Pulmonary HTN and interstitial disease Flashcards

1
Q

Definition of pulmonary HTN

A

mean pulmonary arterial pressure above 25 mmHg at rest

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2
Q

causes of pulmonary HTN

A

idiopathic or secondary to scleroderma, HIV, cirrhosis, anorexigens, congenital heart disease, genetic (linked to TGF-beta),
pulmonary venous HTN is related to CHF or valvular disease

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3
Q

vascular pathology of pulmonary HTN

A

resembles tumor invading the vascualr wall. includes luminal obliteration via vascular smooth muscle cells and endothelial cells. also from deficiency in vasodilators and growth suppressors like NO, prostacyclin, and cGMP.
excess of vasoconstrictors and growth activatos (BMPR, endothelin)

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4
Q

What does endothelin do

A

smooth muscle contraction, fibrosis, smooth muscle prolif and migration, increased sympathetic activity

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5
Q

How does fenfen cause pulmonary HTN?

A

platelet activation and endothelial dysfunction leading to thrombosis and serotonin storage. fenfen releases serotonin and prevents platelet reuptake and increases growth and von Willebrand factor. then , there is an increase in shear forces that promotes growth of smooth muscle cells.

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6
Q

testing for pulmonary HTN

A

6 minute walk, HIV, V/Q scan and pulmonary function testing, echo, tropinin and BMP. right heart catheterization is diagnostic and gives the wedge pressure. if pulmonary HTN is from left heart failure, both pulmonary vein and artery pressures will be high

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7
Q

What are some old ways to treat pulmonary HTN?

A

O2, anticoagulation, diruetics

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8
Q

What is eproprosinol? how does it work>

A

epoprosinol, esp. for stage IV pts. this is a prostacyclin analogue that relaxes smooth muscle, inhibits smooth muscle migration and prolif, decreases platelet aggregation, increases endothelin clearnce and decreases endothelial cell activation.

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9
Q

Epoprostinol: administration and side effects

A

continuous IV infusion, short half life, central access, and can cuase headache, nausea, diarhea, deep bone baine

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10
Q

Where does pleural fluid come from

A

subpleural systemic vessels, not pulmonary vessels. most fluid from the parietal side.

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11
Q

2 physiological alterations that produce pleural effusions

A
  1. increased systemic venous pressure that increases filtration to pleural space and decreases flow to lymphatics
  2. abnomalities of pleural surfaces. may increase filtration or decrease lymphatics
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12
Q

transudate vs. exudate definition

A

transudate: normal capillary permeability to protein
exudate: increased permeability of capillaries and pleural surfaces with spillover into pleural spaces.

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13
Q

4 features that diffecetiate btw transudate and exudate. normal values

A

protein fluid: serum ration; cholesterol; LDH (lactate dehydrogenase), LDH F/S ratio.
Protein ratio: under 0.5 for transudate. LDH ratio under 0.6. LDH is less than 2/3 upper limit for lab. colesheral under 45 mg/dl. If any one criteria not met, this is exudate rather than transudate.

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14
Q

Common etiology for transudate effusions

A

outside the pleural space: CHF, nephrotic syndrome, ascites

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15
Q

Common etiology for exudates

A

problem in the pleural space: malignancy, inflammatory disease like SLE or rheumatoid arthritis, pneumonia/TB

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16
Q

Side effects of thoracentisis

A

bleeding, infection, pneumothorax

17
Q

drug that can cause pleural effusion

A

methotrexate

18
Q

what does low glucose in pleural fluid suggest

A

infection, rheumatoid arthritis

19
Q

empyma necessitans

A

mass-like fluid collection through the chest wall that may rupture spontaneously.