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Yr3 Med Conditions > HAEM > Flashcards

HAEM Flashcards

1
Q

Define Macrocytic Anaemia

A

Anaemia associated with a high MCV of erythrocytes (>100fl in adults)

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2
Q

Aetiology/ Risk Factors of macrocytic anaemia

A

• Megaloblastic - when the bone marrow produces unusually large, structurally
abnormal, immature red cells
o 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
• 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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3
Q

Epidemiology of macrocytic anaemia

A
  • More common in ELDERLY FEMALES

* Pernicious anaemia is the MOST COMMON cause of B12 deficiency in the West

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4
Q

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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5
Q

Signs of macrocytic anaemia on physical examination

A 
•  Signs of Anaemia  
o  Pallor  
o  Tachycardia  
o  Breathlessness  
•  Signs of Pernicious Anaemia 
o  Mild jaundice  
o  Glossitis  
o  Angular stomatitis  
 o  Weight loss  
•  Signs of B12 Deficiency 
o  Peripheral neuropathy  
o  Ataxia  
o  Subacute combined degeneration of the spinal cord   
o  Optic atrophy  
o  Dementia
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6
Q

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 - 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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7
Q

Management plan for macrocytic anaemia

A 
•  Pernicious Anaemia 
o  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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8
Q

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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9
Q

Prognosis for patients with macrocytic anaemia

A

• Majority are treatable if there are no complications

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10
Q

Define microcytic anaemia

A

Anaemia associated with a low MCV (<80 fl)

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11
Q

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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12
Q

Epidemiology of microcytic anaemia

A

• Iron deficiency anaemia is the MOST COMMON form of anaemia worldwide

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13
Q

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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14
Q

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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15
Q

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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16
Q

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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17
Q

Complications of microcytic anaemia

A
  • High-output cardiac failure

* Complications related to the CAUSE

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18
Q

Prognosis for patients with microcytic anaemia

A

• Depends on the CAUSE

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19
Q

Define Normocytic Anaemia

A

Anaemia with a normal MCV (80-100)

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20
Q

Aetiology/ Risk Factors of normocytic anaemia

A

• Causes:
o Decreased production of normal-sized blood cells (e.g. anaemic of chronic disease, aplastic anaemia)
o Increased production of HbS (sickle cell disease)
o Increased destruction of red blood cells (e.g. haemolysis, post-haemorrhagic anaemia)
o Uncompensated increase in plasma volume (e.g. pregnancy, fluid overload) o Vitamin B2 deficiency
o Vitamin B6 deficiency

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21
Q

Epidemiology of normocytic anaemia

A

Common

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22
Q

Presenting symptoms and signs of normocytic anaemia

A

• Typical symptoms and signs of anaemia (depends on severity)
o E.g. breathlessness, fatigue, conjunctival pallor

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23
Q

Investigations for normocytic anaemia

A
  • FBC - check Hb and MCV

* Check history for haemorrhage

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24
Q

Define Aplastic Anaemia

A

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

25
Q

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)

26
Q

Epidemiology of aplastic anaemia

A
  • Annual incidence: 2-4/1,000,000

* Slightly more common in males

27
Q

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
28
Q

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
29
Q

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 cross-linking agents
30
Q

Define Disseminated Intravascular Coagulation (DIC)

A

A disorder of the clotting cascade that can complicate a serious illness.
- DIC can occur in two forms:
• 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

31
Q

Aetiology/ Risk factors 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

32
Q

Pathophysiology of DIC (acute and chronic)

A

o 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
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

33
Q

Epidemiology of DIC

A

Seen in any severely ill patient

34
Q

Presenting symptoms of DIC

A
  • The patients will tend to be severely unwell with symptoms of the underlying disease
  • Confusion
  • Dyspnoea
  • Evidence of bleeding
35
Q

Signs of DIC on physical examination

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 
•  Chronic DIC 
o  Signs of deep vein and arterial thrombosis or embolism 
 o  Superficial venous thrombosis
36
Q

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
37
Q

Define Haemochromatosis

A

An autosomal recessive disease in which increased intestinal absorption of iron causes accumulation of iron in tissues, which may lead to organ damage

38
Q

Aetiology/ Risk Factors of haemochromatosis

A
  • Autosomal recessive
  • Caused be a defect in the HFE gene
  • NOTE: the genetic penetrance of haemochromatosis is complex - not everyone who is homozygous will develop the clinical disease
39
Q

Epidemiology of haemochromatosis

A

• RARE

40
Q

Recognise the presenting symptoms and signs of haemochromatosis

A 
•  Often ASYMPTOMATIC until the late stages of the disease  
•  Symptoms usually start between 40-60 yrs 
•  EARLY symptoms are vague: 
o  Fatigue  
o  Weakness  
o  Arthropathy 
o  Erectile dysfunction   
o  Heart problems  
•  May be an incidental finding (e.g. LFTs, serum ferritin)   
•  LATE symptoms: 
o  Diabetes mellitus   
o  Bronzed skin  
o  Hepatomegaly 
o  Impotence 
o  Amenorrhoea 
o  Hypogonadism 
o  Cirrhosis  
o  Cardiac - arrhythmias and cardiomyopathy   
o  Neurological and psychiatric problems
41
Q

Investigations for haemochromatosis

A

• Haematinics - serum ferritin (HIGH), transferrin (LOW), transferrin saturation (HIGH), TIBC (LOW)
o NOTE: serum ferritin is NOT very specific because it is an acute phase protein
o Serum iron concentration and transferrin saturation do NOT accurately reflect
total body iron stores
• Tests to exclude other causes of high ferritin:
o CRP - inflammation
o Chronic alcohol consumption
o ALT - liver necrosis
• LFTs
• Other investigations for abnormal liver function (e.g. hepatitis serology)
• Genetic testing
• Liver biopsy (rarely required)

42
Q

Define haemolytic anaemia

A

Premature erythrocyte breakdown causing shortened erythrocyte life span (<120 days) with anaemia)

43
Q

Aetiology/ Risk Factors of haemolytic anaemia

A 
•  Hereditary 
o  Membrane Defects  
•  Hereditary spherocytosis   •  Elliptocytosis  
o  Metabolic Defects 
•  G6PD deficiency  
•  Pyruvate kinase deficiency 
 o  Haemoglobinopathies 
•  Sickle cell disease  
•  Thalassemia 
•  Acquired 
o  Autoimmune  
•  Antibodies attach to erythrocytes causing intravascular and extravascular 
haemolysis  
o  Isoimmune 
•  Transfusion reaction 
•  Haemolytic disease of the newborn   
o  Drugs 
•  Penicillin 
•  Quinine  
•  NOTE: this is caused by the formation of a drug-antibody-erythrocyte 
complex  
o  Trauma 
•  Microangiopathic haemolytic anaemia (caused by RBC fragmentation in  abnormal microcirculation) 
   !  E.g. haemolytic uraemic syndrome, DIC, malignant hypertension  
o  Infection 
•  Malaria 
•  Sepsis  
o  Paroxysmal nocturnal haemoglobinuria
44
Q

Epidemiology of haemolytic anaemia

A

• COMMON
• Genetic causes are prevalent if African, Mediterranean and Middle Eastern
populations
• Hereditary spherocytosis is the most common inherited haemolytic anaemia in northern Europe

45
Q

Presenting symptoms of haemolytic anaemia

A
  • Jaundice
  • Haematuria
  • Anaemia
46
Q

Signs of haemolytic anaemia on physical examination

A
  • Pallor
  • Jaundice
  • Hepatosplenomegaly
47
Q

Investigations for haemolytic anaemia

A 
•  Bloods 
o  FBC:  
•  Low Hb  
•  High reticulocytes  
•  High MCV  
•  High unconjugated bilirubin  
•  Low haptoglobin (a protein that binds to free Hb released by red blood 
cells)   
o  U&amp;Es 
o  Folate  
•  Blood Film 
o  Leucoerythroblastic picture  
o  Macrocytosis  
o  Nucleated erythrocytes or reticulocytes  
o  Polychromasia  
o  May identify specific abnormal cells such as: 
•  Spherocytes  
•  Elliptocytes  
•  Sickle cells  
•  Schistocytes  
•  Malarial parasites  
•  Urine 
o  High urobilinogen 
o  Haemoglobinuria 
o  Haemosiderinuria  
•  Direct Coombs' Test 
o  Tests for autoimmune haemolytic anaemia  
o  Identifies erythrocytes coated with antibodies   
•  Osmotic fragility test or Spectrin mutation analysis  
o  Identifies membrane abnormalities  
 •  Ham's Test 
o  Lysis of erythrocytes in acidified serum in paroxysmal nocturnal haemoglobinuria  
•  Hb Electrophoresis or Enzyme Assays 
o  To exclude other causes  
•  Bone Marrow Biopsy (rarely performed)
48
Q

Define Haemolytic Uraemic Syndrome and Thrombotic Thrombocystopaenic Purpura (HUS and TTP)

A

Definition: triad of :

  • microangiopathic haemolytic anaemia (MAHA)
  • acute renal failure
  • thrombocytopenia

There are two forms of HUS:

  • D+ = diarrhoea- associated form
  • D- = no prodromal illness identified

HUS overlaps with TTP , which has additional features of

  • fever
  • fluctuating CNS signs
49
Q

Aetiology/ Risk Factors for HUS and TTP (Haemolytic Uraemic Syndrome and Thrombotic Thrombocystopaenic Purpura)

A
  • Endothelial injury results in platelet aggregation and the release of unusually large vWF multimers and activation of platelets and the clotting cascade
  • This leads to small vessel thrombosis
  • The glomerular-afferent arteriole and capillaries are particularly vulnerable - they undergo fibrinoid necrosis
  • This leads to renal ischaemia and acute renal failure
  • The thrombi also promote intravascular haemolysis
•  CAUSES: 
o  Infection  
•  Escherichia coli O157 
•  Shigella 
•  Neuraminidase-producing infections  
 •  HIV  
o  Drugs 
•  COCP 
•  Ciclosporin   
•  Mitomicin 
•  5-fluorouracil 
o  Others: 
•  Malignant hypertension   •  Malignancy 
•  Pregnancy  
•  SLE  
•  Scleroderma
50
Q

Epidemiology of HUS and TTP (Haemolytic Uraemic Syndrome and Thrombotic Thrombocystopaenic Purpura)

A
  • UNCOMMON
  • D+ HUS often affects YOUNG CHILDREN
  • It is the most common cause of acute renal failure in children
  • TTP mainly affects ADULT FEMALES
51
Q

Presenting symptoms of HUS and TTP (Haemolytic Uraemic Syndrome and Thrombotic Thrombocystopaenic Purpura)

A 
•  GI 
o  Severe abdominal colic  
o  Watery diarrhoea that becomes bloodstained  
•  General 
o  Malaise  
o  Fatigue  
o  Nausea  
o  Fever < 38 degrees (D+)  
•  Renal 
o  Oliguria or anuria 
o  Haematuria
52
Q

Signs of HUS and TTP on physical examination

A 
•  General 
o  Pallor  
o  Slight jaundice (due to haemolysis)   
o  Bruising  
o  Generalise oedema  
o  Hypertension  
o  Retinopathy 
•  GI 
o  Abdominal tenderness  
•  CNS Signs 
o  Occurs in TTP 
o  Weakness  
o  Reduced vision  
o  Fits  
o  Reduced consciousness
53
Q

Investigations for HUS and TTP

A 
•  FBC 
o  Normocytic anaemia  
 o  High neutrophils  
o  Very low platelets  
•  U&amp;Es 
o  High urea  
o  High creatinine  
o  High K+  
o  Low Na+  
•  Clotting 
o  Normal APTT and fibrinogen levels (abnormality may indicate DIC) 
•  LFTs 
o  High unconjugated bilirubin   
o  High LDH from haemolysis  
•  Blood cultures  
•  ABG 
o  Low pH  
o  Low bicarbonate   
o  Low PaCO2 
o  Normal anion gap  
•  Blood Film 
o  Schistocytes  
o  High reticulocytes and spherocytes  
•  Urine 
o  1+ g protein/24 hrs  
o  Haematuria 
•  Stool Samples  
o  MC&amp;S 
•  Renal Biopsy 
o  Can distinguish between D+ and D- HUS
54
Q

Define Haemophilia

A

Bleeding diatheses resulting from an inherited deficiency of a clotting factor
• Haemophilia A: MOST COMMON - deficiency in factor 8
• Haemophilia B: deficiency in factor 9
• Haemophilia C: RARE - deficiency in factor 11

55
Q

Aetiology/ Risk Factors of haemophilia

A
  • Haemophilia A and B have X-linked recessive inheritance
  • 30% of cases are new mutations
  • Due to its inheritance pattern, Haemophilia is mainly seen in MALES
56
Q

Epidemiology of haemophilia

A
  • Haemophilia A incidence: 1/10,000 males
  • Haemophilia B incidence: 1/25,000 males
  • Haemophilia C is more common in Ashkenazi Jews
57
Q

Presenting symptoms of haemophilia

A

• Symptoms usually begin in early childhood
• Swollen painful joints occurring spontaneously or with minimal trauma
(haemarthroses)
• Painful bleeding into muscles
• Haematuria
• Excessive bruising or bleeding after surgery or trauma
• FEMALE carriers are usually asymptomatic, but may experience excessive bleeding
after trauma
• Generally speaking, bleeding in haemophilia is DEEP (into muscles and joints)

58
Q

Recognise the signs of haemophilia on physical examination

A 
•  Multiple bruises  
•  Muscle haematomas 
•  Haemarthroses (right) 
•  Joint deformity  
•  Nerve palsies (due to nerve compression by 
haematomas)  
•  Signs of iron deficiency anaemia
59
Q

Identify appropriate investigations for haemophilia

A
  • Clotting screen (high APTT)
  • Coagulation factor assays (low factor 8, 9 or 11 (depending on type of haemophilia))
  • Other investigations may be performed if there are complications (e.g. arthroscopy)

Yr3 Med Conditions (9 decks)

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