Chapter 32 Flashcards by Brian Adams

What are the types of arteriosclerosis?

Atherosclerosis:
Most common form of arteriosclerosis.
Thickening of the intima with plaques.
Arteriosclerosis obliterans:
Medium and large arteries of the lower extremity.
Medial calcific sclerosis (Monckeberg’s calcific sclerosis):
In the elderly.
Arteries of the thyroid and uterus.
Hyaline arteriolosclerosis:
Thickening of the walls of arterioles by deposition of hyaline material.

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What are the stages fo atherosclerosis?

Initiation and formation.
Adaptation.
Clinical.

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Why are cytokines and monocyts attracted to LDL area

Beacause of epithieal tissue damage

LDL enter intima, oxidized by free radicals.
Oxidized LDLs and lipoproteins induce tissue damage.
Inflammatory response releases cytokines that attract monocytes.
Monocytes differentiate into macrophages.
Macrophages engulf lipid droplets.
Become foam cells.
https://youtu.be/wbShOXhO6p8

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In atherosclerosis the foam cells oxidized lipoproteins stimulate release:
Inflammatory mediators.
TNF-a.
Interleukin-1.
interferon-a.

what do these growth factors stimulate the proliferation of?

Smooth muscle cell proliferation

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In the development of atherosclerosis what happends after the stimulation of smooth muscle cell proliferation

Fibrous plaque forms.
Fatty streak develops.
Angiotensin II released:
Abnormal vasoconstriction.

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What stage of atherosclerosis is this:

Plaque protrudes into lumen.
Artery wall remodels to maintain lumen size.
Cannot compensate when plaque occupies 50% diameter.

Adaptation stage

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What stageof atherosclerosis is this

Hemorrhage into plaque.
Surface ulceration.
Fissure formation.
Calcification.
Plaque rupture.

Clinicial stage

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What can the following cause?

Leakage of plasma proteins into interstitial fluid.
Myexedema.
Decreased plasma [protein].

Edema

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what are 95% of all HTN cases

and what is cause

Primary HTN

No cause clearly identified

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What does vasoconstriction of veins do to blood return to the heart

Improves blood return

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How does plaque effect NO

Covers up endotheial lining which is what releases NO

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How does hyperthyroidism effect HTN

Increases HR

Increases force of contraction of the heart

Therefore increases BP

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How does cortisol effect HTN

Acts simular to aldersterone

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What are these causes most identifiable with?

Renal artery stenosis.
Diabetes mellitus.
Cushing syndrome.
Hyperthyroidism.

CAUSES OF SECONDAY HTN

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Enlarged boxcar shaped nuclei are seen in myocardial cells with what?

Hypertrophy of left ventricular walls

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What does rapid progression vascular compromise with onset of symptomatic diseases of brain, heart, kidney. AND a diastolic pressure > 140mmHg indicate?

Malignant HTN

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These pathophysiology signs indicate what?

Microvascular pathological changes.
Renal microaneurysms.
Scarring of retina.
Segmental dilation due to necrosis of smooth muscle.
Malignant nephrosclerosis.

Malignant HTN

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What is orthostatic hypotension

Decrease in both systolic and diastolic pressures on standing.

Systolic pressure decrease of 20 mmHg or diastolic pressure decrease of 10 mmHg within 3 minutes of standing

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The following describe what type of orthostatic hypotension

Normal regulator mechanism decrease:
Anatomic variation.
Altered body chemistry.
Drug action.
Antihypertensives or antidepressants.
Prolonged immobility.
Starvation.
Volume depletion.
§Venous pooling.

Acute

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The following describe what type of orthostatic hypotension

Idiopathic or primary:
No known cause.(can happen normally w age)
Secondary due to a specific disease:
Endocrine (adrenal insofuency Diabeties).
Metabolic.
Central or peripheral nervous system.

Chronic

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The following would describe what afflection:

Atherosclerosis.
Deficiencies in wall collagen.
Elastin failure due to protease activity or aging.
Increased turnover of aortic collagen.
Marfan syndrome.

aneurysms

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What is a false aneurysm (pseudoaneurysm)

the blood leaks into the surrounding tissue

Does not involve distortion of vessel

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What are saccular or berry aneurysms the result of

Congenital abnormalities in the arterial wall

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What is fusiform (giant) aneurysms the result of

Result of diffuse arteriosclerotic changes

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What are mycotic aneurysms caused by

Arteritis caused by bacterial emboli.

The follwing describes what Hemorrhage into the arterial wall as it dissects a path along the length of the vessel

Dissecting aneurysm

what is the most common source of embolism

Mitral or artic valvular disease (abnormal heart rhythms)

What is the most common cause of endocarditis?

Bacterial embolism

What is Thromboangiitis Obliterans?

ALSO CALLED BUERGER DISEASE Inflammatory disease of peripheral arteries. Accompanied by thrombi and arterial vasospasm. Can occlude portions of small arteries in the feet and sometimes hands.

What is the etiology of buerger disease (Thromboangiitis Obliterans )

T-cell activation, autoimmunity Associated with smoking

What is primary Raynauds Disease

Vasospasm in small arteries and arterioles in fingers (less common in toes). **_Etiology:_** Vasospastic attacks triggered by brief exposure to cold or emotional stress. Endothelial dysfunction with decreased NO production.

What is secondary Raynauds due to

Vascular disease Pulmonay hypertension Myexdema

Name the disease that goes with the following etiology ## Footnote **_Primary:_** Genetic. **_Secondary:_** Increase in cholesterol only. Increase in triglycerides only. Mixed: increase in both cholesterol and triglycerides.

Dyslipidemia

Lipid transport Exogenous is what? Endogenous is what?

**_Exogenous:_** Processes lipids absorbed from the diet. Exogenous fat is carried from small intestines by chylomicron. **_Endogenous:_** Shuttles fats and cholesterols back and forth between the liver and the peripheral tissues.

What are lipoproteins?

They are the transport for both exgenous and edogenous The are : Chylomicrons (picture) VLDL LDL HDL

What is lipoprotein lipase

This is anenzyme found on the capillary walls that when activated will break down (hydorlyze) the lipoproteins (chylomicoron and VLDL) It helps them digest the contents of lipoproteins into the cell

What is apoprotein (apoCII)?

This is the molecule that is on the surface of the chylomicron that reacts with lipoprotein lipase (which is found on the capillary wall)

Chylomicrons are the transporters of exogenous. What are the transporters of endogenous?

VLDL Also activated by apoprotein

What happends to VLDL as it hydrolyes?

Changes to LDL ast it unloads fat

What other structure bears apoprotein receptors and can absorb cholesterol

Macrophages

What is the job of HDL

HDL particles shuttle cholesterol back to the liver where they are degraded. and form bile acids which are then conveted to bile salts

does fats travel in the venous system 1st?

No Lymph system

What is C-reactive protein and what can it indicate?

is an annular (ring-shaped), pentameric protein found in blood plasma, the levels of which rise in response to inflammation It is a good indicator of risk of CAD

What is Hyperhomocysteinemia

associated with an increase in LDL and a decrease in vasodiators Risk factor for CAD

How does smoking increase risk of CAD

Promotes the release of Epi and NE This increases HR and Contration strenghen This requires more O2

What are the risk factors of CAD the make up metabolic syndrome

Dyslipidemia HTN Diabetes Mellitus Obesity

What are the 2 factors that reduce blood flow in myocardial ischemia?

**_Hemodynamic factors:_** §Increased resistance in coronary vessels, hypotension, or decreased blood volume (e.g., hemorrhage). §Most common cause is atherosclerosis (increased resistance). §Narrowing of a major coronary artery by more than 50% impairs blood flow sufficiently to produce myocardial ischemia. **_Cardiac factors:_** §Decrease in diastolic filling time, increase HR, or valvular incompetence. §Fibrillation. This reduces EDV = reduces Stroke volume = Cardiac output

What is Stable Angina

Transient pain resulting from myocardial ischemia. Symptomatic when luminal cross -sectional area is reduced by 50 or 75% .

How is the incidence of stable angina seen diffrently in men and women

Incidence of angina continuously rises with age in women. In men the incidence of angina peaks between 55 and 65 years of age, declines.

What does the pain come from in stable angina

Abnormal stretching of the ischemic myocardium irritates nerve fibers that enter spinal cord from C3 to T4 Discomfort may radiate to the neck, lower jaw, left arm, left shoulder or to the back

How long does stable angina usually last

3-5 min

The following cause what? Hyperactivity of sympathetic nervous system. Increased influx of Ca2+. Impaired production of prostaglandin or thromboxane

Prinzmetal (variant) angina

When does the chest pain of Prinzmetal (variant) angina almost exclusively take place

At Rest Pain occurs during REM sleep, cyclic in nature

The following describe what? Presence of a global or regional abnormality in left ventricular sympathetic innervation. Metabolic dysfunction in diabetes mellitus. Following CABG (coronary artery bypass grafting). Cardiac transplant. Mental stress.

Silent Ischemia

What does silent ischemia increse your risk for

Maked increase for cardiovascular death

Sudden coronary circulation obstruction caused by thrombus or a ruptured or ulcerated atherosclerotic plaque describes what?

Acute Coronary Syndromes

New onset of angina that occurs at rest when it used to just occur at exercise

Unstable angina

Occlusion that results in posterior (inferior) MI

From the Right Coronary Artery

Occlusion that causes infract of massive anterolateral section would be from what artery

Left coronary artery

Infarct of the Anteroseptal portion of the heart is from what artery

Left anterior descending artery

Infract of Lateral Left Vent is from occlusion of what artery

Left circumflex coronary artery

the following describe what type of MI Necrosis limited to inner layers of the heart. Arises within area of one of the major epicardial coronary arteries. Circumferential involving subendocardial areas of multiple coronary arteries. Consequence of hypoperfusion of the heart

Subendocardial infarct

The following describes what type of MI Involves the full left ventricular wall thickness. Usually follows occlusion of a coronary artery. Right coronary artery. Left anterior descending (LAD) coronary artery. Left circumflex coronary artery.

Transmural infarct

How long of hypoxia before you can see EKG changes

After 1 min

How long can the tissue remain viable without O2

20 min

How long after MI are polymorphonuclear leukocyts visible? Muscle cell nuclei disappear?

2-4 days

The following are all characteristics of post MI of how long? Few PMNs remain. Phagocytosis of dead tissue by macrophages. Fibroblasts proliferate. New collagen deposited

4-10 days

Myocardial stunning and hibernating myocardium changes are more consistant with what?

Sustained ischemia (not true MI yet)

MI tissue changes associated with myocardial remodeling are what?

Angiotensin II, Epi and NE, adenosine, inflammatory cytokines : * Myocyte hypertrophy. * Loss of contractile function. These are more consistant with what type of MI tissue changes?

Myocardial remodeling

What type of patients are common to see silent MI

Common in diabetic patients with autonomic dysfunction

Drop in BP. Elevated plasma glucose. Elevated troponin I and T. Transient rise in LDH, CK isoenzymes. **Are clinical manifestations of what?**

What is a characteristic feature of reperfusion of ischemic tissue that displaces as thick irregular eosinophilic bands of necrotic tissue: Small groups of hyper-contracted , disorganized sarcomeres with thickened Z lines. Massive infusion of Ca2+ due to reactive oxygen species

Contract Band Necrosis

Disorders of the pericardium are usually localized manifestaions of other disorders. Name them?

Neoplasm. Trauma. Infection. Immunologic

If you have sudden severe chest pain that worsens with respiratory movements or lying down. Dysphagia. Restlessness, irritability, anxiety. Sinus tachycardia. Friction rub (roughened pericardial membranes rubbing against each other) ## Footnote **You might have what?**

Acute pericarditis

paricarditis can lead to?

pericardial effusion

The following clinical finding indicate what? Pulsus paradoxus: Arterial blood pressure during expiration exceeds arterial pressure during inspiration. Impairment of diastolic filling of right ventricle and decreased filling in all 4 chambers. Muffled heart sounds, poorly palpable apical pulse, dyspnea on exertion

pericardial effusion

Chronic disorder. Idiopathic associated with: * Radiation exposure. * Rheumatoid arthritis. * CABG. Synonymous with TB (years ago). **_Pathophysiology_**: Fibrous scarring with calcification of pericardium . Visceral and parietal layers to adhere. Encases heart like fibrous shell. **_Clinical manifestation_**s: Fatigue and anorexia. Gradual, exercise intolerance. Distention of jugular vein

Constrictive pericarditis

What is the most common cause of cardiomyopathies?

Ischemic or valvular heart disease or virus

Excess alcohol consumption can lead to what

Cardiomyopathies

What does cardiomyopathies cause

overall weaking of the cardiac muscle

What is hypertrophic cardiomyopathy

Idiopathic cardiomyopathy with thickening of myocardium. Usually from autosomal dominat disorder that alters sarcomer function

The following etiolgies indicate what? Amyloidosis. Hemochromomatosis. Glycogen storage disease

Restrictive cardiomyopathies

The myocardium becomes rigid and noncompliant which impairs diastolic function This almost always progresses to CHF

Restrictive cardiomyopahties

What is left heart failure associed with

Increase preload Increase after load Ventriculr remodeling

Does left heart failure cause increase or decreased urine output

Decreased

pulmonary congestion despite normal SV and CO is considered what?

Isolated diastolic heart failure

The following describe what? Pathophysiology: Decreased compliance of left ventricle. Increased left EDV pressure. Clinical manifestations: Dyspnea on exertion. Fatigue. Pulmonary edema. Pleural effusion.

Isolated diastolic heart failure

The following describe what? Inability of the heart to adequately supply the body with blood-borne nutrients, despite adequate blood volume. Etiology: Septicemia, disturbed metabolism, inflammatory processes. Hyperthyroidism. Beriberi. Pathophysiology: Metabolic acidosis. §HR and SV increase. §Impaired cardiac metabolism.

High output heart failure