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Medical Studies 1 > Week 10 Haematology > Flashcards

Week 10 Haematology 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 (eg granulocytes, monocytes, erythrocytes, platelets)

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3
Q

define lymphopoiesis

A

formation of blood cells in the lymphoid cell line (B cells, T cells and NK cells)

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4
Q

outline the haematopoesis pathway

A

-haematopoietic stem cell (hemocytoblast)
-common myeloid progenitor and common lymphoid progenitor cells
-lymphoid progenitors –> NK, T,B, Plasma cell
-common myeloid progenitor–> erythrocyte, mast, basophil, neutrophil, eosinophil, macrophage

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5
Q

where do lymphoid progenitors differentiate

A

Bone marrow (B precursors) and thymus (t precursors)

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6
Q

features of haematopoietic stem cells

A

-precursors to blood cells
-differentiate into progenitor cells
-self renewing
-pluripotent
-mostly found in bone marrow

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7
Q

features of progenitor cells

A

-multipotent
-limited self renewal
-located in bone marrow
-differentiate into myeloid or lymphoid cells

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8
Q

where is the site of haematopoiesis in embryo (0-3 months)

A

yolk sac and then the liver

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9
Q

where is the site of haematopoiesis in foetus (3-7 months)

A

spleen

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10
Q

where is the site of haematopoiesis in foetus (7-9 months)

A

begins to occur in bone marrow

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11
Q

where is the site of haematopoiesis in birth to maturity

A

bone marrow and tibia/femur

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12
Q

where is the site of haematopoiesis in adults

A

bone marrow of skull, ribs, sternum

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13
Q

over production and under production of erythrocytes

A

polycythaemia and anaemia

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14
Q

over production and under production of platelets

A

thrombocythaemia/thrombocytosis and thrombocytopenia

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15
Q

over production and under production of leukocytes

A

leukocytosis and leukopenia

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16
Q

over production and under production of neutrophil

A

neutrophillia and neutropenia

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17
Q

over production and under production of lymphocytes

A

lymphocytosis and lymphopaenia

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18
Q

over production and under production of monocyte

A

monocytosis and monocytopaenia

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19
Q

over production and under production of eosinophil

A

eosinophilia and eosinopaenia

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20
Q

over production and under production of basophil

A

basophilic and basopaenia

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21
Q

proportion of WBC in body from most to least abundant

A

never let monkeys eat bananas

neutrophil-60%
lymphocyte-30%
monocyte-6%
eosinophil-3%
basophil-1%

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22
Q

lifespan of neutrophils

A

2-5 days

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23
Q

lifespan of lymphocyte

A

long-lived

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24
Q

lifespan of monocyte

A

2-5 days

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25
Q

lifespan of eosinophil

A

7-12 days

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26
Q

lifespan of basophil

A

12-15 days

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27
Q

function of mast cells

A

Releases histamine, promotes inflammation, and recruits immune cells.

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28
Q

function of dendritic cells

A

Captures antigens, presents them to T cells, initiates immunity.

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29
Q

function of macrophages

A

Engulfs pathogens, removes debris, and activates immune response.

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30
Q

CD4 T cell=

A

T helper cell

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31
Q

CD8 T cell =

A

T cytotoxic cell

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32
Q

B cell=

A

plasma cell

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33
Q

what are the primary lymphoid organs

A

thymus and bone marrow

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34
Q

what are the secondary lymphoid organs

A

lymph nodes, spleen, MALT

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35
Q

list the structures of the lymph node

A

cortex and paracortex
follicles
medulla
sinuses
antibodies
afferent vessels
efferent vessels
trabecular

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36
Q

what is the cortex and paracortex in the lymph node

A

-cortex contains follicles with B cells
-paracortex contains T cells
-this allows for interactions between these cells and initiates immune response

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37
Q

what are the follicles in the lymph node

A

-areas of the cortex where B cells proliferate and produce antibodies as part of AIR (adaptive immune)

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38
Q

what is the medulla in the lymph node

A

-contains plasma cells that produce antibodies and macrophages phagocytose

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39
Q

what are the sinuses in the lymph node

A

-spaces within lymph nodes where lymph circulates and immune cells meet antigens carried by lymph
-allows for immune surveillance and response

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40
Q

what are the afferent vessels in lymph node

A

-bring lymph along with pathogens and antigens into lymph node for filtration and immune initiation

