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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
aortic dissection vascular wall quality
1. normal vascular wall in 80% | 2. cystic medial necrosis in 20%
26
what is cystic medial necrosis with aortic dissection
clefts/defects in elastin and smooth muscle filled with amorphous basophilic material absence of inflammation usually in Marfan's syndrome
27
outcome of aortic dissections ruptures (5)
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
what is Marfan's syndrome
- 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
clinical features of aortic dissection
sudden excruciating pain in anterior chest radiating to back and moving downward ( you may think its an MI)
30
prognosis of aortic dissection
65-75% | -can be fixed with immediate surgery or anti-HTN meds
31
definition of hypertensive heart dz
LVH in individual with HTN without other reason for ventricular hypertrophy (ex. aortic stenosis or hypertrophic cardiomyopathy)
32
pathogenesis of hypertensive heart dz
- 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
hypertensive heart dz can lead to what 3 things
CHF MI Arrhythmias
34
morphology of hypertensive heart dz
grossly - increased heart weight, LVH, dilation with longstanding RVH microscopically - hyperchromatic box car nuclei, interstitial fibrosis
35
clinical features of hypertensive heart dz
no signs and symptoms until CHF develops | -angina, renal damage, CVA, sudden cardiac death
36
definition of cor pulmonale
- 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
2 definitions of cor pulmonale
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
definition of CHF
- 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
causes of left heart failure
1. HTN 2. Mitral valve disease 3. aortic valve dz 4. IHD 5. primary myocardial dz
40
causes of RHF
1. left heart failure 2. cor pulmonale 3. pulm vascular dz 4. pulm valve dz 5. tricuspid valve dz 6. congenital heart dz
41
what is the major cause of right heart failure
LEFT HEART FAILURE
42
what are compensatory mechanisms of heart failure
1. increased sympathetic nervous system activity | 2. hypertrophy - try to contract more forcefully
43
affect of heart failure from heart to venous
decreased CO = increased EDV = increased EDP = increased VP
44
what is backward failure
failure of the heart causes failure of the venous system
45
evolution of RHF from LHF
LHF = passive pulm congestion = pulm edema = increased pulm resistance = RHF = venous congestion
46
morphology of CHF with LVF
dilated, hypertrophied heart boggy lungs with frothy edema fluid pulm vascular congestion/edema alveolar hemorrhage
47
morphology of CHF - right ventricular failure
soft tissue edema abdominal visceral congestion - nutmeg liver cavity fluid cardiac cirrhosis
48
what is a nutmeg liver
caused by RVF - speckled hemorrhagic
49
clinical features of LHF
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
clinical features of RHF
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
definition of HTN
BP of >140/>90

Clin Med - Cardio I (7 decks)

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