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Cardiovascular > Primary and Secondary Hypertension > Flashcards

Primary and Secondary Hypertension Flashcards

1
Q

Proportion of population 20-79 with HTN

A

20%

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2
Q

Proportion people over 60 with HTN

A

~50%

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3
Q

Hypertension and Atherosclerosis

A
  • HTN accelerates atherosclerosis

- atherosclerosis puts pt at risk for cardiovascular disease

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4
Q

Relationships between hypertension and coronary artery disease

A

Linear

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5
Q

HTN Co-morbities that increase risk of CVD

A
  • Type II DM
  • obesity
  • hypercholeterolemia
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6
Q

Diagnosis of HTN

A
  • moving target, important to check guidelines
  • want to expedite diagnosis and get treatment started in high-risk pt’s
  • three visits, week apart each with three readings of systolic >160 or diastolic >100
  • five visits 140-160 and 90-100
  • ambulatory monitoring - mean awake BP >135 or diastolic >85
  • pt’s with diabetes/chronic renal disease, HTN = >130/80
  • HTN >180/100 diagnosed on first office visit
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7
Q

Two pathways that work to control BP

A
  • neural

- humoral

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8
Q

Neural Pathway

A

-sympathetic nervous system

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9
Q

Humoral Pathway

A

-Renin-Angiotensin-Aldosterone System

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10
Q

RAAS System

A
  • decrease in perfusion pressure at macula densa in distal tubule causes release of renin from juxtaglomerular apparatus
  • renin converts circulating angiotensinogen to angiotensin I
  • angiotensin converting enzyme in pulmonary capillary endothelium converts angiotensin I to angiotensin II
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11
Q

Effects of Angiotensin II

A
  • release of aldosterone from adrenal cortex
  • vasoconstriction
  • hypothalamus - induces release of AVP and induces thirst
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12
Q

Effect of AVP

A

-increased reabsorption of water, more water into extracellular space

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13
Q

Effect of Aldosterone

A

-increased sodium reabsorption, more sodium in EC space, more water pulled out of urine

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14
Q

Primary HTN

A
  • also known as essential HTN
  • HTN with no obvious cause to explain it
  • most common cause of HTN
  • underlying mechanism unknown
  • genetic factors play a role
  • linked with obesity, diabetes mellitus, dyslipidemia
  • could be due to enhanced response to catecholamines
  • people who migrate take on HTN prevalence of the country migrated to
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15
Q

Secondary HTN

A
  • HTN due to an underlying obvious cause

- 1-10% of HTN pt’s have secondary HTN

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16
Q

Circumstances where you suspect secondary HTN

A
  • when it occurs as extremes of age with unexpected target organ damage
  • when it occurs abruptly
  • when it occurs with renal failure
  • when response to tx is atypical
  • when hypokalemia or hypercalcemia is present
17
Q

Potential Causes of Secondary HTN (A)

A

Accuracy of BP measurements
Primary aldosteronism
Obstructive sleep apnea

18
Q

Potential Causes of Secondary HTN (B)

A

Bruits in renal arteries, indicates stenosis of vessels, may result in chronic activation of RAS
Bad kidneys, renal failure and HTN have strong link

19
Q

Potential Causes of Secondary HTN (C)

A

Catecholamine release (excessive) due to potentially a pheochromocytoma
Coarctation of aorta, congenital narrowing of aorta immediately after left subclavian A branches off, produces HTN in upper limbs
Cushing’s syndrome, excessive cortisol release leads to increased sodium and water retention

20
Q

Potential Causes of Secondary HTN (D)

A 
Diet, excessive sodium intake (>2300 mg)
Prescription Drugs (NSAIDs, high estradiol dose oral contraceptives, corticosteroids)
Drugs (nicotine, herbal medications containing ephedra, methamphetamines, cocaine)
21
Q

Potential Causes of Secondary HTN (E)

A

Erythropoietin, increased viscosity of blood due to increased hematocrit
Endocrine disorders, hyperthyroidism, hypothyroidism, hyperparathyroidism

22
Q

Target Organ Damage to HTN

A

Eyes (hypertensive retinopathy)
Kidneys (hypertensive nephrosclerosis)
Brain (cerebrovascular disease)
Heart (hypertensive heart and coronary artery disease)

23
Q

Hypertensive Retinopathy

A
  • vessels of retina change as HTN progresses
  • initially, get spasms and narrowing of arteries, fibrosis leads to focal narrowing
  • as HTN progresses, get vascular remodeling and thickening of arteriolar wall, leading to arterio-venous nicking where arteries cross veins
  • examine retina with ophthalmoscope, looking at fundus (central retina)
  • pt’s don’t usually report visual changes
24
Q

Cerebrovascular Disease

A
  • stroke, 3rd most common cause of death in NA
  • due to thrombosis (occlusion of blood vessel) or intracerebral hemorrhage (rupture of blood vessel)
  • HTN is #1 risk factor for stroke, 2-3 mm Hg reduction in systolic BP reduces stroke risk by 10%
25
Q

Hypertensive Heart Disease

A
  • HTN increases afterload on heart
  • increased after load eventually results in left ventricular hypertrophy, leading to increased risk of stroke, MI, sudden death
  • LVH can be sussed out on physical exam
26
Q

Hypertensive Renal Disease

A
  • HTN is second leading cause of end stage renal disease
  • leads to vascular remodeling that impairs autoregulation of kidneys
  • increased vascular resistance leads to scarring (nephrosclerosis) and loss of blood flow through certain regions (rarefaction)
  • disrupts water and mineral handling
  • get protein in urine (microalbuminuria)
27
Q

Autoregulation

A
  • blood flow to certain organs maintained across range of blood pressures
  • found in kidneys, brain
28
Q

Hypertensive Emergencies

A
  • blood pressure exceeds auto regulation capacity, no longer able to control perfusion, get organ dysfunction
  • usually 250 systolic or 140 diastolic
29
Q

Effect on Brain

A
  • hypertensive encephalopathy

- coma, seizures, headache, confusion, vomiting

30
Q

Effect on Heart

A
  • increases afterload, makes myocardium work harder
  • in pt’s with underlying coronary artery disease, get hypoperfusion of myocardium, producing angina pectoris (chest pain) and or SOB
  • can also lead to reduced left ventricular contractility, get congestion of blood in pulmonary circuit, plasma moves out into pulmonary interstitial and alveoli (CHF)
31
Q

Effect on Aorta

A
  • can lead to aortic dissection (separation between intima and media)
  • puts pt at increased risk of aortic rupture and/or interruption of blood flow to major branch arteries
32
Q

Effect on Kidney

A
  • usually silent
  • acute renal failure can manifest as confusion, swings in BP, fluid collection in pericardial sac, edema, electrolyte disturbances, increases in renal indices
33
Q

Acute Elevation of Bp

A
  • without target organ damage, does not require immediate trip to family doctor or ER
  • headache, dizziness, epistaxis, palpitations, tingling in extremities not indicators of target organ damage

Cardiovascular (8 decks)

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