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1A+B Flashcards

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1
Q

How many and what are the pathways involved in coagulation?

A

3: intrinsic, extrinsic and common

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2
Q

Describe the extrinsic pathway

A

Caused by tissue injury
Causes the expression of tissue factor and factor VII
Tissue factor along with Factor VIIa which activate factor X to become Xa

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3
Q

Describe the intrinsic pathway

A

Activated when blood is exposed to a negative surface
XII -> XIIa,
XI -> XIa,
IX -> IXa
VIII -> VIIIa
Activated factor VIIIa activated factor X to become Xa

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4
Q

Describe the common pathway

A

Factor Xa and Va (cofactor) activate PT II -> thrombin IIa which converts fibrinogen I to fibrin Ia
Activates platelets
This reinforced the platelet plug to stop bleeding

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5
Q

Risk factors of vit B12 deficiency

A

Gastritis
Age
Vegan/ vegetarian/Diet
Hx of gastric or intestinal surgery
Pernicious anaemia
Drugs: metformin, anticonvulsants
Crohn’s or coeliac disease

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6
Q

Presentation of Vit B12 deficiency?

A

Neurological symptoms: parathesia, numbness, delayed reflexes
Visual changes
Cognitive impairment: memory issues

Pallor
Fatigue
SOB
Chest pain
Glossitis
Petechiae
Anorexia
Weight loss
Infertility

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7
Q

DDx vit B12 deficiency

A

Folic acid deficiency
Alcoholic liver disease
Hypothyroidism
Diabetic neuropathy
Depression
Alpha thalassaemia

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8
Q

Examination of vit 12 deficiency

A

Angular stomatitis
pale pallor
Conjunctival pallor

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9
Q

Investigation for Vit B12 deficiency?

A

FBC- elevated MCV, low haematocrit
Peripheral blood smear- Megacities, hyper-segmented polymorphonucleated cells
Serum vit B12 <200picograms/mL
Reticulocyte count- differentiate from haemolytic anaemia

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10
Q

Management of vit B12 deficiency

A

Treat cause

Dietary: oral replacement cyanocobalamin 50-150 mcg

If pernicious anaemia or severe B12 deficiency: 1mg of IM hydroxocobalamin TDS for 2 weeks then every 3 months.

If neurological symtoms: 1mg IM hydroxocobalamin every other day then every 2 months

If not responding, refer to haematology
If malabsorption or IBD refer to gastro

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11
Q

If a patient with vit B12 deficiency also has a folate deficiency, which one should be corrected first? Why?

A

B12 deficiency first to prevent subacute combined degeneration of the cord (complication of B12 deficiency)

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12
Q

What is the management of B12 deficiency for patients with pernicious anaemia? why?

A

1mg IM hydroxocobalamin 3 times a week for 2 weeks
In pernicious anaemia, patients have problem with absorption of B12 therefore B12 supplements (cyanocobalamin) is not sufficient

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13
Q

Complication of B12 deficiency

A

Neurological symptoms
Weight loss
Memory loss

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14
Q

Importance of folate

A

Involved in cell processes including DNA and RNA synthesis, metabolising amino acids for cell division

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15
Q

Pathophysiology of folate deficiency

A

Inadequate dietary intake
Body gets rid of more than normal
Malabsorption
Drugs
Antifolate medication
Alcohol intaje

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16
Q

Where is folate stored?

A

Liver

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17
Q

Where is Vit B12 and B9 absorbed?

A

B9 (folate)- jejunum
B12- ileum

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18
Q

Sources of folate?

