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Clinical Haematology Flashcards

Week 4 (87 cards)

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1
Q

What are 4 lab tests involved in clinical Haemotology?

A

Reticulin stain
flow cytometer
blood smear
bone marrow smear

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2
Q

What does a reticiulin stain do?

A

shows Reticulocytes and polychromatic EBs as blue

Reticulocytes should be greater than 100

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3
Q

When …. and/or … are low = anemia diagnosis?

A

Hb and/or HCT/PCV

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4
Q

What 2 anaemia have normal looking RBCs?

A

Acute bleeding
hypoplastic/aplastic

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5
Q

What type of anemias are due to nutrient deficiency and what are the deficient in?

A

Iron Deficiency

Megaloblastic

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6
Q

What is the deficiency and pathogenesis of Common Microcytic anemia?

A

Iron deficiency

Patho
Decreased Hb and cytoplasm –> smaller RBCs (normal number) = hypochromic and microcytic RBCs

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7
Q

What is the morphology of RBCs with microcytic anemia and what are the clinical features?

A

Morphology
microcytic, hypochromic, normal WBCs and PLTs, pencil cells

Clinical features
Koilonychia, glossitis, stomatitis

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8
Q

What is the cause and pathogensis of Megaloblastic anemia?

A

Caused
folic acid and folate deficiency
cancer/ GIT disorders

Patho
decreased V B12 + folate = decreased DNA synthesis = Decreased divisions = large, nucleated hematopoietic cells

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9
Q

what is the morphology and clinical features of megaloblastic anaemia?

A

Morphology: normochromic but macrocytic, hyper- segmented neutrophils, MCV greater than 110, increased MCH

Clinical features: mild jaundice, glossitis stomatitis and cheilitis.

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10
Q

Defintion of:

a) glossitis

b) Stomatitis

c) Cheilitis

A

Glossitis = inflammation of the tongue

stomatitis = inflammation of the membrane around the mouth

cheilitis inflammation of lips

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11
Q

What type of anemias can occur due to hemopoietic cell defects?

A

Anaemia of chronic disease (ACD)

Aplastic Anaemia

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12
Q

What are the causes and clinical features of Aplastic Anaemia?

A

Caused by: Bone marrow failure from drugs, autoimmune or viral infections

Clinical features: anaemia , infections and bleeding

Weakness, pallor, dyspnoea, thrombocytopenia, neutropenia

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13
Q

What are the two major types of Haemolytic anemias? what are their three subtypes?

A

Acquired (Ext)
Autoimmune
Drugs
Infections

Congenital (Int)
Defective membrane
Defective Hb
Defective enzyme

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14
Q

What defect produces hereditary spherocytosis?

A

Membrane defecetive

Gradual loss of ankyrin and spectrin with ageing of the RBCs → small spherocytes
- lysed in the blood or phagocytised by splenic macrophages

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15
Q

Example of a disease caused by Defective membrane.

A

Hereditary Spherocytosis:

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16
Q

Example of disease casued by defective Hb (Haemolytic Anaemia)

A

Sickle cell
thalassemia

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17
Q

Example of disease caused by defective enzyme (haemolytic anaemia)

A

G6DP deficiency

= vulnerable to oxidative stress

= blister cells, Heinz bodies, episodic haemolysis splenomegaly and gall stones.

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18
Q

Clinical features of extravascular haemolytic anemias.

A
  • marrow expansion (response to RBC loss)
  • hemolytic jaundice (unconjugated bilirubin)
  • bilirubin gallstones + cholecystitis
  • splenomegaly
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19
Q

Clinical features of Intravascular Haemolytic anemias

A

decreased haptoglobin (free Hb carrier protein)

  • hemoglobinuria (kidney failure)
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20
Q

How is bilirubin normally metabolised?

A

unconjugated bilirubin → liver (glucuronide conjugation = soluble) → intestine (oxidised to urobilinogen)

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21
Q

Hemolytic jaundie (what)

A
  • unconjugated hyperbilirubinemia
  • urine and stool normal
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22
Q

Hepatic Jaundice

A
  • mixed conjugation hyperbilirubinemia
  • dark urine and normal/ pale stool
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23
Q

Obstructive/ posthepatic jaundice

A
  • conjugated hyperbilirubinemia
    • dark urine and pale stool
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24
Q

What is the Leukemoid reaction and what is it caused by?

A

Increased WBCs with many immature forms

Due to severe trauma, infections and septicaemia

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25
What is Leukaemia and what is its most common type?
Cancer of bone marrow blast cells Chronic Lymphocytic Leukaemia (CLL)
26
What are the three consequences of decreased Normal haematopoiesis
-decreased erythropoiesis ∴ anemia decreased leukopoiesis = infections decreased thrombopoiesis = bleeding
27
What are the clinical features of Leukaemia?
Bone marrow expansion Splenohepatomegaly Lymphadenopathy ( more common in lymphoid cancer)
28
What are the 4 types of leukaemia?
Acute lymphatic Chronic lymphatic acute myeloid Chronic myeloid
29
What are the clinical features and common patient age of Acute Lymphatic Leukaemia?
Anaemia, bleeding, infections Hepatosplenomegaly and lymphadenopathy Children
30
What are the clinical features and common patient age of Chronic Lymphatic L
Anaemia, bleeding, infections Hepatosplenomegaly and lymphadenopathy >70yrs
31
What are the clinical features and common patient age of Acute myeloid L
Anaemia, bleeding infections Hepatosplenomegaly Rare LD Adults
32
What are the clinical features and common patient age of Chronic Myeloid L?
Hepatosplenomegaly Adults
33
lymphadenopathy
swollen or enlarged lymph nodes
34
Hepatosplenomegaly
Enlarged liver
35
Multiple Myeloma
Cancer of MATURE B lymphocytes, bone marrow and lymph nodes CF: multiple lytic bone lesions (fractures), infections. Hypercalcemia and renal failure.
36
Multiple myeloma vs Leukaemia?
Both blood cancers M= affects plasma ells L= affects IMMATURE blood cells
37
What are myeloproliferative disorders?
blood cancers that occurs when bone marrow produces too many RBCs, WBCs or PLTs - pre-leukemic conditions
38
What are the clinical features of Myeloproliferative disorders?
Hypercellular bone marrow Hepatosplenomegaly Red skin
39
what are the subtypes of myeloproliferative disorders? and their associated cells?
Polycythemia rubra vera RBCs CML WBCs Essential Thrombocythemia PLTs Myelofibrosis Fibroblasts
40
Hodgkins vs non Hodgkins lymphoma.
H= Reed Sternberg cell + all B cell lymphomas Non H= no RS cells + most commonly B cell lymphomas
41
Burkitts Lymphoma
Non Hodgkins Caused by EBV in children Affactes mandible/maxilla
42
What are the three classifications of Anemia according to morphology?
Microcytic Macrocytic Normocytic
43
Describe microcytic anemias (2)
Defective heme synthesis - Iron deficiency – most common * Defective globin chain - Thalassemia
44
What is Macrocytic and what are its 2 subtypes/
Larger than normal red cells and MCV >100 fL Megaloblastic – Large nucleated red cell precursors Non-megaloblastic – Large nucleated red cells with normal DNA synthesis
45
What are the two subtypes of normocytic anemia w abnoral shapes?
Haemolytic (Hereditary spherocytosis, sickle cell disease) Nonhemolytic (Blood loss, aplastic anemia, anemia of chronic disease)
46
Cause and pathophysiology of Pernicious Anemia
Vitamin B12 deficiency Cause: Autoantibodies against intrinsic factor and gastric parietal cells  Patho: decreased intrincic factor --> decreased Vit 12 absorption --> decreased DNA synthesis for RBCs
47
Cause, patho and histo of Sickle Cell Anemia
Cause: inherited mutation of B-globin in HbS Patho: single amino substitution of B-globin. Deoxy HbS self-associates w polymers and completely replaces HbA. Histology: elongated, crescentic or sickle shaped RBCs. Rapid Haemolysis.
48
morphology and clinical features of thalassemia
Morphology: Microcytic and hypochromic, poikilocytosis, anisocytosis and target cells have increased SA = cytoplasm in a dark red puddle. Clinical features: splenomegaly, hepatomegaly and lymphadenopathy.
49
What is Leukopenia
Reduced WBC count (<4000/uL)
50
What can cause Neutropenia?
marrow hypoplasia (chemo/ aplastic anemia), extensive replacement of marrow by a tumour (leukaemia) Neoplastic proliferation of cytotoxic T cells and natural killer cells.
51
Cause and cases of Neutrophilic Leukocytosis
Acute bacterial infections sterile inflammation (tissue necrosis
52
Causes of Eoisinophilc Leukocytosis
Allergic disorders (asthma, hay fever, allergic skin diseases) Parasitic infestations; drug reactions and hodgkin/ non H lymphomas
53
Cause and cases of Basophilic Leukocytosis
Rare - often indicative of a myeloproliferative neoplasm (chronic myeloid leukemia)
54
Cause and cases of monocytosis
Chronic infections (tuberculosis), bacterial endocarditis, and malaria; collagen vascular diseases and IBD
55
Cause and cases of lymphocytosis
Associated with chronic immunologic stimulation (tuberculosis, brucellosis); viral infections (Hep A)
56
What are the 4 main clinical features of Bleeding Disorders
Petechiae Purpura Echymoses Hematoma
57
What is Petechiae and what is it caused by?
Nopalpable, red, pinpoint macules Capillary inflammation and hemorrhage
58
What is Prupura and what is it caused by?
Purple red, cutaneous or mucosal lesion (0.2-1cm) extravastation of blood to skin or mucous membrane
58
What is Echymoses and what is it caused by?
bruise collection of blood under skin from extravastation of nearaby blood vessels
59
What is hematoma and what is it caused by?
collection caused by bleeding into SubCut tissue, muscle,, organ tissue or cavity
60
What are acute clinical manifestations of Anaemia?
SoB, Organ Failure and shock
61
What is the impact of: a) Less Hb b) increased Resp drive c) increased sympathetic stimulation
a) pale, glossitis b) SoB and tachypnoea c) tachycardia
62
What is the impact of: a) cerebral hypoxia b) generalised hypoxia c) myocardial hypoxia
a) dizziness and light headaches b) extreme tiredness/ fatigue b) chest pain in severe anaemia
63
describe the pancytopenia in Megaloblastic anaemia.
Pancytopenia: increased MCH, decreased leucocytes and PLTs
64
Describe the intrinsic and extrinic pathways of Aplastic Anaemia
Extrinsic Immune-mediated suppression of marrow progenitors Intrinsic Abnormality of stem cells
65
What is the primary polycythemia n known as?
Polycythemia vera
66
Polycythemia vera
increased RC mass from autonomous proliferation of erythroid progenitors from a gain of function mutation on JAK2 gene
67
Describe Secondary Polycythemia
Excessive proliferation from elevated levels of EPO due to: lung disease, high-altitude living or EPO secreting tumours
68
Neutropenia (what and cause)
reduction in No. of granulocytes severe= agranulocytosis Cause Decreased granulocyte production (marrow hyperplasia, extensive replacement of marrow by tumour) increased granulocyte destruction
69
Outline the pathophysiology of Leukemia
uncontrolled proliferation of Leukemic blasts decreased normal blood production anaemia, leukopenia and thrombocytopenia
70
Differentiate between superficial bleeding and deep bleeding
S= bleeding disorder (pri Haemostasis) D= coagulation disorder
71
What are the 4 disorders of Haemostasis?
1. vascular 2. PLT disorders 3. Coagulation disorders 4. Mixed haemostatic disorder
72
what is secondary thrombocytopenic purpura due to?
Drug admin (asprin) Decreased PLT production (leukemia, aplastic anaemia) Large amount of Destruction of PLTS(hypersplenism)
73
What are the lab findings in Immune Thrombocytopenia Purpura
Thrombocytopenia, giant immature PLTs, PT and PTT normal, increase in megakaryocytes
74
What are the three types of VWF disease
TI: Most common= reduced vWF TII: Dysfunctional vWF TIII: Complete absence of vWF and FVIII
75
Lab diagnosis of vWF disorder
normal PLT number, prolonged PTT (VIII), prolonged PT
76
Characteristics of Haemophilia
Deep bleeds within joints Spontaneous hemorrhage, recurrent bleeds and easy bruising
77
Lab findings in Haemophilia
Increased aPTT, low FVII/FIX
78
Describe Disseminated Intravascular COagulation
- systemic activation of extrinsic cascade - PLTs and Coagulation factors consumed - fibrinolysis activated
79
What are the two overall causes of DIC?
a) release of tissue Factor or thromboplastic substances (extrinsic) b) Widespread endothelial cell damage
80
Lab diagnosis of DIC
increased a PTT and PT decreased FI increased Bleeding Time decreased FV and VIII
81
explain chronic Disease anemia and what class it is
Haemopoietic in chronic conditions chemical signals mess with bone marrow = harder to make RBCs, RBCs live shorter and harder for the body to use iron to make RBCs.
82
How can you distinguish between a pri / sec haemostatic disorder by looking at the lab findings?
Pri= PLT disorder or vascular with increased bleeding Sec= PT or aPTT will be affected
83
Morphology of Pernicious anaemia
Megabolstic anaemia - macrocytic, poikocytosis and anisocytosis
84
How can you distinguish between Vitamin K deficiency, liver disease, and disseminated intravascular coagulation (DIC)
VK= PT and INR affected, corrected with Vit K LD: some coagulation parameters affected (aPTT, PT, INR and some variability in PLTS) DIC= ALL coagulation parameters affected. elevated D-dimer, decreased fibrinogen
85
Pathophysiology of Haemophila B
Mutation on FIX --> IXa work with VIIIA to produce X in intrinsic --> reduced intrincic pathway --> impacts common pathway --> decreased throbin --> failure to produce stable clot
86
what are two hallmark findings in aplastic anameia?
hypocellular bone marrow and a decrease in all hematopoietic cells

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