Brainscape's Knowledge GenomeTM

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


See full index

VTS(ECC) Preparation > Haemophilic emergencies & Transfusion medicine > Flashcards

Haemophilic emergencies & Transfusion medicine Flashcards

1
Q

How many recognized canine blood types currently exist?
a. 3
b. 5
c. 7
d. 13

A

B

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

How many recognized feline blood types currently exist?
a. 1
b. 3
c. 5
d. 7

A

B

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

To ensure blood recipient health, which of the following pathogens should be screened for prior to blood donation?
a. Borrelia burgdorferi
b. Dirofilaria immitis
c. West nile virus
d. Brucella canis

A

D

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

Which of the following statements is true regarding blood transfusions in canines?
a. Dogs do not have naturally occurring alloantibodies to the DEA 1 group
b. For the first transfusion, the patient does not need to be typed or cross-matched
c. The DEA 1 group can cause a delayed antigenic reaction after a single transfusion
d. If a patient is cross-matched as compatible to a donor, there is no chance of a transfusion reaction

A

C

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

Which of the following blood components provides functional platelets?
a. Packed red blood cells
b. Fresh whole blood
c. Fresh frozen plasma
d. Cryoprecipitate

A

B

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

Both acute and delayed hemolytic transfusion reactions can be treated via which therapy?
a. Corticosteroids
b. Antihistamines
c. Supportive care
d. IVIG

A

C

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

Which blood type in felines could be thought of as a universal recipient?
a. Type A
b. Type B
c. Type AB
d. Type O

A

C

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

A major crossmatch examines the compatibility between which components?
a. Recipient plasma and donor RBCs
b. Donor plasma and recipient RBCs
c. Recipient plasma and recipient RBCs
d. Donor plasma and donor RBCs

A

A

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

Cryoprecipitate would be the treatment of choice for which coagulopathy?
a. Von Willebrand’s disease
b. Hemophilia B
c. DIC
d. Vitamin K1 antagonist rodenticide ingestion

A

A

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

he idea of using individual blood components as opposed to blood in its entirety for transfusion is referred to as what?
a. Component therapy
b. Novel transfusion
c. Tailored transfusion plan
d. Law of veterinary transfusion

A

A

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

Broad indications for transfusions

A
  • Anaemia
  • Coagulopathies
  • Thrombocytopaenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

RBC transfusion

A

Treats anaemia and increases the oxygen carrying capacity of the blood and indicated where there is >20% acute blood loss, low RBC and evidence of transfusion triggers.

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

What percentage blood loss can healthy animals generally tolerate?

A

20%
(20ml/kg BW dogs; 10ml/kg BW cats)

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

PCV requirement for patients undergoing surgery/anaesthesia

A

At least 20% to ensure adequate O2 carrying capacity

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

When is an FFP transfusion indicated?

A

Coagulopathies with extensive bleeding
Colloidal oncotic pressure support
Hypoproteinaemia or hypoalbuminaemia (large volumes required)

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

Cryoprecipitate

A

fibrinogen-rich, factor VIII and vWF and useful in patients with factor deficiencies, plasma & protein deficiencies

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

Cryo-poor plasma indications

A

Coagulopathic and hyproteinaemic patients

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

Platelet transfusions are….

A

Rarely performed due to short storage life (<8 days) or <8h at room temperature.
FWB transfusion preferred method to give platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blood typing & cross-matching

A
  • performed before any transfusion
  • cross matching performed on any patient with unknown or known previous transfusion history
  • blood typing identifies a patient’s blood group but cross-matching does not but will detect presence of alloantibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Massive transfusion

A

Required for near exsanguination where half to full blood volume is transfused
90mL/kg dogs
66mL/kg Cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complications of massive transfusion

A

Electrolyte disturbances
Metabolic acidosis
Coagulopathy
Hypothermia
TRALI
Immunosuppression
Transfusion reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Erythrocytes developed by

A

haemopoietic progenitor cells via erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

EPO

A

Erythropoietin
Released from the liver in response to a drop in oxygenation and is the primary hormone responsible for the production and regulation of RBC within the bone marrow.
Release of EPO begins a biochemical cascade which results in erythropoiesis and the production of new RBC to increase oxygen levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Determination of blood type

A

Presence or absence of antigens on the surface of RBC
positive = antigen present
negative = antigen absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which of IgM and IgG produces a more severe reaction?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Haemophilia affects which coagulation pathway?

A

Intrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TACO & TRALI occur within….

