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HAEM Flashcards

1
Q

Define Von Willebrand disease

A

Bleeding disorder which may present with mucocutaneous bleeding (mouth, epistaxis, menorrhagia), increased bleeding after trauma and easy bruising

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2
Q

What are the 3 types of VWD

A

There are THREE types of von Willebrand disease:
o Type 1 - the von Willebrand factor works well but there isn’t enough of it
o Type 2 - there are normal levels of von Willebrand factor but it is abnormal and doesn’t function correctly
o Type 3 - there is NO von Willebrand factor

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3
Q

What does vWF normally do?

A

vWF is an adhesive bridge between platelets and the damaged subendothelial collagen
vWF also binds to factor VIII and prevents its degradation

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4
Q

What are the genetics of vW disease

A
  • Caused by abnormality in the expression/function of vWF

* Usually autosomal dominant

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5
Q

Recognise the signs and presenting symptoms of von Willbrand disease

A
  • Easy bruising
  • Epistaxis - hard to stop
  • Prolonged bleeding from gums after dental procedures • Heavy or prolonged menstrual bleeding
  • Blood in stools
  • Blood in urine
  • Heavy bleeding from a cut or other accident
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6
Q

Identify appropriate investigations for von Willebrand disease AND their results.

A
  • Bleeding time - HIGH
  • APTT - HIGH
  • Factor VIII - LOW
  • vWF - LOW
  • Ristocetin cofactor - reduced platelet aggregation by vWF in the presence of ristocetin
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7
Q

What’s APTT

A

The activated partial thromboplastin time (aPTT or PTT) is a functional measure of the intrinsic and common pathways of the coagulation cascade. … The aPTT test measures the length of time (in seconds) that it takes for clotting to occur when reagents are added to plasma (liquid portion of the blood) in a test tube

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8
Q

44yo asian female presents with 2 months of SOB and lethargy
She recently became a vegetarian
Blood film: elliptocytes
Bloods: Low Hb, Low MCV, Low Ferritin

A

Fe Deficiency anemia
classic
the most common microcytic anemia
she became a vegetarian = reduced Fe intake.

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9
Q

Explain the aetiology/risk factors of microcytic anaemia

A

• Iron Deficiency - MOST COMMON
o Iron deficiency can be caused by:
• Blood loss (e.g. GI)
• Reduced absorption (e.g. small bowel disease)
• Increased demands (e.g. growth, pregnancy)
• Reduced intake (e.g. vegans)

• Anaemia of Chronic Disease
o Microcytic anaemia in a patient with chronic disease

• Thalassemia

• Sideroblastic Anaemia
o Abnormality of haem synthesis
o It can be inherited or it can be secondary (e.g. to alcohol, drugs)

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10
Q

Recognise the presenting symptoms of microcytic anaemia

A 
•  Non-Specific 
o  Tiredness  *
o  Lethargy   
o  Malaise  
o  Dyspnoea  *
o  Pallor 
o  Exacerbation of ischaemic conditions (e.g. angina, intermittent claudication)  
•  Lead Poisoning - can cause microcytic anaemia 
Symptoms of lead poisoning  
o  Anorexia 
o  Nausea/Vomiting  
o  Abdominal pain  
o  Constipation  
o  Peripheral nerve lesions
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11
Q

Recognise the signs of microcytic anaemia on physical examination

A 
•  Signs of anaemia 
o  Pallor  
o  Brittle nails and hair   
o  Koilonychia (if severe) 
•  Glossitis 
• Angular stomatitis  
•  Signs of thalassemia  
•  Lead poisoning signs:  
o  Blue gumline  *
o  Peripheral nerve lesions (causing wrist or foot drop)  
o  Encephalopathy 
o  Convulsions  
o  Reduced consciousness
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12
Q

Identify appropriate investigations for microcytic anaemia

A 
BLOODS
o  FBC 
•  Low Hb  
•  Low MCV  
•  Reticulocytes  
o  Serum iron (low in iron deficiency) 
o  Total iron binding capacity (high in iron deficiency)  
o  Serum ferritin (low in iron deficiency) 
o  Serum lead  
BLOOD FILM
o  Iron deficiency anaemia: 
•  Microcytic  
•  Hypochromic  
•  Anisocytosis   
•  Poikilocytosis  
o  Sideroblastic anaemia: 
•  Dimorphic blood film  
•  Hypochromic microcytic cells  
o  Lead poisoning: 
•  Basophilic stippling

• Hb Electrophoresis
o Checking for haemoglobin variants and thalassemia

• Sideroblastic Anaemia
o Ring sideroblasts in the bone marrow

• Special investigations for iron deficiency anaemia if > 40 yrs and post-menopausal women
These are considered if no obvious cause of blood loss is identified
o Upper GI endoscopy
o Colonoscopy
o Haematuria

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13
Q

Generate a management plan for microcytic anaemia

A

• Iron Deficiency - oral iron supplements

• Sideroblastic Anaemia
o Treat the cause
o Pyridoxine used in inherited forms
o Blood transfusion and iron chelation can be considered if there is no response to other treatments

• Lead Poisoning
o Remove the source
o Dimercaprol
o D-penicillinamine

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14
Q

Identify possible complications of microcytic anaemia

A
  • High-output cardiac failure

* Complications related to the CAUSE

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15
Q

Explain the 2 main types of macrocytic anaemia and their RF/aetiology

A

MEGALOBLASTIC- when the bone marrow produces unusually large, structurally abnormal, immature red cells
–> Caused by deficiency of B12 or folate required for the
conversion of deoxyuridate to thymidylate, DNA
synthesis and nuclear maturation

o Causes of Vitamin B12 Deficiency:
• Reduced absorption (e.g. post-gastrectomy, pernicious anaemia, terminal ileal resection or disease)
• Reduced intake (vegans)
• Abnormal metabolism (congenital transcobalamin II deficiency)

o Causes of Folate Deficiency:
• Reduced intake (alcoholics, elderly, anorexia)
• Increased demand (pregnancy, lactation, malignancy, chronic inflammation)
• Reduced absorption
• Jejunal disease (e.g. coeliac disease)
• Drugs (e.g. phenytoin)
o Drugs
• Methotrexate (dihydrofolate reductase inhibitor)
• Hydroxyurea
• Azathioprine (Crohn’s, UC)
• Zidovudine

NON MEGALOBLASTIC 
o  Alcohol excess  
o  Liver disease  
o  Myelodysplasia 
o  Multiple myeloma 
o  Hypothyroidism  
o  Haemolysis (shift to immature red cell form - reticulocytosis)   
o  Drugs (e.g. tyrosine kinase inhibitor)
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16
Q

Recognise the presenting symptoms of macrocytic anaemia

A

• Non-specific symptoms of anaemia:
o Tiredness
o Lethargy
o Dyspnoea
• Family history of autoimmune disease
• Previous GI surgery
• Symptoms of the CAUSE (e.g. weight loss, diarrhoea)

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17
Q

Recognise the signs of macrocytic anaemia on physical examination

A 
•  Signs of Anaemia  
o  Pallor  
o  Tachycardia  
o  Breathlessness  
•  Signs of Pernicious Anaemia (IF)
o  Mild jaundice  
o  Glossitis  
o  Angular stomatitis  
o  Weight loss  
•  Signs of B12 Deficiency 
o  Peripheral neuropathy * "cant sit up from chair"
o  Ataxia  
o  Subacute combined degeneration of the spinal cord   
o  Optic atrophy  
o  Dementia
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18
Q

Identify appropriate investigations for macrocytic anaemia

A

BLOODS
o FBC
• High MCV
• Pancytopaenia in megaloblastic anaemia
• Different degrees of cytopaenia in myelodysplasia
• Exclude reticulocytosis
o LFT - High bilirubin (due to ineffective erythropoiesis or haemolysis)
o ESR
o TFT
o Serum vitamin B12
o Red cell folate
o Anti-parietal cell and anti-intrinsic factor antibodies
o Serum protein electrophoresis M looking for a dense band in myeloma

BLOOD FILM
o  Large erythrocytes 
o  In megaloblastic anaemia: 
•  Megaloblasts  
•  Hypersegmented neutrophil nuclei *

• Schilling Test
o Method of testing for pernicious anaemia
o B12 will only be absorbed when given with intrinsic factor
• Bone Marrow Biopsy (rarely needed)
• Investigations for the cause

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19
Q

Generate a management plan for macrocytic anaemia

A

• Pernicious Anaemia - IM hydroxycobalamin for life

• Folate Deficiency
o Oral folic acid
o If B12 deficiency is present, it must be treated before the folic acid deficiency

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20
Q

Identify possible complications of macrocytic anaemia

A
  • Pernicious anaemia –> increased risk of gastric cancer

* Pregnancy - folate deficiency increases the risk of neural tube defects

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21
Q

Classic presentation of b12 deficiency

A

Middle aged/elderly female
Complains of tiredness, dyspnoea, easily fatigues “difficulty getting up the chair” “difficulty holding her books”
Noticed tingling sensation in her fingers

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22
Q

Anaemia of chronic disease mechanism

A

An underlying disease causes and inflammatory process involving cytokines to occur. CRP and ESR are raised.
The effect of these cytokines is to interrupt the homeostasis of iron.
EPO is inhibited, iron is unable to flow out of RBC, ferritin production is increased and RBC death is increased.

This results in anaemia with raised ferritin levels (and in prolonged cases low serum Fe)

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23
Q

Where is b12 absorbed?

A

Terminal ileum

Crohns

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24
Q

Where is folate absorbed?

A

Proximal duodenum

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25
Q

Define DIC

A

• A disorder of the clotting cascade that can complicate a serious illness.

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26
Q

What are the 2 forms of DIC?

A

ACUTE OVERT FORM where there is bleeding and depletion of platelets and clotting factors

CHRONIC NON OVERT FORM where thromboembolism is accompanied by generalised activation of the coagulation system

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27
Q

Explain the aetiology for DIC

A

• Infection - particularly GRAM-NEGATIVE sepsis

• Obstetric Complications
o Missed miscarriage (when the foetus dies but the body doesn’t realise it and the placenta continues to release hormones)
o Severe pre-eclampsia
o Placental abruption (separation of the placenta from the wall of the uterus during pregnancy)
o Amniotic emboli

• Malignancy
o Acute promyelocytic leukaemia - ACUTE DIC
o Lung, breast and GI malignancy - CHRONIC DIC

  • Severe trauma or surgery
  • Others: haemolytic transfusion reaction, burns, severe liver disease, aortic aneurysms, haemangiomas
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28
Q

Explain the pathophysiology of DIC for ACUTE DIC

A

Acute DIC
• Endothelial damage and the release of granulocyte /macrophage procoagulant substances (e.g. tissue factor) lead to activation of coagulation
• This leads to explosive thrombin generation, which depletes clotting factors and platelets, whilst also activating the fibrinolytic system
• This leads to bleeding in the subcutaneous tissues, skin and mucous membranes
• Occlusion of blood vessels by fibrin in the microcirculation leads to microangiopathic haemolytic anaemia and ischaemic organ damage

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29
Q

Explain the pathophysiology of CHRONIC DIC

A

o Chronic DIC
• IDENTICAL process to acute DI
• Happens at a slower rate with time for compensatory responses
• The compensatory responses diminish the likelihood of bleeding but give rise to hypercoagulable states and thrombosis can occur

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30
Q

Summarise the epidemiology of DIC

A

• Seen in any severely ill patient

31
Q

Recognise the presenting symptoms of DIC

A
  • The patients will tend to be severely unwell with symptoms of the underlying disease
  • Confusion
  • Dyspnoea
  • Evidence of bleeding
32
Q

Recognise the signs of DIC on physical examination for ACUTE DIC

A
  • Signs of underlying disease
  • Fever
  • Evidence of shock (hypotension, tachycardia)
•  Acute DIC 
o  Petechiae, purpura, ecchymoses   
o  Epistaxis  
o  Mucosal bleeding  
o  Overt haemorrhage  
o  Signs of end organ damage   
o  Respiratory distress  
o  Oliguria due to renal failure
33
Q

Recognise the signs of DIC on physical examination for CHRONIC DIC

A

• Chronic DIC

o Signs of deep vein and arterial thrombosis or embolism o Superficial venous thrombosis

34
Q

Identify appropriate investigations for DIC

A 
BLOODS
o  FBC 
•  Low platelets  
•  Low Hb  
•  High APTT/PT 
•  Low fibrinogen 
•  High fibrin degradation products   
•  High D-dimers

PERIPHERAL BLOOD FILM
o Schistocytes

35
Q

Microcytic anemia differentials

A

Fe deficiency anemia
Anemia of chronic disease
Thalassaemia

36
Q

What does tea have to do with anemia/deficiencies?

A

Tea is alkaline and reduces the body’s ability to effectively absorb iron.

37
Q

If you suspect Fe defiiciency anemia in a newly vegan young woman, which test is the bst to do?

A

Serum ferritin

It provides an accurate reflection of the body’s iron stores since the serum ferritin originates from the storage pools in the bone marrow, spleen and liver.

Serum ferritin measurements are only accurate when the CRP is normal because both ferritin and CRP are acute phase protein reactants.

38
Q

Why is serum iron level a poor reflection of iron stores?

A

Because it can change dependent on disease states.
In Fe deficiency anemia the serum iron and iron stores are low
In Anemia of chronic disease though iron stores are increased yet the serum iron level is reduced.

39
Q

What does the Fe total binding capacity indicate

A

ITBC saturated transferrin in order to measure the iron-carrying capacity in the body rather than the stores.

40
Q

Define myelofibrosis

A

• Disorder of haematopoietic stem cells characterised by progressive bone marrow fibrosis in associated with extramedullary haematopoiesis and splenomegaly

41
Q

Whats the pathogenesis of myelofibrosis

A

o Abnormal megakaryocytes release cytokines that stimulate fibroblast proliferation and collagen deposition in bone marrow
o This results in extramedullary haematopoiesis in the spleen and liver

42
Q

Explain the aetiology/risk factors of myelofibrosis

A
  • Primary stem cell defect is UNKNOWN
  • It results in increased numbers of abnormal megakaryocytes with stromal proliferation secondary to growth factors released by megakaryocytes
  • 30% of patients have a previous history of polycythaemia rubra vera or essential thrombocythaemia (overproduction of platelets by the bone marrow)
43
Q

Recognise the presenting symptoms of myelofibrosis

A

• ASYMPTOMATIC - diagnosed after routine blood count • Systemic Symptoms

o  COMMON: 
•  Weight loss  
•  Anorexia 
•  Fever  
•  Night sweats   
•  Pruritis  
o  UNCOMMON:  
•  LUQ pain  
•  Indigestion (due to massive splenomegaly)   
•  Bleeding  
•  Bone pain  
•  Gout
44
Q

Recognise the signs of myelofibrosis on physical examination

A
  • SPLENOMEGALY

* Hepatomegaly (present in 50-60%)

45
Q

Identify appropriate investigations for myelofibrosis

A

• Bloods
o FBC
• Initially variable Hb, WCC and platelets
• Later stages –> anaemia, leukopaenia, thrombocytopaenia
o LFTs - abnormal
• Blood Film
o Leucoerythroblastic changes (red and white cell precursors in the peripheral blood)
o ‘Tear drop’ poikilocyte red cells
• Bone Marrow Aspirate or Biopsy
o Aspiration usually unsuccessful - ‘dry tap’ (due to fibrosis)
o Trephine biopsy shows fibrotic hypercellular marrow, with dense reticulin fibres on silver staining

46
Q

What happens in pernicious anaemia?

A

An autoimmune disease whereby antibodies bind IF produced by the parietal cells in the gastric fundus.
IF is essential to the absorbtion of b12 via the terminal ileum

47
Q

Define polycythaemia

A

• An increase in haemoglobin concentration above the upper limit of normal for a person’s age and sex.

48
Q

What is polycythaemia classified into?

A 
Classified into: 
o  Relative Polycythaemia = normal red cell mass but low plasma volume  
o  Absolute (True) Polycythaemia = increased red cell mass
49
Q

Explain the aetiology of the 3 types of polycythaemia

A

• Polycythaemia Rubra Vera
o Characterised by clonal proliferation of myeloid cells
o They have varied morphologic maturity and haematopoietic efficiency
o Mutations in JAK2 tyrosine kinase are involved

• Secondary Polycythaemia

o Appropriate increase in erythropoietin
• Due to chronic hypoxia (e.g. chronic lung disease, living at high altitude)
• This leads to upregulation of erythropoiesis

o Inappropriate increase in erythropoietin
• Renal (carcinoma, cysts, hydronephrosis)
• Hepatocellular carcinoma
• Fibroids
• Cerebellar haemangioblastoma
• Secondary polycythaemia may be due to erythropoietin abuse by athletes

•  Relative Polycythaemia 
o  Dehydration (e.g. diuretics, burns, enteropathy)  
o  Gaisbock's syndrome  = Occurs in young male smokers with hypertension, which results in a  decrease in plasma volume and an apparent increase in red cell count
50
Q

Whata the peak incidence age for polyc. ?

A

45-60yo

51
Q

Recognise the presenting symptoms of polycythaemia

A
  • Headaches *
  • Dyspnoea
  • Tinnitus
  • Blurred vision
  • Pruritis after hot bath *
  • Night sweats
  • Thrombosis (DVT, stroke)
  • Pain from peptic ulcer disease
  • Angina
  • Gout
  • Choreiform movements
52
Q

Recognise the signs of polycythaemia on physical examination

A
  • Plethoric complexion (red, ruddy)
  • Scratch marks from itching
  • Conjunctival suffusion (redness of the conjunctiva)
  • Retinal venous engorgement
  • Hypertension
  • Splenomegaly (in 75% of cases)
  • Signs of underlying aetiology in secondary polycythaemia
53
Q

Identify appropriate investigations for polycythaemia

A 
•  Required for Diagnosis  
o  FBC  
•  High Hb **
•  High haematocrit **  
•  Low MCV

• Isotope Dilution Techniques
o Allows confirmation of plasma volume and red cell mass
o Distinguishes between relative and absolute polycythaemia

•  Polycythaemia Rubra Vera  
o  High WCC *
o  High platelets  
o  Low serum EPO 
o  JAK2 mutation *
o  Bone marrow trephine and biopsy shows erythroid hyperplasia and raised megakaryocytes

• Secondary Polycythaemia
o High serum EPO
o Exclude chronic lung disease/hypoxia
o Check for EPO-secreting tumours

54
Q

Name a few diseases which ahve massive splenomegaly OE

A

Polycythyaemia
Myelofibrosis
Thalassemia

55
Q

Define aplastic anaemia

A

• Characterised by diminished haematopoietic precursors in the bone marrow and deficiency of all blood cell elements (pancytopaenia)

56
Q

Explain the aetiology/risk factors of aplastic anaemia

A

• Idiopathic (> 40%)
o May be due to destruction or suppression of stem cells via autoimmune mechanisms

• Acquired
o Drugs (e.g. chloramphenicol, sulphonamides, methotrexate)
o Chemicals (e.g. benzene, DDT)
o Radiation
o Viral infection (e.g. parvovirus B19)
o Paroxysmal nocturnal haemoglobinuria

• Inherited
o Fanconi’s anaemia
o Dyskeratosis congenita (a rare, progressive bone marrow failure syndrome)

57
Q

Recognise the presenting symptoms of aplastic anaemia

A

• Can be both slow-onset (months) or rapid-onset (days)\

• Anaemia Symptoms:
o Tiredness
o Lethargy
o Dyspnoea

• Thrombocytopaenia Symptoms:
o Easy bruising
o Bleeding gums
o Epistaxis

• Leukopaenia Symptoms:
o Increased frequency and severity of infections

58
Q

Recognise the signs of aplastic anaemia on physical examination

A

• Anaemia Signs:
o Pallor

• Thrombocytopaenia Signs:
o Petechiae
o Bruises

• Leukopaenia Signs:
o Multiple bacterial and fungal infections
o No hepatomegaly, splenomegaly or lymphadenopathy

59
Q

Identify appropriate investigations for aplastic anaemia

A 
BLOODS
o  FBC 
•  Low Hb 
•  Low platelets  
•  Low WCC 
•  Normal MCV  
•  Low or absent reticulocytes

BLOOD FILM
o Exclude leukaemia (check for abnormal circulating white blood cells)

• Bone Marrow Trephine Biopsy

• Fanconi’s Anaemia
o Check for presence of increased chromosomal breakage in lymphocytes cultures in the presence of DNA crossMlinking agents

60
Q

What is AML?

A

• Malignancy of primitive myeloid lineage white blood cells (myeloblasts) with proliferation in the bone marrow and blood

61
Q

Explain the aetiology/risk factors of acute myeloblastic leukaemia

A
  • Myeloblasts undergo malignant transformation and proliferation
  • This leads to replacement of normal marrow and bone marrow failure
62
Q

Summarise the epidemiology of acute myeloblastic leukaemia

A
  • MOST COMMON acute leukaemia in ADULTS
  • Incidence INCREASES with age

middle aged males.

63
Q

Recognise the presenting symptoms of acute myeloblastic leukaemia

A

• Symptoms of Bone Marrow Failure:
o Anaemia (lethargy, dyspnoea)
o Bleeding (due to thrombocytopaenia or DIC)
o Opportunistic or recurrent infections

• Symptoms of Tissue Infiltration:
o Gum swelling or bleeding
o CNS involvement (headaches, nausea, diplopia)

PANCYTOPAENIA SYMPTOMS

64
Q

Recognise the signs of acute myeloblastic leukaemia on physical examination

A 
•  Signs of Bone Marrow Failure: 
o  Pallor  
o  Cardiac flow murmur  
o  Ecchymosis  
o  Bleeding  
o  Opportunistic or recurrent infections (e.g. fever, mouth ulcers, skin infections)

• Signs of Tissue Infiltration:
o Skin rashes
o Gum hypertrophy
o Deposit of leukaemic blasts in the eye, tongue and bone (RARE)

PANCYTOPAENIA SIGNS

65
Q

Identify appropriate investigations for acute myeloblastic leukaemia

A

• Bloods
o FBC - low Hb, low platelets, variable WCC
o High uric acid
o High LDH
o Clotting studies, fibrinogen and D-dimers (to check for DIC)

• Blood Film
o Myeloblasts

• Bone Marrow Aspirate or Biopsy
o Hypercellular with > 20% blasts *

•  Immunophenotyping 
o  Antibodies against surface antigens used to classify the lineage of the abnormal 
clones   
•  Cytogenetics 
 •  Immunocytochemistry
66
Q

What is INR? What does it represent?

A

International normalised ratio
It’s the ratio between the PT compares to a control sample and provides a means of monitoring bleeding risk*

Normal INR: 0.9-1.3
Target INR for rheumatic valve disease + AF: 2-3

67
Q

Define multiple myeloma

A

• Haematological malignancy characterised by proliferation of plasma cells resulting in
bone lesions and the production of a monoclonal immunoglobulin (paraprotein, usually IgG or IgA)

68
Q

Explain the aetiology/risk factors of multiple myeloma

A
  • UNKNOWN
  • Possible viral trigger
  • Chromosomal aberrations are frequent
  • Associated with ionising radiation, agricultural work or occupational chemical exposures
69
Q

Summarise the epidemiology of multiple myeloma

A
  • Annual incidence: 4/100,000
  • Peak incidence: 70 yrs
  • Afro-Caribbean > White People > Asians
70
Q

Recognise the presenting symptoms of multiple myeloma

A

• May be an INCIDENTAL finding on routine blood tests

• Bone Pain
o Usually in the back * (gradually increasing) and ribs
o Sudden and severe bone pain may be caused by a pathological fracture

• Infections - often recurrent

•  General 
o  Tiredness  
o  Thirst  
o  Polyuria 
o  Nausea  
o  Constipation 
o  Mental change (due to hypercalcaemia)

• Hyperviscosity
o Bleeding
o Headaches
o Visual disturbance

71
Q

Recognise the signs of multiple myeloma on physical examination

A
  • Pallor
  • Tachycardia
  • Flow murmur
  • Signs of heart failure
  • Dehydration
  • Purpura
  • Hepatosplenomegaly *
  • Macroglossia
  • Carpal tunnel syndrome
  • Peripheral neuropathies
72
Q

Identify appropriate investigations for multiple myeloma

A

• Bloods
o FBC - low Hb, normochromic normocytic
o High ESR (and possible high CRP)
o U&Es - high creatinine, high Ca2+**
o Normal ALP

• Blood Film
o Rouleaux ** formation with bluish background (suggests high protein)

• Serum or Urine Electrophoresis
o Serum paraprotein
o Bence-Jones protein** (monoclonal immunoglobulin light chain that’s found in the urine and suggests multiple myeloma)

• Bone Marrow Aspirate and Trephine
o High plasma cells (usually > 20%)

• Chest, Pelvic or Vertebral XJRay
o Osteolytic lesions without surrounding sclerosis
o Pathological fractures (lumbar spine or limbs)

73
Q

What antibodies will you test for pernicious anaemia?

A

• Pernicious Anaemia Tests
o Anti-intrinsic factor antibodies
o Anti-parietal cell antibodies

500 SBA's (12 decks)

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