Brainscape's Knowledge GenomeTM

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


See full index

Dylan's flashcards > haem > Flashcards

haem Flashcards

1
Q

Acanthocytes
(Spur/spike cells)

A

RBCs show many spicules

Liver disease, hyposplenism, abetalipoproteinaemia (rare)

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

Basophilic RBC stippling

A

Accelerated erythropoiesis or defective Hb synthesis, small dots at the periphery are seen (rRNA)

Lead poisoning, megaloblastic anaemia, myelodysplasia, liver disease, haemoglobinopathies e.g. thalassaemia

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

Burr cells
(Echinocyte)

A

Like a sea urchin with regular spicules

Often an artefact if blood has sat in EDTA prior to film being made.
Uraemia, renal failure, GI bleeding, stomach carcinoma

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

Heinz bodies

A

Inclusions on very edge of RBCs due to denatured Hb

Glucose-6-phosphate dehydrogenase deficiency, chronic liver disease

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

Howell-Jolly bodies

A

Basophilic (purple spot) nuclear remnants in RBCs

[Note: much bigger purple spots in nucleated RBCs)

Post-splenectomy or hyposplenism (e.g. sickle cell disease)
Megaloblastic anaemia
hereditary spherocytosis

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

Leucoerythroblastic

A

A phrase to denote the presence of nucleated red blood cells and myeloid precursors in peripheral blood

Bone marrow infiltration i.e. myelofibrosis, malignancy

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

Pelger Huet Cells

A

Hyposegmented neutrophil with 2 lobes like a dumbbell
Pseudo-pelger huet cells are also hypogranular

Congenital (lamin B Receptor mutation)
Acquired (myelogenous leukaemia and myelodysplastic syndromes [pseudo-pelger in MDS])

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

Polychromasia

A

Bluish red blood cells due to presence of DNA. Polychromatic cells are usually reticulocytes which are immature RBCs

Usually increased naturally in response to shortened RBC life
↑in haemolytic anaemias
↓aplastic anaemia, chemo

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

Right shift

A

Hypermature white cells - hypersegmented polymorphs (>5 lobes to nucleus)

Megaloblastic anaemia, uraemia, liver disease

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

Rouleaux formation

A

Red cells stacked on each other

Chronic inflammation,
paraproteinaemia,
multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Schistocytes

A

Fragmented parts of RBCs – typically irregularly shaped with sharp edges and no central pallor

Microangiopathic anaemia, e.g. DIC, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, pre-eclampsia

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

Spherocytes

A

Sphere shaped RBCs
Often a little smaller

Hereditary spherocytosis,
Autoimmune Haemolytic Anaemia

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

Stomatocytes

A

Central pallor is straight, curved or rod-like shape. RBCs appear as ‘smiling faces’ or ‘fish mouth’

Can be an artefact during slide preparation.
If not: Hereditary stomatocytosis, high alcohol intake, liver disease

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

Target cells (codocyte)

A

Bull’s-eye appearance in central pallor

Liver disease, hyposplenism, thalassaemia, IDA

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

poikilocytosis

A

(shape) pencil cells

in iron deficiency anaemia

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

Sideroblastic Anaemia

A

Ineffective erythropoiesis → iron loading (bone marrow) causing haemosiderosis (endocrine, liver, and cardiac damage due to iron deposition).
* Diagnosis: Ring sideroblasts seen in the bone marrow (erythroid precursors with iron deposited in mitochondria in a ring around the nucleus).
* Causes: myelodysplastic disorders, following chemotherapy, irradiation, alcohol excess, lead excess, anti-TB drugs or myeloproliferative disease.
* Treatment: Remove the cause and consider Pyridoxine (vitamin B6 promotes RBC production). Consider giving EPO.

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

what does Megaloblastic blood film mean?

A

= Hypersegmented polymorphs, leukopenia, macrocytosis, anaemia, thrombocytopenia with megaloblasts. Megaloblasts are red cell precursors with an immature nucleus and mature cytoplasm. B12 and folate are required for nucleus maturation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how to manage pernicious anaemia ?

A

Treatment: Replenish stores with IM hydroxocobalamin (B12) in 6 injections over 2 weeks.
NICE recommend testing for anti-parietal cell / anti-intrinsic factor antibodies as if there is an autoimmune cause rather than dietary, patients will need 3-monthly IM injections.

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

inheritance of G6pD

A

X linked recessive

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

Pyruvate Kinase Deficiency (inheriatnce, features, treatment)

A
  • Autosomal recessive (but autosomal dominant has been observed with the disorder)
  • Clinical features: can be severe neonatal jaundice, splenomegaly, haemolytic anaemia
  • Treatment: most do not require treatment (can incl blood transfusion or splenectomy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how is sickle cell diagnosed ?

A

Diagnosis: sickle cells and target cells on blood film, sickle solubility test, Hb electrophoresis, Guthrie test (birth) to aid prompt pneumococcal prophylaxis (+FHx)

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

inheritance of factor 8 and fatcor 9 defiicney

A

X linkned recessive

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

diagnosis of haemophilia A?

A

Diagnosis: ↑APTT, normal PT and ↓ factor VIII assay.

24
Q

DVT prophylaxis:
*

A

Daily subcutaneous LMWH (prophylactic dose), TED stockings
o Note: Some DOACs are now licensed for DVT prophylaxis e.g. in post-op ortho patients

25
Q

Treatment of DVT/PE:

A

LMWH (treatment dose) followed by Warfarin or Apixaban/Rivaroxaban/Edoxaban (DOACs)

  • LMWH stopped once INR in therapeutic range (2-3) (with some DOACs LMWH can be stopped immediately)
  • Reason for continuing LMWH while warfarin started: Warfarin also affects protein C/S and often leads to procoagulant state in the first few days before anticoagulant effect

Duration of treatment:
* 3 months minimum
* For clearly provoked VTE consider stop at this point
* Unprovoked VTE needs anticoagulation for 6 months
* Otherwise, needs a clinical decision to be made: there are risk stratification tools used for this. Young men and patients with high baseline D-Dimer are at greater risk.
* Recurrent VTE usually needs lifelong treatment

26
Q

Warfarin mechnaism
*

A

Inhibits the vitamin K epoxide reductase enzyme responsible for regenerating the active form of vitamin K and therefore inhibits the synthesis of factors 2, 7, 9, 10 and proteins C, S and Z

27
Q

Heparin mechanism

A
  • Potentiates antithrombin III which inactivates thrombin, and factors 9, 10, 11
28
Q

haem changes in pregnancy

A

plasma volume increase
red cell mass increase
MCV increase
WCC increase

haemoglobin decrease
haematocrit decrease
platelets decrease

29
Q

Auer rods

A

acute myeloid leukaemia

Auer rods are cytoplasmic inclusions containing enzymes such as MPO

30
Q

t(9;22) BCR-ABL1 (Philadelphia chromosome)

A

chronic myleoid leukaemia

31
Q

massive splenomegaly in blood cancer what is it?

A

chronic myeloid leukaemia

32
Q

common mutation in CML

A
  • Ph+ve (Philadelphia chromosome) in 80% = chromosomal translocation (9;22)
    o Using FISH
  • PCR for BCR-ABL (Philadelphia Chr) fusion gene
    o Monitor disease and therapeutic response by monitoring BCR-ABL levels
33
Q

chemo for chronic myeloid leukaemia

A

Tx = imatinib (BCR-ABL tyrosine kinase inhibitor

34
Q

Richter’s transformation

A

– whereby CLL transforms to more aggressive large cell lymphoma

35
Q

smear cells

A

CLL

36
Q

staging for CLL

A

Binet Staging A, B & C (Rai Staging I-IV could also be used)
Stage A
o High WBC
o <3 groups of enlarged lymph nodes
o Usually no treatment required

Stage B
o >3 groups of enlarged lymph nodes

Stage C
o Anaemia or thrombocytopenia

37
Q

different types of non-hodgkins lymphoma and how aggressive / bad they are ?

A

o High Grade
Very Aggressive – Burkitt’s
Aggressive – Diffuse Large B-Cell, Mantle Cell

o Low Grade
Indolent – Follicular, Marginal Zone, Small Lymphocytic

  • HIGHER GRADE LYMPHOMAS ARE EASIER TO TREAT!
38
Q

staging of non hodskins lymphoma

A
  • Staging Lugano
39
Q

“Starry sky” appearance on blood film

A

burkitt’s lymphoma (non hodkins lymphoma)

NOTE: starry sky describes macrophages filled with cellular debris

40
Q

“Angular/
clefted nuclei”

A

Mantle cell lymphoma

41
Q

“Sheets of large lymphoid cells”

A

Diffuse Large
B-cell (DLBC)

42
Q

“Follicular pattern”
“Nodular appearance”

A

Follicular

43
Q

HTLV-1 infection

A

Adult T cell leukaemia/lymphoma

44
Q

lymphoma Associated with mycosis fungoides

A

Cutaneous T Cell Lymphoma

45
Q

t(8;14)

A

burkitts

46
Q

t(11;14)

A

mantle cell

47
Q

t(14;18)

A

follicular

48
Q

t(2;5)

A

anaplastic large cell lymphoma

49
Q

what is multiple myeloma - what proteins invovled ?

A

Multiple Myeloma: neoplasia of plasma cells (effector B cells antibodies) of BM.
Production of monoclonal immunoglobulin - “paraprotein” → IgG most common.
Middle-Aged to Elderly.
Increased incidence in Afro-Caribbeans.

50
Q

Myelodysplastic Syndromes

A
  • Characterised by: peripheral cytopenia; qualitative abnormalities of cell maturation; risk of AML transformation
  • Typically seen in the elderly; symptoms usually develop over weeks/months (incidental)
  • By definition all patients have <20% blasts (>20% blasts = acute leukaemia)

Clinical Features
* BM failure and cytopenias  infection, bleeding, fatigue
* Hypercellular BM
* Defective cells:
o RBCs e.g. ring sideroblasts (abn nucleated blast surrounded by iron granule ring)
o WBCs – hypogranulation, Pseudo-Pelger-huet anomaly (hyposegmented neutro)
o Platelets – micromegakaryocytes, hypolobated nuclei
N.B. In the exam – use an ‘investigative approach’ to pick out clues that lead to classification

51
Q

polycythaemia vera mutation

A

JAK2 (V617F).

52
Q

raised red cells causes ?

A

Primary causes:
* Polycythaemia vera
* Familial polycythaemia

Secondary causes ( EPO):
* Disease states (renal Ca), high altitude, chronic hypoxia e.g. COPD

Relative (Pseudo) Polycythaemia
Red cell mass normal but plasma volume is reduced.
* Dehydration, burns, vomiting, diarrhoea, cigarette smoking

53
Q

masive icnrease in platelets what is it ?

A

Essential Thrombocythaemia (or Thrombocytosis)

An MPD where megakaryocytes dominate the BM.
50% associated with JAK2.

Also associated with MPL mutation and CALR.
Clinical features
* Incidental finding in 50%
* Venous and arterial thrombosis (stroke & MI), gangrene and haemorrhage
* Erythromelalgia
* Splenomegaly, dizziness, headaches, visual disturbances
Investigations
* Platelet count >600x109
* Blood film – large platelets and megakaryocyte fragments
* Increased BM megakaryocytes (not reactive)

Treatment
* Aspirin
* Anagrelide – reduce formation of platelets from megakaryocytes
* Hydroxycarbamide

54
Q

TACO vs TRALI?

A

trali = fever, no heart failure, normal or negative fluid balance, no peripheral oedema

55
Q

trali what does it stand for ?

A

transfusion related acute lung injruy

56
Q

Taco what does it stand for ?

A

transfusion associated cirulatory overload

57
Q
A

Dylan's flashcards (14 decks)

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