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.
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
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
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
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)
6
Q
What is the most common congenital bleeding disorder?
A
Type I Von Willebrand Disease
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)
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
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
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)
11
Q
What do PTT and PT (INR) measure?
A
PTT –> intrinsic pathway (8/9/11/12)
PT (INR) –> extrinsic pathway (7)
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)
13
Q
What could be a cause of an abnormal PTT/INR?
A
- traumatic venipuncture, heparin contamination, hemolysis, lipemia, increased hematocrit, hyperbilirubinemia
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
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)
16
Q
What is Virchow’s triad?
A
- factors leading to thrombophilia
1. Endothelial injury
2. Stasis
3. Hypercoagulability
17
Q
What are some factors that can cause thrombophilia?
A
- Cancer, pregnancy, OCPs, androgens, post-op, myeloproliferative neoplasm
18
Q
What are two cofactors involved in the coagulation pathway?
A
calcium and phospholipids
19
Q
What can cause superficial vein thrombosis?
A
IV/catheters/etc.
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
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
22
Q
Symptoms of a DVT?
Symptoms of a PE?
A
- swelling, painful, red, warm
- SOB, chest pain (pleuritic), hemoptysis
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
24
Q
What is a measure of DVT likelihood?
A
Well’s Score
25
When should you consider hereditary testing for VTE?
- unprovoked, recurrent, family Hx, purpura fulminans in young
26
How long should DVT treatment be? What can you give for prophylaxis?
- 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
27
What reverses warfarin? Heparin
Warfarin --> vitamin K
Heparin --> protamine
28
What is the MOA of DOACs?
Which DOACs can be given as monotherapy for VTE?
- 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
Benefits of DOAcs
Cons of DOACs (who cannot take them?)
(+) --> 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
Definition of pulmonary HTN
- Mean pulmonary pressure (PAP) greater than 20mmHg
- Note: this is in the pulmonary circulation, not bronchial
31
What is the transpulmonary gradient? How is it calculated? What is a normal value?
- 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
How do you calculate pulmonary vascular resistance? What is a normal value?
PVR = TPG/CO
- normal is 150-250
33
Different Groups of Pulmonary Hypertension
Which groups do pre-capillary HTN and isolated post-capillary PH belong to?
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
Pre-capillary PH vs isolated post-capillary PH?
pcPH --> increased TPG (arterial)
ipcPH --> normal TPG (venous)
35
How does Pulmonary HTN kill you?
- 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
Symptoms of Pulmonary Hypertension?
How to diagnose?
Treatment?
- 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
What does a long history of productive cough suggest?
Chronic bronchitis often secondary to smoking
38
Causes of bronchiectasis?
Causes of hemoptysis?
Causes of atelectasis?
- 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
Which cancer is often linked to smoking and is more common in men?
What are histo signs of this cancer?
- Squamous cell carcinoma
- single cell keratinization, keratin pearls, intercellular bridges
40
Which cancers are centrally located?
- Squamous cell carcinoma
- Small cell carcinoma
41
What are common lung metastases sites?
- Brain, Bone, Liver, Adrenal gland
42
What does an adenocarcinoma look like? What does small cell cancer look like?
- glandular appearance, mucus formation
- small dark cells in non-cohesive clusters, hyperchromatic nuclei, absent nucleoli, scant cytoplasm, crush artifact (DNA strands)
43
What is Pancoast syndrome?
- 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
What is extrinsic allergic alveolitis?
- hypersensitivity pneumonia (i.e. mushrooms)
- chronic interstitial inflammatory infiltrate, granulomas
- treat w steroids
45
Heparin
- how does it work?
- different forms?
- 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
Pros of LMWH
Cons of LMWH
(+) --> decreased risk of thrombocytopenia compared to unfractionated heparin, good for chronic use
(-) --> injection
47
Warfarin (aka Coumadin)
- how does it work?
- 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
Pros of Warfarin
Cons of Warfarin
(+) --> 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
Percutaneous Coronary Intervention (PCI)
Percutaneous Transluminal Coronary Angioplasty (PTCA)
- 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
P2Y12ADP Receptor Inhibitors
Which can you not give in surgery
- 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
Thrombin receptor antagonist
- voraxapar
- cannot use if active stroke or bleeding, VERY high risk of bleeds
52
Clot busters (thrombo/fibrinolytics)
- TPA --> activates plasmin
- need catheter access
- use during MI/ stroke/ VTE/ PE if severe risk outweighs the increased bleed risk
53
How does dosing of warfarin with LMWH work?
- 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
What are some anticoagulant drug limitations based on kidneys/ liver/ blood?
- LMWH and DOACs are dependent on renal excretion
- DOACs are dependent on liver metabolism
- microcytic anemia may indicate active bleeding
55
Which anticoagulants are often first line/ safest in terms of major bleeds?
Which anticoagulant can be taken in pregnancy?
- DOACs
- LMWH
56
What treatments are appropriate for cancer associated thrombosis?
- DOACs as long as there is no increased risk of bleeds
- If there is a high bleeding risk or GI cancer --> LMWH
57
Stable vs unstable CAD
- stable --> lifestyle disease, plaques, 70%+ occlusion
- unstable --> morbid disease, thrombus (due to shear stress, oxidative stress, inflammation), any size
58
Treatments for CAD
- 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
What are some platelet agonists?
- serotonin, epinephrine, ADP, TXA2, collagen, thrombin, tissue factor
60
Aspirin (ASA)
- How does it work
- When is it recommended
- concerns
- 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
Explain the mechanism behind SOB in P/E
Acute hypoxemia due to V/Q mismatch --> chemoreceptors --> increased respiratory drive
62
CHADS65 Criteria
CHADS2 Criteria
- 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
What factors can affect INR?
- Diet (low vitamin K intake when sick)
- Interactions (metronidazole will increase INR)
- Diarrhea
- Non-compliance with medication
64
Course of action if INR is minorly supratherapeutic (under 5)?
omit one dose or lower dose
65
What is bridging?
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
Proximal deep veins
Distal deep veins
Superficial veins
- 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
What are DOAC contraindications?
- liver disfunction, eGFR <30, pregnant or breastfeeding, extremes of body weight, impaired absorption in the stomach or small intestine
68
What is the indication for an IVC filter?
- acute VTE and anticoagulation contraindication
- can provoke thrombosis itself, take out ASAP
