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Pharm 2 > Anticoag and fibrinolytics > Flashcards

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
Q

Anticoagulant therapy: Bivalirudin (Angiomax) and argatroban (Acova)

A

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
Q

Anticoagulant therapy: Fondaparinux (Arixtra)

A

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
Q

Direct Oral Anticoagulants (DOAC)

A

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
Q

DOACS- Dabigatran (Pradaxa)

A

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
Q

DOACS- Dabigatran (Pradaxa)

A

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
Q

Vitamin K antag- Warfarin (Coumadin)

A

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
Q

Fibrinolytics

A

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
Q

Absolute contraindications for fibrinolytics

A
  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
Q

Fibrinolytics Major SE

A

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
Q

Acute Coronary Syndrome (ACS) overview

A

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
Q

STEMI

A

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
Q

STEMI reperfusion Therapy

A
  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
Q

STEMI Anticoagulation and Antiplt

A

STEMI pt = RECEIVE BOTH ANTICOAG AND ANTIPLT REGARDLESS OF PCI OR TPA INITIATED

Aspirin/Clopidogrel + Heparin

37
Q

STEMI- Dual Antiplt therapy (DAPT)

A

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
Q

STEMI - Anticoagulation

A
  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
Q

NSTEMI overview

A

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
Q

TX of NSTEMI ACS on risk stratification

A
  1. TIMI
  2. GRACE
  3. HEART
41
Q

Unstable angina UA

A

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
Q

Post acute Coronary Syndrome

A
  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
Q

DVT/PE: Venous thromboembolic disease (VTE)

A

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
Q

DVT tx

A

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
Q

PE

A

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
Q

Anticoag in Afib

A

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
Q

Peripheral Arterial Disease

A

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
Q

Anticoag in valvular heart disease

A

Mechanical: WARFARIN ONLY, NO DOACS lifelong-> INR 2.5-3.5
Bioprosthetic: Porcine valve-> 3-6 month of anticoag= Warfarin or DOAC

49
Q

Anticoag in pregnancy

A

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
Q

What to do when things go wrong!!!!

A
  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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