A

6h of a blood product transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment of mild transfusion reactions

A

antihistamines and stop transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment of moderate transfusion reactions

A

fluid boluses to 1/2 shock doses
Stop transfusion
Antihistamines (may not prove beneficial)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of severe transfusion reactions

A

Stop transfusion
epinephrine 0.01mg/kg IV
1/2 shock bolus of crystalloids
Oxygen (cats)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

FFP contains

A

All coagulation factors
Fibrinogen and antithrombin III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Major crossmatch

A

recipient plasma against donor RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Minor crossmatch

A

Donor plasma againts recipient RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Common additive to closed collection blood bags

A

CPDA-1
Citrate-phosphate-dextrose-adenine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Open collection system for cats CPDA-1 ratio

A

1ml CPDA to 9mL blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How FFP stored

A

Collection > separated/centrifuged > frozen to -20 within 8h of collection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

PCV monitoring for transfusions

A

Before
During
6h after transfusion
24h after transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

FFP standard dose

A

10ml/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

pRBC dose

A

vol (ml) = 2 X Desired PCV X BW
equiv. 2ml/kg = 1% rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Monitoring and rate of blood transfusion

A

1-3ml for 5min
1-2ml/kg for next 15min
Complete over 4 hours

Monitoring continuous first 15min then hourly until finished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Standard filter size for blood

A

170um

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When is warming of RBC indicated

A

Neonates, massive transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Occurence of transfusion reactions

A

3-13% may be under represented due to clinical signs similar to critical illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Top Immunological reaction to blood products

A

FNHTR & Urticaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Top Non-immunological reaction to blood products

A

Infectious disease, sepsis, citrate toxicity, circulatory overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

FNHTR

A

Thought to be due to WBC inducing cytokine release, immunosuppression, thrombocytopaenia, TRALI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Intravascular haemolysis due to transfusion

A

Antibodies in recipient react with RBC surface antigen of donor and an IgG or IgM reaction activates the complement system forming a membrane attack complex leading to intravascular haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Severity of haemolytic reation

A

Amount of transfused blood
Amount of recipient alloantibodies
IgG or IgM response
Antibody cold or warm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Storage lesions causes and effects

A

Haemolysis
Microparticle aggregation
Decreased viability
Proinflammatory substances
Release of free Fe
Free Hb > reduced tissue perfusion > MODS
Induction of hypercoagulability

  • Day 14-35 of storage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Leukoreduction

A

Eliminates inflammatory response to WBC and resultant immunosuppresion.
- reduces FNHTR
- reduced haemolysis
- reduces microparticle formation
- reduces cytokine reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hypercoagulobility

A

Inappropriate thrombosis where the balance of anticoagulation and procoagulation is disrupted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Virchow’s triad

A

Hypercoagulobility
Blood stasis
Endothelial damage

53
Q

Glycocalyx

A

Large mesh work of glycosaminoglycans, proteoglycans and glycoproteins that is both a mechanoreceptor and crucial to coagulation.

54
Q

Endothelial disruption

A

Exposes procoagulant substances to circulating blood I.e. tissue factor (TF) and activates the extrinsic pathway to start coagulation.

55
Q

Endogenous anticoagulants

A

Restrict coagulation to the site of injury to prevent procoagulant state or systemic dissemination of coagulation.

Antithrombin, protein C, tissue factor pathway inhibitor (TFPI)

56
Q

Antithrombin

A

Inhibits thrombin via factors 7, 9, 10 and is most defective when bound to heparin. AT is decreased in inflammation leading to bleeding.

57
Q

Protein c

A

Inhibits factors 5 and 8a reducing fibrinolysis and is less functional in the face of systemic inflammation

58
Q

Fibrinolysis

A

The final step to prevent vascular occlusion

59
Q

Diagnosis of hypercoagulobility

A

Often diagnosed when a thrombotic event occurs in an at risk patient
Can look at factor levels and TEG as well as other methods

  • Tests used to identify hypocoagulable states ineffective (PT/aPTT)
60
Q

Systemic inflammation effect on coagulobility

A

Increases TF expression
Activates endothelial cells
Disrupts the glycocalyx
Impairs anticoagulation
Abates fibrinolysis

61
Q

Coagulation in septic patients

A

Usually initially a short state of hypercoagulobility but then followed my a much longer period of hypocoagulobility

62
Q

Types of conditions that are prone to hypercoagulobility

A

PLN
IMHA
Hypercortisolaemia/hyperadrenocorticism
Cardiomyopathies (HCM particularly)
Neoplasia
Isolated brain injury

63
Q

Treatment of hypercoagulable states

A

Antithrombotics i.e. clopidogrel, rivaroxaban, aspirin and LMWH may be indicated for for PLN, ATE, IMHA and neoplasia but in instances of systemic inflammation, HAC TBI these may be contraindicated

64
Q

Bleeding disorders

A

Disruption of haemostatic mechanisms which lead to bleeding

65
Q

Haemostasis and fibrinolysis maintain…

A

Integrity of the close, high-pressure circulatory system after vascular damage

66
Q

Primary v. secondary haemostasis

A

Primary: injury > clot formation (interactions between platelets and endothelium)
Secondary: proteolytic reactions that involve clotting factors

67
Q

Fibrinolysis

A

Dissolution of the fibrin clot to restore normal vascular patency

68
Q

Cell based coagulation model

A

TF initiates coagulation on TF-bearing cell surface generating thrombin which amplifies initial signal by activating PLT & co-factors. Complexes from application propagate on the surface of the activated platelet and large scale thrombin formation occurs > large quantities of fibrin to stabilise a thrombus.

** INITIATION, AMPLIFICATION AND PROPAGATION **

69
Q

Platelet count and enumeration

A

Quantitative measure on the number of platelets

PLT a estimate = PLT/hpf X 15,000/uL

70
Q

BMBT

A

The only reproducible and reliable method in small animals to identify primary haemostatic disorder I.e. vWD or NSAID thrombopathia
Gauze around maxilla to occlude upper lip > two 1mm deep incision not where vessels located > blot shedded blood carefully > record time

71
Q

PT/aPTT

A

Used to identify secondary haemostatic defect of extrinsic or intrinsic pathway.
PT = extrinsic = fVII, vit K deficiency
aPTT = intrinsic
Not predictive of bleeding and if only slightly prolonged may not be completely accurate

72
Q

Fibrin split products (FSPs)

A

Occur when fibrin is lysed by plasmin and tested with agglutination testing
High FSP can indicate: DIC, neoplasia, IMHA, TE, hepatic dysfunction, SIRS, trauma, HF, GDV…

73
Q

D-dimers

A

Produced when soluble fibrin is cross-linked with fXIII and indicate the activation of thrombin and plasmin (active coagulation and fibrinolysis)

74
Q

Critical patients are often? (haemostasis)

A

Hypocoagulable so are at risk of spontaneous bleeding that is either direct or induced. Secondary factors like dilution, acidaemia and hypothermia increase the chances of a bleed in these patients

75
Q

Dilutional coagulopathy

A

In hypovolaemic shock there is a drop in intravenous hydrostatic pressure and when a patient is resuscitated with factor-deficient fluid (crystalloid/colloids/MT) there is low circulating factors and platelets resulting in bleeding. Fibrinogen is the first factor affected and therefore will rely on other factors to keep up with consumption however once breakdown>synthesis clot stability is reduced.

76
Q

What fluid has the most profound haemodilution effect and why

A

Hetastarch because affects vWF and fVIII

77
Q

Hypothermia in relation to hypocoagulopathy

A

Platelets are very sensitive to temperature changes even between 33-37. Under 33 degrees there is reduced platelet function, reduced enzyme activity and reduced TF-fVIIa complexes > coagulopathy

78
Q

Acidaemia in relation to hypocoagulopathy

A

Acidaemia occurs with hypoperfusion and MT of stored CPDA cells which increases fibrinogen degradation and impaired coagulation
pH 7.2 = <50% reduction in fX and fV activity (70% reduction at 7.0)
pH 7.0 = <90% reduction in fVIIa

** can not be reversed using a buffer **

79
Q

Antifibrinolytics in the management of bleeding disorders

A

TXA/EACA
Aprotonin

80
Q

Thrombocytopenia

A

Low platelet count and spontaneous bleeding can occur when reduced <30,000 and 50,000/uL

81
Q

Thrombopathia

A

May have adequate platelets but platelets can be non-functional.
Hereditary, NSAIDs, ehrliciosis, drugs, snake envenomation, DIC, hypothermia, anaemia….

82
Q

Inherited coagulopathies

A

Usually just involve one factor however can have rare deficiency of vitamin k factors (II, VII, IX and X) I.e. Devon Rex
Most are identified within first year of life
fVII may be diagnoses later on in life = extrinsic only = PT prolonged
Haemophilia = intrinsic factors = aPTT prolonged

83
Q

Cryoprecipitate use for bleeding disorders

A

fVIII and hypofibrigenaemia

84
Q

Cryosupernatant for bleeding disorders

A

Vit K deficiency (FFP alternatively)

85
Q

Vitamin K deficiency

A

Involves factors: II, VII, IX, X and alters secondary haemostasis
PT will be prolonged first but as factor depletion occurs there will be prolongation of aPTT as well, then the common pathway.

