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Haemotology > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Haemostasis

A

The arrest of bleeding and

the maintenance of vascular patency

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2
Q

Components of Normal Haemostatic System

A

1) Formation of platelet plug = Primary Haemostasis
2) Formation of fibrin clot = Secondary Haemostasis
3) Fibrinolysis
4) Anticoagulant Defences

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3
Q

How are platelets formed?

A

Platelets are formed in the bone marrow by ‘budding’ from megakaryocytes

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4
Q

Platelet structure

A

Platelets are small anucleate discs with a mean life-span of 7-10 days.

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5
Q

Platelet function

A

Endothelial damage exposes collagen and releases Von Willebrand Factor (VWF), and other proteins to which platelets have receptors – platelet adhesion at the site of injury.
There is then secretion of various chemicals from the platelets, which leads to aggregation of platelets at the site of injury.

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6
Q

Failure of Platelet Plug Formation - causes

A

Vascular
Platelets - Reduced number (thrombocytopenia)/Reduced function
Von Willebrand Factor

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7
Q

Consequences of failure of Platelet Plug Formation

A

Spontaneous Bruising and Purpura
Mucosal Bleeding
Intracranial haemorrhage
Retinal haemorrhages

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8
Q

Mucosal bleeding types

A

Epistaxes
Gastrointestinal
Conjunctival
Menorrhagia

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9
Q

Hemostasis includes three steps that occur in a rapid sequence: what are they?

A

(1) vascular spasm, or vasoconstriction, a brief and intense contraction of blood vessels; (2) formation of a platelet plug; and (3) blood clotting or coagulation, which reinforces the platelet plug with fibrin mesh that acts as a glue to hold the clot together.

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10
Q

What are platelets made up of?

A

Fibrin - can be broken own by fibrinolytic drugs

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11
Q

Platelets contain granules that they release to attract more platelets (aggregation of platelets) at site of injury; what are the chemicals released?

A

ADP (adenosine diphosphate), serotonin, and thromboxane A2 (which activates other platelets).

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12
Q

Steps of the coagulation cascade (3rd step of haemostasis)

A

First, blood changes from a liquid to a gel.. Damaged vessels and nearby platelets are stimulated to release prothrombin activator, which in turn activates the conversion of prothrombin into thrombin. This reaction requires calcium ions.

Thrombin facilitates the conversion of fibrinogen into long, insoluble fibers or threads of the protein, fibrin. Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot.

This net of fibers traps and helps hold platelets, blood cells, and other molecules tight to the site of injury, functioning as the initial clot.

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13
Q

What are the main components of the coagulation cascade?

A

Prothrombin, thrombin, and fibrinogen are the main factors involved in the outcome of the coagulation cascade.

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14
Q

Where are Prothrombin and fibrinogen produced?

A

Prothrombin and fibrinogen are proteins that are produced and deposited in the blood by the liver.

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15
Q

What kind of molecule is thrombin?

A

Enzyme that converts fibrinogen to fibrin.

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16
Q

Function of pro-thrombin activator?

A

Activates the conversion of prothrombin, a plasma protein, into an enzyme called thrombin.

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17
Q

Function of fibrin

A

Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot. This net of fibers traps and helps hold platelets, blood cells, and other molecules tight to the site of injury, functioning as the initial clot. This temporary fibrin clot can form in less than a minute and slows blood flow before platelets attach.

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18
Q

How do healthy undamaged vessels prevent abnormal haemostasis and clotting reactions?

A

The endothelial cells of intact vessels prevent clotting by expressing a fibrinolytic heparin molecule and thrombomodulin, which prevents platelet aggregation and stops the coagulation cascade with nitric oxide and prostacyclin.

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19
Q

Failure of Fibrin Clot Formation - causes

A

Single clotting factor deficiency eg Haemophilia

Multiple clotting factor deficiencies, usually acquired eg Disseminated Intravascular Coagulation

Increased fibrinolysis - usually part of complex coagulopathy

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20
Q

Thrombophilia

A

Deficiency of naturally occuring anticoagulants - may be hereditary
Increased tendency to develop venous thrombosis (deep vein thrombosis/pulmonary embolism)

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21
Q

Common Pathway

A

In the final common pathway, prothrombin is converted to thrombin. When factor X is activated by either the intrinsic or extrinsic pathways, it activates prothrombin (also called factor II) and converts it into thrombin using factor V. Thrombin then cleaves fibrinogen into fibrin, which forms the mesh that binds to and strengthens the platelet plug, finishing coagulation and thus hemostasis.

