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pathophysiology > diseases of the veins - Sheet1 > Flashcards

diseases of the veins - Sheet1 Flashcards

1
Q

What are varicose veins?

A

Visible veins where blood has pooled, causing distortion, leakage, increased pressure, and inflammation.

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2
Q

What causes varicose veins?

A

Incompetent venous valves, venous obstruction, epithelial muscle pump dysfunction, or a combination of these.

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3
Q

What is the mechanism behind varicose veins?

A

Increased venous pressure leads to thickening of the basement membrane, capillary elongation, and visible skin changes.

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4
Q

What percentage of varicose veins involve superficial veins?

A

88% of cases involve superficial veins alone or both superficial and deep veins.

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5
Q

What are the manifestations of varicose veins?

A

Visible distention of veins, itching, burning/throbbing pain, and leg fatigue.

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6
Q

How are varicose veins diagnosed?

A

History and physical examination, venous duplex scan.

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7
Q

What is chronic venous insufficiency?

A

A severe form of venous hypertension characterized by edema, skin changes (erythema/ulceration), and poor wound healing.

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8
Q

What worsens the symptoms of chronic venous insufficiency?

A

Prolonged standing or walking.

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9
Q

What is Deep Vein Thrombosis (DVT)?

A

A clot in a deep vein that obstructs blood flow, leading to increased hydrostatic pressure.

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10
Q

What are the risk factors for DVT?

A

Sedentary lifestyle, obesity, cancer, smoking, hypertension, long-haul air travel, estrogen contraceptives, pregnancy, hormone replacement, surgery, trauma, and others.

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11
Q

What is Virchow’s triad?

A

Venous stasis, venous epithelial damage, and hypercoagulable state.

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12
Q

What can happen if a DVT thrombus detaches?

A

It can become a thromboembolus and lead to pulmonary embolism.

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13
Q

What are the manifestations of DVT?

A

Unilateral leg edema, pain/cramping (often in the calf), red/purple skin color changes, warmth on the affected leg.

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14
Q

How is DVT diagnosed?

A

History and physical exam, D-dimer test, venous duplex Doppler study.

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15
Q

What is Superior Vena Cava Syndrome (SVC)?

A

Obstruction of venous drainage from the upper body, causing increased venous pressure and dilation of collateral circulation.

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16
Q

What are the causes of SVC syndrome?

A

Venous compression from malignant tumors or a large clot at the tip of a central line.

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17
Q

What are the manifestations of SVC syndrome?

A

Edema and venous distention in the face, neck, trunk, and upper extremities; dyspnea, cerebral edema (headaches, confusion, vision changes), dysphagia.

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18
Q

How is SVC syndrome diagnosed?

A

History and physical exam, CT scan to identify the cause.

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19
Q

What is Coronary Artery Disease (CAD)?

A

A vascular disorder that narrows or occludes coronary arteries, leading to an imbalance between coronary blood supply and myocardial oxygen demand.

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20
Q

What is the most common cause of CAD?

A

Atherosclerosis.

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21
Q

What are the nonmodifiable risk factors for CAD?

A

Advanced age, family history, male gender, or women after menopause.

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22
Q

What are the modifiable risk factors for CAD?

A

Dyslipidemia, hypertension, smoking, diabetes, obesity, sedentary lifestyle, atherogenic diet.

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23
Q

What is dyslipidemia?

A

An imbalance of lipids, including very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL).

24
Q

What is the role of VLDL?

A

VLDL carries triglycerides and lipoproteins, delivering triglycerides to tissues.

25
Q

What is the role of LDL?

A

LDL delivers cholesterol to tissues and contributes to plaque formation in arteries.

26
Q

What is the role of HDL?

A

HDL removes excess cholesterol from arterial walls and transports it to the liver for elimination.

27
Q

What is myocardial ischemia?

A

Insufficient blood flow to the heart muscle, leading to oxygen supply not meeting demand.

28
Q

What causes myocardial ischemia?

A

Atherosclerosis, coronary spasming, hypotension, dysrhythmias, anemia, and hypoxemia.

29
Q

What are the manifestations of myocardial ischemia?

A

Angina (chest pain).

30
Q

What are the classifications of angina?

A

Stable angina (predictable, relieved by rest), unstable angina (unpredictable, may need medication or intervention), Prinzmetal angina (unpredictable, often at night due to SNS activity or other factors).

31
Q

What is Acute Coronary Syndrome (ACS)?

A

Sudden coronary obstruction due to thrombosis over a ruptured atherosclerotic plaque.

32
Q

What happens if ACS is not treated in time?

A

It can result in a myocardial infarction (MI).

33
Q

What is the difference between reversible and irreversible damage in ACS?

A

Ischemic tissue is potentially salvageable, but infarcted tissue has irreversible damage.

34
Q

What is unstable angina?

A

A red flag for a potential infarction, with increased risk of progression to MI.

35
Q

What are the two types of myocardial infarction (MI)?

A

NSTEMI (non-ST elevation MI) and STEMI (ST elevation MI).

36
Q

What is the mechanism behind myocardial infarction (MI)?

A

Prolonged ischemia causes irreversible damage (myocyte necrosis) to the heart muscle.

37
Q

What are the classic manifestations of an MI?

A

Sudden, severe chest pain radiating to the jaw, shoulder, or back, nausea, vomiting, diaphoresis, agitation, confusion, and “I am going to die” feeling.

38
Q

What are the key diagnostic indicators for MI?

A

History and physical (H&P), elevated troponin levels, and 12-lead EKG changes.

39
Q

What are the structural and functional changes after an MI?

A

Myocardial stunning, hibernating myocardium, and myocardial remodeling.

40
Q

What is myocardial stunning?

A

Temporary loss of contractile function that persists for hours to days after perfusion restoration.

41
Q

What is hibernating myocardium?

A

Persistently ischemic tissue that adapts metabolically to prolong survival.

42
Q

What is myocardial remodeling?

A

Inflammatory process leading to myocyte hypertrophy, scarring, and loss of contractile function after MI.

43
Q

How does angiotensin II contribute to MI complications?

A

It increases myocardial work, peripheral vasoconstriction, and fluid retention, exacerbating damage.

44
Q

What are the complications after an MI (DARTH VADER)?

A

Death, arrhythmias, rupture, tamponade, heart failure, valve disease, aneurysm, Dressler’s syndrome (pericarditis), embolism, recurrence.

45
Q

What is acute rheumatic fever?

A

A diffuse inflammatory disease caused by a delayed immune response to group A beta-hemolytic streptococci infection.

46
Q

What can acute rheumatic fever lead to if untreated?

A

Rheumatic heart disease, characterized by inflammation of the endocardium, myocardium, and pericardium.

47
Q

What causes valve damage in rheumatic heart disease?

A

Inflammation of the endocardium causes swelling of the valve leaflets, frequently leading to heart valve damage.

48
Q

What are the common manifestations of rheumatic fever?

A

Fever, lymphadenopathy, and heart murmurs.

49
Q

How is rheumatic fever diagnosed?

A

History and physical exam (H&P), echocardiogram (ECHO), and transesophageal echocardiogram (TEE) for better visualization of heart valves.

50
Q

What is infective endocarditis?

A

Infection caused by microorganisms that circulate in the bloodstream and attach to the endocardial surface, often affecting heart valves.

51
Q

Which heart valve is most commonly affected by infective endocarditis?

A

The mitral valve.

52
Q

What are vegetations in infective endocarditis?

A

Infectious lesions on the heart valves.

53
Q

What are the risk factors for infective endocarditis?

A

IV drug use, prior prosthetic heart valve implantation, rheumatic fever.

54
Q

Which pathogens are commonly responsible for infective endocarditis?

A

Staphylococcus aureus and Streptococcus.

55
Q

What are the classic manifestations of infective endocarditis?

A

High fever, chills, night sweats, cough, weight loss, fatigue, new heart murmurs, signs of heart failure, septic emboli, hemorrhagic lesions on palms/soles, red-purple lesions on fingers/toes, retinal hemorrhages.

56
Q

How is infective endocarditis diagnosed?

A

History and physical exam (H&P), blood cultures, transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) for better visualization of vegetations.

pathophysiology (56 decks)

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