Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 9 Week 3 > Vascular Lung Disease- Baker 3 > Flashcards

Vascular Lung Disease- Baker 3 Flashcards

1
Q

Blood clots in the pulmonary arterial system are almost always (blank). 90% are from a (blank)

A

embolic

DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Does a DVT= PE?

A

no, DVT 2x more frequent than PE

BUT you cant get a PE without having a DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the morbidity associated with PE?

A

1/2 have long term complications (post-thrombotic syndrome):
-pain, swelling, discoloration
1/3 have recurrence over 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mortality associated with PE?

A

50-100k deaths per year

  • 10-30% die within one month of diagnosis
  • 25% first “symptom” is sudden death
  • cause of or contributes to 10% of hospital deaths
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DVT with a PFO will give you a (blank) pattern rather than a PE

A

stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the risk factors for PE?

A

Virchow’s triad

1) endothelial injury
2) blood stasis/turbulent flow
3) hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the ways that you can get endothelial injury in virchows triad?

A

trauma
vasculitis
hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the ways that you can get blood stasis/turbulent flow in virchows triad??

A
  • immobility (post operative, orthopedic conditions, illness)
  • venous compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the ways that you can get hypercoagulability in virchows triad?

A
  • genetic predisp (factor v leien, prothrombin gene mutation, protein C/S deficiency, AT III deficiency)
  • cancer
  • immobilization
  • pregnancy, HRT, OCP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two main issues in PE pathology?

A
  • respiratory compromise

- hemodynamic compromise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes respiratory compromise?

A
  • V (ventilation) not equal Q (perfusion) mismatch

- allows for VQ study that diagnoses PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes hemodynamic compromise?

A

lack of blood flow to the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Severity of symptoms and PE syndrome is all a matter of (blank) of PE

A

size (clot burden)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If you have a large embolic causing a PE what will result?

A

complete loss of blood flow

-acute hypoxemia, right heart failure, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is one of the few causes of instantanous death?

A

large PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can smaller PEs do?

A

travels deeper into the periphery, less likely to cause death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

PEs can cause a hemmorrhagic lesion in (blank) percent of cases, When will this occur? Where does it typically occur?

A

10%
Usually only when underlying cardiopulmonary conditions are present (inability of the bronchial arteries to compensate)

-typically occurs in lower lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the clinical features of PE?

A 
Tachycardia
Chest pain
Tachypnea
Dyspnea
Hypoxemia 
± cough
± Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common EKG finding with a patient with a PE?
What are some other associated findings?

A

tachycardia!
non-specific ST segment changes and T wave changes
S1Q3T3= right ventricular dilation (present in 12% of massive PE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What willl a chest x ray look like with a person who has PE?

What will the CT scan look like?

A
  • variable. possibly will show a wedge-shaped infiltrate (infarction)
  • gray spots in white arteries demonstrating perfusion defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is normal pulmonary arterial pressure?

A

15-30/4-12 (mean 8-18 mmHg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do you calculate MAP?

A

(2x diastolic + systolic) / 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pulmonary htn is when you have a sustained elevation of mean pulmonary arterial pressure to more than (blank) at rest or to more than (blank) with exercise

A

25 mm Hg

30 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 2 types of pulmonary htn?

A

Primary
-idiopathic pulmonary arterial htn
Secondary
-many causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the histopathology of PAH (pulmonary arterial htn)?

A
  • medial hypertrophy of muscular and elastic arteries
  • plexiform lesion
  • pulmonary artery atheromas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

(blank) are present in idiopathic and familial pulmonary htn (not clear if it is caused of or a result of PH)

A

plexiform lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the five PAH clinical classifications based on similiarites in pathophysiology, clinical presentation and therapy?

