Vascular Flashcards by Jacqueline Dinh

Clinical classification of GPA

Nasal involvement
cartilaginous involvement (hearing loss, hoarseness, endobronchial, saddle nose)

+C ANCA or PR3
pulm nodules, mass or cavitation
granulomas or giant cells on biopsy
pauci-immune glomerulonephritis

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Maintenance therapy for GPA

RTX or MTX or AZA

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Treatment of severe GPA/MPA

RTX (preferred over CYC)
and reduced dose GC

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Indications for plasma exchange in DAH

Anti GBM + ANCA
salvage therapy
Trying to prevent dialysis

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Treatment for non-severe GPA

GC + MTX

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When to avoid rivaroxaban

Hepatic impairment
CrCl<30
CYP3A4 inducers or inhibitors

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When to avoid dabigatran

CrCl <30

Better for liver

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When to avoid apixaban

severe hepatic impairment

Better for kidneys because ok until CrCl <15

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When to avoid Edoxaban

Hepatic impairment
use of rifampin

better for bad kidneys b/c ok until CrCl <15

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Treatment of VTE in malignancy

1st line - LMWH (enoxaparin)
2nd line - oral factor Xa agents (edoxaban, apixaban, rivaroxaban)

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YEARS criteria for work up of PE in pregnancy

3 criteria: 1. signs of DVT 2. hemoptysis 3. PE as most likely diagnosis

If none of criteria met and D dimer <1000 PE ruled out

If one or more of 3 criteria met and D dimer <500 PE ruled out

Most effective during 1st trimester
D-dimer should not be used alone

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Treatment of PAH in pt with sickle cell disease

endothelin-1 receptor antagonists

(ambrisentan, bosentan, macitentan

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Why avoid sildenafil in pt with PAH and ssd

increased pain crisis

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When to use calcium channel antagonist in PAH?

If patient has vasoreactivity in reponses to inhaled NO (ie pulm vaso dilator) – reduction of PAP by >10 and reaching absolute mean PAP <40

Never use for pts with RHF

preferred agents - amlodipine, dilt, nifedipine

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Endothelin receptor antagonist
Names and side effects

Anemia
Teratogenic
Bosentan– Liver injury
ambrisentan
Macitentan

DDI - cyclosporine
Bosentan - hormonal contraception, ritinovir

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Phosodiesteras type 5 inhibitor
Names and side effects

Sildenafil
Tadalafil

Hypotension
visual changes, priapism

DDI- nitrates, riociguat, alpha blockers

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Soluble guanylate cyclase stimulator

Name, effect, side effects

Riociguat
vasodilation

SE: teratogenic
hypotension, bleeding, PVOD, hemoptysis

DDI: Nitrate, PDE-5i, cigarette smoking, Maalox

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Prostacyclin analog

Name, admin route, SE

Epoprostenol – IV
Iloprost - Inhaled
Treprostinil - oral, Inhaled, IV and SC

SE: vasodilatory effects – headache, flushing, jaw pain, limb pain, n, diarrhea, dizziness
thrombocytopenia
rebound PH

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Prostacyclin receptor agonist

Selexipag

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Causes of pulmonary artery pseudoaneurysm

Infection (septic emboli, TB, syphilis pyogenic bactria and fungi (mucor and aspergillosis), most common)
Iatrogenic
trauma
Bronchogenic squamous cell carcinoma
sarcoma and metastatic sarcoma

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Treatment of pulmonary artery Pseudoaneurysm

Embolization direct coil or of the feeding vessel
Stent

First line treatment of PE in pregnancy

Low molecular weight heparin (enoxaparin, dalteparin, tinzaparin)

Duration of therapy - at least 3-6 mo and continues for at least 6 weeks postpartum

Plt threshold for VTE ppx in pt with ITP

> 30 (usually >50 for pts w/o ITP)

Markers of Heritable PAH

BMPR2
ALK-1

Markers of HHT and PAH

Alk 1 BNPR1B

Mutation in PVOD and PCH

EIF2AK4

Characteristics of pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis

PAH + venous involvement Low DLCO, out of proportion hypoxemia No left sided heart disease Mutation EIF2AK4 Lack of response or development of pulmonary edema with PAH-specific therapy CT with diffuse interlobular septal thickening, ggo mosaic, pleural effusion, enlarged PA

disease with endoglin mutation (ENG gene)

Hereditary hemorrhagic telangiectasia

Disease with FLCN gene mutation

Birt-Hogg-Dube syndrome (cystic lung disease, fibrofolliculomas, kidney tumor)

Drugs that cause PAH

Fenfen stimulants -- meth, cocaine chemo interferon alpha and beta hep c treatment

Primary treatment for CTD PH

Ambisartan and tadalafil

Risk factors for PH in HIV pt

IVDU Female cocaine use Hep C

PE characteristics that increase risk of CTEPH

unprovoked Increased BNP RH strain initial PASP on TTE >50 Delayed diagnosis of PE History of VTE or recurrent VTE

Treatment for CTEPH

Riociguat Macitentan SQ trprostinil Balloon pulm angioplasty -------------------------------- NOT sildenafil or bosentan

Group 5 PH causes

Heme dz (SSD) Metabolic disorders Chronic renal failure fibrosing mediastinitis pulmonary tumor thrombotic microangiopathy

RHS on EKG

ST depression, TWI in V1-3 R axis deviation dominant R wave in V1 Dominant S wave V5 or V6

CO calculation

SV x HR

PVR calculation

(mPAP-PAWP)/CO

SVR calculation

SVR= (mSAP-RAP)/CO

PAH risk assessment tool REVEAL lite

eGFR<60 NYAH functional class Systolic BP HR 6MWT proBNP Low risk /= 9 used for monitoring treatment

PAH risk assessment 4 STRATA (or 3 Strata)

Estimate 1-yr mortality WHO-FC 6MWT BNP Low risk 0-3% inter-low 2-7% Inter-high 9-19% High >20%

initial tx for pt w/o cardiopulm comorbid and low/intermediate risk PAH

Endothelia receptor antagonist + PDE5i

initial tx for pt w/o cardiopulm comorbid and High risk PAH

ERA + PDE5i +/- IV/SQ Prostacyclin analog

initial tx for pt with cardiopulm comorbid and low/intermediate risk PAH

Monotherapy with PDE5i or ERA

If low intermediate on strata 4 what changes to make to PAH meds

Add PRA OR switch from PDE5i to sGCs

If High intermediate or high on strata 4 what changes to make to PAH meds

Add IV/SQ PCA and/or eval for lung transplant

Who needs indefinite AC for VTE?

Men - unprovoked Women with risk factors - hyperpigmentation, edema or redness of leg - D-dimer >250 while on AC - Obesity (BMI>30) -Older age (>65) If low risk (0-1 risk factor) and unprovoked in women can stop after 3 mo

Predictors of respiratory failure in ANCA vasculitis DAH

SpO2/FiO2 <450 Elevated CRP >25 Elevated neutrophils BAL >30%

What % of hemosiderine laden mac on BAL suggestive of DAH

>20%

DAH in HF

Capillary stress failure (bland hemorrhage) NOT treated with steroids

Curaçao diagnostic classification involves four criteria—recurrent and spontaneous epistaxis; multiple telangiectasias on the skin of hands or face, or inside the nose or mouth; AVMs or telangiectasias in one or more organs, including lungs, brain, liver, intestines, stomach, and spinal cord; and a family history of HHT in a first-degree relative—with three positive criteria required for a definite clinical diagnosis of HHT.