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Pathophysiology - Respiratory > Pulmonary Vascular Diseases > Flashcards

Pulmonary Vascular Diseases Flashcards

1
Q

What is the definition of pulmonary hypertension (PH)? What is the gold standard for its diagnosis?

A

Mean pulmonary artery pressure >= 25 mmHg measured by right heart catheterization
-> Right heart cath required for definitive diagnosis

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2
Q

How can you tell if pulmonary hypertension is due to left ventricular disease or not? What are these two subsets of pulmonary hypertension called?

A

Pulmonary venous hypertension (postcapillary): If PCWP > 15 mmHg, LAP must be elevated, and thus it is likely due to LV disease

Pulmonary arterial hypertension (precapillary): If PCWP < 15 mmHg, LAP must not be elevated, and thus it is likely cor pulmonale

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3
Q

What are Groups I and II Pulmonary Hypertension?

A

Group I - Pulmonary Arterial Hypertension, can be idiopathic or have a known gene / cause behind it

Group II - Pulmonary Venous Hypertension - generally due to left heart failure

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4
Q

How is group II PH treated?

A

Treat the underlying cause

-> usually LV failure

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5
Q

What is the cause of Group III pulmonary hypertension?

A

Pulmonary diseases causing chronic hypoxemia, and pulmonary vasoconstriction results. Can be irreversible over time.

Causes include:
COPD, interstitial lung disease, high altitude exposure, alveolar hypoventilation disorders

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6
Q

How is Group III pulmonary hypertension treated?

A

Treat the underlying cause, give supplementary O2 if needed.

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7
Q

What is Group IV pulmonary hypertension?

A

Chronic Thromboembolic Disease
-obstruction of proximal or distal pulmonary arteries by PE’s from DVT’s, tumor, parasites, or foreign material leads to obstruction of blood flow or reorganization.

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8
Q

How is Group IV pulmonary HTN managed?

A

Anticoagulants, surgical removal of PE’s, and Riociguat (nitric oxide mechanism)

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9
Q

What is Group V pulmonary hypertension?

A

HTN due to miscellaneous or multifatorial issues, such as hematologic disorders, systemic disorders (sarcoidosis), glycogen storage diseases, tumor obstruction, chronic renal failure
-> treat underlying cause

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10
Q

What are the classical causes of Group I pulmonary hypertension?

A
  1. Idiopathic pulmonary hypertension
  2. Familial pulmonary hypertension (may be related to gene mutations)
  3. Associated with other conditions

etc

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11
Q

What are some “associated conditions” which PH is found with? Why are these important?

A

Congenital heart disease, collagen vascular disease (CT disease or autoimmune), HIV, drugs / toxins, portal hypertension (cirrhosis), Schistosomiasis, sleep disordered breathing

Important because these need to be ruled out as causes by various tests (i.e. LFT’s for suspected portal hypertension) when diagnosing idiopathic pulmonary hypertension

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12
Q

What is the proposed pathogenesis of idiopathic pulmonary hypertension and the prognosis?

A

Imbalance of humoral mediators:
increased TXA2, endothelin, and 5-HT which vasoconstrict

Decreased prostacyclin and NO which vasodilate

This decreases luminal size of pulmonary arteries and eventually results in medial proliferation and right heart failure

-> survival is less than 2-3 years untreated

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13
Q

What specific histological changes can be seen in idiopathic pulmonary hypertension? Who tends to get this disease?

A

More common in women. Think of girl holding two tennis rackets in sketchy

  1. Hyperplasia of intima with fibrosis
  2. Hypertrophy of the media -> SM cells
  3. In situ thrombi from endothelial / platelet dysfunction
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14
Q

What are the telltale symptoms of pulmonary hypertension?

A

Early on, patients have no symptoms.

Later, develop dyspnea or fatigue with heavy exertion. Then at rest.

RV will begin to fail, and they complain about leg edema / abdominal swelling

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15
Q

What is the most ominous symptom that PH has progressed very far?

A

Patient starts fainting (syncope) due to lack of blood flow to left heart and then brain
-> RV can not push against this high afterload

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16
Q

What are classic signs of pulmonary hypertension?

A

Loud P2 due to high backpressure causing closing of the pulmonic valve to sound very loud.

Tricuspid regurg murmur may be heart if RV has dilated enough

Signs of right heat failure

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17
Q

What will ECG show in pulmonary hypertension?

A

Enlarged P waves due to RA hypertrophy

Large R in V1, and T-wave inversion in V1-V3 showing RV strain and hypertrophy

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18
Q

Why are pulmonary function tests and ventilation perfusion (V/Q) scans important when diagnosing PH?

A

Pulmonary function tests - can rule out a Group III disorder

Ventilation perfusion scan - can rule out thromboembolic disease (Type IV) as a cause

19
Q

Why is ECG important for PH diagnosis?

A

Looks for LV function

-> can differentiate from Group II disease

20
Q

What is the treatment of pulmonary hypertension based on, and what test is used to determine this?

A

Treatment is based on functional classes: level of dyspnea with physical activity (Class I-IV)

Six minute walk test while measuring oxygen saturation and heart rate
-> prognosis is worse in patients with short walking distances

21
Q

What is the general treatment used for ALL groups of PH?

A

Supplemental O2 (keep above 90%) and diuretics

22
Q

What classes of drugs are used to treat Group I pulmonary artery hypertension?

Know everything on this

A
  1. Endothelin receptor antagonists (bosentan) - end of the line for boss man Stan
  2. PDE5 inhibitors (sildenafil, tadalafil)
  3. Guanylate cyclase stimulators (riociguat, also used for Type IV)
  4. Prostacyclin derivatives - i.e. think iLow to ePro! epoprostenol, iloprost
  5. DHP calcium channel blockers (rarely) - almost never works
23
Q

What are the clinical sydromes associated with venous thromboembolism (VTE)?

A

Remember the 7 P’s

  1. Proximal DVTs / pelvic thromboses
  2. Post-thrombotic syndromes - venous insufficiency / swelling
  3. Predisposition to future VTE
  4. Pulmonary embolism
  5. Pulmonary hypertension - (Group 4)
  6. Paradoxical emboli
  7. Perish - sudden death
24
Q

What is Virchow’s triad which can predispose to DVT’s?

A
  1. Stasis
  2. Endothelial injury
  3. Hypercoagulable states
25
Q

What are common causes of stasis and endothelial injury?

A

Stasis - surgery requiring > 30 min anesthesia, sitting, stroke, heart failure

Endothelial injury - Injury, inflammation, toxins

26
Q

What specific hospital patient groups are at highest risk of DVT?

A

Orthopedic procedures (hip or knee), major trauma, and spinal cord injury

27
Q

When are you most susceptible to VTE during pregnancy?

A

Near term or immediately post-partum

-> when you are most immobile

28
Q

What are the most classic signs of pulmonary embolism?

A

Chest pain, dyspnea, hemoptysis (from lung infarcts), tachypnea

29
Q

What diagnostic test effectively rules out pulmonary embolism if it comes back negative (very sensitive)?

A

D-dimer

  • > a product of fibrinolysis
  • > not specific
30
Q

What tests are used in the differential of PE to rule out other possible / likely conditions with these symptoms but will not definitively diagnose PE?

A

CXR - findings may be subtle or absent, but can rule out pneumonia or pnuemothorax

ECG - can rule out AMI or pericardial effusion. For PE, EKG would show tachycardia, and signs of RV strain

ABG - nonspecific, but if PaO2 >80, PE is unlikely

31
Q

What is viewed as basically the most clinically practical method for diagnosis of PE and what are its main drawbacks?

A

A contrast CT scan of the chest

Problems:
Morbidly obese patients may not fit
Renal insufficiency - contrast can put them in renal failure
Contrast allergy
Dyspneic patients who keep moving
Low sensitivity for very small PE's
32
Q

What should be done if a patient has renal insufficiency and you need to diagnose PE?

A

Ventilation perfusion scans

  • > also used in Group IV PH
  • > ventilation by radioisotopes will be much greater than perfusion

-> results are often intermediate and inconclusive

33
Q

What is legitimately the gold standard for diagnosis of PE which is rarely done? Why?

A

Pulmonary angiogram
-> will show an intravascular fillding defect in area of clot

It is invasive, technically difficult, and very expensive

34
Q

What is typically used for a proxy for definitive diagnosis of PE?

A

Definitive diagnosis of DVT -> much easier to diagnose, and anticoagulation treatment is the same

35
Q

How is DVT typically diagnosed?

A

Doppler ultrasound

  • > easy to do with high sensitivity and specificity
  • > CT scan is almost never done
36
Q

How is VTE diagnosed in pregnancy?

A

Doppled ultrasound of the leg first. If cannot find DVT, do CT angiogram of chest
-> mom dying is worse than possible fetal issues

37
Q

How is DVT / PE generally treated?

A

Initiate heparin or heparin derivative immediately

Start oral anticoagulants with warfarin or newer agents, make sure to overlap therapy with heparin while warfarin comes online (bridge therapy)

38
Q

What are the main advantages of the Xa and IIa inhibitors over warfarin?

A

No need to check the INR

39
Q

When is the only time you use thromobolytic therapy?

A

Generally, only give alteplase if the patient is hemodynamically unstable (severe cardiovascular compromise, or risk of limb loss with DVT)
-> high risk of bleeding

40
Q

What are the contraindications for thrombolytic therapy?

A

Recent intracranial bleeding, surgery, stroke

41
Q

What are the prophylaxis procedures for VTE in general surgery, orthopedic surgery, and medical patients who are very immobile (CHF, respiratory disease)

A

General surgery: moderate / high risk patients get UFH or LMWH

Orthopedic surgery: LMWH, fondaparinux, AND warfarin

Medical patients: Low dose UFH or LMWH (same as surgery)

42
Q

What is a general added intervention done if patient has chronic thromboembolism with pulmonary hypertension and a PE (Group IV PH)?

A

Surgery!

Very rarely done for acute PE

43
Q

If anticoagulation is contraindicated, what can be done to prevent DVT / PE?

A

Inferior vena cava filter

-basic which is inserted in IVC and catches any clots coming from legs or pelvic area

44
Q

How long should patients with PE / DVT continue on anticoagulation therapy?

A

Give oral anticoagulation for minimum 6 months (or 3 if there was a clear transient risk factor), or lifelong if there are persistent risk factors

Pathophysiology - Respiratory (24 decks)

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