A
  1. Pulmonary Arterial
    Hypertension
  2. PH with left heart disease
  3. PH associated with lung disease / hypoxemia
  4. PH due to chronic thrombotic/embolic disease
  5. Miscellaneous PH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How can you cause secondary PAH? Give me 5 examples

A

anything that increases pressure can lead to PAH

  • CHRONIC LUNG DISEASE
  • HEART DISEASE
  • thromboemboli
  • CT disease
  • OBSTRUCTIVE SLEEP APNEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

In chronic lung disease, you can get (blank) destruction, fewer (blank), and increased (blanK)

A

parenchymal destruction
capillaries
increased resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What types of heart disease can cause secondary PAH?

A

left heart failure and mitral stenosis

31
Q

How will thromboemboli cause secondary PAH?

A

-reduced cross-sectional area, increased resistance

32
Q

What CT disease will cause secondary PAH?

A

Systemic sclerosis-> leads to vascular inflammation, intimal fibrosis, medial hypertrophy

33
Q

How does OSA cause secondary PAH?

A

increased pulmonary pressure

34
Q

When you have an obstructive pulmonary artery thrombus what happens?

A

you get a narrowed lumen which increased flow resistance and increases pulmonary artery BP

35
Q

What causes primary PAH (idiopathic PAH)?

A

mutation of BMPR2 (bone morphogenetic protein receptor 2) leads to proliferation of vascular smooth muscle cells (may be some association with environmental factors)

36
Q

In whom does primary PAH usually occur in?

A

females between 20-40 years of age

37
Q

What are the early clinical signs of primary PAH?

What is like as the disease progresses?

A
  • dyspnea, fatigue, anginal chest pain

- respiratory distress, cyanosis, RVH and death from cor pulmonale

38
Q

What is the mortality of primary PAH?

A

usually die within 2-5 years of diagnosis (80%)

39
Q

What are the conventional therapies of PAH?

A 
conventional therapies:
O2
CCBs
digoxin
diuretics
40
Q

What are the newer specific therapies of PAH?

A
  • prostacyclin analogues
  • endothelial receptor antagonist
  • inhaled NO
  • phosphodiesterase-5 inhibitors
41
Q

What is the most radical therapy of PAH?

A

lung transplant

42
Q

What are the diffuse pulmonary hemorrhage syndromes?

A
  • goodpasture syndrome
  • idiopathic pulmonary hemosiderosis
  • Vasculitits associated hemorrhage
43
Q

What are the three diseases associated with vasculitis associated hemorrhage?

A
  • Wegener Granulomatosis
  • Hypersensitivity angiitis
  • Lupus erythematosus
44
Q

What is this:
autoimmune disorder-autoantibodies against the basement membrane in alveoli and glomeruli.

What can goodpasture syndrome cause?

A

Goodpasture syndrome

  • hemorrhagic interstitial pneumonitis
  • rapidly progressive glomerulonephritis (RPGN)
45
Q

Who typically gets goodpasture syndome?

What is it caused by?

A

Males> female; teens to 20s typically

-etiology of antibodies is uknown (viral infections, toxic exposures, smoking)

46
Q

What will the histology look like in good pasture syndrome?

A
  • alevolar wall necrosis w/ intra alveolar hemorrhages
  • hemosiderin laden macrophages
  • linear Ig and complement deposits in BM
47
Q

What does good pasture syndrome intially present with?
What will an x ray show?
What happens after the initial signs?

A
  • hemptysis
  • focal pulmonary consolidations
  • renal manifestations folllow-> rapidly progressive glomerulonephritis (RPGN)-> uremia-> death
48
Q

How do you treat goodpasture syndrome?

A
  • Renal Replacement therapy (dialysis) for severe AKI
  • Plasmapheresis= removes circulating anti-BM antibodies
  • Immunosuppression
49
Q

What is this:
intermittent, diffuse alveolar hemorrhage
Who does it typically affect?

A

Idiopathic pulmonary hemosiderosis

-usually young children

50
Q

What is the clinical course of idiopathic pulmonary hemosiderosis?

A

productive cough
hemoptysis
anemia
weight loss

51
Q

Idiopathic pumonary hemosiderosis is very similiar to good pasture syndrome but it has no (blank)

A

anti-BM antibodies

52
Q

How do you treat idiopathic pulmonary hemosiderosis?

A

immunosuppression

53
Q

What is the new term for Wegener’s granulomatosis?

A

granulomatosis with polyangitis

54
Q

How does granulomatosis with polyangitis (wegener’s granulomatosis) cause vasculitis?

A

C-ANCA activates neutrophils which cause free radicals and protolytic enzymes-> leads to inflammatory cells and vasculitis

55
Q

How does wegener granulomatosis present?

How do you diagnose it?

A
  • necrotizing vasculitis
  • present w hemoptysis

-transbronchial biopsy

56
Q

Granulomatosis with polyangitis also frequently affects the (blank) giving rise to (blank) clinically. Also the (blank) is frequently affected and here mucosal ulcers are seen.

A

sinuses
chronic sinusitis
nasopharynx

57
Q

What causes increased lymphatic drainage in noncardiogenic pulmonary edema?

A

DISRUPTED ENDOTHELIAL BARRIER w/ normal hydrostatic pressure
increased permeability-> dirupted epithelial barrier-> neutrophils squeeze in and causes alveolar flooding -> you get increased alveolar edema due to lack of salt transports-> increased lymphatic drainage

58
Q

What is this:
engorged alveolar capillaries
intra-alveolar pink precipitate
heart failure cells

A

Cardiogenic pulmonary edema

59
Q

What are heart failure cells and what will you see them in?

A

Hemosiderin-laden macrophages from alveolar microhemorrhages

-cardiogenic pulmonary edema

60
Q

What are the clinical signs of PE?

A

SOB, DOE, orthopnea, PND, crackkles on ausculatation

61
Q

Where will fluid initially accumulate in PE?

If you have chronic PE what can happen?

A

lower lobes first

lead to fibrosis and thickening of alveolar wall

62
Q

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

A

Kerley’s B lines

63
Q

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

A

Kerly A lines

64
Q

What are the 3 causes of noncardiogenic pulmonary edema?

A
  • acute lung injury (ALI)
  • Acute Respiratory Distress Ayndrome
  • Acute interstitial pneumonia
65
Q

What is severe acute lung injury?
What is normal acute lung injury?
What is acute lung injury without an identified cause?
What do they look like histologically?

A
  • ARDS (acute respiratory distress syndrome)
  • Noncardiogenic pulm edema
  • Acute interestitial pneumonia
  • Diffuse alveolar damage (DAD)
66
Q

What are the causes of ALI/ARDS?

A
  • sepsis
  • diffuse pulmonary damage
  • mechanical trauma, including head injuries
67
Q

What does diffuse alveolar damage look like?

A
  • interstitial edema
  • intra-alveolar edema
  • inflammation
  • fibrin deposition
  • hyaline membranes
68
Q

What do hyaline membranes look like?

A

fibrin rich edema fluid mixed w/ remnants of necrotic epithelia cells

69
Q

Whats happens to you alveoli in acute lung injury?

A

you get injured, swollen endothelial cells-> neutrophil migration into alveolus-> cytokines + proteases + leukotrienes + Platelet activating factor-> inactivated surfactant-> sloughed bronchial epithelium

70
Q

SARS demonstrates DAD, what else does?

A

influenza A

71
Q

What does ALI/ARDs cause, systemic or local insults?
Endothelial or epithelial damage?
Results in an imbalance between (blank and blank) mediators

A

both
both
pro and anti-inflammatory

72
Q

How does ALI/ARDS damage the endothelium or epithelium?

A
  • increase vascular permeability
  • alveolar flooding
  • reduced diffusion capacity
  • microthrombi
73
Q

What are the clinical features of ALI/ARDS?

What is the mortality percentage?

A

-rapid onset
-profound dyspnea
-tachypnea
-severe cyanosis
-respiratory failure
-diffuse bilateral pulmonary infiltrates
VERY VERY SICK!

40% mortality

74
Q

In infants what causes ARDS?

What causes ARDS in adults?

A

lack of surfactant

secondary disorder

Block 9 Week 3 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions