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Haemotology > Anaemia/iron/haemochromatosis > Flashcards

Anaemia/iron/haemochromatosis Flashcards

1
Q

When do you look for iron deficiency

A

Microcytic anaemia
Symptoms of
At risk of/prev IDA- heavy menstrual, veggie
Pre surgery - avoid transfusion
Standard pregnancy management - booking and 28 weeks

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2
Q

Iron deficiency symtpoms

A

Anaemia
Fatigue, poor conc, low mood
Hair thinning
Itch
Restless legs
Koilonychia, glossitis, pica

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3
Q

causes IDA

A

Diet - veggie
blood loss
malabsorption
Increased requirement for iron eg pregnancy

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4
Q

Blood loss causing IDA

A

Menstrual
GI bleed - ulcers, malignancy, inflammation, parasites
Blood donation

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5
Q

Who qualifies for an endoscopy/colonsocopy from IDA

A

All men and post menopausal women considered unless clearly non GI bleed

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6
Q

Investigation of IDA

A

Colonsocopy, endoscopy
Malabsorption - coeliac screen, helicobacter pylori
Urinalysis
Blood tests

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7
Q

What see on FBC in IDA

A

Hb - low or nomal
MCV<80 (some may be normal)
MCH <27
RBC - low/normal, RDW - normal/high

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8
Q

Blood film IDA

A

Hypochromia, microcytosis, pencil cells

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9
Q

Why does a normal or high ferritin not necessarily exclude IDA

A

High with inflammation and liver disease

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10
Q

What ferritin evels suggest IDA

A

<15 = no stores - pathogonomic
<30 - IDA
30-50 borderline/probable
<100 - = inflammation = possible IDA

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11
Q

Iron studies

A

Serum iron
Total binding iron capacity
Transferrin saturaiton
Not very useful IRL

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12
Q

Secondary tests for iron deficiency

A

Iron studies
Reticulocyte Hb <28
% hypochromic cells >6%
Zinc protoporphyrin >80
Oral trial of iron - improves by 20g/L in 3 weeks/Hb increases

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13
Q

Low MCV causes

A

IDA
Thalassemia/Hbinopathy
Anaemia of chronic disease
Lead poisonning
Inherited sideroblastic anaemia

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14
Q

Treating IDA

A

Diet
100-200mg elemental iron per day, 3 months after normal Hb
Aim for ferritin >50

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15
Q

What dietary iron is best absorbed

A

Haem iron from meat or fish

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16
Q

How is iron absorbed better

A

Prior to food - acid stomach
With vit C - fresh orange juice
Avoid antacids and tannins

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17
Q

What to do if oral iron not tolerated

A

Reduce dose to alternate days
Lower elemental iron/change formulation
Take w vit C, with food
Treat inflam conditions
Laxatives if constipated
Ensure compliance and no malabsorption, no haematinic deficiency

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18
Q

How does parenteral difffer to oral iron in terms of Hb

A

May initially work faster
4-6 weeks similar levels of Hb to oral iron

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19
Q

When is parenteral iron useful

A

Inflammation
Dialysis
Not tolerated oral despite trying
High levels of blood loss eg HereditaryHT elagniectasia

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20
Q

Complications pareneteral iron

A

Rare anyphylaxis, Low PO4, extravasation

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21
Q

What is hyperferritinaemia

A

Ferritin levels are high, doesnt necessarily mean iron is high

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22
Q

Causes of hyperferritinaemia

A

Inflammation incl AI disease, infection, malignancy
Liver disease, metabolic syndrome
Genetic haemohc=chromatosis
Renal failure
Myedodysplasia
THalassemia intermedia/major + other rare anaemias
Chronic blood transfusion
Porpphyria cutanea tarda
Other rare syndromes eg hereditary hyperferritenemia cataract syndrome, gauchers, acaeruloplasminaemia, friedrichs ataxia

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23
Q

What is high ferritin in men vs women

A

> 300 men
200 women

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24
Q

What do next when raised ferritin

A

Check FBC, U+Es, LFs, inflam markers, transferrin saturation

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25
Q

What does a high ferritin and abnormal FBC warrant investigatio for

A

Iron loaing apaemia
Haemolysis
Myedoplasia Thalassemia

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26
Q

When test for genetic haemochromatosis when high ferritin?

