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Pharm II > Lecture 6 (Vascular)-Exam 3 > Flashcards

Lecture 6 (Vascular)-Exam 3 Flashcards

1
Q

Endocarditis MC organism:
* What are the mc Staphylococcus species?
* What is the MC streptoococcus species?
* When is enterococcus occur?

A

PWID = Persons who inject drugs, PV = prosthetic valve, PVE = prosthetic valve endocarditis, NVE = native valve endocarditis

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2
Q

Endocarditis: Native valve endocarditis
* MCC?
* What is another one?

A
  • MCC=S. aureus
  • Strep viridans
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3
Q

Endocarditis: Injection drug users
* MCC?
* What is another one?
* What is the MC valve affected?
* What can happen with tricuspid infection?

A
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4
Q

Left-Sided IE (MC 80-90%)
* What are the risk factors? (2)
* What valves are affected? (2)
* What is common sxs? (4)

A

Risk factors:
* IVDA (20%)
* Prior IE

Valves: Mitral and aortic

Common Sxs: Fever-MCS (90%), chills, anorexia, weight loss

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5
Q

Left-Sided IE
* What are the common signs? (2)
* What is a common association?

A
  • Common sign: Petechiae, splinter hemorrhages
  • Common Associations: cardiac murmurs
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6
Q

Right-Sided IE (10% of all IE cases)
* What are the RFs (4)
* What is the MCC organism?
* What is a common association?

A
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7
Q

Right-Sided IE
* What are the common sxs? (8)
* What are the uncommon associations? (2)

A
  • Common sxs: Fever-MCS (90%), chills, anorexia, myalgias, headaches, night sweats, SOB, abd pain
  • Uncommon Associations: Detectable heart murmurs & peripheral embolization
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8
Q

Endocarditis Clinical presentation:
* What are the MC signs (2)
* MC with what?
* PWID may present what?

A

Not specific / variable
* MC – Fever (90%)
* Second MC – murmur (85%)

MC insidious with gradual onset

PWID may present with sepsis

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9
Q

What are the cutaneous stigmata? (6)

A

“FROM JANE”

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10
Q

What do you need to do for labs of endocarditis

A

The hallmark laboratory finding is continous bacteremia: set of of blood cultures should be collected over 24 hours (2 needs to be positive)

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11
Q
A
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12
Q

Treatment plan:
* What do you need to do besides meds? (3)
* What is the empiric therapy?

A
  • Hospitalization, ID consult, Cardiovascular surgery consult
  • Empiric therapy: Vancomycin IV and ceftriaxone IV or gentamicin IV
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13
Q

What is the definitive treatment depend on?

A

Culture and sensitivity

Valve type – native vs prosthetic
* Prosthetic Valve IE -> Surgical replacement + antibiotics for 6 weeks

Extent of valve involvement=> need valve replacement, medication, or thromectomy?

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14
Q

Surgical Management recommended for IE is what? (5)

A
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15
Q

What is the MC streptococcal endoarditis

A

Viridans group most common (mouth flora)

Include:
* ­S. viridans
* ­S. sanguinis
* ­S. oralis
* ­S. salivarius
* ­S. mutans
* ­Gemella morbillorum

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16
Q

STREPTOCOCCAL ENDOCARDITIS
* Found where? Cause what?
* Common cause of what?
* Complicated or uncomplicated?
* Sensitive to what?

A
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17
Q

Streptococcus spp txt:
* What are the 3 primary antibiotics? What is the timeline of those?

A
  • Penicillin (q6h=4weeks, q4h=2weeks)
  • Ceftriazone (only is 4 weeks) +/- Gentamicin (added is 2 weeks)
  • Vancomycin (only if have resistant bug or allergy=>4weeks)
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18
Q

How does treatment timeline change based on Native valve and prosthetic valve IE?

A
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19
Q

Strep spp txt:
* What happens when you use double therapy? (2)

A
  • Faster vegetation sterilization in animal models
  • Enhanced activity with beta lactam + aminoglycosides
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20
Q

Native valve of streptococcus spp:
* how long is treatment?
* What groups should not get the shorter therapy?
* Vancomycin is for who?

A
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21
Q

Staphlococcus spp txt
* What is the mc organism? MC in who?
* What is another organism that is common? MC in who? Mortality rate?
* Duration of therapy?

A
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22
Q

Staph spp txt of natvie valve:
* What do you give for methicillin sensitive spp? For how long?
* What do you give for methicillin resistant? For how long?

A
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23
Q

Staph spp txt: Prosthetic valve
* What is the txt for methicillin sensitive?
* What is the txt for methicillin resistant?

A
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24
Q

Endocarditis prophylaxis:
* Antibiotic prophylaxis is reasonable before what? (6)

A

Antibiotic prophylaxis is reasonable before manipulation of gingival (gum) tissue or the periapical region (area around the roots) of teeth, or perforation of the oral mucosa for people with heart valve disease who have any of the following:
1. Prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts
2. Prosthetic material used for heart valve repair, such as annuloplasty rings, chords or clips
3. Previous infective endocarditis
4. Unrepaired cyanotic congenital heart defect (birth defects with oxygen levels lower than normal)
5. Repaired congenital heart defect, with residual shunts or valvular regurgitation at the site adjacent to the site of a prosthetic patch or prosthetic device
6. Cardiac transplant with valve regurgitation due to a structurally abnormal valve,

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25
Q

Antibiotic prophylaxis before dental procedures is not recommended for who?

A

is not recommended for any other types of
congenital heart disease.

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26
Q

antibiotic prophylaxis is not recommended for patients with what?

A

with valvular heart disease who are at high risk of IE for nondental procedures (e.g., TEE, esophagogastroduodenoscopy, colonoscopy, or cystoscopy) in the absence of active infection.

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27
Q
A
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28
Q

When and when not is AP suggested for dental procedures?

A
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29
Q
A
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30
Q

How long does acute pericarditis last?

A

under 4-6 weeks

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31
Q

Acute Pericarditis:
* Treat how?
* What do you give/restrict?

A
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32
Q

Acute pericarditis:
* Addition of colchinine, reduces what?
* Full dose of NSAIDS until when?
* When can you taper?

A
  • Addition of colchicine – reduced recurrence rates, low adverse events
  • Full dose NSAIDS until symptom resolution for at least 24 hours and CRP normalized
  • Taper NSAIDS – 2 to 4 weeks
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33
Q

Give all the different choices of NSAIDs with colchicine and doeses

A

Colchicine dose reduced to once daily for patients < 70 kg

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34
Q

Acute pericarditis:
* Consider what type of protection with what group?
* Corticosteroids reserved for patients with what?
* Aspirin is the DOC when?
* When should patients be evaluated for other causes?

A
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35
Q
A
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36
Q
  • What is released in rsponse to inflammation? What does this do?
A
  • Phospholipase A2 released in response to inflammation
  • Converts phospholipids into arachidonic acid
  • Arachidonic acid is a substrate for two enzymes
    * 5-lipoxygenase (5-LOX)
    * Cyclooxygenase (COX-1 and COX-2)
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37
Q
  • COX 1 is always what?
  • What does thromboxane and prostaglandins/prostacyclins do?
A

COX-1 always circulating and active
* Thromboxane: Promotes platelet aggregation
* Prostaglandins and prostacyclin
* Secretion of protective gastric mucosa
* Maintaining renal blood flow

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38
Q

COX 2 activated where? What does it mediate?

A
  • COX-2 activated at sites of inflammation
  • Mediates inflammation, pain, and fever
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39
Q

What does NSAIDs block? What does it cause?

A

NSAIDs block COX-1 and COX-2
* Reduce prostaglandin, thromboxane, prostacyclin synthesis
* Reduce inflammation, pain, and fever

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40
Q

NSAID SE:
* MC SE is what? Why?

A
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41
Q

What are the Other gastrointestinal adverse effects of NSAIDS?

A
  • Dyspepsia
  • Abdominal pain
  • Nausea / vomiting
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42
Q

NSAIDS: SE
* How does NSAIDS effect the kidneys?

A
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43
Q

What can happen to the skin due to NSAIDs?

A

Rash – hypersensitivity reactions rare / cross sensitivity

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44
Q

Black box warnings of NSAIDs:
* What are the serious CV events? (2)
* What Increased risk of what?
* Avoid in who?

A

Serious CV events:
* Increased risk of embolic events including myocardial infarction and stroke
* Contraindicated in the setting of coronary artery bypass surgery

Increased risk of serious gastrointestinal adverse events
* Bleeding, ulceration, perforation
* Elderly at greatest risk

Pregnancy Considerations
* Avoid if possible; especially in first and third trimesters

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45
Q

What are the CI of NSAIDs (4)

A
  • Aspirin allergy – watch for patients with Samter’s triad
  • Peptic ulcer. GI bleed or perforation
  • Advanced renal impairment
  • Cerebrovascular bleeding
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46
Q

Colchicine:
* What is the MOA?
* What is contraindicated?

A

Mechanism of action
* Anti-inflammatory – disrupts microtubule formation preventing activation, degranulation, and migration of neutrophils

Contraindications
* P-glycoprotein or strong CYP3A4 inhibitors – mostly protease inhibitor used for the treatment of HIV (e.g., ritonavir)

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47
Q

What are the SE of colchicine? (4)

A
  • Diarrhea
  • Nausea / vomiting
  • Pharyngolaryngeal pain
  • Bone marrow suppression (leukopenia, granulocytopenia, thrombocytopenia, aplastic anemia)
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48
Q

What is type I, II, III, IIIa, IIIb aortic dissection?

A
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49
Q

Aortic dissection:
* What is the txt of type A/DeBakey I or II?
* What is the txt of type B/DeBakey IIIa or IIIb?

A
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50
Q

Aortic dissection type III or B- Medical treatment
* What is the first line therapy?
* What is the goal?

A

First-line therapy – IV beta-blockers
* Goals: HR < 60, SBP < 100 to 120 mmHg

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51
Q

Aortic dissection type III or B- Medical treatment
* What is the DOC? Titrate to what?
* What is the alternative?
* What is second line?
* What else should you give?

A

Esmolol = DOC
* Titrate to HR

Labetalol = alternative

Second-line: verapamil / diltiazem

Adjuvant therapy: opioids for pain control

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52
Q

Giant cell/temporal arteritis?
* What is it?
* What arteries are affected?
* Typically in who?

A
  • Granulomatous vasculitis of the extracranial branches of the carotid artery
  • Temporal, occipital, ophthalmic and posterior ciliary artery
  • Typically ages > 50
    * May coexist with polymyalgia rheumatica
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53
Q

GCA txt:
* What is the txt with a patient with no vision loss or signs of ischemia?

A
  • Prednisone 1 mg/kg PO daily (max 60 mg/day) x 2 to 4 weeks then
  • Prolonged taper ( 6 to 12 months)
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54
Q

GCA txt:
* What is the txt with a patient with threatened or established vision loss?

A
  • Methylprednisolone 500 to 1000 mg IV Q24H x 3 days then
  • Prednisone 1 mg/kg PO daily (max 60 mg/day) x 2 to 4 weeks then
  • Prolonged taper (6 to 12 months)
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55
Q

What is second line for GSA? Why?

A
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56
Q

GCA tapering is guided by what?

A
  • Taper guided by ESR and CRP
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57
Q

Steroids:
* Endogenous steroids produced where?
* Steroids released when?
* What effects?

A
  • Endogenous steroids produced in the adrenal gland (MC cortisol)
  • Released in response to stress and inflammation
  • Anti-inflammatory and immunosuppressive effects
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58
Q

What is the MOA of steroids? (cytokines and mediators)

A

Inhibit the production of inflammatory cytokines
* Bind to glucocorticoid receptors inside cells
* Bind to sites on DNA
* Down regulate cytokine production

Inhibit the production of inflammatory mediators
* Inhibit phospholipase A2
* Prevents the production of arachidonic acid
* Decreasing prostaglandins, leukotrienes, thromboxane

Immunosuppression

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59
Q

Steroids effects:
* What do they suppress?

A

Suppress inflammatory response to all noxious stimuli
* Pathogens
* Chemical / physical
* Immune mediated / hypersensitivity

60
Q

How does steroids reduce inflammation? (4)

A

Reduce inflammation by DECREASING:
* Cytokine production – including various interleukins, tumor necrosis factor alpha
* Recruitment of WBCs and monocytes to sites of inflammation (neutrophil demargination)
* Lymphocyte, monocytes, basophil, eosinophil, mast cell production / function-> T-lymphocyte activity
* Production of prostaglandins, bradykinins, leukotrienes (inhibition of phospholipase A2)

61
Q

T/F: Steroids corrects the underlaying cause of disease

A

False

62
Q

What are the short term steroids effects? (6)

A
63
Q

What are the long term steroids effects? (8)

A
64
Q

Steroids tapering:
* Recommended following prolonged use / higher doses. Explain (3)
* Used to avoid what?
* What is the general taper duration rule?

A
65
Q

What are the sxs for steroid withdrawal?(7)

A
66
Q

Tocilizumab (actemra)
* What is the drug?
* What is the MOA?
* What are teh contraindications?

A
  • Biologic DMARD
  • MOA: IL-6 antagonist
  • Dose: 162 mg once weekly subcutaneous injection
  • Contraindications: Sepsis
67
Q

TOCILIZUMAB (ACTEMRA)
* What is the BBW?
* What is the SE?
* How do we monitor?

A
  • BBW: At risk for serious infections including TB, fungal, bacterial and other opportunistic infections
  • Adverse reactions: injection site reactions, hypersensitivity reactions, hepatotoxicity, neutropenia, thrombocytopenia, constipation, increases lipids
  • Monitoring: Baseline CMP; signs/symptoms of infection
68
Q

PAD:
* MC form of what?
* What is it?
* What is equivalent?

A
69
Q

PAD:
* What is the MC characterisitc? Explain what it is?
* Resting pain=

A

MC characteristic = intermittent claudication (IC) and pain at rest in risk lower extremities
* Reproducible fatigue, discomfort, cramping, pain or numbness in affected extremities that resolves with rest
* Limited blood flow and decreased oxygen delivery to extremities in response to increased demand
* Resting pain = late disease

70
Q

What does the history and PE show for PAD?

A
71
Q

How do you dx PAD? What are other tools?

A

Ankle-Brachial Index (ABI)
* ≥ 90 % sensitive and specific
* Important screening tool

Other tools:
* ­CTA
* ­ MRI
* ­ Angiography

72
Q
A
73
Q
  • What is the txt for PAD?
  • What are the goals? (4)
A

Aimed at decreasing functional impairment associated with IC and minimize CV risk factors

Goals
* ­Increase walking distance, duration and pain-free walking
* Control comorbid conditions
* ­Improve QOL
* ­Decrease CV complications and death

74
Q

Treatment of PAD:
* What are the lifestyle modications?

A
75
Q

Adjuvant txt of PAD;
* What do you need to control?
* What should you inhibit and how?
* How do you treat HLD?
* What should the A1C be?
* WHAT TYPE OF THERAPY?

A
76
Q

Antiplatelet therapy:
* Recommended for who?
* What does it recude?

A

Recommended for all patients with symptomatic PAD
* Asymptomatic patients treated on a case-by-case basis

Significantly reduces the risk of future adverse cardiac events
* MI, stroke, vascular death

77
Q

What is the first line for antiplatelet therapy for PAD?

A

Aspirin or Clopidogrel
* Dual antiplatelet therapy NOT recommended

78
Q
A
79
Q

What is steps one, two, and three of primary homeostasis?

A

(1) Vasoconstriction – endothelin
* Reflexive contraction of vessel
* Decreased blood flow (dec. bleeding)

(2) Exposure – exposed collagen from damaged endothelium releases vWF
* vWF binds to the exposed collagen

(3) Adhersion-platelets bind to vWF via glycoprotein 1B (GP1B)
* After vWF is bound to collagen

80
Q

What is step 4 of primary hemostasis?

A

Activation – active platelets change shape (release chemicals)
* Release more vWF, serotonin, ADP, and thromboxane A2, Ca (important for clotting)
* ADP and thromboxane A2
* Activate more platelets
* Stimulate expression of glycoprotein IIB/IIIA on platelet membrane surface

ADP = adenosine diphosphate

81
Q

What is step five of primary hemostasis?

A

Aggregation – GPIIB/IIIA links platelets together via fibrinogen and form a platelet plug

Platelet plug to move to secondary hemostasis

82
Q

Antiplatelet therapy: Aspirin
* What is the MOA of aspirin?
* What type of drug is it?

A
  • Activated platelets release arachidonic acid
  • AA is onverted to prostaglandins via COX1 -> prostaglandins releases thromboxane A2
  • Thromboxane A2 promotes activation of more platelets and activation of glycoprotein 2b/3a
  • Aspirin is an irreversible COX inhibitor
83
Q

Antiplatelet therapy: Aspirin
* Blocks what for and for how long?
* First line for what?

A
  • Blocks thromboxane platelet activation for the life of the platelet (7-10 days)
  • First-line prophylactic antiplatelet therapy
84
Q

Antiplatelet therapy: ADP receptor inhibitors (P2Y12 inhibitors)
* What are the examples?
* Second line for what?
* What can it be combined with?

A
  • Clopidogrel, ticagrelor, ticlopidine, prasugrel
  • Second-line prophylactic antiplatelet therapy
  • Combined with aspirin for dual antiplatelet therapy (DAPT)
85
Q

What is the MOA of ADP receptor inhibitors (P2Y12 inhibitors)?

A
  • Bind to the P2Y12 ADP receptor and prevent ADP from binding
  • No ADP binding = no formation of glycoprotein 2b/3a receptors on the surfaced of activated platelets
  • No platelet aggregation
86
Q

Treatment for intermittent claudiccation
* What is first line?
* What is second line?

A
  • First-line: Supervised exercise program and lifestyle modifications
  • Second-line: Cilostazol
87
Q

What is the MOA and effects of cilostazol?

A

Increased cAMP->decreased intracellular calcium
* Vasodilation
* Decreased platelet activation
* Improves symptoms and increases walking distance in
patients with IC

88
Q

Cilostazol
* What is the dose?
* Discontinue if what?
* use limited by what?

A
  • 100 mg PO BID (30 min before or 2 hours after meals)
  • Discontinue if symptoms not improved after 3 months
  • Use limited by adverse effects and CI in heart failure
89
Q
  • What are the Symptoms of Bleeding – low or dysfunctional platelets? (5)
  • Serious bleeding rare – MC when combined with what?
  • Antiplatelets agents CI when?
A
90
Q

Antiplatelet therapy for PAD/IC
* ASA: MOA, SE and CI?

A
91
Q

Antiplatelet therapy for PAD/IC
* Clopidogrel: MOA, SE and comments?

A
92
Q

Antiplatelet therapy for PAD/IC
* Cilostazol: MOA, SE and comments?

A
93
Q

Acute limb ischemia:
* What is the initital txt? DOC?
* What should you manage?

A
  • Initial treatment: anticoagulation
  • Heparin – DOC
  • Pain management
94
Q

Acute limb ischemia: Heparin
* What is the dose?
* Dose titrated to what?
* Alternative parenteral agent may be used when?
* Decreases what?
* Preserves what?

A
  • 60 to 80 U/kg IV bolus followed by 12 to 18 unit/kg/hr continuous infusions
  • Dose titrated to aPTT or anti-Xa levels
  • Alternative parenteral agent may be used for heparin contraindications
  • Decreases further propagation of thrombus
  • Preserves micro circulation
95
Q

Evaluation for limb management:
* Treatment depends on what?
* What is Endovascular techniques with fibrinolytics?
* What are the surgical techniques?

A

Treatment depends on limb evaluation

Endovascular techniques with fibrinolytics
* Cather directed thrombolysis
* Ultrasound accelerated thrombolysis
* Percutaneous thromboaspiration

Surgical techniques
* Embolectomy with stent placement
* Bypass graft

96
Q
A
97
Q

Limb management (after)
* What is recommended for one month?
* What is long term?

A
98
Q

Phlebitis/thrombophlebitis-superficial
* What is it?
* How do you dx? What are the sxs?

A

Phlebitis and thrombosis of the lower extremity superficial veins is generally benign and self- limited

Diagnosis of phlebitis primarily clinical
* Pain, tenderness, induration, and/or erythema along the course of a superficial vein

99
Q

Phlebitis/thrombophlebitis-superficial
* What is the txt?
* When should you reevaluate patient?
* Worsening of clinical symptoms or extension of signs of phlebitis should get what?

A
100
Q

Anticoagulation for treatment of VTE
* Oral anticoagulant monotherapy with what?
* Start parenteral anticoagulant then what?
* Start parenteral anticoagulant x 5 days then switch ?
* Start parenteral* anticoagulant and what?

A
101
Q

Fill in for Venous Thromboembolism treatment (proximal)

A
102
Q

Fill in the HAS-BLED score

A
  • 0 = low bleeding risk
  • 1 to 2 = moderate bleeding risk
  • ≥ 3 = high bleeding risk
103
Q

Isolated distal DVT- First episode:
* Where do they occur?
* What do you do for Asymptomatic patients with low risk of extension?

A
104
Q

What are the risk factors for proximal extension?

A
105
Q

Isolated distal DVT-first episode:
* What do you do for severe symptoms or risk of thrombosis extension?

A

Anticoagulate following proximal vein treatment guidelines

106
Q

ANTICOAGULATION TRANSITIONS
* What is complex?
* What exist?
* What is recommended?

A
107
Q

Treatment of severe vte: Life-threatening pulmonary embolism with hemodynamically unstable patient
* What is first line and second line?

A
  • First-line: IV thrombolytic therapy
  • Second-line: Catheter-directed thrombolytic therapy
108
Q

Massive proximal lower extremity thrombosis or ilio-femoral thrombosis associated with severe symptoms (< 14 days duration)
* What is first line?

A

First-line: Catheter-directed thrombolytic therapy

109
Q

Treatment of severe vte
* What is last line?

A

Embolectomy

110
Q

Tissue plasminogen activator (tpa)
* What is the MOA?
* What is the half-life?
* How do you dose it?

A

MOA
* binds fibrin in a thrombus and converts plasminogen to plasmin; plasmin lyses fibrin and fibrinogen breaking up the clot

Pharmacokinetics:
* Short half-life; less than 5 minutes; 80% cleared within 10 minutes
* Bolus dose followed by continuous infusion

111
Q

Tissue plasminogen activator (tpa)
* What are the adverse effects?

A

Bleeding
* Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age

112
Q

bridging:
* What does it depend on? (3)
* What may be continued?
* Reversal agents should be utilized for what?

A

Bridging with heparin depends on
* Specific surgery
* Patient risk of bleeding
* Patient risk of thromboembolism

Aspirin may be continued

Reversal agents should be utilized for emergent surgeries

113
Q
A
114
Q

Anticoagulation bleeding
* Anticoag are CI with what?
* What is major bleeding?

A

Anticoagulants contraindicated with any active bleeding

Major bleeding
* Gastrointestinal bleeding (MC) – mortality 5%
* Intracranial hemorrhage – less common – mortality 50%
* Patients can be risk stratified by age, organ function, comorbidities

115
Q

Anticoagulation bleeding
* What is minor bleeding?

A
116
Q

CONTRAINDICATIONS TO ANTICOAGULATION
* What are absolute?

A
117
Q

CONTRAINDICATIONS TO ANTICOAGULATION
* What are relative?

A
118
Q

Heparin, LMWH, fondaparinux: Indirect inhibition
* Heparin and low molecular weight heparins (LMWH) bind to what?
* What is ATIII?

A
  • Heparin and low molecular weight heparins (LMWH) bind to antithrombin III and accelerates its activity
  • ATIII is a natural anticoagulant that inactivates factors Xa and thrombin
119
Q

What is the MOA:
* Heparin:
* LMWH:
* Fondaparinux:

A

Heparin
* Accelerates Xa and thrombin inactivation

LMWH
* Selectively accelerates Xa inactivation; minimal effects on thrombin

Fondaparinux
* Specifically accelerates Xa inactivation; no effects on thrombin

120
Q

What can the large molecule (unfractionated)-> Heparin do?

A

able to interact with both antithrombin III and thrombin

121
Q

What are the indications of heparin? (4)

A
  • Short-term anticoagulation (cont infusion)
  • Immediate anticoagulation – rapid onset (seconds)
  • MC life or limb threatening clots; surgical bridging therapy, DVT prophylaxis if other medications contraindicated
  • Safe in pregnancy – does not cross the placenta (since so big)
122
Q

What is the dosing of heparin?

A
  • IV or subcutaneously (SC)
  • IV: given as bolus plus continuous IV infusion (short half-life)
123
Q

What are the monitoring parameter of heparin?

A
  • aPTT [goal = 1.5 to 2.5 times normal (30 to 40 seconds)]
  • Antifactor Xa level (goal=0.3 to 0.7)
  • CBC (hemoglobin, hematocrit, platelets)
124
Q

What are the adverse effects of heparin?

A
  • Bleeding
  • Osteoporosis – long-term therapy
  • Heparin induced thrombocytopenia
125
Q

What is the antidote for heparin?

A
  • Protamine sulfate 1mg neutralizes ~ 100 units heparin
  • Continuous infusions: use heparin dose from preceding 2 to 3 hours
126
Q

How much antidote do you need to give if you give 1200 units of heparin per hour?

A
127
Q

Heparin induced Thrombocytopenia
* What happens with the immune system? What does that cause?

A

Immune system makes antibodies that bind to heparin-platelet factor 4 complexes
* Platelet activation – aggregation (clumping)
* Clots
* Thrombocytopenia

Platelets are dropping but clots are forming

128
Q

Heparin induced Thrombocytopenia
* What are the risk?
* What is the onset?
* How do you dx it? (3)

A
  • Risk: unfractionated heparin > 7 to 10 days (also occurs with LMWH)
  • Onset: 5 to 10 days after heparin initiation

Diagnosis:
* Check 4T score – probably of HIT
* Low score (≤ 3 rules out HIT); look for additional diagnoses
* High score; stop heparin, give alternative, order additional testing

129
Q

HIT – alternative treatments
* What do you give more critcally ill patients?
* What do you give stable patients?

A
130
Q
A
131
Q
A

Discontinue heparin

132
Q

Warfarin
* What is the moa?

A
  • Factors II, VII, IX and X dependent on vitamin K for synthesis
  • Warfarin inhibits vitamin K recycling and synthesis
  • Not available for factor production
133
Q

Warfarin
* What are the indications? (2)

A
  • DVT, atrial fibrillation, prosthetics valves
  • Only oral anticoagulant indicated for patients with mechanical heart valves
134
Q

Warfarin-Pharmacokinetics:
* What is half life? What is onset?
* Requires what?
* How is metabolized?

A
  • Generally long half-life; prolonged onset
  • Requires bridging therapy with heparin or LMWH-> if INR therapeutic for two days then then you can stop
  • Metabolized by CYP2C9 – many drug interactions
135
Q

CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?

A
136
Q

Monitoring Warfarin
* What levels do you need to look at?
* Adjuct dose to what?
* _ algorithms
* initial dose for most patients?
* What do you need to check daily intil therapeutic?

A

PT/INR – goal 2 to 3 in most cases
* Adjust dose to INR
* Evidence-based algorithms
* Initial dose for most patients: 5mg PO daily
* INR daily until therapeutic (then decrease interval of checking)

137
Q

What are the diet issues with warfarin?

A

Vit K needs to be stabilized with txt
* for example: winter vs summer months

138
Q

Warfarin
* What are the SE? (3)
* What is CI (1)?

A
139
Q

Warfarin overdose:
* Txt based on what?

A

Treatment depends on INR level and if patient is bleeding

140
Q

Warfarin overdose:
* What do you with a patient who is not bleeding? (3)

A
  • Hold warfarin
  • Give vitamin K (1 to 5 mg PO)
  • Resume warfarin at lower dose once INR is 2 to 3
141
Q

Warfarin overdose:
* What do you with a patient who is bleeding? (2)

A
  • 4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k

OR
* Fresh frozen plasma (FFP)

142
Q
A

Fresh frozen plasma

143
Q

Direct inhibitors
* What are the two types and their MOA?

A

Factor Xa inhibitors
* Directly bind factor Xa
* Prevent conversion of prothrombin to thrombin

Thrombin inhibitors
* Bind to and inhibit thrombin

144
Q

Fill in for DOACS

A
145
Q
A

Pharm II (14 decks)

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