Brainscape's Knowledge GenomeTM

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


See full index

Yr4: Cancer Care > Anaemias > Flashcards

Anaemias Flashcards

1
Q

What’s the normal HB range and MCV range for:

  • Women
  • Men
A

Women

  • Hb: 120-165g/L
  • MCV: 80-100 femtolitres

Men

  • Hb: 130-180g/L
  • MCV: 80-100femtolitres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Remind yourself of causes of microcytic anaemia

A
  • Thalassaemia
  • Anaemia of chronic disease
  • Iron deficiency
  • Lead poisoning
  • Sideroblastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Remind yourself of causes of normocytic anaemia

*3 A’s and 2H’s

A
  • Acute blood loss
  • Anaemia of chronic disease
  • Aplastic anaemia
  • Haemolytic anaemia
  • Hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Remind yourself of causes of both megaloblastic macrocytic anaemia and normoblastic macrocytic anaemia

A

Megaloblastic (result of impaired DNA synthesis preventing normal cell division resulting in a larger abnormal cell)

  • B12 deficiency
  • Folate deficiency

Normoblastic

  • Alcohol
  • Reticulocytosis (usually from haemolytic anaemia or blood loss)
  • Hypothyroidism
  • Liver disease
  • Drugs e.g. azathioprine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

State some generic symptoms of anaemia

A
  • Tiredness
  • Shortness of breath
  • Headaches
  • Dizziness
  • Palpitations
  • Worsening of other conditions such as angina, heart failure or peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

State some generic signs of anaemia

A
  • Pale skin
  • Conjunctival pallor
  • Tachycardia
  • Raised respiratory rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State some symptoms specific to Fe deficiency anaemia

A
  • Pica (cravings for abnormal things e.g. dirt)
  • Hair loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

State some signs specific to Fe deficiency anaemia

A
  • Koilonychia (spoon shaped nails)
  • Angular chelitis (red patches at corner of mouth)
  • Atrophic glossitis (smooth tongue due to atrophy of papillae)
  • Brittle hair
  • Brittle nails
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

State some signs specific to haemolytic anaemia

A
  • Jaundice
  • Splenomegaly (spleen full of destroyed RBCs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

State a sign specific to thalassemia

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

What initial investigations would you do if you suspect anaemia?

What further investigations may be done if cause is unclear?

A

Initial Investigations

  • FBC: Hb, MCV
  • Haematinics
    • B12
    • Folate,
    • Ferritin
  • Blood film

Further Investigations

  • OGD & colonoscopy: investigate for GI cause of Fe deficiency
  • Bone marrow biopsy: look for abnormalities in bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fe deficiency is a common cause of anaemia but is NOT a diagnosis in itself; there is always a reason as to why they are Fe deficient. State some potential reasons

A
  • Insufficient dietary iron
  • Iron requirements increased e.g. pregnancy
  • Iron being lost e.g. GI cancer, oesophagitis, gastritis, IBD, menorrhagia
  • Inadequate Fe absorption (e.g. Crohn’s disease affecting terminal ileum, PPIs reducing acidity of stomach)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Remind yourself of the absorption of iron

A
  • Fe comes in two forms ferrous (Fe2+) and ferrate (Fe3+)
  • Fe3+ is reduced to Fe2+ in acidic conditions; this if preferable as Fe2+ can be directly absorbed by enterocyte whereas Fe3+ requires conversion
  • Absorption occurs in duodenum & upper jejenum
  • Fe2+ absorbed via DMT1. Fe3+ reduced by duodenal cytochrome B reductase before absorption via DMT1
  • Fe can then either be stored as ferritin or released into bloodstream via ferroportin
  • Hephaestin then oxidises Fe2+ to Fe3+
  • Fe3+ then binds to transferrin and is transported to sites where it is required or stored (most of it goes to bone marrow for erythropoiesis or is taken up by macrophages in RES as storage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do each of the following tests for Fe deficiency measure/indicate:

  • Ferritin
  • Serum iron
  • Total iron binding capacity
  • Transferrin saturation
    *
A
  • Ferritin: form iron takes when deposited and stored in cells. If low it is highly suggestive of Fe deficiency. If it is high it could be numerous things e.g. iron overload, inflammation (e.g. infection or cancer as it is released from cells in inflammation)
  • Serum iron: amount of iron in serum. Varies throughout day with higher level in morning and after eating iron so not very useful.
  • TIBC: directly related to amount of transferrin in blood as this is what Fe binds to be transported
  • Transferrin saturation: serum iron/TIBC. Gives you the proportion of the transferrin molecules that have Fe bound. Normally ~30% but it less Fe in body will be less saturated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Discuss the management of Fe deficiency anaemia

A
  • Oral iron (ferrous sulfate 200mg TDS): slowly corrects deficiency. Can cause constipation & black stools. Not useful if problem due to malabsoprtion.
  • Iron infusion: quickly corrects deficiency. Small risk anaphlyaxis. Don’t use in sepsis as iron feeds bacteria.
  • Blood transfusion: immediately corrects anaemia but has risks and doesn’t always correct underlying cause.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When correcting Fe deficiency anaemia with Fe supplementation, what would you expect Hb to rise by each week?

A

10g/L per week

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

State some inherited causes of haemolytic anaemia

A
  • Hereditary Spherocytosis
  • Hereditary Elliptocytosis
  • Thalassaemia
  • Sickle Cell Anaemia
  • G6PD Deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

State some acquired causes of haemolytic anaemia

A
  • Autoimmune haemolytic anaemia
  • Alloimmune haemolytic anaemia (transfusions reactions and haemolytic disease of newborn)
  • Paroxysmal nocturnal haemoglobinuria
  • Microangiopathic haemolytic anaemia
  • Prosthetic valve related haemolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What might you see on blood film of haemolytic anaemia?

A

Schistocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alongside usual anaemia investigations, what other investigation would you do if you suspect haemolytic anaemia?

A
  • Direct Coombs test to check for autoimmune haemolytic anaemia
21
Q

Describe the direct Coombs test

A
22
Q

Describe the indirect Coombs test

A
23
Q

Compare direct & indirect Coombs test in regards to:

  • What they test for
  • Uses
A
24
Q

For hereditary spherocytosis, discuss:

  • Who common in
  • Mode of inheritance
  • What the problem is
  • How may present if have infection with parvovirus
  • MCHC and reticulocytes findings
  • Treatment
A
  • Northern Europeans
  • Autosomal dominant
  • Sphere shaped RBCs → fragile → breakdown easily
  • Parvovirus → jaundice, gallstones, splenomegaly & aplastic crisis
  • Blood film shows spherocytes
  • MCHC increased, reticulocytes increased
  • Treatment:
    • Long term:
      • Folate supplementation
      • Splenectomy
      • Cholecystectomy if gallstones occur frequently
    • Acute haemolytic crisis:
      • Supportive e.g. with transfusion if necessary
25
Q

For hereditary elliptocytosis, discuss:

  • Problem
  • Inheritance pattern
A
  • RBCs elliptical in shape
  • Autosomal dominant

*Presentation & management same as for hereditary spherocytosis

26
Q

For G6PD deficiency, discuss:

  • Who more common in
  • Inheritance pattern
  • Problem is
  • Triggers
  • Presentation
  • Peripheral blood smear findings
  • Management
A
  • Mediterranean & African
  • X-linked recessive
  • Deficiency in glucose-6-phosphate-dehydrogenase. Enzyme in involved in pentose phosphate pathway and converts glucose-6-phosphate into 6-phosphogluconolactone. Reaction also converts NADP → NADPH. NADPH is important for converting GSSG back to GSH (reduced form) which can protect against oxidative stress
  • Triggers: infections, medications (e.g. primaquine, ciprofloxacin, sulfonylureas, sulfasalazine, sulphonamides), broad beans
  • Presentation:
    • Jaundice (neonatal)
    • Anaemia
    • Splenomegaly
    • Gallstones
  • Blood film= Heinz bodies, blister/bite cells
  • Management:
    • Acute haemolytic event: treat underlying cause (e.g. stop trigger)
    • May need transfusion
27
Q

What is autoimmune haemolytic anaemia?

State the 2 types

Which type is more common

A
  • Body produces antibodies against body’s own RBCs
  • Two types based on temp at which auto-antibodies function: warm & cold
  • Warm is more common
28
Q

For warm type autoimmune haemolytic anaemia, discuss:

  • What temp it occurs at
  • Cause
A
  • At or above normal temp
  • Idiopathic
29
Q

For cold type autoimmune haemolytic anaemia, discuss:

  • What also called
  • What temperatures it occurs at
  • Causes
A
  • Cold agglutin disease
  • Lower temps (e.g. <10 degrees) results in RBCs clumping together “agglutination” which leads to them getting marked by immune system then filtered and destroyed by spleen
  • Often secondary to: lymphoma, leukaemia, SLE, infections (e.g. EBV, CMV, HIV, mycoplasma)
30
Q

Discuss potential management of autoimmune haemolytic aneamia

A
  • Blood transfusions (still have the problem of destroying RBCs but good in emergency)
  • Prednisolone
  • Rituximab
  • Splenectomy
31
Q

What is alloimmune haemolytic anaemia?

A
  • When there’s either a foreign RBC in pt’s blood which pt’s immune system attacks or a foreign antibody in pt’s blood that attacks pt’s RBCs
  • Example scenarios:
    • Transfusion reactions
    • Haemolytic disease of newborn
32
Q

For paroxysmal nocturnal haemoglobinuria, discuss:

  • What the problem is
  • Characteristic presentation
  • Management
A
  • Rare condition. At some point during lifetime, a genetic mutation in hemopoietic stem cells resulting in loss of proteins on RBC surface. The lost proteins usually inhibit complement cascade hence mutation results in activation of complement cascade on RBC surface leading to destruction of RBC
  • Presentation:
    • Red urine in morning (Hb and haemosiderin)
    • Anaemia
    • Predisposition to thrombosis
    • Predisposition to smooth muscle dystonia (e.g. oesophageal spasm, erectile dysfunction)
  • Management:
    • Eculizumab or bone marrow transplant (latter can be curative)

**Eculizumab is a monoclonal antibody targeting complement component C5 resulting in suppression of complement system

33
Q

For microangiopathic haemolytic anaemia, discuss:

  • What the problem is
  • Causes
A
  • Structural abnormalities in small vessels damage and hence destroy RBCs travelling through the them
  • Causes:
    • HUS
    • DIC
    • Thrombotic thrombocytopenic purpura (TTP)
    • SLE
    • Cancer
34
Q

For prosthetic valve haemolysis, discuss:

  • What problem is
  • Management
A
  • Complication of prosthetic heart valves (both bioprosthetic & metallic); turbulence around valve causing collision and damage to RBCs resulting in destruction
  • Management:
    • Monitoring
    • Oral Fe
    • Blood transfusion (severe cases)
    • Revision surgery (severe cases)
35
Q

Describe the absorption of B12

A
  • B12 binds to haptocorrin secreted by salivary glands
  • Complex passes to stomach.
  • In small intestine, B12 released from haptocorrin and binds intrinsic factor produced by parietal cells in stomach
  • IF-B12 complex bind to receptors on terminal ileum
  • B12 absorbed and IF destroyed
  • Once absorbed, B12 forms complex with transcobalamin II which is released into blood for delivery to other tissues
  • Approx half taken up by liver as storage (3-6 years)
  • Low vitamin B12 can be due to: dietary deficiency, lack of intrinsic factor (e.g. pernicious anaemia, gastrectomy), disease of ileum or lack of transcobalamin.
36
Q

Describe pathophysiology of pernicious anaemia

A
  • Autoimmune cause of B12 deficiency anaemia
  • Parietal cells in stomach produce intrinsic factor
  • Intrinsic factor essential for absorption of B12 in the ileum
  • In pernicious anaemia antibodies against parietal cells or intrinsic factor are produced
  • Leads to lack of intrinsic factor
  • And so lack of absorption of B12
37
Q

State some symptoms of B12 deficiency

A
  • Anaemia symptoms (SOB, fatigue, palpitations)
  • Neurological symptoms:
    • Peripheral neuropathy with numbness or paraesthesia (pins and needles)
    • Loss of vibration sense or proprioception
    • Visual changes
    • Mood or cognitive changes
38
Q

What investigations are used to diagnose pernicious anaemia?

A

Usual anaemia investigations then test for:

  • First line= intrinsic factor antibodies
  • Second line= gastric parietal cell antibodies
39
Q

Discuss the management of pernicious anaemia

A
  • Hydroxocobalamin (eventually every 3/12 but at start more frequent)
  • *IM injection of B12. Oral replacement with cyanocobalamin not useful as problem with absorption*
40
Q

Explain the link between B12 and folate deficiency

A

In summary, dietary folate has to be converted into tetrahydrofolate. This conversion rquires the metabolism of homocysteine to methionine and vitamin B12 is a co-factor that catalyses this reaction. Tetrahydrofolate is then incorporated into DNA cycle to help produce DNA.

41
Q

State some potential causes of B12 deficiency

A
  • Insufficient dietary intake
  • Gastric pathology e.g. pernicious anaemia, gastrectomy
  • Small bowel pathology e.g. ileal resection, IBD
42
Q

State some potential causes of folate deficiency

A
  • Reduced dietary intake e.g. alcohol excess, malnutrition
  • Increased metabolic demand e.g. pregnancy, malignancy
  • Malabsorption: IBD
  • Antifolate drugs: methotrexate, trimethoprim
43
Q

If a pt has both B12 and folate deficiency, what should you treat first and why?

A

B12 deficiency as it can lead to subacute combined degeneration of the cord

44
Q

If a pt has B12 deficiency anaemia (not due to problems with absorption) what would you treat them with?

A

Cyanocobalamin (oral replacement)

*unless deficiency severe

45
Q

For pyruvate kinase deficiency, discuss:

  • How it leads to anaemia
  • What you would see on blood film
  • Management
A
  • Mutation in PKLR gene results in pyruvate kinase deficiency. RBCs have no mitochondria hence no other sources of ATP other than glycolysis. Lack of pyruvate kinase means lack of ATP so Na+/K+ ATPase inhibited; the functioning of this transporter maintains the RBCs shape. Hence cells become spiculated (prickle cells or Burr cells) and are destroyed.
  • Blood film= burr cells
  • Management:
    • Mild= none
    • Severe= blood transfusions, splenectomy
46
Q

For sideroblastic anaemia, discuss:

  • Pathophysiology
  • Causes
  • Findings on FBC, Fe studies, blood film
  • Management
A
  • RBCs fail to completely from haem leading to deposition of Fe in mitochondria that then form a ring around nucleus called a ‘ring sideroblast’
  • Causes:
    • Congenital
    • Acquired
      • Alcohol
      • SLE
      • Lead poisoning
      • Anti-TB medications
  • Findings:
    • FBC: microcytic
    • Fe studies: high ferritin, high Fe, high transferrin saturation
    • Bone marrow: prussian blue staining will show ringed sideroblasts
  • Managment:
    • Supportive
    • Treat underlying cause
    • Pyridoxine
47
Q

Describe the pathophysiology of anaemia of chronic disease

A

Often referred to as ‘functional Fe deficiency’. Increased cytokines:

  • Increase hepcidin release which inhibits absorption of Fe in intestine and release of Fe from macrophages in RES
  • Causes haemphagocytosis/reduces lifespan of RBCs
  • Inhibits erythropoietin release
  • Inhibits erythroid proliferation
48
Q

Discuss the management of anaemia of chronic disease

A
  • Treat underlying condition
  • Other options: transfusions, EPO

Yr4: Cancer Care (19 decks)

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