Week 143 Haemostasis Flashcards
(139 cards)
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.
1
Q
What is normal haemostasis
A
quick, efficient, clot formation at the site of a bleed.
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.
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.
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.
5
Q
In deranged haemostasis there is:
A
Abnormal bleeding (excessive prolonged or delayed)
Non-physiological thrombosis
6
Q
Primary haemostasis is __________.
A
The formation of a platelet plug.
7
Q
Secondary Haemostasis is __________.
A
The formation of a fibrin clot.
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.
9
Q
Failure of haemostasis means ____ or ______.
A
Bleeding or pathological thrombosis.
10
Q
Platelets recognise (using glycoprotein 1b/1x/v) VWF (vonwilemhalm factor???) to recognise ______.
A
Areas of damaged endothelium.
11
Q
Which glycoprotein on a platelet binds to vWF?
A
GP1b
12
Q
What is a tissue factor?
A
A Factor released from damaged tissue.
13
Q
The extrinsic pathway of coagulation comes from ______.
A
Tissue factors.
14
Q
The intrisic coagulation cascade is initiatedb y ______.
A
Phospholipid surface.
15
Q
To convert prothrombin to thrombin from the common pathway you need_________.
A
Factor Ten (FX) + Factor Five a (FVa) + PLCa2+.
16
Q
The test for the extrinsic pathway is called the _______.
A
The prothrombin time, normalised with INR.
17
Q
In extrinsic, to activate the normal pathway ________ is formed.
A
Tissue Factor/FVIIa
18
Q
To test the final pathway, you add ______ and assess the ______.
A
Thrombin, and assess clot formation time.
19
Q
To test intrinsic factor, you use __________.
A
Activated partial thromboplastin time (APTT).
20
Q
Intrinsic factors are _______—–>_________—–> _________——-> ___________, which activates normal pathway.
A
FX11–> FX11a –> FX1a –> FIXaFV111a, PLCa2+
21
Q
Site of bleeding for primary haemostasis is _____.
A
Skin, mucous membranes.
22
Q
Primary haemostasis presents with which symptom?
A
Petichae
23
Q
In secondary haemostasis, petichae is _____ _______.
A
Not present.
24
Echymoses means _____. In secondary haemostasis, these are _____. In primary haemostasis these are ___ and ____.
Bruise
Large, palpable
Small, superficial
25
Haemoarthroses/muscle haematomas are ____ in primary and ____ in secondary haemostasis.
Rare in primary
| Common in secondary
26
Bleeding after surgery is ___ and ____ in ______, and _____ and _____ in ______haemostasis.
Immediate and mild in primary
| Delayed and severe in secondary
27
What two reasons will a patient present with purpura?
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
28
Henoch-Schnoleein purpura is a form of ______.
Vaculitis
29
Glanzmann's thrombasthenia is a lack of _____ normally presenting in neonates.
GPIIb/IIIa
30
Vitamin K is needed to make Factors _______ (4 of them).
2, 7, 9, and 10.
31
Defective haemostasis will present with a history of:
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.
32
FBC will detect ____.
Anemia; Red cell fragmentation.
| THROMBOCYTOPAENIA
33
APPT (ACTIVATED PARTIAL THROMBOPLASTIN TIME) DETECTS WHAT?
DEFICIENCY OF ALL COAGULATION FACTORS (EXCEPT VII)
HEPARIN
34
INR (ONE STAGE PROTHROMBIN TIME) WILL DETECT WHAT?
DEFICIENCY OF FACTORS I, II, VII, AND X.
THINK = WARFARIN
35
FIBRINOGEN OR THROMBIN CLOTTING TIME WILL DETECT WHAT?
REDUCED OR ABNORMAL FIBRINOGEN. HEPARIN; FIBRIN DEGRADATION PRODUCTS.
36
BLEEDING TIME (NOT TO BE DONE IF THROMBOCYTOPAENIA) DETECTS WHAT?
TEST PLATELETS - VESSEL WALL INTERACTION.
37
THE SPECIAL TEST OF MIXING TESTS WITH NORMAL PLASMA WILL DO WHAT?
ASSESS IF NORMAL PLASMA CORRECTS PROLONGED APTT AND OSPT.
38
COAGULATION FACTOR ASSAYS ARE USED TO DO WHAT?
ASSESS/CONFIRM COAGULATION FACTOR DEFICIENCY.
39
VON WILLIBRAND FACTORS ASSAYS DO WHAT?
HELP CONFIRM VW DISEASE, IF SUSPECTED.
40
FACTOR VII/OTHER IHIBITO ASSAY IS CONDUCTED IF?
IF YOU SUSPECT ANTIBODY BEING PRODUCED TO COAGULATION FACTOR.
41
PLATELET FUNCTION TESTS TEST _____.
QUALITATIVE PLATELETS DEFECTS.
42
BERNARD-SOULIER DISEASE IS DEFINED AS A LACK OF ____.
GPIb
Will see thrombocytopenia +platelet dysfunction + AB
43
Essential requirements of normal haemostasis are:
Normal blood vessels
Adequate platelet number and fuction
Normal coagulation system
Normal and effective fibrinolytic system
44
Auto-immune thrombocytopaenia is _____. Platelet lifespan is ____ from ____ to 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
45
Inherited coagulation disorders include:
Haemophilia A - Factor VIII def
Haemophilia B - Christmas disease - IX Def
Von Willebrand - Von willebrand factor
46
Most common cause of low platelets is?
Thrombocytopaenia.
47
Purple tops used for?
FBC
48
BLUE TOP MUST BE FILLED TO WHAT?
THE LINE!!!!!
49
PROTHROMBIN TIME IS USED TO CALCULATE WHAT?
INR (WARFARIN MORNITORING)
50
WHAT ARE THE COMPONENTS OF THE HAEMOSTATIC SYSTEM?
PLATELETS
PROTEINS - VWF
DAMAGED ENDOTHELIUM -- PHOSPHOLIPIDS, COLLAGEN, VWF, TF
51
WHERE DO PLATELETS COME FROM?
ORIGANATE FROM MEGAKARYOCYTES (FROM MYELOID PROGENITOR LINEAGE) IN THE BONE MARROW.
BUDS OF GRANULAR CYTOPLASM (CONTAIN CLOTTING FACTORS).
52
WHERE DOES FIBRIN COME FROM?
FIBRINOGEN - CONVERTED TO FIBRIN BY THROMBIN
| THIS IS CAUSED BY CLOTTING CASCADE (EXTRINSIC/INTRINSIC)
53
LIVER DAMAGE WILL RESULT IN (MOST LIKELY)
REDUCTION IN FIBRINOGEN AND CLOTTING FACTORS - LIVER MAKES A LOT OF PROTEINS!
54
PLATELET PHOSPHOLIPID BILAYER DOES WHAT?
EVERTS TO PRESENT A HUGE PHOSPHOLIPID MEMBRANE SURFACE AREA, IN ORDER TO ACTIVATE PROTEINS.
55
HOW DOES WARFARIN WORK?
IT IS A DIRECT INHIBITOR OF VITAMIN K (COMPETITIVE INHIBITION), STOPPING ACTIVATION OF VIT K DEPENDENT FACTORS.
56
WHAT COULD YOU GIVE TO REVERSE THE EFFECTS OF WARFARIN?
PROTHROMBIN COMPLEX CONCENTRATE (PCC) - VIT K DEPENDENT FACTORS
VITAMIN K - SLOWER (OVER 24 HOURS)
57
WHAT IS HEPARIN? HOW DOES IT WORK?
ANTICOAGULANT AGENT
| ?????
58
WHAT IS ASPIRIN? HOW DOES ASPIRIN WORK?
IT IS AN SALICYLATE ANTICOAGULANT. IT INHIBITS PLATELET ACTIVATION.
59
WHAT FACTORS MAKE BLOOD MORE LIKELY TO BE LIQUID?
???
60
WHAT FACTORS MAKE BLOOD MORE LIKELY TO BE SOLID
???
61
WHAT DRUGS INFLUENCE PLATELET FUNCTION AND WHY?
????
62
What does virchow's triad include?
Vessel wall damage (i.e. atherosclerosis)
Altered Blood flow (i.e. stasis)
Increased blood coagulability (i.e. thrombophilia)
63
Define placebo.
A substance or procedure that has no inherent power to produce an effect that is sought or expected.
64
What is a thrombus?
A clot arising in the wrong place.
65
Naturally occuring inhibitors of blood coagulation are ____ and ______.
- Anti Thrombin
| - Protein C System (protein s)
66
What is antithrombin?
- A glycoprotein
- synthesised by liver
- Inhibits FXa and thrombin
- > 2000 fold increase of the T/AT interaction by heparin
67
There is a dose response curve for the ______ _______.
Placebo effect.
68
Which vitamin is vital for coagulation?
Vitamin K
69
Thrombomodulin is linked to which vitamin?
Vit K
70
The protein C system inhibits ______
Va -> VIIIa
71
What three types of thrombus are there?
Arterial
Venous
Microvascular
72
Arterial thrombus is described as a ____ ______. They are made of ______ and ______. They result in _____ and ______, and principally secondary to _______________.
White clot
Platelets and fibrin
Ischaemia & Infarction
Atherosclerosis
73
Name three types of arterial thromboembolism.
Coronary (Mi/Angina)
Cerebrovascular (stroke/transient ischaemia)
Peripheral embolism (Limb ischaemia)
74
Describe microvascular thrombus.
Platelets and/or Fibrin
Results in diffuse ischaemia
Principally in DIC
75
Venous thrombus is describes as a ____ ______. It is made up of ____ and ___ ______ cells. It results in back _____. It is principally due to ____ and ______.
Red thrombus
fibrin and red blood cells
Results in back pressure
due to stasis and hypercoagulability
76
What is the extinction of an association?
The overwriting of pavlovian conditioning. It's NEW learning.
77
Name two important examples of venous thromboemoblism.
Limb deep vein thrombosis
| Pulmonary embolism
78
Name as many risk factors for venous thromboembolism as you can.
```
Immobility
Tissue trauma (surgery)
Pregnancy
Oral CCP
Obesity
MAlignancy
Hyperviscosity
Anti-phospholipid syndrome
```
79
A variant in TPH2 predicts what?
Whether ppl with social anxiety disorder will experience a placebo effect or not.
80
What is Factor V Leiden?
A common heritable thrombophilia.
5% caucasians
7 fold increase of VTE
40 x increase risk in oral contraceptive
81
Name two common heritable thrombophilia?
Factor V Leiden
| Prothrombin G20210A
82
Name 3 rare causes of heritable thrombophilia.
Antithrombin deficiency
Protein C Deficiency
Protein S deficiency
83
What are the clinical diagnostic criteria for antiphospholipid syndrome?
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
What are the laboratory diagnostic criteria for antiphospholipid syndrome?
Anticardiolipin antibodies IgG or IgM
Lupus anticoagulant
Diagnosis req's at least 1 clinical and 1 laboratory confirmed x2
85
The full effect of a drug is:
Placebo + Natural history + Drug
86
What laboratory test would you do to confirm DVT? How would you confirm it?
D-Dimers
| Imaging to confirm (uS)
87
3 or more of WHAT will give high probability of DVT potential?
```
Active Cx in last 6/12
Paralysis
Bad >3d
Swollen leg/calf swolllen > 3cm/Pitting odemea
Tenderness along veins
```
88
What is the nocebo effect?
Same principle as placebo effect, except that outcome is negative.
< anxiety contributes to this.
89
Describe DVT prophylactic treatment.
MObility, hydration
TED stocking, pneumatic compression
Heparin, i.e. LWMH/other agents
90
What is the Hawthorne effect?
An increase in worker productivity produced by the pysch stimulus of being singled out and made to feel important.
91
Unfractionated heparin inactivates what?
IIa and xa
92
What is the difference in molecular weight between UFH and LMWH?
```
UFH = 15
LMWH = 4.5
```
93
What is the difference in half life between UFH and LMWH?
```
UFH = 2 hours
LMWH = 4-8 hours
```
94
When should you suspect pulmonary embolism?
- 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
How does PE present clinically?
```
Tachypnea
Tachycardia
Rales (crackles)
> breath sounds
Jugular venous distension
```
96
What investigations would you conduct to diagnose a PE?
```
ABG
ECG
CXR
U/S lower limbs
D-Dimers
```
97
What is a CT-PA?
83% of patients with PE had a positive scan.
| 96% without had a negative scan
98
What is a V/Q scan?
A normal scan virtually excludes PE
| HIgh probability and clinical sign --> 95% likelihood of PE.
99
What is the gold standard for PE?
Pulmonary angiography.
2% mortality
5% morbidity
100
How would you manage a PE?
```
Resucitation
Anti-coagulation -----> IVC filters when this is contra indicated
-LMWH
- Warfarin
Thrombolysis,
```
101
Describe the extrinsic coagulation pathway.
VII + Tissue factor --> VIIa/TF
VIIa/TF -------Va--------> changes x --> Xa
Xa changes Prothrombin ---> Thrombin
Thrombin changes Fibrinogen ----> Fibrin
102
Describe the intrinsic coagulation pathway.
XII---->X11A CAUSES..
X1---->X1A CAUSES...
IX ---->IXA CAUSES...
THEN IXa----> to X (then goes from there...)
103
THROMBIN CAUSES A _____ FEEDBACK LOOP
POSITIVE
104
DESCRIBE THE CASCADE OF FIBRINOLYSIS.
UROKINASE TPA TURNS PLASMINOGEN INTO PLASMIN
| PLASMIN THEN TURNS FIBRIN INTO FIBRIN DEGRADATION PRODUCTS
105
WHAT IS THROMBOCYTOPAENIA?
BASICALLY, A LOW PLATELET COUNT.
| BRUISING, PETECHIA, NOSEBLEEDS, BLEEDING GUMS
106
WHAT IS VON WILLEBRAND DISEASE?
MOST COMMON HEREDITARY COAGULATION IN HUMANS.
NEEDED FOR PLATELET ADHESION AND BINDS FACTOR 8
SIGNS OF HEAVY BLEEDING AND BRUISING
107
WHAT IS HAEMOPHILIA?
POOR CLOTTING
A = FACTOR 8 DEFICIENCY
B (RARER) = FACTOR 9 DEFICIENCY
RECESSIVE SEX-LINKED X CHROMOSOME DISORDER
108
WHAT IS DISSEMINATED INTRAVASCULAR COAGULATION?
ABNORMAL CLOTTING, CAUSING DISSEMINATE CLOTS THROUGHOUT THE BODY, LOW FIBRINOGEN AND BLEEDING. NOT GOOD!USUALLY INITIATED BY AN UNDERLYING DISORDER.
109
INTRINSIC ATHWAY IS MONITORED BY?
PTT
110
EXTRINSIC PATHWAY IS MONITORED BY
PT
111
IF FDP IS HIGH, CLOTTING SYSTEM IS _____
ACTIVATING LIKE transformer on a Tuesday.
112
what may lead to false fdp elevation?
HEPATIC OR RENAL INJURY/DAMAGE/FAILURE
113
WHAT ARE SHISTOCYTES?
FRAGMENTED RED BLOOD CELLS
114
HOW WOULD YOU TREAT DIC?
TREAT UNDERLYING DISORDER
| MAY NEED TO TRANSFUSE PLATELETS
115
HAEMOPHILIA IS AN ___ LINKED DISORDER
X
116
WHAT ARE THE TYPICAL BLEEDING SYMPTOMS OF PRIMARY HAEMOSTATIC FAILURE?
IMMEDIATE BLEEDING AFTER TRAUMA
MUCOCUTAEN
PURPURA
117
WHAT ARE THE TYPICAL BLEEDING SYMPTOMS OF A COAGULATION FAILURE?
DELAYED BLEEDING AFTER TRAUMA
MUSCLE AND JOINT BLEEDING
BRUISING
118
A HIGH APTT TIME WITH A FAMILY HISTORY MEANS WHAT?
HAEMOPHILIA
119
IN HAEMOPHILIA, WHICH FACTORS DO YOU REPLACE?
8 AND 9
DDAVP (INCREASED BP)
TRANEXAMIC ACID
120
WHAT DOES TRANEXEMIC ACID DO?
INHIBITS ACTIVATION OF PLASMINOGEN TO PLASMIN
121
VON WILLEBRANDS DISEASE IS AN ______ CONDITION.
AUTOSOMAL
122
LOW PLATELETS MEAN WHAT?
THROMBOCYTOPAENIA
123
LOW FIBRINOGEN, HIGH PLATELETS, AND FDPS INCREASED MEANS WHAT?
DIC
124
NORMAL BLEEDING TIME, < TT, FIBRINOGEN = WHAT?
LIVER DISEASE
125
NORMAL BLEEDING TIME, NORMAL TT, NORMAL PT, < APTT, NORMAL FIBRINOGEN = WHAT?
HAEMOPHILIA
126
< BLEEDING TIME, NORMAL TT, NORMAL PT,
von willebrand disease
127
< TT, < PT, < APTT, >Fibrinogen = what?
DIC
128
thrombocytopaenia
129
what are hirudins?
antithrombins
130
WHAT IS THE MAIN SIDE EFFECT OF HEPARIN?
HEPARIN INDUCED THROMBOCYTOPENIA
131
HIT IS BROKEN DOWN INTO TWO TYPES - WHAT ARE THEY?
TYPE 1 - NON IMMUNE
| TYPE 2- IMMUNE --> CAN BE DEVASTATING
132
HOW DOES HIT WORK?
CAUSES PLATELET REMOVAL BY SPLENIC MACROPHAGE
133
HOW DO YOU MANAGE HIT?
DISCONTINUE ALL HEPARIN IMMEDIATELY
AVOID PROPHYLACTIC PLATELET TRANSFUSIONS
MONITOR FOR THROMBOSIS
CONSIDER ALTERNATE COAGULATION
134
WHAT IS FONDAPARINUX?
SIM, TO LMWH
| ANTI Xa ACTIVITY
135
WHAT ARE THE INDICATIONS FOR INDEFINITE ANTICOAGULANT THERAPY?
RECURRENT IDIOPATHIC VTE
INHERITED THROMBOPHILIA
ANTIPHOSPHOLIPID SYNDROME
MALIGNANCY
136
ANTIDOTE TO WARFARIN?
VITAMIN K
137
WHAT IS DABIGATRAN, AND WHAT ARE ITS ADVANTAGES OVER WARFARIN?
```
ANTI THROMBIN
RAPID ONSET
FIXED DOSE
NO FOOD EFFECT AND FEW INTERACTIONS
NO MONITORING AND SHORT OFFSET
```
138
WHAT ARE THE INDICATIONS FOR FIBRINOLYTIC THERAPY?
ARTERIAL THROMBOSIS
CORONARY THROMBOSIS
PE
MAIN SIDE EFFECT IS BLEEDING
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