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22
Q

Extrinsic pathway

A

The main role of the extrinsic (tissue factor) pathway is to generate a “thrombin burst,” a process by which large amounts of thrombin, the final component that cleaves fibrinogen into fibrin, is released instantly. The extrinsic pathway occurs during tissue damage when damaged cells release tissue factor III. Tissue factor III acts on tissue factor VII in circulation and feeds into the final step of the common pathway, in which factor X causes thrombin to be created from prothrombin.

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23
Q

Intrinsic pathway

A

The intrinsic pathway (contact activation pathway) occurs during exposure to negatively charged molecules, such as molecules on bacteria and various types of lipids. It begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and factor XII (Hageman factor). This initiates a cascade in which factor XII is activated, which then activates factor XI, which activated factor IX, which along with factor VIII activates factor X in the common pathway.

24
Q

What are the three pathways present in secondary haemostasis (coagulation cascade)?

A

Intrinsic
Extrinsic
Common

25
Q

What are the 5 types of shock?

A 
Hypovolaemic
Cardiogenic
Distributive
Obstructive
(Endocrine)
26
Q

What is shock?

A

Shock is a critical condition brought on by the sudden drop in blood flow through the body. Shock may result from trauma, heatstroke, blood loss, an allergic reaction, severe infection, poisoning, severe burns or other causes. When a person is in shock, his or her organs aren’t getting enough blood or oxygen.

27
Q

Hypovolaemic shock

A

Most commonly due to acute blood loss - but other causes occur
Volume depletion > reduced SVR > vasoconstriction > reduced preload > reduced CO

28
Q

Cardiogenic shock

A

Cardiogenic shock is a life-threatening condition in which your heart suddenly can’t pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock. Cardiogenic shock is rare.

29
Q

Obstructive shock

A

Mechanical obstruction to normal cardiac output in an otherwise normal heart = Direct obstruction to cardiac output (PE, Air/Fat/Amniotic fluid-embolism)

Restriction of cardiac filling (Tamponade, Tension pneumothorax)

30
Q

Distributive (Vasoplegic) shock

A
  • Hot” Shock
  • Septic, anaphylaxis, acute liver failure, spinal cord injuries
  • Due to disruption of normal vascular autoregulation, and profound vasodilatation.
  • Poor perfusion – despite increased cardiac output
  • Regional perfusion differences
  • Alteration of oxygen extraction

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body’s tissues and organs.

31
Q

Endocrine shock

A

Severe uncorrected hypothyroidism, Addisonian crisis – both reduced CO and vasodilation
Paradoxically – thyrotoxicosis

32
Q

Neuroendocrine response to shock

A

Release of pituitary hormones – ACTH, ADH, endogenous opioids
Release of cortisol – fluid retention, and antagonises insulin
Release of glucagon

33
Q

Haemodynamic Changes in shock

A

Vascular abnormalities – Vasodilatation, or constriction

Maldistribution of blood flow

Microcirculatory abnormalities – AV shunting, “stop-flow” or “no-flow” capillary beds, failure of capillary recruitment, increased capillary permeability.

Inappropriate activation of coagulation system.

34
Q

The classes of hypovolaemia

A 
Class I - monitor 
Class II (mild) - possibly need blood 
Class III (Moderate) - Needs blood
Class IV (Severe) -  Massive transfusion protocol
35
Q

Monitoring of shock

A

Examination – Pale, cold skin, prolonged capillary refill.

Urine output – Sensitive indicator of renal perfusion

Neurological – Disturbed consciousness a good indicator of cerebral hypoperfusion

Biochemical – Acidosis, lactate levels

36
Q

Clinical features of shock

A

The main symptom of shock is low blood pressure. Other symptoms include rapid, shallow breathing; cold, clammy skin; rapid, weak pulse; dizziness, fainting, or weakness.

37
Q

Monitoring cardiac output in shock

A

Gold standard – Thermodilution with a PA catheter
Pulse contour analysis
Doppler ultrasonography

38
Q

General management of all types of shock

A

Prompt diagnosis, and treatment critical
ABC approach
Establishment of reliable, wide bore IV access and resuscitate while investigating
Identify – and treat – underlying cause

39
Q

DO2 equation for oxygen delivery in shock

A

DO2 = CO x (1.39 x Hb x SpO2) + (PaO2 x 0.003)

40
Q

What is DO2?

A

Global oxygen delivery (DO2) is the total amount of oxygen delivered to the tissues per minute irrespective of the distribution of blood flow.

41
Q

Fluid management in shock

A

Increase pre-load
Rapid fluid replacement (minutes)
Balance between rapid volume replacement, and risk of fluid overload.
Shocked patients more susceptible to pulmonary oedema due to microvascular dysfunction.

42
Q

The fluid challenge volumes to use

A

Typically – 300-500ml over 10-20 mins.

Have a target in mind: Increased MAP, Decreased H/r, increased urine output

43
Q

Fluid choices in shock

A

Crystalloids – Convenient, cheap, safe But: Rapidly lost from circulation to extravascular spaces, need significantly larger volumes than loss.

Colloids – Cheap(ish), reduce volumes required But: Can cause anaphylaxis, no evidence of benefit

Blood – oxygen carrying capacity, will stay in circulation. But: a scarce resource, and multiple risks

44
Q

Hypovolaemic shock features

A

Patients are normally tachycardic and peripherally ‘shut down’. This refers to cool peripheries and a prolonged capillary refill secondary to vasoconstriction. Both the increased heart rate and peripheral vasoconstriction are compensatory responses to reduced blood volume.

45
Q

Hemorrhagic shock

A

Is a type of hypovolaemic shock. Caused by volume loss due to acute blood loss. Causes include trauma, self harm, acute GI bleed, obstetric haemorrhage, aneurysm rupture and post-operative bleeding.

46
Q

Non-hemorrhagic shock

A

Another type of hypovolaemic shock

Non-haemorrhagic shock occurs due to reduced volume from increased fluid losses or reduced intake. Examples include DKA, severe burns and severe diarrhoea and vomiting.

47
Q

Neurogenic shock

A

Brain and spinal cord injuries can cause failure of normal autonomic pathways. If caused by a spinal cord injury these tend to be above T6. A failure of sympathetic tone and unopposed vagal tone results in vasodilation, reduced venous return and a fall in cardiac output. Bradycardia may also play a role.

48
Q

Type I hemorrhagic shock

A 
Volume of blood loss (ml): <750
Percentage blood loss (%): <15
Heart rate (beats/min): <100
Blood pressure: normal
Pulse pressure: normal/increased
Respiratory rate (breaths/min): 14-20
Urine output (ml/hour): >30
Mental state: slightly anxious
49
Q

Type I hemorrhagic shock

A

Volume of blood loss (ml): <750
Percentage blood loss (%): <15
Urine output (ml/hour): >30
Mental state: slightly anxious

50
Q

Type II hemorrhagic shock

A

Volume of blood loss (ml): 750-1500
Percentage blood loss (%): 15-30
Urine output (ml/hour): 20-30
Mental state: mildly anxious

51
Q

Type III hemorrhagic shock

A

Volume of blood loss (ml): 1500-2000
Percentage blood loss (%): 30-40
Urine output (ml/hour): 5-15
Mental state: anxious, confused

52
Q

Type IV hemorrhagic shock

A

Volume of blood loss (ml): >2000
Percentage blood loss (%): >40
Urine output (ml/hour): negligible
Mental state: confused, lethargic

53
Q

anaphylactic shock management

A

Adrenaline 0.5 mg intramuscular (IM)

54
Q

Cardiac tamponade shock management

A

Pericardiocentesis and thoracotomy

55
Q

Septic shock management

A

IV antibiotics

Haemotology (9 decks)

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