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
2
Q
Endocarditis: Native valve endocarditis
* MCC?
* What is another one?
A
- MCC=S. aureus
- Strep viridans
3
Q
Endocarditis: Injection drug users
* MCC?
* What is another one?
* What is the MC valve affected?
* What can happen with tricuspid infection?
A
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
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
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
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
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
9
Q
What are the cutaneous stigmata? (6)
A
“FROM JANE”
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)
11
Q
A
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
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?
14
Q
Surgical Management recommended for IE is what? (5)
A
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
16
Q
STREPTOCOCCAL ENDOCARDITIS
* Found where? Cause what?
* Common cause of what?
* Complicated or uncomplicated?
* Sensitive to what?
A
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)
18
Q
How does treatment timeline change based on Native valve and prosthetic valve IE?
A
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
20
Q
Native valve of streptococcus spp:
* how long is treatment?
* What groups should not get the shorter therapy?
* Vancomycin is for who?
A
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
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
23
Q
Staph spp txt: Prosthetic valve
* What is the txt for methicillin sensitive?
* What is the txt for methicillin resistant?
A
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,
25
Antibiotic prophylaxis before dental procedures is not recommended for who?
is not recommended for any other types of
congenital heart disease.
26
antibiotic prophylaxis is not recommended for patients with what?
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.
27
28
When and when not is AP suggested for dental procedures?
29
30
How long does acute pericarditis last?
under 4-6 weeks
31
Acute Pericarditis:
* Treat how?
* What do you give/restrict?
32
Acute pericarditis:
* Addition of colchinine, reduces what?
* Full dose of NSAIDS until when?
* When can you taper?
* 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
33
Give all the different choices of NSAIDs with colchicine and doeses
## Footnote
Colchicine dose reduced to once daily for patients < 70 kg
34
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?
35
36
* What is released in rsponse to inflammation? What does this do?
* 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)
37
* COX 1 is always what?
* What does thromboxane and prostaglandins/prostacyclins do?
COX-1 always circulating and active
* Thromboxane: Promotes platelet aggregation
* Prostaglandins and prostacyclin
* Secretion of protective gastric mucosa
* Maintaining renal blood flow
38
COX 2 activated where? What does it mediate?
* COX-2 activated at sites of inflammation
* Mediates inflammation, pain, and fever
39
What does NSAIDs block? What does it cause?
NSAIDs block COX-1 and COX-2
* Reduce prostaglandin, thromboxane, prostacyclin synthesis
* Reduce inflammation, pain, and fever
40
NSAID SE:
* MC SE is what? Why?
41
What are the Other gastrointestinal adverse effects of NSAIDS?
* Dyspepsia
* Abdominal pain
* Nausea / vomiting
42
NSAIDS: SE
* How does NSAIDS effect the kidneys?
43
What can happen to the skin due to NSAIDs?
Rash – hypersensitivity reactions rare / cross sensitivity
44
Black box warnings of NSAIDs:
* What are the serious CV events? (2)
* What Increased risk of what?
* Avoid in who?
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
45
What are the CI of NSAIDs (4)
* Aspirin allergy – watch for patients with Samter’s triad
* Peptic ulcer. GI bleed or perforation
* Advanced renal impairment
* Cerebrovascular bleeding
46
Colchicine:
* What is the MOA?
* What is contraindicated?
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)
47
What are the SE of colchicine? (4)
* Diarrhea
* Nausea / vomiting
* Pharyngolaryngeal pain
* Bone marrow suppression (leukopenia, granulocytopenia, thrombocytopenia, aplastic anemia)
48
What is type I, II, III, IIIa, IIIb aortic dissection?
49
Aortic dissection:
* What is the txt of type A/DeBakey I or II?
* What is the txt of type B/DeBakey IIIa or IIIb?
50
Aortic dissection type III or B- Medical treatment
* What is the first line therapy?
* What is the goal?
First-line therapy – IV beta-blockers
* Goals: HR < 60, SBP < 100 to 120 mmHg
51
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?
Esmolol = DOC
* Titrate to HR
Labetalol = alternative
Second-line: verapamil / diltiazem
Adjuvant therapy: opioids for pain control
52
Giant cell/temporal arteritis?
* What is it?
* What arteries are affected?
* Typically in who?
* 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
53
GCA txt:
* What is the txt with a patient with no vision loss or signs of ischemia?
* Prednisone 1 mg/kg PO daily (max 60 mg/day) x 2 to 4 weeks then
* Prolonged taper ( 6 to 12 months)
54
GCA txt:
* What is the txt with a patient with threatened or established vision loss?
* 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)
55
What is second line for GSA? Why?
56
GCA tapering is guided by what?
* Taper guided by ESR and CRP
57
Steroids:
* Endogenous steroids produced where?
* Steroids released when?
* What effects?
* Endogenous steroids produced in the adrenal gland (MC cortisol)
* Released in response to stress and inflammation
* Anti-inflammatory and immunosuppressive effects
58
What is the MOA of steroids? (cytokines and mediators)
**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**
59
Steroids effects:
* What do they suppress?
Suppress inflammatory response to all noxious stimuli
* Pathogens
* Chemical / physical
* Immune mediated / hypersensitivity
60
How does steroids reduce inflammation? (4)
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
T/F: Steroids corrects the underlaying cause of disease
False
62
What are the short term steroids effects? (6)
63
What are the long term steroids effects? (8)
64
Steroids tapering:
* Recommended following prolonged use / higher doses. Explain (3)
* Used to avoid what?
* What is the general taper duration rule?
65
What are the sxs for steroid withdrawal?(7)
66
Tocilizumab (actemra)
* What is the drug?
* What is the MOA?
* What are teh contraindications?
* Biologic DMARD
* MOA: IL-6 antagonist
* Dose: 162 mg once weekly subcutaneous injection
* Contraindications: Sepsis
67
TOCILIZUMAB (ACTEMRA)
* What is the BBW?
* What is the SE?
* How do we monitor?
* 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
PAD:
* MC form of what?
* What is it?
* What is equivalent?
69
PAD:
* What is the MC characterisitc? Explain what it is?
* Resting pain=
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
What does the history and PE show for PAD?
71
How do you dx PAD? What are other tools?
Ankle-Brachial Index (ABI)
* ≥ 90 % sensitive and specific
* Important screening tool
Other tools:
* CTA
* MRI
* Angiography
72
73
* What is the txt for PAD?
* What are the goals? (4)
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
Treatment of PAD:
* What are the lifestyle modications?
75
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?
76
Antiplatelet therapy:
* Recommended for who?
* What does it recude?
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
What is the first line for antiplatelet therapy for PAD?
Aspirin or Clopidogrel
* Dual antiplatelet therapy NOT recommended
78
79
What is steps one, two, and three of primary homeostasis?
(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
What is step 4 of primary hemostasis?
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
## Footnote
ADP = adenosine diphosphate
81
What is step five of primary hemostasis?
Aggregation – GPIIB/IIIA links platelets together via fibrinogen and form a platelet plug
## Footnote
Platelet plug to move to secondary hemostasis
82
Antiplatelet therapy: Aspirin
* What is the MOA of aspirin?
* What type of drug is it?
* 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
Antiplatelet therapy: Aspirin
* Blocks what for and for how long?
* First line for what?
* Blocks thromboxane platelet activation for the life of the platelet (7-10 days)
* First-line prophylactic antiplatelet therapy
84
Antiplatelet therapy: ADP receptor inhibitors (P2Y12 inhibitors)
* What are the examples?
* Second line for what?
* What can it be combined with?
* Clopidogrel, ticagrelor, ticlopidine, prasugrel
* Second-line prophylactic antiplatelet therapy
* Combined with aspirin for dual antiplatelet therapy (DAPT)
85
What is the MOA of ADP receptor inhibitors (P2Y12 inhibitors)?
* 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
Treatment for intermittent claudiccation
* What is first line?
* What is second line?
* First-line: Supervised exercise program and lifestyle modifications
* Second-line: Cilostazol
87
What is the MOA and effects of cilostazol?
Increased cAMP->decreased intracellular calcium
* Vasodilation
* Decreased platelet activation
* Improves symptoms and increases walking distance in
patients with IC
88
Cilostazol
* What is the dose?
* Discontinue if what?
* use limited by what?
* 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
* What are the Symptoms of Bleeding – low or dysfunctional platelets? (5)
* Serious bleeding rare – MC when combined with what?
* Antiplatelets agents CI when?
90
Antiplatelet therapy for PAD/IC
* ASA: MOA, SE and CI?
91
Antiplatelet therapy for PAD/IC
* Clopidogrel: MOA, SE and comments?
92
Antiplatelet therapy for PAD/IC
* Cilostazol: MOA, SE and comments?
93
Acute limb ischemia:
* What is the initital txt? DOC?
* What should you manage?
* Initial treatment: anticoagulation
* Heparin – DOC
* Pain management
94
Acute limb ischemia: Heparin
* What is the dose?
* Dose titrated to what?
* Alternative parenteral agent may be used when?
* Decreases what?
* Preserves what?
* 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
Evaluation for limb management:
* Treatment depends on what?
* What is Endovascular techniques with fibrinolytics?
* What are the surgical techniques?
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
97
Limb management (after)
* What is recommended for one month?
* What is long term?
98
Phlebitis/thrombophlebitis-superficial
* What is it?
* How do you dx? What are the sxs?
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
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?
100
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?
101
Fill in for Venous Thromboembolism treatment (proximal)
102
Fill in the HAS-BLED score
* 0 = low bleeding risk
* 1 to 2 = moderate bleeding risk
* ≥ 3 = high bleeding risk
103
Isolated distal DVT- First episode:
* Where do they occur?
* What do you do for Asymptomatic patients with low risk of extension?
104
What are the risk factors for proximal extension?
105
Isolated distal DVT-first episode:
* What do you do for severe symptoms or risk of thrombosis extension?
Anticoagulate following proximal vein treatment guidelines
106
ANTICOAGULATION TRANSITIONS
* What is complex?
* What exist?
* What is recommended?
107
Treatment of severe vte: Life-threatening pulmonary embolism with hemodynamically unstable patient
* What is first line and second line?
* First-line: IV thrombolytic therapy
* Second-line: Catheter-directed thrombolytic therapy
108
Massive proximal lower extremity thrombosis or ilio-femoral thrombosis associated with severe symptoms (< 14 days duration)
* What is first line?
First-line: Catheter-directed thrombolytic therapy
109
Treatment of severe vte
* What is last line?
Embolectomy
110
Tissue plasminogen activator (tpa)
* What is the MOA?
* What is the half-life?
* How do you dose it?
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
Tissue plasminogen activator (tpa)
* What are the adverse effects?
Bleeding
* Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age
112
bridging:
* What does it depend on? (3)
* What may be continued?
* Reversal agents should be utilized for what?
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
114
Anticoagulation bleeding
* Anticoag are CI with what?
* What is major bleeding?
**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
Anticoagulation bleeding
* What is minor bleeding?
116
CONTRAINDICATIONS TO ANTICOAGULATION
* What are absolute?
117
CONTRAINDICATIONS TO ANTICOAGULATION
* What are relative?
118
Heparin, LMWH, fondaparinux: Indirect inhibition
* Heparin and low molecular weight heparins (LMWH) bind to what?
* What is ATIII?
* 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
What is the MOA:
* Heparin:
* LMWH:
* Fondaparinux:
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
What can the large molecule (unfractionated)-> Heparin do?
able to interact with both antithrombin III and thrombin
121
What are the indications of heparin? (4)
* 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
What is the dosing of heparin?
* IV or subcutaneously (SC)
* IV: given as bolus plus continuous IV infusion (short half-life)
123
What are the monitoring parameter of heparin?
* 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
What are the adverse effects of heparin?
* Bleeding
* Osteoporosis – long-term therapy
* **Heparin induced thrombocytopenia**
125
What is the antidote for heparin?
* Protamine sulfate 1mg neutralizes ~ 100 units heparin
* Continuous infusions: use heparin dose from preceding 2 to 3 hours
126
How much antidote do you need to give if you give 1200 units of heparin per hour?
127
Heparin induced Thrombocytopenia
* What happens with the immune system? What does that cause?
Immune system makes antibodies that bind to heparin-platelet factor 4 complexes
* Platelet activation – aggregation (clumping)
* Clots
* Thrombocytopenia
## Footnote
Platelets are dropping but clots are forming
128
Heparin induced Thrombocytopenia
* What are the risk?
* What is the onset?
* How do you dx it? (3)
* 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
HIT – alternative treatments
* What do you give more critcally ill patients?
* What do you give stable patients?
130
131
Discontinue heparin
132
Warfarin
* What is the moa?
* 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
Warfarin
* What are the indications? (2)
* DVT, atrial fibrillation, prosthetics valves
* **Only oral anticoagulant indicated for patients with mechanical heart valves**
134
Warfarin-Pharmacokinetics:
* What is half life? What is onset?
* Requires what?
* How is metabolized?
* 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
CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?
136
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?
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
What are the diet issues with warfarin?
Vit K needs to be stabilized with txt
* for example: winter vs summer months
138
Warfarin
* What are the SE? (3)
* What is CI (1)?
139
Warfarin overdose:
* Txt based on what?
Treatment depends on INR level and if patient is bleeding
140
Warfarin overdose:
* What do you with a patient who is not bleeding? (3)
* Hold warfarin
* Give vitamin K (1 to 5 mg PO)
* Resume warfarin at lower dose once INR is 2 to 3
141
Warfarin overdose:
* What do you with a patient who is bleeding? (2)
* 4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k
OR
* Fresh frozen plasma (FFP)
142
Fresh frozen plasma
143
Direct inhibitors
* What are the two types and their MOA?
Factor Xa inhibitors
* Directly bind factor Xa
* Prevent conversion of prothrombin to thrombin
Thrombin inhibitors
* Bind to and inhibit thrombin
144
Fill in for DOACS
145
