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Pulm Block > Week 5- Pulmonary Vascular Disease > Flashcards

Week 5- Pulmonary Vascular Disease Flashcards

1
Q

Define plasma and serum

A

Plasma: the cell-free fluid of blood with clotting factors intact

Serum: the cell-free fluid of blood with the clotting factors removed (used for most blood tests, except clotting assays)

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2
Q

Define hemostasis and Virchow’s triad of normal hemostasis

A

mechanism that ensures that blood stays within the vascular system.

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3
Q

How does clotting happen?

A

Primary clotting

  • epithelial injury results in activation, adhesion and aggregation of platelets at the site of injury forming a platelet plug

Secondary clotting

  • the clotting cascade results thrombin activation, and in fibrin reinforcing the platelet plug
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4
Q

Describe the clotting cascade in basic terms (initiator, major players)

A

Extrinsic pathway:

  • tissue factor from damaged tissue initiates
  • occurs at plateley membrane

Intrinsic pathway

  • activated by surface contact with the damaged vessel.

Common pathway

  • Converge on factor Xa
  • Both result in prothrombin–>thrombin (factor IIa), fibrinogen–> fibrin
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5
Q

What is the timeline for clotting after vascular injury?

A

The cascade happens in about 30 seconds, and then the extrinsic pathway is inhibited

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6
Q

How is fibrinogen activated?

How is fibrin strengthened?

A
  • Fibrinogen (soluble) is cleaved by thrombin into a fibrin monomer which dimerizes and the polymerizes (insoluble)
  • Factor XIIIa crosslinks fibrin polymers
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7
Q

What is the role of vitamin K in clotting?

A

Vitamin K is required to carboxylate some clotting factors (Glu–>Gla). This modification is necessary to allow the factor to bind calcium, and the calcium is necessary to target the factor to the platelet membrane

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8
Q

How do coumarol drugs work?

How does heparin work?

A

Coumarol drugs inhibit reduction of vitamin K in the liver, thereby stopping the gamma carboxylation of clotting factors, and making them ineffective (inactivatable).

Heparin accelarates antithrombin activity.

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9
Q

How is clotting terminated ?

A
  • antithrombin gets trapped in the clot
  • thrombin will bind thrombomodulin (on endothelial cell membranes) and together activate protein C and protein S, which inactivate the clotting factors found on platelet cell surface. This inactivates prothrombin–> thrombin.
  • Tissue factor pathway inhibitor (TFPI)
  • activated clotting factors that flow past the site of injury are degraded by proteases in the blood so that the clot stays local
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10
Q

How is a clot degraded (fibrionolysis) after clotting has stopped?

A
  • plasminogen (a plasma protein) is activated by somthing (e.g. urokinase, tPA)
  • It cleaves fibrin and produces D-dimer (AKA D2E fragments)
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11
Q

What is prothrombin time? How is it measured? AKA?

A
  • prothrombin time is measured by taking plasma and incubating with thromboplastin (contains tissue factor) and timing how long it takes to clot.
  • Measured extrinsic and common pathways
  • Given as an **international normalized ratio (INR) **
  • Normal is 1, on coumarol INR >1
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12
Q

What is activated partial thromboplastin time (PTT)? How is it measured? What does it measure?

A
  • plasma is incubated with kaolin (clay..) and thromboplastin but no tissue factor and time to clotting is measured
  • measures intrinsic and common pathways
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13
Q

What is the classification of thrombotic disease

A
  • Venous thromboembolism
  • Arterial thrombosis (usually associated with atherosclerosis)
  • Capillary thrombosis (usually associated with hemolytic anemias)
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14
Q

What are the different kind of venous thromboembolism disease?

A
  • superficial vein thrombosis (SVT) (from IV, catheters, etc..)
  • Migratory SVT (sign of malignancy)
  • DVT
  • DVT complications (PE, post-phlebetic syndrome)
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15
Q

What are the heriditary and acquired risk factors for venous thromboembolic disease?

A

Acquired (much more common)

  • Immobility
  • age
  • pregnancy
  • obesity
  • trauma
  • surgery
  • malignancy
  • meds (OCP)
  • inflammation
  • hyperviscosity
  • antiphospholipid syndrome

Hereditary

  • Factor V Leiden (more resistant to breakdown) (5% of gen. pop)
  • prothrombin mutation
  • protein C or S deficiency
  • antithrombin-3 deficiency
  • increased factor 8
  • increased homocysteine
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16
Q

Virchow’s triad for thrombosis and the risk factors that fit under each

A

stasis

  • immobility
  • age
  • pregnancy
  • obesity

vascular injury

  • surgery
  • trauma
  • malignancy
  • inflammation
  • homocysteine

hypercoagulability

  • hereditary thrombophilias
  • preganancy
  • age
  • malignancy
  • hyperviscosity
  • OCP
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17
Q

How does the coexistance of multiple VTE risk factors actually affect risk of VTE?

A

Acquired + acquired

Acquired +heriditary

are the most common combinations. They have supra-additive effect (having 2 risk factors more than doubles risk)

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18
Q

What is the common clinical presentation of DVT?

A
  • unilateral leg swelling, painful, red and warm (inflammation…must rule out cellulitis)
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19
Q

What are typical and atypical presentations of PE?

A

Typical

  • SOB, chest pain, hemoptysis

Atypical

  • abdo pain, syncope, fever, cough, seizures
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20
Q

What is the common clinical presentation of post-phlebitic syndrome? What is the pathophysiology? What is the treatment?

A
  • swelling, pain, ulcers, rash (the ulcers and rash because it is a more chronic thing than DVT)
  • this happens because of valve damage/vavular insufficiency after a DVT
  • compression stockings
21
Q

Which tests can you do for DVT?

A

Radiologic

  • ultrasonography: better for proximal DVTs
  • spiral CT

Less common radiologic

  • V/Q scan (high radiation)
  • angiography (invasive)

D-dimer levels

22
Q

What’s the specificty and sensitivity of D-dimer for DVT?

A

High sensitivity

Low specificity

23
Q

When would you do etiologic testing for DVT? What would you test?

A

In unprovoked and/or recurrent and/or positive family history. BUT inherited thrombophilia unlikely to change treatment.

Test for:

  • antithrombin-3
  • protein C and protein S
  • prothrombin gene mutation
  • acquired causes: lupus inhibitor, antiphospholipid antibodies
24
Q

What is the treatment for DVT?

