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Principles Flashcards

1
Q

What components interact in haemostasis?

A 
platelets
coagulation factors 
coagulation inhibitors
fibrinolytic processes
blood vessels/endothelium/cell membranes
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2
Q

What are the steps haemostasis + what is their timefram

A

Seconds -> minutes (immediate)
= Primary haemostasis
- get platelet plug

Minutes
= Secondary haemostasis
- fibrin network secures clot in place

Mins -> Hrs
Fibrinolysis
- lysis of clot

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3
Q

What occurs in primary haemostasis?

A
  • damaged vessel wall -exposes collagen
    => platelets are activated when bind collagen

platelets release ADP and 5-HT (serotonin)

5-HT = serotonin (5-HT) - powerful vasoconstrictor

ADP - causes other platelets to activate and change shape
- platelet adhesion + aggregation -> plug

platelets also synthesise other mediators - eg thromboxane from arachadonic acid => stimulate further activation of platelets

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4
Q

via what mechanism do platelets aggregate and adhere

A

fibrinogen bridging between GPIIb/IIIa receptors

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5
Q

What happens in secondary haemostasis?

A
  • activation of coagulation factors

- formation of fibrin -> fibrin network => secure clot into place

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6
Q

What happens in fibrinolysis

A

lysis of clot -> back to smooth surface on endothelium wall

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7
Q

What are the components of Virchow’s triad

A

Vessel wall
Blood composition
Blood flow

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8
Q

Virchow’s triangle - vessel wall - describe

what effects can it have on haemostasis

A

endothelial surface of vessel wall is dynamic + active - interacts with blood/subcutaneous tissue

can be anti or pro-thrombolytic (depending on expression of surface proteins/secreted proteins)

the lining differs with location and age

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9
Q

Which components of Virchow’s triad can we test to look at clotting/bleeding disorders

A

Blood composition (cells, plasma)

Blood flow (cardio factors, function)

Can’t test vessel wall integrity

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10
Q

Virchow’s triad - blood composition; what components are important

A

Blood cells

  • RBC
  • WBC
  • platelets

Plastma - coagulation/clotting system

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11
Q

What are the 2 key components of the coagulation system?

A

tissue factor - is released by vessel wall, kicks things off

thrombin - key enzyme that must be controlled
- converts fibrinogen -> fibrin

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12
Q

What are the phases of the coagulation model? What are the steps within each phase

A

(1) Initiation phase
- vessel wall injury - contact between subendothelial cells + blood
- tissue factor is exposed
- tissue factor binds FVIIa - and this activates FIX + FX
- FXa then binds Fva on cell surface

(2) Amplification phase
- the FXa/FVa complex converts a small amount of prothrombin -> thrombin

thrombin activates FVIII, FV, FXI and platelets

then FXIa converts FIX to FIXa

the activated platelets bind FVa, FVIIIa, FIXa

(3) propagation phase = thrombin burst

FVIIIa/FIXa comple activates FX on activated platelet surface

FXa + FVa convert a large amount of prothrombin -> thrombin

=> this leads to the formation of a stable fibrin clot

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13
Q

why is thrombin esential for clot formation?

A

converts fibrinogen -> fibrin

  • clot formation
  • reinforcement of platelet plut
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14
Q

what happens if there is too much thrombin?

or too little?

A

too much = thrombosis

too little = bleeding

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15
Q

how does inactivation of thrombin occur

A

Thrombin inactivation:

(1) negative feedback
= thrombin binds thrombomodulin -> activates protein C
- APC inhibits VIIIa and Va
- APC also inactivates the inhibitor of tissue plasminogen (allowing fibrinolysis)

(2) Other mechanisms
a. enzyme inhibitors
= antithrombin - binding induces irreversible inhibition (accelerated 1000fold by heparin)
b. binding to heparin co-factor II, dermatan sulphate, a-2 macroglobulin

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16
Q

how does heparin work

A

accelerates antithrombin-thrombin binding (irreversible inhibition of thrombin)

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17
Q

what is a fault of haemostatic testing?

A

isn’t a true measure of physiology - usually we are testing one part of the system in isolation

  • however it can hopefully predict clinical ehaviour
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18
Q

what kinds of tests can we use to test haemostasis?

A

can’t test blood vessel wall

can test platelets - number, function, appearance

we have a range of tests for the coagulation system

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19
Q

what are some tests of the coagulation system

A

tests of risk of bleeding
- APTT, INR etc

we can do specific assays on clotting factors, fibrinogen, specific assays

and we can genotype for disorders of clotting

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20
Q

What are some examples of global functional assays for haemostasis?

A

PT = prothrombin time - initiate clotting (calcium, heating) + measure time to make a clot

INR = standardisation of PT

APTT - activated partial thromboplastin time - similar to PT

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21
Q

Why is INR used?

A

Different labs will have different results for prothrombin time (PT) due to use of different reagents

INR gives a way to standardise these results = international normalised ration

INR = (patient PT/mean normal PT)^ISI

where ISI = sensitivity index

INR is used to monitor warfarin use

22
Q

what can APTT tell you about?

A

factor deficiencies (XII, XI, IX, X)
lupus anticoagulant
heparin monitoring

23
Q

Haemostatic disorders what are type I and type II

A

Type I - low amount and function

Type II - normal amount, but non-functioning

24
Q

How does fibrinolysis occur

A

plasmin - dissolves fibrin

25
Q

What are the 2 pathways to the activation of thrombin from prothrombin

A

(1) extrinsic (to blood)
= in vivo: damaged tissues release thromboplastin - stimulates

(2) intrinsic (to blood - will clot in tube)
= in vitro: exposed collagen or other material, negative charges (eg glass)

26
Q

why is coagulation a cascade?

A

each step is a protease -> catalyses another step, and this amplifies

small signal -> large amount of product

27
Q

which pathway is faster to coagulation - extrinsic/intrinsic?

A

extrinsic

28
Q

What are some vessel wall factors that can lead to improper haemostasis

A

vessel damage -> thrombus formation

eg - atherosclerosis

29
Q

what happens to haemostasis if blood composition changes

A

can have hypercoagulability

30
Q

what happens to haemostasis if blood flow stops (blood stasis)

A

thrombus formation

eg. AF, DVT

31
Q

Common causes of anaemia

A
  • iron deficiency (blood loss)
  • iron/vitamin deficiency
  • chronic disease
  • aplastic - infection/drugs/autoimmune
  • bone marrow disease
  • haemolytic
  • sickle cell
32
Q

acute blood loss - what sort of anaemia will you see

A

normochromic

normocytic

33
Q

iron deficiency/blood loss - what sort of anaemia will you see

how might it present clinically

A

microcytic, hypochromic anaemia (can’t produce Hb properly)

might present as pica!

34
Q

folate or B12 deficiency - what sort of anaemia will you see

A

macrocytic

reticulocytopaenia

35
Q

anaemia of chronic disease - waht will the RBC look like

+pathophysiology

which chronic diseases

A

chronic inflammation -> inflammatory mediators (IL6) increase hepatic hepcidin

hepcidin = inhibit iron absorption in gut

ones with chronic inflammation (chronic microbial, chronic immune - RA etc; neoplasms)

36
Q

What is anaemia? How do we measure it

A

Anaemia = reduction of total circulating red cell mass below normal limits

Measured by
↓haematocrit
↓[Hb]

37
Q

What are the classifications of anaemia according to RBC morphology?

A

Size - normocytic/microcytic/macrocytic

Degree of haemoglobinisation (colour) - normochromic, hypochromic

Shape

38
Q

In general, what causes microcytic, hypochromic anaemias?

A

Disorder of Hb synthesis (eg iron deficiency)

39
Q

In general, what causes macroscopic anaemias?

A

Impairment of maturation of erythroid precursors

40
Q

What changes can occur in kidney/liver/myocardium due to anaemia

A

hypoxia -> fatty change

in myocardium: if severe enough - can get cardiac failure (and this compounds the hypoxia)

Myocardial hypoxia may manifest as angina

If there is acute blood loss + shock -> can get oliguria + anuria (renal hypoperfusion)

41
Q

What are the characteristic morphological changes of megaloblastic anaemias?

A

abnormally large erythroid precursors + RBC

42
Q

Why is there pancytopaenia in megaloblastic anaemia?

A

Derangement of DNA synthesis causes most precursors to undergo apoptosis in marrow

43
Q

What is pernicious anaemia?

A

specific form of megaloblastic anaemia caused by autoimmune gastritis -> this impairs production of intrinsic factor -> B12 deficiency

44
Q

Who is at risk of folate deficiency?

A

need grossly deficient diets - very old, chronic alcoholics, indigent

or those that have increased requirement (pregnancy, infancy, haemolytic anaemias, disseminated cancer)

45
Q

causes of iron deficiency anaemia

A

diet
impaired absorption
increased requirement
chronic blood loss

46
Q

What is aplastic anaemia?
Causes

what is the RBC morphology

A

Chronic primary haematopoietic failure + attendant pancytopenia

Causes - many are autoimmune, otherwise drugs, chemicals (eg chemo, benzene), EBV, VZV etc

these cause marrow suppression

RBC morphology (in this + other marrow failures) - low count, but appear normal

47
Q

What is the erythropoiesis pathway? Which factors are required for each step?

A

Multipotent HSC

↓ (Flt3L, Tal1/SCL)

myeloid SC

↓ (EPO - erythropoietin)

erythroprogenitor

↓ EPO

pro-erythroblast

↓

basophilic erythroblast

↓

polyprochromatophilic erythroblast

↓

orthocytochromatic erythroblast (normoblast) – has nucleus and organelles

↓ Fe is important for late erythroblasts – needed for reticulocyte production

[IN BLOOD]
reticulocyte – still some organelles

↓ enucleation

RBC

↓ 120 days

dies

48
Q

What factors determine erythrocyte size?

A

(1) appropriate signalling in erythropoiesis pathway
(2) time of maturation
(3) proteins
(4) Hb formation

(5) genetic abnormalities (eg thalassaemia)
thalassaemia → autosomal recessive → make strange shaped RBCs`

49
Q

what determines concentration of Hb (3)

A

Iron levels

transferrins (carry around iron)

ferritin (intracellular storage)

50
Q

Where are the following stored:

Iron
B12
Folate

A

Iron

  • liver - bound to ferritin
  • Hb
  • myoglobinn
  • bound to transferrin in blood

B12 - liver

Folate - nowhere

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