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HSS 3305 > Lecture 15 > Flashcards

Lecture 15 Flashcards

1
Q

Arteries/arterioles

A

Conduct blood to tissues (away from heart) – maintain BP, lack elasticity so they use smooth muscle cells

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2
Q

Capillaries

A

Thin endothelium lines vessels that deliver nutrients/oxygen and remove waste products from cells

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3
Q

Veins

A

Return blood to heart under low pressure with assistance of one-way valves

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4
Q

Capillary hydrostatic pressure

A

Force pushing fluid from capillaries into extracellular space

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5
Q

Capillary permeability

A

Determines ease of fluid flow through capillary endothelium

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6
Q

Osmotic pressure

A

Water-attracting property of a solution; exerted by proteins in the blood (colloid osmotic pressure) that attract fluid from interstitial space back into the capillaries

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7
Q

Open lymphatic channels

A

Collect fluid forced out of the capillaries by the hydrostatic pressure and return fluid into circulation

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8
Q

Venous thrombosis

A

Normally, blood does not clot within the vascular system but can be precipitated by any number of conditions “Virchow’s triad” (slowing or stasis of blood flow, blood vessel wall damage, and increased coagulability of blood)

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9
Q

Thrombus

A

An intravascular clot; can occur in any vessel or within the heart

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10
Q

Arterial thrombi

A

Related to development of atherosclerosis, formation of lipid plaques causing narrowing and hardening of arteries.

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11
Q

Embolus/Embolism

A

Blood clots becoming detached and block downstream arterial circulation blocking blood flow

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12
Q

Phlebitis

A

Inflammation of vein (from stretching, or blockage)

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13
Q

Varices or varicosities (Varicose viens) + treatment

A

Excessive dilation and tortuosity (many twisting turns), Lack of prevention of retrograde blood flow, varicose veins result if saphenous (large subcutaneous, superficial leg) veins become dilated and valves become incompetent
Treatment: Stocking, limb elevation, surgical removal/ligation in serious cases.

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14
Q

Where can Varicose Viens be found?

A

Leg, lower rectum (hemorrhoids), scrotum (varicocele), esophageal varices

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15
Q

Predisposing factors to clot formation in leg veins…

A

Prolonged bed rest, extended period of inactivity, Cramped position for an extended period , Varicose veins or any condition preventing normal emptying of veins, Risk of clotting in post-op patients (increased clotting factors), confined to bed (stasis)

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16
Q

Presentation and treatment of Venous Thrombosis

A

Leg swelling/pain from partial blockage of venous return in leg, Risk of detachment and further injury causing pulmonary embolism, Treat with anticoagulants – fibrinolytics (tpa – tissue plasminogen activator) and elevate leg

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17
Q

Why does Varicose veins happen

A

Dilated tortuous veins, usually in the leg - resulting from poor blood return, Results from incompetent valves, runs in the family (genetic)

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18
Q

Pulmonary Embolism + symptoms

A

Embolus found in the pulmonary artery, manifestations depend on the size (larger the embolus the worse the outcome - immediate fatality), blood can find ways around the clot and the clot is dissolved
Symptoms: Cyanosis and shortness of breath due to inadequate oxygenation of blood

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19
Q

Large Pulmonary Emboli

A

Complete block of pulmonary artery, Pulmonary artery and right side of heart becomes overdistended (swollen) with blood, causing increased pulmonary pressure, Left ventricle unable to pump adequate blood to brain and vital organs, patient may go into shock

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20
Q

Small Pulmonary Emboli

A

Small emboli may pass through main pulmonary arteries, becoming impacted in peripheral arteries supplying the lower lobes of the lungs, necrosis can occur in the affected area, if no infarct - mild

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21
Q

Pulmonary Infarct symptoms

A

Dyspnea, chest pain, cough, and expectoration of bloody sputum due to leakage of blood from infarcted lung tissue into bronchi

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22
Q

Pulmonary Embolism Diagnosis

A

CTPA (most important test), D-dimer test, chest x-ray, ventilation/perfusion scan

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23
Q

Air Embolism

A

Large amount of air sucked into circulation from lung injury due to a chest wound, prevents filing of heart due to air in the right heart chambers, result: heart is unable to pump blood

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24
Q

Amniotic Fluid Embolism

A

Complication of pregnancy, Fetal cells, hair, fat, and amniotic debris fluid block maternal pulmonary capillaries, leads to disseminated intravascular coagulation syndrome (DIC)

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25
Q

Foreign Particulate Matter Embolism

A

Material injected intravenously and is trapped within small pulmonary blood vessels causing severe respiratory distress

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26
Q

Edema

A

Refers to accumulation of fluid in interstitial tissues, most often noted in ankles and legs from disturbances of extracellular fluid circulation between capillaries and interstitial tissues

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27
Q

Pitting edema

A

Extreme form of edema where a pit or indentation formed when edematous tissue is compressed with the fingertips

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28
Q

Ascites

A

Fluid accumulates in peritoneal cavity (common with liver failure)

29
Q

Hydrothorax

A

Fluid accumulates in pleural cavity – most commonly from cardiac failure

30
Q

Pathogenesis of Edema

A

Increased capillary permeability (increased swelling of tissues with acute inflammation), low plasma proteins (excess protein loss from liver or kidney disease, Inadequate synthesis), Increased hydrostatic pressure (heart failure, blood clot, inferior superior vena cava syndrome), Lymphatic obstruction

31
Q

Acute Pulmonary Edema

A

Manifestation of acute heart failure, right heart pumps blood into lungs faster than left heart can deliver blood to peripheral tissues which engorges lungs with blood.

32
Q

What happens when the lungs are engorged with blood?

A

Increased pulmonary capillary pressure, Leakage of fluid in alveoli, Shortness of breath from fluid accumulation in alveoli and impaired oxygenation

33
Q

Circulatory Disturbances - Shock

A

Blood flow or blood pressure is too low to adequately supply body with blood and circulating blood volume is less than capacity of vascular system - potentially life threatening

34
Q

Hypovolemic shock

A

Low blood volume (blood loss, severe burns, diarrhea, dehydration)

35
Q

Cardiogenic shock

A

Reduced cardiac output (heart failure)

36
Q

Septic shock

A

Excessive vasodilatation secondary to release of microbial toxins and inflammatory mediators

37
Q

Anaphylactic shock

A

Excessive vasodilatation from release of inflammatory mediators

38
Q

Shock prognosis + treatment

A

Prognosis depends on early recognition and rapid, appropriate treatment
Treatment: Drugs that promote vasoconstriction (Epinephrine), Intravenous fluids or blood to restore volume, treat underlying cause

39
Q

Arterial Thrombosis

A

Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial wall with thrombi formation which blocks blood flow causing infarct

40
Q

Infarct in Coronary artery

A

Myocardial infarction

41
Q

Infarct in Major leg artery

A

Gangrene

42
Q

Infarct in Cerebral artery

A

Stroke

43
Q

Intracardiac Thrombosis

A

Clot formation within artria, on the surface of damaged heart valves, and wall of left ventricle; may dislodge into systemic circulation and cause infarction of major organs (Spleen, kidneys, brain, lung, etc.)

44
Q

Thrombosis by Increased Coagulability (when does this happen?)