A

Veg
nuts
liver
yeast

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19
Q

Risk factors of folate deficiency

A

Pregs
Increased cell turnover
haemolysis
renal dialysis
Malabsorption- coeliac disease, Crohns
Drugs- e.g. Valproate, methotrexate
Alcohol

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20
Q

Presentation of folate deficiency

A

Pallor, systolic flow murmur, bpunding pulse
Fatigue
SOB
Angina
Palpitations
Cardiac Failure
Decreased sensation
paresthesia
ataxia
loss of proprioception
Mouth sores
Glossitis
Diarrhoea
Depression

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21
Q

Examination for folate deficiency

A

Glossitis
Pallor, systolic murmur
bounding pulse
Mouth sores
Neurological signs: paresthesia, visual changes

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22
Q

DDx folate deficiency

A

B12 deficiency anaemia of chronic disease
Myelodsplastic syndomes (MDS- bloos cancer)
Acute leukaemia
Alcohol excess
Vit C defiency
Congenital intrinsic factor deficiency

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23
Q

Investigations of folate deficiency

A

FBC: macrocytosis MCV >110
low reticulocyte, increased mcv
Howell-Jolly bodies
Neutrophil: Hyper-segmented polymorphs >6 lobes

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24
Q

Management of folate deficiency

A

5mg Folic acid for 4 months
If the patient also has B12 deficiency, treat that first to reduce risk of spinal cord degeneration

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25
When should a patient with folate deficiency be referred
Haematology: Preg Neurological symptoms Malignancy suspected Does not respond to treatment MCV is persistently high Gastroenterolgy: Malabsorption or IBD suspected pernicious anaemia, GI symptoms, gastric cancer suspected
26
Define macrocytic anaemia. What are the two types? which type is seen in folate deficiency?
1) Macrocytic- increased production or red blood cells 2) Normoblastic and megaloblastic aneamia 3) folate and B12 deficiency are both megaloblastic macrocytic anaemia
27
Where is iron absorbed in the body? What happen to iron once it has been absorbed
Duodenum and upper jejunum HCL and ascorbic acid aid absorption Iron is transported in plasma by protein transferrin - to develop RBC in bone marrow Ferritin or haemosiderin- protein complexes that store unused iron in a non-toxic form
28
Risk factors of Iron deficiency
Age- infants, adolescents, postmenopausal, elderly GI tract: oesophagitis oesophageal varices Hiatus hernia IBD Change in bowel habit Bleeding- malaena, haemorrhoid, malignancy, gastric or bowel surgery Malabsorption: Coeliac disease Gastrectomy Atrophic gastritis Menorrhagia NSAIDs and Aspirin Diet, vegetarian Pregnancy Breast feeding Weaning age Growth spurts
29
Presentation of Iron deficiency
Tiredness lack of energy heart palpitations SOB Palour Headaches, ringing , sore tongue, wanting to eat non-food (e.g. soil (pica)) GI blood loss- Malaena Menstrual losses- menorhagia
30
Examination of iron deficiency
Koilonychia Skin atrophy Angular stomatitis Tachycardia and cardiac failure with severe anaemia Abdominal, rectal examination and sigmoidoscopy Look for source of blood loss
31
Examination of iron deficiency
Koilonychia Skin atrophy Angular stomatitis Tachycardia and cardiac failure with severe anaemia Abdominal, rectal examination and sigmoidoscopy Look for source of blood loss
32
DDx of iron deficiency
Trauma Acute GI bleed Surgery Aneurysm rupture Malnutrition, chemo, radiotherapy, alcohol abuse
33
Investigation of iron deficiency
FBC- low Hb and MCV <80 If both are low, check ferritin <15mcg (If inflammation or infection present ferritin may be >15) Transferrin saturation raised soluble transferrin assay increased hypochromic RBC Bone marrow aspirate- perls stain- absence of stainable iron
34
What is seen in iron deficiency on a blood film?
Target cells hypochromic microcytic (low MCV)
35
Management of iron deficiency
Iron supplements Ferrous Sulphate 200mg TDS recheck FBC within 4 weeks should continue 3 months after Fe levels have been corrected Can consider paraenteral (cosmofer) or IV iron Ferrous fumerate/gluconate is better tolerated than ferrous sulphate
36
Side effects of 200mg TDS ferrous sulphate?
Ab distention, constipation, diarrhoea, black stools If not tolerated reduce to 200mg BD or OD or give ferous fumerate 200mg TDS
37
Complications of Iron deficiency
Thrombocytosis Cardiac problems pregnancy complications Development delayed in children Restless leg syndrome
38
Define Sickle cell anaemia
Deformed/sickle shaped red cells
39
Pathophysiology of SCA
Caused by a point mutation in the beta chain of haemoglobin causing a glutamic acid to valine forming HbS Lack of elasticity, and adherence to the vascular epithelium can lead to vascular occlusion and ischaemia
40
When does HbS turn into sickle celled shaped
They polymerise and deform into sickle shaped when deoxygenated Triggers of deoxygenation: Cold dehydration insomnia alcohol consumption stress overexertion hormonal changes
41
What type of condition is SCA
Autosomal recessive on chromosome 11
42
Risk factors of SCA
African heritage East mediterranean descent
43
What are the different types of SCA
HbSS: homozygous for HbS, chronic haemolytic anaemia HbSC: milder form, heterozygous for HbS + abnormal haemologlobin C HbSA: Carrier : HbS and HbA (normal) HbS beta thalassemia: HbS and one beta thalassemia gene HbSD, HbSE, HbSO: HbS and another abnormal (D,E,O)
44
What are the different types of SCA
HbSS: homozygous for HbS, chronic haemolytic anaemia HbSC: milder form, heterozygous for HbS + abnormal haemologlobin C HbSA: Carrier : HbS and HbA (normal) HbS beta thalassemia: HbS and one beta thalassemia gene HbSD, HbSE, HbSO: HbS and another abnormal (D,E,O)
45
Presentation of SCA
Usually <6 yrs Severe bony pain Dactylitis - swollen dora of hands and feet Fatigue, lathargy, weakness, pallor failure to thrive Activity intolerance Acute chest pain, SOB - activity dyspnea Pain from acute vaso-occlusive crisis Hypersplenism
46
Examination for SCA
Usually unremarkble, may see swellinng of joints
47
DDx of SCA
Gout Septic arthritis osteomyelitis Trauma
48
Investigations for SCA
Prenatal scanning 8-12 weeks Neonatal screening - heel prick test - electrophoresis Hb isoelectric focusing (HBIEF) - determine SCA gene Peripheral blood smear analysis: Howell Jolly bodies
49
Management of SCA
Screen infants, pregs, high risk Prevent crises Regular monitoring Hydroxyurea- break down sickle cells blood transfusion - be aware of iron overload Avoid triggers on pain: exercise and cold weather Increase fluid intake Analgesics fluids analgesics and oxygen during crises May be started on broad spectrum abx since it may be infection driven
50
Symptoms of SCA crisis
Vaso-occlusion causing ischaemia extreme pain haematuria weightloss loin pain fever dehydration acute chest symptoms: SOB, wheeze, severe vomiting and diarrhoea spleen or liver enlargement Jaundice
51
Complications of SCA
Chronic haemolytic anaemia Functional asplenia Renal papillary necrosis Avascular osteonecrosis Recurrent stroke Retinal vessel occlusion
52
Define polycythaemia
increased circulating red blood cells
53
2 types of polycynthaemia ?
Apparent and absolute
54
What is the difference between apparent and absolute polycythaemia
Apparent: raised haematocrit and normal RBC mass: increased alcohol, smoking, HTN, dehydration Absolute: raised haematocrit and red cell mass which can be split into first and second degree Haematocrit is the ratio of vol of RBC to total volume of blood Apparent: less blood volume (plasma) Absolute: more blood cells
55
Define first and second degree absolute polycythaemia
First degree- usually associated with a positive JAK2 gene (problem with cells produced by bone marrow where too many RBC are made (polycythaemia vera)) Second degree- due to hypoxia or abnormal EPO production (due to underlying condition)
56
Risk factors of polycythaemia
Elderly Smoking Excessive alcohol intake Hypertension Dehydration High cholesterol
57
Presentation of Polycythaemia
May be asymptomatic May present symptoms due to thrombosis Fatigue Headache Dizziness Sweating Bleeding/bruising Weight loss Bone pain Swollen joints Pruritus plethoric
58
Examination for polycythaemia
BP- may be raised neurological exam with symptoms of thrombosis Ab exam: splenomegaly
59
DDx of polycythaemia
Chronic myelogenous leukaemia (CML) Thrombosis Acute myeloid leukaemia (AML) COPD Wilms tumour
60
Investigations for polycythaemia
FB: Hb, Haemocrit Special test: JAK2 gene mutation: positive (primary polycythaemia) low ESR
61
Management of polycythaemia
Venesection (reducing RBC) Low dose aspirin: 75mg OD to reduce risk of blood clots Manage CVD: HTN and hyperlipidaemia
62
Complication of Polycythaemia
Stroke Thrombosis Acute myeloid leukaemia
63
Pathophysiology of acute myeloid/myelogenous leukaemia
arrest of cellular differentiation of myeloid cells causing hyperproliferation of myeloblasts (immature myeloid cells)
64
Pathophysiology of chronic myeloid/myelogenous leukaemia
occurs due to chromosomal translocation of chromosome 9 and 22 forming a BCR-ABL oncogene ; Philadelphia chromosome
65
Risk factors of myelogenous leukaemia
Blood disorder (polycythaemia, aplastic anaemia, myelodysplastic syndrome) Radiation Chemotherapy Down syndrome
66
Presentation of myelogenous leukaemia
SOB/ dizziness if anaemic Generalised aches and pains Recurrent infections/fever Easy bruising/bleeding Night sweats Weight loss
67
Examinations of myelogenous leukaemia
Pale Organomegaly Lymphadenopathy Bleeding/swollen gums Bruises
68
Examinations of myelogenous leukaemia
Pale Organomegaly Lymphadenopathy Bleeding/swollen gums Bruises
69
DDx of AML/CML
Lymphoma
70
Investigations of AML/CML
FBC: anaemia, low platelet, (low Hb, could have normal, high or low WCC) Clotting screen LFT, Us & Es Blood film (blast cells) CXR ECG- cardiac damage Bone marrow aspiration
71
Management of AML/CML
Chemo Acute: Tretinoin (all-trans retinoic acid) Chronic: Tyrosine kinase inhibitors - reduce cell growth Surgery: bone marrow transplant
72
Complication of AML/CML
Secondary malignancies
73
What syndrome is associated with AML
Downs syndrome
74
What is seen on a blood film for AML?
Blast cells and auer rods (immature cells with crystallisation inside)
75
What is seen on a blood film for AML?
Blast cells and auer rods (immature cells with crystallisation inside)
76
What is Philadelphia chromosome associated with?
CML
77
Define multiple myeloma
malignant hyperproliferation of plasma cells resulting in abnormal antibody production
78
Risk factors of multiple myeloma
Alcohol obesity FHx Radiation
79
Presentation of multiple myeloma
Bone pain Falls, fractures Bleeding/bruising Lethargy Anorexia Increased thirst, constipation Dizziness/confusion
80
Examination for multiple myeloma
Depends on severity May present with altered mental status, reduced range of movement
81
DDx of multiple myeloma
Leukaemia Lymphoma
82
Investigations for multiple myeloma
FBC- anaemia Us and Es- high Ca, urea/creatinine ESR/plasma viscosity Ig screening (IgG raised) Blood screening- rouleaux (RBC stacking) Bence Jones proteins in urine XR, CT, MRI Bone marrow aspirate- plasma cells
83
Management of multiple myeloma
Referral haematologist Chemotherapy: Bortezomib Immunomodulators: thalidamide Bisphosphonates: prevent bone loss Abx: infections Glucocorticoids: hypercalcaemia
84
Complications of multiple myeloma
Renal failure Infections Death Hyperviscosity syndrome Ig light chain amyloidosis - build up of proteins fragility fracture
85
Define lymphoma
Malignant tumours of lymph nodes
86
Classifications of lymphomas
hodgkin and non-hodgkin
87
Where is folate stored?
Liver
88
Define aplastic anaemia
Bone marrow unable to make new RBC
89
Pathophysiology of aplastic anaemia
Usually idiopathic but can also be Congenital EBV HIV Drugs - chloramphenicol SCA impairs the production of mature RBC
90
Risk factors of Aplastic anaemia
FHx Viral exposure Drugs e.g. chloramphenicol Chemical exposure
91
Presentation of Aplastic anaemia
Failure to thrive in children Jaundice SOB Tiredness
92
Examination of aplastic anaemia
Cardiovascular: flow murmur or signs of heart failure due to anaemia Ab: masses, tenderness or organomegaly Lymphoadenopathy: neck, armpit and inguinal areas
93
DDx of aplastic anaemia
Lymphoma Multiple Myeloma
94
Investigation for aplastic anaemia
FBC- pancytopenia, low neutrophils, platelet and Hb Viral serology (HIV, EBV, Hepatitis) LFT Blood film CXR Ab USS Bone marrow biopsy
95
Management of aplastic anaemia
Refer to haematologist: Blood/platelet transfusion Bone marrow transplant Immunosuppressive therapy
96
Complication of aplastic therapy
Graft vs host disease if bone marrow transplant Bleeding
97
Define Lymphoma
Blood cancer where WBC hyperproliferate
98
Risk factors of Lymphoma
EBV, HTLV, Hep C Immunosuppression HIV FHx Smoking
99
Presentation of Lymphoma
Enlarged lymph node- can be painful after drinking alcohol Cough SOB Night sweats, Fever, weight loss Abdominal mass
100
Examination of lymphoma
Lymphadenopathy organomegaly (liver/spleen) Palpable abdominal mass
101
DDx of lymphoma
Infectious Mononucleosis Leukaemia
102
Investigation of lymphoma
FBC- exclude leukaemia Serology (HIV, hepatitis, EBV) ESR Lactate dehydrogenase (high- produced when cells break down) CXR- may show effusion CT brain CT-CAP Biopsy
103
Management of lymphoma
Refer to oncology Treatment by MDT team Will be counselled on reproductive plans
104
Complication of lymphoma
Spinal cord compression due to vertebral metastasis GI obstruction
105
What is thalassaemia
Autosomal recessive condition whereby there is a mutation in the beta/alpha globin chain
106
What chromosomes are affected in alpha and beta thalassaemia
Alpha- Mutation/defect of chromosome 16 Beta- Mutation/defect of chromosome 11
107
Risk factors of thalassaemia
Asian- Beta African ethnicity Family Hx
108
Presentation of thalassaemia
Sometimes asymptomatic Anaemia: SOB, fatigue, dizziness Jaundice Gallstones: nausea, wind, bloating, abdominal pain Hx of iron supplementations Lethargy Ab distention failure to gain weight short height/stature Pallor Spinal changes- osteopenia due to iton overload Misaligned teeth Hepatosplenomegaly
109
Examination of thalassaemia
Asymptomatic Splenomegaly Ab distention Pallor Short stature Jaundice Growth retardation Misaligned teeth
110
DDx of Thalassaemia
Iron deficiency Lead deficiency Folate/B12 deficiency
111
Investigations for thalassaemia
high: RBC, reticulocyte, LFT- bilirubin, LDH Low: MCV, MCH, Hb Iron, Ferritin, leukocytes, platelet may be normal-elevated Gap-PCR/MLPA detect alpha/beta allele deletions Ab USS- enlarged spleen and liver XR- osteopenia
112
Management of thalassaemia
Depends on severity: Iron/folic supplements Transfusion Chelating agents for iron overload Splenectomy Stem cell transplantation
113
Complication of thalassaemia
Growth retardation Severe anaemia Osteopenia of bones Iron overload
114
Monitoring for thalassaemia and why?
Serum ferritin due to iron overload due to faulty creation of RBC, recurrent transfusions, increased absorption of iron
115
Management of iron overload in thalassaemia
Iron chelation
116
3 types of thalassaemia
Thalassaemia minor: carriers - one normal and abnormal gene: mild microcytic anaemia Thalassaemia intermedia: 2 defective genes (can be 2 defective or 1 defective and 1 deletion) Thalassaemia major: homozogous for deletion genes

Haematology (1 decks)

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