Alterations of cardiac function Flashcards

1
Q

Varicose veins

A
  • Vein in which blood has pooled
  • Distended, tortuous and palpable
  • Cause: Trauma or gradual vein distention
  • Typically the saphenous vein
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2
Q

Chronic venous insufficiency

A
  • Inadequate venous return over a long period due to varicose veins, valvular incompetence
  • Venous stasis ulcers
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3
Q

Venous stasis

A

Venous hypertension, circulatory stasis, and tissue hypoxia leads to an inflammatory reaction that causes fibrosclerotic remodeling of the skin. Ulceration and hyperpigmentation can occur

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4
Q

Deep Venous Thrombosis

A

-Obstruction of venous flow leading to venous pressure.
-Factors (Virchow triad);
Venous stasis, venous endothelial damage, hypercoagulable states
-Post thrombotic syndrome
-Usually asymptomatic: prophylaxis for at risk individuals is crucial

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5
Q

Post thrombotic syndrome

A

-Frequent complication of DVT characterized by chronic, persistent pain, swelling, and ulceration of the affected limb

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6
Q

Thrombus formation

A
  • Blood clot that remains attached to the vessel wall
  • Thromboembolus (detached-has traveled)
  • Arterial thrombi (more serious due to ischemia-Most common from mitral and aorta)
  • Venous thrombi (more common low pressure, low flow system)
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7
Q

Aneursym

A
  • Local dilation or outpouching of a vessel wall or cardiac chamber
  • True aneursym-all 3 layers of the arterial wall (fusiform, circumferential)
  • False aneursyms (saccular) -Usually near a vascular graft and natural artery
  • Most common site is aorta (htn, and arteriosclerosis are risk factors)
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8
Q

Aortic dissection

A

dysphagia, dyspena, tearing of cp

-Infection, collagen disorders like marfans and chest trauma can also cause this

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9
Q

Embolism

A
  • Bolus of matter that circulates in bloodstream, then lodges obstructing blood flow.
  • Dislodged DVT, air bubble, amniotic fluid, aggregate of fat, bacteria, cancer cells, or a foreign substance
  • Many arterial emboli are from the heart (post MI, valve disease, endocarditis, dysrhythmias, HF)
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10
Q

Peripheral artery disease (PAD)

A
  • atherosclerotic disease of arteries that perfuse the limbs (esp lower)
  • Risk factors: esp those with diabetes
  • Intermittent claudication
  • Often asymptomatic
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11
Q

Intermittent claudication

A
  • Obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with ambulation
  • Claudication-gets better with rest
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12
Q

Peripheral artery diseases-Thromboangiitis obliterans (Buerger disease)

A
  • Occurs mainly in young men who smoke
  • Inflammatory disease of peripheral arteries resulting in nonathersclerotic lesions (Digital, tibial, plantar, ulnar, palmar arteries)
  • Obliterates the small and medium sized arteries
  • Produces dry gangrene
  • Causes pain, tenderness, and hair loss in the affected area
  • Symptoms are caused by slow sluggish blood flow
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13
Q

Peripheral artery disease-Raynaud phenomenon or raynaud disease

A
  • Episodic vasospasm (ischemia) in arteries and arterioles of the fingers, less commonly the toes
  • Raynaud’s is secondary to other systemic diseases or conditions
  • Primary vasospastic disorder of unknown origin
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14
Q

Raynaud’s disease

A
  • Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, myxedema, and environmental factors (cold or prolonged to vibrating machinary)
  • Endothelial dysfunction that causes decreased nitric oxide production (this is a potent vasodilator)
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15
Q

Risk factors for hypertension

A
  • Family hx
  • age, gender (male greater than female)
  • Black race, high sodium
  • glucose intolerance
  • heavy alcohol use, obesity, cigarrettes
  • Low K, Mg, Ca
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16
Q

Primary hypertension

A
  • Genetics plus environment
  • Other contributing factors: insulin resistance, dysfunction of SNS, RAAS, adducin, and natriuretic hormone, and inflamamtion
  • This in turn causes vasoconstriction, renal salt and water retention, increased peripheral resistance, and increased blood volume
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17
Q

Treatment of HTN

A

-diuretics, adrenergic blockers, Ca channel blockers, ACE inhibitors, ang 2 receptor blockers.

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18
Q

Arteriosclerosis

A

-Chronic disease of arterial system
-Abnormal thickening, and hardening of vessel walls
-Smooth muscle cells and collagen fibers migrate to the tunica
intima
-This can be an inevitable result of aging w/ cross linking of collagen and deposits of Ca

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19
Q

Atherosclerosis

A
  • Form arteriosclerosis
  • Thickening and hardening by accumulation of lipid-laden macrophages in the arterial wall
  • Plaque development
  • This is leading cause of CAD and CVD
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20
Q

Risk factors of atherosclerosis

A
  • inflammatory disease that begins with endothelial and progresses through several stages of fibrotic plaque
  • elevated CRP, increased serum fibrinogen, oxidative stress, infection, and periodontal disease
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21
Q

Progression of atherosclerosis

A
  • Inflammation of endothelium
  • cellular proliferation
  • macrophage migration
  • LDL oxidation (foam cell formation)
  • Fatty streak
  • Fibrous plaque
  • Complicated plaque
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22
Q

Endothelial injury

A
  • Endothelium stops making normal antithrombotic and vasodilatory subtances, like nitric oxide and prostaglandins
  • Leukocytes and macrophages adhere to the endothelium and release cytokines
  • Oxidation and phagocytosis of LDL
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23
Q

