Vascular Respiratory Path - Parks and Baker Flashcards
1
Q
blood clots in the pulmonary system are almost always (emoblic/thrombotic)
A
embolic
2
Q
T/F: a DVT means that you have a PE
A
false
3
Q
T/F: a PE means that you have a DVT
A
true
4
Q
What percent of pts have long term complications from a dvt?
A
1/2; pain, discoloration, swelling
5
Q
what percent of pts with a DVT will recur in 10 years?
A
1/3
6
Q
what percent of pts present with sudden death from PE?
A
25%
7
Q
how does a DVT lead to a stroke?
A
communication between left and right heart; aka PFO plus DVT
8
Q
why do people die within one month of PE diagnosis?
A
recurrence of another PE
9
Q
What is Virchow’s Triad?
A
- endothelial injry
- blood stasis/turbulent flow
- hypercoagulability
10
Q
what are the three things that lead to endothelial injury?
A
- trauma
- vasculitis
- hypertension
11
Q
what are the two things that lead to blood stasis or turbulent flow?
A
- immobility
2. venous compression
12
Q
what are the four things that lead to a hypercoagulable state?
A
- genetics (factor V)
- cancer
- immobilization
- pregnancy, HRT, OCP
13
Q
what two types of compromise result from PE?
A
respiratory and hemodynamic
14
Q
the severity of the symptoms of a PE are directly related the (blank) of the PE
A
size
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
16
Q
what types of lesions occur in 10% of cases in PE that lead to pulmonary infarct?
A
hemorrhagic lesions
17
Q
What arteries normally compensate for a PE, that if overwhelmed, lead to pulmonary infarct?
A
bronchial arteries
18
Q
which lobes do you normally get a pulmonary infarct?
A
lower lobes
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
20
Q
what does S1Q3T3 tell you about the right heart?
A
right ventricular dilation
NOT RIGHT HEART STRAIN
21
Q
what are the other EKG findings that suggest right heart strain?
A
- right axis deviation
2. RVH with precordial ST depression and T wave inversion
22
Q
what is the most common EKG finding in PE?
A
sinus tachycardia; nonspecific ST segment changes and T-wave changes
23
Q
what is the general presentation of PE?
A
tachycardia chest pain dyspnea hypoxemia cough fever
24
Q
what might you see on CXR for a PE?
A
wedge shaped infiltrate indicating infarction
25
what will you see on CT for PE?
using contrast, a perfusion blank spot where there is no contrast
26
what is the normal pulmonary arterial pressure?
15-30/4-12
| mean is 8-18
27
What is the Dx criteria for pHTN?
sustained elevation of mean pulmonary arterial pressure to more than 25 mm Hg at rest or to more than 30 mm Hg with exercise
28
t/f: All the restrictive and obstructive if left untreated can lead to PAH
true
29
what part of the pulmonary arteries will hypertrophy in PAH?
medial hypertrophy of muscular and elastic arteries
30
as a result of systemic HTN, what will form within the pulmonary arteries?
atheromas
31
in late stage pHTN, what type of lesions will you see?
plexiform lesions
32
what are the five most common causes of secondary pHTN?
1. chronic lung disease
2. heart disease
3. thromboemboli
4. connective tissue disease
5. obstructive sleep apnea
33
what is the MOA of chronic lung disease cuasing pHTN?
parenchymal destruction, fewer capillaries, increased resistance
34
what is the MOA of heart disease cuasing pHTN?
Left Heart Failure, Mitral Stenosis…etc
35
what is the MOA of thrombemboli cuasing pHTN?
reduced cross-sectional area (narrowed lumen), increased resistance
36
what is the MOA of connective tissue disease cuasing pHTN?
esp Systemic Sclerosis, lead to vascular inflammation, intimal fibrosis, medial hypertrophy
37
what is the MOA of obstructive sleep apnea cuasing pHTN?
increased pulmonary pressure
38
what gene is responsible for primary PAH?
BMPR2; leads to proliferation of vascular smooth muscle; may be associated with environmental factors
39
describe the typical patient with primary PAH
female; 20-40
dyspnea, fatigue, anginal chest pain. with progression will lead to Respiratory distress, cyanosis, RVH and death from cor pulmonale
40
what are the conventional therapies for PAH?
O2, calcium channel blockers, digoxin, diuretics
41
what are the newer targeted therapies for PAH?
Prostacyclin analogues, endothelial receptor antagonist, inhaled NO, phosphodiesterase-5 inhibitors
42
T/f: lung transplant is an option for PAH
true
43
is the Ig fluorescence in Goodpasture's linear or granular?
LINEAR Ig
44
where does the Ig deposit in goodpastures?
the basement membrane
45
in what two organs will you see Ig deposition in goodpastures?
alveoli and glomerulus
46
describe the histological changes in goodpastures?
focal aveolar wall necrosis
| intra alveolar hemorrhages
47
what type of special mac's will you see in the alveoli in good pastures?
hemosiderin laded macrophages
48
describe the MOA of the damage in goodpastures
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
what is the first symptom people will have in goodpastures?
hemoptysis
50
What will you see on CXR in goodpastures?
focal pulmonary consolidations
51
Describe the renal progression in goodpastures
RPGN to uremia to death
52
What is the Tx for removing Abs from the circulation in goodpastures?
plasmaphoresis
53
What are the three Tx available for goodpastures?
1. dialysis for AKI
2. plasmaphoresis
3. immunosuppresion
54
What is the histologic difference between goodpastures and idiopathic pulmonary hemosiderosis?
NO ANTI-BM ANTIBODIES
55
T/F: IPH repsonds well to steroids
true
56
describe the presentation of IPH
Insidious onset of productive cough, hemoptysis, anemia and weight loss
57
describe the histology of IPH
intermittent, diffuse alveolar hemorrhage
58
which ANCA is involvedin 90% of the active cases of Wegener's?
PR3-ANCA aka c-ANCA
59
what is the new name for Wegener's?
granulomatosis with polyangiitis
60
t/f: ANCAs may be used for Dx, are part of the pathogenesis, and can be used to measure dz activity
true
61
when would you get a false positive PR3/c-ANCA?
in certain infections and neoplasms
62
the end result of circulating ANCAs is....
vasculitis
63
describe the process of ANCAs causing vasculitis
1. ANCAs activate neutrophils
| 2. neutrophils release ROS and proteases which damage the endothelium
64
Wegener's is a (blank) vasculitis
necrotizing
65
The renal involvement in Wegener's is a focal, (blank) glomerulonephritis
necrotizing
66
How do you Dx Wegener's?
transbronchial Biopsy
67
Wegener's also affects the sinuses and presents with what two symptoms?
chronic sinusitis
| mucosal ulcers
68
What is the first symptom that most patients get with Wegener's?
hemoptysis
69
which pulmonary edema is pressure related and has intact membranes?
cardiogenic
70
which pulmonary edema has normal hydrostatic pressure and damage to the endothelium?
noncardiogenic
71
what drives the removal of alveolar edema in cardiogenic shock?
transport of Na, Cl, and H2O out of the alveolus
72
what type of pulmonary edema has a protein-rich infiltrate?
noncardiogenic
73
in cardiogenic pulmonary edema, the alveolar capillaries will be engorged and there will a pink precipitate where?
intra-alveolar
74
What are heart failure cells?
Hemosiderin-laden macrophages from alveolar microhemorrhages
75
what are the clinical signs of pulmonary edema?
SOB, DOE, orthopnea, PND, crackles on auscultation
76
Where does the fluid normally begin to pool in the lungs?
lower lobes
77
what happens as a result of chronic pulmonary edema?
fibrosis and thickening of alveolar walls
78
What are Kerley's A lines?
linear opacities extending from the periphery to the hila; they are caused by distention of anastomotic channels between peripheral and central lymphatics.
79
what are Kerley's B lines?
short horizontal lines situated perpendicularly to the pleural surface at the lung base; they represent edema of the interlobular septa.
80
What are Kerley's C lines?
reticular opacities at the lung base, representing Kerley's B lines en face.
81
The Kerley's line patterning in the lungs is a process known as...
cephalization
82
Distinguish ALI from ARDS
ALI: noncardiogenic pulmonary edeam
ARDS: severe ALI
83
T/F: ANY noncardiogenic pulmonary edema can be called ALI
true
84
t/f: Regardless of severity you will see the histologic pattern of DAD
true
85
What is acute interstitial pneumonia?
ALI without an identified cause
86
what are the most common causes of ALI/ARDS?
SEPSIS
PNEUMONIA
ASPIRATION
TRAUMA; flooded with inflammatory response
87
What two types of edema do you get with DAD?
interstitial AND intra-alveolar
88
What happens to the interstitium in DAD>?
inflammation and fibrin deposition
89
In DAD, (blank) membranes form which contain Fibrin rich edema fluid mixed with remnants of necrotic epithelia cells
hyaline membranes
90
what four cell types are damaged in DAD?
type I pneumocytes
type II pneumocytes
epithelial cells
endothelial cells
91
why do people die from the flu?
DAD or superimposed bacterial pneumonia
92
what two things in DAD interfere with O2 exchange?
1. blood vessel congestion
| 2. deposition of fibrin and serum proteins in the interstitium
93
t/f: Endothelial or epithelial damage in ARDS is caused by both systemic and local issues
true
94
what are the five causes of endo and epi damage in DAD?
1. increased vascular permeability
2. alveolar flooding
3. reduced diffusion capacity
4. microthrombi
5. Pro/anti inflamm imbalance
95
t/F: primary lung damage is necessary to precipitate ARDS
false; can result from systemic insult
96
describe the clinical presentation of ARDS
```
rapid onset
dsypnea
tachypnea
severe cyanosis
respiratory failure
diffuse bilateral pulmonary infiltrates
```
97
what is the mortality in ARDS?
40%
98
why do the lungs become stiff and hard to ventilate in ARDS?
formation of hyaline membranes; type II cells produce surfactant; because the type II cells have been damaged the lungs aren’t as compliant.
