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Clin Med - Cardio I > Pathology - HTN CV DZ > Flashcards

Pathology - HTN CV DZ Flashcards

1
Q

risks associated with HTN

A
  1. CHD
  2. CVA
  3. CHF
  4. Aortic dissection
  5. renal failure
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2
Q

two clinical courses of HTN

A
  1. benign - modest stable elevation in BP, long life span

2. malignant - 5%, rapidly rising BP, death within 1-2 years

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3
Q

what is the syndrome of malignant HTN

A
  1. severe HTN = diastolic >120mmHg
  2. renal failure
  3. retinal hemorrhages
  4. re existing benign HTN
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4
Q

equation for BP

A

BP = CO x PVR

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5
Q

CO depends of what two factors

A

blood volume and serum sodium

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6
Q

PVR depends on what

A

arteriolar luminal diameter (under control of vasoconstrictors and vasodilators)

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7
Q

examples of vasoconstrictors

A 
angiotensin II
catecholamines
thomboxane 
leukotrienes
endothelin
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8
Q

examples of vasodilators

A 
kinins
prostaglandins
nitric oxide
lactic acid
hydrogen ions
adenosine
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9
Q

blood pressure regulation in the kidney

A
  1. juxtoglomerular apparatus in kidney sense decrease in GFR (due to decrease in BP) and produces renin to stimulate the RAAS system.
  2. RAAS stimulates aldosterone to increase NA + H2O to increase BP
  3. RAAS also stimulates angiotensin II which increases PVR
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10
Q

BP regulation in the heart

A

increased BP stimulates release of ANF (atriopeptin) from heart which is a potent vasodilator

  • works on kidney to decrease NA and H20 resorption
  • also decreases PVR
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11
Q

HTN is an altered relationship bw what two factors

A

blood volume and arterial resistance

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12
Q

pathogenesis of HTN in renal artery stenosis

A

plaque in artery of kidney - kidney thinks low BP so it stimulates RAAS system = vasoconstriction = increased BP

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13
Q

pathogenesis of essential HTN

A

genetic and environmental factors affecting CO and PVR

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14
Q

genetic factors leading to essential HTN

A

single gene defects

  1. defects in aldosterone metabolism = increased aldosterone activity
  2. Liddle syndrome - mutations in epithelial NA channel protein cause increased response to aldosterone
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15
Q

environmental factors leading to essential HTN

A 
stress
obesity
smoking
inactivity
salt intake
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16
Q

2 essential HTN hypotheses

A
  1. primary defect in renal NA homeostasis = incr BP + CO with compensatory increased PVR
  2. primary increase in PVR - vasoconstriction + structural alterations (smooth muscle hypertrophy)
    * **both are aggravated by sodium intake
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17
Q

what is the current hypothesis of essential HTN

A

genetic/environmental influences cause defect in cell cycle genes which stimulate smooth muscle cell growth resulting in vascular wall thickening, increased vascular tone and vasoconstriction

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18
Q

2 HTN vasculopathies in humans

A

hyaline arteriolosclerosis

hyperplastic arteriolosclerosis

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19
Q

what is hyaline arteriolosclerosis

A

age related change
can be in elderly normotensive
causes benign nephrosclerosis with granular texture
-homogenous pink smudgey material that thickens arteriole wall

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20
Q

what is hyperplastic arteriolosclerosis

A

happens with malignant HTN (diastolic BP >120)
onion skinning of the kidney
smooth muscle hypertrophy
fibrous deposition and acute necrosis

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21
Q

What is aortic dissection

A

formation of blood filled channel within the muscle wall of the aorta that usually ruptures
-forms from a tear in the muscle wall

22
Q

groups at risk for aortic dissection

A

men 40-60 with HTN
connective tissue disorders - Marfan’s syndrome
rarely pregnancy

23
Q

classification of type of aortic dissection dependent on what

A

location of the tear

24
Q

DeBaky I, II, III aortic dissection

A

I & II (also called Type A): 90%, tear within 10cm of aortic valve

III (also called Type B): tear in descending thoracic aorta distal to left subclavian artery

25
Q

aortic dissection vascular wall quality

A
  1. normal vascular wall in 80%

2. cystic medial necrosis in 20%

26
Q

what is cystic medial necrosis with aortic dissection

A

clefts/defects in elastin and smooth muscle filled with amorphous basophilic material
absence of inflammation
usually in Marfan’s syndrome

27
Q

outcome of aortic dissections ruptures (5)

A
  1. can rupture proximally to involve coronary arteries = MI
  2. can rupture distally to involve iliac/femoral arteries
  3. can rupture into pericardial sac, pleural or perioneal cavity
  4. can rupture into aortic lumen creating a second lumen (double barrel aorta)
  5. can collapse inner layers of smaller arteries causing obstruction
28
Q

what is Marfan’s syndrome

A
  • genetic defect in fibrillin gene (connective tissue protein necessary in elastic tissue)
  • causes defects in CV, skeletal, and ocular
  • 70-90% have HTN
  • most have cystic medial necrosis
29
Q

clinical features of aortic dissection

A

sudden excruciating pain in anterior chest radiating to back and moving downward ( you may think its an MI)

30
Q

prognosis of aortic dissection

A

65-75%

-can be fixed with immediate surgery or anti-HTN meds

31
Q

definition of hypertensive heart dz

A

LVH in individual with HTN without other reason for ventricular hypertrophy (ex. aortic stenosis or hypertrophic cardiomyopathy)

32
Q

pathogenesis of hypertensive heart dz

A
  • sustained pressure load acts as stimulus causing changes in gene expression of myosin and actin
  • increased metabolic requirements with reduced supply (stiff myocardium with reduced compliance and reduced stroke volume)
33
Q

hypertensive heart dz can lead to what 3 things

A

CHF
MI
Arrhythmias

34
Q

morphology of hypertensive heart dz

A

grossly - increased heart weight, LVH, dilation with longstanding RVH
microscopically - hyperchromatic box car nuclei, interstitial fibrosis

35
Q

clinical features of hypertensive heart dz

A

no signs and symptoms until CHF develops

-angina, renal damage, CVA, sudden cardiac death

36
Q

definition of cor pulmonale

A
  • dz of right heart due to pulmonary HTN due to COPD/CRPD or pulm vascular dz (PE)
  • not due to leart heart dz or congenital heart dz
37
Q

2 definitions of cor pulmonale

A
  1. acute - usually PE or acute RVF - dilated & normal chamber size
  2. chronic - usually due to COPD or chronic RVF - compensatory RVH, increased weight, pulmonary artery stenosis
38
Q

definition of CHF

A
  • multisystem derangement when heart is no longer able to eject blood delivered to it by venous system
  • high output failure due to increased demand by tissues
  • not due to blood loss or venous issues
39
Q

causes of left heart failure

A
  1. HTN
  2. Mitral valve disease
  3. aortic valve dz
  4. IHD
  5. primary myocardial dz
40
Q

causes of RHF

A
  1. left heart failure
  2. cor pulmonale
  3. pulm vascular dz
  4. pulm valve dz
  5. tricuspid valve dz
  6. congenital heart dz
41
Q

what is the major cause of right heart failure

A

LEFT HEART FAILURE

42
Q

what are compensatory mechanisms of heart failure

A
  1. increased sympathetic nervous system activity

2. hypertrophy - try to contract more forcefully

43
Q

affect of heart failure from heart to venous

A

decreased CO = increased EDV = increased EDP = increased VP

44
Q

what is backward failure

A

failure of the heart causes failure of the venous system

45
Q

evolution of RHF from LHF

A

LHF = passive pulm congestion = pulm edema = increased pulm resistance = RHF = venous congestion

46
Q

morphology of CHF with LVF

A

dilated, hypertrophied heart
boggy lungs with frothy edema fluid
pulm vascular congestion/edema
alveolar hemorrhage

47
Q

morphology of CHF - right ventricular failure

A

soft tissue edema
abdominal visceral congestion - nutmeg liver
cavity fluid
cardiac cirrhosis

48
Q

what is a nutmeg liver

A

caused by RVF - speckled hemorrhagic

49
Q

clinical features of LHF

A

dyspnea due to reduced lung compliance with increased stretch receptor activity

  • exertional at first
  • orthopnea
  • PND
  • enlarged heart, tachy, S3, fine rales
  • mitral regurgitation
50
Q

clinical features of RHF

A
  1. distended neck veins
  2. enlarged tender liver
  3. weight gain
  4. dependent edema, effusions
  5. cyanosis and acidosis (reduced perfusion)
  6. ventricular arrhythmias, sudden death
51
Q

definition of HTN

A

BP of >140/>90

Clin Med - Cardio I (7 decks)

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