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ICM-pulmonary > PVD > Flashcards

PVD Flashcards

1
Q

the V shaped structure on a CT scan is

A

the pulmonary artery

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2
Q

aorta is always

A

larger than pulmonary artery

-could mean is pulmonary HTN if larger

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3
Q

in someone with a large pulmonary artery, what could cause shortness of breath?

A

primary pulmonary HTN

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4
Q

how to measure pulmonary HTN

A

cardiac catheterization

  • insert small tube called a catheter, swan gaz catheter-> goes to SVC-> RA-> RV->pulmonary artery
  • read pulmonary wedge pressure
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5
Q

what is PAH?

A

hemodynamic state of stained elevation of pulmonary arterial pressure to 25 mmHg at rest or 30mmHg with exercise
-PCWP <15mmHg

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6
Q

what mimics PPH?

A

CTD, liver disease, HIV

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7
Q

PAH causes?

A
  • idiopathic
  • familial
  • connective tissue disease
  • associated with significant venous or capillary involvement
  • pul HTN with left heart disease
  • pul HTN associated with lung disease and hypoxmia: COPD, emphysema, pulmonary fibrosis, sleep apnea
  • Pul HTN due to chronic thrombotic and/or embolic diseases
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8
Q

leading cause of PAH

A

idiopathic PAH
-more common in women
-mean age of 52
no risk factors, family history or genetic mutation

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9
Q

genetic abnormalities in PAH

A

TGF-B receptor family
bone morphogentic protein receptor type II,
activin receptor like kinase 1

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10
Q

associated PAH

A

CTD: 15%, systemic sclerosis have worst prognosis
HIV 6%
shistosomiasis
sickle cell disease 20%, mild-moderate increase PAP

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11
Q

clinical findings of PAH

A 
increased P2
parasternal lift
TI murmur
Graham steel murmur (diastolic PI)
rS3
cyanosis (late)
*see right heart failure process
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12
Q

physical exam on PAH

A 
RS4
peripheral edema (ankles)
prominent P2 (93%)
pitting edema
RS3
cyanosis 
TR
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13
Q

pathophysiology

A

-Mainly vascular change
-Vasoconstriction
-Smooth muscle cell and endothelial cell proliferation
thrombosis
-Pulmonary endothelial cell injury leading to an imbalance in:
*vasodilators/constrictors
*growth inhibitors/mitogens
*antithrombotic/pro thrombotic factors

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14
Q

cellular mechanism involved in development of PAH include

A

increased endothelin levels

-main factor

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15
Q

APAH

A

HIV (independent of CD4 counts)
CREST
Portal HTN
Drugs and toxin: anorexigens, meth, cocaine, L-tryptophan

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16
Q

IPAH

A

rare
female more prominent
mean age of 37
progressive obliteration of pulmonary vascular bed

17
Q

embolic disease rare forms

A 
septic embolic
amniotic fluid embolism
fat embolism
parasitic embolism
tumor
foreign body
18
Q

Pulmonary HTN left heart disease

A

left ventricular dysfunction

left sided valvular disease: MS/MR, AS

19
Q

most common HF with pulmonary HTN?

A

diastolic

20
Q

pulmonary HTN with lung disease/hypoxemia

A

COPD

21
Q

CTEPH

A

prom

22
Q

PAH

A
  1. loss of cross sectional area
  2. vascular remodeling:
    - medial hypertrophy
    - plexiform lesion
    - intimal fibrosis
  3. excessive vasoconstriction
23
Q

diagnosis of PAH

A

diagnosis of exclusion
-parenchymal disease
alveolar hypoventilation
chronic hypoxemia

24
Q

mechanisms of PAH

A

reduced prostacyclin availability caused by diminished prostacyclin synthesis

25
Q

diagnostic studies for PAH

A 
V/Q
echo
RHC
sleep study
PFT's
26
Q

therapy for PTH

A

vasodilators
coumadin
diuretics?
transplant

27
Q

symtpoms to suspect PAH

A 
exercise intolerance
fatigue
CP
palpitations
NP cough
syncope
tachycardia 
prominent P2, TR, RHF, JVD
hepatomegaly, edema, stasis
28
Q

ECG findings

A

prominent P waves

RVH

29
Q

all patients with evidence of PAH by echo should undergo?

A

Ventilation perfusion scan

-look for embolic process

30
Q

what can confirm PAH

A

right heart catheterization

31
Q

guide for treatment

A

acute vasodilator challenge

-is respond: will respond to treatment

32
Q

kkk

A

mean fall in PA pressure >10mmHg to mean <40mmHg to cardiac output

33
Q

pre-test used to see treatment response

A

6 minute walk test

-afterwards measure oxygen sat values

34
Q

CCB are only given to

A

responders

ICM-pulmonary (12 decks)

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