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
What is the role of LDL?
LDL delivers cholesterol to tissues and contributes to plaque formation in arteries.
26
What is the role of HDL?
HDL removes excess cholesterol from arterial walls and transports it to the liver for elimination.
27
What is myocardial ischemia?
Insufficient blood flow to the heart muscle, leading to oxygen supply not meeting demand.
28
What causes myocardial ischemia?
Atherosclerosis, coronary spasming, hypotension, dysrhythmias, anemia, and hypoxemia.
29
What are the manifestations of myocardial ischemia?
Angina (chest pain).
30
What are the classifications of angina?
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
What is Acute Coronary Syndrome (ACS)?
Sudden coronary obstruction due to thrombosis over a ruptured atherosclerotic plaque.
32
What happens if ACS is not treated in time?
It can result in a myocardial infarction (MI).
33
What is the difference between reversible and irreversible damage in ACS?
Ischemic tissue is potentially salvageable, but infarcted tissue has irreversible damage.
34
What is unstable angina?
A red flag for a potential infarction, with increased risk of progression to MI.
35
What are the two types of myocardial infarction (MI)?
NSTEMI (non-ST elevation MI) and STEMI (ST elevation MI).
36
What is the mechanism behind myocardial infarction (MI)?
Prolonged ischemia causes irreversible damage (myocyte necrosis) to the heart muscle.
37
What are the classic manifestations of an MI?
Sudden, severe chest pain radiating to the jaw, shoulder, or back, nausea, vomiting, diaphoresis, agitation, confusion, and "I am going to die" feeling.
38
What are the key diagnostic indicators for MI?
History and physical (H&P), elevated troponin levels, and 12-lead EKG changes.
39
What are the structural and functional changes after an MI?
Myocardial stunning, hibernating myocardium, and myocardial remodeling.
40
What is myocardial stunning?
Temporary loss of contractile function that persists for hours to days after perfusion restoration.
41
What is hibernating myocardium?
Persistently ischemic tissue that adapts metabolically to prolong survival.
42
What is myocardial remodeling?
Inflammatory process leading to myocyte hypertrophy, scarring, and loss of contractile function after MI.
43
How does angiotensin II contribute to MI complications?
It increases myocardial work, peripheral vasoconstriction, and fluid retention, exacerbating damage.
44
What are the complications after an MI (DARTH VADER)?
Death, arrhythmias, rupture, tamponade, heart failure, valve disease, aneurysm, Dressler’s syndrome (pericarditis), embolism, recurrence.
45
What is acute rheumatic fever?
A diffuse inflammatory disease caused by a delayed immune response to group A beta-hemolytic streptococci infection.
46
What can acute rheumatic fever lead to if untreated?
Rheumatic heart disease, characterized by inflammation of the endocardium, myocardium, and pericardium.
47
What causes valve damage in rheumatic heart disease?
Inflammation of the endocardium causes swelling of the valve leaflets, frequently leading to heart valve damage.
48
What are the common manifestations of rheumatic fever?
Fever, lymphadenopathy, and heart murmurs.
49
How is rheumatic fever diagnosed?
History and physical exam (H&P), echocardiogram (ECHO), and transesophageal echocardiogram (TEE) for better visualization of heart valves.
50
What is infective endocarditis?
Infection caused by microorganisms that circulate in the bloodstream and attach to the endocardial surface, often affecting heart valves.
51
Which heart valve is most commonly affected by infective endocarditis?
The mitral valve.
52
What are vegetations in infective endocarditis?
Infectious lesions on the heart valves.
53
What are the risk factors for infective endocarditis?
IV drug use, prior prosthetic heart valve implantation, rheumatic fever.
54
Which pathogens are commonly responsible for infective endocarditis?
Staphylococcus aureus and Streptococcus.
55
What are the classic manifestations of infective endocarditis?
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
How is infective endocarditis diagnosed?
History and physical exam (H&P), blood cultures, transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) for better visualization of vegetations.