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1 STEP Uworld pulmo > UW pulm physio 2 > Flashcards

UW pulm physio 2 Flashcards

1
Q

Hereditary PAH is most often due to an …………………..

A

Inactivating mutation in BMPR2

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2
Q

Patients with BMPR2 mutation have presdisposition for (2) ……………….

A

dysfunctional epithelium and smooth muscle cell proliferation

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3
Q

What is thought activate disease process in pulmonary hypertension?

A

An insult as infection or drugs

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4
Q

Insults, that activate pulmonary hypertension leads to decreased ………… (2) an increased …………….. (2)

A

decr. vasodilative, antiproliferative mediators eg NO, prostacyclin;
incr. vasoconstrictive, proliferative mediators eg endothelin

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5
Q

Insults, that activate pulmonary hypertension leads to decreased ………… (2) an increased …………….. (2)

A

decr. vasodilative, antiproliferative mediators eg NO, prostacyclin;
incr. vasoconstrictive, proliferative mediators eg endothelin

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6
Q

What is end result that cause pulmonary hypertension?

A

Vasoconstriction with vascular smooth muscle proliferation, intimal thickening and fibrosis + incr. pulm. vasc. resist and progresive pulmonary hypertension

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7
Q

What complication results due to PAH and causes right axis deviation on ECG?

A

PH –> right ventricular hyperthrophy as compensation –> right axis deviation on ECG.

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8
Q

How can be detected pulmonary artery hypertension? (physical examination)

A

Loud pulmonic component of S2

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9
Q

How can be detected pulmonary artery hypertension? (physical examination)

A

Loud pulmonic component of S2

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10
Q

2 steps of hereditary PAH development?

A

Abnormal BMPR2 predisposes to excessive smooth muscle and endotheliai proliferation. Insult such infection of drugs then activate the disease process

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11
Q

What form s in the last stage of PAH pathogenesis in arteries?

A

Capillary tufts (pexiform lesions)

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12
Q

What form s in the last stage of PAH pathogenesis in arteries?

A

Capillary tufts (pexiform lesions)

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13
Q

What triggers remodeling in systemic sclerosis in arteries?

A

Increased proliferation of T cells with secretion of variety cytokines (eg TGF-beta) –> stimulate fibroblasts –> increased collagen and extracellular matrix proteins.
Also, endothelial dysfunction due to inc. endothelin and TXA2 versus NO and prostacyclin

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14
Q

What other changes apart PAH can cause systemic sclerosis in lungs?

A

Interstitial fibrosis –> PAH due to hypoxia-induced vasoconstriction

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15
Q

What disease in chest cavicty also manifest in systemic sclerosis and induce RHF?

A

Pericardial fibrosis –> impaired diastolic dysfunction of RV

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16
Q

What causes loud pulmonic component in PAH?

A

forceful pulmonic valve closure in the setting of high pulmonary arterial pressure

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17
Q

What can create accenuated impulse palpated at the left sternal border in PAH?

A

RV enlargement due to inc. load (ie concentric RV hypertrophy)

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18
Q

What can create accenuated impulse palpated at the left sternal border in PAH?

A

RV enlargement due to inc. load (ie concentric RV hypertrophy)

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19
Q

How is described accenuated impulse felt on left sternal border in PAH?

A

Left parasternal lift due to right ventricular heave

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20
Q

PAH relatively more often afftects what population?

A

young women

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21
Q

What causes fatigue and exertional dyspnea in PAH?

A

Decreased CO

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22
Q

Where happens congestion due to HF in lungs?

A

Pulmonary venous congestion

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23
Q

Where happens congestion due to HF in lungs?

A

Pulmonary venous congestion

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24
Q

Smooth muscle cell proliferation in pulmonary arteries leads to ………… (1)

A

medial hypertrophy

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25
Q

Collagen depositions in pulmonary arteries leads to ………… (2)

A

Intimal thickening and fibrosis

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26
Q

The remodeling in pulmonary arteries is less extensive in PH due to LH or due to primary PAH?

A

in LV induced PAH.
primary is due to genetic mutations

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27
Q

Congenital heart disease that causes …………..shunting (eg, ventricular septal defect, atrial septal defect) can lead to …… via an increase in pulmonary arterial blood flow

A

left-to-right;
pulmonary hypertension

28
Q

Why occurs hypoxic vasoconstriction in pulmonary hypertension?

A

Hypoxic vasoconstriction is a physiologic mechanism unique to lung tissue that helps minimize ventilation-perfusion mismatch and increase overall gas exchange efficiency.

29
Q

An area of ventilation defect without perfusion defect is suggestive of conditions that lead to …………………..

A

acute alveolar filling (pneumonia, pulmonary edema)

30
Q

Pulmonary arterial compliance in pulmonary hypertension?

