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Renal > 22 Hypertension > Flashcards

22 Hypertension Flashcards

1
Q

Hypertension

  • Frequency
  • Pt awareness, treatment, & control
  • BP treatment
A
  • Frequency
    • Common in the US (1/3 of adults)
    • Increases w/ age
    • Affects both genders
  • Pt awareness, treatment, & control
    • 79.6% are aware they have hypertension
    • 70.9% are being treated
    • 47.8% have controlled BP
  • BP treatment
    • BP is a continuous variable so when to treat varies
    • <60yo, CKD, or diabetes: goal < 140/90
    • >60yo: goal < 150/90
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2
Q

Hypertension severity

  • HTN is associated with…
  • As ppl live longer due to decreased death from MI and CVA…
  • As a primary disease, HTN accounts for…
  • Risk of ESRD is associated w/…
  • Management & risk of HTN
  • Who’s at risk for developing HTN
A
  • HTN is associated with…
    • Significant morbidity & mortality
    • Esp cerebrovascular accidents, coronary disease, & renal disease
    • HTN control decreases cerebrovascular accidents (hemorrhagic or ischemic brain damage) & coronary artery disease.
  • As ppl live longer due to decreased death from MI and CVA…
    • They develop the next generation of diseases associated w/ HTN (CHF & renal failure) at an accelerating rate
  • As a primary disease, HTN accounts for…
    • 30% of the ESRD in the US
  • Risk of ESRD is associated w/…
    • Ethnicity
    • Severity of HTN
  • Management & risk of HTN
    • Most common reason for physician visits by non-pregnant adults in the US
  • Who’s at risk for developing HTN
    • 90% of adults >50yo
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3
Q

Pathogenesis of HTN:
Definitions

  • Arterial pressure
  • HTN
  • HTN in adults < 60yo
  • HTN in adults > 60yo
A
  • Arterial pressure
    • Determiend by CO & systemic vascular resistance (SVR)
    • BP = CO * SVR
  • HTN
    • Imbalance b/n CO & SVR
    • Occurs when CO &/or SVR (peripheral resistance) increases
  • HTN in adults < 60yo
    • BP > 140/90
  • HTN in adults > 60yo
    • BP > 150/90
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4
Q

Pathogenesis of HTN:
Cardiac output

  • Rare to find a form of HTN where…
  • Essential (primary) HTN
  • Any sustained rise in BP requires…
  • Role of genetics
    • Sibling of pt w/ HTN
    • Single gene defects
    • Other genes associated w/ HTN
    • HTN transplant
  • Role of excess Na intake
    • Salt vs. HTN/BP
    • Essential HTN
A
  • Rare to find a form of HTN where…
    • Only one of either CO or SVR is abnormal
    • Even in secondary forms of HTN multiple factors play a role
  • Essential (primary) HTN
    • 90-95% of all HTN
    • Cause: multifactorial
  • Any sustained rise in BP requires…
    • Participation of the kidney
  • Role of genetics
    • Sibling of pt w/ HTN has 3.5x risk of HTN than general population
    • Rare instances of single gene defects causing HTN exist
      • Involve increased Na reabsorption due to a primary defect in a Na transport system (e.g. Liddle’s Syndrome affecting ENaC)
    • Other genes associated w/ HTN
      • Polygenic (multiple genes involved)
      • Polymorphisms of ACE & RAAS genes
    • HTN can be transplanted (Salt Sensitive Dahl rat)
  • Role of excess Na intake
    • Salt vs. HTN/BP
      • Increase salt intake –> increase frequency of HTN
      • Dietary Na restriction –> decreased BP
    • Essential HTN
      • Due to an abnormal kidney that’s unwillingn to excrete sodium
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5
Q

Pathogenesis of HTN:
Primary increase in CO

  • Guyton’s animal models
  • Application of Guyton’s model to pts w/ reduced renal function
A
  • Guyton’s animal models
    • Decreased renal mass + volume expansion (i.e., give salt & water) –> BP increases due to increased CO
    • Normal kidney function: CO returns to baseline in a few days
    • Reduced kidney function: BP remains elevated due to increased peripheral vascular resistance
      • Due to autoregulation in vascular beds
      • Increased CO –> increased delivery to vascular bed –> increased total peripheral resistance –> return nutrient & oxygen delivery to vascular bed back to “normal”
  • Application of Guyton’s model to pts w/ reduced renal function
    • Young HTN pts: CO remains w/ normal TPR
    • After years of chronic BP elevation due to chronic high salt intake, CO decreases to low levels but TPR increases
    • Due to cardiac and vascular remodeling
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6
Q

Pathogenesis of HTN:
Cardiac output:
Abnormality in Na excretion (4 hypotheses)

  • Altered pressure natriuresis
  • Deficient natriuretic hormone
  • Renin and nephron heterogeneity (Laragh-Sealy Hypothesis)
  • Reduced nephron number
A
  • Altered pressure natriuresis
    • Normally: increased BP –> increased Na delivery to distal nephron –> increased Na excretion
      • Na loss –> decreased BP back to normal
    • If pressure natriuresis is “reset”
      • Pt will regulate around a higher baseline BP or have decreased sensitivity to volume expansion
      • –> higher pressures
  • Deficient natriuretic hormone
    • Increase volume –> release natriuretic hormone –> inhibits Na-K ATPase –> decreased Na reabsorption
    • Defect in this hormone –> prevent excretion of excess Na loads
  • Renin and nephron heterogeneity (Laragh-Sealy Hypothesis)
    • Sub-population of ischemic nephrons chronically releases renin –> HTN
    • Increase BP –> decrease renin
    • Most pts w/ primary HTN have normal or high renin levels (70%) due to…
      • Nephron heterogeneity (i.e., subgroup of nephrons that are ischemic and release excess renin)
      • RAAS that doesn’t modulate properly
      • Increased sympathetic drive
  • Reduced nephron number
    • Congenital reduction in the # of glomeruli –> fewer nephron units to excrete excess Na loads –> HTN
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7
Q

Pathogenesis of HTN:
Cardiac output:
Role of SNS

  • Baroreceptors
  • Excess stress
  • SNS net effect
A
  • Reset baroreceptors
    • Aortic arch, carotid sinus, & cardiopulmonary baroreceptors
    • Regulate at higher set points of BP
  • Excess stress –> increased SNS
    • Intermittent stress –> Epi release –> increased BP
      • BP remains elevated for some time afterwards
    • Epi acts on pre-synaptic β2 receptor –> NE release
    • Cardiac NE spillover
      • Higher in HTN pts
      • Correlates directly w/ Epi release
    • HTN patients have faulty NE re-uptake
  • SNS net effect
    • –> decreased RBF & GFR
    • –> increased renal Na reabsorption
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8
Q

Pathogenesis of HTN:
Role of total peripheral resistance (TPR)

  • TPR
  • Primary lesion in HTN
    • May be…
    • Possible candidates
  • Arterial stiffness
    • Increase age –>
    • Major determinant of CV risk
  • Cell membrane alterations
A
  • TPR
    • Increased peripheral resistance maintains HTN
    • Regulated by vascular endothelial cell & vascular smooth muscle cell
  • Primary lesion in HTN
    • May be structural remodeling of blood vessels in childhood
    • Possible candidates
      • RAAS
      • Endothelin-1 – high plasma levels in HTN pts
      • Transforming Growth Factor β1
      • Insulin like growth factor
      • Mechanical forces – hemodynamic shear
      • Nitric oxide – whole body NO production is decreased in pts w/ essential HTN
  • Arterial stiffness
    • Increase age –> progressive increase in systolic BP
      • Collagen deposition in the blood vessels
      • Smooth muscle hypertrophy
      • Altered elastin vascular media
      • Age associated endothelial dysfunction
    • Major determinant of CV risk: increasing pulse pressure
  • Cell membrane alterations
    • IC Na is higher in cells from HTN pts
    • Altered Na/H exchange
    • Altered membrane composition
    • Ca transport & binding – calcium content increased in the membranes of HTN pts
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9
Q

