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1 STEP Respiratory patho > Pulm hypertension pathoma and UW 12/12 > Flashcards

Pulm hypertension pathoma and UW 12/12 Flashcards

1
Q

how is defined PH? mmHg

A

nomal pressure 10 mmHg
in PH > 25 mmHg

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2
Q

PH biopsy characterization (pathoma) - 3?

A
  1. Atherosclerosis of the pulmonary trunk
  2. Smooth muscle proliferation (medial hypertrophy)
  3. INTIMAL fibrosis (due to collagen deposition)
    ——> signifficant luminal narrowing
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3
Q

PH characteristic finding? in both primary and secondary

A

Plexiform lesion - severe, long standing disease

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4
Q

PH leads to what?

A

RVH and cor pulmonale

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5
Q

PH symptoms?

A

1.progressive, exertional dyspnea, 2.fatigue,
3.syncope
4. exertional angina

DUE TO DECREASED cardiac output due to inability of the RV to pump blood through the lungs

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6
Q

PH what murmur?

A

due to tricuspid regurgitation -> holosystolic murmur

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7
Q

Primary change - cause?

A

Changes in pulmonary arteries

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8
Q

Secondary changes - causes?

A

due to diseases: LHF, chronic lung hypoxia, chronic thromboembilic diseases.

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9
Q

How to rule out LHF as a cause?
aka increased volume in pulmonary circuit

A

PCWP ir less than 12 mmHg.

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10
Q

What causes chronic lung hypoxia/hypoxemia?

A

eg interstitial lung disease, COPD

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11
Q

Primary PH = pulmonary arterial hypertension. What is mechanism?

A

proliferative vasculopathy aka proloferation of vascular smooth muscles

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12
Q

pulmonary arterial hypertension - causes?

A

hereditary INACTIVATING mutation BMPR2 (proapoptotic), connective tissue diseases (SS, RA), HIV infection.

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13
Q

what ir BMPR2 mutation?

A

inactivating

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14
Q

pulmonary arterial hypertension what population?

A

young females

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15
Q

what mediator promotes vasoconstriction and smooth muscle cells proliferation?

A

Endothelin

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16
Q

Endothelin - what does it?

A

promotes vasoconstriction and smooth muscle cells proliferation (MEDIAL HYPERTROPHY)

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17
Q

PAH - concentration of endothelin?

A

typically PAH patients have high concentration of endothelin

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18
Q

What are endothelin receptor antagonists?

A

bosentan, ambrisentan

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19
Q

bosentan, ambrisentan - what group?

A

endothelin receptor antagonists

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20
Q

Result of endothelin receptor antagonists?

A

Decrease smooth cells proloferation and alleviate vasoconstriction -> lower pumonary arterial pressure -> improve dyspnea

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21
Q

where is proendothelin?

A

in endothelium

22
Q

whats the origin of endothelin 1?

A

proendothelium

23
Q

where are endothelin receptor?

A

in smooth muscles of pulmonary artery

24
Q

proendothelin -> endothelin -> joins endothelin receptors –> effect?

A

smooth muscle cells proliferation and vasoconstriction

25
Q

dyspnea and exercise intolerance in women aged 20-40

A

.

26
Q

Where is L-arginine?

A

in endothelium

27
Q

what 2 products is from L-arginine?

A

L- citruline
NITRIC OXIDE

28
Q

What cyclic molecule participates in NO pathway?

A

cGMP

29
Q

L arginine -> NO -> cGMP -> effect?

A

vasodilation and decreased proliferation of smooth muscles

30
Q

What activates (+) cGMP?

A

Nitrates and Phosphodiesterase inhibitor

31
Q

Where is arachidonic acid?

A

endothelium

32
Q

Arachidonic -> ?

A

prostacyclin (prostaglandin I2)

33
Q

what cyclic molecule is in prostacyclin pathway?

A

cAMP

34
Q

Arachidonic -> prostacyclin -> cAMP -> effect?

A

vasodilation and decreased porliferation

35
Q

what stimulates (+) cAMP?

A

prostacyclin analogues

36
Q

PAH - target treatment?

A

treatment targeted at endothelial dysfunction

37
Q

PH - target treatment?

A

aimed at underlying cause

38
Q

mechanism of decr. CO?

A

RV cannot pump -> decr. LA preload -> decr. LV preload -> decr. SV -> decr. CO

39
Q

what is pulmonary wedge pressure in PAH?

A

decreased (decreased RV pump function)

40
Q

BMPR2 hereditary pattern?

A

autosomal dominant

41
Q

what is tought to activate the process of PAH?

A

an insult (eg drugs, infection) in susceptible patients

42
Q

what mediators are increased and what decreased in PAH?

A

Incr.: endothelin
decr: NO, prostacyclin

43
Q

what is heard on auscultation?

A

loud pulmonic component of S2 - forced by pulmonic valve closure in the setting of high pulmonary arterial pressure

44
Q

RHF clinical?

A

distended jugular veins, nut meg liver (hepatic congestion), pitting edema

45
Q

what unusual clinical presentation may be due to RHF induced concentric hypertrhophy of RV?

A

it can create attenuated impulse palpated at the left sternal border (left parasternal lift due to right ventricular valve heave (RV hypertrophy)).

46
Q

what size arteries are affected in PAH?

A

small-medium sized pulmonary arteries/arterioles

47
Q

Systemic slerosis. what cells increased?

A

proliferation of T cells with secretion of various cytokines (eg TGF-beta)

48
Q

result of T cells + cytokines ->?

A

they stimulate fibroblasts to increase the production of collagen and extracellular matrix proteins.
there is also endothelial dysfunction due to and excess of vasoconstrictive (endothelin, TXA2) relative to vasodilative antiproliferative (NO, prostacyclin) mediators. —-> smooth muscle proliferatio and vasoconstriction

49
Q

why occurs hypoxic vasoconstriction in pulmonary hypertension?

A

Its a physiologic mechanism unique to lung tissue that helps minimize ventilation-perfusion mismatch and incrrase overall gas exchange efifciency

50
Q

what is normal RV thickness and what is in RV hypertrophy?

A

normal 3-4 mm;
in RV hypertrophy - 2 cm

51
Q

prostacyclin analogue?

A

epoprotenol

52
Q

NO enhancing agent?

A

sildenafil

1 STEP Respiratory patho (4 decks)

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