Brainscape's Knowledge GenomeTM

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


See full index

Osha 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

What is myeloma?

A
  • Bone marrow cancer
  • Cancer of differentiated B lymphocytes (plasma cells)
  • leads to large quantities of single type of antibody being produced
  • Multiple myeloma: affects multiple areas of body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the pathophysiology behind myeloma?

A
  • genetic mutation causes uncontrolled multiplication
  • Accumulation of malignant plasma cells leads to progressive bone marrow failure
  • Mostly occurs in IgG
  • Bence Jones protein found in urine of patients (antibody light chains)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for myeloma?

A
  • age
  • male
  • black african
  • family history
  • obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 4 key features of myeloma?

A
  • C: elevated calcium >2.75mmol/l (inc osteoclast activity)
  • R: renal impairment: creatinine >1.73mmol/l
  • A: anaemia
  • B: lytic bone lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is monoclonal gammopathy of undetermined significance (MGUS)?

A
  • clonal antibody produced which doesn’t correlate to particular infection
  • excess of a single type of antibody
  • may progress to myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is smouldering myeloma?

A
  • progression of MGUS
  • premalignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is myeloma investigated?

A
  • serum protein electrophoresis
  • FBC and U&E
  • urine electrophoresis (Bence-Jones proteins)
  • X-ray for osteolytic lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the treatment for myeloma?

A
  • Bisphosphonates
  • thalidomide
  • corticosteroids: dexamethasone - augments action of chemotherapies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is sickle cell anaemia?

A
  • single point mutation in β global gene > HbS
  • Autosomal recessive
  • HbS polymerises when deoxygenated
  • Blocks blood vessels > ischaemia, sequestration (away from organs)
  • chronic haemolysis > low baseline Hb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is sickle cell anaemia diagnosed?

A
  • 1st line: sickle solubility test: cloudy looking
  • Gold: HPLC, capillary electrophoresis (Hb separated based on size and charge)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some complications of sickle cell disease?

A
  • sequestration in liver/spleen
  • thrombosis (DVT, PE)
  • acute chest syndrome
  • aplastic crisis
  • vaso-occlusive crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is lymphoproliferative disease?

A
  • neoplastic, clonal proliferation of lymphoid cells
  • Cancer of the white blood cells
  • 2 categories: Hodgkin’s and non-Hodgkin’s (aggressive or indolent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the aetiology of indolent lymphoma?

A
  • Primary Immunodeficiency
  • Secondary Immunodeficiency e.g. HIV; Recipients of Transplant
  • Infection e.g. EBV; Helicobacter Pylori
  • Autoimmune Disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does lymphoma present?

A
  • lymphadenopathy > neck, armpit, groin
  • non-tender, rubbery nodes
  • b symptoms: fever, night sweats, weight loss
  • pain after drinking alcohol (Hodgkin’s)
  • recurrent infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is lymphoma investigated?

A
  • lymph node biopsy: core needle or excision node
  • lactate dehydrogenase raised
  • Reed-Stenberg test: abnormally large B cells with multiple nuclei: Hodgkin’s (owl eyes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Ann Arbor staging for lymphoma?

A
  • if affected nodes are above or below diaphragm
  • Stage 1: confined to one region
  • Stage 2: in more than one region on same side of diaphragm
  • Stage 3: affects nodes above and below diaphragm
  • Stage 4: widespread involvement inc non-lymphatic organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is lymphoma treated?

A
  • Hodgkin’s: DBVD: doxorubicin, bleomycin, vinblastine, dacarbazine
  • NH: R-CHOP: rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some types of Non-Hodgkin’s lymphoma?

A
  • Burkitt: associated w EBV, malaria, HIV
  • MALT: affects mucosa-associated lymphoid tissue (H. pylori)
  • Diffuse large B cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are risk factors for Non-Hodgkin’s lymphoma?

A
  • HIV, EBV, malaria, H. pylori
  • Hep B/C infection
  • exposure to pesticides and trichloroethylene
  • family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 3 Myeloproliferative Disorders and what is the definition?

A
  • uncontrolled proliferation of a single stem cell type
  • primary myelofibrosis
  • polycythaemia vera
  • essential thrombocythaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is myelofibrosis?

A
  • cytokines released from proliferating cells
  • leads to proliferation of a cell line > fibrosis of bone marrow
  • can cause anaemia and low WBC
  • haematopoiesis occurs in liver and spleen > hepato and splenomegaly > portal hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of cell line does primary myelofibrosis affect and what are the investigations?

A
  • haematopoeitic
  • investigations: anaemia, high/low wbc count, teardrop shaped RBC on blood film, varied rbc size, blast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do Myeloproliferative Disorders present?

A
  • systemic: fatigue, weight loss, night sweats, fever
  • anaemia
  • splenomegaly
  • low wbc (infection)
  • low platelets (bleeding, petechiae)
  • portal hypertension (ascites, varices, abdominal pain)
  • raised rbc (thrombosis, red face)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the cell line affected in polycythaemia vera and what are the investigations?

A
  • erythroid
  • raised Hb ( >16.5g/dL in men or >16g/dL in women)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What cell line is affected in primary thrombocythaemia and what are the investigations?

A
  • megakaryocyte
  • primary thrombocythaemia > 450*10^9/l
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 3 key signs of polycythaemia vera?

A
  • conjunctival plethora
  • ruddy complexion
  • splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How are Myeloproliferative Disorders investigated?

A
  • bone marrow biopsy (aspiration > dry due to scar tissue)
  • JAK2, MPL and CALR gene testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is primary myelofibrosis managed?

A
  • Ruxolitinib
  • erythropoietin injections
  • analgesia for splenic discomfort
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is polycythaemia treated?

A
  • aspirin 75mg daily
  • venesection
  • hydroxycarmabide 500mg daily
  • aim to keep haemtocrit <0.45
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is thrombocytosis treated?

A
  • aspirin 75mg daily: reduces blood clot development
  • hydroxycarmabide 500mg daily
  • aim to keep platelets 150-400
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is pernicious anaemia?

A
  • B12 deficiency
  • parietal cells produce intrinsic factor for B12 absorption in ileum
  • antibodies form against parietal cells or intrinsic factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does pernicious anaemia present?

A
  • peripheral neuropathy, paraesthesia
  • loss of proprioception
  • visual changes
  • mood/cognitive changes
  • lemon yellow skin
  • angular chelitis and glossitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is pernicious anaemia diagnosed?

A
  • testing for auto-antibodies
  • 1st line: intrinsic factor antibody
  • can also test for gastric parietal cell antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is pernicious anaemia treated?

A
  • dietary: oral replacement with cyanocobalamin
  • 1mg of IM hydroxycobalamin every other day/3x weekly depending on severity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is mean corpuscular volume (mcv) and what are the reference ranges?

A
  • microcytic: <80
  • normocytic: 80-95
  • macrocytic: >95
  • normal range: 120-165g/l in women or 130-180g/l in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the causes of microcytic anaemia?

A
  • T – Thalassaemia
  • A – Anaemia of chronic disease
  • I – Iron deficiency anaemia
  • L – Lead poisoning
  • S – Sideroblastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the causes of normocytic anaemia?

A
  • A – Acute blood loss
  • A – Anaemia of Chronic Disease
  • A – Aplastic Anaemia
  • H – Haemolytic Anaemia
  • H – Hypothyroidism
38
Q

What is aplastic anaemia?

A
  • pancytopenia where the bone marrow fails
  • deficiency in red cells, white cells and platelets
39
Q

What is megaloblastic anaemia?

A
  • megaloblastic: results from impaired DNA synthesis. Rather than dividing, the cell continues to grow becoming abnormally large.
  • B12 deficiency
  • folate deficiency
40
Q

What are the causes of normoblastic macrocytic anaemia?

A
  • hypothyroidism
  • alcohol excess
  • liver disease
41
Q

What are the causes of iron deficiency anaemia?

A
  • blood loss: menorrhagia, IBD, GI bleeding
  • dietary insufficiency in children
  • poor iron absorption
  • increased requirements during pregnancy
42
Q

How is iron absorbed in the GI tract?

A
  • mainly absorbed in duodenum and jejunum
  • stomach acid needed to keep iron in soluble Fe2+ form
  • changes to Fe3+ when acid drops so PPIs interfere
  • travels around the blood as Fe3+ bound to transferrin
43
Q

How is iron deficiency anaemia investigated?

A
  • low transferrin saturation and ferritin
  • high total iron binding capacity: space for transferrin molecules to bind
  • FBC
  • blood film: Howell Jolly bodies
44
Q

How is iron deficiency anaemia managed?

A
  • OGD/colonoscopy if no clear cause
  • blood transfusion
  • iron infusion
  • oral iron (ferrous sulphate)
45
Q

How does iron deficiency anaemia present?

A
  • koilonychia (spoon shaped nails)
  • angular chelitis
  • atrophic glossitis
  • brittle hair and nails
46
Q

What is thalassaemia?

A
  • genetic defect in protein chains making up Hb
  • autosomal recessive
  • defects in α chains > α thalassaemia
  • defects in β chains > β thalassaemia
47
Q

What is the presentation of thalassaemia?

A
  • fatigue
  • pallor
  • jaundice
  • gallstones
  • splenomegaly: RBC fragile so more damaged collected by spleen
  • pronounced forehead and cheekbones: bone marrow expands
48
Q

How is thalassaemia diagnosed?

A
  • FBC
  • Hb electrophoresis
  • DNA testing
49
Q

How is α thalassaemia managed?

A
  • monitoring FBC
  • blood transfusions
  • splenectomy
  • bone marrow transplant
50
Q

How is β thalassaemia managed?

A
  • monitoring
  • transfusions
  • iron chelation to prevent overload
51
Q

What is haemolytic anaemia and how does it present?

A
  • destruction of RBC leading to anaemia
  • splenomegaly
  • jaundice: bilirubin released during destruction
52
Q

How is haemolytic anaemia investigated?

A
  • FBC: normocytic anaemia
  • blood film shows schistocytes (fragments)
  • direct Coombs test: +ve in autoimmune haemolysis
53
Q

What investigations other than MCV, Hb and blood film can be done for haemolytic anaemia and what are the results?

A
  • reticulocytes high (immature rbc)
  • haptoglobin low (used up clearing fragments)
  • LDH high (high cell turnover)
  • bilirubin high
54
Q

What are the complications of sickle cell anaemia?

A
  • inc risk of infection
  • avascular necrosis
  • pulmonary hypertension
  • CKD
  • acute chest syndrome
55
Q

How is sickle cell anaemia managed?

A
  • antibiotic prophylaxis prevents against infection
  • hydroxycarbamide stimulates production of HbF
  • blood transfusion
  • bone marrow transplant
56
Q

What are the different types of sickle cell crises?

A
  • vaso-occlusive: sickle shaped cell clogs capillaries
  • aplastic: temporary loss of creation of new RBC
  • splenic sequestration: RBC block flow into spleen > splenomegaly > hypovolaemic shock
57
Q

What is acute chest syndrome?

A
  • results from sickle cell anaemia
  • fever/resp symptoms + new infiltrates on X-Ray
  • can be due to infection or emboli
  • may need antibiotics, transfusion, ventilation
58
Q

What is leukaemia?

A
  • cancer of stem cells in bone marrow
  • classified as acute or chronic
  • myeloid or lymphoid depending on cell line affected
59
Q

What is the pathophysiology behind leukaemia?

A
  • genetic mutation in precursor cells leads to excessive production of single type of abnormal WBC
  • leads to suppression of other cell lines
60
Q

What is the epidemiology of leukaemia?

A
  • MC in Under 5 (and over 45) – acute lymphoblastic leukaemia
    Over 55 – chronic lymphocytic leukaemia
    Over 65 – chronic myeloid leukaemia
    Over 75 – acute myeloid leukaemia
61
Q

How does leukaemia present?

A
  • fatigue
  • fever
  • failure to thrive (kids)
  • lymphadenopathy
  • abnormal bleeding/bruising
62
Q

How is leukaemia diagnosed?

A
  • FBC
  • blood film
  • LDH
  • GOLD: bone marrow biopsy
63
Q

How is leukaemia managed?

A
  • chemotherapy and steroids
  • radiotherapy
64
Q

Describe acute lymphoblastic leukaemia

A
  • malignant change in lymphocyte precursor cell
  • acute proliferation of B-lymphocytes
  • peaks in children 2-4yrs
  • associated with Downs
  • blood film shows blast cells
65
Q

Describe chronic lymphocytic leukaemia

A
  • chronic proliferation of well differentiated lymphocyte: usually B lymphocytes
  • smear or smudge cells on blood film
66
Q

Describe chronic myeloid leukaemia

A
  • chronic, accelerated and blast phase
  • chronic: 5yrs, raised white count
  • accelerated: patients become more symptomatic and immunocompromised
  • blast: even higher proportion of blast cells + blood
  • associated with Philadelphia chromosome (t9:22)
67
Q

Describe acute myeloid leukaemia

A
  • can be transformation from myeloproliferative disorder or myelofibrosis
  • blood film: high proportion of blast cells
  • may have Auer rods in cytoplasm
68
Q

What is PT?

A
  • prothrombin time: the time taken for blood to clot via the extrinsic pathway
  • factor VII is the only factor in this pathway and rarely deficient so this measures overall clothing factor synthesis
  • affected by liver disease, vit K deficiency, warfarin levels
69
Q

What is INR?

A
  • international normalised ratio
  • calculated from PT: 1.0 represents the global average
  • used to monitor patients on warfarin
70
Q

What is APTT?

A
  • activated partial thromboplastin time
  • time taken for blood to clot via intrinsic pathway
  • can indicate issues with factor VIII, vWF, IX and XI
  • heparin can cause prolonged APTT
71
Q

What is von Willebrand’s disease?

A
  • type 1: reduced amount of vWF
  • type 2: defective vWF
  • type 3: little/no vWF
  • important in platelet adhesion and binds to factor VIII
  • autosomal dominant
72
Q

How does von Willebrand disease present?

A
  • bleeding gums with brushing
  • epistaxis (nose bleeds)
  • menorrhagia
  • heavy bleeding
  • family history
73
Q

How is von Willebrand disease investigated?

A
  • APTT prolonged
  • Low factor VIII
  • immunoassay of vWF
74
Q

How is von Willebrand disease managed?

A
  • desmopressin: stimulates release of vWF
  • infused vWF and factor VIII
  • tranexamic acid
75
Q

What is the presentation of haemophilia?

A
  • spontaneous haemorrhage, bleeding into joints and muscles
  • intracranial haemorrhage and cord bleeding in newborns
  • bleeding: gums, GI, urinary tract, retroperitoneal space
76
Q

How is haemophilia diagnosed?

A
  • bleeding scores: prolonged APTT
  • coagulation factor assays (factor VIII/IX)
  • genetic testing
77
Q

How is haemophilia managed?

A
  • prophylaxis: infusions of factor VIII/IX
  • avoid NSAIDs and contact sport
  • desmopressin and tranexamic acid (antifibrinolytic)
78
Q

What is haemophilia?

A
  • X linked recessive inherited bleeding disorders
  • almost exclusively affect males, women would need 2 affected X copies
  • A: deficiency in factor VIII
  • B: deficiency in factor IX
79
Q

What are the normal reference ranges for neutrophils?

A
  • neutrophilia: high - acute bacterial infection
  • neutropenia: low - myeloma, lymphoma
80
Q

What are the normal reference ranges for platelets?

A
  • thrombocytosis: high - myeloproliferative disorders
  • thrombopenia: low - 150x10^9 - ITP
81
Q

What are the normal reference ranges for lymphocytes?

A
  • lymphocytosis: high - leukaemia
  • lymphocytopenia: low - infection
82
Q

What is immune thrombocytopenic purpura (ITP) and who does it affect?

A
  • autoimmune platelet destruction
  • in children 2-6 (post viral infection)
  • in adult women (malignancy, HIV, autoimmune)
83
Q

How does ITP present, how is it diagnosed and how is it treated?

A
  • symptoms: purpuric rash, easy bleeds
  • diagnosis: thrombocytopenia, inc megakaryoblasts
  • prednisolone and IV IgG
84
Q

What is thrombotic thryombcytopenic purpura and how does it present?

A
  • inherited
  • deficiency in enzyme clearing vWF so aggregation at endothelial injury sites
  • symptoms: purpuric rash, menorrhagia, AKI, anaemia, neuro symptoms
85
Q

How is TTP diagnosed and treated?

A
  • diagnosis: thrombocytopenia, schistocytes, dec ADAMTS13
  • treatment: plasmapheresis, prednisolone, rituximab
86
Q

How does malaria present and how is it diagnosed and treated?

A
  • anaemia, blackwater fever, hepatosplenomegaly
  • blood film
  • treatment: quinine and doxycycline
87
Q

What is sideroblastic anaemia?

A
  • ineffective erythropoesis due to defective Hb synthesis
  • leads to inc iron absorption, iron loading in bone marrow
  • cardiac, endocrine and liver damage due to iron deposition
88
Q

What is autoimmune haemolytic anaemia?

A
  • mediated by antibodies causing extravascular haemolysis and spherocytosis
  • divided by optimal binding temp to RBC
89
Q

What are the 2 types of autoimmune haemolytic anaemia and their treatments?

A
  • Cold: IgG mediated - steroids
  • Warm: IgM mediated, keep warm
90
Q

What is tumour lysis syndrome?

A
  • rapid cell death when starting chemo for rapidly proliferating blood cancers
  • causes rise in urate, K, phosphate > renal failure
  • prevention with hydration and allopurinol
91
Q

What is disseminated intravascular coagulopathy?

A
  • widespread activation of coagulation due to release of procoagulant agents
  • clotting factors and platelets consumed > inc risk of bleeding

Osha 2a (15 decks)

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