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competency 10/11 > cardio: thrombosis > Flashcards

cardio: thrombosis Flashcards

1
Q

thrombosis

A

process involved in the formation of a fibrin blood clot, contributed by platelets and clotting factors

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2
Q

embolism

A

process by which any intravascular material migrates from its original location to occlude a distal vessel
- blood clot (thrombosis)
- fat
- air
- amniotic fluid
- tumour

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3
Q

primary hemostasis

A

platelet adhesion, activation, and aggregation

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4
Q

secondary hemostasis

A

clotting cascade
- once activated -> generates thrombin -> fibrin

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5
Q

function of the hemostatic system

A
  • to react to vascular injury
  • to close the vessel wall defect
  • prevent further bleeding
  • maintain our blood in a fluid state
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6
Q

arterial thrombosis, typically caused by

A
  • rupture of the atherosclerotic plaques
  • AF, blood clots from heart (cardioembolic source - use anticoag)
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7
Q

venous thrombosis, typically caused by

A

a combi of factors from the Virchow’s triad

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8
Q

diseases a/w arterial thrombosis

A

ACS, ischemic stroke, limb claudication/ischemia, mesenteric artery ischemia

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9
Q

location of arterial thrombosis

A

left heart chambers, arteries

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10
Q

location of venous thrombosis

A

venous sinusoids of muscles and valves in veins

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11
Q

diseases a/w venous thrombosis

A

dvt, pe

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12
Q

composition and treatment of arterial thrombosis

A

mainly platelets, some fibrin and occasional leukocytes -> antiplatelets

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13
Q

composition and treatment of venous thrombosis

A

mainly fibrin and erythrocytes -> anticoagulation

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14
Q

platelet-rich thrombus

A

‘white clot’
- atherosclerotic plaque rupture
- exposure of lipid core to blood
- platelet activation and aggregation

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15
Q

fibrin-rich thrombus

A

‘red clot’
- AF: formation of LAA (left atrial appendage) thrombus
- activation of coagulation cascade

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16
Q

deep vein

A

iliac, femoral, poplitical, tibial veins
- major role in propelling blood toward the heart (muscles surrounding the deep vein help to force the blood towards the heart, with help of one-way valves)

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17
Q

when circulation of the blood slows down due to illness, injury or inactivity……

A

blood can accumulate or ‘pool’ which provides an ideal setting for clot formation

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18
Q

DVT risk factors

A
  • age: doubles with each decade >50yo
  • venous stasis: immobility, major surgery, general anesthesia for >30min
  • vascular injury: indwelling venous catheters, major orthopedic surgery, trauma
  • hypercoagulability: malignancy, pregnancy/postpartum, clotting factor deficiencies
  • drug therapy: estrogen replacement
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19
Q

s/sx of DVT

A
  • discoloration of the elf: pallor from arterial spasm, cyanosis from venous obstruction, reddish color from perivascular inflammation
  • calf or leg pain or tenderness
  • swelling of the leg or LL
  • warm skin
  • surface veins become more visible
  • leg fatigue
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20
Q

diagnosis of DVT

A
  • clinical features
  • history, risk factors and physical examination
  • tests for definitive dx: venography (x-ray imaging of the leg via injection of contrast), impedance plethysmography (sensing changes in blood vol via use of electrodes)
  • venous ultrasonography (most common, uses ultrasound to see if there is any abnormality in blood flow)
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21
Q

pathophysiology of PE

A

DVT breaks off (embolus) and travel in the circulation, getting trapped in the lung, where it blocks the oxygen supply

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22
Q

risk factors of PE

A
  • hx of vte
  • recent surgery
  • immobilisation
  • stroke
  • obesity
  • htn
  • malignancy
    -> BUT absence of risk factors does not exclude dx of PE (many patients have no identifiable risk factors!)
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23
Q

s/sx of PE

A

SOB, tachycardia (>100bpm), tachypnea (>20bpm), sweating, apprehension (anxiety or a feeling of impending doom), sharp chest pain, cough, blood sputum, fainting

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24
Q

one of the most popular scoring system for PE dx

A

Well’s criteria for predicting the probability of PE
- helps to decide what further diagnostic testing (venous ultrasonography, CT pulmonary angiogram) may be necessary

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25
Q

treatment of VTE

A

anticoagulation:
- SC LMWH
- IV UFH
(after acute phase)
- DOACs
- warfarin

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26
Q

stroke risk factors, modifiable

A

htn, dm, smoking, hld, physical inactivity

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27
Q

stroke risk factors, non-modifiable

A

age>80y, race and ethnicity, sex (generally men>women, except ages 35-44y and >85y), FH and genetic disorders eg, sickle cell disease

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28
Q

stroke diagnosis

A
  • history and physical examination
  • neurologic evaluation: stroke scales
  • brain imaging: NCCT, DW-MRI
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29
Q

treatment of acute ischemic stroke

A

tPA (tissue-type plasminogen activator, recombinant form of endogenous protease)
-> binds to fibrin in thrombus -> converts entrapped plasminogen to plasmin -> initiates local fibinolysis

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30
Q

secondary prevention for non-cardioembolic (atherothrombotic) ischemic stroke

A

antiplatelet (white clot)

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31
Q

secondary prevention for cardioembolic ischemic stroke

A

anticoagulant (red clot)

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32
Q

AF -> ischemic stroke?

A

AF is an independent risk factor for ischemic stroke
- impaired atrial cotnraction -> blood stasis (abnormal blood flow) -> increase thromboembolic risk

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33
Q

DOACs have a lesser risk of ____________ than warfarin

A

intracranial bleeding

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34
Q

use of DOACs vs warfarin, which is preferred in pt with severe renal impairment?

A

warfarin

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35
Q

use of DOACs vs warfarin, which is preferred in pt with valvular AF?

A

warfarin
- AF with rheumatic mitral stenosis, a mechanical or bisprosthetic heart valve, or mitral valve repair
- insufficient evidence for DOACs in this area

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36
Q

indications for anticoagulant therapy

A

pathologic thrombus formation:
- dvt, pe
- acs (unstable angina, acute MI)
- intracardiac thrombus formation

prophylaxis:
- orthopedic, general surgery patients
- bridging therapy
- prophylactic flushes to maintain potency of lumen catheters

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37
Q

full effects of warfarin depends on

A
  • inhibition of vit k-dependent clotting factors production
  • depletion of previously synthesised vit k-dependent clotting factors
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38
Q

early in warfarin treatment (within 24hr), INR can

A

increase, secondary to depletion of factor 2 (shortest t1/2 = 6h)

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39
Q

full anticoagulant effect of warfarin only seen after

A

5-7 days of treatment, when factors 2 and 10 (longest t1/2) are depleted

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40
Q

prothrombin time

A
  • measures how long it take for blood to clot
  • normal: 12sec
  • prolonged by deficiencies of clotting factors SNOT
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41
Q

what is the problem with using PT for lab monitoring?

A

no standardised thromboplastin reagent -> significant variability in PT

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42
Q

INR

A
  • mathematical ‘correction’ of PT
  • baseline: 1
    INR = (PT of patient/PT mean normal)^ISI
    ISI = international sensitivity index used at the local lab to perform the PT measurement
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43
Q

higher the INR

A

greater the anticoagulant effect -> ‘thinner’

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44
Q

HAS BLED score

A

Hypertension (uncontrolled >160mmHg)
Abnormal renal/liver disease - 1 point each
Stroke

Bleeding tendency/predisposition
Labile INR
Elderly>65yo
Drug or alcohol - 1 point each

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45
Q

precautions during initiation of warfarin - assessing patient’s sensitivity to warfarin using these factors (risk of over anticoagulation and bleeding is increased with the following):

A
  • age>70
  • weight<50
  • baseline INR>1.4 or low platelet count<50k
  • history of falls or GI bleed
  • severe CHF or liver disease
  • presence of malignancy
  • malnutrition
  • major surgery within 10-14 days
  • ddi eg, amiodarone, rifampicin
  • HAS BLED >= 3
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46
Q

treatment of overanticoagulation by warfarin

A
  • hold and/or reduce dose
  • vitamin K1 (phytonadione): PO, IV
47
Q

choose dose carefully based on INR level and s/sx of patients to avoid……

A

initial resistance to subsequent warfarin therapy

48
Q

factors affecting warfarin therapy

A
  • age
  • ethnicity: asians tend to have higher warfarin sensitivity
  • gender: F»>M
  • recent surgery: incr risk of bleeding -> incr INR
  • undernourished or NPO x more than 2 days: initiate warfarin at dose of =<5mg
  • fever or diarrhea, incr warfarin sensitivity
  • alcohol: acute incr, chronic decr INR
  • smoking, may incr or decr INR
  • exercise/activity
  • underlying disease states
  • non-adherance
  • diet
  • drug- and herb- interactions
49
Q

factors affecting warfarin therapy: underlying disease states

A
  • CHF/liver disease: initial dose =< 5mg
  • hyperthyroidism, incr INR
  • hypothyroidism, decr INR
50
Q

factors affecting warfarin therapy: diet

A
  • vit k-rich foods, decr INR: dark green, leady vege eg. kale, spinach, turnip greens, chick peas, cauliflwoer, cabbage, asparagus, broccoli, brussels sprouts
  • meat: beef liver, pork liver
  • fruits: avocado, apple, banana, orange, peas
51
Q

drugs that incr INR

A
  • inhibit catabolism of clotting factors: thyroid hormones
  • inhibition of warfarin metabolism (non-PK): paracetamol>2g/d, allopurinol, azithromycin, simvastatin, TCAs, sulfamethoxazole
  • inhibition of warfarin metabolism via 2c9: amiodarone, celecoxib, metronidazole, sulfamethoxazole
  • inhibition of warfarin via cyp3a4: ciprofloxacin, clarithromycin, erythromycin, isoniazid, itraconazole, ketoconazole
  • inhibition of warfarin via 1a2: FQ
52
Q

drugs that decr INR

A
  • incr synthesis of clotting factors: vit K, estrogens
  • decr catabolism of clotting factors: PTU
  • induce warfarin metabolism via 3a4: cbz, rifampin
53
Q

herbs that incr bleeding risk

A

garlic, ginger, gingko

54
Q

herbs that decr INR

A
  • contains vit K derivatives: green tea, coQ10
  • induces cyp3a4: st john’s wort
  • unknown: ginseng
55
Q

warfarin adverse effects

A

most common: bleeding
rare: skin necrosis, purple toe syndrome

56
Q

skin necrosis

A
  • extensive thrombosis of venules and capillaries within SQ fat, involving abdomen, buttocks, thighs or breasts
  • due to protein C or S deficiency
  • onset: within 1-10 days of warfarin initiation
57
Q

purple toe syndrome

A
  • release of atheromatous plaque emboli to cause systemic cholesterol microembolism
  • incr risk in pt with protein C deficiency
  • onset: 3-10 weeks after warfarin initiation
  • toes painful, purple
58
Q

in pt with swallowing difficulties, can dabigatran capsules be opened?

A

no! dabigatran should not be opened in view of the dramatic increase in bioavailability

59
Q

in pt with swallowing difficulties, can rivaroxaban be crushed?

A

yes! suspend in 50ml of water, stable in water for up to 4 hours
- not suitable for feeding tubes that do not terminate in the stomach eg. nasojejunal, PEJ

60
Q

in pt with swallowing difficulties, can apixaban be crushed?

A

yes! may be crushed and suspended in water, or D5W via oral or nasogastric tube, stability up to 4 hours

61
Q

monitoring for anticoagulants

A
  • routine monitoring using clotting test (PT, INR, aPTT, FXa) not recommended
  • renal function: baseline and at least every 3-6 months after, or during acute illness that may worsen renal function
  • liver function: baseline and yearly after, every 3-6months for patients at risk of hepatic dysfunction
  • cbc: baseline and at regular intervals (at least yearly), assess trends in Hb/Hct
  • s/sx of blood loss
62
Q

symptomatic management of bleeding for pt on anticoagulants

A
  • mechanical compression
  • surgical intervention
  • fluids for hemodynamic support
  • blood products
63
Q

antidote for rivaroxaban and apixaban

A

coagulation factor Xa (recombinant), inactivated-zhzo

64
Q

antidote for dabigatran

A

idarucizumab

65
Q

rivaroxaban dose in stroke prevention for non-valvular AF

A

CrCl>50: 20mg OD
CrCl 15-49: 15mg OD

66
Q

rivaroxaban dose in treatment or prevention of DVT

A

day 1-21: 15mg BD
from day 22: 20mg OD
after 6months: 10mg OD or (if high risk of VTE recurrence: complicated comorbidities, recurrent DVT/PE on extended prevention) 20mg OD

67
Q

rivaroxaban dose in prevention of VTE after elective hip or knee replacement surgery

A

10mg OD x5w (hip) or 2w (knee)

68
Q

rivaroxaban, not recommended for use:

A
  • Under 18 years of age
  • CrCl <15 ml/min
  • Concomitant treatment with strong inducers or inhibitors of both CYP3A4 and Pgp
    (e.g. azole, HIV protease inhibitors )
  • Hepatic disease associated with coagulopathy and clinically relevant bleeding
    risk
    –Avoid use in moderate to severe hepatic impairment (Child-Pugh Class B and C cirrhosis)
69
Q

For patients treated for prevention of stroke and systemic embolism, how do we switch from VKA to rivaroxaban?

A

VKA should be stopped and xarelto initiated when the INR =< 3.0

70
Q

For patients treated for DVT and prevention of recurrent DVT and PE, how do we switch from VKA to rivaroxaban?

A

VKA should be stopped and xarelto initiated when INR =< 2.5

71
Q

How do we switch from rivaroxaban to VKA?

A

both given overlapping until inr is >= 2.0

72
Q

converting from parenteral UFH to xarelto

A

xarelto should be started at the time of discontinuation

73
Q

converting from parenteral LMWH to xarelto

A

xarelto should be started 0-2 hours before the time of the next scheduled administration of the parenteral drug

74
Q

converting from xarelto to parenteral anticoagulants

A

discontinue XARELTO and give the first dose of the other anticoagulant at the time that the next XARELTO dose would have been taken.

75
Q

apixaban dose in stroke prevention for non-valvular AF

A

5mg BD, unless…..

at least 2 of the following:
- age >= 80
- weight =< 60
- SCr >= 133umol/L
THEN 2.5mg BD

76
Q

apixaban dose in treatment or prevention of DVT

A

10mg BD x7d -> 5mg BD
after >=6 months or for reduction in risk of recurrent DVT following initial therapy: 2.5mg BD

77
Q

apixaban dose in prevention of VTE after elective hip or knee replacement surgery

A

2.5mg BD x 35d (hip) or 12d (knee)
- starting 12 to 24 hours after the surgery

78
Q

ddi with apixaban - increase exposure and risk of bleeding

A

combined p-gp and cyp3a4 inhibitors
- ketoconazole, itraconazole, ritonavir

79
Q

how to dose adj for coadministraiton of apixaban with combined p-gp and cyp3a4 inhibitors?

A

for pt receiving 5mg or 10mg BD, reduce dose by 50%

for pt receiving 2.5mg BD, avoid!!

80
Q

switching from eliquis to warfarin

A

discontinue eliquis, then begin both parenteral anticoagulant and warfarin at the next dose that would have been taken -> discontinue parenteral anticoagulant when INR reaches acceptable range

81
Q

switching from warfarin to eliquis

A

stop warfarin and start eliquis when INR =< 2

82
Q

what is dabigatran formulated with?

A

tartaric acid - reduce variability of absorption of dabigatran etexilate

83
Q

recommended dose of dabigatran for stroke reduction in NVAF

A

CrCl 15-29ml/min: 75mg BD
CrCl>30: 150mg BD

84
Q

recommended dose of dabigatran for treatment or prevention of DVT

A

150mg BD
- for treatment only: initial use of parenteral anticoagulation for 5-10d

85
Q

recommended dose of dabigatran for post hip surgery DVT prophylaxis

A

110mg, 1-4 hours post-surgery and after achieving hemostasis -> 220mg OD for 28-35d

86
Q

ddi of dabigatran with p-gp inhibitors

A

NVAF: cannot use for CrCl<30
DVT/PE & HIP: cannot use for CrCl<50

87
Q

converting from warfarin to dabigatran

A

discontinue warfarin -> start dabigatrian when INR <2

88
Q

converting from dabigatran to warfarin

A

start warfarin 3d (CrCL>50), 2d (30-50ml/min), 1d (15-30) before discontinuing dabigatran

89
Q

converting from parenteral anticoagulants to dabigatran

A
  • scheduled dosing: initiate dabigatran 0-2h before next dose
  • continuous infusion (UFH): at time of discontinuation
90
Q

converting from dabigatran to parenteral anticoagulants

A

CrCl>= 30: wait 12h after last dose of dabigatran
CrCl =<30: wait 24h after last dose of dabigatran

91
Q

moa of UFH

A

accelerates action of antithrombin (ATIII: a naturally circulating anticoagulant antithrombin made by the liver) to inactivate various clotting factors in the coagulation cascade
- mainly factors 2a (thrombin) and 10a
- also interferes with platelet aggregation

92
Q

does heparin cross the placenta or distribute into breast milk?

A

nope, it is a large molecule

93
Q

clinical indications for UFH

A
  • when immediate anticoagulation is required
  • acute thrombotic conditions: acute DVT/PE, ACS
  • when immediate reversal of anticoagulation therapy is anticipated
  • prophylactic therapy when thromboembolic risks are high
94
Q

aPTT

A

activated partial thromboplastin time
- reflects alterations in intrinsic pathway of the clotting cascade
- mean normal: 24-36s, varied based on reagents used for lab tests
- must wait >= 6 hours to draw aPTT after initiation of heparin

95
Q

UFH adverse effects

A
  • hypersensitivity: allergy to pork products
  • hemorrhages (common): common sits of bleeding incl soft tissues, GI/urinary tract, nose and oral pharynx
  • hyperK (rare): high or low dose, may occur as quickly as within 7 days after heparin initiation
  • oseteoporosis: associated with >20,000IU/day for >= 6 months
  • HIT: type 1 and 2
96
Q

is type 1 or 2 HIT more severe?

A

2 - delayed onset after 5-14 days of heparin initiation, immune-mediated response

97
Q

management of UFH overdose

A
  1. discontinuing heparin
  2. blood transfusion
  3. IV protamine sulfate: bind to heparin to form stable complex, 1mg will neutralise 100U of heparin, t1/2 = 7min
98
Q

adv of LMWH over UFH

A
  • incr plasma half life: longer duration of action
  • superior bioavailability
  • lower incidence of HIT (type 1 or 2)
  • less risk of osteoporosis
  • more predictable dose-response rs
99
Q

anti-Xa monitoring recommended in

A
  • severely obese patients
  • patient with renal insufficiency
  • pregnant
  • patients with prosthetic heart valves
  • high risk for bleeding
100
Q

use LMWH with extreme caution in patient with

A

indwelling epidural catheters - incr risk of spinal or epidural hematomas, resulting in permanent paralysis (BB warning)

101
Q

aspirin MOA

A

irreversibly inhibit platelet COX-1 -> inhibit downstream production of thromboxane A2 (critical inducer of platelet activation and aggregation)

102
Q

adverse effects of aspirin

A

upper GI events eg, gastric ulcers, GI bleeding - since cox-1 is protective of GI lining

103
Q

clopidogrel, prasugrel, ticagrelor: which is reversible?

A

ticagrelor

104
Q

prasugrel is a third gen thienopyridine, developed to __________

A

overcome major short comings of clopidogrel:
- large inter individual response variability (2C19 mediated metabolism to produce active metabolites)
- delayed onset of action
- high proportion of patients with insufficient inhibition of platelet aggregation

105
Q

advantages of prasugrel and ticagrelor over clopidogrel include

A

reduced rates of ischemia and stent thrombosis

106
Q

antiplatelets use in pregnancy

A
  • clopidogrel and prasugrel: cat B, used routinely and safely
  • ticagrelor: cat C, may warrant use
107
Q

vitamin K is a ?-soluble vitamin

A

fat

108
Q

2 forms of vitamin K

A

k1 (phylloquinone): acquired through diet and present in green leafy vege, broccoli, and brussel sprouts
k2 (menaquinone): gut bacteria, especially bacteriodes

109
Q

vitamin D deficiency common in newborns due to

A

insufficient intestinal colonisation by bacteria and inadequate nutritional compensation -> parenteral vit K administered at birth

110
Q

fibrinolysis

A

process of dissolution of fibrin in blood clots to prevent them from growing

111
Q

preferred fibrinolytic drug?

A

tPA&raquo_space;> uPA or streptokinase
- preferentially bind to clot-associated fibrin, localised PLG and tPA on the surface hence localising and enhancing plasmin generation

112
Q

clinical uses of fibrinolytic drugs

A

often used following an acute ischemic stroke, MI or PE

113
Q

absolute contraindications for fibrinolytic drugs

A

patients with prior cranial hemorrhage, ischaemic stroke within the last 3 months, and/or active bleeding

114
Q

antidote for fibrinolytic drugs

A

anti fibrinolytic agents - tranexamic acid (competes with lysine binding sites on plasminogen and plasmin, thus blocking interaction w fibrin) - used to reverse states of excess fibrinolysis

competency 10/11 (31 decks)

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