A

decreases due to vascular remodeeling and stiffening of the walls

31
Q

The main mechanism of pulmonary hypertension in chronic hypoxic diseases?

A

hypoxia induced vasoconstriction

32
Q

Massive PE can lead to sudden occlusion of …..% of the pulmonary arterial circulation

A

> 50proc

33
Q

If CT is contraindicated for PE diagnostics, what method we would use?

A

V/Q scan

34
Q

Low tidal volume ………… dead-space ventilation

A

increases

35
Q

Increases in physiologic dead space occur in many lung diseases, including (3)

A

PE, emphysema, ARDS

36
Q

lower tidal volumes increase the proportion of ………………..

A

each breath composed of dead space

37
Q

minute ventilation formula?

A

tidal volume x RR

38
Q

Why patients with weakened respiratory muscles tend to breath at low tidal volumes?

A

To minimize the work of breathing

39
Q

Patients with weakened respiratory muscles tend to breath at low tidal volume. What is a compensatory response?

A

hypoventilation triggers increase in respiratory drive –> incr. RR to maintain ventilation

40
Q

What is rapid shallow breathing index (RSBI)?

A

Ratio of respiratory rate/tidal volume

41
Q

How is called the ratio of respiratory rate/tidal volume?

A

Rapid shallow breathing index (RSBI)

42
Q

What indicates low RSBI? (3)

A

relatively high tidal volume, relatively efficient breathing and lower likelihood of recurrent respiratory failure once ventilatory support is discontinued.

43
Q

What indicates low RSBI? (3)

A

relatively high tidal volume, relatively efficient breathing and lower likelihood of recurrent respiratory failure once ventilatory support is discontinued.

44
Q

Increases in both respiratory rate and tidal volume result in increased ……………..

A

minute ventilation

45
Q

A decrease in respiratory rate and an increase in tidal volume would ……………

A

keep minute ventilation

46
Q

Decr. RR and inc. tidal volume. Dead space ventilation each breath?

A

decrease

47
Q

Because at low tidal volumes a higher proportion of each breath is composed ……………, it leads to………………

A

Of dead space;
leads to an increase in wasted ventilation (inefficient breathing)

48
Q

Because at low tidal volumes a higher proportion of each breath is composed ……………, it leads to………………

A

Of dead space;
leads to an increase in wasted ventilation (inefficient breathing)

49
Q

How astma changes compliance of the lungs?

A

doesnt change

50
Q

What method is used if patient cannot tolerate CT angiography in PE with IV contrast?

A

V/Q scan - compares regional ventilation and perfussion.

51
Q

V/Q scan in PE. 1 stage - what is used?

A

Radiolabeled aerosol - inhaled and delivered throughout the tracheobronchial tree.

52
Q

V/Q scan in PE. 2 stage - what is used?

A

IV tracer is distributed throughout the pulmonary vasculature.

53
Q

V/Q scan in spontaneous pneumotorax?

A

normal perfusion but impaired ventilation due to compressed lung

54
Q

what is normal thick of the RV wall?

A

3-4mm

55
Q

Long-standing pulmonary hypertension eventually leads to ……………………………right ventricle (cor pulmonale)

A

hypertrophy and/or dilation of the right ventricle

56
Q

What is the most common cause of death in PAH?

A

RHF with circulatory collapse and respiratory failure

57
Q

What is the difference between dilated cardiomyopathy and cor pulmonale due to PAH?

A

dilated cardiomyopathy - all 4 chambers are dilated
RV hypertrophy due due PAH - thick RV wall

58
Q

Gross changes in WPW?

A

none, because it is electrophysical abnormality.

59
Q

Endothelin pathway and result?

A

Proendothelin –> endothelin-1 –> activates endothelin receptor on smooth mucle –> vasoconstriction+proliferation

60
Q

NO pathway and result?

A

L-arginine –> forms NO and L-citruline –> NO converts GTP to cGMP –> vasodilation and decreased proliferation

61
Q

Prostacyclin pathway and result?

A

Arachidonic acid –> prostacyclin –> cAMP –> vasodilation and decr. proliferation

62
Q

What part of vessel proliferates in PAH?

A

Intima

63
Q

What targets PAH therapy?

A

Targets the mediator imbalance created by endothelial dysfunction (inc. vasoconstrictive mediators and decr. vasodilative mediators)

64
Q

What is endothelin receptor antagonist?

A

Bosentan

65
Q

What is prostacyclin analogue?

A

Epoprostenol

66
Q

NO oxide enhancing agent?

A

Sildenafil

67
Q

What is the same effect of all medications used for PAH therapy?

A

All help to reduce tissue proliferation regardless their mechanism of action

1 STEP Uworld pulmo (7 decks)

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