Pathology: Hypertensive and Atherosclerotic Cardiovascular Disease

Question 1

List the finctions of the vasular endothelium in basal state

Answer 1

Maintain a permeability barrier, provide a nonthrombogenic surface to maintain blood In liquid state, elaboration of mediators for hemostasis, produce ECM, modulate blood flow and vasomotor tone by producing relaxing factors (NO) and contracting factors (endothelin) Regulate inflammation, regulate growth by elaboration of growth factors, metabolize some hormones (angiotensin)

Question 2

Endothelial cell activation

Answer 2

in response to certain stimuli (turbulant flow, increased BP, etc) the endothlial cells activat and respond by aquiring new (indicible) properties

Question 3

endothelial cell inducing stimuli

Answer 3

cytokines (bacterial products), hemodynamic stresses and lipid products, advanced glycation end products of DM, viruses, complement components, hypixia

Question 4

Activated endothelia cell response examples

Answer 4

expression of adhesion molecules, production of cytokines, chemokines, growth factors, and vasoactive molecules. Prodcution of MHC molecules, procoagulant and/or anticoagulant molecules and other biologically active molecules

Question 5

Endothelial Dysfunction

Answer 5

endothelium becomes proinflammatory or prothromboyoc. Some forms are slow onset (hours to days) - require alterations in gene expression and protein synthesis othe rforms are rapid onset (minutes) - do not require change in gene extression and protein synthesis

Question 6

what cell type is responsible for vasoconstriction and vasodilation in repons eto pysiologic or phramacologic stimuli (ex: blood pressure

Answer 6

Vascular smooth muslce cells

Question 7

Vascular smooth muscle cells

Answer 7

responsible for vasoconstriction/dilation in response to stimuli, play role in norma vascular repair and pathological proceses, capacity to prolifereate when appropriately stimiled (ex: prolonged HTN) Can synthesize collagen, elastin, and proteoglycans (ground sunstance) and can elaboratte growth factors and cytokines (inflammatory mediators)

Question 8

sterotypical response of vessel wall to injury

Answer 8

intimal thickening

Question 9

Descrive the vascular response to injury

Answer 9

endothelial cell involved in repair migrate to injured areas, smooth muscle or preucursor cells migrate to the intima and proliferate secrete ECM. Neointimal smooth muscle cells are motile and can divide but not contract. Healing process results in permanent intimal thickening. With persistent or recurrent insults excessive thickening can cause narrowing or stenosis of small and medium blood vessels (eg: atherosclerosis) impeding downstream tissue perfusion

Question 10

Main regulation of blood volume

Answer 10

renal sodium excretion or resorption (renin angiotensin aldosterone axis)

Question 11

Normal BP

Answer 11

less than 120/80

Question 12

Elevated BP

Answer 12

systolic between 120-129 and diastolic less than 80

Question 13

Stage 1 BP

Answer 13

Systolic between 130-139 or diastolic between 80-89

Question 14

Stage 2 BP

Answer 14

Systolic at least 140 or diastolic at least 90

Question 15

Hypertensive crisis

Answer 15

Systolic over 180 and/or diastolic over 120 - patinets need prompt changes in medications if there are no other indications of problems or immediate hospitalization if there are signs of organ damage

Question 16

Essential Hypertension

Answer 16

90-95% of cases - cause is unknown: multifactorial (tends to run in families)

Question 17

Secondary hypertension causes

Answer 17

1.) Renal 2.) Endocrine 3.) Cariovascular 4.) Neurologic

Question 18

Renal causes of secondary hypertension

Answer 18

acute glomeronephritis, polycystic disease, renal artery stenosis, renal vasculitis, renin producing tumors

Question 19

Endocrine causes of secondary hyertension

Answer 19

adrenocortical hyperfucntion, exogenous hormones, pheochromocytoma, acromegaly, hyperthyroidism/hypothyroidism, pregnancy induced

Question 20

Cardiovascular causes of secondary hypertension

Answer 20

coarctation of aorta, polyarteritis nodosa, increased intravascular volume (volume overload) aortic rigidity

Question 21

Neurologic causes of secondary hypertension

Answer 21

Psychogenic, increased intracranial pressure, sleep apnea,a cute stress (including surgery)

Question 22

Clinical features of HTN

Answer 22

Most cases are clinically silent for yearts. Headaches, shortness of breath, nosebleeds (nonspecific symptoms that do not show up intil hypertension is severe)

Question 23

Clinical features of malignant hypertension

Answer 23

rapidly rising blood pressure leading to severe hypertension (often leads to death within 1-2 years if untreated) Most commonly is superimposed on chronic hypertension. Renal failure, retinal hemorrhages and exudates, +/- papilledema

Question 24

Complictaions of HTN

Answer 24

Acceleration of atherosclerosis, cardiac hypertrophy and heart failure (hypertensive heart disease), multi-infarct dementia, aortic dissection, renal failure, stroke (hemorrhagic or ischemic)

Question 25

Pathogenesis of renovascular HTN

Answer 25

renal artery stenosis leads to decreased blood pressure and flow in the glomerular afferent arteriole which stimulates renin secretion leading to increased vascular tone and blood volume via the angiotensin aldoserone pathway

Question 26

Monckeberg’s Medical Calcific Sclerosis

Answer 26

Calcific depositis in the muscular arteries in people over the age of 50 (especially women) that does NOT involve the limen. This is the most significant form of arterioscleosis

Question 27

Arteriolosclerosis

Answer 27

diseaseof small vessels and arterioles associated with hypertension and diabetes

Question 28

Hyaline arteriolosclerosis

Answer 28

due to endothelial injury with leakage of plasma into arteriolar walls and increased smooth muscle cell matrix synthesis. Arteriolar wall is thicked with increased plasma protein deposition and markedly narrow lumen (stenosis)

Question 29

Hyperplastic arteriolosclerosis

Answer 29

“onion skinning” causing obliteration of the lumen. Occurs in severe (malignant) HTN

Question 30

which form of arteriolosclerosis occurs in malignant HTN

Answer 30

Hyperplastic arteriolosclerosis

Question 31

what is the most frequent and clinically important pattern of ateriosclerosis

Answer 31

Atherosclerosis

Question 32

foam cells

Answer 32

macrophages stuffed with mdified ingested lipids (seen in atherosclerosis)

Question 33

Early gross changes of atherosclerosis

Answer 33

aorta with fatty streaks mainly associated wit the ostia where blood flow is more tubulent and non-denuding ednothelial damage is most frequent

Question 34

where does athrosclerosis distribule

Answer 34

more in the abdominal aorta than the thoracic aorta. Predilection for the ostia of major branches (points of increased turbulence)

Question 35

modifiable risk factors for atherosclerosis

Answer 35

Hyperlipdemia (even in the absence of other risk factors) Hypertension, cigarette smoking, diabetes mellitus

Question 36

Progression and sequelae of atherosclerosis

Answer 36

1.) calcification, 2.) rupture, ulceration, erosion of plaques, inducing thombosis 3.) Hemorrhage into plaques 4.) Atheroembolism 5.) Aneurysmal dilatation (especially in the abdominal aorta)

Question 37

Hypertensive Heart Disease

Answer 37

Hypertension leads to pressure overlad and ventricular hypertrophy in order to meet the increased demands placed on the heart

Question 38

Minimal criteria for diagnosing Systemic (left sided) hypertensive heart disease

Answer 38

1.) Left ventricular Hypertrophy (usually concentric) in the absence of other cardiovascular pathology (aortic stenosis,etc) 2.) Histroy or Pathologic evidence of hypertension

Question 39

Discribe the gross mophology of systemic (left sided) hypertension

Answer 39

thickened left ventricle (>1.5cm) , ventricle becomes stiff and noncompliant due to interstitial fibrosis leading to ventricular filling defect and often subsequent left atrial enlargement

Question 40

earliest microscopic change seen in systemic hypertensive heart disease

Answer 40

myocyte hypertrophy(increase in the diameter)

Question 41

Potential sequelae of systemic hypertensive heart disease

Answer 41

1.) Ischemic heart disease 2.) Renal damage 3.) Cerebrovascular damage 4.) Progressive heart failure or sudden cardiac death from arrythmia 5.) Development of aneurysms (especially aortic - also can be thoracic)

Question 42

Pulmonary (right sided) HTN disease

Answer 42

stems from pressure overload in the right ventricle. Pulmonary vasculature is typically low pressure and the normal right ventricle is thinner compared to the left ventricle

Question 43

cor pulmonale

Answer 43

isolated pulmonary hypertensive heart disease. Characterized by 1.) Right ventricular hypertrophy (concentric) 2.) Right ventricular dilation (results in venous back up which can cause symptoms such as JVD and ansacara) 3.) Potential right heart failure secondary to pulmonary hypertension

Question 44

MCC of cor pulmonale (isolated pulmonary hypertension)

Answer 44

Lung disease

Question 45

Acute cor pulmonale

Answer 45

marked dilation of the right ventricle (ovoid shape) WITHOUT hypertrophy

Question 46

Chronic cor pulmonale

Answer 46

1.) Right sided ventricular wall thickening 2.) Fat in the walls disappear and fat align themselves circumfrentially 3.) Hypertrophied right ventricle may compress left ventricle or lead to recurgitation and thickening of the tricuspid valve

Question 47

Potential sequelae of Pulmonary Hypertensive Heart Disease

Answer 47

1.) Tricuspid valve Incompetence 2.) right sided heart failure (JVD, ansacara, dyspnea, fatigue, weakness, fainting, palpations and arrythmias)