haemostasis (haematology 14-15) Flashcards
(113 cards)
1
Q
what is haemostasis?
A
haemo - blood, stasis - stop
haemostasis is about the mechanisms that prevent or minimise bleeding (blood clot formation, blood vessel repair)
2
Q
what is the term for an inappropriate blood clot formation?
A
thrombosis
3
Q
what are the three components (Virchow’s triad) that make inappropriate blood clot formation more likely?
A
1 - changes in blood flow (stasis or turbulence)
2. hypercoagulability
3. endothelial damage
4
Q
what is primary haemostasis, essentially?
A
the formation of the platelet plug
5
Q
what is secondary haemostasis, essentially?
A
the formation of fibrin to stabilise the platelet plug
6
Q
what are the five overlapping stages of haemolysis? *these guys are mostly happening at the same time
A
*blood vessel is damaged
1. vasoconstriction (axonal reflex, release of cytokines (cell messengers))
2. platelets are attracted to the area, formation of the platelet plug
3. formation of fibrin to stabilise platelet plug
4. clot removal (fibrinolysis)
5. repair of damaged vessel
7
Q
the end goal of primary haemostasis is the formation of a platelet plug at the site of injury - a process that requires which three components?
A
- platelets
- von Willebrand’s factor (vWF - a large protein)
- blood vessel wall/subendothelial collagen
8
Q
where is von Willebrand’s factor (vWF) NOT found?
a. in the plasma
b. in the subendothelial collagen
c. erythrocytes
d. within endothelial cells
e. within platelets
A
d. within endothelial cells - found everywhere else :)
9
Q
which is the correct order for the steps of primary haemostasis?
a. platelet aggregation, platelet adhesion, platelet activation
b. platelet activation, platelet adhesion, platelet aggregation
c. platelet adhesion, platelet activation, platelet aggregation
A
c. platelet adhesion, platelet activation, platelet aggregation
- stick, activate, aggregate
hint - smallest to largest words lol
10
Q
what is the name of the protein that helps glue platelets to the subendothelial collagen?
A
vWF - von Willibrand’s factor
11
Q
which is NOT one of the three functions of different granules released by platelets during platelet activation?
a. recruiting/attracting passing platelets to the area
b. help with getting blood vessel healing started
c. contribute to secondary haemostasis by releasing coagulation factors
d. signalling for more RBCs to be made
A
d. signalling for more RBCs to be made - that’s EPO from the kidney’s job
12
Q
what does thrombocytopenia mean?
A
not enough platelets
13
Q
other word for platelets (more commonly used in birds and reptiles) is..
A
thrombocyte
14
Q
what does thrombocytopathy mean?
A
platelets not functioning normally (pathy = dysfunctional/disease)
15
Q
what is von Willebrand’s disease?
A
lack of von Willebrand’s factor (vWF, the chunky protein)
16
Q
disorders of primary homeostasis occur when there is a defect in one or more of the main components - which are they? (hint - 3)
A
- platelet problems (thrombocytopenia, thrombocytopathy)
- lack of vWF (von willebrand’s disease)
- defects in vessel wall
17
Q
what is the correct term for the haemorrhages on this heart?
a. eccymoses
b. haematoma
c. petechiae
d. bruising
A
c. petechiae - pin point haemorrhages
18
Q
types of haemorrhage - what is eccymoses?
A
bruising
19
Q
true or false - abnormal primary haemostasis often presents as prolonged post-surgical bleeding and spontaneous small bleeding from capillaries or mucosal surfaces
A
true
20
Q
what is haematuria?
A
blood in urine
21
Q
what is epitaxis?
A
a nose bleed
22
Q
what is haematochezia?
A
fresh blood in faeces - lower GI tract bleed
23
Q
what clinical signs could you get from defects in primary haemostasis of the upper GI tract?
A
a. blood in vomit (coffee ground appearance)
b. melaena (digested blood in faeces)
24
Q
with abnormal primary haemostasis, why do these small bleeds occur even if secondary haemostasis is working fine?
A
fibrin formation takes longer than platelet plug formation, meaning multiple small bleeds occur before secondary haemostasis can catch up
25
which three tests are commonly used for primary haemostasis issues?
1. platelet count
2. buccal mucosal bleeding time
3. von Willebrand factor testing
26
how does buccal mucosal bleeding time (BMBT) test only primary haemostasis and not secondary?
a small incision is made with a special tool (surgicutt) which only cuts to a certain depth, meaning only small capillaries are cut and not large blood vessels - blood clotting then relies on the platelet's plug formation, not the formation of fibrin in secondary haemostasis
27
true or false - any issue with primary haemostasis results in a prolonged BMBT (buccal mucosal bleeding time)
true!
| specifically vWD though
28
which is NOT a defect of primary haemostasis?
a. thrombocytopenia
b. von Willebrand's disease
c. vessel wall defect
d. coagulation factor deficiency
e. abnormal platelet function
d. coagulation factor deficiency - this is secondary haemostasis
29
reference range for platelets at normal, prolonged bleeding and spontaneous bleeding?
the reference range for platelets is 200-500 x10-^9/L but prolonged bleeding with surgery or injury doesn't usually occur until platelets are less than 50 x 10-^9/L and spontaneous bleeding not till 25 x 10-^9/L
30
or example, BMBT will only be prolonged in animals with vWD if the vWF is less than ? percent of normal?
< 20% of normal - but it gives you a rough idea of the animal's ability to form a platelet plug
31
thrombocytopenia - what is the fake (artefactural) version?
pseudothrombocytopenia - occurs with platelet clumping (the analyser doesn't count the clump and records reduced platelets). check for feathered edge of blood smear for clumps - if these are present, patient has enough platelets
32
what are platelets actually, and where are they made?
platelets are blobs of cytoplasm that has been detached from a large cell called a megakaryocyte, and made in the bone marrow (and spleen, in dire circumstances)
33
what are the four true causes of thrombocytopenia?
1. decreased production
2. sequestration (hide more)
3. increased consumption (use more)
d. increased destruction
34
what causes decreased production of platelets? (decreased production based thrombocytopenia)
bone marrow disease - often with this you'll also see pancytopenia (neutropenia and non regenerative anaemia as well as thrombocytopenia). cancer, infectious agents also
35
what is the word for a decrease in all bone marrow cell lines in the bloodstream - erythrocyte, neutrophil and platelet?
pancytopenia - (many cell decrease). this can be caused by drugs eg oestrogen, myotoxins (fungi toxins), ionising radiation.
36
what is myelophthisis?
when all the normal bone marrow cells have been replaced by neoplastic cells - results in pancytopenia, including thromocytopenia
37
what causes the increased sequestration of platelets?
spelomegaly (enlarged spleen, due to congestion or neoplasia) may lead to a greater number of platelets being trapped in the spleen - mild thrombocytopenia
38
what causes increased usage of platelets?
anything that damages the blood vessels and triggers clot formation - increased use of platelets = thromocytopenia
39
what is the most common cause of thrombocytopenia in dogs?
primary immune mediated thrombocytopenia
40
what causes the destruction of platelets?
often immune mediated destruction of platelets (immune mediated thrombocytopenia). can be due to the production of antibodies (primary) or due to viruses, drugs, vaccines, neoplasia (secondary)
41
in an animal with thrombocytopathy, will the platelet numbers be normal or abnormal?
a. normal
b. abormal
a. normal - same amount, the platelets are just dysfunctional
42
In an animal with a thrombocytopathy, will the buccal mucosal bleeding time be normal or increased?
a. Normal
b. Increased
b. Increased - the platelet function is abnormal so the primary platelet plug cannot form
43
von Willebrand's factor is a large protein produced mainly by megakaryocytes and endothelial cells - what is it's function?
vWF acts to glue platelets to exposed subendothelial collagen
44
which dog breed is most commonly affected by vWF disease?
a. husky
b. great dane
c. doberman
d. german shepherd
c. doberman
45
which of the following is NOT a symptom of vWF disease?
a. normal platelet count
b. increased BMBT
c. decreased vWF antigen
d. increased vWF antigen
e. normal clotting times (coagulation panel)
d. increased vWF antigen - von Willebrand's disease occurs when there is a decrease in the amount or function of vWF.
46
von Willebrand's disease - which tests can be done in clinic, and which would have to be sent to a lab?
a. platelet count
b. coagulation panel
c. vWF antigen test
d. buccal mucosal bleeding time (BMBT)
in clinic - platelet count, BMBT
diagnostic lab - coagulation panel, antigen test
note - a dog with vWD will have normal platelet count, increased BMBT, normal coagulation panel, decreased vWF panel
47
what are the clinical signs of vWD (von Willebrand's disease)?
most commonly presents as prolonged bleeding post surgery, after trauma or during parturition
48
why does scurvy (vitamin C deficiency) cause blood vessel defects?
vit C is needed for collagen synthesis, and collagen is the main supporting structure of blood vessels. scurvy = predisposed to haemorrhage (esp around joints) and bone fragility.
49
what lab results would you expect to see with scurvy?
BMBT is prolonged but other tests of coagulation are normal
50
what is Ehlers-Danlos Syndrome (EDS), and how does it relate to blood vessel defects? (violet sorrengail disease lol)
a congenital/hereditary collagen disorder - EDS compromises the structural integrity of blood vessels and connective tissue, resulting in fragile skin, spontaneous hematomas, and excessive bruising.
51
it petechaie more consistent with primary or secondary haemostasis?
primary
52
what does the platelet count, BMBT, vWF antigen and coagulation (clotting) times look like for each of the three diseases of primary haemostasis?
a. thrombocytopenia
b. thrombocytopathy
c. von Willebrand's disease (vWD)
53
secondary haemostasis is all about the formation of fibrin to stabilise the initial platelet plug - this happens at the same time as primary haemostasis, and likewise is divided into three (imaginary) pathways - what are their names?
- intrinsic pathway
- extrinsic pathway
- common pathway
54
which pathway?
a. intrinsic
b. extrinsic
c. common
a. intrinsic - factors 12, 11, 9, 8
55
which pathway?
a. intrinsic
b. extrinsic
c. common
b. extrinsic - factor 7 (and TF, factor 3)
56
which pathway?
a. intrinsic
b. extrinsic
c. common
c. common (factors 10, 5, 2)
57
the end result of the intrinsic/extrinsic =common pathways is thrombin (activated factor 2) - what does it do?
Thrombin converts fibrinogen to insoluble fibrin, which acts like a cement to stabilise the platelet plug - magic step
58
which pathway is the "factor released from trauma" one?
a. intrinsic
b. extrinsic
b. extrinsic - this pathway is activated when tissue factor (TF, factor 3), is released from damaged cells
59
which pathway is the "factor floats into negatively charged surfaces (exposed subendothelial collagen)" one?
a. intrinsic
b. extrinsic
a. intrinsic - pathway is activated when FXII (factor 12) comes into contact with negatively charged surfaces (such as exposed subendothelial collagen)
60
true or false - all clotting factors must be present and functional for clotting to occur?
true
61
Most clotting factors and inhibitors of clotting are synthesised by which organ?
the liver - so normal liver function is essential for haemostasis.
62
The binding of coagulation factors II, VII, IX and X (2, 7, 9, 10) to calcium requires which vitamin as a cofactor?
vitamin K
63
how is fibrin clot formation confined to the platelets?
ome coagulation cascade reactions have to occur on the phospholipid surface of platelets (also known as platelet phospholipid). This confines fibrin clot formation to platelet surfaces.
64
true or false - At the same time as secondary haemostasis is occurring, activation of fibrinolysis occurs. The breakdown of fibrin results in production of fibrin degradation products (FDPs) which inhibit the process of secondary haemostasis.
true - the body is whack
65
which pathway has defects caused by inherited deficiencies in clotting factors (haemophilia?)
a. intrinsic pathway defects
b. extrinsic pathway defects
c. combined intrinsic and extrinsic pathway defects
a. intrinsic pathway defects
66
are extrinsic pathway defects common or rare?
rare - not taught any specific examples
67
what are the three things combined intrinsic and extrinsic pathway defects can result from?
1. rat bait toxicity (vit K antagonism)
2. severe liver disease
3. DIC (disseminated intravascular coagulation)
68
what does abnormal secondary haemostasis tend to present with? (clinical sign)
large amounts of bleeding (haemorrhage) into body cavities and organs
69
what's the term for blood in the abdomen?
haemoabdomen/haemoperitoneum
70
what is haemarthrosis?
term for blood in the joints
71
haematemesis (vomiting blood), melaena (digested blood in faeces), vomiting, diarrhoea...
a. upper gastrointestinal tract haemorrhage
b. lower gastrointestinal tract haemorrhage
a. upper gastrointestinal tract haemorrhage
72
haematochezia (fresh blood in faeces)...
a. upper gastrointestinal tract haemorrhage
b. lower gastrointestinal tract haemorrhage
b. lower gastrointestinal tract haemorrhage
73
The two most commonly used tests of secondary haemostasis are: (hint, a category and a test)
1. Clotting times tests (APTT, PT, TT)
2. In-clinic activated clotting time (ACT)
74
___?___ measures the time required for fibrin clot formation in citrated plasma after addition of FVII (factor 7) activator... which test?
1. APTT
2. PT
3. ACT
4. TT
2. PT - prothrombin time. this is the extrinsic and common pathway test
75
__?____ measures the time required for fibrin clot formation in citrated plasma after addition of a FXII (factor 12) activator.. which test?
1. APTT
2. PT
3. ACT
4. TT
1. APTT - activated partial thromboplastin time. this is the intrinsic and common pathway test (along with ACT)
76
What do you think it would suggest if only the PT was prolonged?
a. extrinsic pathway defect
b. intrinsic pathway defect
c. extrinsic and common pathway defect
d. intrinsic and common pathway defect
e. common pathway defect
c. extrinsic and common pathway defect
77
What do you think it suggests if only the APTT is prolonged?
a. extrinsic pathway defect
b. intrinsic pathway defect
c. extrinsic and common pathway defect
d. intrinsic and common pathway defect
e. common pathway defect
d. intrinsic and common pathway defect
78
What do you think it would suggest if both PT and APTT are prolonged?
a. a defect in both intrinsic and extrinsic pathways or
b. common pathway defect (rare on it's own)
79
___?____ measures the time required for fibrin clot formation in citrated plasma after the addition of thrombin, so measures the conversion of fibrinogen to fibrin.
1. APTT
2. PT
3. ACT
4. TT
4. TT - thrombin time. (common pathway test)
if this is prolonged, either low fibrinogen concentration or something messing with conversion of fibrinogen to fibrin (DIC, probably)
80
what's the name of the test that covers PT, APTT, ACT, TT, platelet count and fibrinogen concentration?
coagulation panel - done at a diagnostic lab
81
test which measures the time required for fibrin clot formation in fresh whole blood?
1. APTT
2. PT
3. ACT
4. TT
3. ACT - activated clotting time (done in clinic). ACT tubes contain a substance that activates factor XII (factor 12), so if prolonged you're looking at a intrinsic or common pathway defect (similar to APTT)
82
which test/s do you do for intrinsic (and common) pathway?
APTT, ACT
83
which tests do you do for extrinsic (and common) pathway?
PT
84
which test do you do purely for common pathway?
TT
85
what colour vacutainer do you use for coagulation panel bloods?
a. red
b. purple
c. green
d. blue
d. blue - sodium citrate tube.
86
Based on the increase ACT clotting time, select the appropriate pathway that has a defect in Jet.
a. Intrinsic
b. Extrinsic
c. Common
a. Intrinsic (common is rare)
87
A follow up coagulation panel at the diagnostic lab was done for Jet. The results showed an increased APTT and PT. Based on this result, select the appropriate combination of pathways that most likely have a defect in Jet.
a. Intrinsic
b. Extrinsic
c. Common
d. Intrinsic and extrinsic
d. Intrinsic and extrinsic
- could be common, but very rare
88
inherited haemostatic disorders (often known as different types of haemophilia) - when are they normally visible in an animal's life stage?
in young animals, or an animal having their first surgery (uncommon to see for the first time in an adult animal)
89
Animals with an inherited FVIII deficiency will have which combination of changes on their clotting times:
a. Normal APTT, ACT, PT, TT
b. Increased APTT, ACT, PT, TT
c. Increased APTT and ACT, normal PT and TT
d. Normal APTT and ACT, increased PT and TT
e. Normal APTT, ACT, TT, increased PT
f. Increased APTT, ACT, PT, normal TT
c. Increased APTT and ACT, normal PT and TT - only the intrinsic pathway is affected
90
why is clotting delayed after a dog eats rat bait?
- vit K is needed for the activation of clotting factors 2, 7, 9, and 10
- rat poison blocks the activation of vit K, clotting factors get depleted over 1-3 days after ingestion
- impaired blood clotting, increased risk of bleeding
91
which test would you use FIRST to check for rat bait toxicity?
a. APTT
b. ACT
c. PT
c. PT - factor 7 has the shortest half life of all the clotting factors, so it runs out first after animal eats rat bait (around 48h later).
92
What will happen with APTT and PT in an animal that is bleeding due to rat bait toxicity? (3 days after ingestion)
a. both prolonged
b. PT prolonged
c. APTT prolonged
a. both prolonged - remember factors 2, 7, 9, and 10 all impacted, 7 just is evident the fastest (PT).
93
There are several reasons why animals may have an increased APTT and PT when they have severe liver disease... list the top three?
1. the liver is where most clotting factors are produced
2. cholestasis (blockage of bile flow) can lead to less intestinal absorption of vit K (it's fat soluble), leading to less production of factors 2, 7, 9, and 10 (vit K dependent ones)
3. fibrin degradation products not cleared by the liver = they can still inhibit coagulation
94
what does DIC stand for?
Disseminated Intravascular Coagulation - known colloquially as Death Is Coming. it's the pathological activation of the coagulation system leading to generalised intravascular coagulation - very bad.
95
what is DIC triggered by?
endothelial damage - exposes tissue factor in multiple places throughout the veins
96
how does DIC cause defects in both primary and secondary haemostasis (consumptive coagulopathy)?
it occurs all over the body, so both platelets (primary) and coagulation factors (secondary) are used up
- patients can be hypo or hyper coagulable depending on the balance of what's left in circulation
97
what clinical signs and/or lesions would you expect to see in a dog with DIC?
1. spontaneous bleeding (either primary - petechiae, or secondary - body cavity haemorrhage)
2. organ necrosis - due to thrombosis and ischaemia
3. lesions associated with whatever the underlying disease is
98
Inguinal skin from a sheep with DIC. what is the term for the lesion present?
petechiae - pinprick haemorrhage, primary haemostatic defect
99
Laboratory findings for DIC can be variable but may include...
- thrombocytopenia (platelets get used up)
- increased PT and APTT (clotting factors used up)
- increased TT (fibrin getting used up)
- schistocytes on blood smear (poor RBCs trying to squeeze past blood clots, fibrin acts like a sieve and cuts fragments off)
- increased fibrin degradation products (FDPs)
fibrinogen - can be increased (from underlying disease inflammation) or decreased (DIC uses it up)
100
what are the components of secondary haemostasis?
- coagulation factors
- calcium (coagulation cascade)
- vitamin K
101
clinical signs of primary haemostasis?
- petechiae or ecchymoses
- mucosal bleeding
- prolonged bleeding after surgery
(more immediate in general)
102
clinical signs of secondary haemostasis?
- cavity bleeding
- haematomas (bleeding under the skin)
- prolonged bleeding after surgery
(more delayed in general, eg bleeding after the initial clot breaks instead of immediate)
103
tests of primary haemostasis?
- platelet count
- BMBT
- vWF assay
103
tests of secondary haemostasis?
- APTT, ACT
- PT
- TT
104
disorders of primary haemostasis?
- decreased numbers of platelets: thrombocytopenia (due to decreased production, increased use, increased sequestration, increased destruction, artefactural)
- weird platelets: thrombocytopathy
- Von Willebrand's disease (vWD)
- DIC
105
disorders of secondary haemostasis?
- intrinsic pathway: inherited factor disorders
- combined intrinsic and extrinsic pathway: rat bait toxicity, severe liver disease, DIC
106
what test results (out of platelet count, BMBT, ACT/APTT, PT, TT, Fibrinogen) would you expect to see with thrombocytopenia?
- decreased: platelet count
- normal: BMBT, ACT/APTT, PT, TT, Fibrinogen
106
what test results would you expect to see with von Willebrand's disease out of platelet count, BMBT, ACT/APTT, PT, TT, Fibrinogen?
increased - BMBT
normal - platelet count, ACT/APTT, PT, TT, Fibrinogen
107
what test results would you expect to see with inherited factor deficiency out of platelet count, BMBT, ACT/APTT, PT, TT, Fibrinogen?
- increased ACT/APTT
- normal platelet count, BMBT, PT, TT, Fibrinogen
108
what test results would you expect to see with vitamin K antagonism (rat bait poisoning) out of platelet count, BMBT, ACT/APTT, PT, TT, Fibrinogen?
- increased ACT/APTT, PT
- normal platelet count, BMBT, TT, Fibrinogen
109
what test results would you expect to see with DIC out of platelet count, BMBT, ACT/APTT, PT, TT, Fibrinogen?
increased - BMBT, ACT/APTT, PT, TT
normal - nothing lol
decreased - platelet count, fibrinogen (normally, can be increased if too much inflammation in the body)
110
An 8 year old corgi cross dog comes into your clinic with a history of epistaxis (nosebleed). On clinical exam you note that it has petechiae on the conjunctiva and the inguinal skin.
What would be the best diagnostic test to perform first on this dog?
most common cause of primary haemostasis (epitaxis, petechiae), is thrombocytopenia (not enough platelets).
- first test: platelet count
111
A 1 year old labrador comes into your clinic with a history of dyspnoea (difficulty breathing). On clinical examination you notice it has pale mucous membranes and a fluid wave in the abdomen. Abdominocentesis reveals the abdominal fluid is frank blood. What test of haemostasis would be useful to perform on this dog?
looks like secondary haemostasis (age, body cavity bleeding) - can do ACT in clinic or a coagulation panel.
- rat bait poisoning most likely ddx
