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Pulmonology > PE/DVT > Flashcards

PE/DVT Flashcards

1
Q

Describe why patients can develop bronchospasm and wheezing in PE?

A

Platelet aggregates and platelet breakdown products can cause bronchoconstriction

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2
Q

What is the reason for hypoxia seen in PE?

A

Dead space ventilation.

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3
Q

What therapy should be started as soon as PE is suspected?

A

anticoagulation therapy (given the patient does not have allergies to anticoagulant medications). do not wait for confirmed diagnosis

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4
Q

Pathognomonic EKG finding seen in minority of patients with PE? Evidence of what?

A

S1Q3T3, evidence of right ventricular strain

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5
Q

90% of emboli originate from where?

A

DVT in legs

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6
Q

Upper extremity vein thrombosis can occur when?

A

if patient has central venous cath placed

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7
Q

Besides blood, what are some other forms of emboli?

A

air, tumor, amniotic fluid, talc, fat

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8
Q

What is one way to prevent patient from getting air emboli if patient is having a central venous line put in?

A

put them in Trendelenburg position. head down increases venous pressure.

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9
Q

Classic example of tumor emboli?

A

renal cell carcinoma, go in IVC

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10
Q

Virchows triad. What is it referring to? What 3 components?

A

3 predisposing factors for clot formation

stasis, hypercoagulable state, endothelial injury

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11
Q

Biggest congenital mutation leading to hypercoaguable state?

A

Factor V Leiden mutation

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12
Q

Besides Factor V Leiden mutation, what other congenital disorders can cause a hypercoaguable state?

A 
Prothrombin G20210A mutation
Protein C & Protein S deficiency
Antithrombin III deficiency
Increased levels of Factor H
Dysfibrinogenemia, Homocystinemia (these 2 less important)
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13
Q

What form of lung cancer causes a hypercoaguable state?

A

adenocarcinomas

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14
Q

Factor V Leiden mutation. How does this cause hypercoaguable state

A

Resistance to activated protein C (natural anticoagulant).

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15
Q

Name most common types of acquired hypercoaguable states?

A 
Estrogen use
hormonal changes of pregnancy
Malignancy (esp adenocarcinoma)
Nephrotic syndrome
Heparin Induced thrombocytopenia
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16
Q

what antibodies are produced in Heparin induced thrombocytopenia? Describe mechanism

A

5-10% of patients that receive heparin developed anti platelet-4 antibodies.

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17
Q

Clinically, what would you observe in patient that possibly has HIT (heparin induced thrombocytopenia)?

A

Gave heparin, patient platelet count drops and they develop arterial or venous clot (as evidenced by UA)

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18
Q

Diagnosed patient with HIT, what are the next 2 steps in order

A
  1. STOP Heparin

2. Give non heparin anticoagulant (Factor X inhibitor, direct thrombin inhibitor)

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19
Q

List common causes of endothelial injury that can increase risk of PE

A

homocystinemia, autoimmune injury, trauma, surgery, malignancy and treatment of malignancy

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20
Q

List determinants of physiologic consequences of PE (i.e. what determines what happens to people)

A
  • Size of the embolus
  • Cardipulmonary status/reserve (80 year old man can’t tolerate the same PE in 20 year old kid)
  • Neurohormonal substances
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21
Q

What happens to pulmonary vascular resistance in PE?

A

Increases

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22
Q

What 2 endogenous compounds are released contributing to vasoconstriction in PE

A

Serotonin (released from platelets)
Endothelin-1 (production increases)
-both of these combine to increase bronchoconstriction & vasoconstriction

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23
Q

PE effect on J receptors?

A

Reflexively stimulated during PE, causing alveolar HYPERventilation

24
Q

Vasodilatation of uninvolved vasculature is a compensatory mechanism in PE. Describe how.

A

Vessels that are distal to site of PE will undergo vasoconstriction (since they aren’t participating in gas exchange currently). Sites that are not affected by PE will undergo vasodilation (increase gas exchange and perfusion); therefore, the overall increase in vascular resistance is not as high as you would think (i.e. a left pulmonary artery PE does not cause vascular resistance to double within the lungs)

25
Q

What gas exchange abnormalities occur with a PE?