Pathogenesis of HTN:
Other factors

  • Weight
    • Framingham study
    • Associated w/…
  • Mineral metabolism
  • Tobacco
  • Caffeine
  • Alcohol
    • Moderate quantities
    • Larger quantities
A
  • Obesity
    • Framingham study: gain 10lb –> increase systolic BP by 4.5 mmHg
    • Associated w/…
      • Increased CO
      • Intravascular volume
      • SNS activity
      • Increased RAAS
      • Diminished NO mediated vasodilation
      • Hyperinsulinemia
  • Mineral metabolism
    • Decreased Ca intake + increased Ca excretion –> increased HTN
    • Decreased dietary K &Mg –> increased BP
    • Lead causes HTN
  • Tobacco
    • BP increases for 30 minutes following tobacco use
  • Caffeine
    • Increases BP
    • Tolerance develops to pressor effect
  • Alcohol
    • Moderate quantities: may contribute to HTN
    • Larger quantities: significant contributor
      • 10% of HTN in men –> directly linked to ethanol
      • BP decreases when heavy drinkers abstain
      • HTN pts should drink < 2 standard drinks / day
        • Standard drink = 12 oz beer, 5 oz wine, 1.5 oz hard liquor
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10
Q

Pathogenesis of HTN:
Secondary causes of HTN

  • Presentation
  • Renal parenchymal disease
  • Renovascular HTN
A
  • Presentation
    • < 35yo with abrupt onset of HTN
    • No family hx of HTN
    • Fail empiric therapy.
  • Renal parenchymal disease
    • Decreased ability to excrete Na & water –> volume expansion & increased CO
    • Autoregulation –> increae TPR –> decrease CO –> HTN
  • Renovascular HTN
    • Caused by > 80% renal artery stenosis
      • 1% of unselected pts w/ HTN have this lesion
      • Surgically correctable
    • Arterial constriction –> decreased renal perfusion –> increased renin & AII –> increase BP
    • Causes
      • Atherosclerosis aortic aneurysm, emboli, and arteritis.
    • Fibromuscular dysplasia: disease of the layers of the blood vessel (usually medial fibroplasia)
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11
Q

Pathogenesis of HTN:
Secondary causes of HTN

  • Adrenal gland causes of HTN
    • Pheochromocytoma
    • Primary aldosteronism
    • Cushing’s syndrome
  • Miscellaneous Causes of secondary HTN
A
  • Adrenal gland causes of HTN
    • Pheochromocytoma
      • Chromaffin cell tumors episodically increase BP
      • Associated w/ tachycardia, sweating, flushing & tremor
    • Primary aldosteronism
      • Due to adrenal adenomas or adrenal hyperplasia
      • Classic features: HTN, hypokalemia, excess urinary K losses, metabolic alkalosis, & hypernatremia
    • Cushing’s syndrome
      • Caused by excess cortisol
      • Due to excess ACTH from the pituitary –> excess adrenal production of cortisol
      • May be from excess unstimulated production of cortisol by the adrenal gland
  • Miscellaneous Causes of secondary HTN
    • Coarctation of the Aorta
    • Hypothyroidism and hyperthyroidism
    • Hyperparathyroidism
    • Sleep apnea
    • Meds
      • Erythropoietin
      • Cyclosporine
      • Tacrolimus (FK 506)
    • Street Drugs
      • Cocaine
      • Bath salts
      • Amphetamines
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12
Q

