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Pathophysiology Semester 1 > Chapter 32 > Flashcards

Chapter 32 Flashcards

1
Q

What are the types of arteriosclerosis?

A

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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2
Q

What are the stages fo atherosclerosis?

A

Initiation and formation.
Adaptation.
Clinical.

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3
Q

Why are cytokines and monocyts attracted to LDL area

A

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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4
Q

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?

A

Smooth muscle cell proliferation

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5
Q

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

A

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

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6
Q

What stage of atherosclerosis is this:

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

A

Adaptation stage

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7
Q

What stageof atherosclerosis is this

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

A

Clinicial stage

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8
Q

What can the following cause?

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

A

Edema

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9
Q

what are 95% of all HTN cases

and what is cause

A

Primary HTN

No cause clearly identified

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10
Q

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

A

Improves blood return

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11
Q

How does plaque effect NO

A

Covers up endotheial lining which is what releases NO

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12
Q

How does hyperthyroidism effect HTN

A

Increases HR

Increases force of contraction of the heart

Therefore increases BP

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13
Q

How does cortisol effect HTN

A

Acts simular to aldersterone

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14
Q

What are these causes most identifiable with?

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

A

CAUSES OF SECONDAY HTN

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15
Q

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

A

Hypertrophy of left ventricular walls

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16
Q

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

A

Malignant HTN

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17
Q

These pathophysiology signs indicate what?

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

A

Malignant HTN

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18
Q

What is orthostatic hypotension

A

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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19
Q

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.

A

Acute

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20
Q

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.

A

Chronic

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21
Q

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.

A

aneurysms

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22
Q

What is a false aneurysm (pseudoaneurysm)

A

the blood leaks into the surrounding tissue

Does not involve distortion of vessel

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23
Q

What are saccular or berry aneurysms the result of

A

Congenital abnormalities in the arterial wall

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24
Q

What is fusiform (giant) aneurysms the result of

A

Result of diffuse arteriosclerotic changes

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25
Q

What are mycotic aneurysms caused by

A

Arteritis caused by bacterial emboli.

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26
Q

The follwing describes what

Hemorrhage into the arterial wall as it dissects a path along the length of the vessel

A

Dissecting aneurysm

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27
Q

what is the most common source of embolism

A

Mitral or artic valvular disease (abnormal heart rhythms)

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28
Q

What is the most common cause of endocarditis?

A

Bacterial embolism

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29
Q

What is Thromboangiitis Obliterans?

A

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.

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30
Q

What is the etiology of buerger disease (Thromboangiitis Obliterans )

A

T-cell activation, autoimmunity

Associated with smoking

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31
Q

What is primary Raynauds Disease

A

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.

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32
Q

What is secondary Raynauds due to

A

Vascular disease

Pulmonay hypertension

Myexdema

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33
Q

Name the disease that goes with the following etiology

Primary:
Genetic.
Secondary:
Increase in cholesterol only.
Increase in triglycerides only.
Mixed: increase in both cholesterol and triglycerides.

A

Dyslipidemia

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34
Q

Lipid transport

Exogenous is what?

Endogenous is what?

A

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.

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35
Q

What are lipoproteins?

A

They are the transport for both exgenous and edogenous

The are :

Chylomicrons (picture)

VLDL

LDL

HDL

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36
Q

What is lipoprotein lipase

A

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

37
Q

What is apoprotein (apoCII)?

A

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

38
Q

Chylomicrons are the transporters of exogenous.

What are the transporters of endogenous?

A

VLDL

Also activated by apoprotein

39
Q

What happends to VLDL as it hydrolyes?

A

Changes to LDL ast it unloads fat

40
Q

What other structure bears apoprotein receptors and can absorb cholesterol

A

Macrophages

41
Q

What is the job of HDL

A

HDL particles shuttle cholesterol back to the liver where they are degraded.

and form bile acids which are then conveted to bile salts

42
Q

does fats travel in the venous system 1st?

A

No

Lymph system

43
Q

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

A

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

44
Q

What is Hyperhomocysteinemia

A

associated with an increase in LDL and a decrease in vasodiators

Risk factor for CAD

45
Q

How does smoking increase risk of CAD

A

Promotes the release of Epi and NE

This increases HR and Contration strenghen

This requires more O2

46
Q

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

A

Dyslipidemia

HTN

Diabetes Mellitus

Obesity

47
Q

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

A

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

48
Q

What is Stable Angina

A

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

49
Q

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

A

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

50
Q

What does the pain come from in stable angina

A

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

51
Q

How long does stable angina usually last

A

3-5 min

52
Q

The following cause what?

Hyperactivity of sympathetic nervous system.
Increased influx of Ca2+.
Impaired production of prostaglandin or thromboxane

A

Prinzmetal (variant) angina

53
Q

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

A

At Rest

Pain occurs during REM sleep, cyclic in nature

54
Q

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.

A

Silent Ischemia

55
Q

What does silent ischemia increse your risk for

A

Maked increase for cardiovascular death

56
Q

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

A

Acute Coronary Syndromes

57
Q

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

A

Unstable angina

58
Q

Occlusion that results in posterior (inferior) MI

A

From the Right Coronary Artery

59
Q

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

A

Left coronary artery

60
Q

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

A

Left anterior descending artery

61
Q

Infract of Lateral Left Vent is from occlusion of what artery

A

Left circumflex coronary artery

62
Q

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

A

Subendocardial infarct

63
Q

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.

A

Transmural infarct

64
Q

How long of hypoxia before you can see EKG changes

A

After 1 min

65
Q

How long can the tissue remain viable without O2

A

20 min

66
Q

How long after MI are polymorphonuclear leukocyts visible?

Muscle cell nuclei disappear?

A

2-4 days

67
Q

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

A

4-10 days

68
Q

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

A

Sustained ischemia (not true MI yet)

69
Q

MI tissue changes associated with myocardial remodeling are what?

A

MI

70
Q

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?

A

Myocardial remodeling

71
Q

What type of patients are common to see silent MI

A

Common in diabetic patients with autonomic dysfunction

72
Q

Drop in BP.
Elevated plasma glucose.
Elevated troponin I and T.
Transient rise in LDH, CK isoenzymes.

Are clinical manifestations of what?

A

MI

73
Q

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

A

Contract Band Necrosis

74
Q

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

A

Neoplasm.
Trauma.
Infection.

Immunologic

75
Q

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)

You might have what?

A

Acute pericarditis

76
Q

paricarditis can lead to?

A

pericardial effusion

77
Q

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

A

pericardial effusion

78
Q

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 manifestations:
Fatigue and anorexia.
Gradual, exercise intolerance.
Distention of jugular vein

A

Constrictive pericarditis

79
Q

What is the most common cause of cardiomyopathies?

A

Ischemic or valvular heart disease or virus

80
Q

Excess alcohol consumption can lead to what

A

Cardiomyopathies

81
Q

What does cardiomyopathies cause

A

overall weaking of the cardiac muscle

82
Q

What is hypertrophic cardiomyopathy

A

Idiopathic cardiomyopathy with thickening of myocardium.

Usually from autosomal dominat disorder that alters sarcomer function

83
Q

The following etiolgies indicate what?

Amyloidosis.
Hemochromomatosis.
Glycogen storage disease

A

Restrictive cardiomyopathies

84
Q

The myocardium becomes rigid and noncompliant which impairs diastolic function

This almost always progresses to CHF

A

Restrictive cardiomyopahties

85
Q

What is left heart failure associed with

A

Increase preload

Increase after load

Ventriculr remodeling

86
Q

Does left heart failure cause increase or decreased urine output

A

Decreased

87
Q

pulmonary congestion despite normal SV and CO is considered what?

A

Isolated diastolic heart failure

88
Q

The following describe what?

Pathophysiology:
Decreased compliance of left ventricle.
Increased left EDV pressure.

Clinical manifestations:
Dyspnea on exertion.
Fatigue.
Pulmonary edema.
Pleural effusion.

A

Isolated diastolic heart failure

89
Q

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.

A

High output heart failure

Pathophysiology Semester 1 (7 decks)

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