Diseases of Vascular Origin Flashcards

1
Q

Where is the usual location where PE’s arise from?

A

Deep leg vv.

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2
Q

What is the main etiology for DVT formations?

A

Immobilization (like in hip Fx)

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3
Q

This is a large emboli inside the bifurcation of the pulmonary a. and its major branches.

A

Saddle embolus

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4
Q

What is the acute problem with a large PE?

A

Sudden death

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5
Q

What is the more chronic problem with a large PE?

A

R sided heart failure (cor pulmonale)

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6
Q

What is the problem with small PE’s?

A

hemorrhage or infarction

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7
Q

Where do 3/4 of infarctions occur in the lungs?

A

Lower lobes

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8
Q

What is the gross morphology of an infarction of the lower lobes of the lung?

A

Wedge infarction with the apex pointing towards the hilus

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9
Q

True or False: there will not be lines of Zahn in the thrombus of the PE.

A

False. There will be.

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10
Q

In infarction, what will be in the pleural surface?

A

Fibrious exudate

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11
Q

Which test can u use to Dx a pulmonary embolus?

A

Spiral CT

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12
Q

At what % of systemic pressure must the pulmonary pressure meet to be termed “primary pulmonary HTN (PH)”?

A

1/4 the systemic levels.

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13
Q

If a pt has familial PH, what the protein that is mutated?

A

BMPR2

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14
Q

What is the fxn of the BMPR2 receptor in the cell?

A

Surface protein important for embryogenesis, apoptosis, and cell proliferation/differentiation

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15
Q

What are some secondary forms of PH?

A

endothelial dysfxn by mechnaical or biochemical injury

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16
Q

What is PH usually associated with?

A

Structural cardiopulmonary conditions that increas pulmonary blood flow or pressure (or both)

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17
Q

Which forms of PH have medial hypertrophy, atheromas of the pulmonary a. and RVH?

A

All forms of PH

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18
Q

What is the tuft of capillary fomrations that look like a web that spans the lumens of dilated thin-walled small arteries called?

A

Plexiform lesion

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19
Q

This is the condition where there’s an autoimmune hemorrhage syndrome of the lungs and kidneys.

A

Goodpastures syndrome

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20
Q

There are autoimmune Ab’s against which structural component of the kidney and lung?

A

Collagen IV

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21
Q

What is the triad of problems in goodpastures?

A
  1. destruction of the basement membrane (anti-GBM)
  2. proliferative and rapid glomerulonephritis
  3. necrotizing hemorrhagic intertitial pneumonitis
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22
Q

What type of hypersensitivity reaction is goodpastures?

A

type II

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23
Q

What is gross morpholgy of the lungs in goodpastures?

A

Heavy with red-brown consolidation

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24
Q

What types of cells are present in the lungs with goodpastures?

A

hemosiderin-laden macrophages

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25
Q

What are the beginning respiratory Sx of goodpastures?

A

hemoptysis

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26
Q

What is teh most common cause of death in goodpastures?

A

uremia

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27
Q

What improves prognosis in goodpastures?

A

Plasmapheresis

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28
Q

This is a rare disorder of intermittent, diffuse alveolar hemorrhage, typically in young children.

A

Pulmonary hemosiderosis

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29
Q

What are the Sx to pulmonary hemosiderosis?

A

productive couhg, hemoptysis, anemia, and weight loss.

30
Q

True or False: there is diffuse pulmonary infiltration in pulmonary hemosiderosis similiar to goodpastures.

A

True.

31
Q

What drugs can u give for the Tx of pulmonary hemosiderosis?

A

Prednisone or azathioprine

32
Q

This is an autoimmune disease with granulomatous inflammation of the upper respiratory tract and necrotizing vasculitis affecting the small vessels.

A

Wegener granulomatosis

33
Q

What type of ANCA do u see with wegener granulomatosis?

A

c-ANCA (PR3)

34
Q

What are the 3 components of the triad to wegener’s granulomatosis?

A
  1. acute necrotizing granulomas of the upper resp tract
  2. necrotizing or granulomatous vasculitis of small-med sized vessels
  3. crescentric glomerulonephritis
35
Q

What is the major Sx of Wegeners?

A

Hemoptysis

36
Q

What do u see in the lungs and kidneys in wegeners?

A

lungs- capillaritis and scattered, poorly formed granulomas

kidneys- necrotizing glomerulonephritis

37
Q

What % of pts die within a year with Wegeners?

A

80%

38
Q

What is the Tx for Wegeners?

A

steroids, cyclophosphamide, and TNF-antagonists

39
Q

At what mean pulmonary arterial pressure (MPAP) is indicative of pulmonary HTN?

A

> 25mmHg

40
Q

What must be NORMAL alongside the ↑ MPAP to be a pulmonary HTN Dx?

A

Pulmonary capillary wedge pressure

41
Q

True or False: there is lower extremity edema in pulmonary HTN.

A

True

42
Q

What is the non-invasive way of diagnosing a DVT?

A

Duplex ultrasonography

43
Q

What are the Sx to a PE?

A

tachypnea, tachycardia, dyspnea, pleuritic pain, hemoptysis, pleural friction rub, wheezing

44
Q

What are the 2 big red flags that point to acute PE?

A

syncope or acute hypoTN

45
Q

Gib me all the tests for a PE Dx.

A
Clinical exam
EKG (S1, Q3, T3)
CXR
Blood gases
BNP
Troponins + ↑ d-dimer
46
Q

What is the gold standard test for a PE?

A

Pulmonary angiography

47
Q

What are the 2 drugs u can give for a PE?

A

Heparin

Warfarin

48
Q

If a pt has a massive PE, what is the class of drugs u should give within 24 hrs?

A

Thrombolytics (streptokinase, urokinase)

49
Q

This type of heparin is used in outpatient therapy or prophylaxis, for proximal DVT or PE, normal v/s, low risk of bleeding, lower incidence of HIT, and rapid onset.

A

LMWH

50
Q

What route must u give unfractionated heparin?

A

IV drip

51
Q

Nasal septal perforation and ulceration of the vomer is a sign of what disease?

A

Wegener’s

52
Q

This is a disease where there is systemic and pulmonary vasculitis, there are extravascular granulomas, and ↑ IgE + eosinophilia.

A

Churg_Strauss syndrome (CSS)

53
Q

CSS occur exclusively in patients with a Hx of what?

A

Asthma or allergies

54
Q

What are the Sx to CSS?

A

resp distress, nasal polyps, allergic rhinitis, nasal mucosa crusting and septal perforations.

55
Q

What do u see on CXR in CSS?

A

patchy + occasiaonally diffuse alveolar infiltrates in perihilar area

56
Q

This is a relapsing chronic multisystemic inflammatory disorder where there is apthous ulcers/stomatitis along with others Sx.

A

Behcet disease

57
Q

How many of these Sx (alongside the apthous ulcers/stomatitis) must the pt have to be diagnosed with Behcet disease?

Apthous ulcerations
Uveitis
Cutaneous nodules/pustules
Synovitis
Meningoencephalitis
A

2

58
Q

What can u see in the upper and lower extremities in Behcet disease?

A

DVT’s

59
Q

True or False: in behcet disease, there is mile hemoptysis.

A

FALSE. ITS SUPER GNARLY.

60
Q

What shows up on CXR in behcet disease?

A

Lung infiltrates, pleural effusions, prominent pulmonary artereis and pulmonary artery aneurysms

61
Q

This is the condition where there is chronic inflammatory disease that affects the primary aorta and major branches. Ella Chan Baek.

A

Takayasu artertitis

62
Q

This is the condition where there is recurrent episodes of purpura, arthralgias, weakness + multiorgan involvement.

A

Mixed cryoglobulinemia

63
Q

What is the mose serious complication to mixed cyroglobulinemia?

A

Glomerulonephritis

64
Q

What Ab do u screen for in goodpastures?

A

Anti-GMB Ab

65
Q

What Ab lines the basement membrane with complement in goodpastures?

A

IgG

66
Q

Which patients with goodpatures get glomerulonephritis and lung hemorrhage?

A

Young men in 20’s

67
Q

Which patients with goodpastures get glomerulonephritis alone?

A

Elderly women

68
Q

What are the classic Sx to goodpastures?

A

Recurrent hemoptysis, pulmonary insufficiency, hematuria, renal failure, anemia

69
Q

This is the condition characterized by vasoconstriction, pulmonary vascular remodeling + thrombosis in situ.

A

Pulmonary Arterial Hypertension (PAH)

70
Q

What are the clinical manifestations of PAH?

A

leads to progressive increase in pulmonary vascular resistnace, RHF, and death.

71
Q

True or False: PAH has non-specific Sx of progressive dyspnea, lower extremity edema, and fatigue.

A

True

72
Q

What is the most common causes of PAH?

A

Idiopathic