Evaluation of HTN:
History

  • Family hx
  • Review of systems (ROS)
  • Evaluate…
  • Diet
  • Meds
A
  • Family hx
    • High BP
    • Early heart disease
    • Cerebrovascular accidents (CVA)
    • Peripheral vascular disease
    • DM
    • Lipid abnormalities.
  • Review of systems (ROS)
    • Emphasis on cardiac & neurologic complaints
    • Previous hx of renal diseases, DM, or lipid abnormalities
    • Previous HTN or anti-HTN therapy
  • Evaluate…
    • Weight hx
    • Smoking
    • Physical activity
  • Diet
    • Fat, alcohol, & Na intake
  • Meds
    • Drugs that increase BP
      • Oral contraceptives
      • Steroids
      • Immunosuppresive drugs
      • NSAIDs
      • Decongestants
      • Appetite suppressants
      • Tricyclic antidepressants
      • Monoamine oxidase inhibitors
    • Street drugs
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13
Q

Evaluation of HTN:
History

  • Symptoms suggestive of secondary HTN (uncommon)
  • When the pt considered to have HTN
A
  • Symptoms suggestive of secondary HTN (uncommon)
    • Episodic tachycardia, tremor, orthostatic HoTN, sweating, pallor & anxiety –> pheochromocytoma
    • Severe HTN in a young pt w/ no family hx of HTN
    • HTN poorly responsive to interventions
    • Well-controlled HTN that becomes poorly controlled
    • Sudden onset of HTN or presentation w/ accelerated or malignant HTN
  • When the pt considered to have HTN
    • Diagnosis not made on basis of single measurement
    • Confirm elevation on > 2 subsequent visits over several weeks
      • Unless BP is in severe or very severe range –> hospitalization or more frequent outpatient visits
    • Severe HTN in presence of target organ damage (TOD)
      • CHF, angina, stroke, or renal failure
      • Indication for hospitalization
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14
Q

Evaluation of HTN:
Measuring & monitoring BP

  • Measuring BP
  • Role of 24 hour ambulatory BP monitoring
    • Why
    • When
  • Advantages of self-measurement
A
  • Measuring BP
    • Pt seated w/ arm bared, supported, & at heart level
    • No nicotine or caffeine within 30 minutes before measurement
    • Measure after 10-15 minutes of rest
    • Use appropriate cuff size
      • Cuff bladder must cover >80% of arm circumference.
    • First appearance of sound is the systolic pressure
    • Disappearance of sound is true diastolic (Phase V)
      • Muffling (Phase IV) is not true diastolic
    • > 2 measurements separated by 2 minutes should be averaged
      • If values differ by > 5 mm Hg –> additional readings
    • Initial exam should include BP in both arms
      • Higher BP = true BP
  • Role of 24 hour ambulatory BP monitoring
    • BP measurements in the office may not reflect the pt’s usual BP
    • When 24 hour ambulatory BP monitoring may be helpful
      • BP elevated on multiple occasions in clinic setting but repeatedly normal out of hospital
        • Aka “white coat” HTN
      • Drug therapy appears to be ineffective
      • Episodic HTN
      • Evaluation of nighttime BP changes
      • Excess anti-HTN effect (i.e., orthostatic HoTN)
  • Advantages of self-measurement
    • Identifies “white-coat HTN”
    • Assess response to meds
    • Improves adherence to treatment
    • Potentially reduces costs
    • Usually provides lower readings than those recorded in clinic
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15
Q

Evaluation of HTN:
Physical & lab exams

  • Physical
  • Labs
A
  • Physical
    • > 2 BP readings > 2 minutes apart w/ pt supine or seated & after standing for > 2 minutes
    • Check opposite arm & use higher value
    • Measure height & weight.
    • Fundoscopic exam
    • Examine neck for carotid bruits, enlarged thyroid, & venous distention
    • Cardiac exam looking for tachycardia, laterally displaced PMI, precordial heave, clicks, murmurs, & S3 / S4 gallops
    • Examine abdomen for bruits (anteriorly and posteriorly), enlarged kidneys, masses, & abdominal aortic pulsation
    • Examine extremities for diminished pulses (coarctation or peripheral vascular disease [PVD]), bruits, or edema
    • Neuro exam
  • Labs
    • Urinalysis for proteinuria
      • Centrifuged urine sediment exam for acute renal disease
    • CBC, glucose, electrolytes, BUN, Creatinine, uric acid, fasting lipid profile & EKG
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16
Q

Evaluation of HTN:
Optional tests & procedures

A
  • Creatinine clearance
  • Microalbuminuria
  • 24-hour urinary protein
  • Serum calcium
  • Serum uric acid
  • Fasting triglycerides
  • LDL cholesterol
  • Glycosolated hemoglobin
  • Thyroid-stimulating hormone
  • Plasma renin activity/ urinary sodium determination
  • Limited echocardiography
  • Ultrasonography
  • Serum Aldosterone
17
Q

Consequences of HTN

  • Cardiac
  • Cerebrovascular
  • Peripheral vasculature
  • Renal
  • Retinopathy
    • Grade 1
    • Grade 2
    • Grade 3
    • Grade 4
    • Grade 3 & 4
A
  • Cardiac
    • Clinical, electrocardiographic, or radiologic evidence of coronary artery disease
    • EKG shows LVH
      • LVH detected by echo is highly predictive of future cardiac events (MI, CHF)
    • CHF and LV dysfunction frequently seen
    • Direct correlation of incidence of coronary heart disease & systolic BP
  • Cerebrovascular
    • Transient ischemic attack (TIA)/CVA
    • Direct correlation of BP elevations & incidence of strokes
    • Anti-HTN therapy has the greatest impact.
  • Peripheral vasculature
    • Accelerated atherosclerosis of distal arteries –> diminished circulation to extremities –> ischemia w/ exertion and pain (claudication)
    • Ischemia at rest –> ischemic ulcers of the toes, feet, lower legs, & fingers
  • Renal
    • Serum Creatinine > 1.5
    • Clinical proteinuria (1+ or more on standard dipstick)
    • Microalbuminuria
  • Retinopathy
    • Grade 1 - first crossing AV nicking
    • Grade 2 - copper wire narrowing of retinal arterioles, second crossing AV nicking
    • Grade 3 - silver wire narrowing of retinal arterioles Cotton wool exudates, hemorrhage
    • Grade 4 - hemorrhage and exudates with papilledema
    • Grade 3 & 4 - high association w/ progressive renal failure
18
Q

Pathophysiology of essential hypertensive renal disease

  • 20-30yo: phase 1
  • 30-40yo: phase 2
  • 40-50yo: phase 3
  • >50yo
    • Phase 4
    • Phase 5
A
  • 20-30yo: phase 1
    • Increase in Renal Vascular Resistance (RVR) due to…
      • Functional disturbance of renal vasculature
      • Over active vasoresponse to endogenous AII
      • NE
  • 30-40yo: phase 2
    • Further increase in RVR w/ both functional & structural disturbances in renal vasculature
    • Decrease in renal perfusion
    • Preservation of GFR (although glomeruli may be ischemic)
    • Increase in FF
    • Microalbuminuria
  • 40-50yo: phase 3
    • Further increase in RVR
    • Structural disturbances involving renal vasculature & glomeruli (arteriolar nephrosclerosis)
    • Decrease in perfusion disproportionately > decrease in filtration
    • Sustained rise in FF
    • Proteinuria
  • >50yo
    • Phase 4
      • Critical decrease in renal mass
      • Decrease in RVR (reduction in afferent arteriolar resistance)
      • Increase in glomerular capillary hydraulic pressure
      • Progressive decrease in GFR
      • Nephrosclerosis
      • Glomerulosclerosis
    • Phase 5
      • Chronic renal insufficiency progressing to ESRD

Renal (24 decks)

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