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Block 9 Week 3 > Vascular Respiratory Path - Parks and Baker > Flashcards

Vascular Respiratory Path - Parks and Baker Flashcards

1
Q

blood clots in the pulmonary system are almost always (emoblic/thrombotic)

A

embolic

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2
Q

T/F: a DVT means that you have a PE

A

false

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3
Q

T/F: a PE means that you have a DVT

A

true

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4
Q

What percent of pts have long term complications from a dvt?

A

1/2; pain, discoloration, swelling

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5
Q

what percent of pts with a DVT will recur in 10 years?

A

1/3

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6
Q

what percent of pts present with sudden death from PE?

A

25%

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7
Q

how does a DVT lead to a stroke?

A

communication between left and right heart; aka PFO plus DVT

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8
Q

why do people die within one month of PE diagnosis?

A

recurrence of another PE

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9
Q

What is Virchow’s Triad?

A
  1. endothelial injry
  2. blood stasis/turbulent flow
  3. hypercoagulability
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10
Q

what are the three things that lead to endothelial injury?

A
  1. trauma
  2. vasculitis
  3. hypertension
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11
Q

what are the two things that lead to blood stasis or turbulent flow?

A
  1. immobility

2. venous compression

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12
Q

what are the four things that lead to a hypercoagulable state?

A
  1. genetics (factor V)
  2. cancer
  3. immobilization
  4. pregnancy, HRT, OCP
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13
Q

what two types of compromise result from PE?

A

respiratory and hemodynamic

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14
Q

the severity of the symptoms of a PE are directly related the (blank) of the PE

A

size

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15
Q

A complete loss of blood flow from a large embolus will have what type of symptoms?

A

acute hypoxemia
right sided heart failure
INSTANT DEATH

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16
Q

what types of lesions occur in 10% of cases in PE that lead to pulmonary infarct?

A

hemorrhagic lesions

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17
Q

What arteries normally compensate for a PE, that if overwhelmed, lead to pulmonary infarct?

A

bronchial arteries

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18
Q

which lobes do you normally get a pulmonary infarct?

A

lower lobes

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19
Q

what is the characteristic EKG finding with PE?

A

S1Q3T3;
prominent S in lead I
Q wave and inverted T in lead III

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20
Q

what does S1Q3T3 tell you about the right heart?

A

right ventricular dilation

NOT RIGHT HEART STRAIN

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21
Q

what are the other EKG findings that suggest right heart strain?

A
  1. right axis deviation

2. RVH with precordial ST depression and T wave inversion

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22
Q

what is the most common EKG finding in PE?

A

sinus tachycardia; nonspecific ST segment changes and T-wave changes

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23
Q

what is the general presentation of PE?

A 
tachycardia
chest pain
dyspnea
hypoxemia
cough
fever
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24
Q

what might you see on CXR for a PE?

A

wedge shaped infiltrate indicating infarction

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25
Q

what will you see on CT for PE?

A

using contrast, a perfusion blank spot where there is no contrast

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26
Q

what is the normal pulmonary arterial pressure?

A

15-30/4-12

mean is 8-18

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27
Q

What is the Dx criteria for pHTN?

A

sustained elevation of mean pulmonary arterial pressure to more than 25 mm Hg at rest or to more than 30 mm Hg with exercise

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28
Q

t/f: All the restrictive and obstructive if left untreated can lead to PAH

A

true

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29
Q

what part of the pulmonary arteries will hypertrophy in PAH?

A

medial hypertrophy of muscular and elastic arteries

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30
Q

as a result of systemic HTN, what will form within the pulmonary arteries?

A

atheromas

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31
Q

in late stage pHTN, what type of lesions will you see?

A

plexiform lesions

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32
Q

what are the five most common causes of secondary pHTN?

A
  1. chronic lung disease
  2. heart disease
  3. thromboemboli
  4. connective tissue disease
  5. obstructive sleep apnea
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33
Q

what is the MOA of chronic lung disease cuasing pHTN?

