Ch. 32 Alterations of Cardiovascular Function Flashcards

(39 cards)

1
Q

What are two causes of Varicose Veins?

A
  1. Injury or disease involving the saphenous vein valves
  2. gradual venous distention caused by the action of gravity on blood in the legs.
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2
Q

Chronic Venous Insufficiency

A

inadequate venous return over a long period of time

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3
Q

Treatment of Varicose Veins

A

elevating the legs, wearing compression bandages or stocking and performing physical exercises

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4
Q

Why are venous thrombi more common than arterial thrombi?

A

flow and pressure are lower in the vein than in the arteries

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5
Q

Triad of Virchow (factors that promote venous stasis)

A
  1. venous stasis
  2. venous endothelial damage
  3. hyper coagulable states
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6
Q

Tissue Factor produced by cancer cells activates…

A

coagulation, fibrin synthesis and platelet activation

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7
Q

Plasminogen activator inhibitor -1

A

produced by cancer cells, inhibit the fibrinolytic system

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8
Q

endothelial protein C receptor (EPCR), also known as the activated protein C receptor (APC receptor)

A

is a transmembrane glycoprotein that plays a crucial role in regulating blood coagulation, inflammation, and vascular integrity by enhancing protein C activation and mediating its cytoprotective effects

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9
Q

The most common inherited hyper-coagulability state

A

factor V leiden mutation, which affects 3% to 8%, cause of 20% to 25% of venous thromboembolism cases

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10
Q

Factor V Leiden results from…

A

single point mutation in the Factor V which causes inadequate anticoagulant response to activated protein C

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11
Q

If D-dimer is elevated, diagnosis of DVT is confirmed by

A

doppler ultransonography

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12
Q

Superior Vena Cava Syndrom

A

progressive occlusion of the the superior vena cava that leads to venous distention in the upper extremities and head.

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13
Q

Most common cause of SVCS

A

bronchogenic cancer followed by lymphomas and metastasis of other cancers

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14
Q

Clinical Manifestations of SVCS are

A

Edema, and venous distention in the upper extremities and face, including the ocular beds

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15
Q

Diagnosis of SVCS

A

chest x-ray, doppler studies, CT, MRI and ultrasound

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16
Q

Treatment of SVCS

A

if malignant disorders radiation therapy, SX, chemotherapy and the administration of diuretics, steroids and anticoagulation therapy

17
Q

What defines hypertension

A

sustained systolic blood pressure of 130mm Hg or a diastolic pressure of 80mm Hg or greater

18
Q

Secondary Hypertension

A

caused by underlying disease process or medication that raises PVR or cardiac output
ex. renal vascular disease, adrenocortical tumors, oral contraceptives, antihistamines

19
Q

Family history
advancing age
cigarrette smoking
obesity
heavy alcohol consumption
sex
black race
high dietary sodium intake
low intake of k+, calcium or magnesiumn
glucose intolerance

A

Risk factors for Primary hypertension

20
Q

The “pressure-natriuresis relationship”

A

describes how the kidneys respond to changes in blood pressure by excreting more or less sodium and water, ultimately influencing blood volume and pressure

21
Q

The primary function of leptin

A

to interact with the hypothalamus to control body weight through appetite inhibition and increased metabolic rate

22
Q

Adiponectin

A

is a hormone your adipose (fat) tissue releases that helps with insulin sensitivity and inflammation.

23
Q

increased leptin and decreased leptin are associated with

24
Q

insulin resistance promotes overactivity of…

25
hypertrophy characterized by
myocardium that is thickened, scarred, and less able to relax during diastole, leading to heart failure with preserved ejection fraction
26
now recognized as an early sign of impending renal dysfunction
microalbuminuria
27
atherosclerosis
caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to plaque buildup
28
Foam cells are
macrophages (white blood cells) that have accumulated large amounts of lipids, primarily cholesterol and triglycerides
29
C-reactive protein (CRP)
is a protein produced by the liver in response to inflammation.
30
what control the serum levels of LDL
the liver, because LDL is controlled by a hepatic receptors
31
"reverse cholesterol transport"
HDL, which returns excess cholesterol from the tissues to the liver for processing or elimination in the bile
32
hs-CRP
protein synthesized in the liver and is used as an indirect measure of atherosclerotic plaque-related inflammation
33
primary used of hs-CRP
aid to decision-making about pharmacologic interventions for individuals with other risk factors for CAD
34
LDL oxidation
is a process in which low-density lipoprotein (LDL), also known as "bad" cholesterol, becomes damaged. This damage can lead to the formation of atherosclerotic plaques, which are deposits of fat and cholesterol in the arteries
35
Takotsubo syndrome
acute reversible heart failure syndrome associated with acute myocardial ischemia but without obstruction of coronary arteries
36
left heart failure
categorized as heart failure with reduced EF
37
normal EF
55% to 70%
38
The Frank-Starling law of the heart
describes the relationship between the force of myocardial contraction and the initial length of the cardiac muscle fibers, stating that as the heart fills with more blood (preload), it contracts with greater force and pumps out more blood (increased stroke volume
39