Vascular Disease Flashcards

1
Q

2 main features of pulm circulation

A

low pressure low resistance

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2
Q

mechs to prevent increased PVR

A

recruitment and distension of vessels

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3
Q

2 types of hypoxic vasoconstriction

A

focal alveolar hypoxia (pneumonia) vasoconstricts upstream of specific area

global alveolar hypoxia (lung disease, altitude)

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4
Q

cutoff for pulm HTN

A

mPAP over 25

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5
Q

3 states that could elevate mPAP

A

left atrial elevation- passive, from heart failure, mitral stenosis

CO elevation- hyperdynami, high flow states

PVR elevation- PE, tumor; PAH, emphysema, ILD; hypoxemia or hypercapnea

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6
Q

WHO group 1 PH

A

pulmonary arterial hypertension- constriction of smooth muscle w/ arterial wall thickening and small lumen, inflammation

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7
Q

WHO group 2 PH

A

from left heart disease, pressure buildup from LA

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8
Q

WHO group 3

A

lung disease- hypoxic constriction, sleep apnea, emphysema, fibrosis

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9
Q

WHO group 4

A

thromboembolic pulm HTN

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10
Q

WHO group 5

A

varied- like sarcoid, myeloproliferative disease, renal failure

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11
Q

physical exam signs of PH

A

loud P2, ejection murmur, parasternal heave

signs of RV failure maybe: JVD, edema, ascites

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12
Q

echo findings for PH

A

can see dilated RA, evidence of high PVR

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13
Q

dx of PH

A

need right heart cath- swan ganz

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14
Q

3 drug pathways for PAH tx

A

endothelin, NO, prostacyclin

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15
Q

target of prostacyclin drugs

A

GCPR in SMC, induce more cyclic AMP and vasodilaiton

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16
Q

target for endothelin drugs

A

antagonize ETA and ETB receptors in SMC- A causes vasoconstriciton and B dilaiton

want to be more selective for A

17
Q

drug targets for NO, examples

A

sildenafil/tadalafil

inhibit PDE 5- causes buildup of cyclic GMP (messenger downstream of NO) leading to dilation

18
Q

moa of riocuat

A

stimulate guanylyl cyclase in SMC, also raises cyclic GMP

19
Q

PH managment (6)

A
  • Ca blocker (group 1 PAH w/ response to vasodilator)
  • diuretics
  • O2
  • anticoag
  • surgery
  • transplant
20
Q

4 pulm pathophys consequences from PE

A
  • increased alveolar dead space
  • hypoxemia (V/Q mismatch, surfactant loss and atelectasis)
  • hyperventilation
  • pulm infarction
21
Q

cardio consequences of PE

A

increased PVR leads to PH, right heart failure, hypotension, shock death

22
Q

sx of acute PE

A

dyspnea, pleuritic pain,hemoptysis (last two w/ infarct), anxiety, syncope

23
Q

4 main Dx tools for PE

A

D-dimer: to rule out in low likelihood pts, if below 500 can exclude

V/Q scanning (looking for discrepancy)

spiral or helical CT

*not for PE, but detection of DVT w/ echo is easy and same Tx

24
Q

4 PE tx options

A

anticoag- heparin, warfarin (after heparin), DOACs

thrombolytics for massive PE w/ hemodynamic compromise

surgery- embolectomy

IVC filter