A

parenchymal destruction, fewer capillaries, increased resistance

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34
Q

what is the MOA of heart disease cuasing pHTN?

A

Left Heart Failure, Mitral Stenosis…etc

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35
Q

what is the MOA of thrombemboli cuasing pHTN?

A

reduced cross-sectional area (narrowed lumen), increased resistance

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36
Q

what is the MOA of connective tissue disease cuasing pHTN?

A

esp Systemic Sclerosis, lead to vascular inflammation, intimal fibrosis, medial hypertrophy

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37
Q

what is the MOA of obstructive sleep apnea cuasing pHTN?

A

increased pulmonary pressure

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38
Q

what gene is responsible for primary PAH?

A

BMPR2; leads to proliferation of vascular smooth muscle; may be associated with environmental factors

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39
Q

describe the typical patient with primary PAH

A

female; 20-40
dyspnea, fatigue, anginal chest pain. with progression will lead to Respiratory distress, cyanosis, RVH and death from cor pulmonale

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40
Q

what are the conventional therapies for PAH?

A

O2, calcium channel blockers, digoxin, diuretics

41
Q

what are the newer targeted therapies for PAH?

A

Prostacyclin analogues, endothelial receptor antagonist, inhaled NO, phosphodiesterase-5 inhibitors

42
Q

T/f: lung transplant is an option for PAH

A

true

43
Q

is the Ig fluorescence in Goodpasture’s linear or granular?

A

LINEAR Ig

44
Q

where does the Ig deposit in goodpastures?

A

the basement membrane

45
Q

in what two organs will you see Ig deposition in goodpastures?

A

alveoli and glomerulus

46
Q

describe the histological changes in goodpastures?

A

focal aveolar wall necrosis

intra alveolar hemorrhages

47
Q

what type of special mac’s will you see in the alveoli in good pastures?

A

hemosiderin laded macrophages

48
Q

describe the MOA of the damage in goodpastures

A
  1. Antibody attaches to basement membrane
  2. Complement is activated
  3. Neutrophils are chemoattracted by C5a and release ROS and proteases and damage the tissue in type II reaction
49
Q

what is the first symptom people will have in goodpastures?

A

hemoptysis

50
Q

What will you see on CXR in goodpastures?

A

focal pulmonary consolidations

51
Q

Describe the renal progression in goodpastures

A

RPGN to uremia to death

52
Q

What is the Tx for removing Abs from the circulation in goodpastures?

A

plasmaphoresis

53
Q

What are the three Tx available for goodpastures?

A
  1. dialysis for AKI
  2. plasmaphoresis
  3. immunosuppresion
54
Q

What is the histologic difference between goodpastures and idiopathic pulmonary hemosiderosis?

A

NO ANTI-BM ANTIBODIES

55
Q

T/F: IPH repsonds well to steroids

A

true

56
Q

describe the presentation of IPH

A

Insidious onset of productive cough, hemoptysis, anemia and weight loss

57
Q

describe the histology of IPH

A

intermittent, diffuse alveolar hemorrhage

58
Q

which ANCA is involvedin 90% of the active cases of Wegener’s?

A

PR3-ANCA aka c-ANCA

59
Q

what is the new name for Wegener’s?

A

granulomatosis with polyangiitis

60
Q

t/f: ANCAs may be used for Dx, are part of the pathogenesis, and can be used to measure dz activity

A

true

61
Q

when would you get a false positive PR3/c-ANCA?

A

in certain infections and neoplasms

62
Q

the end result of circulating ANCAs is….

A

vasculitis

63
Q

describe the process of ANCAs causing vasculitis

A
  1. ANCAs activate neutrophils

2. neutrophils release ROS and proteases which damage the endothelium

64
Q

Wegener’s is a (blank) vasculitis

A

necrotizing

65
Q

The renal involvement in Wegener’s is a focal, (blank) glomerulonephritis

A

necrotizing

66
Q

How do you Dx Wegener’s?

A

transbronchial Biopsy

67
Q

Wegener’s also affects the sinuses and presents with what two symptoms?

A

chronic sinusitis

mucosal ulcers

68
Q

What is the first symptom that most patients get with Wegener’s?

A

hemoptysis

69
Q

which pulmonary edema is pressure related and has intact membranes?

A

cardiogenic

70
Q

which pulmonary edema has normal hydrostatic pressure and damage to the endothelium?

A

noncardiogenic

71
Q

what drives the removal of alveolar edema in cardiogenic shock?

A

transport of Na, Cl, and H2O out of the alveolus

72
Q

what type of pulmonary edema has a protein-rich infiltrate?

A

noncardiogenic

73
Q

in cardiogenic pulmonary edema, the alveolar capillaries will be engorged and there will a pink precipitate where?

A

intra-alveolar

74
Q

What are heart failure cells?

A

Hemosiderin-laden macrophages from alveolar microhemorrhages

75
Q

what are the clinical signs of pulmonary edema?

A

SOB, DOE, orthopnea, PND, crackles on auscultation

76
Q

Where does the fluid normally begin to pool in the lungs?

A

lower lobes

77
Q

what happens as a result of chronic pulmonary edema?

A

fibrosis and thickening of alveolar walls

78
Q

What are Kerley’s A lines?

A

linear opacities extending from the periphery to the hila; they are caused by distention of anastomotic channels between peripheral and central lymphatics.

79
Q

what are Kerley’s B lines?

A

short horizontal lines situated perpendicularly to the pleural surface at the lung base; they represent edema of the interlobular septa.

80
Q

What are Kerley’s C lines?

A

reticular opacities at the lung base, representing Kerley’s B lines en face.

81
Q

The Kerley’s line patterning in the lungs is a process known as…

A

cephalization

82
Q

Distinguish ALI from ARDS

A

ALI: noncardiogenic pulmonary edeam
ARDS: severe ALI

83
Q

T/F: ANY noncardiogenic pulmonary edema can be called ALI

A

true

84
Q

t/f: Regardless of severity you will see the histologic pattern of DAD

A

true

85
Q

What is acute interstitial pneumonia?

A

ALI without an identified cause

86
Q

what are the most common causes of ALI/ARDS?

A

SEPSIS
PNEUMONIA
ASPIRATION
TRAUMA; flooded with inflammatory response

87
Q

What two types of edema do you get with DAD?

A

interstitial AND intra-alveolar

88
Q

What happens to the interstitium in DAD>?

A

inflammation and fibrin deposition

89
Q

In DAD, (blank) membranes form which contain Fibrin rich edema fluid mixed with remnants of necrotic epithelia cells

A

hyaline membranes

90
Q

what four cell types are damaged in DAD?

A

type I pneumocytes
type II pneumocytes
epithelial cells
endothelial cells

91
Q

why do people die from the flu?

A

DAD or superimposed bacterial pneumonia

92
Q

what two things in DAD interfere with O2 exchange?

A
  1. blood vessel congestion

2. deposition of fibrin and serum proteins in the interstitium

93
Q

t/f: Endothelial or epithelial damage in ARDS is caused by both systemic and local issues

A

true

94
Q

what are the five causes of endo and epi damage in DAD?

A
  1. increased vascular permeability
  2. alveolar flooding
  3. reduced diffusion capacity
  4. microthrombi
  5. Pro/anti inflamm imbalance
95
Q

t/F: primary lung damage is necessary to precipitate ARDS

A

false; can result from systemic insult

96
Q

describe the clinical presentation of ARDS

A 
rapid onset
dsypnea
tachypnea
severe cyanosis
respiratory failure
diffuse bilateral pulmonary infiltrates
97
Q

what is the mortality in ARDS?

A

40%

98
Q

why do the lungs become stiff and hard to ventilate in ARDS?

A

formation of hyaline membranes; type II cells produce surfactant; because the type II cells have been damaged the lungs aren’t as compliant.

Block 9 Week 3 (8 decks)

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