A

Rise in coagulation factors following surgery or injury, polycythemia, estrogen in contraceptive pills stimulate synthesis of clotting factors, hereditary gene mutation in clotting factors

45
Q

Polycythemia

A

A rare blood cancer in which bone marrow produces too many red blood cells

46
Q

Hereditary gene mutations in clotting factors

A

Mutation of gene that codes for factor V results in abnormal factor V (more resistant to inactivation, prolonged activity, increased coagulability) and Mutation of gene regulating prothrombin synthesis (risk for venous thrombosis increases as prothrombin level rises)

47
Q

Why are cancer patients more susceptible to thrombosis

A

Increased platelets and coagulation factors due to the release of thromboplastic materials into circulation from tumor (both arterial and venous thromboses; DIC can occur from this)

48
Q

Arteriosclerosis

A

Chronic and progressive degenerative disease of large to mid-sized arteries (thickening/ hardening due to aging)

49
Q

Atherosclerosis

A

Narrowing of arteries from lipid deposits (buildup of fat / cholesterol) from bloodstream

50
Q

Atheroma

A

Necrotic core rich in lipids with fibrous cap containing immune/inflammatory cells, smooth muscle cell and connective tissue

51
Q

Atheromatous Deposits

A

Stable plaque surrounded by fibrous tissue which cause permanent narrowing of the vessel

52
Q

Risk factors for blocked arteries

A

Elevated blood lipids (most significant), High BP, Smoking, Diabetes, and genetics (largest impact (40-60%))

53
Q

Neutral fat

A

Triglyceride (three molecules of fatty acid combined with glycerol) from ingested fat, sugar, and carbohydrates

54
Q

Trans fat and saturated fat

A

Atherogenic

55
Q

Cholesterol

A

Synthesized in body and from diet

56
Q

Low-density lipoprotein (LDL) vs. High-density lipoprotein (HDL)

A

Bad cholesterol and Good cholesterol; protective; increases with regular exercise, smoking cessation, modest alcohol intake

57
Q

C-Reactive Protein (CRP, associated with inflammation)

A

Produced in the liver and released in response to inflammation (accumulation of macrophages, lymphocytes, lipids, and products of tissue injury) - High CRP level predicts high cardiovascular disease risk

58
Q

Homocysteine

A

Sulfur-containing amino acid formed from methionine that is abundant in animal protein (high levels indicate early onset of severe atherosclerosis and risk of cardiovascular disease)

59
Q

Diagnosis and Treatment of CAD

A

Diagnosis (Angiogram – to detect artery obstruction, Echocardiogram – to evaluate blood flow, structural abnormalities, and Stress tests – measure cardiac function (EEG))
Treatment: Lifestyle changes (diet, exercise, stress), Drugs: Anti-anginal drugs (nitroglycerin), anti-arrhythmic, statins (lower blood cholesterol), and Surgical: bypass, angioplasty

60
Q

Hypertension

A

Increased sympathetic stimulation can cause excessive vasoconstriction of small arterioles resulting in increased peripheral resistance; increased diastolic blood pressure, Increased force of ventricular contraction, Compensatory increase in systolic pressure

61
Q

Cardiac effects of hypertension:

A

Increased peripheral resistance → higher workload → heart enlarges → heart failure

62
Q

Vascular effects of hypertension:

A

Increased pressure → premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → rupture and hemorrhage

63
Q

Renal effects of hypertension:

A

Narrowed renal arterioles → decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules → renal failure

64
Q

Secondary hypertension

A

From a known disease (autoimmunity, chronic kidney disease, pituitary or adrenal tumor, hyperthyroidism)

65
Q

Treatment for hypertension

A

Diuretics - to remove salt/water, ACE inhibitors – reduce angiotensin II (potent vasoconstrictor), Calcium channel blockers (inhibit contraction of arteriolar smooth muscle cells)

66
Q

Isolated systolic hypertension

A

Mild to moderate rise in systolic pressure, but low or normal diastolic pressure (Increased rigidity of aorta with age,

67
Q

Aneurysms

A

Dilatation or outpouching of a weakened portion of the arterial wall caused by arteriosclerosis

68
Q

Arteriosclerotic aneurysm

A

Arteriosclerosis causes narrowing, thrombosis, and weakening of vessel wall

69
Q

Aorta aneurysms

A

Most common in distal part of aorta; may rupture, leading to massive and fatal hemorrhage (Degenerative changes over time can cause layers of aorta to separate and blood is forced into the aortic wall)

HSS 3305 (21 decks)

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