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Medicine Year 1 > Week 143 Haemostasis > Flashcards

Week 143 Haemostasis Flashcards

0
Q

42 yr old man with recurrent epistaxis (since teens), with subsequent iron deficiency, and required blood transfusions on occasions.

A family history (father and sister) of nose bleeds. O/E severe lesions on lips and tongue of dilated blood vessels. Nml plt, Nml coag. It’s??

A

Hereditary haemorrhagic talengectasia.

Autosomal dominant condition.

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1
Q

What is normal haemostasis

A

quick, efficient, clot formation at the site of a bleed.

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2
Q

7 Y/O girl chest infection 7/7 ago. Purpura (petichae) on body, particular legs, no meds, no other sig. history. O/I All normal, except low platelet count., blood film = isolated thrombocytopenia. This is likely to be________.

A

Immune thrombocytopaenia.

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3
Q

5/12 YO baby with swollen painful Rt knee. knee bent and stiff, no history of trauma, normal birth, no fmh. IVX show FBC normal, coagulation = Factor VII > 2%. It is likely _________.

A

Severe Haemophilia A.

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4
Q

75 yo woman, collapsed at home. Morning malaena. PMH - AF on long term therapy.
O/E = pale, BP 90/60, PR 124/min
Coagulation - INR 8 (target 2-3) This is likely ______ due to ______.

A

GI bleed due to warfarin od.

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5
Q

In deranged haemostasis there is:

A

Abnormal bleeding (excessive prolonged or delayed)

Non-physiological thrombosis

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6
Q

Primary haemostasis is __________.

A

The formation of a platelet plug.

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7
Q

Secondary Haemostasis is __________.

A

The formation of a fibrin clot.

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8
Q

Plasminogen becomes Plasmin via ______. Plasmin then cleaves Fibrin to form ________. This process can be investigated with the ______ Test.

A

Tissue plasminogen activator
Fibrin degradation products
D-Dimer test.

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9
Q

Failure of haemostasis means ____ or ______.

A

Bleeding or pathological thrombosis.

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10
Q

Platelets recognise (using glycoprotein 1b/1x/v) VWF (vonwilemhalm factor???) to recognise ______.

A

Areas of damaged endothelium.

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11
Q

Which glycoprotein on a platelet binds to vWF?

A

GP1b

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12
Q

What is a tissue factor?

A

A Factor released from damaged tissue.

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13
Q

The extrinsic pathway of coagulation comes from ______.

A

Tissue factors.

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14
Q

The intrisic coagulation cascade is initiatedb y ______.

A

Phospholipid surface.

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15
Q

To convert prothrombin to thrombin from the common pathway you need_________.

A

Factor Ten (FX) + Factor Five a (FVa) + PLCa2+.

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16
Q

The test for the extrinsic pathway is called the _______.

A

The prothrombin time, normalised with INR.

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17
Q

In extrinsic, to activate the normal pathway ________ is formed.

A

Tissue Factor/FVIIa

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18
Q

To test the final pathway, you add ______ and assess the ______.

A

Thrombin, and assess clot formation time.

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19
Q

To test intrinsic factor, you use __________.

A

Activated partial thromboplastin time (APTT).

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20
Q

Intrinsic factors are _______—–>_________—–> _________——-> ___________, which activates normal pathway.

A

FX11–> FX11a –> FX1a –> FIXaFV111a, PLCa2+

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21
Q

Site of bleeding for primary haemostasis is _____.

A

Skin, mucous membranes.

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22
Q

Primary haemostasis presents with which symptom?

A

Petichae

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23
Q

In secondary haemostasis, petichae is _____ _______.

A

Not present.

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24
Q

Echymoses means _____. In secondary haemostasis, these are _____. In primary haemostasis these are ___ and ____.

A

Bruise
Large, palpable
Small, superficial

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25
Q

Haemoarthroses/muscle haematomas are ____ in primary and ____ in secondary haemostasis.

A

Rare in primary

Common in secondary

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26
Q

Bleeding after surgery is ___ and ____ in ______, and _____ and _____ in ______haemostasis.

A

Immediate and mild in primary

Delayed and severe in secondary

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27
Q

What two reasons will a patient present with purpura?

A

thrombocytopaenia - most common cause for sepsis –> if platelet count is low, likely cause.
OR
vasculitis (if platelet count is normal) i.e. Henoch-Schonlein purpura

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28
Q

Henoch-Schnoleein purpura is a form of ______.

A

Vaculitis

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29
Q

Glanzmann’s thrombasthenia is a lack of _____ normally presenting in neonates.

A

GPIIb/IIIa

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30
Q

Vitamin K is needed to make Factors _______ (4 of them).

A

2, 7, 9, and 10.

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31
Q

Defective haemostasis will present with a history of:

A

Abnormal bruising, prolonged bleeding from cuts, nose bleeds, menorrhagia, bleeding after child birth, dental history, bleed post-surgery, previous anaemia and transfusion, drug history and family history.

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32
Q

FBC will detect ____.

A

Anemia; Red cell fragmentation.

THROMBOCYTOPAENIA

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33
Q

APPT (ACTIVATED PARTIAL THROMBOPLASTIN TIME) DETECTS WHAT?

A

DEFICIENCY OF ALL COAGULATION FACTORS (EXCEPT VII)

HEPARIN

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34
Q

INR (ONE STAGE PROTHROMBIN TIME) WILL DETECT WHAT?

A

DEFICIENCY OF FACTORS I, II, VII, AND X.

THINK = WARFARIN

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35
Q

FIBRINOGEN OR THROMBIN CLOTTING TIME WILL DETECT WHAT?

A

REDUCED OR ABNORMAL FIBRINOGEN. HEPARIN; FIBRIN DEGRADATION PRODUCTS.

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36
Q

BLEEDING TIME (NOT TO BE DONE IF THROMBOCYTOPAENIA) DETECTS WHAT?

A

TEST PLATELETS - VESSEL WALL INTERACTION.

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37
Q

THE SPECIAL TEST OF MIXING TESTS WITH NORMAL PLASMA WILL DO WHAT?

A

ASSESS IF NORMAL PLASMA CORRECTS PROLONGED APTT AND OSPT.

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38
Q

COAGULATION FACTOR ASSAYS ARE USED TO DO WHAT?

A

ASSESS/CONFIRM COAGULATION FACTOR DEFICIENCY.

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39
Q

VON WILLIBRAND FACTORS ASSAYS DO WHAT?

A

HELP CONFIRM VW DISEASE, IF SUSPECTED.

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40
Q

FACTOR VII/OTHER IHIBITO ASSAY IS CONDUCTED IF?

A

IF YOU SUSPECT ANTIBODY BEING PRODUCED TO COAGULATION FACTOR.

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41
Q

PLATELET FUNCTION TESTS TEST _____.

A

QUALITATIVE PLATELETS DEFECTS.

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42
Q

BERNARD-SOULIER DISEASE IS DEFINED AS A LACK OF ____.

A

GPIb

Will see thrombocytopenia +platelet dysfunction + AB

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43
Q

Essential requirements of normal haemostasis are:

A

Normal blood vessels
Adequate platelet number and fuction
Normal coagulation system
Normal and effective fibrinolytic system

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44
Q

Auto-immune thrombocytopaenia is _____. Platelet lifespan is ____ from ____ to a _____.

A

Immunological destruction of platelets.
Lifespan reduced from 7-10 days to a few hours.
Destroyed in spleen and liver
Can be acute OR chronic

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45
Q

Inherited coagulation disorders include:

A

Haemophilia A - Factor VIII def
Haemophilia B - Christmas disease - IX Def
Von Willebrand - Von willebrand factor

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46
Q

Most common cause of low platelets is?

A

Thrombocytopaenia.

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47
Q

Purple tops used for?

A

FBC

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48
Q

BLUE TOP MUST BE FILLED TO WHAT?

A

THE LINE!!!!!

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49
Q

PROTHROMBIN TIME IS USED TO CALCULATE WHAT?

A

INR (WARFARIN MORNITORING)

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50
Q

WHAT ARE THE COMPONENTS OF THE HAEMOSTATIC SYSTEM?

A

PLATELETS
PROTEINS - VWF
DAMAGED ENDOTHELIUM – PHOSPHOLIPIDS, COLLAGEN, VWF, TF

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51
Q

WHERE DO PLATELETS COME FROM?

A

ORIGANATE FROM MEGAKARYOCYTES (FROM MYELOID PROGENITOR LINEAGE) IN THE BONE MARROW.

BUDS OF GRANULAR CYTOPLASM (CONTAIN CLOTTING FACTORS).

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52
Q

WHERE DOES FIBRIN COME FROM?

A

FIBRINOGEN - CONVERTED TO FIBRIN BY THROMBIN

THIS IS CAUSED BY CLOTTING CASCADE (EXTRINSIC/INTRINSIC)

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53
Q

LIVER DAMAGE WILL RESULT IN (MOST LIKELY)

A

REDUCTION IN FIBRINOGEN AND CLOTTING FACTORS - LIVER MAKES A LOT OF PROTEINS!

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54
Q

PLATELET PHOSPHOLIPID BILAYER DOES WHAT?

A

EVERTS TO PRESENT A HUGE PHOSPHOLIPID MEMBRANE SURFACE AREA, IN ORDER TO ACTIVATE PROTEINS.

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55
Q

HOW DOES WARFARIN WORK?

A

IT IS A DIRECT INHIBITOR OF VITAMIN K (COMPETITIVE INHIBITION), STOPPING ACTIVATION OF VIT K DEPENDENT FACTORS.

56
Q

WHAT COULD YOU GIVE TO REVERSE THE EFFECTS OF WARFARIN?

A

PROTHROMBIN COMPLEX CONCENTRATE (PCC) - VIT K DEPENDENT FACTORS

VITAMIN K - SLOWER (OVER 24 HOURS)

57
Q

WHAT IS HEPARIN? HOW DOES IT WORK?

A

ANTICOAGULANT AGENT

?????

58
Q

WHAT IS ASPIRIN? HOW DOES ASPIRIN WORK?

A

IT IS AN SALICYLATE ANTICOAGULANT. IT INHIBITS PLATELET ACTIVATION.

59
Q

WHAT FACTORS MAKE BLOOD MORE LIKELY TO BE LIQUID?

A

???

60
Q

WHAT FACTORS MAKE BLOOD MORE LIKELY TO BE SOLID

A

???

61
Q

WHAT DRUGS INFLUENCE PLATELET FUNCTION AND WHY?

A

????

62
Q

What does virchow’s triad include?

A

Vessel wall damage (i.e. atherosclerosis)
Altered Blood flow (i.e. stasis)
Increased blood coagulability (i.e. thrombophilia)

63
Q

Define placebo.

A

A substance or procedure that has no inherent power to produce an effect that is sought or expected.

64
Q

What is a thrombus?

A

A clot arising in the wrong place.

65
Q

Naturally occuring inhibitors of blood coagulation are ____ and ______.

A
  • Anti Thrombin

- Protein C System (protein s)

66
Q

What is antithrombin?

A
  • A glycoprotein
  • synthesised by liver
  • Inhibits FXa and thrombin
  • > 2000 fold increase of the T/AT interaction by heparin
67
Q

There is a dose response curve for the ______ _______.

A

Placebo effect.

68
Q

Which vitamin is vital for coagulation?

A

Vitamin K

69
Q

Thrombomodulin is linked to which vitamin?

A

Vit K

70
Q

The protein C system inhibits ______

A

Va -> VIIIa

71
Q

What three types of thrombus are there?

A

Arterial
Venous
Microvascular

72
Q

Arterial thrombus is described as a ____ ______. They are made of ______ and ______. They result in _____ and ______, and principally secondary to _______________.

A

White clot
Platelets and fibrin
Ischaemia & Infarction
Atherosclerosis

73
Q

Name three types of arterial thromboembolism.

A

Coronary (Mi/Angina)

Cerebrovascular (stroke/transient ischaemia)

Peripheral embolism (Limb ischaemia)

74
Q

Describe microvascular thrombus.

A

Platelets and/or Fibrin
Results in diffuse ischaemia
Principally in DIC

75
Q

Venous thrombus is describes as a ____ ______. It is made up of ____ and ___ ______ cells. It results in back _____. It is principally due to ____ and ______.

A

Red thrombus
fibrin and red blood cells
Results in back pressure
due to stasis and hypercoagulability

76
Q

What is the extinction of an association?

A

The overwriting of pavlovian conditioning. It’s NEW learning.

77
Q

Name two important examples of venous thromboemoblism.

A

Limb deep vein thrombosis

Pulmonary embolism

78
Q

Name as many risk factors for venous thromboembolism as you can.

A 
Immobility
Tissue trauma (surgery)
Pregnancy
Oral CCP
Obesity
MAlignancy
Hyperviscosity
Anti-phospholipid syndrome
79
Q

A variant in TPH2 predicts what?

A

Whether ppl with social anxiety disorder will experience a placebo effect or not.

80
Q

What is Factor V Leiden?

A

A common heritable thrombophilia.
5% caucasians
7 fold increase of VTE
40 x increase risk in oral contraceptive

81
Q

Name two common heritable thrombophilia?

A

Factor V Leiden

Prothrombin G20210A

82
Q

Name 3 rare causes of heritable thrombophilia.

A

Antithrombin deficiency
Protein C Deficiency
Protein S deficiency

83
Q

What are the clinical diagnostic criteria for antiphospholipid syndrome?

A

Vascular thrombosis
Complications of pregnancy:
- 3 or more unexplained consecutive abortions <10w
- 1 or more loss after 10w
- 1 or more unexplained premature birth Up to 34 w

84
Q

What are the laboratory diagnostic criteria for antiphospholipid syndrome?

A

Anticardiolipin antibodies IgG or IgM
Lupus anticoagulant

Diagnosis req’s at least 1 clinical and 1 laboratory confirmed x2

85
Q

The full effect of a drug is:

A

Placebo + Natural history + Drug

86
Q

What laboratory test would you do to confirm DVT? How would you confirm it?

A

D-Dimers

Imaging to confirm (uS)

87
Q

3 or more of WHAT will give high probability of DVT potential?

A 
Active Cx in last 6/12
Paralysis
Bad >3d
Swollen leg/calf swolllen > 3cm/Pitting odemea
Tenderness along veins
88
Q

What is the nocebo effect?

A

Same principle as placebo effect, except that outcome is negative.
< anxiety contributes to this.

89
Q

Describe DVT prophylactic treatment.

A

MObility, hydration
TED stocking, pneumatic compression
Heparin, i.e. LWMH/other agents

90
Q

What is the Hawthorne effect?

A

An increase in worker productivity produced by the pysch stimulus of being singled out and made to feel important.

91
Q

Unfractionated heparin inactivates what?

A

IIa and xa

92
Q

What is the difference in molecular weight between UFH and LMWH?

A 
UFH = 15
LMWH = 4.5
93
Q

What is the difference in half life between UFH and LMWH?

A 
UFH = 2 hours
LMWH = 4-8 hours
94
Q

When should you suspect pulmonary embolism?

A
  • Always in sudden collapse 1-2 weeks after surgery
  • Dyspnoea at rest or with exertion (usually in seconds or minutes)
  • Pleuritic pain
  • cough
  • Calf/thigh pain/swelling
  • Wheezing
95
Q

How does PE present clinically?

A 
Tachypnea
Tachycardia
Rales (crackles)
> breath sounds
Jugular venous distension
96
Q

What investigations would you conduct to diagnose a PE?

A 
ABG
ECG
CXR
U/S lower limbs
D-Dimers
97
Q

What is a CT-PA?

A

83% of patients with PE had a positive scan.

96% without had a negative scan

98
Q

What is a V/Q scan?

A

A normal scan virtually excludes PE

HIgh probability and clinical sign –> 95% likelihood of PE.

99
Q

What is the gold standard for PE?

A

Pulmonary angiography.
2% mortality
5% morbidity

100
Q

How would you manage a PE?

A 
Resucitation
Anti-coagulation -----> IVC filters when this is contra indicated
-LMWH
- Warfarin
Thrombolysis,
101
Q

Describe the extrinsic coagulation pathway.

A

VII + Tissue factor –> VIIa/TF
VIIa/TF ——-Va——–> changes x –> Xa
Xa changes Prothrombin —> Thrombin
Thrombin changes Fibrinogen —-> Fibrin

102
Q

Describe the intrinsic coagulation pathway.

A

XII—->X11A CAUSES..
X1—->X1A CAUSES…
IX —->IXA CAUSES…
THEN IXa—-> to X (then goes from there…)

103
Q

THROMBIN CAUSES A _____ FEEDBACK LOOP

A

POSITIVE

104
Q

DESCRIBE THE CASCADE OF FIBRINOLYSIS.

A

UROKINASE TPA TURNS PLASMINOGEN INTO PLASMIN

PLASMIN THEN TURNS FIBRIN INTO FIBRIN DEGRADATION PRODUCTS

105
Q

WHAT IS THROMBOCYTOPAENIA?

A

BASICALLY, A LOW PLATELET COUNT.

BRUISING, PETECHIA, NOSEBLEEDS, BLEEDING GUMS

106
Q

WHAT IS VON WILLEBRAND DISEASE?

A

MOST COMMON HEREDITARY COAGULATION IN HUMANS.
NEEDED FOR PLATELET ADHESION AND BINDS FACTOR 8

SIGNS OF HEAVY BLEEDING AND BRUISING

107
Q

WHAT IS HAEMOPHILIA?

A

POOR CLOTTING
A = FACTOR 8 DEFICIENCY
B (RARER) = FACTOR 9 DEFICIENCY
RECESSIVE SEX-LINKED X CHROMOSOME DISORDER

108
Q

WHAT IS DISSEMINATED INTRAVASCULAR COAGULATION?

A

ABNORMAL CLOTTING, CAUSING DISSEMINATE CLOTS THROUGHOUT THE BODY, LOW FIBRINOGEN AND BLEEDING. NOT GOOD!USUALLY INITIATED BY AN UNDERLYING DISORDER.

109
Q

INTRINSIC ATHWAY IS MONITORED BY?

A

PTT

110
Q

EXTRINSIC PATHWAY IS MONITORED BY

A

PT

111
Q

IF FDP IS HIGH, CLOTTING SYSTEM IS _____

A

ACTIVATING LIKE transformer on a Tuesday.

112
Q

what may lead to false fdp elevation?

A

HEPATIC OR RENAL INJURY/DAMAGE/FAILURE

113
Q

WHAT ARE SHISTOCYTES?

A

FRAGMENTED RED BLOOD CELLS

114
Q

HOW WOULD YOU TREAT DIC?

A

TREAT UNDERLYING DISORDER

MAY NEED TO TRANSFUSE PLATELETS

115
Q

HAEMOPHILIA IS AN ___ LINKED DISORDER

A

X

116
Q

WHAT ARE THE TYPICAL BLEEDING SYMPTOMS OF PRIMARY HAEMOSTATIC FAILURE?

A

IMMEDIATE BLEEDING AFTER TRAUMA
MUCOCUTAEN
PURPURA

117
Q

WHAT ARE THE TYPICAL BLEEDING SYMPTOMS OF A COAGULATION FAILURE?

A

DELAYED BLEEDING AFTER TRAUMA
MUSCLE AND JOINT BLEEDING
BRUISING

118
Q

A HIGH APTT TIME WITH A FAMILY HISTORY MEANS WHAT?

A

HAEMOPHILIA

119
Q

IN HAEMOPHILIA, WHICH FACTORS DO YOU REPLACE?

A

8 AND 9
DDAVP (INCREASED BP)
TRANEXAMIC ACID

120
Q

WHAT DOES TRANEXEMIC ACID DO?

A

INHIBITS ACTIVATION OF PLASMINOGEN TO PLASMIN

121
Q

VON WILLEBRANDS DISEASE IS AN ______ CONDITION.

A

AUTOSOMAL

122
Q

LOW PLATELETS MEAN WHAT?

A

THROMBOCYTOPAENIA

123
Q

LOW FIBRINOGEN, HIGH PLATELETS, AND FDPS INCREASED MEANS WHAT?

A

DIC

124
Q

NORMAL BLEEDING TIME, < TT, FIBRINOGEN = WHAT?

A

LIVER DISEASE

125
Q

NORMAL BLEEDING TIME, NORMAL TT, NORMAL PT, < APTT, NORMAL FIBRINOGEN = WHAT?

A

HAEMOPHILIA

126
Q

< BLEEDING TIME, NORMAL TT, NORMAL PT, <APTT AND NORMAL FIBRINOGEN = WHAT?

A

von willebrand disease

127
Q

< TT, < PT, < APTT, >Fibrinogen = what?

A

DIC

128
Q

<bleeding time, Normal TT, Normal PT, Normal APTT, Normal Fibrinogen =

A

thrombocytopaenia

129
Q

what are hirudins?

A

antithrombins

130
Q

WHAT IS THE MAIN SIDE EFFECT OF HEPARIN?

A

HEPARIN INDUCED THROMBOCYTOPENIA

131
Q

HIT IS BROKEN DOWN INTO TWO TYPES - WHAT ARE THEY?

A

TYPE 1 - NON IMMUNE

TYPE 2- IMMUNE –> CAN BE DEVASTATING

132
Q

HOW DOES HIT WORK?

A

CAUSES PLATELET REMOVAL BY SPLENIC MACROPHAGE

133
Q

HOW DO YOU MANAGE HIT?

A

DISCONTINUE ALL HEPARIN IMMEDIATELY
AVOID PROPHYLACTIC PLATELET TRANSFUSIONS
MONITOR FOR THROMBOSIS
CONSIDER ALTERNATE COAGULATION

134
Q

WHAT IS FONDAPARINUX?

A

SIM, TO LMWH

ANTI Xa ACTIVITY

135
Q

WHAT ARE THE INDICATIONS FOR INDEFINITE ANTICOAGULANT THERAPY?

A

RECURRENT IDIOPATHIC VTE
INHERITED THROMBOPHILIA
ANTIPHOSPHOLIPID SYNDROME
MALIGNANCY

136
Q

ANTIDOTE TO WARFARIN?

A

VITAMIN K

137
Q

WHAT IS DABIGATRAN, AND WHAT ARE ITS ADVANTAGES OVER WARFARIN?

A 
ANTI THROMBIN
RAPID ONSET
FIXED DOSE
NO  FOOD EFFECT AND FEW INTERACTIONS
NO MONITORING AND SHORT OFFSET
138
Q

WHAT ARE THE INDICATIONS FOR FIBRINOLYTIC THERAPY?

A

ARTERIAL THROMBOSIS
CORONARY THROMBOSIS
PE

MAIN SIDE EFFECT IS BLEEDING

Medicine Year 1 (39 decks)

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