A

When trasnferrin saturations also high
eg >50% in men >40% in women
Check HFE genotyping

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27
Q

What can causes an isolated high ferritin

A

inflammation, malignancy, liver disease, metabolic syndrome etc

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28
Q

Genetic haemochromatosis why often not diagnosed

A

Often no clinically significnat iron overloading

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29
Q

Iron overlaoding symtpoms in haemochromatosis

A

Joint damage, osteoporosis
Endocrine - diabetes, gonadal sailure
Bronzed skin
Liver failure/cirrhosis HCC
Cardiac iron loading

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30
Q

Does high ferritin always cause iron overloading symptoms

A

No - only in people who have genetic haemochromatosis

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31
Q

Managment of haemochromatoss

A

Venesection 3-4 x a year aim for ferritin <50ug/L
Check for complications, family
Iron chelation if cant do venesection
Avoid vit C, reduce alcohol

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32
Q

Four initial tests for anaemia

A

Hb
MCV
Reticulocyte count
#Blood film/smear

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33
Q

If MCV <80 what differnetial anaemias suspect

A

IDA
Thalassemia
Anaemia of chronic disease
Lead poisonning
Sideroblastic

34
Q

What does a normal MCV and low reticulocyte count suggest differentials

A

Bone marrow failure
BM infiltration
Organ failure/endocrinopathy

35
Q

What does a normal MCV and high reticulocyte count suggest differentials

A

Bleeding
Haemolysis
Treated nutritionaldeficinecy

36
Q

What differentials when MCV >100 eg macrocyticc

A

B12/folate deficinecy
Liver disease
Alcohol
Drugs - methotraxtae, sulfasalazine, ART
thryoid disease

37
Q

What reticulocyte level would you expect in an anaemic patient with a healthy bone marrow response?

A

High - increased erythropoiesus

38
Q

What are reticulocytes

A

Immature RBCs

39
Q

Clinical features of haemolytic anaemias

A

Pallor
Jaundice
Gallstones pigmenet
Splnomegaly, may have hepatomegaly

40
Q

3 lab features common to all haemolytic anaemias

A

Reticulocytosis
Elevated LDH
Eleated indirect - conjugated - bilirubin

41
Q

What ceclls see in warm AI haemolytic anaemia (WAIHA)

A

Spherocytes

42
Q

What morpholoy see in cold AIHA

A

Agglutination

43
Q

What cells see in microangiopathic haemolytic anaemia -MAHA

A

Shistocytes, some spherocytes

44
Q

What cells see in oxidative haemolyiss

A

Bite cells

45
Q

What does intravascular haemolysis occur in

A

ABO incompatability
G6PD defiency
PNH - Paroxysmal nocturnal hemoglobinuria (complement destorys RBC)
PCH - AI after cold exposure, also complement
Clostridial sepsis (c.difficile)
Mechanical valve
Severe burns

46
Q

Characteristics of IV haemolysis

A
  • plasma free haemoglobin (hemoglobinemia)
  • decreased haptoglobin (bound by free Hb)
  • increased methaemoglobin (heme with Fe3+)
  • haemoglobinuria and hemosiderinuria
  • chronically, may lead to iron deficiency
47
Q

What conditions see extravascular haemolysis in

A

RES, most causes of haemolytic anaemia

48
Q

Intrinsic RBC anaemia - congenital - where effected in cell by what disease

A

1) membrane – hereditary spherocytosis, elliptocytosis
2) haemoglobin – sickle cell disease, thalassaemia’s
3) enzymes – G6PD, PK deficiency

49
Q

Secondary causes of WAIHA

A

Lymphoma
Drugs
Connective tissue disease
Causes IgG AB to antigen on RBC

50
Q

Treating WAIHA

A

Primarily extravascular haemolysis
- Treatment: steroids, treat underlying cause
- Azathioprine, cyclophosphamide, etc for steroid-sparing

51
Q

Secondary causes Cold AIHA

A

lymphoma (adults), infections (children; EBV, Mycoplasma pneumoniae)

52
Q

Antibodies CAIHA vs WAIHA

A

cold = IgM, antibody target I or i
warm = IgG, many targets incl Rh

53
Q

How does CAIHA work

A
  • Primarily intravascular haemolysis; degree of haemolysis determined by thermal amplitude of cold agglutinin
54
Q

Treatment CAIHA

A

NOT STEROIDS - dont work
Supportive in children
underlying cause adults
Cyclophosphamide
TRANSFUSE through blood warmer

55
Q

Paroxysmal cold haemoglobinuria summary

A

– IgG Ab against p (globoside) antigen, binds RBC at 4C, activates complement when re-warmed to 37C: associated with viral infections, syphilis.

56
Q

Alloimmune anaemias

A

haemolytic transfusion reactions (acute and delayed),
haemolytic disease of the new born.

57
Q

Summary of PNH

A

– acquired defect in PIG-A gene, unable to anchor proteins that require PIP, complement-mediated
chronic intravascular haemolysis marked by acute attacks

58
Q

Drug induced haemolysis causing drugs

A

Drug absorption (penicillin)
ii. Membrane modification (cephalosporin)
iii. Immune complex (quinine)
iv. Autoantibody – levodopa, methyldopa

59
Q

Non immune mediated anaemias

A

RBC fragmentation syndrome
Infection
Toxins
Chemical agents eg copper, arsenic, hypophosphatemia
Burns, downing, march heamoglobinuria

60
Q

RBC fragmentation syndromes

A

Cardiac (valves, bypass, AVMs)
ii. MAHA – TTP/HUS, malignant HTN, DIC, HELPP, pre-eclampsia

61
Q

When do you suspect Beta thalassemia in Hb electrophoresis

A

Hb A2<3.5%

62
Q

Electrophoresis and microcytic anaemia

A
  • Suspect β thalassaemia when Hb A2 >3.5%
    Normal Hb electrophoresis does not exclude α thalassaemia or iron deficiency
     In concomitant iron deficiency, Hb electrophoresis may be falsely normal; therefore, it should be repeated once iron stores are replete
     If α-thalassaemia suspected, order DNA testing
63
Q

What rule out in microytic anaemia

A

 GI investigations, rule out intravascular haemolysis, celiac disease, H .pylori, congenital

64
Q

When expect Hb to respond to iron in IDA

A

4-6 weeks
If doenst further investigations

65
Q

What decereases iron absorption

A

 Inhibited by calcium, tea, coffee, phytic acid (grains, legumes) and
 decreased gastric acidity (proton pump PPI)

66
Q

Side effects of iron

A

nausea, vomiting, dyspepsia, constipation, diarrhoea, dark stools; generally dose-related and usually subside with continued therapy (except dark stools)

67
Q

Oral preps of iron

A

 Fumarate 210mg = 65 mg elemental iron
 Gluconate 300mg = 35 mg elemental iron
 Sulphate 200mg = 65 mg elemental iron
 Feredetate 190 mg/5ml = 27.5 mg/5ml elemental iron
 Maltol 30mg = 30 mg elemental iron

68
Q

What is HHT

A

Hereditary hemorrhagic telangiectasia, also known as Osler–Weber–Rendu disease and Osler–Weber–Rendu syndrome, is a rare autosomal dominant genetic disorder that leads to abnormal blood vessel formation in the skin, mucous membranes, and often in organs such as the lungs, liver, and brain.
cause bleeding, known as arteriovenous malformations (AVMs).

69
Q

Normal HbA1c

A

Men - 130g/L
Women - 115g/L
Varies with age

70
Q

Lifespan of RBC

A

3 weeks for erythropoeisis
3 month life cycle in circulation

71
Q

What stimulates erythropoietin release

A

Decreased oxygen

72
Q

Causes of deveased RBC production

A

Reduced EPO response - kidney or chronic inflammation
Raw material deficiencies eg chronic inflam - less use iron
Reduced bone marrow production - infiltration (cancer, infection), aplastic anaemia, myelosupression (drug, infection)

73
Q

INfections and drugs causing myelosupression

A

Chloramphenicol, alcohol
Chemo
DMARDs
Propothyouracil, carbimaxole
Tacrolimus
Hydroxyurea
Parvovirus

74
Q

Causes increased RBC destruction

A

Haemolytic anaemias - AI, drug induced, hered spherocytosis
Haemoglobinopathies
Hypersplenism - RBCs out of circulation eg portal hypertenion

75
Q

What can low folate indicate

A

Increased demand for RBC eg pregnancy, lactating

76
Q

investigations in microcytic anaemia

A

Ferritin/iron studies
Further depends on symptoms
Consider haemoglobinopathy screen

77
Q

investigations for normocytic anaemia

A

Blood film, reticulocytes (low - bone marrow)
U+Es, LFTs
CRP
Ferritin/B12/folate
HIV

78
Q

Macrocytic anaemia investiations

A

Blood film
Reticulocutes
B12/folate
LFTs, U+Es
LDH, haptoglobin
DAT - haemolysis
Consider myeloma screen - serum Igs and serum free light chains
HIV

79
Q

Anaemia of chronic disease why and treatment

A

Inadequate usage of stored iron
Inadequate eryhtropoietin response to anaemia
RBC life span
Treat - underlying cause, IV iron, EPO injections

80
Q

Hypersegmented neutrophils ass with

A

Haemotinic deficiencies

81
Q

Pernicious anaemia markers

A

Low B12
Intrinsic factor
Parietal cell antibodies

82
Q

Why need to do endoscopy in B12 deficiency anaemia

A

Ass w gastric cancer

Haemotology (19 decks)

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