Brainscape's Knowledge GenomeTM

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


See full index

Integrative > Anaemia & Abnormal Cell Counts > Flashcards

Anaemia & Abnormal Cell Counts Flashcards

1
Q

What are some of the abnormalities seen in red cells on histology?

A

Normal = RBCs have central pallor on blood film (no nucleus)

Spherocytes = no area of central pallor, smaller and denser

Acanthocytes = spiky appearance; usually reactive to something (i.e. not hereditary)

Target cells = central pallor and dark centre (“sombrero-shaped”); can be cause by liver disease, alcohol, thalasseamias

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

How are RBCs removed? Which RBCs are removed?

A

Reticuloendothelial system

  • removal of antibody-coated RBCs (e.g. autoimmune haemolytic anaemias, transfusion reaction)
  • removal of damaged RBCs (e.g. mechanically damaged by trying to bypass clots in DIC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why can splenomegaly cause anaemia?

A

RBCs spend more time in splenic circulation than systemic circulation

Increased breakdown of RBCs

Dilutional effect

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

Outline the cycle of RBCs. How can each step be affected?

A

Erythropoiesis —> bone marrow

Haemoglobin synthesis —> bone marrow

Bone marrow —> peripheral RBCs —> removal by reticulo-endothelial system (after 120 days)

Erythropoiesis inhibited by:

  • EPO deficiency
  • haematinic deficiency
  • bone marrow failure

Haemoglobin synthesis affected by:

  • thalassaemias
  • porphyrias
  • structural Hb variants

Structure of peripheral RBCs affected by:

  • hereditary elliptocytosis
  • hereditary spherocytosis

Metabolism in peripheral RBCs inhibited by:

  • G6PD deficiency
  • pyruvate kinase deficiency

Removal of RBCs stimulated by:

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

What are some of the functions of iron?

A

Formation of haemoglobin (oxygen transport to tissues)

Formation of myoglobin (oxygen use and storage in muscles; hence why iron deficiency causes muscle aches)

Formation of cytochromes (electron transport in cells)

Enzyme reactions

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

What are the reference ranges for anaemia?

A

Adult men = less than 130g/l

Adult women = less than 115g/l

Children = less than 110g/l

Newborns = less than 150g/l

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

What are some of the physiological adaptations to anaemia?

A

Increased cardiac output (increased stroke volume and tachycardia)

Increased EPO production (providing adequate renal function)

Shift in Hb-O2 dissociation curve

note: depends on age, severity, and speed of onset

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

What are the signs and symptoms of anaemia?

A
  • shortness of breath
  • weakness, lethargy, reduced exercise tolerance
  • palpitations
  • headaches
  • angina
  • heart failure
  • claudication
  • confusion
  • pallor
  • tachycardia
  • systolic flow murmur
  • koilonychia (iron deficiency)
  • glossitis (pernicious anaemia)
  • angular stomatitis (iron deficiency)
  • leg ulceration (chronic anaemia)
  • untreated thalassaemia —> expansion of bone marrow —> bossing and increased size of maxillary sinuses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some of the general causes of anaemia? How can these be differentiated by the FBC results?

A

Reticulocyte count

LOW (due to reduced Hb production)

  • haematinic deficiency
  • bone marrow failure (abnormal platelets and WCC)

HIGH (increased RBC removal)

  • bleeding
  • destruction (autoimmune or mechanical)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the appearance of reticulocytes on histology?

A

Hypochromic (pale) due to reduced iron

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

What is haematocrit?

A

Proportion of blood filled by RBCs

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

Give some examples of specific causes of anaemia with reticulocytosis.

A

Bleeding

Splenic sequestration

Haemolysis

  • hereditary (red cell membrane e.g. hereditary spherocytosis; red cell enzymopathies e.g. G6PD deficiency; abnormal haemoglobin e.g. sickle cell disease)
  • alloimmune (incompatible transfusion, haemolytic disease of the newborn e.g. Rhesus factor)
  • autoimmune
  • mechanical damage e.g. thrombotic thrombocytopenic purpura (TTP), haemolytic uraemic syndrome, microangiopathic haemolytic anaemia, mechanical heart valves, sepsis, malaria, hypersplenism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some important investigations to screen for haemolysis?

A

Blood film

  • ?spherocytes
  • ?schistocytes (red cell fragments)
  • ?polychromasia (increased no. of reticulocytes)

Direct Coombs test (look for Igs on RBCs)

Bilirubin

LDH (RBCs full of LDH, so haemolysis causes increased LDH in blood)

Haptoglobin (haem carrier protein which recovers free haem in blood; reduced haptoglobin in haemolysis as it binds to Hb and is removed)

Reticulocyte count

+/- haemosiderin

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

What are the causes of microcytic anaemias?

A

TAILS =

  • Thalassaemias
  • Anaemia of chronic disease
  • Iron deficiency
  • Lead and other heavy metal poisoning
  • Sideroblastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline the causes, investigations, and treatment of iron deficiency anaemia.

A

Causes:

  • inadequate iron intake
  • increased iron loss e.g. GI bleeding
  • increased iron use e.g. pregnancy

Investigations:

  • ferritin (acute phase protein; can also be raised in inflammation or malignancy)
  • serum iron
  • %transferrin saturation

Treatment:

  • oral iron supplements (3/day) taken with orange juice (vitamin C aids absorption)
  • OR IM/IV iron
  • transfusion can be used to temporarily improve oxygen carrying capacity (but does not treat iron deficiency)

note: Hb should increase by 20g/l in 3 weeks with increased MCV and serum ferritin

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

Give some examples of ADRs associated with oral iron supplements.

A

Black faeces

Constipation

Abdominal cramps

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

What are some of the causes of macrocytic anaemia? What is seen on histology?

A

Histology: hypersegmented neutrophils

Vitamin B12 deficiency (years)

  • vegans
  • gastric cause

note: treated with IM hydroxycobalamine

Pernicious anaemia (autoantibody to intrinsic factor)

Folate deficiency (months)

  • dietary (esp. alcoholics)
  • malabsorption
  • excess use (due to chronic haemolysis)
  • drugs e.g. anticonvulsants, cotrimoxazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some important investigations in macrocytic anaemia?

A

Check B12/folate

TFTs & LFTs (can be caused by hypothyroidism, liver disease, and alcohol)

Igs (myeloma)

?referral for bone marrow aspiration

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

What are some of the causes of normocytic normochromic anaemia?

A

Bleeding

Haemolysis

Anaemia of chronic disease

Iron deficiency or vitamin B12/folate deficiency (MCV is averaged out as normal; can identify RBC width distribution using blood film)

Bone marrow failure

Renal disease

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

Outline the pathophysiology of anaemia of chronic disease

A

Associated with chronic inflammation/infection

Cytokines drive increased hepcidin —> reduced iron absorption in gut —> recycled iron pushed into stores —> reduced [iron]serum (but normal or raised ferritin and normal %transferrin saturation)

Reduced EPO production

Reduced RBC lifespan

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

Give some examples of causes of neutrophilia.

A
  • INFECTION (most common)
  • drugs/reactive
  • acute haemorrhage
  • myeloproliferative disease e.g, CML
  • smoking
  • tissue damage
  • acute inflammation
  • cytokines e.g. G-CSF
  • metabolic/endocrine disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give some examples of causes of monocytosis.

A
  • chronic infection e.g. TB
  • chronic inflammatory conditions e.g. rheumatoid arthritis, SLE, Crohn’s, ulcerative colitis
  • carcinoma
  • myeloproliferative disorders/leukaemias
23
Q

Give some examples of causes of eosinophilia.

A
  • allergic disease e.g. asthma, eczema, urticaria, hayfever, aspergillosis
  • drug hypersensitivity e.g. penicillin
  • Churg-Strauss syndrome = diffuse vasculitic disease (small and medium arteries) associated with asthma
  • parasitic infection e.g. roundworm, tapeworm, flukes
  • skin disease e.g. bullous pemphigoid (chronic, autoimmune, subepidermal blistering)
  • Hodgkin’s lymphoma (reactive; not part of clonal cells)
  • other leukaemias/myeloproliferative disorders
24
Q

Give some examples of causes of basophilia.

A

REACTIVE:

  • immediate hypersensitivity reactions
  • ulcerative colitis
  • rheumatoid arthritis

PROLIFERATIVE:
- myeloproliferative disorders

25
Q

Give some examples of causes of lymphocytosis.

A
  • viral infections (esp. in children)
    REACTIVE:
  • bacterial infections (esp. pertussis)
  • stress related e.g. MI, cardiac arrest
  • splenectomy (lymphocytes usually pool in spleen —> circulate once asplenic)

LYMPHOPROLIFERATIVE:

  • chronic lymphocytic leukaemia (CLL)
  • lymphoma
26
Q

Give some examples of causes of thrombocytosis.

A

REACTIVE:

  • infection
  • inflammation
  • post-op
  • malignancy
  • bleeding
  • iron deficiency
  • splenectomy

PRIMARY HAEMATOLOGICAL DISORDERS:

  • essential thrombocythaemia
  • CML
  • polycythaemia rubra vera (myeloproliferative disorder)
  • myelofibrosis
27
Q

What is a leucoerythroblastic blood film appearance? What can it indicate?

A

Increased granulocyte precursors and nucleated RBcs

  • bone marrow infiltration (carcinoma or haematological malignancy)
  • sepsis/shock
  • severe megaloblastic anaemia (vitamin B12/folate deficiency)
  • storage disorders
  • primary myelofibrosis
  • AML/MDS
28
Q

What might the abnormal blood results be in renal disease?

A

RBCs:

  • anaemia = of renal failure, of chronic disease, blood loss, haematinic cause, cardiac cause, bone marrow infiltration
  • polycythaemia = post-renal transplant, renal tumour

WCCs:

  • high = inflammation, acute/chronic infection
  • low = sepsis, bone marrow infiltration

Platelets:

  • high = reactive, bleeding, iron deficiency
  • low = uraemia, drugs, haemolytic uraemic syndrome

note: anaemia is common in renal failure (CKD = 3+ indicated EPO + iron infusion)

29
Q

What might the abnormal blood results be in rheumatoid arthritis?

A

RBCs:
- anaemia = of chronic disease, blood loss, haematinic causes, immune-mediated, viral infection, etc.

WCCs:

  • high = inflammation, acute/chronic infection, drug reactions, etc.
  • low = sepsis, drugs e.g. methotrexate etc.

Platelets:

  • high = reactive, bleeding, iron deficiency related to NSAID use, etc.
  • low = drugs, immune, splenomegaly (Felty’s syndrome = triad of rheumatoid arthritis, neutropenia, and splenomegaly)
30
Q

What is thrombin burst?

A

Widespread activation of clotting factors once prothrombin (II) is converted to thrombin (IIa)

31
Q

How do the vessels damaged in trauma activate the clotting cascade?

A

Vasoconstriction

Production of von Willebrand’s factor

  • –> platelet adhesion
  • –> VIII protection

Exposure of collagen and tissue factor —> initiates activation of clotting factors

32
Q

What is the function of platelets when vessels are damaged by trauma?

A
  • adhesion to vessel wall at site of injury
  • secretion of ADP, thromboxane, and fibrinogen to encourage further aggregation
  • aggregation at site of injury —> platelet plug —> fuse together to improve stability
  • site for coagulation factor activation
  • secretion of some coagulation factors from internal stores
33
Q

Give some examples of vessel wall disorders. What are the signs and symptoms?

