Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Phase 1b - Cardiovascular & Respiratory Medicine > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Define haemostasis.

A
  • The cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the function of haemostasis (3)?

A
  • Prevention of blood loss from intact vessels
  • Arrest bleeding from injured vessels
  • Enable tissue repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline the process of haemostasis (4 stages).

A
  • Vessel constriction
  • Primary haemostasis: Formation of an unstable platelet plug
  • Secondary haemostasis: Stabilisation of the plug with fibrin
  • Fibrinolysis: Vessel repair and dissolution of clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the first step of haemostasis (vessel constriction) (1A / 1E).

A

Action:
* Vascular smooth muscle cells contract locally

Effect:
* Limits blood flow to injured vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the second step of haemostasis (primary haemostasis) (2A / 2E).

Primary haemostasis: Formation of an unstable platelet plug

A

Action:
* Platelet adhesion
* Platelet aggregation

Effect:
* Limits blood loss
* Provides surface for coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the third step of haemostasis (secondary haemostasis) (1A / 1E).

Secondary haemostasis: Stabilisation of the plug with fibrin

A

Action:
* Blood coagulation

Effect:
* Stops blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the fourth step of haemostasis (fibrinolysis) (2A / 1E).

Fibrinolysis: Vessel repair and dissolution of clot

A

Action:
* Cell migration / proliferation
* Fibrinolysis

Effect:
* Restores vessel integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the disorders of primary haemostasis divided into (cause specific) (3)?

A
  • Platelets caused
  • Von Willebrand Factor caused
  • Vessel wall caused
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the platelet caused disorders of primary haemostasis (2)?

A
  • Thrombocytopenia (low numbers)
  • Impaired platelet function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causes of thrombocytopenia leading to disorders of primary haemostasis (3)?

A
  • Bone marrow failure:
    • e.g. Leukaemia / B12 deficiency
  • Accelerated clearance:
    • Immune Thrombocytopenia (ITP) / Disseminated Intravascular Coagulation (DIC)
  • Pooling and destruction in an enlarged spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of impaired platelet function leading to disorders of primary haemostasis (2)?

A
  • Hereditary absence of glycoproteins or storage granules
  • Acquired due to drugs:
    • Aspirin / NSAIDs / Clopidogrel (common)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the Von Willebrand factor caused disorder of primary haemostasis (1)?

A
  • Von Willebrand disease

VWF has two functions in haemostasis:
* Binding to collagen and capturing platelets
* Stabilising Factor VIII
* Factor VIII may be low if VWF is very low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the causes of Von Willebrand disease (2)?

A
  • Hereditary decrease of quantity and / or function (common)
    • Deficiency of VWF (Type 1 or 3)
    • VWF with abnormal function (Type 2)
  • Acquired due to antibody (rare)

VWF has two functions in haemostasis:
* Binding to collagen and capturing platelets
* Stabilising Factor VIII
* Factor VIII may be low if VWF is very low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the vessel wall caused disorders of primary haemostasis (2)?

A
  • Inherited connective tissue disorders (rare):
    • Hereditary haemorrhagic telangiectasia / Ehlers-Danlos syndrome
  • Acquired (common):
    • Steroid therapy / Ageing (‘senile’ purpura) / Vasculitis / Scurvy (Vitamin C deficiency)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How would a patient with suspected primary haemostasis disorder present (8)?

A

Typical primary haemostasis bleeding:
* Immediate
* Prolonged bleeding from cuts
* Nose bleeds (epistaxis): prolonged > 20 mins
* Gum bleeding: prolonged
* Heavy menstrual bleeding (menorrhagia)
* Bruising (ecchymosis), may be spontaneous / easy
* Prolonged bleeding after trauma or surgery

Skin signs:
* Petechiae
* Purpura

Petechiae and Purpura are caused by bleeding under the skin Purpura do not blanch when pressure is applied
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What investigations are suggested in suspected primary haemostasis disorder (5)?

