-139 OR DBP 80-89

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5
Q

stage 2 HTN

A

SBP 140+ OR DBP 90+

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6
Q

primary (essential) HTN - defined

A

*unknown cause
*likely genetic & environmental influences

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7
Q

secondary HTN - defined & when to suspect it

A

*due to an identifiable cause
*consider secondary HTN if…
-refractory or resistant HTN
-young age of onset (<30 in adults)
-associated hypokalemia
-abrupt onset or significant increase in HTN in a short period of time
-very severe HTN

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8
Q

refractory/resistant hypertension - defined

A

*blood pressure that is still not at goal despite treatment with 3 medications at max tolerated dose, all from different classes, including a diuretic

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9
Q

hypertensive urgency vs. emergency

A

*both have severe HTN: BP 180/120 or higher
*HTN urgency: no end organ damage
*HTN EMERGENCY: SIGNS OF END ORGAN DAMAGE:
-pulmonary edema
-papilledema, ICH
-MI/elevated troponins
-AKI
-aortic dissection

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10
Q

white coat hypertension - defined

A

*HTN only seen in doctor’s office
*normal BP at home, however, pt is more nervous in medical setting, so blood pressures are higher
*this can be confirmed with 24h ambulatory BP monitoring

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11
Q

masked hypertension - defined

A

*opposite of white coat HTN
*blood pressure is NORMAL in the doctor’s office but runs HIGH AT HOME
*detected through 24h ambulatory BP monitoring

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12
Q

lifestyle interventions to treat HTN

A

*WEIGHT LOSS
*heart healthy diet (ex. DASH diet)
*low salt diet
*exercise/increased physical activity
*decrease alcohol consumption
*treatment of OSA with CPAP

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13
Q

suspected pathogenic mechanisms in HTN

A
  1. abnormal kidney handling of sodium & plasma volume
  2. activation of sympathetic nervous system
  3. activated RAAS
  4. likely other environmental & genetic factors
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14
Q

effects of abnormal kidney handling of sodium & plasma volume → HTN

A

*excess Na+ (and thus excess water) content in blood → higher blood pressure

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15
Q

pressure natriuresis

A

*mean arterial pressure increases as sodium intake increases

*2 clinical categories:
1. salt sensitive:
-more likely to respond to diuretic and dietary salt restriction
-have lower renin levels
2. salt insensitive:
-more likely to respond to RAAS blockade
-have higher renin levels

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16
Q

effects of RAAS → HTN

A

angiotensinogen → angiotensin I → angiotensin II → aldosterone
*end result = INCREASED BLOOD PRESSURE / VOLUME

*rate limiting step = RENIN RELEASE (recall: renin converts angiotensinogen to angiotensin I)

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17
Q

angiotensin II - effects leading to increased blood pressure

A

*sodium reabsorption
*water reabsorption (increased ADH)
*vasoconstriction
*increased sympathetic tone
*increased salt appetite
*increased thirst drive

end result: increased BP/blood volume

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18
Q

aldosterone - effects leading to increased blood pressure

A

*salt reabsorption → increased blood volume
*potassium excretion
*acid excretion

end result: increased BP/blood volume

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19
Q

factors that cause renin release

A

*decreased renal perfusion (systemic hypotension or low afferent arteriole pressure)
*increased sympathetic activity/tone
*decreased flow through tubules or decreased distal Na+ delivery (detected by macula densa)
*beta1 adrenergic stimulation
*low sodium diet

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20
Q

effects of aldosterone in the principal cell in the collecting duct

A

aldosterone (made by adrenal cortex) binds mineralocorticoid receptor (MR) inside principal cells → increased activity of Na+/K+ ATPase AND increased activity of ENaC → increased reabsorption of sodium into blood & wasting of potassium in urine

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21
Q

medications that turn off steps of RAAS cascade

A
  1. ACE inhibitors (-prils) - block conversion of Ang I to Ang II
  2. ARBs (-sartans) - block conversion of Ang II to aldosterone
  3. aldosterone antagonists (spironolactone, epleronone) - block effects of aldosterone
22
Q

effects of increased salt intake on RAAS activity

A

*as salt intake increases, the RAAS system should be turned OFF

23
Q

risk factors for HTN

A

*obesity
*decreased nephron number
*family hx of HTN
*race (more common in Black pts)
*increasing age
*smoking
*male sex
*substantial alcohol use
*sedentary lifestyle
*low SES
*insulin resistance
*high dietary sodium intake

24
Q

genetic disorders associated with HTN

A
  1. Liddle Syndrome
  2. Syndrome of Apparent Mineralocorticoid Excess (SAME)
  3. Pseudohypoaldosteronism type 2 / Gordon Syndrome
  4. Glucocorticoid Remediable Hyperaldosteronism (GRA)
25
Liddle Syndrome - inheritance pattern & genetics
*autosomal dominant ***gain of function mutation of the ENaC channel** located in the apical membrane on the principal cell in the collecting duct *results in **excessive Na+ reabsorption and excessive K+ wasting**
26
Liddle Syndrome - electrolyte impacts
1. **excessive Na+ reabsorption** 2. **hypokalemia** (excessive K+ wasting) 3. **metabolic alkalosis** 4. **hypertension** 5. low-to-normal serum aldosterone
27
Liddle Syndrome - clinical presentation
*young person with high blood pressure *family hx of HTN (particularly at a young age) *hypokalemia *metabolic alkalosis (due to K+/H+ exchange in the alpha-intercalated cells) ## Footnote **METABOLIC ALKALOSIS + HYPOKALEMIA + HTN (low serum aldosterone)**
28
Liddle Syndrome - effects on RAAS
***gain of function of ENaC channels → excessive Na+ reabsorption → volume expansion → DECREASED RENIN** *decreased renin → decreased Ang II → decreased aldosterone
29
Liddle Syndrome - treatment
*block ENaC: **potassium sparing diuretics: amiloride, triamterene**
30
primary hyperaldosteronism vs. Liddle Syndrome
*both: HTN, hypokalemia, metabolic alkalosis *Liddle Syndrome: LOW ALDOSTERONE *primary hyperaldosteronism: HIGH ALDOSTERONE
31
Syndrome of Apparent Mineralocorticoid Excess (SAME) - inheritance pattern & genetics
*autosomal recessive ***mutation of 11 beta-hydroxysteroid dehydrogenase**, causing it to be inactivated *this enzyme normally converts cortisol to cortisone; inactivation of enzyme → **activation of mineralocorticoid receptors by excess cortisol** *notably - a LOT of **black licorice ingestion** can cause a similar phenotype (**glycyrrhizic or glycyrrhetinic acids** in licorice inhibits the same enzyme)
32
Syndrome of Apparent Mineralocorticoid Excess (SAME) - clinical features
*infants with low birth weight, failure to thrive ***severe HTN *hypokalemia *metabolic alkalosis** *low serum aldosterone (cortiol tries to be the SAME as aldosterone)
33
Syndrome of Apparent Mineralocorticoid Excess (SAME) - effects on RAAS
*cortisol is stimulating the mineralocorticoid receptor (same receptor that aldosterone stimulates) *increased Na+ reabsorption → volume expansion → **decreased renin** *decreased renin → decreased Ang II → decreased aldosterone
34
pseudohypoaldosteronism type 2 / Gordon Syndrome - inheritance pattern & genetics
*autosomal dominant ***gain of function mutation of the Na+/Cl- cotransporter in DCT** (opposite of thiazide diuretics; opposite of Gitelman syndrome)
35
pseudohypoaldosteronism type 2 / Gordon Syndrome - electrolyte impacts
*excessive Na+ reabsorption → increased blood volume *less delivery of Na+ to the cortical collecting duct, so K+ cannot be excreted
36
pseudohypoaldosteronism type 2 / Gordon Syndrome - clinical presentation
*HTN *HYPERKALEMIA *metabolic acidosis *normal kidney function
37
pseudohypoaldosteronism type 2 / Gordon Syndrome - treatment
*thiazide diuretics
38
glucocorticoid remediable hyperaldosteronism (GRA) - inheritance pattern & genetics
*autosomal dominant *genetic crossover between 2 genes causes the creation of a chimeric aldosterone synthase gene which is controlled by ACTH release instead of Ang II
39
glucocorticoid remediable hyperaldosteronism (GRA) - clinical presentation
*HTN (resistant, often at a young age) *metabolic alkalosis *family hx of HTN and/or premature hemorrhagic stroke
40
glucocorticoid remediable hyperaldosteronism (GRA) - treatment
*glucocorticoids to suppress ACTH release
41
Bartter Syndrome - inheritance pattern & genetics
*autosomal recessive ***inactivating mutation in the NKCC channel in thick ascending loop of Henle** (loop diuretic channel) note - this is a cause of HYPOtension
42
Bartter Syndrome - clinical presentation
*presents in infancy/childhood *growth delay *volume depletion *hypokalemia, hypomagnesemia, hypochloremia, metabolic alkalosis *HYPERCALCIURIA *usually HYPOTENSION or normotension remember - pts with Bartter Syndrome act like they have been on LOOP diuretics ## Footnote **metabolic alkalosis + hypokalemia + hypercalciuria + hypotension**
43
Gitelman Syndrome - inheritance pattern & genetics
*autosomal recessive *inactivating mutation in the **Na+/Cl- cotransporter in the DCT** *acsts like a **thiazide** diuretic (causes hypercalcemia) *opposite of Gordon syndrome note - this is a cause of HYPOtension
44
Gitelman Syndrome - clinical presentation
*usually presents in childhood, teen, or early adult years *volume depletion *hypokalemia, hypomagnesemia, hypochloremia, metabolic alkalosis *HYPOCALCIURIA *usually HYPOTENSION or normotension remember - pts with Gitelman Syndrome act like they are on THIAZIDE diuretics ## Footnote **metabolic alkalosis + hypokalemia + hypocalciuria + hypomagnesemia + hypotension**
45
Bartter Syndrome vs. Gitelman Syndrome
*HIGH URINE CALCIUM (**hypocalcemia**) = Bartter (acts like a **loop** diuretic) *LOW URINE CALCIUM (**hypercalcemia**) = Gitelman (acts like a **thiazide** diuretic)
46
pseudohypoaldosteronism type 1 - inheritance pattern & genetics
*autosomal dominant or sporadic ***loss of function defect in ENaC or mineralocorticoid receptor** *essentially, **unresponsive to the effects of aldosterone**
47
pseudohypoaldosteronism type 1 - clinical presentation
*presents in neonatal period or early infancy *salt wasting, failure to thrive *HYPOTENSION *hyperkalemia
48
pseudohypoaldosteronism type 1 - treatment
high salt diet/NaCl supplements
49
monogenic disorders of BP regulation: ENaC channel in principal cells of collecting duct
*Liddle's Syndrome = gain of ENaC function → hypertension *Pseudohypoaldosteronism type I = loss of ENaC function → hypotension
50
monogenic disorders of BP regulation: NKCC channel in loop of Henle
*Bartter's Syndrome = loss of NKCC function → hypotension
51
monogenic disorders of BP regulation: Na+/Cl- cotransporter in DCT
*pseudohypoaldosteronism type 2 (Gordon) = gain of NCC function → hypertension *Gitelman's syndrome = loss of NCC function → hypotension

Renal Exam (44 decks)

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