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Anticoag and fibrinolytics Flashcards

1
Q

Rheumatic Heart disease- patho

A

Patho: AI to M protein of Group A Beta Hemolytic Streptococcus (GABHS)

-> attacks Strep proteins then glycoproteins = Molecular Mimicry-> lead to inflam carditis w/ valvular damage

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2
Q

Rheumatic Heart Disease prevention and tx

A

Primary prevention: Rec GABHS early w/ ABX (strep pharyngitis)= Penicillin V
Secondary prevention: previous RF @ high risk for it again following repeat GABHS infection- PCN

TX: w/ or w/out active carditis during or following GABHS infection

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3
Q

Acute Rheumatic Fever

A

Jones criteria- 2 major or 1 major and 2 minor

Acute GABHS infection Primary prevention: most common GABHS infxn= pharyngitis= TX PENICILLIN V or G

Acute RF: ABX + ASA (aspirin for adults) or NSAIDS

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4
Q

RHD secondary prevention

A

RH but no carditis= PCN for 5 yrs or until age 21 (whichever is longer)

RF with carditis but NO RHD (valve damage)= PCN for 10 yrs or until 21 (whichever longer)

Carditis with RHD= PCN for 10 yrs or until age 40 (whichever is longer)

compliance= better with IM duh
peds= weight based

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5
Q

Angina

A

transient ischemia in the setting of a supply and demand mismatch

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6
Q

Stable angina

A

usually in the setting of coronary artery disease with narrowed vessels limiting blood flow.

Rest good/ bad exertion

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7
Q

Unstable angina

A

new onset symptoms or now occurring at rest, increasing in severity (crescendo), increasing frequency

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8
Q

tx of chronic stable angina- goals of therapy

A
  1. Reduce myocardial oxygen demand (workload)- afterload- PAMP
  2. Vasodilate to improve BF to the myocardium
  3. Improve pt function/capacity
    - short acting nitrates-> acute sympt relief
    -beta blockers-> prevention (decrease symp)
    -Long acting nitrates-> prevention
    -calcium channel-> prevention
    -Ranexa (sodium calcium channel blocker)->SM relaxation= lower afterload
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9
Q

Chronic Stable angina- Nitrates

A

Nitrates (nitroglycerin)- Short acting (sublingual tab or spray) 0.4 mg every 5 min up to 3 doses

SM relaxation (arteries and veins)-> VD and improved BF in narrowed vessels

Less preload and afterload-> less myocardial workload

Long acting nitrates: goal for prevention of symptoms and improve exercise tolerance
ISOSORBIDE MONONITRATE (ER)

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10
Q

Chronic stable angina-transdermal topical nitrates

A

Nitro-Bid
slow absorption over time for hospitalized pts- SQUEEZE OUT IN INCHES

can easily be removed by wiping off skin b4 becoming Hypotensive
DONT GET ON HANDS

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11
Q

Nitrate overview

A
  1. frequent use-> tolerance= cant use 24 hours a day
  2. SE: headache, hypotension-> low BP and vd
    3.NO PDE5 INHIBITORS-> VIAGRA/CIALIS: profound hypotension
  3. NO USE WITH RV INFARCT/ INFERIOR WALL MI
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12
Q

Chronic stable angina: Beta Blockers

A

1st line: PREFERRED PRIMARY PREVENTION AGENT IN ANGINA

Reduced HR and BP= less workload-> reduced myocardial oxygen demand

Meds: atenolol or metoprolol

SE: Bradycardia, hypotension, fatigue

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13
Q

Chronic stable angina: Calcium channel blockers

A

Second line: prevention

MOA: block Calcium influx-> decrease contractility

reduced HR and BP
SM relaxation-> vasodilation-> less afterload
decreased inotropy-> decreased workload

EX: Diltiazem (Cardizem), Amlodipine (Norvasc)
SE: Bradycardia, hypotn, peripheral edema (stasis in legs), headache, WORSEN CHF bc low contractility and no squeeze

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14
Q

Chronic stable angina: Ranolazine (Ranexa)

A

Sodium/calcium exchange pump blocker-> less intracellular calcium and sm relaxation

LAST DITCH MED AFTER ALL OTHERS WITH REFRACTORY SIMPTOMS

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15
Q

Prinzmetal (Variant) Angina

A

Secondary to Coronary Vasospasm-> from CAD or healthy
SS: at rest, night, triggered by stimulants: cocaine

Vasospasm: produce distal ischemia and typical EKG findings
TX:
Nitrates- for acute relief
Calcium channel blockers- Amlodipine

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16
Q

Thromboembolic conditions

A
  1. Acute myocardial infarction (STEMI/NSTEMI)
  2. Acute pulmonary embolism (PE)
  3. Acute Deep Vein Thrombosis (DVT)
  4. Acute arterial occlusion
  5. Acute thromboembolicm CVA (ischemic CVA)
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17
Q

Antiplatelet therapy

A
  1. Aspirin (ASA)
  2. P2Y12 inhibitors- Plavix, Effient, Brilinta
  3. GP 2B/3A inhibitors- Abciximab (Reopro), Eptifibatide (Integrillin)
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18
Q

Antiplatelet therapy- acetylsalicylic acid (ASA)/Aspirin

A

Indications: Primary therapy for ACS presentations, 2ndary prevention for all cardiovascular disease

MOA: irreversible COX-1 enzyme blocking-> inhibit arachidonic acid to thromboxane A2 which then inhibits platelet activation and vasoconstriction EFFECT REMAINS FOR LIFE OF PLT (7 DAYS)

Pill: NON ENTERIC COATING, CHEWED AND SWALLOWED

SE: GI upset/ulcer, TINNITUS (AT TOXIC DOSES)

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19
Q

Arachidonic acid pathway

A

tissue injury-> injury to phospholipid membrane-> phospholipase A2-> Arachidonic Acid which goes to Cox 1 and 2 + lipooxygenase pathway

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20
Q

Antiplatelet therapy- P2Y12 inhibitions

A

Indications: Primary tx- pts undergoing PCI, Secondary- pts w/ high risk CVD condition or stent placement

MOA: irreversibly bind to P2Y12 receptor on plt ADP binding-> decreased plt activation and aggregation

Clopidogrel- Plavix- commonly used, generic, cheapest
prodrug and metab to its active form via Cytochrome P450 pathway-> some pts are resistant bc theres doesnt work well

Prasugrel (Effient) and Ticagrelor (Brilinta) newer more costly
decreased CHANCE OF RESISTANCE THO
INCREASED RISK OF BLEEDING COMPARED W/ CLOPIDOGREL

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21
Q

Anticoagulant therapy- secondary hemostasis

A
  1. Heparins- Intrinsic pathway
  2. Vitamin K pathway- extrinsic
  3. Direct Oral Anticoagulants (DOACs)-> Direct thrombin inhibitors and Factor Xa Inhibitors= Common Pathway
22
Q

Anticoagulant therapy- Unfractionated Heparin UFH

A

found naturally in human mast cells and basophils
heparin- derived from pic intestine mucosa in china
MOA: binds and catalyzes Antithrombin 3 -> inactivate 2, 7, 9, 10

Indications: Primary tx of ACS, PE/DVT, Peripheral arterial thrombosis, DVT prophylaxis
Dosing: weight-based and condition based
SE: BLEEDING, HEPARIN INDUCED THROMBOCYTOPENIA (HIT), hypersens rxn
Reversal agent: Protamine sulfate-> binds and neutralizes

23
Q

Anticoagulant therapy- Low Molecular Weight Heparin

A

Enoxaparin (Lovenox)-> heparin molecule chopped into smaller fragments

MOA: binds and potentiates Antithrombin 3-> inhibits Prothrombin-> Thrombin conversion

less effect on clotting factors and plasma proteins than UFHmaking its anticoagulation effects more predictable-> Routine lab monitoring is not needed in most instances

Indications: same as UFH
Primary tx of ACS, PE/DVT, Peripheral arterial thrombosis, DVT prophylaxis
Dosing: weight based and condition based- MUST MOD DOSE WITH RENAL DYSFUNCTION
SE: BLEEDING AND HIT- LESS THAN UFH THO
Reversal agent: Protamine sulfate

24
Q

Heparin induced Thrombocytopenia- HIT

A

life-threatening for small percentage
Secondary to autoantibody formation to Platelet Factor 4 (PF4)
1. if plt count drops after initiation of UFH or LMWH= monitor closely- if persistent decline to < 100K= stop heparin
2. Check HIT antibody (lab test) to confirm that this is the cause
3. Switch to non heparin -> Direct thrombin inhibitors (Argatroban), Fondaparinux

25
Anticoagulant therapy: Bivalirudin (Angiomax) and argatroban (Acova)
Indications: tx of acute STEMI in pts undergiong PCI, ALTERNATIVE FOR HIT PATIENTS MOA: direct thrombin inhibitor-> prevents fibrinogen-> fibrin Dosing: iv only SE: BLEEDING, hypersens reaction n/v Reversal agent: NONE-> short half life = wait and pray
26
Anticoagulant therapy: Fondaparinux (Arixtra)
Indications: tx of acute DVT/PE, prophyl DVT, alt for HIT MOA: binds antithrombin 3 and produces selective inhibition of factor Xa SE: BLEEDING Reversal: NONE
27
Direct Oral Anticoagulants (DOAC)
Meds: Rivaroxaban (Xarelto) and Apixaban (Eliquis) Indications: acute DVT/PE tx and maintenance, DVT prophyl, stroke prophyl in pts with Afib MOA: inhibit Factor Xa and Prothrombinase SE: BLEEDING, hypersens Reversal agent: andexanet alfa (AndeXanet)-> recomb but inactive Xa acts as decoy and sequesters drug. Can give PCC or FFP
28
DOACS- Dabigatran (Pradaxa)
Indications: tx of DVT/PE, DVT prophylaxis, prophyl of stroke afib MOA: thrombin inhibitor SE: BLEEDING Reversal: idarucizummab (Praxbind)-> monoclonal ab binds to drug and neut
28
DOACS- Dabigatran (Pradaxa)
Indications: tx of DVT/PE, DVT prophylaxis, prophyl of stroke afib MOA: thrombin inhibitor SE: BLEEDING Reversal: idarucizummab (Praxbind)-> monoclonal ab binds to drug and neut
29
Vitamin K antag- Warfarin (Coumadin)
Indications: Tx DVT/PE, stroke prophy with Afib and Valvular heart dz MOA: antagonist for clotting factor activation and synth in liver 2, 7, 9, 10 Dosing: low and titrate to goal INR - DVT/PE goal INR= 20-3.0 -Stroke prophylaxis in Afib= 2.0-3.0 -Mechanical heart valve goal INR= 2.5-3.5 SE: BLEEDING, GI upset, alopecia, hypersens rxn Reversal: Vitamin K (doesnt work quick), FFP, PCC
30
Fibrinolytics
Alteplase (Activase), tenecteplase (TNKase), reteplase (Retavase) Indications: acute STEMI WHEN PCI NOT AVAILABLE acute massive PE- saddle embolism Acute non hemorrhagic-> ischemic cva MOA: recombinant tPA (tissue plasminogen activator LOTS OF CONTRAINDICATION= ALWAYS LOOK UP
31
Absolute contraindications for fibrinolytics
1. any prior hemorrhagic stroke- any head bleed ever 2. Ischemic stroke w/in 3 months 3. intracranial neoplasm or arteriovenous malformation 4. Active internal bleeding 5. Aortic dissection 6. considerable facial trauma or closed head trauma in past 3 months 7. intracranial or intraspinal surgery within 2 months (epidurals) SEVERE UNCONTROLLED HTN (sYSTOLIC > 180 MMHG OR DIASTOLIC >110 HGMM numerous relative contraindications
32
Fibrinolytics Major SE
BLEEEEEEEDING 1. INTRACRANIAL HEMORRHAGE (IS THE MOST FEARED 2. GI bleed 3. GU bleed 4. Respiratory bleeding 5. Gingival bleeding 6. Epistaxis 7. bleeding from every orifice
33
Acute Coronary Syndrome (ACS) overview
1.Unstable Angina UA- new onset of angina at rest, increased freq and severity-> infarct has not occurred but could be imminent 2. Non-ST Segment Elevation Myocardial Infarction (NSTEMI)- Incomplete occlusion of coronary vessel but reduction in flow to distal-> ischemia and ultimate infartction= EKG NON DIAGNOSTIC AND DIAGNOSED WITH LAB BIOMARKERS= TROPONIN 3. ST Segment Elevation Myocardial Infarction- acute and COMPLETE occlusion of distal flow beyond area of thrombosis-> + EKG and + Biomarkers
34
STEMI
usually = acute plaque rupture -> thrombus formation at site *Acute ST elevation in contiguous (grouped)-> leads on EKG or new LBBB findings Initial management- IV, Monitor, CONSIDER NTG, BB, Morphine for pain, O2 ONLY IF NEEDED LESS THAN +92% iNITIATE ANTICOAG AND ANTIPLT
35
STEMI reperfusion Therapy
1. Primary Percutaneous Coronary Intervention (PCI)- GOLD STANDARD FOR TX GET IN UNDER 90 MIN= ballon and sten positioned into artery and expand-> remove balloon with in place 2. Fibrinolysis (tPA)- 2nd line-> if PCI not available or not enough time
36
STEMI Anticoagulation and Antiplt
STEMI pt = RECEIVE BOTH ANTICOAG AND ANTIPLT REGARDLESS OF PCI OR TPA INITIATED Aspirin/Clopidogrel + Heparin
37
STEMI- Dual Antiplt therapy (DAPT)
Aspirin: 325 mg PO adult or 4* 81 mg Baby aspirin = NON ENTERIC COATED CHEWED AND SWALLOWED + Clopidogrel (Plavix)-> loading dose of 300 mg then 75 mg daily Prasugrel (Effient) -> loading dose of 60 mg then 10 mg daily Ticagrelor (Brilinta)-> loading dose 180 mg then 90 mg twice daily
38
STEMI - Anticoagulation
1. IV Unfractionated Heparin (UFH)= (short half life and stop dose) IV as a bolus= in Units= then continuous drip over 24-48 hours following reperfusion therapy 2. IV/SC LMWH= enoxaparin (Lovenox) or fractionated heparin More bioavailable, no continuous lab monitoring, decreased HIT risk
39
NSTEMI overview
EKG- nonspecific finding-> maybe normal maybe ST depression, inverted t wave Diag: Biomarkers- TROPONIN LEVELS (rise in hours following infarct) Initial therapy: BB, NTG, Morphine, O2 IF NEEDED, High dose statin, ASA NO FIBRINOLYTICS look at old ekg for comparison
40
TX of NSTEMI ACS on risk stratification
1. TIMI 2. GRACE 3. HEART
41
Unstable angina UA
may look like NSTEMI symp and ekg but NO BIOMARKER ELEVATION BC HAVENT INFARCTED Initial tx: BB, Nitrates, Morphine, O2 if needed, High does statin therapy Risk stratify: intermediate-> High= Antiplt w/ ASA/P2Y12 + anticoag UFH or LMWH Consult cardiology: plan for early coronary angio and PCI
42
Post acute Coronary Syndrome
1. High dose Statin therapy-> goal LDL less than 70 mg/dL 2. DAPT= ASA + P2Y12 (plavix) 3. Beta blocker 4. ACE Inhibitor- added once the dust settles and assess LV function
43
DVT/PE: Venous thromboembolic disease (VTE)
LE and pelvic veins, some upper extremity virchows triad: 1. Increased coaguability 2. BV injury 3. Stasis TX: anticoag to prevent further clot- not breaking it up Provoked DVT- clear reason= anticoag for 3-6 months Unprovoked= unclear- may need workup for underlying hypercoag disease pts w/ multi DVT or hypercoag disorder= anticoag for life
44
DVT tx
Initial tx: IV first then switch to oral - DOAC or Warfarin 1. UFW wt based Or LMWH wt based 2. DOAC- Rivaroxaban (Xarelto) or Apixaban (Eliquis)- Factor Xa inhibition Prophylaxis: nearly all hospitalized pts: MC is LMWH via sc injection daily Ortho pts: replacements high risk for DVT -> 30-35 days after surgery
45
PE
risks like DVT- originate from extremity of pelvic vein Diag: Chest CT Pulmonary Angiography CTPA TX: based on severity-> hemodynamically stable (anticoag) or unstable (tPA) Fibrinolytics-> for large clot burden and compromised- tPA: Alteplase (Activase) or Tenecteplase (TNKase) Anticoag required unless contraindicated-> UFH, LMWH, or DOAC= continue for 3-6 months depending on risk assessment
46
Anticoag in Afib
increased risk for embolic stroke-> assess pt risk pros and cons CHA2DS2-VASc Score- estimate risk 0-1= just ASA and not full anticoag >1 male= rec full oral anticoag- DOAC or Coumadin >2 female= rec full oral anticoag- DOAC or Coumadin
47
Peripheral Arterial Disease
equivalent to Coronary heart disease when assessing overall cardiovas risk Clinical findings: Claudicaiton (intermittent pain)- muscles during exercise and resolves with rest 2ndary to atherosclerosis in periph arteries-> ischemia TX: lifestyle, exercise, smoking cessation *Statin therapy *Antiplt therapy- ASA *OR* Plavix *Cilostazol (Pletal)= Phosphodiesterase 3 inhibitor -> vasodilation and improve claudication
48
Anticoag in valvular heart disease
Mechanical: WARFARIN ONLY, NO DOACS lifelong-> INR 2.5-3.5 Bioprosthetic: Porcine valve-> 3-6 month of anticoag= Warfarin or DOAC
49
Anticoag in pregnancy
Contraindicated: DOACs and Warfarin Safe: UFW or LMWH= dont cross placenta UFW preferred around 36+ weeks bc has the shortest half life= may still allow for spinal anesthesia/epidural
50
What to do when things go wrong!!!!
1. UFH or LMWH *stop drug immed *Protamine sulfate 2. DOACS *stop immed * give AndexXa, FFP, PCC, Pradaxa, or Praxbind 3. Antiplt drugs *stop immed *PLT transfusion???-> little evidence-> pray 4. Vitamin K antagonists *stop drug *PCC or FFP *Vitamin K replacement IV or SC

Pharm 2 (15 decks)

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