A

Hypocapnia (due to hyperventilation)
Hypoxemia (due to low O2 in blood)
Wide A-a gradient

26
Q

What is the most favorable outcome that occurs with clots in the lung? (don’t overthink)

A

Fibrinolysis,
- Smaller the clots, easier it is to break them up. Normal healthy patients have small PEs all the time that are broken down via fibrinolysis

27
Q

Best radiologic test for diagnosing PE?

A

Helical (Spiral) CT: CT Pulmonary angiography

28
Q

Most common complaint from a patient with acute PE?

A

SOB

29
Q

In PE: What happens to each (increase or decrease)?

HR, RR, CO2, O2

A

HR, RR Increase

CO2, O2 decrease

30
Q

t-PA (tissue plasminogen activator) is best used in acute PE associated with ___?

A

shock. If patient has PE & goes into shock, give t-PA. otherwise, use anticoagulant therapy

31
Q

CXR of patient with acute PE most likely to reveal ___?

A
  • nothing, will be normal (most common)

- Atelectasis or decrease in lung volume (next most common, but much less common than CXR being normal)

32
Q

PE: PaO2 low or high?

A

low

33
Q

PE: PaCO2 low or high?

A

low

34
Q

PE: A-a gradient?

A

increased

35
Q

PE: WBC count?

A

normal or slightly elevated

36
Q

PE: What lab value is elevated as a result of fibrinolysis?

A

D-dimer

37
Q

PE: What peptide is elevated? Why?

A

BNP (brain natriuretic peptide) due to right ventricular stretch

38
Q

PE: What cardiac protein can be elevated? Why?

A

Troponin, if coronary circulation becomes compromised

39
Q

Fact. PE can cause elevated LDH and bilirubin with normal transaminases

A

Know this. couldn’t think of a way of asking it in flashcards

40
Q

(High or low?) clinical suspicion + (high or low?) probability V/Q scan = confirms PE?

A

High CS + High probability V/Q scan confirms PE

41
Q

(High or low?) clinical suspicion + (high or low?) probability V/Q scan = excludes PE?

A

Low CS + Low probability V/Q scan excludes PE

42
Q

Gold standard for diagnosing PE? Downside to this gold standard? Alternative used now (best choice)

A

pulmonary angiography. Downside: Invasive. Helical CT scanning used

43
Q

Normal perfusion scan and PE?

A

Excludes it.

44
Q

> 90 % of PE comes from (upper or lower) extremities?

A

lower

45
Q

Recurrent emboli are rare if ___?

A

rare if there is no proximal lower extremity DVT

46
Q

TEST QUESTION: In low clinical probability setting, what 2 factors are important to essentially rule out PE or DVT?

A

If perfusion scan is normal and d-dimer less than 500 –> possibility for DVT is really low

47
Q

PE causes interventricular septum to usually move in what direction?

A

towards left ventricle. back pressure builds up in right ventricle, causing septum to push into left ventricle

48
Q

Best diagnostic modality for DVT?

A

B mode ultrasonography to demonstrate noncompressibility

49
Q

Best pharmacologic prophylaxis to prevent DVT in ICU patient?

A

5000 IU subcutaneous heparin every 8 hours (also low molecular weight heparin good too i.e. enoxaparin)

50
Q

Ex of low molecular weight heparin?

A

Enoxaparin

51
Q

Best assay to monitor low molecular weight heparin adequacy ?

A

Factor Xa activity

52
Q

Best assay to monitor warfarin adequacy?

A

Prothrombin Time (PT)

53
Q

Best assay to monitor heparin adequacy?

A

activated Partial Thromboplastin Time (aPTT) or Factor Xa activity

54
Q

Most common reason for failure in treating patients for PE?

A

not giving anticoagulant therapy within the 1st 24 hours

55
Q

Triad of Fat Embolism?

A

Mental status changes, thrombocytopenia, petechiae in the chest and neck

Pulmonology (31 decks)

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