A
  • Platelet count
  • Platelet morphology
  • Bleeding time (PFA100 in lab)
  • Assays of von Willebrand Factor
  • Clinical observation

N.B. Coagulation screen (PT, APTT) is normal (except more severe VWD cases where FVIII is low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the management principles of primary haemostasis disorder (6)?

A

Failure of production/function:
* Replace missing factor / platelets e.g. VWF containing concentrates
* Prophylactic
* Therapeutic
* Stop drugs e.g. aspirin/NSAIDs

Immune destruction:
* Immunosuppression (e.g. prednisolone)
* Splenectomy for ITP

Increased platelet consumption:
* Treat cause
* Replace as necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What haemostatic treatments are used in the management of primary haemostasis disorder (4)?

A
  • Desmopressin (DDAVP)
    • Vasopressin analogue
    • 2-5 fold increase in VWF (and FVIII)
    • Releases endogenous stores (so only useful in mild disorders)
  • Tranexamic acid
    • Antifibrinolytic
  • Fibrin glue / spray
  • Other approaches e.g hormonal (oral contraceptive pill for menorrhagia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the disorders of secondary haemostasis divided into (cause specific) (3)?

A
  • Deficiency of coagulation factor production
  • Dilution of coagulation factor
  • Increased consumption of coagulation factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the deficiency-of-coagulation-factor-production-caused disorders of secondary haemostasis (4)?

A

Hereditary:
* Factor VIII/IX: haemophilia A/B (respectively)

Acquired:
* Liver disease - decreased production
* Most coagulation factors are synthesised in the liver
* Anticoagulant drugs
* Warfarin
* Direct Oral Anticoagulants (DOACs)

Deficiency of coagulation factor:
* Factor VIII and IX (Haemophilia)
* Severe but compatible with life
* Spontaneous joint and muscle bleeding
* Prothrombin (Factor II)
* Lethal
* Factor XI
* Bleed after trauma but not spontaneously
* Factor XII
* No bleeding at all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the dilution-of-coagulation-factor-caused disorder of secondary haemostasis (1)?

A

Acquired:
* Blood transfusion
* Red cell transfusions no longer contain plasma
* Major haemorrhage requires transfusion of plasma as well as red cells and platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the increased-consumption-of-coagulation-factor-caused disorders of secondary haemostasis (2)?

A

Acquired:
* Disseminated intravascular coagulation (DIC) (common)
* Immune – autoantibodies (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How would a patient with suspected secondary haemostasis disorder present (8)?

A
  • Superficial cuts do not bleed (platelets)
  • Bruising is common
  • Nosebleeds are rare
  • Spontaneous bleeding is deep, into muscles and joints -> muscle wasting
  • Bleeding after trauma may be delayed and is prolonged
  • Bleeding frequently restarts after stopping
  • Chronic haemarthrosis: The hallmark of haemophilia.
Haemarthrosis
24
Q

How would one make the clinical distinction between bleeding due to platelet and coagulation defects?

A

Platelet / Vascular:
* Superficial bleeding into skin, mucosal membranes
* Bleeding immediate after injury

Coagulation:
* Bleeding into deep tissues, muscles, joints
* Delayed, but severe bleeding after injury; bleeding often prolonged

