Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PT prep > Haematology > Flashcards

Haematology Flashcards

(77 cards)

Start Studying
1
Q

Aetiology of microcytic anaemia

A

Iron deficiency
Thalassaemia
Sideroblastic
Chronic disease (can be normocytic)

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

Aetiology of normocytic anaemia

A 
Acute blood loss
Anaemia of chronic disease
Bone marrow failure
Renal failure
Hypothyroidism
Haemolysis
Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aetiology of macrocytic anaemia

A 
B12 or folate deficiency (or anti-folate drugs)
Alcohol excess or liver disease
Reticulocytosis 
Cytotoxic drugs 
Myelodysplastic syndromes
Marrow infiltration 
Hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When is transfusion in acute anaemia indicated?

A

<70g/L

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

How is red cell distribution width RDW useful in anaemia

A

If simultaneous pathology is occurring such as poor absorption of iron and folate (coeliac disease) then this may be shown in a greater volume distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of chronic iron-deficiency anaemia

A

Koilonychia
Atrophic glossitis
Angular stomatitis
Post-cricoid webs (Plummer-Vinson)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathophysiology of anaemia of chronic disease

A

1) Poor use of iron in erythropoiesis
2) Cytokine induced shortening of RBC survival
3) Decreased production of and response to erythropoietin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Microcytic anaemia not responding to iron think

A

Sideroblastic anaemia

Ineffective erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Howell-Jolly bodies

A

Seen post-splenectomy and in hyposplenism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of hyposplenism

A 
Sickle-cell disease
Coeliac diseaase
Congenital
IBD
Myeloproliferative disease
Amyloid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Reticulocytes

A

Young, large, immature RBC
Indicate active erythropoiesis
Increased in haemorrhage, haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Schistocytes

A

Fragmented RBCs in intravascular haemolysis- DIC, haemolytic anaemic syndrome, thrombotic thrombocytopenic purpura TTP, pre-eclampsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Spherocytes

A

Autoimmune haemolytic anaemia or hereditary spherocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When are target cells seen (Mexican hat cells)

A

Liver disease
Hyposplenism
Thalassaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cabot rings

A

Pernicious anaemia
Lead poisoning
Bad infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Macrocytic megaloblastic causes of anaemia

A

B12 and folate deficiency

Nuclear maturation is delayed compared with the cytoplasm

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

Non-megaloblastic macrocytic anaemia

A 
Alcohol excess
Reticulocytosis 
Liver disease
Hypothyroidism
Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antibodies in pernicious anaemia

A

Parietal cell antibodies in 90%

IF antibodies- more specific but less sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When is the indirect Coombs test used?

A

Pre-natal testing to see if there are antibodies against RBCs that are free in the serum

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

Causes of haemolytic anaemia

A 
Acquired
Immune mediated- Coomb's +
Coomb's -ve
Microangiopathic haemolytic anaemia
Infection- malaria
Paroxysmal nocturnal haemoglobinuria 
Hereditary
Enzyme defects- G6PD deficiency 
Hereditary spherocytosis 
Hereditary elliptocytosis 
Haemoglobinopathy- sickle cell disease, thalassaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Warm AIHA

A

IgG mediated

Lymphoproliferative disease- CLL, lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cold AIHA

A

IgM mediated, bind at lower temperatures
Often following infection
Associated with chronic anaemia, Raynaud’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Haemolytic anaemia that is coomb’s direct test positive

A

AIHA
Drug-induced- penicillin, quinine
Acute transfusion reaction
Haemolysis of the newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sickle cell vaso-occlusive crises precipitated by

A

Hypoxia
Cold
Dehydration
Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Hereditary haemorrhagic telangiectasia
Osler-Weber-Rendu syndrome | Abnormal blood vessel development in the cutaneous tissue and mucous membranes
26
Haemophilia A inheritance
X-linked recessive 50% of sons affected 50% of daughters carriers
27
Christmas disease
Haemophilia B
28
Liver disease bleeding pathology
Decreased synthesis of clotting factors Decreased absorption of vit K Abnormalities of platelet function
29
Alteplase MOA
Recombinant tissue plasminogen activator Converts plasminogen into plasmin Degrading fibrin cross-linking Bind fibrin so localise to the area of the clot
30
Immune thrombocytopenia
Anti-platelet antibodies | IV immunoglobulin may be used to temporarily raise the platelet count- ie for pregnancy or surgery
31
PT factors tested
Extrinsic and common | I, II,V,VII,X
32
APTT factor tested
I, II, V, VIII, IX, X, XI, XII
33
How should crossmatch blood be taken?
From one patient at a time and labelled immediately
34
When is Fresh Frozen Plasma used?
To correct clotting defects | DIC, TTP, liver disease, when vitamin K would be too slow
35
Complications of transfusion
Early- within 24 hours Acute haemolytic reactions, anaphylaxis, bacterial contamination, febrile reactions, allergic reactions, fluid overload, transfusion related acute lung injury Delayed- after 24 hours Infections, iron overload, post-transfusion purpura, potentially lethal fall in platelet count
36
What is a massive blood transfusion?
Replacement of an individuals entire blood volume within 24 hours
37
What is autologous blood transfusion?
Patients blood is stored pre-op for their own use later
38
TRALI management
STOP the transfusion Give 100% oxygen Treat as ARDS with respiratory and circulatory support and close monitoring for sepsis Donor should be removed from donor panel
39
LMWH
Preferred preventative anticoagulant Inactivated factor Xa but not thrombin Half life 2-4 fold longer than standard heparin and response is more predictable
40
Unfractioned heparin MOA
Binds antithrombin- increasing ability to inhibit thrombin, factor Xa and IXa Rapid onset and short half-life
41
How often do DOACs need monitoring?
Every 3 months an assessment and an annual blood test
42
Target INR for warfarin for PE/DVT/AF/aortic valve replacement
2-3
43
Target INR for warfarin for mitral valve replacement
2.5-3.5
44
INR 5-8, no bleed
Withhold warfarin and restart at lower dose once <5
45
INR 5-8 minor bleed
Stop warfarin and admit for urgent IV vit k | Restart warfarin <5 INR
46
INR >8 no bleed
Stop warfarin | Haematology advice
47
INR >8 minor bleed
Stop warfarin and admit for urgent IV vit k Restart warfarin <5 INR Daily check of INR
48
Any major bleed on warfarin
STOP warfarin Give Prothrombin Complex Concentrate and IV vit K Discuss with haematology
49
Types of leukaemia
Chronic lymphoblastic leukaemia Chronic myeloid leukaemia Acute lymphoblastic leukaemia Acute myeloid leukaemia
50
Commonest cancer of childhood
Acute lymphoblastic leukaemia
51
Signs and symptoms of ALL
Marrow failure- anaemia, infection and bleeding Infiltration- hepatosplenomegaly, lymphadenopathy- superficial or mediastinal, orchidomegaly, CNS involvement- cranial nerve palsies, meningism
52
Treatment for ALL
Educate and motivate patient to get involved with treatment Support- blood/platelet transfusion, IV fluids, allopurinol (tumour lysis syndrome prevention) Infections- immediate antibiotics and start neutropenic regimen Chemotherapy
53
Philadelphia chromosome
Reciprocal change of information between 22 and 9 Results in chronic myeloid leukaemia and is associated with some forms of ALL 22t(9:22)
54
What are myelodysplastic syndromes?
Disorders that manifest as bone marrow failure- life threatening infection and bleeding
55
AML differentiated from ALL
Auer rods on biopsy
56
Commonest acute leukaemia in adults
AML
57
CML presentation
Mostly chronic and insidious- weight loss, tiredness, fever, sweats Features of gout due to purine breakdown Bleeding- anaemia and bruising Abdominal discomfort from splenic enlargement
58
Most common leukaemia
Chronic lymphocytic leukaemia | Progressive accumulation of a malignant clone of functionally incompetent B cells
59
CLL presentation
Often none- surprise on a routine FBC Can have constitutional symptoms or anaemic or infection prone Enlarged, rubbery, non-tender nodes Hepatosplenomegaly
60
Characteristic Hodgkin's lymphoma cells
Reed-Sternberg cells
61
Risk factors for Hodgkin's lymphoma
Affected sibling EBV SLE Post-transplantation
62
Symptoms and signs of Hodgkin's lymphoma
``` Enlarged, non-tender, rubbery, superficial lymph nodes- usually cervical but can be axillary or inguinal 25% have constitutional upset Alcohol induced lymph node pain Mediastinal lymph node involvement Cachexia, anaemia, organomegaly ```
63
Tests for Hodgkin's lymphoma
Blood- FBC, film, ESR, LFT, LDH, urate, Ca2+ | Imaging- CXR, CT TAP
64
Staging system used in Hodgkin's lymphoma
Ann-Arbor system
65
MALT lymphoma
Mucosa-associated lymphoid tissue | Gastric is caused by H. pylori
66
Burkitt's lymphoma
Non-Hodgkin's lymphoma Childhood disease Characteristic jaw lymphadenopathy
67
Causes of polycythaemia
Relative- low plasma Absolute- primary- Polycythaemia vera, secondary- hypoxia or inappropriate erythropoietin secretion
68
Mutation in polycythaemia vera
JAK2 | >95%
69
Presentation of polycythaemia vera
Asymptomatic and detected on FBC or Hyperviscosity related- headaches, dizziness, tinnitus, visual disturbance Itching after a hot both and erythromelalgia (burning sensation in fingers and toes) Signs Facial plethora, splenomegaly, gout from increased urate from RBC turnover Arterial or venous thrombosis may be present
70
Treatment of polycythaemia vera
Venesection to keep the risk of thrombosis down Aspirin 75mg daily If higher risk (>60 years old or previous thrombosis) then hydroxycarbamide Alpha-interferon in women of childbearing age
71
Treatment for essential thrombocythaemia
Aspirin 75mg daily
72
Clinical features of myeloma
Osteolytic bone lesions- backache, pathological fractures, vertebral collapse Hypercalcaemia- increased osteoclastic activity Anaemia, neutropenia or thrombocytopenia from marrow infiltration by plasma cells Recurrent bacterial infections Renal impairment from light chain deposition in the distal loop of Henle
73
Tests for multiple myeloma
FBC, raised ESR, raised urea and calcium, alk phos normal unless healing fracture Film Bone marrow biopsy- increased plasma cells Serum/urine electrophoresis Xray- lytic lesions, pepperpot skull, vertebral collapse, fractures, osteoporosis
74
Treatment for multiple myeloma
Supportive- analgesia (avoid NSAIDs- renal function), bisphosphonate, local radiotherapy Transfusion for anaemia Renal failure- rehydration and ensure adequate fluid intake Rapid infection control Chemotherapy
75
Causes of massive splenomegaly
CML Myelofibrosis Malaria Leishmaniasis
76
Protein C & S action
Vitamin K dependent factors that act together to cleave and neutralise factors V and VIII Deficiency causes thrombophilia
77
Activated protein C resistance/ factor V leiden syndrome
Single point mutation in factor 5 so that this clotting factor is not broken down by APC 5 fold increase risk of DVT/PE if heterozygous

PT prep (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions