Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med School > DVT > Flashcards

DVT Flashcards

1
Q

Tobacco Use Disorder (DSM-5)

A
  • at least 2 of the following over 12 months:
  • larger amounts, longer period, craving, time spent obtaining, affects life, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Treatments for smoking cessation? Side effects?

A
  • interventional and behavioural support VERY effective (advice from doctors helps people quit! brief intervention, etc.)
  • NRT –> transdermal patch, gum, lozenge, inhaler, etc. (no superiority of one over the other)
  • skin reactions due to adhesives, insomnia, heart palpitations, chest pain, N/V, GI, mouth ulcers, hiccups
  • Vareniciline –> partial agonist (release of DA) and antagonist (reduces effect of nicotine) at the alpha-4-beta-2 receptor, effect increases if taken with NRT
  • nausea, insomnia, constipation, weird dreams
  • Buproprion –> serotonin/NE re-uptake inhibitor
  • only given if varenciline/NRT contraindicated
  • insomnia, dry mouth, decreased appetite
  • cannot give to patients w seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stages of change in motivational interviewing?

A
  • Pre-contemplation (no intent to change)
  • Contemplation (aware of issue)
  • Preparation (intent on taking action)
  • Action
  • Maintenance
  • Repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe primary hemostasis

A
  • occurs in minutes
  • vessel wall injury –> vasoconstriction –> circulating VWF binds to sub-endothelial collagen –> VWF binds GPIb on platelets –> platelets are activated leading to a hemostatic plug at the site of injury
  • platelets aggregate via GPIIbIIIa receptors and fibrinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are signs of defects in primary hemostasis? What are possible etiologies?

A
  • excessive bruising, mucosal bleeds (epistaxis, gums, GI, menses), post-operative bleeds
  • PLATELET ISSUE –> either quantitative (thrombocytopenia) or qualitative (platelet function defect aka PFD)
  • VON WILLEBRAND DISEASE –> either quantitative (type I which is moderate, type III which is severe, or acquired/autoimmune) or qualitative (type II)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common congenital bleeding disorder?

A

Type I Von Willebrand Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What tests could you order to assess primary hemostasis issues?

A
  • CBC (platelet count)
  • Aggregometry (ability to aggregate with platelet agonists)
  • VWF testing - quantity with Ag, quality with VWF and F8 activity (VWF stabilizes F8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe secondary hemostasis

A
  • occurs over hours
  • cascade of coagulation factors leading to a fibrin net that stabilizes the hemostatic plug
  • TF (F7a) from endothelium binds F8a –> cleaves F10 to F10a
  • F10a cleaves prothrombin (F2) to thrombin (F2a)
  • Thrombin cleaves fibrinogen to fibrin, activates platelets via PAR receptors, and produces F11a which drives more thrombin production
  • Fibrin and F13a link to produce an insoluble fibrin clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe fibrinolysis.
What is an example of an antifibrinolytic drug?

A
  • occurs over days/weeks
  • tPA released by endothelium converts plasminogen to plasmin which breaks down the fibrin clot
  • this results in fibrin degradation products such as D-dimer (reflects systemic clotting activity, really only useful in ruling things OUT if low pre-test probability i.e. high sensitivity)
  • tranexamic acid (TXA)
  • Alpha-2-PI inhibits plasmin and PAI inhibits plasminogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are signs of a defect in secondary hemostasis? What could possible etiologies be?

A
  • umbilical stump bleed, joint or IM bleeds, delayed post-operative bleeding
  • Hemophilia A (F8) and Hemophilia B (F9) (both x-linked recessive)
  • An acquired inhibitor (most common is against F8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do PTT and PT (INR) measure?

A

PTT –> intrinsic pathway (8/9/11/12)
PT (INR) –> extrinsic pathway (7)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is INR standardized for? What is considered normal?

A

Standardized for warfarin therapy (should be 2-3)
1 is considered normal (including if on DOAC/ heparin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What could be a cause of an abnormal PTT/INR?

A
  • traumatic venipuncture, heparin contamination, hemolysis, lipemia, increased hematocrit, hyperbilirubinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do the results of a PTT mixing study indicate?

A
  • Mix patient and normal plasma
  • If clot time corrects it is a factor issue
  • If it does not correct there is an inhibitor present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some examples of natural coagulation inhibitors?

A
  • Protein C and S (inactivate F5a and F8a, vitamin K dependent)
  • Antithrombin (prevents cleaving of prothrombin to thrombin)
  • Tissue factor pathway inhibitor (TFPI - inhibits TF aka F7a)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Virchow’s triad?

A
  • factors leading to thrombophilia
    1. Endothelial injury
    2. Stasis
    3. Hypercoagulability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some factors that can cause thrombophilia?

A
  • Cancer, pregnancy, OCPs, androgens, post-op, myeloproliferative neoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are two cofactors involved in the coagulation pathway?

A

calcium and phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can cause superficial vein thrombosis?

A

IV/catheters/etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors for VTE?

A
  • immobility (in-patient hospitalization), age, pregnancy, obesity, trauma, surgery, malignancy, OCPs, inflammation, antiphospholipid Ab syndrome
  • hereditary causes –> protein C/S/antithrombin deficiencies, factor V Leiden, increased F8
  • these risks are supra-additive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Post-Thrombotic Syndrome

A
  • chronic venous insufficiency leading to venous HTN
  • edema, hypoxia, inflammation, swelling, pain, ulcers, rash/ skin changes
  • consider TPA to prevent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Symptoms of a DVT?
Symptoms of a PE?

A
  • swelling, painful, red, warm
  • SOB, chest pain (pleuritic), hemoptysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Best imaging methods for DVT? P/E?

A
  • Compression U/S best for proximal DVT
    - if (+), venous compression will be limited or gone
  • CT pulmonary angio for P/E
    - will see filling defect, failure of PA opacification
    - V/Q scan is an alternative (no contrast or radiation
    but takes longer and less accesible)

*VQ scan is best screening tool for CTEPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a measure of DVT likelihood?

A

Well’s Score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When should you consider hereditary testing for VTE?

A
  • unprovoked, recurrent, family Hx, purpura fulminans in young
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How long should DVT treatment be? What can you give for prophylaxis?

A
  • 3-6 months for DVT/ transient factor
  • 6-12 months fro PE
  • indefinite if high risk/ unprovoked/ persistent factor/ cancer assx thrombosis
  • LMWH or DOACs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What reverses warfarin? Heparin

A

Warfarin –> vitamin K
Heparin –> protamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the MOA of DOACs?
Which DOACs can be given as monotherapy for VTE?

A
  • direct inhibitors of thrombin (Dabigatran) (good if antithrombin deficient)
  • direct inhibitors of Factor 10a (Rivaroxaban, Apixaban, Edoxaban)
  • only rivaroxaban and apixaban are given for VTE
    *DOACs are dosed differently for different indications
29
Q

Benefits of DOAcs
Cons of DOACs (who cannot take them?)

A

(+) –> faster acting, no monitoring, fewer dietary and drug interactions
(-) –> expensive, cannot give if renal insufficiency, only Dabigatran is reversible, cannot give if antiphospholipid syndrome/ mechanical heart valves/ on rifampin or phenytoin

30
Q

Definition of pulmonary HTN

A
  • Mean pulmonary pressure (PAP) greater than 20mmHg
  • Note: this is in the pulmonary circulation, not bronchial
31
Q

What is the transpulmonary gradient? How is it calculated? What is a normal value?

A
  • Pressure decreases as the blood flows from the R heart across the pulmonary circulation to the L heart due to resistance

TPG = mean pulmonary artery pressure (mPAP) - mean left atrial pressure (LAP)

*mPAP = 2/3 dPAP + 1/3 sPAP
*LAP estimated from pulmonary capillary wedge pressure (PCWP), arterial puncture, or LVEDP via L heart catheter

  • normal is under 10mmHg
32
Q

How do you calculate pulmonary vascular resistance? What is a normal value?

A

PVR = TPG/CO
- normal is 150-250

33
Q

Different Groups of Pulmonary Hypertension

Which groups do pre-capillary HTN and isolated post-capillary PH belong to?

A

Group 1 –> pulmonary arterial HTN (increased resistance to flow)
- intima proliferation, medial hypertrophy
- CT disease, HIV, portal HTN, congen heart disease

Group 2 –> Left heart disease (high back pressure from the left heart)

Group 3 –> Lung Disease/ Hypoxia (destruction of pulmonary parenchyma)

Group 4 –> Pulmonary Artery Obstructions
- Chronic Thromboembolic PH (CTEPH)
- P/E increases PVR (mPAP over 20) leading to small
vessel arteriopathy

Group 5 –> Unclear/ Multifactorial

pcPH –> 1/3/4/5
IpcPH –> 2/5

34
Q

Pre-capillary PH vs isolated post-capillary PH?

A

pcPH –> increased TPG (arterial)
ipcPH –> normal TPG (venous)

35
Q

How does Pulmonary HTN kill you?

A
  • overtime get increase PAP/ PVR and decreased CO
  • this leads to systemic hypotension –> decreased RV tissue perfusion –> RV ischemia –> right heart dysfunction with increased right arterial pressure
  • RV overload leads to RV dilation –> LV compression
36
Q

Symptoms of Pulmonary Hypertension?
How to diagnose?
Treatment?

A
  • SOBOE, fatigue, palpitations, hemoptysis, weight gain, syncope
  • echocardiogram (will see increased systolic peak tricuspid regurgitation velocity)
  • 1 –> neurohormonal (target endothelin/ prostacyclin/ NO-SGC-cGMP pathways)
  • 2 –> underlying cause
  • 3 –> underlying cause
  • 4 –> surgical endarterectomy, balloon angioplasty (+/- NH modulation)
  • 5 –> underlying cause
37
Q

What does a long history of productive cough suggest?

A

Chronic bronchitis often secondary to smoking

38
Q

Causes of bronchiectasis?
Causes of hemoptysis?
Causes of atelectasis?

A
  • obstruction, CF, measles, pertussis
  • pneumonia, TB, bronchiectasis, cancer, SLE, trauma, P/E, left heart failure, aortic rupture, mitral stenosis, cocaine
  • obstruction or compression i.e. mucus/ malignancy/ fluid/ foreign body/ hemo or pneumothorax
39
Q

Which cancer is often linked to smoking and is more common in men?
What are histo signs of this cancer?

A
  • Squamous cell carcinoma
  • single cell keratinization, keratin pearls, intercellular bridges
40
Q

Which cancers are centrally located?

A
  • Squamous cell carcinoma
  • Small cell carcinoma
41
Q

What are common lung metastases sites?

A
  • Brain, Bone, Liver, Adrenal gland
42
Q

What does an adenocarcinoma look like? What does small cell cancer look like?

A
  • glandular appearance, mucus formation
  • small dark cells in non-cohesive clusters, hyperchromatic nuclei, absent nucleoli, scant cytoplasm, crush artifact (DNA strands)
43
Q

What is Pancoast syndrome?

A
  • Horners (anhydrosis, ptosis, constricted pupils) AND brachial plexus issues
  • Commonly caused by an apex lung tumor (OFTEN squamous cell carcinoma)
  • Will see a cavitary pancoast tumor
44
Q

What is extrinsic allergic alveolitis?

A
  • hypersensitivity pneumonia (i.e. mushrooms)
  • chronic interstitial inflammatory infiltrate, granulomas
  • treat w steroids
45
Q

Heparin
- how does it work?
- different forms?

A
  • endogenously released by mast cells
  • potentiates antithrombin I/III which inactivates 9/10/11/12 and thrombin
  • unfractionated, LMWH (dalteparin, enoxaparin), fondaparinux (only anti-10a)
46
Q

Pros of LMWH
Cons of LMWH

A

(+) –> decreased risk of thrombocytopenia compared to unfractionated heparin, good for chronic use
(-) –> injection

47
Q

Warfarin (aka Coumadin)
- how does it work?

A
  • vitamin K antagonist (essential for 2/7/9/10) - all of these factors must be depleted for it to work, although INR will increase if even one is
48
Q

Pros of Warfarin
Cons of Warfarin

A

(+) –> easily reversed, cheap, no renal excretion, effective and familiar
(-) –> slow acting so must be given with LMWH, requires monitoring, drug and dietary interactions, difficult to use with procedures, chemo interactions, nausea and vomiting

*note antigoagulants protein C+S are also vitamin K dependent

49
Q

Percutaneous Coronary Intervention (PCI)
Percutaneous Transluminal Coronary Angioplasty (PTCA)

A
  • minimally invasive but can cause restenosis, manageable with antiplatelets but more issues if diabetic
  • often use with dual antiplatelet therapy for 3m-2y post
50
Q

P2Y12ADP Receptor Inhibitors
Which can you not give in surgery

A
  • block platelet activation (primary hemostasis)
  • used in PCI
  • often part of dual antiplatelet therapy with aspirin
  • clopidogrel, ticagrelor, prasugrel
  • cannot give clopidogrel in surgery
51
Q

Thrombin receptor antagonist

A
  • voraxapar
  • cannot use if active stroke or bleeding, VERY high risk of bleeds
52
Q

Clot busters (thrombo/fibrinolytics)

A
  • TPA –> activates plasmin
  • need catheter access
  • use during MI/ stroke/ VTE/ PE if severe risk outweighs the increased bleed risk
53
Q

How does dosing of warfarin with LMWH work?

A
  • looking for therapeutic INR range of 2-3
  • have to give LMWH for a minimum of 5 days no matter what (or longer if still not therapeutic)
  • also need at least 2 days of therapeutic overlap
54
Q

What are some anticoagulant drug limitations based on kidneys/ liver/ blood?

A
  • LMWH and DOACs are dependent on renal excretion
  • DOACs are dependent on liver metabolism
  • microcytic anemia may indicate active bleeding
55
Q

Which anticoagulants are often first line/ safest in terms of major bleeds?
Which anticoagulant can be taken in pregnancy?

A
  • DOACs
  • LMWH
56
Q

What treatments are appropriate for cancer associated thrombosis?

A
  • DOACs as long as there is no increased risk of bleeds
  • If there is a high bleeding risk or GI cancer –> LMWH
57
Q

Stable vs unstable CAD

A
  • stable –> lifestyle disease, plaques, 70%+ occlusion
  • unstable –> morbid disease, thrombus (due to shear stress, oxidative stress, inflammation), any size
58
Q

Treatments for CAD

A
  • antithrombotics/ antiplatelets (revascularization)
    • clopidogrel has a 2 step metabolism, slower onset
      than prasugrel and ticagrelor
    • if high bleed risk do not continue dual anti-platelet
      therapy (DAPT) for long
  • anti-ischemics (pre/afterload, HR, contractility)
  • anti-arrhythmics/ anti-inflammatory (cardioprotection)
59
Q

What are some platelet agonists?

A
  • serotonin, epinephrine, ADP, TXA2, collagen, thrombin, tissue factor
60
Q

Aspirin (ASA)
- How does it work
- When is it recommended
- concerns

A
  • inhibits TXA2
  • better for MI in males and ischemic stroke in females
  • only recommended for males 45+ if MI risk is greater than GI hemorrhage and woman if ischemic CVA risk is greater
  • do NOT use for CV protection in women under 55 and men under 45
  • increases risk of serious bleeding events with age
61
Q

Explain the mechanism behind SOB in P/E

A

Acute hypoxemia due to V/Q mismatch –> chemoreceptors –> increased respiratory drive

62
Q

CHADS65 Criteria
CHADS2 Criteria

A
  • If over 65 (OAC), if under 65 but stroke/TIA/HTN/CHF/DM (OAC), if under 65 but CAD/arterial vascular disease (ASA)

CHF
HTN
Age over 65
DM
Stroke/TIA (2)

63
Q

What factors can affect INR?

A
  • Diet (low vitamin K intake when sick)
  • Interactions (metronidazole will increase INR)
  • Diarrhea
  • Non-compliance with medication
64
Q

Course of action if INR is minorly supratherapeutic (under 5)?

A

omit one dose or lower dose

65
Q

What is bridging?

A

Substituting LMWH for warfarin when warfarin is interrupted –> this shortens the period of time that a patient is not anticoagulated
- warfarin has a long t1/2 so it takes 5 days to normalize after starting/stopping
- especially needed if at high risk for thromboembolism i.e. mechanical mitral valve

66
Q

Proximal deep veins
Distal deep veins
Superficial veins

A
  • external iliac, femoral, popliteal (70-80%)
  • anterior tibial, peroneal, posterior tibial (20-30%)
  • greater and lesser saphenous veins

*distal DVT and superficial vein thrombosis dont always need anticoagulation

67
Q

What are DOAC contraindications?

A
  • liver disfunction, eGFR <30, pregnant or breastfeeding, extremes of body weight, impaired absorption in the stomach or small intestine
68
Q

What is the indication for an IVC filter?

A
  • acute VTE and anticoagulation contraindication
  • can provoke thrombosis itself, take out ASAP

Med School (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions