Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MD2 > Haematology > Flashcards

Haematology Flashcards

1
Q
  • Severe nose bleeds and post-surgery bleeding (predominantly mucosal bleeding)
  • Autosomal dominant inheritance
  • Mildly elevated APTT

What is the provisional diagnosis and what test would confirm this??

A

Mild type 1 vWF deficiency

Confirm via blood tests for:
vWF Ag levels
vWF activity or function tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  • X-linked inheritance
  • Characterised by joint bleeding! (often post-trauma)
  • Mildly elevated APTT

What is the provisional diagnosis and what test would confirm this?

A

Mild Type Haemophilia

Confirm via blood tests for factors 8 (deficiency=Type A) and 9 (deficiency=Type B)
And/or genetic tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • Bruising and petechiae on skin +/- Blood blisters on palate/mucosal surfaces, epistaxis, menorrhagia, GI bleeding, intracranial bleeding…
  • Previously well with no medications
  • Only abnormality on investigation is thrombocytopenia

What is the provisional diagnosis?
Treatment for this?

A

Immune Thrombocytopenia Purpura (ITP)

Diagnosis of exclusion!

Make sure to do FBE, blood film, U&Es, LFTs (can lead to renal failure), ANA, serology for EBV & CMV

Treatment:

  • High dose steroids
  • IV Ig if bleeding
  • Splenectomy if life-threatening bleeding
  • DO NOT give plts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  • Arterial or venous blood clots
  • Mixing study not correctable - what does this mean and what further bloods would you order for diagnosis?

What is the provisional diagnosis ?

A

indicating presence of an inhibitor rather than factor deficiency
-Blood tests positive for anticardiolipin and antiphospholipid Ab

Antiphospholipid syndrome (primary or secondary to SLE or induced by drugs such as Quinine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • HX severe trauma, obstetric complications, sepsis, allergic/toxic reaction, cancer
  • Investigations reveal: Low Hb and Plt; high APTT and PT; low fibrinogen; positive D dimer

What is the provisional diagnosis ? What is the underlying pathophys?

A

Disseminated Intravascular Coagulation

Widespread activation of clotting cascade results in formation of clots in microvasculature around body, leading to organ infarct and coagulation factor deficiency which leads to bleeding at other sites.

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

Causes microcytic anaemia

A

Iron deficiency (slow chronic bleed or nutrient deficiency)

Anaemia of chronic disease

Thalassaemia

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

Causes normocytic anaemic

A

Hypoproliferative

  • leukaemia
  • aplastic anaemia
  • pure red cell aplasia

Hyperproliferative

  • haemmhorage/bleed
  • haemolytic anaemia (sickle cell, thalassaemia, spherocytosis, G6DP deficiency, haemolytic uraemia, DIC, TTP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes macrocytic anaemia

A

Megaloblastic
-B12/folate deficiency

Non-megaloblastic

  • cirrhosis, liver failure
  • alcoholism
  • myelodysplastic syndrome
  • congenital bone marrow failure syndrome
  • myeloproliferative disorders
  • myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are 2 common causes of acute decline in CML?

A

Developing Largre B Cell lymphoma

Infection from immunocompromised state (few white cells)

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

Casues of mediastinal obstruction

A
  • Massive lymphadenopathy
  • Thyroid (neoplasm or goitre)
  • Thymus (neoplasm)
  • Teratoma (germ cell neoplasm)
  • Terrible lymphoma (lymphoma or lymphoblastic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the name of the cells characteristically found on Hodgkins lymphoma histopath?

A

Reed Sternberg cells.

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

35 year old female w erythema nodosum, SOB (CT chest shows pulmonary nodules)
What are 2 probable diagnoses and what histo path pattern would you see on biopsy?

A

Sarcoidosis or Tb.

Granulomatous inflammation on biopsy.

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

Pathophys of ITP

A

Patient develops autoantibodies for glycoprotines (Ag) on platelet membranes -> platelets targeted to the spleen for sequestration -> destroyed (phagocytosed) by mononuclear macrophages

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

Signs and symptoms of ITP

A

Petechiae and ecchymoses
Gingival bleeding
Haemorrhagic bullae
Occurs in otherwise healthy person (no splenomegaly, wasting, signs of chronic disease/infx)

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

MX ITP

A

Prednisone + IV Ig

DO NOT infuse platelets - they will be destroyed by immune response!

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

DDX for petechiae/purpura/ecchymosis

A
  1. Thrombocytopenia
    - ITP
    - Secondary to meds, leukaemia, SLE, APL syndrome, vWF deficiency
  2. Vascular disorders
    - Senile purpura, HTN, Henoch Schonlein purpura
  3. Coagulation problem
    - DIC or Scurvey
  4. MENINGOCCOCEMIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Extrinsic pathway:

  1. which blood test measures this?
  2. what drug acts on this pathway?
A
  1. INR /PT

2. Warfarin

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

Intrinsic pathway:

  1. which blood test measures this?
  2. what drug acts on this pathway?
A
  1. APTT

2. Heparin

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

What is primary haemostasis?

How do you test this?

A

Vasoconstriction, platelet adhesion and activation via binding vWF, and pletelet aggregation to form plug.

Triggered by exposure of collagen and subendothelial matrix from vessel injury

Test via platelet count.

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

WHat is secondary haemostasis and how do you test it?

A

Reinforcement of platelet plug by formation of fibrin meshwork via extrinsic and intrinsic pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does the extrinsic pathway differ from intrinsic pathway in how they start, and where do yhey join up with the common pathway?

A

Extrinsic: starts w tissue damage & exposure of Tissue factor

Intrinsic: starts with conversion of factor 12 to 12a

Common pathway: conversion of factor 10 to factor 10a

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

How long does clopidogrel stay in system for?

A

10-12 days. essentially a long-acting aspirin

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

What can you do for bleeding due to drugs?

  1. dabigatran
  2. warfarin
  3. clopidogrel/aspirin
A
  1. prothrombinex and activated factor 7
    + antidote for dabigatran
  2. give vitamin K, Or FFP and prothrombinex
  3. Give platelet transfusion (aspirin and clopidogrel affect platelets for extent of life span) and FFP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Differentials for abnormal bleeding

A 
Haemophilia A or B
vWF disorder
Other factor deficiency
Platelet disorder 
Anticoag/antiplatelet drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Investigations to order for bleeding disorders
FBE - plts, Hb Coags Factor VIII, IX levels (factor 8 levels give indicator of vWF levels; haemophilia A and B) vWF Ag vWF activity or function test Blood group (group 0 have lower levels vWF) Genetic studies
26
Type 1 vs Type 2 vWF deficiency
type 1- partial deficiency | type 2-complete vWF deficiency
27
Treatment for vWF disease
Treat only if symptomatic Desmopressin - releases stores of vWF and factor 8 OR replacement therapy (recombinant factor 8/vWFAg concentrate or recombinant vWF Ag or cryoprecipitate) Antifibrinolytics to symptomatically treat tranexamic acid
28
What are the hallmarks of haemophilia?
X linked (in males) Haemarthrosis Subcutaneous and intramuscular haematomas Poor wound healing Abnormal APTT but normal INR (factor 8 and 9 only involved in intrinsic pathway)
29
Treatment of haemophhilia
Replace factor 8 or 9
30
Treatment of DIC
Treat the underlying cause REsusitation and resp/circ support Cryoprecipitate - rich in blood factors
31
Causes of DIC
``` cancer obstetric complications massive tissue injury sepsis transfusion reaction Large aortic aneurysm Severe allergic/toxic reaction ```
32
Causes of B12 deficiency
Absorption of B12 requires gastric acid and IF 1. Atrophic gastritis (autoimmune - autoantibodies targeting IF) 2. Pancreatic failure 3. Post-gastrectomy -lack IF 4. Crohn's or resection of ileum 5. Coeliac 6. Vegan diet
33
What causes folate deficiency anaemia?
Alcoholics Malnourished patients Pregnancy
34
What is myelodysplastic syndrome? Who gets it and what might it progress on to?
Haemopoietic stem cell disorders resulting in ineffective production of one or more blood cell lines - fail to mature properly 90% cases over 60 May progress onto AML
35
What type of anaemia does myelodysplasic syndrome cause?
Macrocytic
36
Symptoms of anaemia
Fatigue, weakness Dizziness, syncome SOB, decr exercise tolerance Palpitations, tachycardia
37
THings to ask about on anaemia history
``` Bleeding, menstruation Systemic/chronic illness Family HX Medications (L-DOPA, penicillin, quininine, NSAIDs, paracetamol) Diet, alchohol ```
38
Clues to haemolytic anaemia
Incr red cell breakdown: - incr bilirubin, urinary urobilinogen - incr serum LDH Incr red cell production - incr reticulocytes Extravascular -splenomegaly Intravascular - incr free plasma Hb - decr plasma Haptoglobin - Haemoglobinuria (red-brown urine ) - haemosiderinuria (occurs after haptoglobin binding capacity is exceeded)
39
What is the most common leukaemia in children?
ALL
40
What is the most common acute leukaemia in adults?
AML
41
What is the most common leukaemia?
CLL
42
What syndrome is associated with ALL?
Down syndrome and Fanconi's anaemia
43
Acute vs chronic leukaemia pathophsy
Acute- overproduction of malignant IMMATURE WBCs (Blasts) Rapidly multiply in bone marrow, suppressing normal function and spill into blood crowing out healthy cells. CHRONIC: abnormal WBC blasts fail to die and accumulate in blood, bone marrow and related organs
44
What cells are affected by AML and CML?
erythrocytes, mast cells, thrombocytes (plt), basophils, neutrophils, eosinophils, macrophages and monocytes
45
What cells are affected by ALL and CLL?
ALL - B cells, T cells, NK cells | CLL- B cells mostly
46
What is myeloma?
Neoplastic disease of plasma cells (Ab producing mature B lymphocytes) Neoplastic plasma cells produce PARAPROTEIN (abnormal Abs consisting of light protein only)
47
SX of myeloma
Calcium levels high Renal failure - proteinuria Anaemia (tiredness and fatigue) Bony pain (back pain, fractures) - lytic lesions on x-ray (CRAB)
48
What is Lymphoma?
Neoplastic disease of mature lymphocytes in lymphoid tissue (lymph nodes, spleen, tonsils, MALT)
49
What is Leukaemia?
Acute - Neoplastic disease of IMMATURE cells (blasts) in bone marrow. affects myeloid or lymphoid progenitor cells Chronic - neoplastic disease of MATURE white blood cells in the bone marrow. Affects more mature cells You have too many WCCs but they are dysfunctional so immune function is impaired.
50
Which leukaemia might transform into which other leukaemia?
CML may transform into AML (blast crisis)
51
what is Myeloproliferative disease. name 3 examples
Neoplastic proliferation of platelets, RBCs or fibroblasts (everything other than WBCs) 1. RBCs: polycythaemia rubra vera 2. Plts: Essential thrombocythaemia 3. Fibroblasts: myelofibrosis
52
What is myelodysplastic syndrome?
Pre-cancerous disease of bone marrow here dysplastic cells may cause abnormal or inadequate blood cell production. May progress to acute leukaemia. Often occurring in old people. Often results in anaemia, thrombocytopenia, requiring regular blood transfusions.
53
How does MM lead to lytic bony lesions?
neoplastic plasma cells increase osteoclastic activity and reduce osteoblastic activity via secretion of inflammatory IL cytokines -> leads to bone breakdown and hypercalcacemia
54
What is the protein in the urine from MM called?
Benz Jones protein
55
How does MM lead to renal failure?
Paraprotein (M protein) or free light chains in blood can deposit in organs and cause dysfunction
56
Investigations for MM
BMAT Bone marrow biopsy Xray (osteoporosis) and CT (bony lesions) Blood and urine: - FBE - UEC and BUN - Electrophoresis looking for paraprotein and urinary Bence jones protein
57
What are Auer Rods a sign of?
AML (almost sounds like auer)
58
Which leukaemia is the philidelphia chromosome associated with and what does this indicate?
CML in all cases. ALL in some cases. Philadelphia chromosome: t(9,22) causing production BCR-ABL gene which makes tyrosine kinase enzyme which leads to CML Indicates good prognosis due to drug (TK inhibitors (imatinib) selectively kill CML cells)
59
Symptoms/signs of Leukaemia
- SX of anaemia - dizzy, SOB, fatigue, tachycardia etc (decr RBC) - Easy bleeding, bruising (decr Plts) - Freq infections, slow healing (defective WBCs) - Lymphadenopathy (lumps) - Hepatosplenomegaly - GUM HYPERTROPHY + bleeding WITH AML - MASSIVE splenomegaly with CML - Weight loss, night sweats with CML and CLL
60
Investigations for Leukaemia
Blood film FBE Coags Bone marrow aspirate
61
What leukaemia are smear/smudge cells (on blood film) associated with?
CLL.
62
Which leukaemia are more associated with old people?
CML and CLL.
63
What are reed-sternberg cells characteristic of?
Hodgkin's lymphoma
64
What does high LDH indicate in lymphoma, leukaemia?
High risk of CNS involvement and tumor lysis
65
How do you diagnose lymphoma?
Core or excision biopsy of lymph nodes (or other lymphoid tissue involved)
66
What is the Ann Arbour staging system used for? What are the stages and how do you determine this.
Hodgkin and non-hodgkin lymphoma Determine stage via CT/PET and BMAT 1. Confined to single lymph node region 2. 2/more nodal areas involved on same side of diaphgragm 3. Nodes on both sides of diaphragm involved 4. Spread beyond lymph nodes (liver, bone marrow etc) ◊ Every stage is either A: no systemic symptoms present other than pruritis B: systemic symptoms (fever, night sweats, weight loss) present Worse disease
67
How might Hodgkin's lymphoma present?
YOUNG person. Enlarged rubbery lymph nodes non-painful Becomes tender after drinking alcohol Systemic symptoms May get SVC obstruction SX from mass effect
68
What are examples of low grade (1) and high grade (2) non-hodgkin lymphoma Which has best cure rates?
Low grade: Follicular lymphoma -Indolent course but often wide-spread at diagnosis so non-curable. High grade: Diffuse large B cell lymphoma, Burkitt lymphoma -Best cure rates because more aggressive but treatable.
69
what is MGUS?
Low levels of serum monoclonal protein with NO EVIDENCE of end-organ damage (no CRAB)
70
When does myeloma become symptomatic?
>10% malignant monoclonal plasma cells in bone marrow and/or tissue biopsy Myeloma-related organ dysfunction (CRAB) present.
71
What will serum and urine electrophoresis in MM show?
□ Low IgG (2/3) and IgA (1/3) □ High serum free light chains (free kappa and free lambda) □ High paraprotein/M protein (Ig produced by a single clone of plasma cell) = “Bence Jones protein” in urine
72
Treatment of MM
Chemotherapy and radiation Bisphosphonates Transfusions and epo (anaemia) May need dialysis if end-stage RF
73
Anaemia with rouleaux on blood film with unexplained hypercalcaemia, renal failure and fracture/bony pain. What do you suspect?
Multiple myeloma

MD2 (16 decks)

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