Complications of atherosclerosis

A
  • Calcification of fibrous plaque
  • Rupture or ulceration of plaque
  • Hemorrhage of plaque
  • Embolization of fragments
  • Weakening of vessel wall
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24
Q

Coronary artery disease

A
  • Any vascular disorder that narrows or occludes the coronary arteries
  • Atherosclerosis is most common cause
25
Q

Risk factors for CAD

A

-Dyslipidemia, hypertension, smoking, DM, Obesity, defect in the production of precursor endothelial cells

26
Q

Non-traditional risk factors for CAD

A
  • Markers of inflammation of thrombosis
  • C reactive protein, fibrinogen, protein C, and plasminogen and activator inhibitor
  • Infections
  • Hyperhomocysteinemia
27
Q

Lipids

A
  • Strong link between lipoproteins and CAD
  • Fat metabolism
  • Dietary fat package in chylomicrons for absorption in small instenstine
  • Good cholesterol in transported lipids to the liver for disposal
28
Q

Triglycerides

A

-In chylomicrons

29
Q

VLDL

A

-Mainly triglycerides + carrier protein

30
Q

LDL

A

-Mainly cholesterol + carrier protein

31
Q

HDL

A

Mainly phospholipids + carrier protein

32
Q

Coronary arteries

A

-Two major left main and RCA

33
Q

Left main coronary artery

A
  • LAD supplies to LV, RV and septum

- Circumflex supplies LA and lateral wall

34
Q

RCA

A

-Supplies posterior RV, and some to the LV

35
Q

Prinzmetal angina

A

-abnormal vasospasm of coronary vessels results in unpredictable chest pain

36
Q

Silent ischema

A

-MI that doesn’t cause detectable symptoms

37
Q

Myocardial ischemia

A
  • When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs-MI
  • Two major types of MI
38
Q

Two types of MI: Subendocardial infarction and transmural infarction

A

-in addition to myocyte necrosis other changes in the heart with MI include hibernating, stunning and remodeling

39
Q

Acute coronary symptom assessment

A

-measuring serum enzymes such as creatinine kinase and troponins and ECG changes (ST elevation)

40
Q

Acute coronary syndromes

A
  • Transient ischemia
  • Unstable angina
  • Sustained ischemia
  • MI
  • Myocardial inflammation and necrosis
41
Q

Unstable angina

A
  • Partially occlusive thrombus. EKG shows no ST elevation, no elevation in troponin
  • Presents with chest pain, can occur at rest, usually a new onset and severe pain (NSTEMI)
42
Q

MI

A
  • cellular injury, cellular death,
  • structural and functional changes (2-hibernating myocardium, 3-myocardial remodeling, 1-myocardial stunning)
  • Repair
43
Q

Clinical eval of MI

A
  • ECG changes
  • Cardiac enzymes (Troponins-see in 2-4 hours and can be elevated for 7-10 days)
  • CK-MB (see in 2-4 hours, peaks in 24 hours)
  • LDH (hyperglycemia 72 hours post MI)
  • Creatinine kinase
  • Complications: dysrhythmias, congestive HF, and death
44
Q

Disorders of heart wall: Pericardium

A
  • acute pericarditis (drug therapy, infections, tumors)
  • Pericardial effusions (tamponade)
  • constrictive pericarditis
45
Q

Disorders of myocardium: Cardiomyopathies

A
  • Dilated cardiomyopathy (congestive cardiomyopathy)
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
46
Q

Hypertrophic cardiomyopathy

A
  • asymmetric septal hypertrophy cardiomyopathy

- Hypertensive (valvular hypertrophic) cardiomyopathy

47
Q

Dilated cardiomyopathy

A
  • increase in radius with no change in wall thickness
  • greater the wall tension generated greater myocardial O2 demand. If blood supply doesn’t meet o2 demand pump will eventually fail
  • More prone to fail
48
Q

Hypertrophy

A

-increase in absolute wall thickness

49
Q

Restrictive cardiomyopathy

A
  • infiltration of myocardium and reduced compliance
  • Ventricular filling is reduced
  • Systolic functions and myocardium wall thickness are normal or near normal
50
Q

Disorders of the endocardium

A
  • Valvular dysfunction
  • Valvular regurg
  • Mitral valve prolapse syndrome
51
Q

Valvular Stenosis

A

Mitral stenosis

Aortic stenosis

52
Q

Valvular regurg

A

Aortic regurg
Mitral regurg
Tricuspid regurg

53
Q

Rheumatic fever

A
  • Diffuse inflammatory disease caused by a delayed response to infection by group A beta-hemolytic streptococci
  • Febrile illness (Inflammation of joints, skin, nervous system, and heart)
  • If left untreated can result in rheumatic heart disease
54
Q

Infective endocarditis

A
  • Inflammation of endocardium
  • Agents (bacteria, virus, fungi, rickettsiae, and parasites)
  • Sources (prothestic valves, indwelling catheters, open heart surgery)
  • Pathogensis (Prepared endocardium, blood-borne microorganism adherence, proliferation of microorganisms)
55
Q

Congestive HF

A
  • Systolic HF

- Diastolic HF

56
Q

Systolic HF

A

Inability of the heart to generate adequate CO to perfuse tissues

57
Q

Diastolic HF

A

Pulmonary congestion despite SV and CO

58
Q

Right HF

A
  • Commonly caused by a diffuse hypoxic pulmonary disease
  • Can result from increase in LV filling pressure that’s reflected back in pulmonary circulation
  • Can occur from LHF, diffuse hypoxic disease (pulmonary, COPD, cystic fibrosis, ARDS)