Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Coagulation studies > Flashcards

Coagulation studies Flashcards

1
Q

when is aPTT used? (active partial thromboplastin time)

A
  1. Identify factor deficiencies in intrinsic pathway (XII, XI, IX, VIII, X, V, II, I)
  2. Monitor heparin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is PT used? (prothrombin time)

A
  1. Identify factor deficiencies in extrinsic pathway (VII, X, V, II, I)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is clotting factor I & function

A

Fibrinogen

> thrombonin substrate

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

What is clotting factor II & function

A

Prothrombonin

> serine protease

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

What is clotting factor III & function

A

Tissue factor

> co-factor to inc. enzymatic activity

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

What is clotting factor IV & function

A

Calcium

> mineral

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

Why is citrate the anticoagulant of choice when testing clotting functions in specimens*

A

because it reversibly binds to Ca2+ unlike EDTA

- add more Ca2+ so citrate unbounds

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

Hypercholesterolemia & cause

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

friedwald equation

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperlipidemia / Hyperlipoprotemia . cause

A

. hi cholesterol OR TG

  1. familial cholesterolemia
  2. diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Combined Hyperlipidemia / Hyperlipoprotemia

A

Hi choesterol AND hi TG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypolipoproteinemia / Hypolipidemia

A

.

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

Hypertriglyceridemia

A

.

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

Define Pupura

A

bleeding under the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define petechiae

A

small bleeds under skin (3mm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define ecchymoses

A

larger bleeds under skin (>3mm)

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

Define haemarthrosis

A

bleeding into joint = joint swelling

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

Define epistaxis

A

nose bleed

19
Q

Define haematemesis

A

vomiting of blood

20
Q

Define haematoma

A

bleeding confined to particular organ

21
Q

Define Maelena

A

blood in faeces

22
Q

Define menorrhagia

A

heavy menstrual bleeding

23
Q

What does the 1º & 2º haemostasis involve?

A

1º: platelets

2º: plasma coagulation factors- requiring +ve & -ve charges = complexes

24
Q

How does the 1º haemostatic plug form?

A
  1. vasular injury = endothelial damaged= exposes collagen
  2. von Willebrand factor (vWF) (in blood/released from damaged endothel) sticks to collagen (subendothelial matrix) & elonagate = expose binding sites
  3. Plt bind to vWF via glycoprotein (GP) 1b-V-IX => plt become activated = change shape = discoid (flat shape) 4. GP IIb-IIIa exposed on plt => fibrinogen binds to these on adjacent plt > stabilise plt
  4. procoagulant contents released => recruit more plt & further aggregation
25
Q

What do activated plt release?

A
  • Dense bodies: Seretonin, ADP, Ca2+
  • Alpha granules: fibrinogen, vWF, PF4, PDGF, thrombospondin
  • thromboxane A2 > activate more plt
26
Q

what is Fibrinolysis & Describe process

A

a. digestion of fibrin clot

b. plasminogen activated to plasmin => digest fibrinogen & fibrin

27
Q

3 phases of fibrinogen formation ie. endpoint of 2º haemostasis

A
  1. proteolysis
  2. polymerisation: form fibrin polymers
  3. stabilisation: FXIIIa forms covalent bonds in b/w D-dimers ≠ break = stable fibrin polymer
28
Q

Describe how you form fibrin from fibrinogen w/ thrombin

A

thrombin cleaves Fibrino peptides on E domain of fibrinogen => E domain is +ve charged & D domain is -ve

29
Q

Describe the intrinsic & common pathway (T E N = X)

A
  1. FXII is activated by -ve charged surface => FXIIa
  2. FXIIa activates FXI => FXIa
  3. FXIa activates FIX => FIXa:FVIII complex (or intrinsic tenase)
  4. Complex activates FX => FXa:FV
  5. FXa:FV activates prothrombin => thrombin (enzyme)
  6. Thrombin cleaves fibrino peptides on E domain of fibrinogen => fibrin
30
Q

Describe the extrinsic & common pathwaay

A
  1. Vessel injury
  2. Tissue release factor (or intrinsic tenase) like thromboplastin (tiss. factor on PL)
  3. TF:FVIIa complex is formed => activating FX => FXa:FV
  4. FXa:FV activates prothrombin => thrombin (enzyme)
  5. Thrombin cleaves fibrino peptides on E domain of fibrinogen => fibrin
31
Q

3 roles of haemosatic system

A
  • keep blood & prevent excess blood loss
  • keep thrombosis to the site
  • fibrinolysis (digest fibrin clot for remodelling)
32
Q

4 substances that activate plt

A
  • thromboxane a
  • ADP
  • Collagen
  • Thrombin
33
Q

a deficiency in vWF can lead to a deficiency of F_ because _

A

FVIII

bc vWF cirlulates (bound to) FVIII

34
Q

plt aggregates by

A

fibrinogen binding to GP IIb-IIa on adjacent plt

35
Q

which measurement to use to determine platelet function

A

platelet aggregation

36
Q

list th 5 laboratory assays for 1º haemostasis

A
  1. [ptl] (150-400 x10^9/L)
  2. bleeding time
  3. plt function analyser (measure clot time w/ PFA-100)
  4. vWF
  5. plt aggretonomy
37
Q

list the clotting factors from I-VII

A 
I: fibrinogen
II: prothrombin
III: tissue factor
IV: Calcium
V: labile factor (cofactor)
VII: stable factor (serine protease)
* NO FACTOR VI
38
Q

characteristics of Fibrinogen group

A
  • FI, V, VIII, XIII

- procoag. factors => thrombosis

39
Q

characteristics of Prothrombin group

A
  • FII, VII, IX, X
  • Vitamin K dependant
  • stable in blood storage
  • inhibited by warafin (PT = ext.)
40
Q

characteristics of contact group

A
  • FXI, XII

- activated when in contact with -ve charged surfaces

41
Q

list th 5 laboratory assays for 2º haemostasis

A
  1. PT
  2. aPTT
  3. thrombin time
  4. factor assays
  5. Fibrinogen assays
42
Q

organ/site of production for factors

A

liver

43
Q

Why is vitamin K important for FII, VII, IX, X?

A
  • bc is required to make FII, VII, IX, X functional
  • bc Vit. K is needed by glutamic acid (Gla) => undergo gamma carboxylation so that Ca2+ can bind to Gla => complex can bind to -ve PL (remain at site of damage)
44
Q

4 Things to avoid when preparing coagulation assays

A
  • use citrate not EDTA
  • use plastic tubes not glass (bc can activate CF)
  • mix well to prevent specimens clotting
  • avoid under-filling tubes = keep ratio constant ie 9 blood : 1 citrate

Haematology (15 decks)

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