25
What investigations are suggested in suspected secondary haemostasis disorder (5)?
* Screening tests (‘clotting screen’) * **Prothrombin time (PT)** * **Activated partial thromboplastin time (APTT)** * Full blood count **(FBC)** (platelets) * **Coagulation factor assays** (for Factor VIII etc) * Tests for **inhibitors**
26
* PT: 10.6 secs (9.6 - 11.6) * APTT: 85 secs (26 - 32) What could cause these results (4)?
* Haemophilia A * Haemophilia B * Factor XI deficiency * Factor XII deficiency
27
* PT: 26 secs (9.6 - 11.6) * APTT: 29 secs (26 - 32) What could cause these results (1)?
* Factor VII deficiency
28
* PT: 26 secs (9.6 - 11.6) * APTT: 49 secs (26 - 32) What could cause these results (4)?
* Liver disease * Anticoagulant drugs e.g. warfarin * DIC (platelets and D dimer) * Dilution following red cell transfusion
29
What are the management principles of secondary haemostasis disorder (3)?
Failure of production/function: * **Replace missing factor / platelets** e.g. VWF containing concentrates * Prophylactic * Therapeutic Increased platelet consumption: * **Treat cause** * **Replace as necessary**
30
What treatments are used in the management of secondary haemostasis disorder (4)?
* **Plasma** (fresh frozen plasma FFP) * Contains all coagulation factors * **Cryoprecipitate** * Rich in Fibrinogen, FVIII, VWF, Factor XIII * **Factor concentrates** * Concentrates available for all factors except factor V * Prothrombin complex concentrates (PCCs) - Factors II, VII, IX, X * **Recombinant forms of FVIII and FIX** are available * ‘On Demand’ to treat bleeds * Prophylaxis to prevent bleeds
31
What haemostatic treatments are used in the management of secondary haemostasis disorder (2)?
* **Desmopressin (DDAVP)** * Vasopressin analogue * 2-5 fold increase in VWF (and FVIII) * Releases endogenous stores (so only useful in mild disorders) * **Tranexamic acid** * Antifibrinolytic
32
Outline the pathophysiology of thrombosis (causes 4 diseases).
Can cause to: * Pulmonary Embolism **(PE)** * Deep Vein Thrombosis **(DVT)** * **Heart Attack** * **Stroke**
33
How would pulmonary embolism (PE) present (6)?
* **Tachycardia** * **Hypoxia** * **Shortness of breath** * Chest **pain** * **Haemopysis** * **Sudden death**
34
How would deep vein thrombosis (DVT) present (6)?
* **Painful** leg * **Swelling** * **Red** * **Warm** * **May embolise to lungs** * **Post thrombotic syndrome**
35
The pathogenesis of venous thrombosis can be broken down to Virchow’s triad. What makes up Virchow's triad? ## Footnote **Virchow’s triad:** the three contributory factors to thrombosis
* **Blood:** dominant in venous thrombosis * **Vessel wall:** dominant in arterial thrombosis * **Blood flow:** contributes to both arterial and venous thrombosis
36
Describe the pathogenesis of thrombosis that makes up the blood from Virchow's triad (1). ## Footnote Dominant in venous thrombosis.
**Increased coagulant factors platelets:** * Factor VIII * Factor II * Factor V Leiden * (increase activity due to activated protein C resistance) * Myeloproliferative disorders (plts increase)
37
Describe the pathogenesis of thrombosis that makes up the vessel wall from Virchow's triad (1). ## Footnote Dominant in arterial thrombosis.
* Many proteins active in coagulation are expressed on the surface of endothelial cells and their expression altered in **inflammation** (TM, EPCR, TF) ## Footnote We know little about the role of the vessel wall in venous thrombosis.
38
Describe the pathogenesis of thrombosis that makes up the blood flow from Virchow's triad (1). ## Footnote Contributes to both arterial and venous thrombosis.
* Reduced flow **(stasis)** increases the risk of thrombosis * e.g. surgery, long haul flight, pregnancy
39
What is used in the therapeutic management of venous thrombosis (Initial 4 / Long 2)?
* **Initial treatment** (surgery / angiograph) to minimise clot extension / embolisation (< 3 months): * **DOAC** or **LMWH** for first few days followed by **DOAC** or **Warfarin** * **Long term treatment** to reduce risk of recurrence * **DOAC** or **Warfarin**
40
What is used in the therapeutic management of atrial fibrillation (2)? ## Footnote Why is atrial fibrillation managed? * To reduce risk of embolic stroke
**DOAC** or **Warfarin**
41
What is used in the therapeutic management of mechanical prosthetic heart valve (1)?
**Warfarin** (DOACs not effective and should be avoided)
42
What is used in the preventative (thromboprophylaxis) management of venous thrombosis (Surgery 2 / Hospital 1 / Pregnancy 1)? ## Footnote E.g. following surgery, during hospital admission, during pregnancy
* Following surgery: **LMWH** or **DOAC** * During hospital admission: **LMWH** (DOACs not effective for use as medical thromboprophylaxis) * During pregnancy: **LMWH** (DOACs not safe in pregnancy)
43
What are the 2 forms of heparin?
* Unfractionated heparin (UFH) * Low molecular weight heparin (LMWH)
44
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to molecular weight?
* As the name suggests, UFH is unfractionated, meaning it has a variable molecular weight. In contrast, **LMWH** is a fractionated form of heparin with a **lower molecular weight**.
45
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to mechanism of action?
* Both UFH and LMWH inhibit clotting factors by binding to antithrombin III, but the binding is **more specific and longer-lasting with LMWH**.
46
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to administration?
* **UFH** is administered through injection into a **vein** or under the skin, whereas **LMWH** can be given **subcutaneously**.
47
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to monitoring?
* **UFH** requires **regular monitoring** of its effect on blood clotting through **aPTT** (activated partial thromboplastin time) tests, whereas **LMWH** typically **does not require monitoring**.
48
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to reversal?
* In cases of bleeding or overdose, **UFH can be reversed** using **protamine sulfate**, while there is **no specific reversal agent for LMWH**.
49
What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to indications?
* **UFH** is commonly used in the treatment of acute **thrombotic events**, whereas **LMWH** is often used for **prophylaxis** against deep vein thrombosis (DVT) and pulmonary embolism (PE) after surgery.
50
What is the mechanism of action of warfarin [Vitamin K Antagonists (VKA)] (3)?
1. **Competes with Vitamin K** – complicated metabolism 1. **Reduces** production of **functional coagulation factors** 1. **Induces** an **anticoagulated state slowly** ## Footnote * **Many** dietary, physiological and drug **interactions** * **Narrow therapeutic index and requires monitoring**
51
What is the mechanism of reversing action of warfarin [Vitamin K Antagonists (VKA)] (Slowly 1 / Rapidly 2)?
* Reversed **slowly** by **Vit K administration** – takes several hours to work * Reversed **rapidly** by **infusion of coagulation factors:** * **PCC** (Prothrombin Complex Concentrate- contains Factors II, VII, IX and X) * **FFP** (Fresh Frozen Plasma)
52
What are the adverse effects of warfarin [Vitamin K Antagonists (VKA)]?
* **Bleeding** * Minor 5% pa * Major 0.9 – 3.0% pa * Fatal 0.25% pa * **Skin Necrosis** * **Purple toe syndrome** * **Embryopathy** – Chondrodysplasia punctata
53
Warfarin [Vitamin K Antagonists (VKA)] requires monitoring when administer. What equation is used for that?
**INR (International Normalised Ratio)** ## Footnote * ISI = International Sensitivity Index * Indicates sensitivity of particular thromboplastin for warfarin Unanticoagulated normal INR = 1.0 Target INR usually 2-3
54
What factors can lead to warfarin [Vitamin K Antagonists (VKA)] resistance (4)?
* **Lack of patient compliance** * Measure warfarin levels * Proteins Induced by Vitamin K Absence (PIVKA) * Diet, **Increased Vit K intake** * Increased metabolism **Cyt P450** (CYP2C9) * **Reduced binding** (VKORC1)
55
What are the differences between warfarin [Vitamin K Antagonists (VKA)] and direct oral anticoagulants (DOACs) when it comes to: * Onset / Offset * Dosing * Food effect * Interactions * Monitoring required * Renal dependence * Reversibility

Phase 1b - Cardiovascular & Respiratory Medicine (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions