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Medical Studies 1 > Haem Week 10 > Flashcards

Haem Week 10 Flashcards

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USMLE® Step 1 flashcards
1
Q

Define haematopoiesis

A

Formation of the cellular components of red blood cells

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2
Q

Define myelopoiesis

A

Formation of blood cells in the myeloid line (e.g granulocytes, monocytes, erythrocytes and platelets)

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3
Q

Define lymphopoiesis

A

Formation of blood cells in the lymphoid cell line (e.g B cells, T cells, NK cells)

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4
Q

Outline the haematopoiesis pathway

A

All blood cells are derived from haematopoietic stem cells

This HSCs then differentiate into lymphoid or myeloid lineage by forming common lymphoid or common myeloid progenitor cells

Lymphoid progenitor cells differentiate within the bone marrow (B precursors) and thymus (T precursors, while myeloid progenitor cells on differentiate in the bone marrow only

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5
Q

Describe haematopoietic stem cells

A

Precursor cell to blood cells

High self renewal tendency

Located in bone marrow

Pluripotent

Differentiate into progenitor cells

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6
Q

Describe progenitor cells

A

Immediate product of HSC differentiation

Located in bone marrow

Limited self-renewal tendency

Differentiate into myeloid or lymphoid cells

Multipotent

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7
Q

Where is the site of haematopoiesis in an embryo 0-3mo

A

Yolk sac and then liver

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8
Q

Where is the site of haematopoiesis in a foetus 3-7mo

A

Spleen

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9
Q

Where is the site of haematopoiesis in a foetus 7-9mo

A

Begins to occur in the bone marrow

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10
Q

Where is the site of haematopoiesis from birth to maturity

A

Bone marrow and tibia/femur

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11
Q

Where is the site of haematopoiesis in an adult

A

Bone marrow of skull, ribs, sternum

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12
Q

Describe primary lymphoid organs

A

Where lymphocytes undergo ontogeny (they are made and develop into mature B and T cells)

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13
Q

Describe lymphocytes ontogeny

A

B and T cells make unique B cell receptors (BCRs) and T cell receptors (TCRs)

BCRs and TCRs are tested; cells w receptors that recognise itself are eliminated before further differentiation can occur to prevent autoimmune conditions

Then, mature antigen-responsive lymphocytes are released into circulation

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14
Q

Describe secondary lymphoid organs

A

Sites where mature lymphocytes encounter an antigen or differentiate into effector cells

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15
Q

What are the primary lymphoid organs

A

Thymus

Bone marrow

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16
Q

What are the secondary lymphoid organs

A

Lymph nodes

Spleen

Mucosal-associated lymphoid tissue (MALT)

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17
Q

What is the function of the cortex and paracortex of the lymph node structure

A

Cortex contains follicles w B cells

Paracortex contains T cells

Facilitates interactions between immune cells and the initiation of immune response

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18
Q

What is the function of follicles in the lymph node structure

A

In cortex of lymph node where B cells proliferate and produce antibodies

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19
Q

What is the function of the medulla in the lymph node structure

A

Contains plasma cells that produce antibodies and macrophages that phagocytose pathogens and debris

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20
Q

What is the function of sinuses in the lymph node structure

A

Spaces within lymph nodes where lymph circulates and immune cells meet antigens carried by lymph

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21
Q

What is the function of afferent vessels in the lymph node structure

A

Bring lymph, along with pathogens and antigens, into the lymph node for filtration and immune response initiation

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22
Q

What is the function of efferent vessels in the lymph node structure

A

Carry filtered lymph, including immune cells and antibodies, away from lymph nodes

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23
Q

What is the function of trabecula in the lymph node structure

A

Fibrous CT partitions within lymph nodes that provide structural support and contain blood vessels that supply nutrients to lymph node

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24
Q

Describe the spleen and its function

A

Responsible for filtering blood-borne antigens

Consists of white pulp for immune responses and red pulp for filtration

T cell area containing dendritic cells which surrounds arterioles as a periarteriolar lymphoid sheath (PALS)

