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Phase 2a Basic Knowledge > Haematology > Flashcards

Haematology Flashcards

1
Q

When are eosinophils elevated

A

Parasitic infections

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2
Q

What is elevated in myelodysplastic syndrome

A

Monocytes

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3
Q

Define thrombocytosis

A

Too many platelets

> 400 x 10^9 / L

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4
Q

Define thrombocytopenia

A

Platelet deficiency

<150 x 10^9 / L

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5
Q

Define lymphocytosis

A

Too many lymphocytes

> 3.5 x 10^4

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6
Q

Define lymphocytopenia

A

Less lymphocytes

<1.3 x 10^4 / L

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7
Q

Define neutrophilia

A

Increased neutrophils

> 7.5 x 10^9 / L

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8
Q

Define neutropenia

A

Low neutrophil count

<2 x 10^9 / L

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9
Q

What might give you neutrophilia

A

Acute bacterial infection

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10
Q

What might give you neutropenia

A

Myeloma
Lymphoma

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11
Q

What might cause lymphocytosis

A

Chronic infection

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12
Q

What is clotting screening

A

AKA a coagulation screen…

a group of tests used for haemostatic assessment. The screen consists of the Prothrombin time, INR, APTT, APTT ratio and derived fibrinogen

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13
Q

What is prothrombin time

A

PT / INR shows…
Coagulation speed through the EXTRINSIC PATHWAY

PT:10-13.5s

Normal INR: 0.8-1.2 ; if on warfarin: 2-3!!!

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14
Q

Define INR

A

International normalised ratio

Ratio of…
Tested PT / Normal PT

I.e.
Patient PT / Reference PT

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15
Q

What factors are included in the extrinsic coagulation cascade

A

3 … 7 … 10

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16
Q

What clotting factors are included in intrinsic coagulation cascade

A

12 … 11 … 9 … 8 … 10

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17
Q

What increases INR

A

Remember when using warfarin… INR is HIGHER (from 0.8-1.2 to 2-3)
So INR is higher the LESS coagulative the blood is…

Vit K deficiency
Anticoagulants
Liver disease
DIC (Disseminated intravascular coagulation)

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18
Q

What is APTT

A

Activated Partial Thromboplastin Time
Coagulation speed through intrinsic pathway

35-45s ; if on heparin: 60-80s

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19
Q

Which diseases is APTT affected by

A

Haemophilia A (factor 8)
Haemophilia B (factor 9)
VWF disease

All these condition cause PT normal & prolonged APTT!!

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20
Q

Define thrombin time

A

AKA bleeding time
Measure of how long the blood’s plasma takes to form a clot.
This test shows how long it takes fibrinogen to turn into fibrin

12-14s

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21
Q

What is the common pathway of coagulation cascade

A

10 .… 2 … 1
|
5

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22
Q

What is mean corpuscular volume

A

Size and volume of RBC

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23
Q

What are the ranges for MCV and what do they indicate

A

Microcytic [< 80]

Normocytic [80-95]

Macrocytic [> 95]

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24
Q

Types of microcytic anaemia

A

Thalassaemia Alpha / Beta (actually haemolytic too)

Anaemia of chronic disease

Iron deficiency anaemia

Lead poisoning

Sideroblastic anaemia

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25
Q

Types of normocytic anaemia

A

Haemolytic:
Sickle cell anaemia
G6PD deficiency
AHA (autoimmune haemolytic anaemia)
Hereditary spherocytosis

Non-haemolytic:
Aplastic
Chronic disease [esp. CKD]
Pregnancy
Myelophthisic anaemia

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26
Q

What happens to Reticulocyte in Normocytic anaemia

A

In haemolytic anaemia get raised Reticulocytes
[lots of RBC death BUT as compensation, get good bone marrow response]

In non-haemolytic anaemia get reduced reticulocytes
[due to failing bone marrow]

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27
Q

Normal lifespan of RBC

A

120 days

I.e. 3 months

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28
Q

Lifespan of RBC in haemolytic anaemia

A

5-10 days!!!

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29
Q

What’s haemoglobin range for anaemia

A

Men < 130 g/L

Women < 120 g/L

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30
Q

For anaemia when should transfusions be considered

A

When…
Hb < 70

Or

Hb < 80 + cardiac comorbidity

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31
Q

Types of Macrocytic anaemia

A

Megaloblastic:
B12 deficiency
Folate deficiency

Non-Megaloblastic:
Alcohol
Hypothyroidism
Non-alcoholic liver disease [NALD]

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32
Q

General symptoms of anaemia

A

Pallor
Fatigue
Exertional SoB

Chest pain + Tachycardia + hypotension + palpitations

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33
Q

What is most common anemia worldwide

A

Iron deficiency

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34
Q

Epidaemiology of iron deficiency anaemia

A

Most common anaemia

F>M

Over 500 million cases

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35
Q

Causes of iron deficiency anaemia

A

Malnutrition / less iron intake in diet
[seen in vegetarians]

Malabsorption
[coeliac / IBD]

Severe blood loss
[trauma / menorraghia (F) / hookworm (most common worldwide for GI blood loss) / colon cancer (RED FLAG for elderly > 60y/o with iron deficiency]

increased requirement - pregnancy

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36
Q

Pathophysiology of iron deficiency anaemia

A

Non-inherited iron deficiency leads to impaired synthesis of haemoglobin
Iron is an important component of heme which is used in the haemoglobin to help carry O2
Absorption in duodenum / proximal jejunum - where its slightly acidic
Iron either travels around the blood as ferric ions [Fe3+] bound to transferrin protein , stored as ferritin or incorporated into Hb!!
When your iron is deficient, there’s less heme groups synthesis and therefore smaller RBC - microcytic Anaemia

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37
Q

Signs and symptoms of iron deficiency anaemia

A

General anaemia +

Koilonchya (spoon-shaped nails)
Angular stomatitis (mouth corner ulceration)
Atrophic glossitis (tongue enlargement)
Hair loss … Brittle hair + nails

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38
Q

Diagnosis and investigation of iron deficiency anaemia

A

1st line:
FBC - microcytic anaemia

Blood film
Hypochromic, target cells, Howell jolly bodies
Fe studies
low serum iron, ferritin, transferrin saturation
high TIBC

Gold standard:
Bone marrow biopsy is for when all other cause for iron deficiency have been ruled out…
idiopathic iron deficient anaemia

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39
Q

Iron deficiency anaemia for investigation for > 60y/o

A

Endoscopy - high risk of colon cancer

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40
Q

What’s are target cells

A

Non-specific bulls eye pattern RBC

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41
Q

What are howell jolly bodies

A

Non-specific uncleared RBCs
Where remanent of DNA is not removed via spleen

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42
Q

Treatment for iron deficiency anaemia

A

Treat underlying cause + oral iron…

ferrous sulphate

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43
Q

Side effects of ferrous sulphate

A

Given in iron deficiency

black stool
Diarrhoea / constipation
GI upset

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44
Q

If ferrous sulphate is poorly tolerated, what is an alternative

A

Ferrous gluconate
Then…
CosmoFer (injection version if tablets can’t be taken)
remember: risk of anaphylaxis & avoid during sepsis

If all else fails…
Give blood transfusion

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45
Q

Condition which is autosomal recessive haemoglobinopathy

A

Thalassaemia

Can also be Sickle Cell Anaemia

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46
Q

Epidaemiology for Thalassaemia

A

Autosomal recessive

Mediterranean ancestry
Prevalent where malaria is (carrier of Thalassaemia - protective against malaria)

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47
Q

Types of haemoglobin

A

HbF
X2 Alpha
X2 Gamma chains

HbA
X2 Alpha
X2 Beta chains

HbA2
X2 Alpha
X2 delta chains

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48
Q

Pathophysiology alpha Thalassaemia

A

4 genes on chromosome 16
deletion of these genes causes defect in alpha globin chains

Associated with HbH - an abnormal Hb isoform where beta tetromers are formed

1 gene deletion
carrier
asymptomatic

2 gene deletion
alpha Thalassaemia minor
The deletion could be ‘Cis’ or ‘Trans’ :
Cis - deletion is on same chromosome - Prevalent in Asian populations
Trans - deletion is on each chromosome - Prevalent in African population

3 gene deletion
HbH disease - marked anaemia

HbH causes hypoxia in 2 ways :
Haemolysis
Intramedullary haemolysis - Breakdown of RBC in bone marrow
Extravascular haemolysis - Breakdown of RBC by macrophages in spleen
HbH has high O2 affinity
Oxygen isn’t released to tissues as readily

That means that because of the hypoxia the extramedullary tissues (liver & spleen) compensate by increasing RBC production
Overworking the bone marrow, liver and spleen as compensation causes them to enlarge

4 gene deletion
Hb BART’s hydrops fetalis
When all 4 alpha genes are deleted, as a foetus you end up with 4x gamma chain tetromer
This has extremely high O2 affinity (100x more) so, the tissue is supplied with little to no oxygen —> severe hypoxia
The hypoxia leads to heart failure, Hepatosplenomegaly, kidney failure
All of this causes full body oedema in foetus
Incompatible with life in utero or soon after birth

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49
Q

Signs and symptoms of alpha Thalassaemia

A

General anaemia Sx
Pallor, Exertional dyspnoea, fatigue, tachycardia+hypotensive, chest pain

+

Skeletal deformities
Hepatosplenomegaly

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50
Q

Investigations / diagnosis of alpha Thalassaemia

A

FBC + blood film
Hypochromic RBCs, target cells, microcytic anaemia with increased reticulocytes [haemolytic anaemia]

Hb electrophoresis (diagnostic)
Shows Hb type populations

Genetic testing - definitive diagnosis
Prenatally this can be done via fetal DNA :
- Using chorionic villus sampling
- Amniocentesis

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51
Q

Treatment for Alpha Thalassaemia

A

Mild
usually doesn’t need treating

Severe Thalassaemia
Blood transfusions
May need iron chelating to trap excess iron (prevent iron overload) - desfemoxamine

If Dx Hb BARTS hydops fetalis prenatally, can give Tx of intrauterine transfusion
Later on can give bone marrow transplant

Splenectomy - wait till after 6y/o (has defensive role using encapsulated bacteria

Definitive / curative = Bone marrow transplant (risky)

Haemolytic anaemia so give folate supplements

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52
Q

Give an iron chelating drug + its side effect

A

Desfemoxamine

Side effect : deafness, cataracts

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53
Q

Chromosome affected in alpha Thalassaemia

A

Chromosome 16

4 genes ; Mutations leading to gene deletion

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54
Q

Chromosome affected in beta Thalassaemia

A

Chromosome 11

2 genes ; mutations lead to defective genes

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55
Q

Pathophysiology for beta Thalassaemia

A

You have normal Hb isoform, just depleted beta chains
B- = reduced beta chain gene coding
B0 = absent beta chain gene coding

BB- / BB0 === carrier / asymptomatic (thalassaemia minor)

B-B0 / B- B- === marked anaemia (Thalassaemia intermediate)

B0B0 === severe anaemia (thalassaemia major)

When RBCs are Beta globin chain deficient, free alpha chains build up in them causing inclusions

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56
Q

What are RBC inclusions ad when are they seen

A

Seen When RBCs are Beta globin chain deficient, free alpha chains build up in them causing inclusions

Inclusions damage cell membrane of RBCs therefore the RBCs need to be broken down by either…
Haemolysis (in the bone marrow)
This results in the contents of the RBC to flow in the blood plasma.
Haem is recycled into unconjugated bilirubin and iron

Excess unconjugated bilirubin over time leads to jaundice
Iron deposits that can the lead to haemochromatosis
Haemochromatosis = An iron storage disorder that results in excessive total body iron and deposition of iron in tissues

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57
Q

Complication of beta thalassaemia

A

Arrythmias, Pericarditis, Cirrhosis, hypothyroidism and D.M

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58
Q

Investigation / diagnosis for beta thalassaemia

A

FBC + blood film
Hypochromic RBCs, target cells, microcytic anaemia with increased reticulocytes [haemolytic anaemia]

Haemoglobin electrophoresis (diagnostic)
- Low HbA
- High HbF and HbA2
Remember this is because excess Alpha chains end up binding to the gamma and delta chain

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59
Q

Treatment for beta thalassaemia

A

Beta-Thalassaemia doesn’t always need Treatment but for intermedia and major…

Regular blood transfusion

Prevent iron overload using iron chelating agents

Could do splenectomy when splenomegaly causes extra haemolysis.

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60
Q

In which condition is chipmunk facies seen in

A

Beta thalassaemia major

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61
Q

Signs and symptoms for beta thalassaemia

A

Mild, moderate may be asymptomatic

General anaemia Sx (pallor, dyspnoea and fatiguability)
+
bone deformities
Chipmunk Facies
- Enlarged forehead and enlarged cheekbones
- This is because for chronic anaemia the body compensated for the reduced RBC and undergo extramedullary haemopoesis + bone marrow expansion - as RBCs are produced from these sites.
+
Other signs and symptoms it causes:
Hepatosplenomegaly
Jaundice
Gall stones - Px might present with RUQ pain / swollen abdomen (haemolysis of RBC causes an increased breakdown of them releasing uric acid leading to gall stones and gout)

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62
Q

Define Sideroblastic anaemia

A

Microcytic
Defective Hb synthesis because of pathological accumulation of iron in RBC mitochondria with the inability for iron to be incorporated in the Hb as its trapped in mitochondria

Lack of incorporation due to ALA synthetase deficiency

I.e. functional Fe3+ deficiency

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63
Q

Enzyme deficiency in Sideroblastic anaemia

A

ALA synthetase deficiency

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64
Q

Inheritance pattern for siderblastic anaemia

A

X linked

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65
Q

Investigation / diagnosis for Sideroblastic anaemia

A

FBC + blood film
Microcytic with ringed siderblasts + basophilic stippling [increased basophilic granules]

Iron studies
High serum Iron
High ferritin
High transferrin
Low TIBC

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66
Q

What type of anaemia is sickle cell anaemia

A

Normocytic

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67
Q

Inheritance pattern for sickle cell anaemia

A

Autosomal recessive

Haemoglobinopathy

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68
Q

Which chains are affected in SS anaemia

A

Beta globin chains

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69
Q

Epidaemiology for SS anaemia

A

Commonest in Africa - antimalarials properties as carrier against falciparum malaria

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70
Q

Affected genotype for SS anaemia

A

HbS HbS - sickle cell disease (autosomal recessive)

HbS - the abnormal variant for sickle cell haemoglobin

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71
Q

Chromosome affected leading to HbS in sickle cell anaemia

A

Chromosome 11 - beta globin chain defect

same in beta thalassaemia

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72
Q

Pathophysiology for sickle cell anaemia

A

GAG to GTG (Glutamic acid - Valine) on 6th codon of beta globin gene
causes
Irreversible RBC sickling

More fragile RBC -> less efficient and more likely to get stuck in capillaries
Risk of sequestration

SS anaemia = haemolytic
Intravascular - inside vessels (marked by increased haptoglobin)
Extravascular - outside vessel (@ spleen)

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73
Q

Signs and symptoms of SS anaemia

A

General Sx of anaemia (pallor, dyspnoea, fatigue)
+ jaundice (haemolytic anaemia = pre-hepatic)
+ splenomegaly

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74
Q

Complication of SS anaemia

A

Splenic sequestration - can cause autosplenectomy

Vaso-occlusive crisis - clogging capillaries causing distal ischaemia + polymerise & trap in long bone blood vessel

acute chest crisis - pulmonary vessel Vaso-occlusion + cause of resp. Distress ; emergency

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75
Q

What is SS anaemia precipitated by

A

infection
cold
hypoxia
acidosis

Dehydration

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76
Q

Which anaemia is osteomyelitis

A

Common in sickle cell

Osteomyelitis is usually due to S. Aureus, but in those with SS = salmonella

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77
Q

Investigation / diagnosis for sickle cell anaemia

A

Heel prick test (tests for sickle cell, hypothyroidism, cystic fibrosis)

FBC + Blood films (normocytic normochromic with increased reticulocytes)
Sickled RBCs + Howell jolly bodies

Hb electrophoresis = diagnostic ; proportion of Hb (90% HbS)

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78
Q

Treatment of SS anaemia

A

For acute complicated attacks :
IV fluids + analgesia (NSAIDs) + O2 + (antibiotic for infection)

Avoid precipitants
Hydroxycarbamide (aka hydroxyurea) + Folic acid supplement
transfusion + Fe chelation
Last resort - bone marrow transplant

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79
Q

Inheritance pattern for G6PDH deficiency

A

X linked recessive

Enzymopathy

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80
Q

Role of G6PDH

A

G6PDH is protective against oxidative damage

It’s involved in glutathione synthesis
Which protects against reactive oxidative species like H2O 2

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81
Q

Epidaemiology of G6PDH deficiency

A

Causes half lifespan and degradation of RBC
Africa & Asia

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82
Q

Signs & symptoms of G6PDH deficiency

A

Asymptomatic unless precipitated

Could cause an attack
rapid anaemia
Jaundice

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83
Q

Type of haemolysis in G6PDH deficiency

A

Intravascular haemolysis

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84
Q

Precipitating factors for G6PDH deficiency

A

FAVA / BROAD beans - metabolised into R.O.S
Anti-malarials (e.g. quinine)
Nephthelene - in moth balls & pesticide (major cause)
Nitrofurantoin - Antibacterial for UTIs
Aspirin

The key piece of knowledge for G6PD deficiency relates to triggers. In your exam look out for a patient that turns jaundice and becomes anaemic after eating broad beans, developing an infection or being treated with antimalarials. The underlying diagnosis might be G6PD deficiency.

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85
Q

Investigation / diagnosis for G6PDH deficiency

A

FBCS + blood films:
Normal in between attacks
During attacks : Normocytic Normochromic with increased reticulocytes
Heinz bodies + bite cells

Remember : beans means Heinz!!! —— Bite beans to eat them

decreased G6PDH level

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86
Q

Treatment for G6PDH deficiency

A

Avoid precipitants
Blood transfusion when attacks ensure

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87
Q

Inherited pattern for hereditary spherocytosis

A

Autosomal dominant

Membranopathy

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88
Q

Epidaemiology of hereditary spherocytosis

A

N. Europe + America

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89
Q

Define hereditary spherocytosis

A

Deficiency in structural membrane protein spectrin
Makes RBCs more spherical & rigid
… leads …
Increased splenic recycling causes splenomegaly as rigid cells get stuck in spleen (risk of autosplenctomy)

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90
Q

Signs & symptoms of hereditary spherocytosis

A

General anaemia symptoms (pallor, dyspnoea, fatigue)

+

Neonatal jaundice
Splenomegaly
Gallstones (50%)

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91
Q

Investigation / diagnosis for hereditary spherocytosis

A

FBC + blood film
Normacytic normochromic + increased reticulocytes
Spherocytes

Direct Coombs -ve ;
+ve in AHA (autoimmune haemolytic anaemia!!!)

92
Q

Treatment for hereditary spherocytosis

A

Splenectomy
Wait till at least 6y/o due too sepsis risk - spleen fights off encapsulated bacteria

In neonatal jaundice - Tx = phototherapy
If untreated, risk of **kernicterus ** - bilirubin accumulates in CNS basal ganglia ; CNS dysfunction + death

93
Q

Type of haemolysis in hereditary spherocytosis

A

Extravascular haemolysis

94
Q

Subtypes of autoimmune haemolytic anaemia (AHA)

A

Warm (most common) - It is usually idiopathic

Cold - the antibodies against red blood cells attach themselves to the red blood cells and cause them to clump together (agglutination) - triggers immune system against RBC clumps and increased spleen degredation of RBC

95
Q

What other conditions is Cold type AHA secondary too

A

Lymphoma, leukaemia, systemic lupus erythematosus and infections (EBV, CMV, HIV)

96
Q

Type of haemolysis in AHA

A

Extravascular + intravascular haemolysis

97
Q

Investigation / diagnosis for AHA

A

Direct Coombs +ve
(as there’s agglutination of RBCs with Coombs reagent)

Remember Coombs -ve in hereditary spherocytosis

98
Q

Types of non-haemolytic anaemia

A

All normocytic

CKD
Aplastic Anaemia
Myelophthisic anaemia

99
Q

What is bone marrow activity in CKD and why

A

Reduced bone marrow activity because CKD is a cause of non-haemolytic anaemia
Due to decreased erythropoietin secretion, reduced stimulation for erythropoiesis…

In non-haemolytic there is no stimulation / turnover of RBC in Bone Marrow but in haemolytic anaemias, increased reticulocytes…

100
Q

Define aplastic anaemia

A

Pancytopenia - where bone marrow fails so no production of heamopoetic stem cells

101
Q

Aetiology / cause of aplastic anaemia

A

Idiopathic (mostly)
Might be triggered by infection (parvovirus, EBV)

102
Q

Investigation / diagnosis of aplastic anaemia

A

FBC - normocytic anaemia with reduced reticulocytes

Bone marrow biopsy - hypocellularity

103
Q

Treatment for aplastic anaemia

A

Increased risk of infection (neutropenia) - give broad spec Antibiotic
+
Bone marrow transplant

104
Q

Define Myelophthisic anaemia

A

Normocytic non haemolytic anaemia
When bone marrow is replaced with something else like malignancy

105
Q

What type of anaemia is pernicious anaemia

A

Macrocytic Megaloblastic anaemia

106
Q

Give types of Macrocytic anaemia

A

Megloblastic :
Pernicious / B12 deficiency
Folate deficiency

Non-megaloblastic / Normoblastic Macrocytic :
Alcohol
Liver disease
NALD - non-alcoholic liver disease
Hypothyroidism

107
Q

What does it mean if RBCs are non Megaloblastic but are Normoblastic Macrocytic?

A

Megloblastic = impaired DNA synthesis causes cell to enlarge but not end up dividing

But Normoblastic Macrocytic is when the cell DNA synth is functional, RBCs just have high MCV

108
Q

How does alcohol cause anaemia

A

Toxic to RBC
Also depletes folate (+ B1 -Thiamine)

109
Q

How does hypothyroidism lead to anaemia

A

Interference with EPO ; multi factorial

110
Q

How does liver disease lead to anaemia

A

Decompensated liver cirrhosis (HBV associated +/- HCC) - strongly linked to Macrocytic anaemia

Short-term predictor of mortality
Several factors- increased LDL deposition on RBC surface;increasing MCV…OR… Related to b12 and folate deficiency

111
Q

Define pernicious anaemia

A

AKA B12 deficiency

112
Q

Epidaemiology of B12 deficiency

A

Older patients - takes years to develop
Increased in long-term vegans

113
Q

Causes of B12 deficiency

A

Malnutrition
Malabsorption - Crohns
Pernicious anaemia (antibodies against parietal cells + Intrinsic Factor)

114
Q

Which cells are produced to help with b12 absorption

A

Parietal cells in stomach

Produce intrinsic factor

115
Q

Where is b12 absorbed

A

Ileum

116
Q

Pathophysiology of b12 deficient anaemia

A

Typically, b12 binds to transcolbamin-1 in saliva (protection against stomach acid)
Binds to intrinsic factor in duodenum
Absorbed as b12-IF complex in ileum
but
autoimmune condition where antibodies form against the parietal cells or intrinsic factor. A lack of intrinsic factor prevents the absorption of vitamin B12 and the patient becomes vitamin B12 deficient.

117
Q

Signs and symptoms of b12 deficiency anaemia

A

General anaemia Sx (pallor, dyspnoae, fatigue) +

Lemon yellow skin
Angular glossitis + stomatitis
If severe :
Neurological Sx -
Symmetrical paraesthesia (pins & needles),
Loss of proprioception / vibration
muscle weakness

  • For your exams remember testing for vitamin B12 deficiency and pernicious anaemia in patients presenting with peripheral neuropathy, particularly with pins and needles.
118
Q

Why does Px present with angular stomatitis / glossitis in pernicious anaemia

A

B12 helps cell division by helping synthesis of DNA precursor

Deficiency interrupts cell division… esp rapidly dividing ones
(Hence pancytopenia)

Tongue mucosa is rapidly dividing too so when damaged, cells aren’t replaced leading to inflammation etc…

119
Q

Cause of neurological Sx in pernicious anaemia

A

Small amounts of methylmalonic acid is produced during metabolism (too much is harmful) - b12 is used to metabolise it

Deficiency means a build up of methylmalonic in myelin sheath of neuron - causing degeneration of myelin sheath

Communication between neurons gets significantly slower, which leads to impairment of neurological and muscle function.

120
Q

Investigation / diagnosis for b12 deficiency anaemia

A

FBC + blood film:
Macrocytic anaemia
Megaloblasts - hypersegmented nucleated neutrophils (> 6 lobes)
more lobes = more immature cell, as DNA mature becomes compact

Serum b12 (low)

Auto Antibodies -
anti-intrinsic factor antibodies (diagnostic - but not present in all Px)
Anti-parietal antibodies

121
Q

Treatment for pernicious anaemia

A

Dietary advice (salmon, eggs)
+
B12 supplements (PO, hydroxycobalamin)

122
Q

Name for vitamin b12

A

Cobalamin

123
Q

Time of development for folate deficiency

A

Months

B12 deficiency takes years

124
Q

Causes of folate deficiency anaemia

A

Malnutrition

pregnancy

Malabsorption

Drugs - trimethoprim + methotrexate + sulfasalazine
They are dihydrofolate reductase inhibitors … so …
mTHF ——x——> THF (THF is what folate is converted to in the lining to be used for DNA synthesis)

125
Q

Signs and symptoms of folate deficiency anaemia

A

General Sx of anaemia (pallor, dyspnoea, fatigue)
+
Angular glossitis / stomatitis (like b12 deficiency anaemia)

(Do not see neurological Sx or lemon yellow skin - only seen in b12 deficiency)

In babies: if the embryo was folate deficient… baby may present with spina bifida / anencephaly because neural tube defect

126
Q

Investigation / diagnosis of folate deficiency anaemia

A

FBC + blood film:
Macrocytic anaemia
Megaloblasts

Serum folate (low)

127
Q

Treatment of folate deficient anaemia

A

Dietary advice (leafy greens, brown rice)
Folate supplements

note: if accompanied with b12 deficiency… treat b12 FIRST - because giving folate first depletes b12 more (complex DNA synthesis pathway)

For pregnant women: prophylactic folate 400mg for first 12 weeks

128
Q

Complication for folate deficient anaemia

A

Ischaemic heart disease
Ischaemic Stroke

129
Q

What is the most inherited bleeding disorder

A

Von willebrands disease

130
Q

Give types of bleeding disorders

A

Von willebrands
Haemophilia a
Haemophilia b
DIC (disseminated intravascular coagulopathy)

131
Q

Inheritance pattern for VWF disease

A

Autosomal dominant mutation on VWF gene

Chromosome 12

132
Q

Define VWF disease

A

Responsible for basis of platelet plug so decrease in VWF means more spontaneous bleeds + bruising

133
Q

Investigation or diagnosis of VWF disease

A

Normal PT
Increased APTT
Normal factor 8/9 assay

Decreased VWF

134
Q

Treatment for VWF disease

A

Not curable but managed

Desmopressin
Helps increased VWF from endothelial Weibel palade bodies!!