A

CONGENITAL:

  • hereditary haemorrhagic telangiectasia = autosomal dominant; dilated microvascular swellings increase with time; GI haemorrhage can cause iron deficiency anaemia
  • connective disorders e.g. Ehlers-Danlos

ACQUIRED:

  • senile purpura = weakened collagen with age (vessels more easily damaged)
  • steroids
  • infection e.g. measles, meningococcus
  • Henoch-Schonlein purpura = immune complex deposition in vessels —> extensive bruising (classically buttocks and extensor surfaces), joint swelling, haematuria, abdominal pain, renal failure
  • scurvy (vitamin C deficiency —> defective collagen production)

S&S:
- easy bruising due to spontaneous bleeding from small vessels (in skin +/- mucous membranes)

34
Q

Give some examples of platelet disorders. What are the signs and symptoms?

A

CONGENITAL:

  • Bernard-Soulier syndrome = autosomal recessive; deficiency of receptor for von Willebrand’s factor —> impaired platelet granule content release
  • von Willebrand’s disease = abnormal platelet adhesion to vessel wall and reduced amount and activity of factor VIII

ACQUIRED:

  • aspirin, NSAIDs, clopidogrel
  • uraemia
  • hypergammaglobulinaemia e.g. myeloma
  • myeloproliferative disorders

S&S:

  • skin and mucous membrane bleeding e.g. epistaxis, gum bleeding, bruising
  • prolonged bleeding after trauma e.g. menorrhagia, post-op, post-dental extraction
  • spontaneous joint or muscle bleeding (RARE!)
35
Q

Give some examples of coagulation factor disorders. What are the signs and symptoms?

A

CONGENITAL:

  • haemophilia A (factor VIII deficiency)
  • haemophilia B (factor IX deficiency)

ACQUIRED:

  • liver disease
  • vitamin K deficiency
  • warfarin

S&S:

  • recurrent haemoarthroses and muscle haematomas (COMMON!)
  • joint pain/deformity
  • prolonged bleeding post-dental extraction
  • life threatening post-op and post-trauma bleeding
  • intracerebral haemorrhage
36
Q

Give some examples of causes of bloody diarrhoea (dysentery).

A

Infectious:

  • CMV (owl’s eye appearance on histology)
  • Campylobacter jejuni
  • Salmonella
  • E. coli
  • Shigella
  • Clostridium difficile
  • Entamoeba histolytica
  • Schistosomiasis
  • Ebola

Autoimmune:

  • Crohn’s disease
  • ulcerative colitis

Colorectal cancer

Trauma

Iatrogenic:

  • chemotherapy
  • antibiotics
37
Q

Contrast blood transfusions and whole blood transfusions.

A

“Blood transfusion” = packed RBCs (no WBCs)

“Whole blood transfusion” = RBCs + WBCs + plasma + platelets

38
Q

What is haemosiderin? When is it elevated?

A

Ferritin + Haemoglobin (minus most Fe2+) stored in squamous cells and macrophages

NOT a good available supply of iron

Elevated in haemorrhage (phagocytosis of RBCs and haemoglobin by macrophages) and haemosiderosis (autoimmune or transfusion-related; accumulates excessively in other tissues e.g. lungs, liver, pancreas, kidneys)

39
Q

What treatment should take place prior to commencing chemotherapy?

A

Treat any present infections (IV antibiotics)

Screen for present/latent infections e.g. TB

Check baseline obs (LFTs, U&Es)

Ensure well hydrated

Obtain consent for (multiple) blood transfusions

Ask about freezing sperm/eggs (chemo will reduce fertility)

40
Q

What signs on examination of a patient with swollen joints may indicate the differential diagnoses?

A

Bruising (trauma, ?reduced clotting function)

Displaced limbs (?hip dysplasia, ?fracture, ?osteogenesis imperfecta)

Eczema (?associated rheumatoid arthritis)

Active bleeding sites e.g. gums (reduced clotting function)

Temperature of joints (hot joints —> ?septic arthritis)

41
Q

What are some important questions/examinations when establishing increased bleeding tendency?

A

?family history of haemophilias/thrombocytopenias

?frequent epistases

?menorrhagia

?joint swellings

42
Q

What are the possible causes of a raised APTT, and what does this indicate?

A

Raised activated clotting time

von Willebrand disease (deficient/abnormal vWf): von Willebrand’s factor is required to attract platelets to sites of damage (formation of platelet plug) and protect factor VIII from premature destruction (stabilisation)
—> mucosal bleeding

43
Q

What is more common: haemophilia A or von Willebrand’s disease?

A

Haemophilia A: 1/4,000 (0.0025%)

von Willebrand’s disease: 1%-2% (but some asymptomatic)

44
Q

What is INR? Why does it have no units?

A

Clotting time (prothrombin)

Ratio of patient’s prothrombin time to the norm (therefore can sometimes vary depending on what control value is used)

45
Q

Give some examples of causes of a raised INR but normal APTT.

A
  • warfarin
  • vitamin K deficiency
  • sepsis (—> DIC)
46
Q

Give some examples of causes of a normal INR but elevated APTT.

A
  • heparin

- isolated factor deficiency involved in intrinsic pathway e.g. haemophilia A

47
Q

Give some examples of causes of a raised INR and APTT.

A
  • liver failure (reduced production of all clotting factors)
  • DIC (clotting factors activated then used up)
  • isolated factor deficiency involved in common pathway
  • heparin overdose
  • warfarin overdose
  • dilutional
48
Q

Give some examples of causes of thrombocytopenia.

A
  • DIC (activates platelets but then uses them up)
  • drugs e.g. chemotherapy
  • haemolytic uraemic syndrome
  • HELLP syndrome (in pregnancy = Haemolysis, Elevated LFTs, Low Platelet count)
  • HIT (heparin-induced thrombocytopenia)
  • autoimmune e.g. SLE, rheumatoid arthritis, sarcoidosis
  • liver disease
  • post-transfusion
  • TTP (thrombotic thrombocytopenic purpura)
  • congenital e.g. Bernard-Soulier syndrome, Fanconi’s anaemia, von Willebrand’s disease
  • bone marrow disorders e.g. leukaemia, viral infections,
  • cardiopulmonary bypass
  • hypersplenism/splenomegaly
49
Q

Give examples of causes of DIC.

A
  • infection
  • malignancy
  • trauma (crush syndrome and burns)
  • connective tissue disorders e.g.
  • pregnancy complications e.g. placental abruption, amniotic fluid embolism, HELLP syndrome, severe hypertension of pregnancy
  • incompatible blood transfusion
  • heat stroke
  • dissecting aortic aneurysm
50
Q

What are the blood abnormalities in myeloma?

A

Plasma cell tumour —> synthesises monoclonal Ig or light chains (M-component/paraprotein)

  • usually elevated IgG
  • can be elevated IgA or Ig light chains (kappa or lamda)
  • elevated IgM commonly due to Waldenstrom’s macroglobulinaemia
  • plasma conc. of unaffected Igs is often markedly suppressed (immune paresis)
51
Q

What are the specific investigations for myeloma?

A

Electrophoresis = shows “M spike” due to increased abnormal Ig

Measure serum/urine levels of Ig by nephelometric method (measure water turbidity in sample using angled light) to calculate free:light chain (kappa and lamda) - tumour marker used to measure response to treatment

note: free light chains small enough to enter the urine - Bence-Jones protein

52
Q

What is monoclonal gammopathy of unknown significance?

A

Stable paraproteinaemia without immune paresis or symptoms of multiple myeloma/lymphoproliferative disease in elderly patients

53
Q

What are the specific investigations for pheochromocytoma?

A

Measure metanephrines (breakdown product of catecholamines) in plasma or 24hr urine collection

54
Q

What are the specific investigations for neuroblastoma?

A

Measure metanephrines (breakdown product of catecholamines), vanillylmendelic acid, and homovanillylmendelic acid.

Integrative (10 decks)

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