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Patho > Week 10: Cardiovascular > Flashcards

Week 10: Cardiovascular Flashcards

1
Q

What are the two laws that describe the resistance and pressure gradient needed for the CV system to function?

A

Ohm’s law: pressure gradient

Poiseuille’s law: resistance

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2
Q

What is the most important variable that determines the flow of the CV system?

A

radius of the blood vessels

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3
Q

How do you calculate: stroke volume, cardiac output, ejection fraction and MAP?

A

Stroke volume = EDV - ESV
Cardiac output = HR x SV
Ejection fraction = SV/EDV
MAP = CO x TPR

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4
Q

Define edema, what are the major causes (4)

A

accumulation of excess fluid in the interstitial space
Causes:
Heart failure: increased hydrostatic pressure as fluid accumulates from fluid backup
Increased hydrostatic pressure: increased arterial or venous pressure or arterial dilation
Decreased osmotic pressure: decreased plasma proteins or increased permeability to proteins
Obstruction: lymph failure

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5
Q

What is the role of the lymphatic system (3)

A
  1. function to maintain BV
  2. important in defense and fat absorption
  3. Return excess fluid from the interstitium to the circulatory system through vein-like vessels
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6
Q

Define lymphedema

A

excessive accumulation of lymph due to damaged or obstructed lymph vessels

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7
Q

Define acute lymphangitis

A

acute inflammation of lymph vessels; lymphadenitis if nodes are involved

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8
Q

What is the role of the venous system? What is important to maintain venous return?

A
  1. return blood to the heart through low-resistance blood conduits
  2. maintain blood pressure
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9
Q

How do: sympathetic stimulation; skeletal muscle pump; and respiratory pump help maintain venous return?

A

Sympathetic stimulation: contracts smooth muscle to raise venous pressure

Skeletal muscle pump: muscle contraction constricts veins and raises venous pressure

Respiratory pump: during inspiration, thoracic cavity expands, reducing pressure in the R atrium at the same time that abdominal pressure increases, helping generate a pressure gradient to drive blood return to the heart

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10
Q

How does digitalis work to help with CV function?

A

inhibits Na-K-ATPase, increased NA to exchange with Ca2 - increases intracellular Ca2
Strengthens contractions

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11
Q

How does nitroglycerin work to help with CV function?

A

increases vasodilation and increases blood flow to the heart

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12
Q

How do calcium channel blockers work to help with CV function?

A

disrupt the movement of calcium through calcium channels, relaxes blood vessels

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13
Q

How do beta-adrenergic antagonists work to help with CV function?

A

Reduces myocardial oxygen demands + Increase ventricular filling by relaxing the obstructing muscle. Reduces contractility and heart rate

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14
Q

How do ACE inhibitors work to help with CV function?

A

reduce afterload through vasodilation, by blocking the formation of Angiotensin II

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15
Q

How do diuretics work to help with CV function?

A

reduce fluid retention

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16
Q

Define hyperlipidemia, what is an associated disease that increases r/f CVD?

A
  1. lipids collect in the blood normally transported by proteins
  2. atherosclerosis
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17
Q

Which form of hyperlipidemia may have a genetic basis? Which form is associated with lifestyle choices - obesity, sedentary lifestyle, etc.?

A
  1. primary

2. secondary

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18
Q

Chylomicrons: percentage of triglycerides/protein; where are they synthesized?

A

80-90% triglycerides, very little protein 2%

Synthesized in small intestine as part of fat reabsorption process

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19
Q

Very-low density lipoproteins (VLDL): percentage of triglycerides/cholesterol/protein

A

55-65% triglycerides, 10% cholesterol and 5-10% protein

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20
Q

Low-density lipoproteins (LDL): percentage of triglycerides/cholesterol/protein; what is this the main carrier of?
Is this considered “good” or “bad” cholesterol?

A
  1. 10% triglycerides, 50% cholesterol, 25% protein
  2. Cholesterol
  3. Bad as it carries more cholesterol
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21
Q

High-density lipoproteins (LDL): percentage of triglycerides/cholesterol/protein; What is the major role of this lipoprotein?
Is this considered “good” or “bad” cholesterol?

A
  1. 5% triglycerides, 20% cholesterol, 50% protein
  2. reverse carrier, brings cholesterol from tissues to liver, allows body to recycle cholesterol
  3. Good cholesterol - carries less cholesterol
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22
Q

Where are LDL/HDL synthesized and released?

A

Liver

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23
Q

Ideal levels of LDL, HDL, total cholesterol, triglycerides

What level does LDL get to to be classified as hypercholesterolemia?

A 
LDL < 100mg/dL
HDL > 40-60 mg/dL
Total cholesterol < 200mg/dL
Triglycerides < 10-150mg/dL
Hypocholesteremia = LDL 70-130mg/dL
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24
Q

How do the following agents help lower lipids: Statins, sequestrants, absorption inhibitors, fibrates, niacin/nicotinic acid, omega-3 supplements

A

Statins: prevent liver from manufacturing cholesterol
Sequestrants: prevent body from absorbing cholesterol
absorption inhibitors: limit body’s absorption of cholesterol
Fibrates: decrease synthesis of VLDL by liver, stimulate triglyceride clearance
Niacin/nicotinic acid: blocks synthesis and release of VLDLs from liver, reduces VLDL and LDL level, increase HDL concentrations
omega-3 supplements: decreases rate at which the liver synthesizes triglycerides

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25
Q

Define atherosclerosis, risk factors, patho, consequences on CV function

A

series of arterial disorders that have degenerative changes in arteries, leading to a decrease in blood flow through blood vessels

Key risk factors: hypercholesteremia, hypertension, smoking (nicotine promotes vasoconstriction), obesity, diabetes (sugar attach to proteins that are associated with changes), sedentary lifestyle

Pathogenesis: deposition of lipids leads to decrease in radius, eventual occlusion of blood flow and hypertrophy of vessels, loss of elasticity

Consequences on CV function: CAD, TIAs, CVAs, renal stenosis, arterial occlusive disease

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26
Q

Define aneurysm, where do they typically form? Risk factors, major concern

A
  1. change in dilation of blood vessel wall, can lead to rupture and bleeding
  2. aorta
  3. Underlying risk factors: congenital defects, trauma, infection, atherosclerosis that leads to hypertension
  4. Major concern: massive blood loss particularly if aneurysm present in a large vessel
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27
Q

True vs. false aneurysm

A

True: aneurysm bounded by complete vessel wall and all blood remains in that vascular compartment

False: localized dissection or tear in the wall of the vessel that forms a hematoma outside the vessel, enlarging it

28
Q

What are 4 classifications of aneurysms?

A

Berry: small spherical dilatation of vessel at a bifurcation point - seen in structures likes the Circle of Willis

Fusiform: involves entire circumference of vessel, characterized by gradual, progressive dilation

Saccular: extends over part of circumference of vessel, appears like a sac

Dissecting: false aneurysm resulting from a tear in tunica intima, allows blood to enter vessel wall and creates pocket filled with blood

29
Q

Define vasculitides, what are typical causes (4)

A
  1. group of diseases that cause inflammatory injury and possible necrosis of blood vessel walls
  2. direct injury, infectious agent, immune processes, s/t other diseases
30
Q

Define peripheral vascular disease. Which demographic does it affect most, what are risk factors?

A
  1. atherosclerosis distal from the arch of aorta, gradual vessel occlusion - leads to ischemic pain at rest, damage and ulceration of blood vessels, gangrene can develop due to decreased perfusion
  2. older men in 60s or 70s
  3. Risk factors include cigarette smoking, diabetes
31
Q

Define thromboangiitis obliterans. Clinical manifestations? Which demographic does it affect most, what is the major risk factor?

A
  1. vasculitis that affects medium-size arteries, usually found in plantar or digital vessels
  2. significant pain, impaired circulation, sensitivity to cold, ulceration and gangrene
  3. Men 25-40
  4. smoking
32
Q

Define Raynaud phenomenon, potential causes, affected demographic.
What are some examples of secondary causes? What is a disease where this almost always occurs?

A
  1. functional disorder caused by intensive vasospasm of arteries and arterioles, typically in fingers, less often in toes
  2. Cold exposure, potential hormonal involvement
  3. young women
  4. previous vessel injury or occupational trauma/use of vibrating tools, collagen disorders and occlusive disorders
  5. Scleroderma
33
Q

Define hypotension, causes, patho

A
  1. low BP
  2. Causes: massive vasodilation from allergic response, absolute losses of fluids (sweating, burns, diarrhea, hemorrhage)
  3. Baroreceptor response will initiate and attempt to increase BV by shifting fluid from the interstitium to the blood vessels
34
Q

Define syncope, causes

A
  1. progressive, sudden loss of consciousness

2. Causes: vasovagal response, postural syncope, carotid sinus syncope

35
Q

Define hypertension. Major underlying cause, impact on CV function, medications (3)

A
  1. elevation in BP or MAP
  2. Underlying cause: generally due to increase in TPR, usually result of reduced vessel radius
  3. Impact of CV function: atherosclerosis, increases afterload
  4. Drugs: aimed at reducing TPR - B-adrenergic blockers, calcium channel blockers, ACE inhibitors
36
Q

Define primary/essential HTN, what are major causes

A

Primary: chronic elevation of BP without other evidence of disease (90%)
Causes: genetic factors, sodium intake, DM, smoking, alcohol

37
Q

What are secondary causes of HTN? (3)

A

adrenal tumor that releases catecholamines, increase in aldosterone, stress

38
Q

Define hypertensive crisis, when does this occur (4)? What body systems can this damage if left untreated?

A
  1. sudden elevation in MAP
  2. May occur with extreme ischemia, chest pain, pulmonary edema, intracerebral hemorrhage
  3. renal, cardiac, cerebral
39
Q

Hypertension staging

A 
Staging:
Normal <120 SBP and <80 DBP
Prehypertension 120-139 SBP 80-89 DBP
Stage 1 140-159 SBP or 90-99 DBP
Stage 2 >160 SBP or >100 DBP
40
Q

Define varicose veins

A

dilated, tortuous veins - may lead to edema and stasis ulcers as a result of chronic venous insufficiency

41
Q

Define chronic venous insufficiency

A

chronic venous disease of the lower extremities characterized by venous hypertension, varicose veins, venous ulcers due to venous insufficiency

42
Q

Define venous stasis ulcers

A

fluid shifting leads to edema that gives rise to skin breakdown and ulcer formation, at risk for necrosis and infection

43
Q

Define venous thrombosis

A

thrombus in a vein and the accompanying inflammatory response in the vessel wall - can develop in superficial or deep veins
embolism

44
Q

What are the three issues that make up Virchow’s triad

A

Trauma
Venous stasis
Altered coagulability

45
Q

Define: acute pericarditis; restrictive/constrictive pericarditis; pericardial effusion; and, cardiac tamponade

A
  1. acute pericarditis: acute inflammatory response results in exudate accumulation around the heart
  2. restrictive/constrictive pericarditis: formation of scar tissue between pericardial layers
  3. pericardial effusion: accumulation of fluids in the pericardial sac
  4. cardiac tamponade: accumulation of exudates in pericardial sac, under pressure
46
Q

Distinguish between ischemia, injury and infarction

A

Ischemia: decrease in blood flow, leading to decrease in O2 delivery
Injury: ischemia that can compromise or lead to cell injury
Infarction: death of myocardial cells - irreversible

47
Q

Define coronary artery disease. How can nitrites help?

A
  1. atherosclerosis to coronary arteries

2. Potent vasodilators which can help reperfuse blocked tissues

48
Q

Define angina pectoris, myocardial infarction, heart failure

A

angina pectoris: Mild ischemia
myocardial infarction: ischemic death of myocardial tissue
heart failure: R cor pulmonale or L sided CHF

49
Q

What disease processes are included in acute coronary disease? What are risk factors?

A

MI, STEMI, NSTEMI, unstable angina

Risk factors: diabetes, hypertension, obesity, smoking, high fat-to-carb ratio in diet, family history of heart disease

50
Q

Define cardiomyopathy.

What is this the second leading cause of?

A
  1. disease of the heart muscle fibers that usually affects cardiac performance
  2. sudden death (50%)
51
Q

Define dilated cardiomyopathy. What is this disease process a common indication of, presentation, causes, and inheritance pattern

A
  1. dilation of the heart chambers impairing the function of the heart as a pump
  2. Common indication for heart transplantation
  3. Presentation: variable degrees of cardiac enlargement, evidence of CHF
  4. Causes: damage to the heart from toxic, metabolic, or infectious agents
  5. Inheritance pattern: Disease is heterogenous and commonly shows - autosomal dominant or X-linked recessive pattern
52
Q

Define hypertrophic cardiomyopathy, inheritance pattern, s/s (5)

A
  1. hypertrophy of the muscle mass that can lead to obstruction of blood filling
  2. Genetic mutations that may be inherited or acquired: autosomal dominant inheritance pattern
  3. S/S: dyspnea, chest pain, palpitations, syncope, sudden cardiac death
53
Q

Define restrictive cardiomyopathy, characteristics, causes (primary vs. secondary), s/s (5), tx (3)

A
  1. extremely rigid ventricular walls that restrict blood filling but spare contractile properties of the muscle
  2. Characteristics: reduced preload and end-diastolic volumes with back-up of blood flow in the circulation, eventually resulting in heart failure
  3. Causes: Primary: endocarditis; Secondary: amyloidosis, hemochromatosis, sarcoidosis
  4. S/S: dyspnea, edema, ascites, fatigue and weakness
  5. Treatment: diuretics, calcium channel blockers, usually eventually require heart transplant
54
Q

Cardiomyopathies:
Which can have a genetic etiology?
Which is associated with exposure to toxins or infection?
Which is fairly rare?

A
  1. Dilated, hypertrophic
  2. Dilated, restrictive
  3. Restrictive
55
Q

Define endocarditis. Which population does it commonly affect? What is the usual infectious agent?
Prognosis?

A
  1. infection of the endocardium, heart valves or cardiac prosthesis resulting from bacterial or fungal invasion
  2. IV drug users
  3. Staph aureus
  4. If treated - 70% recover, fatal if untreated
56
Q

Define bacteremia

A

infection causes fibrin and platelets to aggregate on the valve tissue further causing growths on the valves and lining of the heart with leads to ulceration and necrosis, can embolize to the spleen, kidneys, CNS or lungs

57
Q

Define valvular stenosis vs. valvular insufficiency. Which valves are commonly impacted?

A

Stenosis: narrowing of valve opening leads to greater resistance to blood flow through the valve
Insufficiency: failure of the valve to close completely results in backflow of blood to previous compartment
Which valves are commonly impacted: mitral and aortic valves

58
Q

How do valvular diseases occur in adults vs. children?

A 
Rheumatic fever (adults): inflammatory destruction of valve in response to b-hemolytic strep is a common cause
Valvular disorders (children/adolescents): most commonly occur as a result of congenital heart defects
59
Q

Define heart failure, what are common causes

A

heart cannot pump sufficient blood to meet metabolic demands of the body
Causes: CAD, hypertension, dilated CM, valvular heart disease

60
Q

L sided heart failure: definition, causes (3) and consequences

A

definition: ineffective left ventricular contractile function
Causes: HTN, acute MI, valvular defects
consequences: back-up of fluids into pulmonary circulation which can give rise to pulmonary edema

61
Q

Define shock, consequences

A

reduced tissue and organ perfusion and eventually organ dysfunction and failure, acute life-threatening condition where body tissues are inadequately perfused or unable to use O2
Consequences: cell death, lactic acidosis, reperfusion injury

62
Q

What are the different types of shock (4)?

A

Distributive, cardiogenic, hypovolemic, obstructive

63
Q

What are the major consequences of shock on body systems (5)?

A 
acute respiratory distress syndrome
acute renal failure
GI ulceration
DIC
multiple organ dysfunction syndrome
64
Q

R sided heart failure: Definition, causes and major consequences (3)

A

definition: ineffective R ventricular contractile function
cause: cor pulmonale: occurs in response to chronic pulmonary disease
consequence: fluid back-up into systemic and hepatic venous systems resulting in edema or ascites, jugular vein distention

65
Q

Systolic heart failure: Definition, causes and major consequences (2)

A

definition: left ventricle can’t pump enough blood into the systemic circulation during systole and EF falls
Causes: ischemic heart disease, cardiomyopathy
consequence: deceased contractility and EF

66
Q

Diastolic heart failure: Definition, causes and major consequences (1)

A

definition: ability of the L ventricle to relax and fill during diastole is reduced and SV falls
causes: any condition that impedes expansion of the ventricles
consequence: decreased CO

Patho (14 decks)

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