Haematology Flashcards

1
Q

Hematocrit

A

Vol of RBC

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2
Q

Leukocyte function

A

Destroys microorganism at site of infection, found in buffy coat

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3
Q

Leukocytosis

A

Increase WBC count, normal response to stressor and can also occurs in leukaemia

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4
Q

Leukopenia

A

Decrease number of WBC, caused by radiation, chemo, SLE

decrease in response to infection as they are all in the same place

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5
Q

Eosinophil function

A

Destroys parasites in GI, ovary, uterus, spleen

For allergy, eczema, asthma

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6
Q

Eosinopenia

A

Decrease in Eosinophils in blood usually caused by stress, steroids, Cushing’s syndrome, shock, trauma, burns

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7
Q

Eosinophilia

A

High number of eosinophils in blood eg allergies, asthma, hay fever, drug allergies, dermatitis, HIV, parasitic infection, blood cancers

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8
Q

Basophil function

A

Involved in allergic reaction and inflammation

Release of histamine, large granules

1-2 days

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9
Q

Heparin function

A

Prevents clotting

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10
Q

Basopenia

A

Decrease basophils, seen in hives anaphylaxis, hyperthyroidism

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11
Q

Elements of blood (3)

A

Plasma 55%- water, proteins, salts

Buffy coat- wbc, platelets

Erythrocytes- RBC

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12
Q

Mast cell function

A

Found in tissue
Ige Receptor
Similar to basophils
Antibodies attach to mast cells release histamine when allergen encountered

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13
Q

Mastocytosis

A

Too many
Excessive histamine release
Increase itching, anaphylactic shock, pigmentosa

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14
Q

Neutrophil function

A
4-5 days 
50-70% of WBC
Phagocytic
Destroys harmful microorganism, foreign material
Acute inflammation- pus 
Antibacterial
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15
Q

Neutropenia

A

Decrease in neutrophil

Causes: cancer, radiation, haemodialysis

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16
Q

Neutrophilia

A

Increase neutrophils, occurs in first stage of infection if demand is high, immature ones will be released, maybe be because of appendicitis, malignancy and splenectomy

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17
Q

Monocyte function

A

Largest WBC
Phagocytic
Can change into dendritic/macrophages these cells then stimulate lymphocytes

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18
Q

Monocytosis

A

Increased monocytes caused by infection e.g leukaemia

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19
Q

Monocytopenia

A
Decreased monocytes 
Rare
E.g
Acute infection
Drugs
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20
Q

Dendritic cell function

A

Stimulates lymphocytes

Resides in lymph nodes, nose, lungs, stomach, intestines

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21
Q

Erythropoiesis

A

Production of RBC
starts as a stem cell
B2,9,12 cause cell maturity
The hormone EPO CONTROLS this process and produced mainly in kidney

It boost RBC
Delays fatigue
Increase aerobic capacity

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22
Q

Polycythemia

A

Increase in RBC due to drug doping or physiological factors such as altitude, hypoxic disease( COPD, hypoxic sleep apnoea) or genetics

Ss -headache
Vertigo 
Enlarged spleen
Liver
Itchiness
Red skin
Ringing in ears
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23
Q

What is anemia

A

Reduction in total number of erythrocytes
Decrease in quality and quantity of haemoglobin
decrease blood vol

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24
Q

Causes of Anaemia

A
Blood loss
Altered haemoglobin
Stem cell dysfunction 
Renal disease
Altered DNA synthesis 
Increase RBC destruction
Bone marrow infiltration
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25
Q

Iron deficiency anaemia

A

Most common
Common in women
Impairs o2 carriage
Due to haemorrhage, chronic infection, diet, diarrhoea, vomitting

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26
Q

Ss of Fe deficiency anaemia

A
Fatigue
Lethargy
Sob
Pale earlobes 
Impaired capillary circulation 
Difficulty in swallowing
Enzyme changes
Mental confusion
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27
Q

Pernicious anaemia

A

-Caused by B12 deficiency, impaired uptake
Maybe be genetic, autoimmune factors, gastrectomy, pancreatitis

Due to lack of intrinsic factor in gastric mucosa
Cannot bind to B12 to protect it
DNA synthesis impaired

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28
Q

Ss of pernicious anaemia

A

Mood swings
Memory loss
Psychosis
Can lead to death

29
Q

Macrocytic anaemia- folate deficiency

A

Folic acid deficiency which is important for RBC development
Absorption in upper GI
Stored in liver, more easily depleted than B12

30
Q

Thalassaemia

A

Inherited autosomal recessive blood disorder,
Originated in Mediterranean region
Variant/missing genes- affects haemoglobin production

31
Q

Beta- thalassaemia

A

Too little of one type of chain and excess of non- deficient chains

Defective haemoglobin
Extra chains aggregate within cells and make them prone to haemolysis or destruction in the bone marrow

Can be
Minor- a symptomatic normal life expectancy, one chain

Intermediate- manage normal life, occasional transfusion, 2 chains

Major- two mutations, impairs growth, skeletal abnormalities, bronze colours skin, change in gonads

32
Q

Alpha- thalassaemia

A

Deficient/absent in alpha chains( excess beta)

Variety of clinical syndromes depending on how many genes are defective

Common in Asian/African population

33
Q

Types of alpha- thalassaemia

A

Silent- no anaemia, no tx

Minor- minimal/absent anaemia, no symptoms, no tx required

Hb H disease- common in Asian populations 
3 alpha genes deleted
Abnormal red cells 
Breakdown of RBC 
TX- folate 

Hb Barts Hydrops foe tails- all 4 alpha genes deleted, high oxygen affinity, cannot release oxygen

34
Q

Definition of bleeding

A

Loss of blood escaping from circulatory system

Internal- blood vessel
External- mouth, nose, ear, vsgina, anus,skin break

35
Q

Classes of bleeds

A

Class 1- 15% of blood vol eg subconjunctival hemorrhage

Class 2- 15-30% of blood vol eg stomach cancer, bleeding

Class 3- 30-40% of blood vol eg pulmonary hemorrhage

36
Q

Causes of bleeding

A

Traumatic injury
Medical condition
Intravascular changes- within vessel
Intramuscular- changes of wall within vessels
Extravascular: changes outside blood vessels

37
Q

Haemostasis

A

Stopping or controlling of bleeding

VASOSPASM- construction of blood vessels, first response to injury, chemicals released by endothelial cells and platelets

FORMATION OF PLATELET PLUG

ACTIVATION OF COAGULATION CASCADE- platelets adhere to site of vascular injury, clotting factor released, fibrinogen-fibrin strands precipitate, form clot)

FORMATION OF CLOT

CLOT RETRACTION- shrinking of clot, pull edges of wound together. Occurs due to: contraction of platelets, intergrins anchor platelets to fibrin threads

CLOT DISSOLUTION

38
Q

Mast cell function

A

IgE receptor
Found in tissue
Antibody attaches to mast cell and mast cells release histamine when allergen encountered

39
Q

Mastocytosis

A

Too many mast cells
Excessive histamine release
Increased itching

40
Q

Neutropenia

A

Decreased neutrophils

Causes include cancer, haemodialysis, radiation

41
Q

Neutrophil function

A

50-70% of WBC
destroys harmful micro organisms, foreign material
Acute inflammation, pus

42
Q

Neutrophilia

A

Increased neutrophils
Occurs in first stage of infection, if demand is high immature ones will be released

May be because of appendicitis, malignancy, splenectomy

43
Q

Monocytes function

A

Largest WBC
moves to site of infection and increase in size
Change into dendritic/macrophages
APC Cells stimulate lymphocytes

44
Q

Monocytosis

A

Increase in monocytes

Caused by infection, leukaemia, autoimmune, neutropenia

45
Q

Monocytopenia

A

Decreased monocytes, rare

46
Q

Dendritic cell function

A

Stimulates the immune system

Reside in lymph nodes, nose,lungs,stomach,intestines

47
Q

Erythropoiesis

A

Production of RBC
starts from a stem cell
B2,9,12 stimulates cell maturity

The hormone EPO controls Erythropoiesis

Production mainly in kidneys

EPO - boosts RBC

  • increased aerobic capacity
  • delays fatigue
48
Q

Polycythemia

A

Increase in RBC
due to drug doping,physiological factors such as altitude, hypoxic disease (COPD), genetics, disease related ( abnormal bone marrow

Ss headache, vertigo, enlarged spleen, liver, itchiness, red skin, ringing in ears

49
Q

Anaemia definition

A

Reduction in total number of erythrocytes
Decrease in quality and quantity of haemoglobin
Decrease in RBC vol

50
Q

Causes of Anemia

A
Blood loss
Altered haemoglobin synthesis
Stem cell dysfunction
Renal disease
Decrease production of RBC
altered DNA synthesis
Increased RBC destruction 
bone marrow infiltration
51
Q

Iron deficiency anaemia

A

Most common, and in women
Impairs 02 carriage

Due to haemorrhage, diet,diarrhoea, vomiting, chronic infection

Ss: fatigue, lethargy, SOB, pale earlobes, difficulty in swallowing, enzyme changes, mental confusion

Ss fatigue , lethargy, SOB, pale earlobes, sore tongue, difficulty in swallowing, mental confusion, memory loss, increase infection

52
Q

Pernicious anaemia

A
  • Cause by vit B12 deficiency, impaired uptake of Vit B 12

- genetic ,autoimmune factors, gastroectomy, pancreatitis may be involved

53
Q

Macrolytic anaemia- folate deficiency

A

Folic acid deficiency- important for RBC development

Absorption in upper SI

54
Q

Normocytic Anaemia- increase RBC destruction

A

Increase in haemolysis

Can be caused by trauma, infection, sickle cell

55
Q

Thalassaemia

A

Inherited autosomal recessive blood disorders
Originated in Mediterranean region
Weakening and destruction of RBC
variant/ missing gene which affect haemoglobin production

56
Q

Beta- Thalassaemia

A

Too little of one type of chain and excess of non-deficient chains
Defective haemoglobin
Extra chains aggregate within cells and make them prone to haemolysis or destruction in bone marrow/spleen

57
Q

Types of beta Thalassaemia

A

Minor- a symptomatic, normal life expectancy
Intermediate- manage normal life, occasional transfusions, two chains have mutation
Major- two mutations, impairs growth, skeletal abnormalitites, bronze coloured skin, progresses to death

58
Q

Alpha Thalassaemia

A

Deficient/absent in alpha chains, excess beta
Variety of clinical syndromes depending on how many genes are defective
Common in Asian, African populations

59
Q

Types of alpha Thalassaemia

A

Silent- no anaemia, no Tx

Minor- minimal/absent anaemia, no symptoms/Tx

Hb H disease- 3 alpha genes deleted, abnormal RBC cells, break down of RBC, Mid-life threatening

Hb Barts Hydrops foe tails( major)- all 4 alpha genes deleted
High oxygen affinity, cannot release oxygen

60
Q

Causes of bleeding

A
Traumatic injury
Medical conditions
Intravascular changes
Intramuscular changes 
Extravascular changes
61
Q

Haemostasis

A

Vasospasm- constriction of blood vessels, first response to injury, chemicals released by endothelial cells and platelets

Formation of platelet plug

Activation of coagulation cascade-platelets adhere to site of vascular injury,clotting factor released, fibrinogen-fibre strands precipitate, form clot

Formation of clot

Clot retraction- shrinking of clot, pull edges of sound together occurs due to contraction of platelets, intergrins anchor platelets to fibrin threads

Clot dissolution (fibrinolysis)

62
Q

Haemophilia

A

A-genetic deficiency in clotting factor VIII, increased bleeding, inherited x linked, can lead to joint deformity

B- deficiency of IX, X linked recessive, several mutations, effects ranging from a symptomatic to severe haemorrhage
Ss: unexplained excessive bruising, blood in faeces, pooling of blood, prolonged bleeding from cuts

C- herditary deficiency of factor XI,milder disease

63
Q

Leukaemia

A

Cancer of WBC
Affects ability to produce normal blood cells
Bone marrow makes abnormally large number of immature WBC

SS: weight loss, SOB, pain/bone tenderness, muscle weakness, fatigue, loss of appetite, night sweats, easy bruising/bleeding

Causes: radiation, chemicals,viruses, mostly unknown, genes

64
Q

Acute leukaemia

A

Rapid increase in the number of Immature blood cells
Immediate treatment required due to rapid progression and accumulation of malignant cells
Most common form in children
Can kill you fast

2 forms
Acute lymphoblastic leukaemia
60% of cases, overproduction of immature WBC, common in kids
Ss: growth failure, fever, anaemia,bleeding

Acute mylenogenous leukaemia
Overproduction of immature WBC
More common in adults, 3 subtypes
Ss: anaemia, fever,bleeding

65
Q

Chronic leukAemia

A
Excessive build up of relatively mature, but still abnormal WBC
takes month to years to progress
Mostly I'm older people
High white blood cell count
Kills you slowly

Chronic lymphoblastic leukaemia
Very close growing
Incurable
Treatment based on age and presentation

Chronic mylenogenous leukaemia
Increased proliferation of the granulocytic cell without the loss of their capacity to differentiate
Increase mylenoid, erythroid, platelets in blood
Originates in a single abnormal stem cell

66
Q

Leukaemogenesis

A

The development of leukaemia

67
Q

Lymphoma

A

Cancer of lymphatic system- lymph nodes,spleen, thymus,tort tissue
Tend to be solid tumours

68
Q

Non-hodgkins lymphoma

A

Risk factors
Environmental agents e.g radiation
Inherited genetic abnormalities
Males, >50

Ss
Fever, night sweats, weakness
Weight loss
Abdo pain
Eosinophilia
Lymphadenopathy
69
Q

Hodgkin’s lymphoma

A

Cancer originates from lymphocytes
Characterised by the orderly spread of disease from one lymph node group to another

Ss: enlarged painless mass in neck, skin lesions, itching, scratching, body weight loss

Treatment
Chemo, radiation, stem cell transplant