Block I - CVS, Wound Healing, Vasculitis, etc. Flashcards

1
Q

What is the most important mediator in the healing process?

A

FGF. Earliest growth factor in healing; stimulates macrophages and MMPs

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2
Q

What does TGF-beta do?

A

Causes fibrosis and some angiogenesis

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3
Q

What synthesizes the extracellular matrix?

A

Fibronectin; responsible for cross-linking

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4
Q

What secretes PDGF?

A

Activated platelets and macrophages.

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5
Q

What does PDGF do?

A

Induces vascular remodeling, smooth muscle cell migration, sand stimulates fibroblast growth for collagen synthesis

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6
Q

What is responsible for attachment of epithelium to extracellular matrix?

A

Integrin

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7
Q

What is the maximum wound strength possibility?

A

85%; at around 4 months

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8
Q

What is responsible for would contraction in burns?

A

Myofibroblasts

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9
Q

What is the first step in healing?

A

Clot formation

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10
Q

What would you expect to see 0-4 hours in healing?

A

Waviness of fibers

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11
Q

What would you expect to see 12-23 hours in healing?

A

Contraction band necrosis

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12
Q

What would you expect to see 2-3 days in healing?

A

Neutrophils peaking; causing increased vessel permeability and migration into tissue

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13
Q

What would you expect to see 3-7 days into healing?

A

Macrophages predominating; clear debris via mediators and MMP to eat collagen

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14
Q

What would you expect to see 7-21 days into healing?

A

Granulation tissue & Type III Collagen; angiogenesis, and wound contraction via myofibroblasts

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15
Q

What would you expect to see 6-7 weeks into healing?

A

Scar formation; when repair cannot be done by cell generation alone.

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16
Q

What does collagenase require in order to break down Type III collagen?

A

Zinc

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17
Q

What is Keloid?

A

Abnormal scar formation due to proliferation of Type I and Type III collagen; grows outside of border of normal wound.

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18
Q

How does diabetes cause problems in wound healing?

A

Enzymatic Glycosylation

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19
Q

What is a Desmoid Tumor?

A

Abnormal growth from connective tissues that provide strength and flexibility; seen in bones, ligaments, muscles. Break sutures, fibroid tissue into infiltrate.

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20
Q

What phase must a cell be in for regeneration?

A

G1

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21
Q

How does an atheroma develop?

A

Injury to endothelial cell

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22
Q

Differentiate between an atheroma and fatty streak:

A

Atheroma has a necrotic core and cholesterol clefts while fatty streak does not.

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23
Q

What presents with a “beading appearance?”

A

Fibromuscular Dysplasia

24
Q

In renal artery stenosis, in which kidney is the renin level increased?

A

Increased renin in the affected kidney; causes unilateral atrophy

25
Q

What is the main cause of an abdominal aortic aneurysm?

A

Atherosclerosis

26
Q

What are two complications of an abdominal aortic aneurysm?

A
  1. Formation of mural thrombus leading to impotence and gangrene.
  2. Rupture if greater than 5cm in diameter.
27
Q

What is the most common cause of sudden adult death, and how does it occur?

A

Ventricular aneurysm caused by ischemia.

28
Q

A vasculitis involving small vessels, causing a necrotizing granuloma; presence of C-ANCA is what?

A

Wegeners; commonly in middle-aged male, will have nosebleeds, sinusitis, hemoptysis with bilateral lung infiltrates.

29
Q

The most common form of arteritis in adults greater than 50; commonly found in the carotid artery is what, and what is a complication?

A

Giant (Temporal) Cell Arteritis; can lead to blindness. Will have ESR levels very high usually above 100.

30
Q

What vasculitis is a granulomatous vasculitis, commonly seen in young, Asian females?

A

Takayasu; presents with weak or absent pulse in upper extremities.

31
Q

What is the main cause of aortic dissection and what is it due to?

A

Cause: HTN
Due: Endothelial tear.

32
Q

What has a sharp, severe chest pain that radiates to the back, and can cause pericardial tamponade leading to death?

A

Aortic Dissection

33
Q

What are the components of Tetralogy of Fallot?

A
  1. VSD
  2. Overriding Aorta
  3. Pulmonary HTN
  4. RVH
34
Q

What is the main cause of Eisenmerger?

A

Pulmonary HTN

35
Q

What is commonly seen in Marfan’s, and describe the murmur.

A

Mitral Valve Prolapse; mid-systolic click followed by a late systolic murmur best heard at the base of the apex

36
Q

What happens to the Mitral Valve Prolapse murmur on standing or valsalva?

A

Increases; earlier systolic click, and longer murmur (note this is opposite in aortic stenosis)

37
Q

Describe the Mitral Regurgitation murmur:

A

Seen in Rheumatic Fever and chordae tendinae rupture; is a holosystolic, blowing, high-pitched murmur that radiates to the left axilla.

38
Q

Describe the Mitral Stenosis murmur:

A

Apical, mid-diastolic rumble; seen in RHD and Pulmonary HTN

39
Q

Describe the Aortic Regurgitation murmur:

A

Decrescendo, diastolic murmur present with head-bobbing, Waterhammer pulse, and pulsation of retinal arteries; also seen in Marfan’s and syphilis.

40
Q

Describe the Aortic Stenosis murmur:

A

Harsh, systolic, crescendo-decrescendo with radiation to the carotids.

41
Q

What amyloid is seen in age-related amyloidosis of the heart?

A

Transthyretin

42
Q

What amyloid is seen in Multiple Myeloma?

A

Light-chain

43
Q

Describe a Ventricular Rhabdomoma:

A

Tuberosclerosis, hypopigmentation of the skin, ash-leaf spot, and kidney tumor; seen in children commonly at left ventricle.

44
Q

What causes endocarditis of healthy adults and IV drug users?

A

Staph Aureus

45
Q

What causes endocarditis of previously damaged heart valves?

A

Strep Viridans; alpha-hemolytic

46
Q

What are Roth spots and Osler’s nodes due to?

A

Immune Complex Deposition

47
Q

What are Janeway lesions due to?

A

Thromboembolism

48
Q

What are the tumors of VHL?

A

Hemangioblastoma, angioma of the retina, and bilateral renal carcinoma.

49
Q

In a capillary hemangioma where the parents are worried about appearance of the child, what should you suggest?

A

Do nothing; will go away on it’s own while surgical intervention can leave a scar

50
Q

What are two late complications of MI?

A

Free wall rupture (3-5 days) due to LAD occlusion, presenting with cardiac tamponade and Dressler Syndrome (5 weeks) which is pericarditis due to immune response with chest pain and fever.

51
Q

Pulmonary edema is caused by what?

A

Increased hydrostatic pressure

52
Q

What causes HOCM?

A

Obstruction of aortic outflow due to septum being too thick, and the anterior and posterior leaflets coming together to completely block outflow

53
Q

What does HOCM sound like on auscultation; and what effect does valsalva/standing have?

A

Aortic Stenosis; will increase this murmur on standing/valsalva (aortic stenosis would decrease)

54
Q

What genetic effect causes HOCM, and what does HOCM lead to?

A

Beta-myosin mutation; creates cardiac tissue with several branches, thicker, tighter muscle. Leads to death during exercise; Autosomal Dominant.

55
Q

Describe concentric hypertrophy:

A

Pressure overload (narrowing the lumen); seen in aortic stenosis or HTN

56
Q

Describe essentric hypertrophy:

A

Volume overload; seen in aortic regurgitation

57
Q

What is nutmeg liver?

A

Due to passive venous congestion; typically seen in Congestive Heard Disease, presents with fatty change around portal triad. Never caused by alcohol or hypoxia.