A

heparin and coumadin with 5 days overlap, then on coumadin for 6 months

25
What is the mechanism of action of heparin? Is there any difference between unfractionated heparin (UH) and LMW heparin?
MOA * activates antithrombin III (1000x increase), which inhibits factor Xa and thrombin * UH inactivates both * LMWH inactivates factor Xa really well, but less than half the chains are long enough to inactivate thrombin too. SE * heparin induced thrombocytopenia
26
What are the advantages of LMWH over UH? Disadvantages?
LMWH has: * decreased heparin resistance * doesn't need laboratory monitoring * higher bioavailability * longer half life * less inhibition of platelet function * lower incidence of thrombocytopenia (HIT) BUT * UH can be more readily reversed with protamine sulfate * UH is safe in patients with renal failue
27
What is the antidote for heparin?
Protamine sulfate \*\*UH is easier to reverse than LMWH\*\*
28
How soon does heparin start working? How soon does warfarin start working? Why?
Heparin * immediately Warfarin * ~72 hr delay while the vitamin-k dependent clotting factors are cleared from the blood.
29
What are the indications for warfarin?
* DVT prophylaxis +/- treatement * AFib prophylaxis * valvular stenosis * heart valve replacement * MI * antiphospholipid syndrome
30
What are contraindications for warfarin?
* hypersensitivity to warfarin * hermorrhagic tendency or risk * inadequate lab monitoring available * vitamin K deficiency Drugs * NSAIDs * Cholestid (binds Cho in the gut)
31
What are side effects of warfarin?
* hemorrhage * skin necrosis * purple toe syndrome * microembolization * tetratogen
32
what are 2 important pharmacokinetic features of warfarin?
* highly bioavailable * 99% protein bound * can be antagonized by vitamin K
33
What are thrombolytic agents? What are indications and side effects of thrombolytic agents?
Thrombolytic agents are plasminogen activators * tissue plasminogen activator (tPA) * streptokinase * urokinase They are indicated in submassive and some massive PE. Must be judicious because sometimes they just accelarate the clot break-down but at increased risk of intracranial bleed. They are contraindicated in patients on warfarin or heparin. Main side effect is hemorrhage especially intracranial.
34
What veins to DVTs usually happen in?
Iliac Femoral Popliteal Tibial
35
What is the clinical presentation of a PE?
* new onset dyspnea, or subacute (exertional) dyspnea * chest pain * hemoptysis
36
What is the differential for a suspected DVT?
* cellulitis * muscle pull or tear * joint related * ruptured Baker's cyst * peripheral edema (this is usually bilateral)
37
What is the diagnostic approach to DVT?
* Symptoms & SIgns--\> Well's criteria gives low, moderate or high score * D-dimer (negative test rules out, positive test warrants imaging) * U/S of the leg (look for thrombus, or no "wink" when vessel is compressed * If still not conclusive, repeat U/S after 7 days.
38
What is the diagnotic approach to PE?
* Signs & symptoms --\> Well's criteria gives low, moderate or high risk * D-dimer (negative test rules out) * Imaging: CT scan (1st line), V/Q scan (if CT contraindicated) * Further imaging if inconclusve
39
What is the treatment for venous thromboembolism? (common Tx, for submassive, and massive PE, recurrent PE)
1. Anticoagulation * heparin +warfarin, then warfarin for 3-6 months * rationale: heparin works immediately, warfarin takes 72h and may have a transient hypercoaguable state * once thrombus is there, _high risk of extension_. * monitor for bleeding, HIT 2. Thrombolytic therapy * for sub-massive and some massive PE (e.g. hypotensive/hypoxemic/RHF) 3. Thrombectomy * Only for acute, massive PE (e.g. saddle embolus). Rarely used 4. IVC filters * when anticoagulants are contraindicated * when emboli are recurrent
40
What is the route of administration of UH and LMWH?
UH: IV LMWH: subcutaneous injection
41
What happens when patients develop HIT?
Heparin-induced thrombocytopenia: immune-mediated destruction of platelets. Patient must be taken off heparin and put on a different anticoagulant. They can never be on heparin again.
42
What are two new oral anticoagulants to be aware of?
Dabigatran: direct thrombin inhibitor Rivaroxiban: factor Xa inhbitor
43
IVC filters prevent _______ but increase the risk of \_\_\_\_\_\_\_
PE DVT
44
What is the pulmonary pathophysiology of acute left ventricular failure?
Pressure/volume are increased in the left heart, which is continous with the pulmonary capillary beds. This causes pulmonary congestion..the alveoli fill with fluid (messes with surfactant and gaa exchange ability), RBCs escape capillaries.
45
What is the pulmonary physiology of chronic left ventricular failure?
Alveoli are still very congested, but the RBCs are mostly contained within capillaries. Microhemorrhage of these will give rusty colored sputum
46
What will the sputum look like in acute vs. chronic heart failure
Acute: more likely to be pink and frothy Chronic: more likely to be rusty colored
47
What is the pulmonary pathophysiology of masive, medium and small emboli?
Massive: obtructs major pulmonary arteries--\>dyspnea and death Medium: obtructs medius pulmonary arteries. More likely to infarct with pre-existing lung disease. Often wedge infarcts Small: obstructs small vessels --\> fibrosis of the obstructed vessel, recanulization around blocked vessel (but doesn't return ot original function)
48
What is cor pulmonale?
Hypertrophy of the right ventricle in response to pulmonary hypertension (increase in myocyte size)
49
What can happen to the right ventricle in acute obstruction?
RV failure due to increased pressure (afterload).

Pulm Block (10 decks)

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