86
Q

The liver in haemostasis

A

The liver synthesises clotting factors, coagulation inhibitors and fibrinolytic proteins and thus liver dysfunction may result in bleeding or deficiencies.
In saying this 70% of hepatic mass is lost before evidence of this due to large reserve stored within it but fVII will be the first to go.
< 93% of patients with liver disease will have haemostatic dysfunction

87
Q

To combat potential resuscitation associated coagulopathy (RAC)

A

Permissive hypotension (50mmHg MAP)
FFP:RBC 1:1
CP = 1u/7-10kg
Use TEG to guide treatment

88
Q

DIC

A

Systemic activation of coagulation that leads to widespread micro vascular thrombosis, compromising organ perfusion and inducing MODS. Mostly associated with SIRS and sepsis

89
Q

Diagnosis of DIC

A

Underlying dz with risk of DIC + 1 or more of the following:
- thrombocytopaenia
- prolonged PT
- prolonged aPTT
- elevated D-dimers
- hypofibrinogenaemia
- reduced antithrombin
- schistocytes

90
Q

Delayed bleeding in greyhounds

A

Occurs in about 26% of greyhounds 36-72h post surgery and is accompanied with illness, widespread bleeding, haemolysis, mildly low platelet, increased hepatic and muscle enzymes and is considered a fibrinolytic system anomaly due to it NOT reflecting a primary or secondary haemostatic disorder.
Treated by prophylactic EACA for 5 days before undergoing elective procedures.

91
Q

Normal values for BMBT, PT, aPTT

A

BMBT 1.7-4.2 sec; 1.4-4.2
PT 6-12
aPTT 10-25

92
Q

Normal PLT count

A

200-800 X 10^9/L
8-15/hpf

93
Q

Signs of thrombocytopaenia

A

Petechiae & ecchymoses
Mucosal bleeding
Epistaxis
Hyphema
Haematochezia
Melena
Haematuria
CNS abnormalities
Excessive bleeding at venipuncture sites

94
Q

Large platelets on smear

A

May indicate regeneration from bone marrow but could be normal for some breeds

95
Q

Mechanisms of thrombocytopaenia

A
  1. Increased production
  2. Consumption
  3. Sequestration
  4. Increased destruction
96
Q

Interventions for thrombocytopaenia

A

Depends on the cause but sometimes no therapeutic measures are needed or aimed at treating underlying disorder. If <30X10^9/L therapy generally indicated. Some options (depends on cause but focused on immune mediated):
- glucocorticoids: pred 2-4mg/kg/day
- immunomodulation; IVIG, cyclosporine, azathioprine, mycophenalate
- chemo agents: vincristine 0.02mg/kg IV
- splenectomy
- platelet transfusions (fWB usually used)

97
Q

Platelet transfusion

A

Can increase PLT number < 40X10^9/L

98
Q

Extrinsic v. intrinsic platelet disorders

A

Extrinsic - lack of functional protein required for adhesion and aggregation therefore normal platelet structure and function. I.e. vWD where vWF is dysfunctional
Intrinsic - inherent to platelets I.e. Chediak-hibachi syndrome and glanzmann’s thromboaesthesia

99
Q

vWD

A

Dysfunction of vWF that normally mediates platelet function and stabilises fVIII. It is autosomal dominant or recessive, resulting in suspicious bleeding during or shortly after surgical procedures. There is no petechiae and ecchymoses generally and can be confirmed with BMBT and lab testing.
BMBT usually 6-11min
Type 3 = absolute deficiency of vWF

100
Q

Some examples of acquired platelet disorders

A

Uraemia, vWD, drugs

101
Q

Treatment options for platelet disorders

A

Avoid trauma
fWB
Cryoprecipitate 1u/10kg
DDAVP 1u/kg SQ
Identify and treat underlying cause
Testing for disorder I.e. vWD

102
Q

Anaemia

A

Reduction in the oxygen-carrying capacity of the blood that results from low haemoglobin and low RBC mass
1. Blood loss
2. Reduced erythropoiesis
3. Haemolysis

103
Q

Haemophilia A and B only affect

A

Male dogs

104
Q

Clinical signs of anaemia

A

Pallor
Icterus
Pigmenturia
Hypovolaemia
Lethargy
Tachycardia
Tachypnoea
Signs of haemorrhage
Petechiae/ecchymoses

105
Q

Minimum database for anaemic patients

A

PCV/TS
CBC/Smear
Biochemistry
Coagulation profile
Agglutination test
Imagine
Blood typing
Faecal exam

106
Q

Polychromasia

A

May indicate regenerative anaemia when accompanied by reticulocytes

107
Q

Rouleaux formation

A

Stacking of RBC

108
Q

Hypochromasia

A

May indicate a chronic anaemia

109
Q

Spherocytes

A

Often seen and associated with IMHA

110
Q

Schistocytes

A

DIC

111
Q

Heinz bodies

A

Indicative of toxic and oxidative damage

112
Q

What are some other causes of haemolytic anaemia that aren’t IMHA

A

Chemical induced or oxidative injury - onions, zinc, copper, hypophosphataemia
Hereditary - phosphofructokinase deficiency, pyruvate kinase deficiency
Infectious process
Haemolysis

113
Q

Therapeutic approaches to anaemic patients

A

Depends on their presentation and what their underlying disorder is.
- Oxygen
- supportive care
- blood products
- surgery
- vitamin K 2-5mg/kg
- DDVAP 1-4ug/kg
- Pred 2-4mg/kg/day
- AB
- parasitic treatment

114
Q

Haemolysis

A

Premature destruction of RBC either in the extra vascular or intra vascular space

115
Q

Haemolytic anaemia

A

Occurs when destruction of RBC exceeds the rate of production and can be due to many things and either classed as regenerative or non regenerative

116
Q

Signs of haemolytic anaemia

A

Decrease O2 carrying capacity and delivery of O2
- exercise intolerance
- anorexia
- malaise
- syncope/collapse
- pallor +- icterus
- tachycardia
- tachypnoea
- bounding pulse
- soft, systolic murmur

117
Q

IMHA

A

Antibody mediated destruction of a patients own RBC and either primary or secondary due to drug, infection or cancer. Female dogs over-represented.
Treatment involves immunosuppressive agents (pred, dex, cyclosporine), IVIG, blood products, supportive care, anticoagulants

118
Q

Anticoagulant rodenticides

A

Antagonise action of vitamin K factors (II, VII, IX, X) inducing coagulopathy. There is a lag of 3-5 days whilst factor VII depletes and then clinical signs of bleeding into lungs, abdomen, CNS, joints and trachea occurs. Treatment with initial decontamination, activated charcoal, Vit K and FFP. Monitor PT.

119
Q

Cholecalciferol rodenticides

A

Increase iCa as rapidly absorbed and converted by hepatocytes and further converted into the kidneys and therefore there is reduced excretion, increased Ca GIT absorption and resorption from the bone. Commonly prevents with AKI and cardiac arrhythmias. Labs include: low phos, inc Ca, metabolic acidosis, inc protein, azotaemia. Can have soft tissue mineralisation. Treatment with 0.9% saline to increase caliuresis0, furosemide, pamidroante, glucocorticoids

120
Q

Bromethalin

A

Uncouples oxidative phosphorylation reducing ATP > CA forced into cells > cellular swelling > inc ICP > neurological signs, hyperthermia, hyperexcitability, paresis/paralysis.

121
Q

fWB components

A

All factors, RBC and platelets if used within 8h of collection

122
Q

FFP components

A

Contains all labile and non-labile factors but not platelets
If stored > year is classed as FP and this will have loss of factors 8 & vWF V and IX (still has II, VI and X)

123
Q

Liquid plasma components

A

Kept at 1-6 degrees
Has factors V and VIII for 14 days

124
Q

Facts about FNHTR

A

Usually self limiting and due to incompatibility to donor WBC & PLT
Over 1 degree temp rise usually within 1-2h of transfusion; usually resolves within 12-24h
Use leukoreduction filters

125
Q

DHTR

A

Usually occur over 24h after transfusion finished (most common 3-5 days)
Antibody production to foreign antigen I.e. DEA -ve given DEA +ve blood
Jaundice, fever, anorexia
Decreasing RBC lifespan (normal 4-6weeks)

126
Q

AHTR

A

RB-antigen incompatibility leading to an inflammatory response, haemolysis and SIRS
Usually occurs within 20-30min of transfusion but occur <24h after
Very severe in cats

127
Q

Type III sensitivity reaction

A

Formation and depositing of immune complexes in areas like the glomeruli, endothelial cells, lymph nodes, and synovium leading to neutrophil migration, activation and inflammation

128
Q

Citrate toxicity

A

Normal citrate processing by the liver overwhelmed > hypocalcaemia > seizures, panting, pyrexia, PU/PD etc

129
Q

Hyperammonaemia

A

Breakdown of stored RBC release potassium and ammonia > hepatic disease and hepatic encephalopathy especially if patient already has liver dysfunction

VTS(ECC) Preparation (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions