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HYMS Y1 > Block 4 W1 > Flashcards

Block 4 W1 Flashcards

1
Q

What is the composition of blood?

A
  1. Liquid composition - 55% plasma

2. Formed elements - 45% RBC + WBC + platelets

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2
Q

Outline the components of plasma.

A

92% water
7% plasma proteins - albumin, globulins
1% other substance - electrolytes, hormones, nutrients

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3
Q

Describe the function of plasma.

A

ECM of blood - keeps blood cells in suspension.

Serum is plasma devoid of clotting factors.

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4
Q

Where is the site of haematopoiesis prenatally?

A

Yolk sac -> liver and spleen

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5
Q

Where is site of haematopoiesis post-birth?

A

Bone marrow

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6
Q

How is haematopoiesis controlled?

A

By environment within bone marrow i.e. stromal cells and growth factors and cytokines:

  • EPO, erythropoietin - RBC
  • TPO, thrombopoietin - platelets
  • Interleukin, G-CSF, GM-CSF and SCF - WBCs
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7
Q

Where is the site of erythropoiesis?

A

Bone marrow - 2.5x10^6 new RBC/sec

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8
Q

How is erythropoiesis initiated?

A

Hypoxia detected by kidney -> releases EPO into blood -> binds erythropoietin receptor on progenitor cells.

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9
Q

Describe the process of erythropoiesis.

A

Multipotent stem cell -> common myeloid progenitor -> proerythroblast -> phase 1 ribosome synthesis (basophilic erythroblast) -> phase 2 haemoglobin accumulation (polychromatic erythroblast) -> phase 3 nucleus rejection (orthochromatic erythroblast) > reticulocyte -> erythrocyte.

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10
Q

Describe haemoglobin.

A

4 global polypeptide chain - 2alpha and 2beta -> each associated with haem.
HB - binds O2 for transportation and CO2 for removal.

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11
Q

Describe haem.

A

Porphyrin ring + iron molecule as cofactor.

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12
Q

Describe structure and function of erythrocytes.

A

RBC
Bi-concave, no nucleus for optimal O2 function and flexibility.
Lifespan - 120 days
Damaged cells removed by macrophages in spleen.

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13
Q

Describe structure and function of thrombocytes.

A

Platelets
Small, no nucleus
Initiates blood clotting at site of injury.
Lifespan - 7-10 days

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14
Q

Describe thrombopoiesis.

A

10^11 made/day
1 megakaryocyte generates 5000 platelets -> fragment to make platelets.
30% stored in spleen.

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15
Q

Where is TPO made?

A

Liver and kidney

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16
Q

List innate immune cells.

A 
Neutrophils 
Eosinophils
Basophils
Monocytes
NK cells
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17
Q

Describe neutrophils.

A

Lifespan - 5 days
60-70% of WBC (most common)
Phagocytes - ingest and kill pathogens and damaged cells. Initiate inflammatory process.

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18
Q

Describe eosinophils.

A

Lifespan - 2-5 days
0.2%
Phagocytic against helminths

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19
Q

Describe basophils.

A

Lifespan - 1-2 days
0.2%
Allergic reactions

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20
Q

Describe monocytes.

A

Lifespan - 1-7 days
2-10%
Phagocytic and differentiate to become macrophages.

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21
Q

Describe natural killer cells.

A

Lifespan - 14 days
15%
Kill virally infected cells

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22
Q

Describe lymphocytes.

A

Adaptive immune cells
T and B cells
Lifespan - weeks to years
20-40%

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23
Q

Describe haematocrit test.

A 
Separates blood into 3: plasma + WBC and platelets + RBC
F = 37-47%
M = 42-52%
Reduced - anaemia
Increased - polycythaemia
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24
Q

Define polycythaemia vera.

A

Primary form of myeloproliferative disorder.
Increased Hb, PCV and RBC.
95% due to mutations in JAK2 gene.

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25
Q

Define essential thrombocythaemia.

A

Secondary form of myeloproliferative disorder.
Normal Hb and WBC but increased platelets.
JAK2 mutations.

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26
Q

Define myelofibrosis/myelosclerosis.

A

Elevated WBC and platelet count.

JAK2 mutations.

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27
Q

How does JAK2 gene mutation cause myeloproliferative disorders?

A

Janus kinase 2 acts in signalling pathway downstream of EPO and TPO receptors.
Point mutation -> constitutively activates receptors in absence of EPO.

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28
Q

What are the treatments of polycythaemia?

A
  1. Venesection
  2. Chemotherapy - hydroxycarbamide
  3. Low dose aspirin
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29
Q

What is the ABO blood group?

A

2 antigens on surface of RBCs determines a persons blood type.

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30
Q

What are A and B antigens?

A

Carbohydrate structures present on RC membrane glycoproteins and glycolipids.

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31
Q

What are the major carriers of A and B antigens?

A 
N-glycosylated glycoproteins
Anion exchanger
Glucose transporter (GLUT 1)
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32
Q

What do the types A, B and O gene encode?

A

A - N-acetylgalactosaminyltransferase
B - galactosyltransferase
O - no transferase

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33
Q

Describe the inheritance of ABO.

A

Ch 9 -> 3 allelic variants
i, IA and IB
IA and IB co-dominant
4 blood groups, A, B, AB and O.

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34
Q

What are rhesus D antigens?

A 
Expressed on RBC surface.
5 major Rh antigens: D, C, E, c and e.
D = most immunogenic
RhD- = no expression of antigen.
85% RhD+ 15% RhD-
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35
Q

Describe the gene of RhD.

A

Encoded by RHD and RHCE gene.

No anti-D antibodies present in blood.

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36
Q

How does haemolytic disease of the newborn (HDN) occur?

A
  1. Rh+ father
  2. Rh- mother carrying her first Rh+ foetus. Rh antigens from foetus enters mothers blood during pregnancy.
  3. Mother makes anti-Rh antibodies and becomes sensitised.
  4. If mother pregnant with another Rh+ foetus, anti-Rh antibodies crosses placenta and damages foetal RBCs.
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37
Q

What are the complications of HDN?

A

Range: mild anaemia -> intrauterine death at 18 weeks (hydrops fetalis).
Kernicterus - severe jaundice causes brain damage or deafness.

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38
Q

What is the prevention of HDN?

A

Routine antenatal serology + prophylaxis anti-D therapy.

Anti-D immunoglobulin binds and neutralises any RhD+ cells preventing formation of maternal antibodies.

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39
Q

What do incompatible blood transfusions cause?

A 
Agglutination - IR facilitated by antibody-antigen interactions.
Haemolysis
Renal failure
Shock
Death
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40
Q

Define anaemia.

A

Reduced no. of RBC or decreased HB -> reduced levels of oxygen delivery.

41
Q

What are the signs of anaemia?

A 
Pallor
Tachycardia
Glossitis
Koilonychia - spoon nails
Dark urine
42
Q

What are the symptoms of anaemia?

A 
Lethargy
Dizziness
SOB
Chronic fatigue
Poor concentration
43
Q

What are the severe symptoms of anaemia?

A

Jaundice, splenomegaly
Hepatomegaly, angina
Cardiac failure, fever

44
Q

How does changes in bone marrow cause anaemia?

A

Pure red cell aplasia (PRCA) - conditions affecting specifically erythropoiesis in bone marrow.
Pancytopenia - affecting production of RBCs, WBCs and platelets.

45
Q

Give an example of congenital PRCA.

A

Diamond Blackfan anaemia - reduced proliferation of erythroblasts.

46
Q

What conditions causes acquired PRCA?

A

Infections: EBV, HIV, Hep B
Malignancy: solid tumours, haematological tumours.
Autoimmune disease: SLE, RA.
Other causes: drugs (methotrexate), pregnancy.

47
Q

How does pancytopenia occur due to changes in bone marrow?

A

No self-renewal stage of haematopoietic stem cell -> exhaustion.

48
Q

Define haemolytic anaemia.

A

Premature destruction of RBC by extrinsic/instrinsic mechanisms i.e. drugs, abnormal types of Hb.

49
Q

Define allo-immune haemolysis.

A

Alloantibodies are made in response to immune recognition of foreign erythrocyte introduced via blood transfusion or pregnancy.
e.g. HDN

50
Q

Define auto-immune haemolysis.

A

Patient’s IS produces antibodies that recognise own RBCs as foreign and destroys. 3 causes:

  1. idiopathic
  2. secondary - other illness e.g. lymphoproliferative disorders, SLE, Crohn’s.
  3. drug-induced - alpha-methyldopa and penicillin.
51
Q

How is haemolytic anaemia diagnosed on blood films?

A

Schisocytes, polychromasia, nucleated erythrocytes and spherocytes.

52
Q

Define haemoglobulinopathy.

A

Autosomal co-dominant genetic defects -> abnormal structure of globin chains in Hb.
e.g. sickle cell anaemia

53
Q

Why are iron, vitamin B12 and 6 and folic acid need for erythrocyte function?

A

These essential micronutrients are needs for the metabolism of haem and formation of Hb.

54
Q

What are the likely causes of lack of essential micronutrients?

A

Malabsorption

Malnutrition

55
Q

How can iron deficiency anaemia be diagnosed on blood films?

A

Hypochromic (pale) and microcytic (small).

56
Q

Define sideroblastic anaemia.

A

Failure to incorporate iron into haem in erythrocyte precursor cells -> iron-rich mitochondria

57
Q

Where is haem synthesised in RBCs?

A

Cytoplasm and mitochondria.

58
Q

What are the dietary sources of iron?

A

Dark-green leafy veggies, whole grains, beans, nuts, meat.

59
Q

What makes iron absorption difficult?

A

Tea and coffee, PPI, Calcium, antacids, wholegrain cereals.

60
Q

What are the main causes of deficiency of iron.

A

Poverty, helminths, pregnancy, occult bleeding, vegan/vegetarian.

61
Q

Why is vitamin B12, 6 and folic acid required?

A

For maturation of RBCs and DNA synthesis in erythrocyte proliferation.
Patients have abnormally low reticulocytes.

62
Q

What are the dietary sources of vitamin B12, 6 and folic acid?

A

Meat, salmon, milk, eggs, soy products.

63
Q

What are the causes of deficiency of vitamin B12, 6 and folic acid?

A

Malnutrition and malabsorption, poverty, pregnancy, drugs, pernicious anaemia (deficiency of gastric intrinsic factor), gastrectomy, fish tapeworm, pancreatitis.

64
Q

Define megaloblastic anaemia.

A

Due to inhibition of DNA synthesis in erythropoiesis due to deficiency in folate and B12, caused by malnutrition or malabsorption.
Characteristic - megaloblasts and hypersegmented neutrophils.

65
Q

Define pernicious anaemia.

A

Caused by lack of intrinsic factor - required to absorb B12.

Due to autoimmune condition targeting gastric parietal cells.

66
Q

Define thalassemia.

A

Occurs when body is unable to produce enough Hb.

Target cells, Heinz bodies.

67
Q

Define aplastic anaemia.

A

Bone marrow and haematopoietic stem cells damaged so inability to make mature blood cells.

68
Q

Where is vitamin B12 absorbed and stored?

A

B12 binds intrinsic factor in stomach and is absorbed in terminal ileum.
Stored in liver.

69
Q

Where is folate absorbed and stored?

A

Absorbed in duodenum/proxmial jejunum.

Stored in liver.

70
Q

Define primary lymphoid tissues.

A

Sites for development of lymphocytes and where lymphocytes differentiates to express antigen receptors.

71
Q

Give examples of primary lymphoid tissues.

A

Thymus - T cells

Bone marrow - B cells

72
Q

Define secondary lymphoid tissues.

A

Specialised sites for turning on the adaptive IR. T and B cells are educated to respond to specific antigens.

73
Q

Give examples of secondary lymphoid tissues.

A

Lymph nodes
Spleen
Mucosal associated lymphoid tissue (MALT)

74
Q

Draw simple diagrams of thymus, lymph node, spleen and Peyer’s patch.

A

PIC

75
Q

What are the 3 components that all lymphoid tissues have?

A

Capsule
Vascular
Compartments

76
Q

What is the role of lymph nodes?

A

Filter lymphatics

Anatomical meeting place for cells of IS and their exposure to antigen for IR.

77
Q

Describe the events in a lymph node.

A

Afferent lymph comes from periphery. APCs sample antigens of incoming microbes. D cells pick up antigens from periphery and transport to LN -> LN concentrated in antigens so its easier for lymphocyte activation in same area. Lymphocytes and APCs leave via efferent lymph.

78
Q

Describe the functions of the spleen.

A

Looks for infection in systemic circulation as directly connected to blood vessels.

  • directs IR to antigens in blood (white pulp)
  • destruction of RBC (red pulp)
79
Q

What do the presence of Howell-Jolly bodies (erythrocyte with nuclear fragments) indicate?

A

Hyposplenism

Not fatal but pre-disposes to infections.

80
Q

Where is spleen located?

A

Left hypochondria regions of abdominal cavity.

12x7x2.5

81
Q

What are MALTs?

A

Aggregates of lymphocytes in reticular mesh.
Sites of IR to antigens that breach epithelia.
No incoming lymphatic vessels.

82
Q

Define lymphatics.

A

Drainage system involved in regulating fluid balance, returning the fluid to blood i.e. excess interstitial fluid and plasma proteins.

83
Q

Describe lymph capillaries.

A

Originates as closed tubes except in CNS, epidermis and cartilage.
Wall - overlapping endothelial cells that respond to fluid pressure.
Lymph capillaries anastomose to form lymphatics.

84
Q

Where do superficial lymphatics drain into?

A

Superficial lymphatics follow superficial veins - flow into lymph nodes in axillary + cervical + inguinal -> drains into deep lymphatics.

85
Q

Where do deep lymphatics drain into?

A

Deep lymphatics follow main vessels.
Lymph from 3/4 of body drains into left brachiocephalic veins via thoracic duct.
Lymph from upper right quadrant enters rights brachiocephalic vein.

86
Q

Outline the dual circulatory route.

A

This allows immunological surveillance throughout the body:

  • pathogens from site of infection reach LN via lymphatics.
  • naive lymphocytes arrive at LN in arterial blood.
  • lymphocytes and lymph return to blood via lymphatics
  • venous blood returns to heart.
87
Q

Define innate immunity.

A

Non-specific first line defence.
Prevents pathogen establishment and limits multiplication.
Early protection while adaptive reacts.
No memory and low specificity.

88
Q

Define adaptive immunity.

A

Specific, delayed immune response.
Contains immunological memory.
Uses lymphocytes.

89
Q

What are the components of innate immunity?

A

Physical barriers - mucous, epithelia, cilia
Complement system
IS cells - neutrophils, monocytes, basophils, eosinophils, NK cells, D cells, mast cells.

90
Q

Describe the complement system.

A

Multi-catalytic system which enables amplification of IIR by enzymatic cascade. 3 pathways:
- Alternative -> activation by pathogen surfaces
- Lectin -> activation by lectin binding mannose on pathogen.
- Classical -> activation by antibody-antigen complexes.
C3a + C5a -> inflammatory and phagocytic function.
C3b -> opsonisation
C5b - C9 membrane lysis.

91
Q

Describe the acute inflammatory process in the complement system.

A

Bacteria activates alternative pathway, recognised by C3 -> generates C3 fragment products.
C3b sticks to surface of bacteria.
C5a + C3a recruit inflammatory cells via mast cells -> degranulates and allows histamine to make endothelial walls more permeable to inflammatory cells.

92
Q

Describe membrane lysis in the complement system.

A

C5b binds C6 and C7 -> complex C5b67 binds membrane via C7 -> C8 binds to complex and inserts into membrane -> C9 binds complex and polymerises -> pore -> lysis.

93
Q

Describe opsonisation in the complement system.

A

C3b coats membrane of target cell - promotes binding of microbes to phagocytes -> microbe rapidly ingested.

94
Q

How do macrophages recognise bacteria?

A

Distinguishes different classes of microbes due to PAMPs and PRRs e.g. LPS and glucan receptors.

95
Q

Describe phagocytosis.

A
  1. Attachment via PRR
  2. Pseudopodia forming a phagosome
  3. Granule fusion and phagolysosome - allows for antigen presentation to lymphocyte
  4. Release of microbial products.
96
Q

Define cytokines and chemokine.

A
  • Hormones of IS
  • Allows communication between variety of immune and non-immune cells.
  • Chemokine - further family of chemotactic cytokines.
  • Designed to work over short distances but can have systemic effects.
  • Opposing effects of cytokines on macrophage function.
97
Q

What are the roles of macrophages?

A
  1. phagocytosis
  2. recruitment - releases cytokines to induce inflammation
  3. presentation - APC
  4. extravasation
98
Q

Outline the events in systemic acute phase response.

A

Trauma, stress, inflammation -> local réponse to make proinflammatory cytokines -> causes hepatocyte to modulate protein synthesis -> acute phase response (leukocytosis, complement activation, clotting and opsonisation -> resolution.

99
Q

Describe the acute inflammatory response.

A

Damage:

  • release of cytokines and chemokine which attracts leukocytes (leukocyte chemotaxis)
  • mast cell degranulation of histamine -> causes vasodilation and increased permeability of capillaries.
  • releases inflammatory mediators i.e. bradykinin and prostaglandins -> increases pain sensitivity.

HYMS Y1 (25 decks)

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