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Clinical Pathology 2 > Haematology > Flashcards

Haematology Flashcards

Uni of Leeds Lectures

1
Q

Causes of splenomegaly

A

C- Cancer
H - Haematology (CML, Myelofibrosis, CLL, Hairy cell Leukaemia, Beta Thalassemia)
I - Infection (Schistosomiasis, Malaria, Leishmaniasis, EBV)
C - Congestive (Liver disease/Portal)
A - Autoimmune (haemolysis, SLE)
G - Glycogen Storage disorders
O - Other (amyloid, sarcoid)

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2
Q

CML is characterised by

A

Increased granulocytes, splenomegaly and anaemia.

It occurs due to cytogenic abberation (philadelphia chromosome 22) resulting in BCR-ABL fusion.

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3
Q

CML is treated with what type of medication

A

Imatinib (gleevac) which is a tyrosine kinase inhibitior as the BCR-ABL product is a tyrosine kinase.

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4
Q

What are the symptoms of CML and causes of them?

A

Abdominal discomfort/pain due to Splenomegaly and Splenic infarct
Fatigue due to anaemia, catabolic state
Gout due to hyperuricaemia
Venous occlusion from DVT, retinal vein or priapism

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5
Q

There are currently no reported cases of imatinib resistance. True or False?

A

False. activating loop mutions in bcr-abl confer resistance & loss of disease control

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6
Q

How long to RBCs last for?

A

120 days

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7
Q

How long can RBCs for transfusion be stored for

A

35 days

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8
Q

What are the indications for RBC transfusion

A

Bleeding, acute/chronic/sever symptomatic anaemia

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9
Q

Platelets can be collected in which ways?

A

A)Pooled
1 unit from 1 whole blood
4-6 units pooled together usually form diff donors into a single pack
B)Apheresis
Apheresis machine used, platelets removed & all other blood returned to the donor. This is equivalent to 4-6 units from random donors.

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10
Q

Usual transfusion time for RBC & Platelets

A

RBCs: (1.5-3 hours) Max 4 hours
Platelets: 30mins/Unit

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11
Q

Dose for adult recieving platelets

A

4-6 units

This is equivalent to pooled platelets (4-6) or a single round of apheresis

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12
Q

Shelf life of platelets

A

5 days

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13
Q

Indications for transfusion with platelets

A

Treatment/Prevention of bleeding due to severe thrombocytopenia
Prevention of bleeding can be for cases of prophylaxis for surgery or bone marrow failure

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14
Q

Contraindication for transfusion of platelets

A

Immune thromobocytopenia Prupura
Thrombotic thromobocytopenia Prupura
Heparin induced thromobocytopenia & thrombosis

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15
Q

Types of plasma transfusion

A

A. Fresh frozen plasma (FFP); stored at -30 degree celcius. liquid portion of whole blood. It is used to treat conditions in which there are low blood clotting factors (INR>1.5) or low levels of other blood proteins.
B. Cryoperciptate; stored at -30 degree celcius, 3 yr shelf life if frozen. contains: vWF, factor VIII and XIII
C. Fractionations of e.g. albumin, immunoglobulin, factor complexes (VII, IX, prothrombin complex)

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16
Q

Fresh Frozen plasma and cryopercipitate indications

A

A. Fresh frozen plasma (FFP);
Indication: Bleeding with clotting factor deficiencies/abnormalities OR prophylaxis for surgery for ppl with abnormal clotting results

B. Cryoperciptate;
Indications: source of fibrinogen in acquired coagulopathies i.e. massive haemorrhage, DIC

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17
Q

How to reverse warfarin?

A

Prothrombin complex cencentrate (factor IX concentrate) that contains II, VII, IX, X, Vit K (i.e. vit K dependent factors)

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18
Q

Fresh frozen plasma can be used to reverse warfarin. TRUE/False

A

False. Prothrombin complex cencentrate (factor IX concentrate) that contains II, VII, IX, X, Vit K (i.e. vit K dependent factors)

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19
Q

Fresh Frozen plasma indications and contraindications

A

A. Fresh frozen plasma (FFP);
Indication: Bleeding with clotting factor deficiencies/abnormalities OR prophylaxis for surgery for ppl with abnormal clotting results
Contraindications: single factor deficiencies, to correct abnormal clotting in ppl that arent bleeding, to reverse warfarin

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20
Q

Risks of transfusion can be

A

immunological or non-immunological

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21
Q 
Transfusion reactions are known as delayed if they occur:
A. >6hours
B. >12hours
C.>24hours
D.>36hours
E.>48hours
A

C - 24 hours

<24hours is acute transfusion reaction

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22
Q

Types of non-immunological transfusion reaction

A

Transfusion transmitted viral/prion infection
Transfusion transmitted bacterial infection
Transfusion associated circulatory overload (TACO)
Febrile non-haemolytic transfusion reaction

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23
Q

Transfusion transmitted prion infection can be prevented with

A

Methylene Blue

usually the prion is vCJD (no case since 1999)

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24
Q

Types of immunological transfusion reactions

A

Acute haemolytic transfusion reaction
Delayed haemolytic transfusion reaction
Post transfusion purpura
Allergic/anaphylactic reaction
Transfusion related acute lung injury (TRALI)
Transfusion associated graft vs. host disease (TA-GvHD)

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25
Q

Prevention of Acute haemolytic transfusion reaction is done by

A

1) Pre-transfusion testing of: ABO group, Rh (D) status and RBC antigen detection
2) Cross-matching (only for RBC transfusions); mix patient blood with aliqoutes of donor blood to see if there are any signs of cross reactivity

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26
Q

Delayed haemolytic transfusion reaction

A

due to post-transfusion formation of IgG ab against RBC antigens other than ABO

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27
Q

Direct anti-globulin test is used to detect

A

antibodies on the surface of RBCs (Coomb’s) as anti(h)-globulin adhere together with RBCs to form visible agglutinations

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28
Q

Who is at increased risk of anaphylactic reaction related to trasfusion reactions

A

ppl with IgA deficiency or anti-IgA antibody

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29
Q

Criterion for Transfusion related acute lung injury (TRALI) diagnosis

A

sudden onset of acute lung injury within 6 hours of transfusion

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30
Q

Transfusion related acute lung injury (TRALI) occurs due to

A

anti-HLA and anti-HNA

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31
Q

Transfusion related acute lung injury (TRALI) can be prevented by

A

taking plasma only from male donors

bec risk of anti-HLA higher in females with prev pregnancies

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32
Q

Testing for haemoglobinpathies

A

Antenatal: booking visit discuss and screen parents
Prenatal: High risk preg = counsilling and offer prenatal diagnostic test (chronic villus biopsy and genetic testing at 8-12 weeks) +/- termination
Postnatal: 5 days post-partem (heal prick test)

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33
Q

Haematological changes during preg

A

*Macrocytic anaemia and physiological anaemia:
1. Plasma expansion by up to 50%
2. Red cell mass expands by 25%
3. haemodilution occurs maximally at 32 weeks.
4. Mean cell volume increases physiologically
*Leukocytosis
Mainly a neutrophilia, rising from the 2nd month to a peak range of around 9-15 in the 2nd-3rd trimester
Left shift may also be seen (myelocytes/metamyelocytes)
*Gestational thrombocytopenia
No pathological significance for mother or fetus
Recovers rapidly following delivery
Main issue in management is differentiation from other causes
*Evidence of platelet activation
*Increase in many procoagulant factors
*Reduction in some natural anticoagulants
*Reduction in fibrinolysis
*Rise in markers of thrombin generation
*Coagulation factors (plasma fibrinogen, vWF, factors V, VII, VIII, X, XII, initail increase in XIII (then halved to pre-preg value), small decrease in XI and minimal increase in IX

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34
Q

Usual cause for macrocytic anaemia in pregnancy

A
  1. need for folic acid and preg increases need for folate

2. Fe defiency as preg increases need for fe and mobilises iron stores

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35
Q

Gestational thrombocytopenia does not need to be managed. TRUE or FALSe

A

TRUE. it has no functional consequence on foetus or mother but needs to be distinguished from other causes

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36
Q

SICKLE CELL DISEASE – acute complications:

A

a. Vaso-occlusive crisis - hands and feet (dactylitis), chest syndrome, abdominal pain (mesenteric), bones (long bones, ribs, spine), brain, priapism (painful erection)
b. Septicaemia
c. Aplastic crisis (failure of the bone marrow to produce any red blood cells - should not be confused with anaemia)
d. Sequestration crisis (spleen, liver)

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37
Q

SICKLE CELL DISEASE –chronic complications:

A

a. Hyposplenism: due to infarction and atrophy of spleen.
b. Renal disease: medullary infarction with papillary necrosis. Tubular damage - can’t concentrate urine (bed-wetting at night). Glomerular – chronic renal failure/dialysis
c. Avascular necrosis (AVN): femoral/humeral heads
d. Leg ulcers, osteomyelitis, gall stones, retinopathy, cardiac, respiratory

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38
Q

TREATMENT OF SICKLE CELL DISEASE

A

Penicillin etc from 6 months (neonatal screening)
Acute crisis
* vaso-occlusive - analgesia (usually opiates), hydration (to maintain red cell water), treatment of precipitants
* Priapism – education. Acute (minor/major, intracorporeal phenylephrine), Recurrent – etilefrine?
* Respiratory – ECHO screening, O2 Sats
* Transfusion because of:
Top up: splenic sequestration, aplastic crisis, pre-operative, acute chest crisis (usually when Hb <50g/l)
Exchange: Acute chest crisis, acute stroke, pre-operative.
Regular exchange: Primary and secondary stroke prevention, (chronic organ damage?)
Hydroxycarbamide
Increases Hb F (time delay to polymerisation, reduced adhesion to endothelium, enhances NO)
consider if >3 admissions with painful crisis in 12 months or 2 chest crisis (MSH study 1995)
CHRONIC
Transcranial doppler (annual from 3 years), STOP trial
AVN – MRI, may need joint replacement
*Perioperative care – Transfusion, avoid local tourniquet
*Cholecystectomy for symptomatic biliary disease
*Renal disease – U&E, BP, Ix haematuria. role of ACE Inhibitors for proteinuria?
*Ophthalmic – annual review
***
____Curative__________
Bone Marrow Transplant from normal donor, Gene therapy
____Prevention_________
Genetic counselling/prenatal diagnosis, avoiding precipitants

39
Q

You should treat sickle cell anaemia with Hydroxycarbamide in what case

A

if >3 admissions with painful crisis in 12 months or 2 chest crisis because it increases Hb F (time delay to polymerisation, reduced adhesion to endothelium, enhances NO)

40
Q

True or false? Preganacy is a pro-thrombotic state despite there is gestational thrombocytopenia

A
  • Evidence of platelet activation
  • Increase in many procoagulant factors
  • Reduction in some natural anticoagulants
  • Reduction in fibrinolysis
  • Rise in markers of thrombin generation
  • Coagulation factors (plasma fibrinogen, vWF, factors V, VII, VIII, X, XII, initail increase in XIII (then halved to pre-preg value), small decrease in XI and minimal increase in IX
41
Q

What is erythropoietin (EPO)’s function and where is it produced

A

Production of erythrocytes is controlled by erythropoietin (EPO) produced in kidneys in response to tissue oxygen concentration

42
Q

Hb globin chains are encoded by whick two chromosomes

A

16 alpha chains encoded here

11 gamma, delta and beta chains encoded here

43
Q 
Which Hb chains make up:
HbA
HbA2
HbF
HbS
A 
Adult
  HbA: alpha2 and beta2 
  HbA2: alpha2 delta2
Foetal 
  HbF: alpha2 gamma2
Sickle
  HbS:usually a single base substitution in globin gene altered structure/function
44
Q

True or false. Worldwide distribution of Haemoglobin

disorders mirrors falciparum malaria

A

TRUE

45
Q

DIAGNOSIS OF HAEMOGLOBINOPATHIES

A

FBC/Film

Haemoglobin electrophoresis
Isoelectric focusing
High performance liquid chromatography (HPLC)

Heat stability, isopropanol (unstable Hb’s)
Oxygen dissociation curve (p50, high affinity)
DNA analysis (genetic counseling, prenatal Dx)
Mass spectometry
Kleihauer testing, Supravital staining, Sickle solubility

46
Q

HbA/S describes what haemoglobinopathy?

A

SICKLE CELL TRAIT i.e. heterozygous (Hb A/S)

Blood count: normal

Hb Electrophoresis: Hb-S 45%, Hb-A 55%

Clinical picture: no problems except when extreme hypoxia/dehydration (eg very bad anaesthetia, flying unpressurised military aircraft)

47
Q

Pathogenesis of sickle cell anaemia

A 
Sickle Hb (Hb-S) polymerises to form long fibrils which distort the red cell membrane and produce the classical sickle shape
The sickled red cells have a short lifespan in the blood – haemolytic anaemia

n.b: Polymerisation is reduced if other haemoglobins are present in the red cell e.g. Hb-F in fetus or neonate. Hydroxycarbamide can be used to treat acute complications of sickle cell anaemia as it increases Hb F.

48
Q

Other causes of sickle cell disease

A

Co-inheritance of βs and another β chain abnormality

  • SC disease – fewer crisis, higher risk AVN and retinopathy
  • S/O-Arab (severe)
  • S/β-thalassaemia, S/Lepore, S/D-punjab (moderate)
  • S/HPFH, S/δβ0, S/E (mild)
49
Q

Thalassaemia grouping

A

Divided into α, β, δβ and γδβ according to which globin chain is reduced
In some, no globin chain is produced (e.g. α0), in others they are produced at a reduced rate (e.g. α+)

50
Q

α -THALASSAEMIA

A

Most serious forms restricted to SE Asia and some Mediterranean islands
Both Hb A and F have α chains
*Hb Barts (homozygous inheritance of α0) - hydrops fetalis
*Hb H disease
*α-trait

51
Q

β-THALASSAEMIA

A

Reduced rate of production of beta-globin chains (pathology caused by excess alpha chains)
Many molecular variants arising in different locations worldwide
-includes β-Thalassaemia Major and Trait

52
Q

β-Thalassaemia Trait

A

Blood picture resembles
iron deficiency (small,
pale red cells)

Total Hb level normal
or only slightly reduced

Hb-A2 level >3.5%

“target cells” on film

No clinical problems

53
Q

Haemoglobinopathy described by no absolute requirement for regular transfusions in order to survive during the first 3-5 years of life

A

The clinical picture and genetic basis can be highly variable
All should be genotyped

54
Q

β-THALASSAEMIA MAJOR

A

present with very
severe anaemia at
1 to 2 years of age

blood film very
abnormal with lots
of *nucleated red cells

clinical features due
to severe anaemia & attempt to make more red cells in marrow to compensate

55
Q

Nucleated red cells is a sign of which of the following haemoglobinopathy?

  • sickle cell anaemia
  • alpha THALASSAEMIA
  • beta THALASSAEMIA Major
  • THALASSAEMIA intermedia
A 
beta THALASSAEMIA Major
\_\_\_\_\_\_\_\_\_
present with very
severe anaemia at
1 to 2 years of age

blood film very
abnormal with lots
of *nucleated red cells

clinical features due
to severe anaemia & attempt to make more red cells in marrow to compensate

56
Q

Hydrops fetalis occurs in what type of thalassaemia

A

α -THALASSAEMIA: Hb Barts (homozygous inheritance of α0) - hydrops fetalis

57
Q

Pathology of beta THALASSAEMIA Major caused by

A
  • Excess alpha chains cause ineffective erythropoiesis (red cells die in marrow) & shortened RBC life span(haemolysis) -> anaemia
  • Increased marrow activity results in skeletal deformity, stunted growth, increased iron absorption and
    organ damage (exacerbated by blood transfusion),protein malnutrition
  • Enlarged and overactive spleen results in increased transfusion requirement and pooling of red cells (increased anaemia)
58
Q

The following featres are a characteristic of:
Short stature and distorted limb growth due to premature
closure of epiphyses in long bones
Enlarged liver and spleen “extramedullary haemopoiesis”

A

beta THALASSAEMIA Major

59
Q

Hair on skull appearance on X-ray is a result of

A

widening of diploic cavities by marrow expansion in β-THALASSAEMIA MAJOR

60
Q

β-THALASSAEMIA MAJOR clinical features

A

Short stature and distorted limb growth due to premature
closure of epiphyses in long bones
Enlarged liver and spleen “extramedullary haemopoiesis”
THALASSAEMIC FACIES:maxillary hypertrophy, abnormal dentition and frontal bossing due to expanded bone marrow
Hair on skull appearance on X-ray due to widening of diploic cavities by marrow expansion

61
Q

β-THALASSAEMIA MAJOR treatment

A

TRANSFUSION:
to maintain mean Hb 120 g/l (pre-transfusion Hb 95-100)
suppresses marrow red cell production and prevents skeletal
deformity and liver/spleen enlargement
3 to 4 weekly transfusions from 1st year of life

Consequences
*by 10-12 years of age there is severe iron overload and toxicity:
gonads/hypothalamus – failure of puberty, growth failure
pancreas – diabetes
heart – dilated cardiomyopathy and heart failure
liver - cirrhosis

  • Monitoring chelation - Ferritin (acute phase), liver biopsy, MRI (T2*)
  • Infection – decreased CD4/8 ratio and defective neutrophil chemotaxis, increased virulence with excess iron (yersinia and DFO), line infections, transfusion transmitted infection.
  • Endocrine complications – Growth and development, -> screening for glucose intolerance, hypothyroidism and hypoparathyroidism
62
Q

β-THALASSAEMIA MAJOR is treated with transfusions however this can result in iron overload, how is this counteracted?

A

To prevent death from iron overload patients are started on IRON CHELATION THERAPY from 2nd year of life to promote excretion of iron in urine and faeces:

Desferrioxamine is given by 8-12 hourly subcutaneous infusion via a syringe-pump as home-treatment on at least 5 nights a week to prevent the accumulation of iron

New Oral Iron Chelators include Deferiprone and Deferasirox

Target Ferritin around 1000-1500µg/L

63
Q

Haemoglobinopathies testing

A

Universal antenatal & newborn screening for genetic haemoglobin disorders.

  • *If antenatal testing positive: counseling +/- partner testing
  • *Options: pre-implantation diagnostic testing or choriovillus biopsy +/- termination
64
Q

Physiological changes that may occur in pregnancy

A

Physiological changes that may occur are:

  • *Anaemia (macrocytosis), thrombocytopenia
  • *Neutrophilia (and left shift)
  • *Increased pro-coagulant factors & ↓ fibrinolysis
65
Q

Sickle Cell Disease

A

A common resessive disorder of the β globin gene
Vascular occlusion but also a chronic inflammatory state with haemolysis induced haemostatic activation
During hospital admission, look for development of acute complications (e.g. chest crisis, CNS, priapism)
Good analgesia but also careful to avoid toxicity

66
Q

Thalassaemia

A

Genetically and clinically variable

Main focus on good iron chelation to prevent cardiac and liver failure

67
Q

Myeloma

A

An incurable malignant disorder of clonal plasma cells

Now appreciated that is preceded by asymptomatic

68
Q

Epidemiology of Myeloma

A
  • Median age 70 yo

* Higher incidence in Afro-Caribbean ethnic groups compared with Caucasians

69
Q

Myeloma is on a spectrum of severity what are the extremes (begnin to malignant),

A

Begnin: MGUS in all patients before myeloma presents

this spectrum of plasma cell dyscrasias – “paraproteinaemias” the more plasma cells the more malignant

70
Q

Immunofixaction is a technique that enables the detection and identification of monoclonal immunoglobulins. What pattern would be expected in myelmas?

A

monoclonal gammopathy as an antigen–antibody reaction should take place. After washing to remove unbound antibodies, the gel paper is stained, which allows identification of a specific isotope of the monoclonal protein.

71
Q

what is protein electrophoresis?

A

The laboratory technique whereby serum is placed in a gel and exposed to an electric current
Five major fractions are normally identified:
Serum albumin
Alpha-1 globulins
Alpha-2 globulins
Beta blogulins
Gamma globulins

72
Q

What is a normal pattern of Gamma globulins (IMMUNOGlobulins) on protein electrophoresis?
vs. in Myeloma

A

polyclonal distribution
vs.
M-spike

73
Q

Myeloma diagnostic criteria

A

Clonal Bone Marrow (BM) plasma cells >10% or biopsy-proven bony or extramedullary plasmacytoma AND any one or more of:

  • CRAB features
  • Myeloma Defining Events (MDE’s)
74
Q

CRAB Features can be seen in myeloma, what are they?

A

C – hypercalcamia (>2.75mmol/L)
R – renal insufficiency (creat clearance <40ml/min or serum creat >177micromol/L)
A – anaemia (Hb<100g/L)
B – bone lesions (one or more osteolytic lesions on skeletal radiography, CT, or PET/CT

75
Q

MDE (myeloma defining events) are features can be seen in myeloma, what are they?

A

Myeloma-defining events (MDEs):
> 60% clonal plasma cells on BM biopsy
SFLC ratio >100mg/L provided the absolute level of the involved LC is >100mg/L
>1 focal lesion on MRI measuring >5mm

76
Q

If a patient is assymptomatic but, on MRI, 2 (6mm) focal lesion are seen, is myeloma diagnosed?

A

Only if there is Clonal Bone Marrow (BM) plasma cells >10% or biopsy-proven bony or extramedullary plasmacytoma as MDE feature seen.

MDE >1 focal lesion on MRI measuring >5mm = treatment

77
Q

True or False, Myeloma commonly causes renal insufficiency

A

TRUE
50% have renal insufficiency at some point during their disease course
50% will have persistent renal impairment despite therapy
20-25% of patients have renal insufficiency at diagnosis

78
Q

Myeloma investigations

A

FBC: Hb (CRAB), WBC, platelets and blood film (rolo)
U&Es (CRAB)
Calcium (CRAB)
CRP (?active infection)
Ig Levels (immunofixation)
Plasma electropheresis (m-spike seen if myeloma)
Imaging: Whole-body CT or MRI +/- (some PET scans positive not all)

79
Q

Management of Myeloma

A

STEROIDs
Early diagnosis and intervention – STEROIDS!
Simple measures: hydration, avoid nephrotoxics and appropriate chemotherapy (attenuated dosing)

ACUTE KIDNEY INJURY WITH SUSPECTED MYELOMA IS A MEDICAL EMERGENCY

80
Q

What is MGUS?

A

Monoclonal gammopathy of undetermined significance (MGUS) is a condition in which an abnormal protein — known as monoclonal protein or M protein — is in your blood. The protein is produced in a type of white blood cell (plasma cells) in your bone marrow. MGUS usually causes no problems. Begnin and MGUS is seen in all patients before myeloma.
Diagnostic criteria:
*Serum M-protein <30g/L
*<10% clonal plasma cells in the bone marrow
*Absence of end-organ damage (CRAB)

81
Q

MGUS most commonly progresses. TRUE OR FALSE

A

FALSE. Approx. 1% per year

Of the 1% that progress, majority progress to myeloma

82
Q

MGUS can progress to:

A

majority progress to myeloma or
Waldenstrom’s macroglobulinaemia
Primary AL amyloidosis
Lymphoproliferative disorders

83
Q

AL Amyloidosis

A

Light chain fragments misfold and self-aggregate to form beta-pleated fibrils then deposit in organs

84
Q

Possible causes of a neck mass?

A

Malignant: lymphoma, chronic lymphocytic leukaemia, metastatic cancer of the lung/breast/cervix
Non-malignant: infective (bacterial, viral, mycobacterial), inflammatory (sarcoidosis), lipoma, fibroma, haemangioma

85
Q

During a VTE assesment, pts on asprin and clopidigrol should not be put of prophylaxis. TRUE OR FALSE

A

FALSE. these are antiplatelets, pts need anticoagulants

86
Q

Arterial thrombosis vs Venous

A

Arterial vs. Venous
Platelet aggregation vs. fibrin deposit
Antiplatelets used vs. anticoagulants
Retrograde vs. with blood flow
Atherosclerosis vs. venous stasis
Grey/Whitish vs. Red blue with fibrin

87
Q

VTE prophylaxis

A 
"low dose" LMW heparin
Fondaparinux
New anticoags:
* direct FXa inhibitor: Rivaoxaban (apixaban)
* direct thrombin inhibitor: Dabigatran
88
Q

diagnosis of VTE can be done by

A 
Exclusion tests:
1.Wells score
2.D-dimer
Duplex scan
VQ (ventilation - perfusion) scan
Multislice CT results
89
Q

VTE treatment

A

LMWH (low molecular weight heparin) OR unfractionated heparin (if needs to be STAT) for at least 5 days
Warfarin (overlap warfarin with LMWH until INR>2 for 2 days)

90
Q

Antiphospholipid Syndrome diagnosis depends on

A

Antiphospholipid (lupus anticoagulant/ anticardiolipin ab) antibodies detected on at least 2 occasions 8 weeks apart
+ venous/arterial thrombosis or recurrent fetal loss

91
Q

Factor V leiden

A

High factor V causes thrombophilia, mostly congenital. Most common familian thrombophilia
Factor V lieden increases due to resistance to active protein C (APC) which breaks it down int its inactive form

92
Q

Are Protein C and Protein S procoagulant/anticoagulant?

A

Both are anticoagulants

Hint to remember:
Protein Stop Coagulant
I.e. protein S and C

93
Q

Antiphospholipid Syndrome

A

Is an acquired thrombophilia. This means people with APS are at greater risk of developing conditions such as: deep vein thrombosis (DVT), a blood clot that usually develops in the leg.

94
Q

Prothrombin 20210

A

heritable thrombophilia caused by mutation in 3’ UTR resulting in high prothrombin. causing X3 increase in venous thrombosis

Clinical Pathology 2 (1 decks)

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