135
Q

Signs / symptoms for VWF disease

A

Patients present with a history of unusually easy, prolonged or heavy bleeding:

Bleeding gums with brushing
Nose bleeds (epistaxis)
Heavy menstrual bleeding (menorrhagia)
Heavy bleeding during surgical operations

136
Q

Define disseminated intravascular coagulopathy

A

A crisis

Massive activation of coagulation cascade
* increased clotting in the blood cells leads to platelets being used up unnecessarily
* lack of systemic available platelets means increased bleeding risk

137
Q

Causes / triggers DIC

A

Trauma

Sepsis (e.g. meningococcal meningitis — non-Blanching Petechiae rash)

Malignancy

138
Q

Investigation / diagnosis of DIC

A

FBC / lab findings

Decreased platelets
Decreased fibrinogen

Increased D-DIMER (the more clots the more break-down byproducts of a clot) - also seen in DVT & PE

139
Q

Treatment of DIC

A

FFP (fresh frozen plasma) - to replace clotting factors
Cryoprecipitate (replace fibrinogen)

Platelet transfusion + RBC transfusion (if needed)

140
Q

Inheritance pattern for haemophilia A and B

A

X linked recessive

141
Q

Epidaemiology for haemophilia

A

Haemophilia A is more common than B

Exclusively affects males for both - as its x linked recessive and men only have 1 X-chromosome

For a female to be affected they would require an affected father and a mother that is either a carrier or also affected.

142
Q

Define both haemophilia

A

Haemophilia A is caused by a deficiency in factor VIII.

Haemophilia B is caused by a deficiency in factor IX.

143
Q

Signs and symptoms of haemophilia

A

Spontaneous bleeding — joints (haemoathrosis) and muscles

Epistaxis

Very easy bruising

episodic

144
Q

Investigation / diagnosis for haemophilia

A

Normal PT + increased APTT (factor 8/9 is a part of the intrinsic pathway which is why APTT is prolonged)

Low f8 / f9 assay

145
Q

Treatment for haemophilia

A

Haemophilia A : IV factor 8 + desmopressin (releases factor 8 stores from vessel wall)

Haemophilia B : IV factor 9

146
Q

Give 3 conditions in which desmopressin can be used as treatment

A

Diabetes insipidus
VWF disease
Haemophilia A

147
Q

Define polycythaemia

A

Erythrocytosis (increased RBC production) of any cause

148
Q

Aetiology of polycythaemia

A

Primary - polycythaemia vera
JAK2 V617 mutation (accounts for 95% cases)

Secondary
Hypoxia
Ectopic EPO (renal cell carcinoma)
Dehydration
Alcohol

149
Q

Signs and symptoms of polycythaemia Vera

A

Itchy after bath

Erthyromelalgia - burning fingers and toes

Conjunctival plethora (excessive redness to the conjunctiva in the eyes) - blurred vision

A “ruddy” complexion - reddish / purply complexion

Splenomegaly

Features of hyperviscosity - increased RBCs —> increased haematocrit —> more solid mass of blood

150
Q

Investigation / diagnosis of polycythaemia Vera

A

FBC :
Increased RBC, WBC, platelets
Increased Hb

Bone marrow biopsy - ‘dry’ bone marrow due to scar tissue development

genetic testing
+ve for JAK2 V617

151
Q

Treatment for polycythaemia Vera

A

Non - curative but managed
1st line = VENESECTION + aspirin

Consider chemotherapy - hydroxycarbamide (aka hydroxyurea) : in high risk patients

152
Q

Define a myeloma

A

Malignancy of plasma cell (a a type of B lymphocyte producing antibodies) leading to bone marrow failure

Multiple myeloma is where the myeloma affects multiple areas of body

As a definition learn it as…
neoplastic monoclonal proliferation of a plasma cell

153
Q

Complication of polycythaemia Vera

A

Thromboemboli

154
Q

Pathophysiology of myeloma

A

There is a genetic mutation in a specific type of plasma cell

Leads to production and proliferation of abnormal antibody (i.e. immunoglobulin — 50%: IgG ; 20% IgA) by all the identical cancerous plasma cells

Can be called a monoclonal paraprotein single type of abnormal protein

155
Q

Risk factors for multiple myeloma

A

Older age (70y/o)
Male
Black African ethnicity

Family history
Obesity

156
Q

Signs and symptoms of multiple myeloma

A

Remember as OLD CRAB

Old - 70+ y/o

Calcium raised —— remember the Sx of Hypercalcaemia
Bones, stones, Abdo groans, Psych moans

Renal failure

Anaemia

Bone pain / lesions

157
Q

Why is Hypercalcaemia seen in myeloma

A

Increased osteoclast activity leads to increased calcium reabsorption from bone resorption - also leads to the bone pain and bone lesions (because bone resorption is in patches)

  • the monoclonal proliferation of a single plasma cell leads to increased cytokine release from these plasma cells ; cytokines stimulate osteoclast activity
158
Q

Why is renal failure seen in m. Myeloma

A

Hypercalcaemia from bone resorption can lead to calcium oxalate renal stones

Increased immunoglobulin light chains Kappa deposition in kidneys
- Nephrotoxic
- Sub-unit of these light chains = Bence-Jones protein - this is a marker found in urine

159
Q

Why would m. Myeloma lead to anaemia

A

B cells produced in Bone marrow… malignancy of one type of plasma cell in bone marrow leads to bone marrow infiltration

Causing suppression of other cell lines
- anaemia
- neutropenia
- thrombocytopenia

160
Q

Investigations / diagnosis of m. Myeloma

A

FBC + blood film
Normocytic + normochromic RBCs
- ROULEAUX FORMATION - aggregation of RBC (pathognamonic)
Raised ESR

Urine dipstick / electrophoresis
Bence-jones proteins

serum protein electrophoresis
Xray
Osteolytic lesions —> punched out holes
Skull —> raindrop skull

bone marrow biopsy : > / = 10% plasma cells

Nice recommend - full body MRI to see systemic bone marrow filtration

161
Q

What is differential diagnosis for m . Myeloma

A

MGUS - Monoclonal Gammopathy of Undermined Significance

162
Q

Give 3 features of MGUS

A

< 10% plasma cells in bone marrow

Little / no paraprotein spike

Asymptomatic

163
Q

What is MGUS

A

MGUS - Monoclonal Gammopathy of Undermined Significance

A precursor of myeloma

164
Q

Treatment of m. Myeloma

A

Chemotherapy
Bisphosphonates (for bone protection) - alendronate
Dialysis

Consider bone marrow stem cell transplant

165
Q

Define lymphoma

A

Lymphomas are a group of malignancies that affect the lymphocytes inside the lymphatic system

166
Q

Types of lymphomas

A

2 types :

———— Reed sternberg cells = Hodgkin’s
———— Non reed sternberg = Non-Hodgkin’s

167
Q

Give 3 examples/types of Non-Hodgkin’s lymphoma

A

Low grade = follicular

High grade = diffuse large B cell (most common- 80%)

Very high grade = burkitts

168
Q

Epidaemiology of Hodgkin’s

A

Bimodal ; ** Teens and Elderly** (to peaks of increased incidence)

Associated with EBV (aka glandular fever)

169
Q

What are B symptoms for lymphomas

A

Fever
Night sweats
Unintentional weight loss

+

Lymphadenopathy

170
Q

Signs and symptoms of Hodgkin’s lymphoma

A

B symptoms (fever, night sweats, unintentional weight loss)

+

painless rubbery lymphadenopathy - painful after drinking alcohol

171
Q

Investigation / diagnosis of Hodgkin’s lymphoma

A

Lymph node biopsy :
reed sternberg +ve - diagnostic

Note: a subtype of Hodgkin’s can also show popcorn cell (reed sternberg cell variant)

blood test
raised LDH (Lactate dehydrogenase)
Raised ESR
Low Hb

CT / MRI / PET - for staging lymphoma

172
Q

What staging is used for lymphomas

A

Ann arbour staging (1-4)

173
Q

Describe Ann arbour staging

A

Ann arbour staging (1-4)
1 : Single lymph node
2 : > / = 2 lymph nodes on same side of diaphragm
3 : Lymph nodes on both sides of diaphragm
4 : Spread to extra-nodal organs

+ either…
A : without “B” symptoms
Or
B : with “B” symptoms

174
Q

Treatment for hodgkins lymphoma

A

ABVD chemotherapy

175
Q

Side effects for ABVD chemotherapy

A

Alopecia
Nausea + vomiting
Infection
Myelosupression / bone marrow failure

176
Q

Complication of chemo

A

Febrile neutropenia

Huge risk in patients who had recent / high dose chemo (/ on carbimazide)

Px : fever, tachycardia + pnoea, sweats, rigors
Tx : immediate broad spec antibiotics (amoxicillin + fluoroquinolone)

177
Q

What can burkitts lymphoma cause

A

Jaw lymphadenopathy in children

Linked to EBV

178
Q

Signs / symptoms of non-hodgkins lymphoma

A

B symptoms

+

Painless rubbery lymphadenopathy - not affected by alcohol

Symptoms vary on subtypes

179
Q

Investigation / diagnosis of non-hodgkins lymphoma

A

lymph node biopsy - diagnostic
No reed sternberg cells
Helps confirm subtypes (e.g. burkitts = ‘stormy sky’ biopsy)

CT / MRI / PET for staging - Ann Arbour

180
Q

Treatment for non-hodgkins lymphoma

A

R-CHOP chemotherapy

181
Q

Risk factors for lymphomas

A

FHx
EBV
HIV

+

Hodgkin’s :
autoimmune condition

Non- hodgkins :
Hep b/c
H. Pylori

182
Q

Give examples of anti coagulation meds

A

Aspirin (COX inhibitor)

Heparin / LMWH (binds to antithrombin 3 & inhibits factor X)

Clopidogrel (P12Y12 inhibitor) - antiplatelet

Thrombolytics (Alteplase)

183
Q

Define leukaemia

A

A form of malignancy of WBC lines (myeloblasts ; lymphoblast) in bone marrow

A genetic mutation in one of the precursor cells in the bone marrow leads to excessive production of a single type of abnormal white blood cell

184
Q

Does leukaemia lead to anaemia and why

A

Yes
Leukaemia leads to anaemia but also pancytopenia (anaemia, neutropenia, thrombocytopenia) -

The excessive production of a single type of cell can lead to suppression of the other cell lines causing underproduction of other cell types

185
Q

Types of leukaemia

A

Acute lymphoblastic leukaemia (ALL)

Chronic lymphocytic leukaemia (CLL)

Chronic myeloid leukaemia (CML)

Acute myeloid leukaemia (AML)

186
Q

Age acute lymphoblastic leukaemia presents

A

Remember ALL CeLLmates have CoMmon AMbitions

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

187
Q

Age acute myeloid leukaemia presents

A

Remember ALL CeLLmates have CoMmon AMbitions

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

188
Q

Age chronic lymphocytic leukaemia presents

A

Remember ALL CeLLmates have CoMmon AMbitions

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

189
Q

Age chronic myeloid leukaemia presents

A

Remember ALL CeLLmates have CoMmon AMbitions

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

190
Q

Define A. L. Leukaemia

A

Neoplastic lymphoblasts (immature) proliferation
Mostly B cells
Has good prognosis

191
Q

Most common childhood malignancy

A

Acute lymphoblastic leukaemia
75% cases
> / = 6y/o

192
Q

Translocation for ALL

A

T(12:21)

193
Q

Condition associated with ALL

A

Down syndrome; x30 risk

+

Radiation

194
Q

General signs & symptoms of leukaemia

A

Fatigue
Fever
Failure to thrive (children)
Pallor due to anaemia
Petechiae and abnormal bruising due to thrombocytopenia
Abnormal bleeding
Lymphadenopathy

195
Q

Signs and symptoms of ALL

A

General leukaemia Sx:

6y/o with Down syndrome
Hepatosplenomegaly

196
Q

Investigation and diagnosis of ALL

A

FBC:
Pancytopenia

Blood film:
Increased lymphoblasts

Bone marrow biopsy (diagnostic) :
> / = 20% lymphoblasts

197
Q

Treatment for ALL

A

Chemotherapy (+/- allopurinol)

198
Q

Define chronic lymphocyte leukaemia

A

Chronic neoplastic proliferation of lymphocytes - mainly b cells

199
Q

Most common type of leukaemia

A

Chronic lymphocyte leukaemia

200
Q

CLL prognosis

A

75% with 5 year survival

201
Q

Signs and symptoms of CLL

A

men with general anemia Sx
+ lymphadenopathy (non tender)
+ Hepatosplenomegaly

Often it is asymptomatic but it can present with infections, anaemia, bleeding and weight loss. It can cause warm autoimmune haemolytic anaemia

202
Q

Investigation and diagnosis of CLL

A

FBC:
Pancytopenia

Blood film:
smudge/smear cells

Immunoglobulin:
Hypogammaglobulinaemia - B cells proliferate but dont differentiate to plasma cells so no immunoglobulin production

203
Q

Treatment for CLL

A

It’s progressive so give
Chemo + palliative care (if old)

Also, if hypogammaglobinaemia give IV Ig

204
Q

Complication for CLL

A

Richter transformation

B cells massively accumulate in lymph nodes —> leading to lymphadenopathy
+ transformation from CLL —> aggressive lymphoma

205
Q

Define acute myeloid leukaemia

A

Neoplastic myeloblasts (immature)proliferation

206
Q

Translocation mutation of AML

A

T(15;17)

207
Q

Prognosis for AML

A

Has rapid progression
If not treated ASAP; 3 year survival = only 20%

Therefore v. Severe

208
Q

Risk factors for AML

A

Pre-existing myeloproliferative disorders - polycythaemia Vera

Congenital disorders - Down’s syndrome

Prior chemo / radiation

209
Q

Signs and symptoms of AML

A

General leukaemia Sx +

Hepatosplenomegaly

210
Q

Investigations / diagnosis for AML

A

FBC :
Pancytopenia

Blood smear :
AUER RODS and +ve myeloperoxidase
Auer rods = myeloperoxidase cytoplasmic aggregates in neutrophils

Bone marrow biopsy :
> / = 20% myeloid blasts

211
Q

Give a subtype of AML

A

Acute promyelocytic leukaemia

It is : AML + DIC

212
Q

Treatment for AML

A

Chemotherapy + allopurinol
+ ATRA

Consider prophylaxis for neutropenia / transfusion for anaemia

Last resort = bone marrow transplant

213
Q

What is given with chemotherapy for leukaemia

A

Allopurinol

Prevent tumour lysis syndrome (chemo releases uric acid from cells, so can accumulate in kidney / cause gout) - allopurinol prevents uric acid build up

214
Q

Define CML

A

Neoplastic proliferation of myelocytes - baso / eosino / neutrophils

215
Q

Genetic translocation mutation for CML

A

T(9;22)
Philadelphia chromosome

BCR-ABL gene fusion causes tyrosine kinase irreversibly switched on

216
Q

Role of tyrosine kinase

A

Increased cell proliferation

217
Q

Sign and symptoms of CML

A

General Sx of leukaemia - weight loss, fatigue, fever, infections, bruising, excessive bleeding
+ huge Hepatosplenomegaly

218
Q

Investigation / diagnosis of CML

A

FBC:
Pancytopenia
But granulocytosis (increased proliferation of eosinophils/baso/neutrophils)
Blood blast cell % =
> 10% (better prognosis) //// < 20% (blast crisis)

Bone marrow biopsy : increased granulocytes
philadelphia chromosome genetic testing

219
Q

Treatment of CML

A

Chemo +

IMANTINIB - Tyrosine kinase inhibitor

Also, consider allopurinol

if not treated, risk of progression onto AML

220
Q

Define RBC inclusions

A

When RBCs are Beta globin chain deficient, free alpha chains build up in them causing inclusions

221
Q

Side effect to thrombolysis

A

Major bleed - if given in PE might leads to intracranial bleed

222
Q

When in if piperacillin and tazobactam given

A

Give if px has fever 7-14 days after chemotherapy… neutropenia sepsis

223
Q

In a px with iron deficiency when would ferritin be high

A

Ferritin would be falsely high when theres an infection
As its an acute phase reactant

224
Q

What do you haem arthritis in and epistaxis

A

Haemophilia a and b

225
Q

Give an example antifibrynolytic agent and where is it given

A

Tranexamic acid
Haemophilia A/B and VWF disease

226
Q

Give the drugs name that opposite action to alteplase

A

Tranexamic acid

227
Q

Give 3 sign of essential thrombocytosis

A

Splenomegaly
Erthromelagia (discolouration and burning peripheries)
Livedo reticularis (purple rash)

Phase 2a Basic Knowledge (13 decks)

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