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1st Year Med > Haematology > Flashcards

Haematology Flashcards

1
Q

what are the main functions of blood?

A

O2 transport
clotting
healing/infection
transport system
homeostasis

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2
Q

what is the function of haemostasis?

A

limits blood loss (haemorrhage) following vascular damage without compromising blood fluidity

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3
Q

what are the 3 phases of haemostasis?

A

vasoconstriction
platelet plug
coagulation

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4
Q

what compound is used in blood storage to prevent coagulation?

A

sodium citrate

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5
Q

what is the extrinsic pathway initiated by and how can it be tested?

A

tissue factors released by damaged cells

tested using prothrombin time (PT)

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6
Q

what is the intrinsic pathway and how can it be tested?

A

initiated by active platelets

tested using activated partial thomboplastin time (APTT)

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7
Q

what 3 things are required to carry out the intrinsic and extrinsic pathways?

A

clotting factors
Ca ions
negatively charged lipid surfaces

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8
Q

how long should each pathway test take?

A

extrinsic (PT): 10-14 seconds
extrinsic (APTT): 30-45 seconds

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9
Q

explain the final common pathway in coagulation

A

platelets release prothrombin activator
(turns prothrombin -> thrombin)
thrombin turns soluble fibrinogen into insoluble fibrin
factor 8 cross links fibrin which then strengthens the clot

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10
Q

what is fibrinolysis?

A

process of clot removal

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11
Q

where is plasminogen synthesised and where does it circulate?

A

synthesised - liver

circulated - plasma

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12
Q

what is plasminogen activated by?

A

a serine protease called tissue plasminogen activator (tPA)

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13
Q

what does tPA do?

A

converts plasminogen into plasmin which breaks down fibrin mesh

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14
Q

what is thrombosis?

A

occlusion of a blood vessel (venous or arterial) by an intravascular blood clot or platelet lump

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15
Q

what is intravascular blood coagulation inhibited by and how does it inhibit it?

A

non-thrombogenic surface of endothelium
prostacyclin (PGI2)
NO

inhibits platelet aggregation and adhesion to vascular wall
inhibits natural anticoagulants (antithrombin III)

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16
Q

explain the process of platelet adhesion

A

adhere to sub-endothelial collagen to activate
platelet surface integrin GPIb permits adhesion to collagen in vessel wall through von willebrand factor bridge

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17
Q

how do platelets promote vasoconstriction?

A

release agents (thromboxane, ADP) promoting vasoconstriction and aggregation
thromboxane initiates arachnoid acid metabolism (vasoconstriction)

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18
Q

what changes are seen in platelets after activation?

A

shape change (discoid -> spherical)
pseudopodia development
expose cell surface integrin GPIIb/IIIa cross linking to fibrinogen

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19
Q

what does blood coagulation involve?

A

coagulation factors (plasma proteins)
phospholipids (platelet surface)
Ca ions

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20
Q

what activated plasma proteins?

A

proteolic cleavage to become active proteases

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21
Q

name 4 blood clotting disorders and the factor they lack

A

von willebrand disease (von willebrand)
haemophilia A (8)
haemophilia B (9)
haemophilia C (11)

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22
Q

explain the formation of venous thrombosis

A

formed by intravascular blood clot in deep veins (often legs)
a fragment may break off (embolus) and block the blood vessel, often the pulmonary artery (DVT)

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23
Q

explain the causation of arterial thrombosis

A

caused by platelet aggregate at side of ruptured atherosclerotic plaque which is then encapsulated by a clot
common in coronary arteries causing MI, or cerebral artery causing theombotic stroke

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24
Q

what medications are used to treat thrombosis?

A

anticoagulant - inhibit coagulation cascade
antithrombotics - inhibit platelet activation
thrombolytics - dissolve clots

25
Q

give an example of anticoagulants and explain their mechanism of action

A

heparin (sulphated GAG)
binds to antithrombin III (anticoagulant)
complex binds to/inhibits clotting factors (IIa, IXa, Xa, XIa, XIIa)
imediate effect
low molecular weight heparin inhibits Xa mostly

26
Q

how do the 2 types of heparin differ?

A

2 forms: UFH (unfractionated) and LMWH

LMWH has more consistent chain length

27
Q

explain the administration of heparin

A

intravenously or subcutaneously
cant cross placenta or BBB
used for DVT or pre-eclampsia

28
Q

what are the side effects of heparin?

A

allergic reactions
hyperkalaemia
haemorrhage
heparin-induced thrombocytopaenia (HIT)

29
Q

explain the mechanism of action of oral anticoagulants

A

warfarin
blocks synthesis of coagulation factors in liver
reduces vitamin K reductase blocking carboxylation resulting in no Ca binding to factors II, VII, IX and X

30
Q

when is warfarin used?

A

venous thrombosis
pulmonary embolism prevention (especially in AF patients)
thrombosis prophylaxis after prosthetic insersion (valves)

31
Q

what are the side effects and disadvantages of warfarin?

A

active in vivo, not in vitro
effects delayed

can cause haemorrhage
crosses placenta/BBB

32
Q

explain the INR

A

measurement of clotting time or ratio of prothrombin to control
target: 2-3

high INR: haemorrhage risk
low INR: thrombosis risk

33
Q

what are the advantages of new anticoagulants? (+ example)

A

rivaroxaban (Xa inhibitor)

active imediately
dont involve antithrombin III

34
Q

what is the function of andexanet?

A

reverses factor X inhibitors

35
Q

how does low dose aspirin act as an anti-thrombotic?

A

irreversibly inhibits cyclooxygenase which causes acetylation of terminal serine which inhibits synthesis of thrombxane A2 and prostacyclin

36
Q

what are thrombolytic agents used for?

A

venous thrombosis, MI or thrombotic stroke

never haemorrhagic stroke (side effect is haemorrhage)

37
Q

what is shock?

A

life threatening, generalised form of acute circulatory failure with inadequate O2 delivery and utilisation by cells

38
Q

name 4 markers indicating shock

A

CV status (BP/HR)
respiratory rate
lactate levels
urine output

39
Q

what are the 4 types of shock?

A

distributive
hypervolaemic
cardiogenic
obstructive

40
Q

what are the causes of distributive shock?

A

vasoregulation failure (vasodilation)

sepsis (toxic inflammatory response)

anaphylaxis (biochemical mediator release)

neurogenic (spinal injury)

41
Q

what are the causes of hypervolaemic shock?

A

loss of intravascular volume
haemorrhage (trauma, GI bleeding)
non haemorrhage (burns)

42
Q

what are the causes of cardiogenic shock?

A

pump failure
MI
arrythmias (toxins, medications, valve problems)
mechanical

43
Q

what are the causes of obstructive shock?

A

barriers to cardiac flow/filling
pulmonary embolism
cardiac tamponade
pneumothorax

44
Q

how is distributive shock treated?

A

fluids
vasosuppressors (targets peripheral vasodilation)
antibiotics

45
Q

how is hypervolaemic shock treated?

A

fluid
blood
stop blood loss

46
Q

how is cardiogenic shock treated?

A

vasosuppressors
inotropes
fluids

47
Q

how is obstructive shock treated?

A

improve obstruction (needle/thrombolysis)

48
Q

what are the main components of blood?

A

RBC
WBC
platelets
plasma (water, proteins, coagulation factors etc.)

49
Q

name the 5 steps of blood loss in order

A

intravascular volume loss
decreased CO
impaired tissue oxygenation
end organ dysfunction
death

50
Q

explain the vivious cycle of blood loss

A

hypothermia = decreased coagulation (clotting problem)
clotting problem = increased lactic acid in blood (blood more acidic)
acidic blood = heart performance decrease resulting in hypothermia

51
Q

what levels of blood loss are seen with each stage of shock?

A

S1: 750ml (15%)
S2: 750-1500ml (15-30%)
S3: 1500-2000ml (30-40%)
S4: >2000ml (>40%)

52
Q

what pulse and BP observations are seen in each stage of shock?

A

S1: pulse below 100, BP normal
S2: pulse 100-120, BP normal
S3: pulse 120-140, BP lower
S4: pulse 140+, BP low

53
Q

what respiratory rates and urine outputs are seen in each level of shock?

A

S1: RR 14-20, UO >30ml/h
S2: RR 20-30, UO 20-30ml/h
S3: RR 30-40, UO 5-15ml/h
S4: RR >40, UO negligible

54
Q

what is the emergency treatment for a catastrophic haemorrhage?

A

A - airway (c-spine control)
B - breathing (oxygenation)
C - circulation (haemorrhage control)
D - disability
E - exposure

55
Q

what is an abrasion wound and how would you treat it?

A

superficial/deep, dragged against irregular surface

remove debris and dress wound

56
Q

what is a laceration wound and how would you treat it?

A

blunt force trauma causing skin to tear/split at tissue bridging
ireegular edges and depth levels

irrigate and clean, close wound with glue, staple/suture wound

57
Q

what is an incision wound and how would you treat it?

A

sharp/penetrating trauma (slash/stab), clean edges, uniform shape

investigate for underlying damage

58
Q

what is a degloving wound?

A

skin/blood supply torn off by major trauma and severe injuries
could be limbs/digits entirely

59
Q

what is a bite wound and how would you treat it?

A

small entry wound prone to infection
possibly deep penetration with foreign body

test for human blood borne viruses (tetanus), antibiotics, ensure vaccinations up to date, delay closure, irrigate

1st Year Med (52 decks)

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