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CPR Exam 1 > Hypertensive Vascular Dz, Blood Pressure Regulation > Flashcards

Hypertensive Vascular Dz, Blood Pressure Regulation Flashcards

1
Q

Describe the negative side affects to high blood pressure.

A

End organ damage

Major risk factor in atherosclerosis

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2
Q

What is the BP value associated with increased risk of atherosclerosis?

A

Sustained >89/>139

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3
Q

What is secondary HTN associated with? Give examples.

A

Associated with underlying renal and adrenal dz

Ex: Primary aldosteronism, Cushing syndrome, Pheochromacytoma

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4
Q

Describe how secondary HTN occurs. How can you diagnose it during a physical exam?

A

Increased production of renin from ischemic kidney causes renal artery stenosis

A bruit can be heard on auscultation of affected kidney

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5
Q

Essential HTN is idiopathic (arises spontaneously, cause unknown). However, what are the risk factors that may lead to this dz?

A

Prevalence and vulnerability increases with age and African-american ethnicity

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6
Q

What other health problems may arise from essential HTN?

A 
Cardiac hypertrophy,
Heart failure (hypertensive heart dz)
Multi-infarct dementia
Renal failure
Aortic dissection
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7
Q

What happens with untreated HTN patients?

A

1/2 dies of ischemic heart dz or congestive heart failure

1/3 die of stroke

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8
Q

What is the BP value associated with malignant HTN?

A

> 200/>120

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9
Q

Describe what occurs with malignant HTN.

A

Rapid increase in BP, death within 1-2 yrs

Severe HTN
Renal failure
Retinal hemorrhage and exudates +/- papilledema

Often superimposed on pre-existing benign HTN

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10
Q

What is the most common type of HTN?

A

Essential HTN (~90-95%)

Secondary HTN (~5%)
Malignant HTN (~5%)
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11
Q

What is BP a function of? What influence it?

A

BP = Cardiac output (CO) X Peripheral Resistance

Influenced by multiple genetic and environmental factors

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12
Q

What is cardiac output?

A

Heart rate and stroke volume

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13
Q

What influences stroke volume?

A

Influenced by blood volume

BV regulated by renal sodium excretion or resorption (also mineralocorticoids and ANP)

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14
Q

Where is vascular resistance regulated? What influences it?

A

Regulated at level of arterioles

Influenced by neural and hormonal inputs

  • Neural = a/B-adrenergic
  • Humoral = Constrictors (angiotensin 2, thromboxane, etc.), Dilators (Prostagladins, Kinins, NO)
  • Local factors = auto regulation, pH, hypoxia
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15
Q

How does the body regulate LOW blood pressure?

A

In states of low volume or low peripheral resistance (or a decreased glomerular filtration rate), RENIN is released by juxtaglomerular cells in the afferent arterioles in kidneys.

Angiotensinogen –> Angiotensin 1 by Renin

Angiotensin 1 –> Angiotensin 2 by ACE (endothelium)

A2 causes:

  • Vasoconstriction
  • Aldosterone by adrenal gland causing kidneys to reabsorb sodium and water –> increase in BP
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16
Q

How does the body regulate HIGH blood pressure?

A

Volume expansion induces myocardial release of ANP leading to:

  • Na excretion and diuresis
  • Vasodilation
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17
Q

HTN is occasionally controlled by ___?
HTN is secondary to ___?
Sustained HTN requires participation of ___?

A

Controlled by single gene DO

Secondary to renal dz, adrenal dz, and endocrine DO

Sustained HTN requires participation of Kidneys

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18
Q

What are the 2 forms of small blood vessel dz?

A

Hyaline arteriosclerosis

Hyperplastic arteriosclerosis

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19
Q

Describe Hyaline arteriosclerosis. How is it involved in nephrosclerosis?

A

Increase in smooth matrix synthesis
Plasma protein leakage across damaged endothelium

In nephrosclerosis due to chronic HTN, arteriolar narrowing of hyaline arteriosclerosis –> diffuse impairment of renal blood supply and glomerular scarring

20
Q

What is the histologically significant of hyaline arteriosclerosis?

A

Homogenous pink (hyaline) thickening of vessel wall –> luminal narrowing

21
Q

Describe Hyperplastic arteriolosclerosis.

A

Occurs in severe HTN

In malignant HTN, laminations are accompanied by fibrinoid deposits

22
Q

What is the histologically significant of hyperplastic arteriolosclerosis?

A

Smooth muscle cells form concentric lamellations (“onion skinning”) –> luminal narrowing

In malignant HTN, laminations are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), particularly in kidney

23
Q

What is Arteriosclerosis?

A

“Hardening of arteries” (Large/middle arteries)

Arterial wall thickening and loss of elasticity

24
Q

What is Arteriolosclerosis?

A

Affects middle/small sm arteries and arterioles, may cause downstream ischemic injury

25
Q

What is Monckeberg medial sclerosis?

A 
Affects = >50 years old 
Calcification of muscular arteries
Internal elastic membrane involved
No narrowing of lumen 
No clinical significance
26
Q

What is Atherosclerosis?

A

“Gruel”, “Hardening” - PROCESS

Most frequent and clinically important pattern

27
Q

Atherosclerosis underlies the pathogenesis of?

A

Primary coronary, cerebral, and peripheral vascular dz

28
Q

In simple terms, what is the general worldwide distribution of patients suffering from atherosclerosis?

A

Extremely common, especially in the DEVELOPED world - this may be due to bad diets and decreased exercise

Roughly 1/2 of all deaths in western world
MI = 1/4 of all deaths in US

29
Q

Describe the overall pathogenesis of atherosclerosis.

A

Over time, vessel wall (endothelium) gets damaged. This caused build of fat, which later gets oxidized. This causes macrophage to travel to site and change into “foamy” macrophages. This begins to form a plaque. At the same, smooth muscle cells from layer underneath will travel towards the lumen and form a fibrotic cap around the macrophages.

30
Q

What is an atheroma? Why is it dangerous?

A

It is an atherosclerotic plaque.
Raised lesion with soft grumous core of lipid covered by a fibrotic cap

Besides mechanically obstructing blood flow, atherosclerotic plaques can rupture leading to catastrophic obstructive vascular thrombosis

Plaque can also increase diffusion distance from lumen to media leading to ischemic injury and weakening of vessel wall, changes that may result in aneurysm formation

31
Q

Describe how age is a risk factor for atherosclerosis.

A

40-60 year old incidence increases by 5x
Death rates from ischemic heart dz increase each decade

premenopausal women are somewhat protected - possibly due to atheroprotective effect of estrogen

32
Q

Describe hypercholesterolemia and metabolic syndrome in regards to atherosclerosis.

A

Both are major risk factors for atherosclerosis

HC is a major risk factor even in absence of other factors - it is sufficient to initiate lesion development

Metabolic syndrome: assoc w/ central obesity
Insulin resistance, HTN, dyslipidemia ( in. LDL, dec. HDL), hypercoagulability, & proinflammatory state may contribute to endothelial dysfunction and/or thrombosis

33
Q

What are some nonmodifiable risk factors for Atherosclerosis?

A

Genetic abnormalities
Family HX
increasing age
Male gender

34
Q

What are some modifiable risk factors for Atherosclerosis?

A 
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes (incidence of MI 2X higher in pts W/ DM than in those w/o)
Inflammation
35
Q

What molecule may be used to predict cardiovascular risk?

A

C-reactive protein (CRP)

36
Q

Where is endothelial injury more likely to occur in terms of atherosclerosis?

A

Hemodynamic turbulence
Does not occur randomly or everywhere uniformly
Most lesions tend to occur @ openings of existing vessels, branch points, posterior abd aorta - due to flow disturbances normally seen in these locations

37
Q

Describe how circulating lipids play a role in atherosclerosis.

A

Lipids in atheromatous plaques are predominantly cholesterol & cholesterol esters

Accumulate in the intima, are taken up by macrophages & partially oxidized

This modified LDL further accumulates w/in macrophages & smooth muscle cells, forming foam cells & a lesion known as a “fatty streak”

This stimulates an inflammatory response to accumulation of this toxic form of LDL

38
Q

Describe the inflammatory process that occurs once macrophages detect the site of injury.

A

Accumulation of cholesterol crystals w/in macrophages is recognized by the inflammasome, which leads to IL-1 secretion

More macrophages & T-cells are recruited & activated

Inflammatory cytokines further activate endothelial cells, & growth factors stimulate smooth muscle cells to migrate to the intima & proliferate

39
Q

Name the molecules associated w/ smooth muscle proliferation.

A

PGDF (released by locally adherent platelets)
Macrophages
Endothelial cells
Fibroblast growth factor
Transforming growth factor - alpha (TGF-a)

40
Q

Describe what happens during smooth muscle migration, proliferation, & matrix deposition.

A

Smooth muscle cells proliferate and synthesize ECM, including collagen

Atheromatous plaque = intimal expansion from foam cells & ECM, recruited inflammatory & smooth muscle cells, increased ECM

The fibrofatty plaque becomes covered w/ a fibrous cap (dense collagen fibers)

Center of plaque is necrotic, containing lipid, debris, foam cells & thrombus, surrounded by a none of inflammatory & smooth muscle cells

41
Q

What are the common sites of atherosclerotic involvement? (decreasing order)

A 
Abdominal aorta
Coronary arteries
Popliteal arteries
Internal carotid arteries
Circle of Willis
42
Q

What are the complications of atherosclerotic plaque?

A

Rupture & ulceration - may lead to thrombosis

Hemorrhage - may follow plaque rupture

Embolism - may follow plaque rupture

Aneurysm formation

43
Q

What are the consequences of atherosclerosis?

A

Stenosis of the arterial lumen

Acute plaque change

44
Q

Describe what happens during stenosis of the arterial lumen.

A

Plaques tend to continuity grow because of repeated cycling through the injury-healing process

The lumen of the affected vessel gradually shrinks, eventually leading to ischemia downstream (a point known as critical stenosis - approx. 70% occluded)

This may lead to chronic ischemia of myocardium, bowel, brain, the extremities, etc.

45
Q

Describe what happens with acute plaque change.

A

An acute thrombus may form over the plaque, occluding the artery. This may occur secondary to:

  • rupture of the plaque
  • erosion or ulceration of the plaque surface

Hemorrhage into the plaque may acutely expand its volume

46
Q

Some plaques are more prone to rupture than others. Why?

A

Fibrous cap is continually degraded and resynthesized (remodeled)

Increased inflammation in the plaque can accelerate fibrous cap degradation and inhibit its resynthesis; thus decreased collagen in the cap and weakening it

Physical stresses can cause plaque rupture:

  • change in BP
  • vasoconstriction
47
Q

What are atherosclerotic emboli composed of? What happens when an embolus breaks off?

A

May be composed of fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, even or even foreign bodies.

Emboli travel through the blood until they encounter vessels too small to permit further passage, causing partial or complete vascular occlusion

CPR Exam 1 (11 decks)

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