Adjacent to the PALS are follicles in the B cell area

PALS and follicles form a complex that is enveloped by a plexus of veins aka marginal sinus

Marginal zone surrounds marginal sinus

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25
Q

What are colony-stimulating factors

A

CSFs are factors that stimulate certain elements of erythropoiesis, enabling the differentiation of HSCs into monocytes, granulocytes, platelets

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26
Q

What are 4 types of CSF

A

M-CSF

GM-CSF

G-CSF

Thrombopoietin

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27
Q

What is the function M-CSF

A

Stimulates production + differentiation of monocytes and macrophages from HSC

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28
Q

What is the function of GM-CSF

A

Promotes growth + maturation of WBC, including granulocytes and macrophages

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29
Q

What is the function of G-CSF

A

Stimulates production and release of neutrophils from bone marrow

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30
Q

What is the function of thrombopoietin

A

Regulates production + maturation of platelets from megakaryocytes in the bones marrow, maintaining platelet levels in the blood

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31
Q

Outline the production pathway of mast cell

A

HSC

Then, common myeloid progenitor

Then, mast cell

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32
Q

What are 4 functions of blood and give a brief description of each

A

Nutrition - gas exchange, providing oxygen to cells and tissues

Waste removal - regulate homeostasis of pH by removing CO2

Thermoregulation - regulating internal temp of body via vasodilation/constriction

Distribution - of immune cells, cytokines, hormones, immunoglobulins

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33
Q

What are 3 major components of blood

A

Plasma

Buffy coat

Red cells

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34
Q

What proportion of blood does plasma comprise

A

55% of blood volume

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35
Q

What proportion of blood does buffy coat comprise

A

Insignificant proportion of blood volume

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36
Q

What proportion of blood does red cells comprise

A

45% of blood volume

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37
Q

Describe the structure of bone marrow

A

Bony trabeculae - seen as thick pink ‘stripes’ / structure of the bone itself

Active marrow - pink/purple cellular elements of the bone marrow

Dissolved fat - leaves behind gaping white spaces

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38
Q

Outline haeme synthesis

A

Succinyl-CoA and glycine combine to form delta-aminolaevulinic acid (ALA)

Then, ALA is transported into cytoplasm

Then, series of enzymatic reactions in the cytoplasm and mitochondria lead to formation of porphyrin ring, known as porphobilinogen (PBG)

Then, 4 PBG molecules combine to from hydroxymethylbilane (HMB), which is then converted into uroporphyrinogen lll

Then, uroporphyrinogen lll is converted into coproporphyrinogen lll

Then, coproporphyrinogen lll is further modified to form protoporphyrin IX

Then, iron is incorporated into protoporphryin IX to produce haeme

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39
Q

Describe the structure of haemoglobin

A

Tetrameric protein consisting of 4 subunits

These subunits can be divided into 2 alpha-like subunits and 2 beta-like subunits

Each subunit is complexed w a haeme molecule containing iron; the haeme molecule is crucial for binding and transport of O2 in haemoglobin

Iron in the haeme group is capable of binding to O2, allowing haemoglobin to carry and release O2

Haemoglobin’s quaternary structure facilitates cooperative binding and release of O2

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40
Q

What are two predominate types of haemoglobin

A

HbA (adult)

HbF (foetal)

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41
Q

Describe HbA

A

Composed of 2 alpha and 2 beta haemoglobin chains

Present birth onwards

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42
Q

Describe HbF

A

Composed of 2 alpha and 2 gamma haemoglobin chains

Greater affinity to O2 compared to HbA as it allows the foetus to extract O2 from placenta where PO2 is lower

They are present from conception to 6mo-post birth

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43
Q

What are 3 key physiological properties of haemoglobin and provide a brief description of each

A

O2 transport - primary function is to bind to O2 in lungs and release into body tissues

CO2 transport - binds to CO2 aiding in its removal from tissues

Cooperative binding - haemoglobin exhibits cooperativity, meaning that as one subunit binds to oxygen, it increases the affinity of the other subunits for oxygen, hence this enhances oxygen carrying capacity

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44
Q

Describe steady state haematopoiesis

A

Formed elements of blood have high turnover

Due to high turnover of granulocytes, it is estimated that 10^13 myeloid cells are produced per day

Thus bone marrow must have high constant output to maintain normal cell counts

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45
Q

Describe stress haematopoiesis

A

At times of increased demand, output is increased rapidly in the bone marrow

Normal stresses include pregnancy and vigorous exercise/aerobic activity

Abnormal stresses include blood loss and infection

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46
Q

Describe haematopoietic growth factors

A

Glycoproteins that regulate growth, proliferation, differentiation, and function of progenitor cells and blood cells

They act locally or can circulate through bloodstream

Released by T cells, monocytes, and stromal cells

The kidney is a major source of erythropoietin

The liver is a major source of thrombopoietin

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47
Q

What four parameters cause a right shift on the oxygen-haemoglobin dissociation curve indicating a decreased affinity for O2

A

Increased pCO2

Increased H+

Increased temp

Increased 2,3-DPG

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48
Q

Describe the structure of the thymus

A

Small, bi-lobed organ

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49
Q

Where is the thymus located

A

In the anterior mediastinum of the chest, behind the sternum and just above the heart

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50
Q

Where is the spleen located

A

Intraperitoneal in the left upper quadrant of the abdomen, long axis parallel to the 10th rib

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51
Q

What is the function of the white pulp in the spleen

A

Serves as the immune response centre, initiating and coordinating immune reactions against blood-borne pathogens and antigens

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52
Q

What is the function of the red pulp

A

Primarily functions to filter and remove damaged or aged red blood cells from the circulation, as well as to store platelets

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53
Q

What is the function of the capsule of the lymph node structure

A

Outer protective covering of the lymph node

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54
Q

What is the function of the subcapsular sinus of the lymph node structure

A

Drains lymph into the node and filters it

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55
Q

Outline the flow of lymph through the lymph node

A

Lymph enters through the afferent lymphatic vessels, flowing into the subcapsular sinus

Then, lymph flows through the subcapsular sinus where it is filtered

Then, lymph flows into the cortex where B cells in the lymphoid follicles produce antibodies

Then, lymph flows into the paracortex where T cells enable cell mediated immune responses

Then, lymph enters the medulla, where dendritic cells/macrophages process antigens

Then, lymph exists via the efferent lymphatic vessel and returns to circulation

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56
Q

The right lymphatic duct collects lymph from…

A

Upper right side of the body

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57
Q

The thoracic duct collects lymph from…

A

The rest of the body (so everywhere except the upper right side of the body as this is where the right lymphatic duct collects from)

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58
Q

The thoracic duct empties into…

A

The left subclavian vein

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59
Q

In the occipital area, what lymph nodes are there (deep and/or superficial)

A

Superficial - occipital nodes

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60
Q

What structures in the occipital area drain into the occipital nodes

A

Scalp

Posterior neck

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61
Q

What lymph nodes are there in the auricular area (superficial and/or deep)

A

Superficial - Pre-auricular, Post-auricular, Parotid nodes

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62
Q

What structures drain lymph into the auricular area

A

External ear

Temple

Cheek

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63
Q

What lymph nodes exist in the cervical area (superficial and/or deep)

A

Superficial - anterior cervical, posterior cervical, supraclavicular nodes

Deep - deep cervical nodes

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64
Q

What structures drain lymph into the cervical area

A

Head and neck

Superficial structures

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65
Q

What lymph nodes exist in the axillary area (superficial and/or deep)

A

Superficial - pectoral, subscapular, humeral nodes

Deep - central axillary nodes

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66
Q

What structures drain lymph into the axillary area

A

Upper limb

Breast

Superficial thorax

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67
Q

What lymph nodes exist in the mediastinal area (superficial and/or deep)

A

Deep - tracheobroncial, paratracheal nodes

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68
Q

What structures drain lymph into the mediastinal area

A

Lungs

Bronchi

Oesophagus

69
Q

What lymph nodes exist in the inguinal area (superficial and/or deep)

A

Superficial - superficial inguinal nodes

Deep - deep inguinal nodes

70
Q

What structures drain lymph into the inguinal area

A

Lower limb

External genitalia

Lower abdominal wall

71
Q

What lymph nodes exist in the coeliac region (superficial and/or deep)

A

Deep - coeliac nodes

72
Q

What structures drain lymph into the coeliac area

A

Stomach

Liver

Pancreas

Spleen

Upper duodenum

73
Q

What lymph nodes exist in the external iliac area (superficial and/or deep)

A

Superficial - superficial external iliac nodes

Deep - deep external iliac nodes

74
Q

What structures drain lymph into the external iliac area

A

Lower abdominal wall

Perineum

External genitalia

75
Q

What lymph nodes exist in the common iliac area (superficial and/or deep)

A

Deep - common iliac nodes

76
Q

What structures drain lymph into the common iliac area

A

Pelvic viscera

Upper thigh

77
Q

What lymph nodes exist in the popliteal area (superficial and/or deep)

A

Superficial - popliteal nodes

Deep - deep popliteal nodes

78
Q

What structures drain lymph into the popliteal area

A

Foot

Calf

Posterior knee

79
Q

Generally speaking, which groups of lymph nodes does the head/neck drain into

A

Occipital, auricular, cervical

80
Q

Generally speaking, which groups of lymph nodes do the upper limbs drain into

A

Axillary

81
Q

Generally speaking, which groups of lymph nodes does the thorax drain into

A

Axillary, mediastinal

82
Q

Generally speaking, which groups of lymph nodes does the abdomen drain into

A

Coeliac, superior mesenteric, inferior mesenteric

83
Q

Generally speaking, which groups of lymph nodes does the pelvis drain into

A

External iliac and common iliac

84
Q

Generally speaking, which groups of lymph nodes do the lower limbs drain into

A

Popliteal

85
Q

Describe Fe3+

A

Obtained from plant products

High solubility

Low O2 affinity

86
Q

Describe Fe2+

A

Obtained from animal products

Low solubility

High O2 affinity

87
Q

What is DMNT-1

A

A transporter protein that converts Fe3+ into Fe2+ as Fe3+ has a lower binding affinity to O2

88
Q

What is ferroportin

A

Transporter protein that enables Fe2+ to travel from enterocytes into the bloodstream

89
Q

What is transferrin

A

Transporter protein that oxidises iron to the ferric state of Fe3+ thus enabling higher solubility in the blood

When the body needs more iron, like during periods of increased demand or when iron stores are low, the liver produces more transferrin to carry additional iron

90
Q

What is hepcidin

A

Regulatory protein that is produced by the liver, but actively degrades ferroportin (thus entrapping iron in the enterocytes and preventing uptake into the bloodstream)

91
Q

Outline the iron metabolism pathway

A

Fe2+ from animal products and Fe3+ from plant products are both converted into Fe2+ by DNMT-1

Then, the Fe2+ is transported from the enterocytes into the bloodstream using ferroportin

Then, transferrin oxides iron into Fe3+ for increased solubility in the blood

92
Q

How does hypoxia affect iron absorption

A

Increased DNMT-1 leads to decreased hepcidin, which then leads to increased absorption of iron

93
Q

How does increased EPO affect iron absorption

A

Decreased hepcidin leads to increased release of iron into bloodstream

94
Q

How does inflammation affect iron absorption

A

Increased hepcidin which leads to decreased release of iron into bloodstream

95
Q

How does haemochromatosis affect iron absorption

A

Decreased hepcidin, which leads to increased release of iron into bloodstream

96
Q

What is the role of ferritin

A

It is a globular protein that is common to most living organisms

Its primary role is iron storage (one ferritin molecule carries 4500 elemental units of iron)

Patients w a functional iron deficiency may have high levels of ferritin (this may be due to action of hepcidin)

97
Q

What is apo-ferritin

A

Empty ferritin

Circulates blood as a key player in acute inflammatory responses

Apo-ferritin levels indicate the amount of full ferritin, which can provide an insight into the demand for ferritin and thus iron

98
Q

What is the role of transferrin

A

Primary function is to transport iron from the sites of absorption (mainly small intestine) and storage (mainly liver and spleen) to the cells that require iron for various metabolic processes

It helps maintain iron homeostasis by controlling the amount of iron available for cells to use

99
Q

what is the diagnostic anaemic Hb value for males

A

<130 g/L

100
Q

what is the diagnostic anaemic Hb value for females

A

<120 g/L

101
Q

what is the diagnostic anaemic Hb value for pregnant females

A

<110 g/L

102
Q

what is the MCV for macrocytic anaemia

A

> 100 fL/cell

103
Q

what are 3 causes of macrocytic anaemia

A

B12 deficiency

folate deficiency

alcoholic liver disease

104
Q

what is the MCV for normocytic anaemia

A

80-100 fL/cell

105
Q

what are 3 causes of normocytic anaemia

A

renal failure

anaemia of chronic disease

leukaemia

106
Q

what is the MCV for microcytic anaemia

A

<80 fL/cell

107
Q

what are 2 causes of microcytic anaemia

A

iron deficiency

anaemia of chronic disease

108
Q

what does mean cell volume (MCV) mean

A

average size or volume of a RBC

109
Q

what does mean cell haemoglobin (MCH) mean

A

average amount of Hb in a red cell

110
Q

what does mean corpuscular haemoglobin concentration (MCHC) mean

A

amount of Hb per unit volume in a red cell

111
Q

what is thalassaemia

A

reduction or absence of synthesis of a globin chain resulting in an imbalance of alpha and beta globin chains

112
Q

what are haemoglobinopathies

A

mutations in the Hb genes resulting in changes in the normal amino acid sequence of a globin chain, resulting in an abnormal structure

113
Q

what is alpha+ thalassaemia

A

reduced or partial production of alpha globin chains

114
Q

what is alpha-0 thalassaemia

A

absence of production of alpha globin chains

115
Q

what is beta+ thalassaemia

A

reduced or partial production of beta goblin chains

116
Q

what is beta-0 thalassaemia

A

absence of production of beta globin chains

117
Q

outline the pathogenesis of anaemia due to thalassaemia

A

absence of beta globin chains or reduction of beta globin chains leads to excess of alpha globin chains

then, absence of B-globin leads to precipitation in erythroid precursors within bone marrow which results in ineffective erythropoiesis / reduction of B-globin leads to membrane damage to peripheral RBCs which results in hemolysis

then, this results in anaemia

118
Q

what are 4 clinical symptoms associated with thalassaemia

A

pallor - anaemia and reduced O2 supply

jaundice - due to breakdown of RBC

splenomegaly - resulting from spleen’s increased workload filtering abnormal RBC

dyspnea - due to reduced O2 carrying capacity in blood

119
Q

outline the consequence of genetic alterations as a result of alpha and beta thalassaemia on RBCs

A

both alpha and beta types results in genetic alterations that affect the production of alpha and beta globin chains of Hb, leading to abnormal Hb molecules

this can cause structural changes in RBC, making them fragile and prone to hemolysis

this leads to anaemia, as RBC have shorter lifespan and reduced O2 carrying capacity

120
Q

what is thalassaemia minor

A

when an individual carries one normal and one mutated gene

121
Q

what is thalassaemia major

A

when an individual inherits two mutated genes

122
Q

what are 6 consequences of iron overload in beta thalassaemia major and provide a brief description of each

A

cardiac complications - Fe overload in heart > cardiomyopathy and HF which can be life-threatening

liver damage - Fe deposits in liver > liver fibrosis > cirrhosis > impaired liver fn

endocrine disorders - disrupt hormone regulation > growth and puberty delays, diabetes, thyroid dysfunction

bone marrow suppression - Fe accumulation in bone marrow can interfere w RBC production, exacerbating anaemia

weakened immune system - Fe excess impair immune system fn which increases susceptibility to infections

skin discolouration - bronze or slate-grey hue due to Fe deposits

123
Q

what are 5 causes of iron deficiency anaemia

A

chronic blood loss

diet

malabsorption

increased iron demand

impaired iron recycling

124
Q

outline the pathophysiology of lack of dietary Fe leading to iron deficient anaemia

A

lack of dietary Fe

leads to, depleted Fe reserves in the body

leads to, reduced Fe absorption

leads to, Fe deficiency anaemia

125
Q

outline the pathophysiology of chronic blood loss leading to iron deficient anaemia

A

chronic blood loss

leads to, Fe removal without replenishment

leads to, depleted Fe reserves in the body

leads to, reduced Fe absorption

leads to, Fe deficiency anaemia

126
Q

outline the pathophysiology of increased Fe demand leading to iron deficient anaemia

A

increase in Fe demand

leads to, Fe removal without replenishment

leads to, depleted Fe reserves in the body

leads to, reduced Fe absorption

lead to, Fe deficiency anaemia

127
Q

outline the pathophysiology of malabsorption/absorption pathologies leading to iron deficient anaemia

A

absorption pathology e.g coeliac disease

leads to, reduced Fe absorption

leads to, Fe deficiency anaemia

128
Q

outline the pathophysiology of impaired Fe recycling leading to iron deficient anaemia

A

impaired Fe recycling

leads to, Fe removal without replenishment

leads to, depleted Fe reserves in the body

leads to, reduced Fe absorption

leads to, Fe deficiency anaemia

129
Q

outline the pathophysiology of inflammation causing anaemia

A

inflammation

leads to, release of cytokines

leads to, increased activity of hepcidin

leads to, inhibited release of recycled iron from macrophages causing functional iron deficiency, thus creating erythroid hypoproliferation

leads to, reduced EPO production

leads to, increased production of myeloid lineage cells

leads to, increased myeloid cells and decreased erythrocytes (due to TNFa inhibiting erythropoiesis and activating macrophages for erythrophagocytosis)

130
Q

what percentage of the global population is anaemic

A

24.8%

131
Q

what is the highest prevalence of anaemia

A

pre-school aged children - 47.4%

132
Q

what is the most common cause of anaemia in the world

A

iron deficiency, comprising ~50% of all cases

133
Q

what are 6 risk factors for anaemia

A

malnutrition

comorbidities

GI disorders

menstruation

pregnancy

surgery/trauma

134
Q

Describe the role of vitamin B12 in erythropoiesis and what a deficiency can potentially lead to

A

Plays a role in DNA synthesis, maturation of RBC and health of nerve tissues

A deficiency can result in megaloblastic anaemia and neurological complications, affecting the nerves that control muscle mvmt

135
Q

Where is vitamin b12 found mainly

A

Primarily in animal-based foods such as meat, fish, dairy products and eggs

It is not naturally present in plant based food which makes it essential for vegetarians and vegans to obtain b12 from fortified food or supplements

136
Q

Describe the role of folate in erythropoiesis and what a deficiency can potentially lead to

A

Aka vitamin b9 is crucial for DNA synthesis, rapid cell division, and production of RBC

A deficiency can lead to megaloblastic anaemia characterized by large immature RBCs

137
Q

What kind of food sources can folate be obtained from

A

Variety of foods including leafy greens, legumes, citrus fruits, fortified cereals

Also available in supplement form and is a key nutrient for pregnant women to prevent neural tube defects in foetus

138
Q

Outline the pathogenesis of macrocytic anaemia

A

Folate deficiency leads to impaired DNA synthesis / B12 deficiency leads to reduced conversion of m-CoA to s-CoA

Leads to, formation of macrocytic cells

Leads to, low Hb concentration

Leads to, macrocytic anaemia

139
Q

What are two megaloblastic causes of macrocytic anaemia

A

B12 deficiency

Folate deficiency

140
Q

What are 4 non-megaloblastic causes of macrocytic anaemia

A

Alcohol

Reticulocytosis

Liver disease

Hypothyroidism

141
Q

What is haemolytic anaemia

A

Anaemia due to premature destruction of RBCs

The reticuloendothelial system (spleen and liver) is operating in overdrive which enables and increased volume of haemolysis

Leads to release of LDH which is a useful measure when diagnosing haemolytic anaemia

142
Q

What does intrinsic haemolytic anaemia mean

A

Haemolytic anaemia occurring due to abnormalities within the RBCs themselves

143
Q

What does extrinsic haemolytic anaemia mean

A

Haemolytic anaemia occurring due to abnormalities outside of RBCs

144
Q

What are 2 intrinsic causes of haemolytic anaemia

A

Thalassaemia

G6PD deficiency

145
Q

What are 3 extrinsic causes of haemolytic anaemia

A

Stress from mechanical valves

Thrombotic state

Infectious agent

146
Q

Outline the pathophysiology behind stress from mechanical valves causing haemolytic anaemia

A

Shear force exerted upon RBCs by valves

Leads to, haemolysis

Leads to, decreased RBC count

Leads to, haemolytic anaemia

147
Q

Outline the pathophysiology behind a thrombotic state causing haemolytic anaemia

A

Shear force exerted upon RBCs by thrombotic state

Leads to, haemolysis

Leads to, decreased RBC count

Leads to, haemolytic anaemia

148
Q

Outline the pathophysiology behind an infectious agent causing haemolytic anaemia

A

Agent invades RBCs

Leads to, haemolysis

Leads to, decreased RBC count

Leads to, haemolytic anaemia

149
Q

Outline the pathophysiology behind thalassaemia causing haemolytic anaemia

A

Impaired Hb content

Leads to, haemolysis

Leads to, decreased RBC count

Leads to, haemolytic anaemia

150
Q

Outline the pathophysiology behind G6PD deficiency causing haemolytic anaemia

A

Exposure to trigger

Leads to, haemolysis

Leads to, RBC count decrease

Leads to, haemolytic anaemia

151
Q

What is intravascular haemolytic anaemia

A

Haemolysis occurring within the vasculature ie within the bloodstream

152
Q

What is extravascular haemolytic anaemia

A

Haemolysis occurring outside of the vasculature ie in the reticuloendothelial system

153
Q

Describe sickle cell disease

A

Caused by specific mutation in the HBB gene, which encodes the beta-globin subunit of Hb

In this mutation, a single base pair change results in the substitution of glutamic acid w valine at position 6 of the beta-globin chain

Inherited in an autosomal recessive manner

Mutation leads to production of abnormal Hb variant call haemoglobin S (HbS) > can polymerise and cause RBC to deformation in characteristic sickle shape, leading to vasoocclusive events and other complications

154
Q

What are 5 physiological consequences of sickle cell disease and provide a brief description of each

A

Hb structure - abnormal HbS formed due to substitution of valine for glutamic acid W

RBC morphology - HbS polymerisation causes RBC to become rigid and have sickle shape

O2 transport - sickle cells have reduced flexibility and difficulty passing through small vessels therefore impairs O2 delivery to tissues

Haemolysis - sickle cells have shorter lifespan so they are more prone to rupture

Blood viscosity - increase blood viscosity due to sickle cells

155
Q

What are 8 signs and symptoms of anaemia and link them to the underlying pathological process

A

Fatigue - reduced O2 carrying capacity

Pallor - decreased Hb levels, and hence less O2

Dyspnoea - heart has to work harder resulting in rapid or laboured breathing

Weakness - insufficient O2 to muscles and tissues

Tachycardia - HR increase as compensatory

Jaundice - haemolysis leads to release of bilirubin

Splenomegaly - spleen may enlarge to compensate for anaemia by produce more RBC or filet abnormal ones

Glossitis - inflammation of tongue’s mucous membrane can occur

156
Q

What are 5 investigations that can be done for the diagnosis of anaemia and link it to the aetiology

A

CBE - classify micro/macro/normocytic

Iron studies - low serum iron or ferritin suggests iron deficiency anaemia

B12/folate - low levels of B12 or folate may indicate megaloblastic anaemia

LDH - high LDH may suggest haemolytic anaemia due to various causes, including hereditary or acquired conditions

Hb electrophoresis - helps diagnose + differentiate types of haemoglobinopathies such as sickle cell disease or thalassaemia

157
Q

What are 5 management options for anaemia

A

Diet control

Oral iron

IV iron therapy

B12/folate

Blood transfusion

158
Q

What is one indication and one contraindication for use of diet control as a management option for Rx of anaemia

A

Indication = demonstrated deficiency

Contraindication = non-iron deficient anaemia

159
Q

What is one indication and one contraindication for the use of oral iron as a management option for Rx of anaemia

A

Indication = severe iron deficiency

Contraindication = malabsorption-based iron deficiency

160
Q

What is one indication and one contraindication for the use of IV iron therapy as a management option for the Rx of anaemia

A

Indication = unable to receive transfusions

Contraindications = hypersensitivity prone individuals

161
Q

What is one indication and one contraindication for the use of B12/folate as a management option for Rx of anaemia

A

Indication = demonstrated deficiency

Contraindication = other unrelated causes

162
Q

What is one indication and one contraindication of using blood transfusions as a management option for Rx of anaemia

A

Indications = anaemia w acute threat

Contraindication = Jehovah’s Witness

163
Q

Describe the recommended follow-up for a Pt w anaemia

A

Dependent on underlying cause and severity of the anaemia

Frequency of blood tests needed can vary greatly b/w causes and should be assessed on a case-by-case basis

In anaemia due to acute leukaemia, bloods may be needed multiple times per day; in iron-deficient anaemia, every 4 months may be sufficient

164
Q

What are 4 periods in ones lifetime where iron demands increase (vulnerable stages of life to iron dependency)

A

Infancy - rapid growth and development

Adolescence - growth spurt and increased physical activity

Pregnancy - support growing foetus

Menstruation - monthly blood loss

165
Q

What are 6 food sources of dietary iron

A

Red meat

Seafood

Fortified cereals

Poultry

Legumes

Dark leafy greens

166
Q

What are 6 factors that affect the bioavailability of iron in different food sources

A

Fe2+ vs Fe3+ - haeme iron (animal based) more readily absorbed compared to non-haeme iron (plant based)

Vitamin C - enhances the absorption of non-haeme iron

Calcium - inhibit absorption of both haeme and non-haeme iron

Tannins - in tea and coffee > can interfere with iron absorption

GI disorders - e.g coeliac disease and inflammatory bowel disease can affect iron absorption

Cooking method - cooking in iron cookware can increase iron content of food; overcooking can reduce iron content

167
Q

Outline the concept of food pairing to maximise iron absorption

A

Involves combining foods in a way that enhances the body’s ability to absorb non-haeme iron

Strategies to improve iron absorption include the use of vitamin C and iron cookware, in the absence of calcium and tea/coffee

168
Q

What are 2 causes of B12 deficiency

A

Nutritional e.g veganism

Malabsorption e.g pernicious anaemia, gastrectomy

169
Q

What are 4 causes of folate deficiency

A

Nutritional e.g poverty, famine

Malabsorption e.g gluten induced enteropathy

Excess utilisation e.g pregnancy, cancer

Drugs e.g anticonvulsants

Medical Studies 1 (16 decks)

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