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41
Q

what are the efferent vessels in lymph node

A

carry filtered lymph, including immune cells, and antibodies away from Ln to body

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42
Q

what is the trabecular in lymph node

A

-fibrous CT partitions within lymph nodes that provide structure support and nutrients to Ln

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43
Q

what is lymph

A

-tissue fluid carries antigens from the periphery, to the local draining lymph nodes

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44
Q

function of spleen

A

-filters blood borne antigens

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45
Q

structure of spleen

A

-white pulp (immune responses) and red pulp (filtration)
-T cell area containing Dc cells which surround periarteriolar lymphoid sheath (PALS)
-adjacent to PALS are follicles in B cell area
-PALS + follicles –> marginal sinus (veins)
-marginal zone surrounds this sinus

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46
Q

what are Colony stimulating factors

A

factors that stimulate certain elements of erythropoiesis, enabling the differentiation of HSC’s

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47
Q

list the CSF’s

A

M-CSF
GM-CSF
G-CSF
Thrombopoietin

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48
Q

Function of M-CSF

A

stimulates the production and differentiation of monocytes and macrophages from haematopoietic stem cells

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49
Q

Function of GM-CSF

A

promotes growth and maturation of WBC’s, including granulocytes (neutrophils, eosinophils, and basophils)

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50
Q

Function of G-CSF

A

specifically stimulates the production and release of neutrophils from the bone marrow, helping the body fight infection

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51
Q

function of thrombopoietin

A

regulates the production and maturation of platelets from megakaryocytes in the bone marrow, maintaining appropriate platelet levels in the blood

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52
Q

what is lymphoid ontogeny

A

process by which lymphocytes are made and developed into mature b and T cells

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53
Q

describe what happens in lymphoid ontogeny

A

-B and T cells make unique BCR’s and TCR’s
-these are tested by body before further differentiation to prevent AI conditions

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54
Q

list the functions of blood

A

nutrition
waste removal
thermoregulation
distribution

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55
Q

describe nutrition as a function of blood

A

gas exchange, providing oxygen to cells and tissue

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56
Q

describe waste removal as a function of blood

A

regulating homeostasis of pH and electrolytes; removal of CO2

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57
Q

describe thermoregulation as a function of blood

A

regulating the internal temperature of the body via vasodilation and vasoconstriction

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58
Q

describe distribution as a function of blood

A

distribution of immune cells, cytokines, hormones and immunoglobulins

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59
Q

list the components of blood

A

plasma
Buffy coat
red cells

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60
Q

what is plasma’s proportion in the blood

A

-55% of blood volume
(91% water, 7% proteins and 2% nutrients)

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61
Q

what is the Buffy coats proportion in the blood

A

insignificant proportion of blood volume (made of cells)

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62
Q

what is the red cells proportion in the blood

A

45% of blood volume (haematocrit)

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63
Q

what are the features of bone marrow structure

A

-bony trabecular
-active marrow
-dissolved fat

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64
Q

what is the bony trabecular of the bone marrow

A

seen as thick ‘pink’ stripes, structure of the bone itself

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65
Q

what is the active bone marrow in bone marrow

A

pink/purple cellular elements of the bone marrow

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66
Q

what is the dissolved fat in the bone marrow

A

leaves behind gaping white spaces (CIRCLES)

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67
Q

where does heme synthesis occur

A

mitochondria (early and late stages) and cytoplasm (intermediate stages)

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68
Q

Outline the steps in heme synthesis

A

1.Succinyl-CoA and glycine combine to form delta-aminolaevullinic acid (ALA)
2.ALA is transported into cytoplasm
3.A series of enzymatic reactions in the cytoplasm and mitochondria lead to the formation of porphyrin ring, known as propobilinogen (PBG)
4.Four PBG –> hydroxymethylbilane (HMB), –> urophyrinogen III
5. urophyrinogen III i–> coproporphyrinogen III
6. coproporphyrinogen III i–> protoporphyrin IX
7.iron + protoporphyrin IX –> heme

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69
Q

Describe the structure of haemoglobin

A

-tetrameric protein with 4 subunits
-2 alpha-like and 2 beta-like subunits , each subunit contains a Fe molecule
-the Fe in heme group is able to bind to oxygen, allowing Hb to carry and release O2 as needed
-Hg has a quaternary structure

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70
Q

features of HbF

A

-has two alpha and two gamma haemoglobin chains
-present from conception to 6 months

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71
Q

features of HbA

A

-has two alpha and two beta haemoglobin chains
-present from birth onwards

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72
Q

list the properties of Hb

A

O2 transport
CO2 transport
cooperative binding

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73
Q

describe O2 transport as a property of Hb

A

Hb’s primary function is to bind to oxygen in the lungs (oxyhemoglobin) and release it in the body’s tissues (deoxyhemoglobin) to facilitate oxygen transport

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74
Q

describe CO2 transport as a property of Hb

A

Hb can bind to Co2, aiding in it’s removal from tissues, some CO2 binds directly to Hb, forming carbaminohemoglobin

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75
Q

describe cooperative binding as a property of haemoglobin

A

Hb exhibits cooperativity, meaning that s one subunit binds to oxygen, it increases the affinity of the the other subunits for oxygen, enhancing its oxygen carrying capacity

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76
Q

what is the Bohr effect vs Haldane effect

A

Bohr: High CO₂ or low pH encourages O₂ release (tissues).

Haldane: Oxygen binding encourages CO₂ release (lungs).

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77
Q

describe the maturation of erythroblasts to erythrocytes

A

-born with 300 HSC, they divide once or twice per year (lessens risk of mutations)
-with successive cell divides, the progeny stem cells become committed to a specific lineage
-mature cells lose proliferative potency and acquire specific characteristic functions akin to their type

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78
Q

what is the turnover of red cells

A

120 days

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79
Q

what is the turnover of granulocytes

A

few hours (10^13) produced daily)

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80
Q

what is the turnover of platelets

A

5-10 days

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81
Q

describe stress haematopoiesis

A

-at times of increased demand, output is increased rapidly in bone marrow
-stress includes exercise and pregnancy
-abnormal stress includes blood loss and infection

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82
Q

source of erythropoietin

A

kidney

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83
Q

source of thrombopoietin

A

liver

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84
Q

what is 2,3-DPG

A

2,3-diphosphoglycerate

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85
Q

increased PCO2 leads to …

A

right shift (decreased O2 affinity)

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86
Q

increased H+/decreased pH leads to…

A

right shift (decreased O2 affinity)

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87
Q

increased temperature leads to

A

right shift (decreased O2 affinity)

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88
Q

increased 2,3-DPG leads to

A

right shift (decreased O2 affinity)

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89
Q

describe the structure of the thymus

A

small, bilobular structure

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90
Q

describe the location of the thymus

A

in the anterior mediastinum of the chest, behind the sternum (breastbone) and just above the heart

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91
Q

describe the structure of the spleen

A

white pulp (lymphoid tissue, T cells, b cells, Dc)
red pulp (splenic sinusoids, macrophages)

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92
Q

describe the location of the spleen

A

intraperitoneal in the left upper quadrant of the abdomen, long axis parallel to the 10th rib, mobile with respiration

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93
Q

function of the white pulp

A

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

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94
Q

function of the red pulp

A

primarily functions to filter and remove damages or aged RBC’s from the circulation, as well to store platelets

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95
Q

structure of the capsule in lymph node

A

outer protective covering the lymph node

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96
Q

function of the sub capsular sinus

A

drains lymph into the node and filters it

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97
Q

describe the flow of lymph through the lymph node

A
  1. lymph enters through the afferent lymphatic vessels, flowing into the sub capsular sinus
    2.lymph flows through the subcapsular sinus where it is filtered (debris/pathogens are trapped)
    3.lymph flows into cortex, where B cells in lymphoid produce antibodies
    4.lymph flows into the paracortex where T cells enable Cell mediated response
    5.Lymph enters the medulla, where dendritic cells macrophages process antigens
    6.lymph exits via the efferent lymphatic vessel and returns to circulation
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98
Q

function of the right lymphatic duct vs thoracic duct

A

collects lymph from the upper right side of the body vs thoracic duct collects lymph from the rest of the body

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99
Q

what lymph nodes are in the occipital area

A

superficial: occipital nodes

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100
Q

what nodes do scalp and posterior neck drain into

A

occipital nodes

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101
Q

what lymph nodes are in the auricular area

A

superficial: pre auricular, post auricular , parotid nodes

102
Q

what lymph nodes are in the cervical area

A

superficial: anterior cervical, posterior cervical, supraclavicular nodes
Deep: deep cervical nodes

103
Q

what nodes do external ear, temple, and cheek drain into

A

superficial: pre auricular, post auricular , parotid nodes

104
Q

what nodes do head, neck and superficial structures drain into

A

superficial: anterior cervical, posterior cervical, supraclavicular nodes
Deep: deep cervical nodes

105
Q

what lymph nodes are in the axillary area

A

Superficial: pectoral, sub scapular, humeral nodes , apical
deep: central axilliary nodes

106
Q

what structures do the the upper limb, breast and superficial thorax drain into

A

Superficial: pectoral, sub scapular, humeral nodes
deep: central axilliary nodes

107
Q

what lymph nodes are in the mediastinal area

A

deep: tracheobronchial and paratracheal nodes

108
Q

what nodes do the lungs, bronchi and oesophagus drain into

A

deep: tracheobronchial and paratracheal nodes

109
Q

what lymph nodes are in the inguinal area

A

superficial: superficial inguinal nodes
deep: deep inguinal nodes

110
Q

what nodes do the lower limb, external genitalia, lower abdominal drain into

A

superficial: superficial inguinal nodes
deep: deep inguinal nodes

111
Q

what lymph nodes are in the coeliac area

A

deep: celiac nodes

112
Q

what nodes do the stomach, liver, pancreas, spleen and upper duodenum drain into

A

deep: celiac nodes

113
Q

what lymph nodes are in the external iliac area

A

superficial: superficial external iliac nodes
deep: deep external iliac nodes

114
Q

what do the lower abdominal wall, perineum and external genitalia drain into

A

superficial: superficial external iliac nodes
deep: deep external iliac nodes

115
Q

what lymph nodes are in the common iliac area

A

deep: common iliac nodes

116
Q

what do the pelvic viscera, upper thigh drain into

A

deep: common iliac nodes

117
Q

what lymph nodes are in the popliteal area

A

superficial: popliteal nodes
deep: deep popliteal nodes

118
Q

what do the foot, calf, posterior knee drain into

A

superficial: popliteal nodes
deep: deep popliteal nodes

119
Q

features of Fe3+

A

-obtained from plant products
-High solubility
-low oxygen affinity

120
Q

features of Fe2+

A

-obtained from animal products
-low solubility
-high oxygen affinity

121
Q

Describe iron metabolism

A

*Fe³⁺ is reduced to Fe²⁺ by an enzyme, which is then transported into cells by DMT-1.
*Fe2+ then can be converted into Fe3+ and stored as ferritin or
*Ferroportin transports Fe²⁺ from cells (like enterocytes) into the bloodstream.
*Transferrin binds to Fe²⁺ and oxidises it to Fe³⁺, increasing its solubility, so it can transport it through blood
*Hepcidin regulates iron homeostasis by degrading ferroportin, preventing iron release into the bloodstream.

Cells can later reduce Fe³⁺ back to Fe²⁺ if they need it for active processes, like heme synthesis.

122
Q

list the factors effecting iron absorption

A

hypoxia
increased erythropoietin
inflammation
haemochromatosis

123
Q

describe how hypoxia influences iron absorption

A

increased DMT-1
decreased hepcidin
increased iron absorption

124
Q

describe how a need for increased erythropoietin influences iron absorption

A

decreased hepcidin
increased release of iron into blood stream

125
Q

describe how inflammation influences iron absorption

A

increased hepcidin
decreased release of iron into bloodstream

126
Q

describe how haemochromatosis influences iron absorption

A

decreased hepcidin
increased release of iron into bloodstream

127
Q

what is the role of ferritin

A

globular protein found in most organisms, primarily stores/contains iron and, in its empty form , circulates in the blood, reflecting iron demand

128
Q

role of transferrin

A

blood glycoprotein that transports Fe3+ throughout the body (from site of absorption and site of storage to cells)

129
Q

ferric vs ferrous

A

Ferric =Fe3+
Ferrous = Fe2+

130
Q

what is the male anaemic haemoglobin

A

<130 g/L

131
Q

what is the female anaemic haemoglobin

A

<120 g/L

132
Q

what is the pregnant female anaemic haemoglobin

A

<110 g/L

133
Q

what is macrocytic anaemia + eg’s

A

> 100 fL/cell
FAT RBC

foetal
alcohol
thyroid disease
reticulocytosis
b12/folate
cirrhosis and liver disease

134
Q

define mean cell volume

A

average size or volume of a red blood cell

135
Q

define mean cell haemoglobin

A

average amount of Hb in a red cell

136
Q

define mean corpuscular Hb concentration(MCHC)

A

amount of Hb per unit volume in a red cell

137
Q

what is thalassemia

A

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

138
Q

what are haemoglobinopathies

A

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

139
Q

what is alpha thalassaemia (a+)

A

reduced or partial production of alpha globin chains

140
Q

what is alpha thalassaemia (a0)

A

absence of production of alpha globin chains

141
Q

what is beta thalassaemia (b+)

A

reduced or partial production of beta globin chains

142
Q

what is beta thalassaemia (b0)

A

absence of production of beta globin chains

143
Q

what is normocytic anaemia + eg’s

A

80-100 fL/cell

acute blood loss
bone marrow defieincy
chronic disease of anaemia
destruction of RBC’s (hemolytic)
enzymatic

144
Q

what is microcytic anaemia +eg’s

A

<80 fL/cell

thalassemia, anaemia of chronic disease, iron deficiency, lead poisoning, seroblastic anaemia (TAILS)

145
Q

what is the main difference between alpha and beta thalassaemia

A

-alpha thalassaemias are mostly due to deletions in the Hb alpha locus (chromosome 16)
-beta thalassemia is due to mutate in Hb beta gene locus (chromosome 11)

146
Q

what are the consequences of thalassaemia on red blood cells

A

-genetic alterations that affect the production of alpha and beta globin chains of Hb, leading to abnormal Hb molecules
-RBC’s become fragile and prone to hemolysis
-leading to anaemia as RBC have shorter lifespan and reduced oxygen carrying capacity

147
Q

list the clinical exam presentation of thalassaemia

A

pallor
jaundice
splenomegaly
dyspnoea

148
Q

describe pallor in thalassaemia

A

skin appears usually pale due to anaemia and reduced oxygen supply

149
Q

describe jaundice in thalassaemia

A

yellowing of the skin and eye caused by breakdown of RBC’s (bilirubin increases=yellow)

150
Q

describe splenomegaly in thalassaemia

A

an enlarged spleen is common, enlarged due to increased workload in filtering abnormal red blood cells

151
Q

describe dyspnoea in thalassaemia

A

SOB, especially during physical exercise, due to reduced oxygen carrying capacity in blood

152
Q

Outline the severity of thalassaemia

A

-determined by the specific mutations in the alpha or beta globin chains
-thalassemia minor if individuals carries one normal and one mutated gene (heterozygous)
-thalassaemia major if individuals inherit two mutated genes (homozygous)
-intermediate is between the two above

153
Q

what is iron overload

A

-occurs when body absorbs too much iron from the diet, often when there is no efficient mechanism for iron regulation
-can be due to genetic mutations or medical conditions

154
Q

list the consequences of iron overload in beta thalassaemia major

A

cardiac complications
liver damage
endocrine disorders
bone marrow suppression
weakened immune system
skin discoularation

155
Q

describe cardiac complications as a result of iron overload in beta thalassaemia major

A

iron overload in the heart can result in cardiomyopathy and HF, which can be life threatening

156
Q

describe liver damage as a result of iron overload in beta thalassaemia major

A

iron deposits in the liver can lead to liver fibrosis, cirrhosis, and impaired liver function

157
Q

describe endocrine disorders as a result of iron overload in beta thalassaemia major

A

iron overload can disrupt hormone regulation , causing growth and puberty delays, diabetes and thyroid dysfunction

158
Q

describe bone marrow suppression as a result of iron overload in beta thalassaemia major

A

iron accumulation in the bone marrow can interfere with red blood cell production, exacerbating anaemia

159
Q

describe weakened immune system as a result of iron overload in beta thalassaemia major

A

iron excess can impair the immune system function, increasing susceptibility to infections

160
Q

describe skin discolouration as a result o firon overload in beta thalassaemia major

A

skin may developer a bronze or slate-grey hue due to iron deposits

161
Q

what are the causes of iron deficiency anaemia

A

chronic blood loss
diet
malabsorption
increased iron demand
impaired iron recycling

162
Q

how does diet lead to Fe deficiency anaemia

A

-lack of dietary Fe
-depleted Fe reserved in the body
-decreased Fe absorption
-Fe defieicny anaemia

163
Q

how does chronic blood loss lead to Fe deficiency anaemia

A

-chronic blood loss
-Fe removal without replenishment
-depleted Fe reserved in the body
-decreased Fe absorption
-Fe deficiency anaemia

164
Q

how does increase in Fe demand lead to Fe deficiency anaemia

A

-increased Fe demand
-Fe removal without replenishment
-depleted Fe reserved in the body
-decreased Fe absorption
-Fe deficiency anaemia

165
Q

How does malabsorption lead to Fe defiency anaemia

A

-absorption pathologies eg coeliac
-decreased Fe absorption
-Fe deficiency anaemia

166
Q

how does impaired Fe recycling lead to Fe deficiency anaemia

A

-impaired Fe recycling
-Fe removal without replenishment
–depleted Fe reserved in the body
-decreased Fe absorption
-Fe deficiency anaemia

167
Q

what is coeliac disease, briefly

A
  • autoimmune disorder in which the immune system mistakenly reacts to the consumption of gluten, causing damage to the small intestine.
  • Celiac disease can cause malabsorption of nutrients, including iron (Fe), in the small intestine.
  • Damage to the intestinal villi reduces the surface area available for nutrient absorption.
  • In coeliac disease, the immune system’s reaction to gluten can create chronic inflammation, exacerbating the
    anaemia.
168
Q

Describe the pathogenesis of anaemia of inflammation/ anaemia of chronic disease

A

-inflammation
-release of cytokines (IL-6)
-increased hepcidin produced (decreases Fe availability for pathogens)
-hepcidin inhibits the release of recycled iron from macrophages causing decreased serum iron
-decreased serum iron
-reduced EPO production
-bias of hamaetopoiesis towards myeloid cell production
-TNFa molecule inhibits erythropoiesis and promotes erythrophagocytosis
-more myeloid cells and less erythrocytes are produced

169
Q

features of iron deficiency anaemia (Hb, MCV/MCH, Ferritin, Transferrin)

A

low Hb
low MCV/MCH
low Ferritin
high transferrin/low transferrin saturation

170
Q

features of thalassaemia (Hb, MCV/MCH, Ferritin, Transferrin)

A

low Hb
low MCV/MCH
high Ferritin
low transferrin

171
Q

features of iron overload (Hb, MCV/MCH, Ferritin, Transferrin)

A

high Hb
normal MCV/MCH
high Ferritin
low transferrin

172
Q

features of chronic inflammation anaemia (Hb, MCV/MCH, Ferritin, Transferrin)

A

low Hb
low MCV/MCH
high Ferritin
low transferrin

173
Q

epidemiology of anaemia

A

Globally, 24.8% of the population are anaemic; the highest prevalence is pre-school age children (47.4%).
* most common cause of anaemia in the world is iron deficiency, (approximately 50% of all cases)
.

174
Q

list the risk factors for anaemia

A

malnutrition
commorbidities
GI disorders
menstruation
pregnancy
surgery/trauma

175
Q

how is malnutrition a risk factor for anaemia

A

-inadequate intake of key nutrients like iron, vitamin B12, folate, necessary for RBC production

176
Q

how are comorbidities a risk factor for anaemia

A

CKD, cancer, inflammatory conditions can disrupt RBC production or lifespan of RBC

177
Q

how are GI disorders risk factors for anaemia

A

conditions like celiac disease or crohns can impair nutrient absorption, leading to anaemia

178
Q

how is menstruation a risk factor for anaemia

A

heavy prolonged menstrual bleeding in women can result in iron deficiency anaemia

179
Q

how is pregnancy a risk factor for anaemia

A

increased iron demands during pregnancy can lead to anemia if dietary intake is insufficient

180
Q

how is surgery/truama a risk factor for anaemia

A

acute blood loss due to surgery or GI bleeds can readily deplete RBC’s or anaemia

181
Q

Describe the process of erythropoiesis

A

-Driven by hypoxia and low renal perfusion
-renal release of EPO
-EPO extends pro-erythrocyte life in bone marrow to increase chance of maturation
-increased RBC production
-HSC differentiates into myeloid/lymphoid progenitor
-myeloid progenitor–>erythroblast–>pro-erythrocyte–>reticulocyte–>erythrocyte

182
Q

Describe the red blood cell breakdown

A

involves the phagocytosis of aged or damaged RBCs by macrophages, degradation of hemoglobin into globin and heme, conversion of heme into bilirubin, and recycling of iron for new red blood cell synthesis.

183
Q

describe the role of iron in erythropoiesis

A

iron is required to produce haemoglobin, and it’s deficiency leads to reduced oxygen carrying capacity to anaemia

184
Q

describe the role of vitamin B12 in erythropoiesis

A

vitamin B12 or cobalamin, plays a role in DNA synthesis and the maturation of red blood cells, a deficiency can result in megaloblastic anaemia and neurological complications, affecting the nerves that control muscle movement

185
Q

describe the role of folate in erythropoiesis

A

folate, also known as vitamin B9, is essential for DNA synthesis, which is critical in the rapid cell division that occurs during erythropoiesis, a deficiency can lead to megaloblastic anaemia, characterised by large, immature red blood cells

186
Q

outline the pathophysiology of macrocytic anaemia (B12)

A

-B12 deficiency leads to reduced conversion of m-CoA to s-CoA
-formation of macrocytic cells
-low Hb concentration

187
Q

outline the pathophysiology of macrocytic anaemia (folate)

A

-folate deficiency leads to impaired DNA synthesis
-formation of macrocytic cells
-low Hb concentration

188
Q

sources of vitamin B12

A

-meat/poultry/fish
-dairy
-algae/seweed
-mushrooms

189
Q

sources of folate

A

-leafy green (spinach, kale)
-legumes
-fortified grains/cereals
-sunflower seeds

190
Q

examples of megaloblast macrocytic anaemia

A

-B12 deficiency eg pernicious anaemia
-Folate deficiency eg dietary insufficiency

191
Q

examples of non megaloblast macrocytic anaemia

A

-alcohol
-reticulocytosis (haemolytic)
-liver disease
-hypothyroidism

192
Q

intrinsic vs extrinsic haemolytic anaemia

A

intrinsic is due to abnormalities within the RBC itself whereas extrinsic is due to abnormalities outside the RBC’s

193
Q

intrinsic causes of haemolytic anaemia

A

thalassaemia
G6PD deficiency

194
Q

extrinsic causes of haemolytic anaemia

A

stress from mechanical valve
thrombotic state

195
Q

pathophysiology of haemolytic anaemia from mechanical valves and thrombotic state

A

-mechanical valves and/or thrombotic state
-shear force exerted upon RBC’s
-premature RBC breakdown (haemolysis)
-RBC count reduction
-haemolytic anaemia

196
Q

pathophysiology of haemolytic anaemia from infectious agent

A

-infectious agent
-agent invades RBC’s
-premature RBC breakdown (haemolysis)
-RBC count reduction
-haemolytic anaemia

197
Q

pathophysiology of haemolytic anaemia from thalassaemia

A

-impaired Hb content
-premature RBC breakdown (haemolysis)
-RBC count reduction
-haemolytic anaemia

198
Q

pathophysiology of haemolytic anaemia from G6PD deficiency

A

-exposure to trigger
-premature RBC breakdown (haemolysis)
-RBC count reduction
-haemolytic anaemia

199
Q

describe the difference between intravascular and extravascular haemolytic anaemia

A

intravascular=haemolysis occurring within the vasculature (i.e in the bloodstream)
extravascular=haemolysis occurring outside the vasculature (reticuloendothelial system)

200
Q

what is sickle cell anaemia

A

-caused by specific genetic mutation in the HBB gene (which encloses the beta globin subunits of Hb)
-single base pair change results in sub of glutamic acid wth valine at position 6 on beta-globin chain
-inherited autosmal recessive
-the mutation leads to the production of HbS
-this can lead to RBC deformities into a sickle shape-> vasocclusive events

201
Q

list the consequences of sickle cell disease

A

-Hb structure
-RBC morphology
-Oxygen transport
-haemolysis
-blood viscosity

202
Q

describe abnormal Hb structure in sickle cell disease

A

Substitution of valine for glutamic acid at position 6 of the beta-globin chain results in
the formation of abnormal haemoglobin S (HbS). HbS tends to polymerise under
certain conditions.

203
Q

describe RBC morphology in sickle cell disease

A

HbS polymerisation causes red blood cells to become rigid and assume a sickle
shape, leading to the characteristic sickling of cells.

204
Q

describe oxygen transport in sickle cell disease

A

Sickle-shaped cells have reduced flexibility and difficulty passing through small blood
vessels, leading to vaso-occlusive events. This impairs oxygen delivery to tissues and
organs, contributing to tissue damage and pain.

205
Q

describe haemolysis in sickle cell disease

A

sickle cells have a shorter life span and are more prone to rupture, leading to haemolysis and chronic anaemia

206
Q

describe blood viscosity in sickle cell disease

A

sickle cell increases blood viscosity, making it more difficult for blood to flow through the vessels, which can further impede circulation and contribute to complications

207
Q

list the symptoms and signs of anaemia

A

fatigue
pallor
dyspnoea
weakness
tachycardia
jaundice
splenomegaly
glossitis

208
Q

how does anaemia present with fatigue

A

reduced oxygen carrying capacity of blood (anaemia) leads to tissue hypoxia and fatigue

209
Q

how does anaemia present with pallor

A

Anaemia results in decreased haemoglobin levels, causing pale skin due to reduced
oxygen delivery to tissues.

210
Q

how does anaemia present with dyspnoea

A

Anaemia forces the heart to work harder to compensate, resulting in rapid or laboured
breathing.

211
Q

how does anaemia present with weakness

A

Insufficient oxygen supply to muscles and tissues due to anaemia leads to overall
weakness.

212
Q

how does anaemia present with tachycardia

A

Anaemia triggers the release of compensatory hormones, increasing heart rate to enhance oxygen delivery.

213
Q

how does anaemia present with jaundice

A

Haemolysis (red blood cell breakdown) in certain anaemias results in the release of
bilirubin, causing yellowing of the skin and eyes.

214
Q

how does anaemia present with splenomegaly

A

The spleen may enlarge to compensate for anaemia by producing more red blood
cells or by filtering abnormal ones

215
Q

how does anaemia present with glossitis

A

When iron levels are low in the blood, myoglobin, a protein necessary for muscle formation, including the tongue muscle, is low
affecting taste and appearance

216
Q

list the investigations of anaemia

A

CBE
iron studies
B12/Folate
LDH
Hb electrophoresis
haptoglobin studies
blood films

217
Q

why do CBE in anaemia

A

classification of aetiology via microcytic/macrocytic/normocytic

218
Q

why do iron studies in anaemia

A

low serum iron or ferritin suggests iron deficiency anaemia

219
Q

why do B12/folate studies in anaemia

A

low levels of B12 or folate may indicate megaloblastic anaemia (pernicious anaemia due to B12 deficiency)

220
Q

why do LDH studies in anaemia (lactate dehydrogenase)

A

High LDH may suggest haemolytic anaemia due to various causes, including hereditary disorders or acquired conditions.

221
Q

why do Hb electrophoresis in anaemia

A

helps diagnose and differentiate types of haemoglobinopathies such as sickle cell or thalassemia

222
Q

why do haptoglobin studies in anaemia

A

test for sickle cell anaemia (haptoglobin is released from haemolytic anaemia)

223
Q

why do blood film in anaemia

A

checks for abnormalities in red cell shape, size etc

224
Q

indications and contraindications for diet control in treating anaemia

A

-indication is iron deficiency -contraindications are non iron deficient anaemia

225
Q

indications and contraindications for oral iron in treating anaemia

A

-indications are severe iron deficiency
-contrainidcations are Malabsorption-based iron-deficiency

226
Q

indications and contraindications for IV iron therapy in treating anaemia

A

-indications are pt who are Unable to receive transfusions
-contraindications are Hypersensitivity prone individuals

227
Q

indications and contraindications for B12/folate supplement in treating anaemia

A

-indications are b12/folate deficiency
-contraindiications are unrelated causes of anaemia

228
Q

indications and contraindications for blood transfusion

A

-indication are anaemia with acute threat
-contraindications are Jehovah witness

229
Q

describe the recommended follow up for a patient with anaemia

A

-depends on cause and severity of anaemia
-the frequency of blood tests needed vary greatly between causes and should be assess case-by-case
-in anaemia due to acute leukaemia, bloods needed multiple times day, in iron deficient bloods needed multiple times per day

230
Q

why is infancy a vulnerable stage of life to iron dependency

A

rapid growth and development, high iron needs for building RBC’s and the brain

231
Q

why is adolescence a vulnerable stage of life to iron dependency

A

period of growth spurt and increased physical activity, which requires additional iron for muscle growth and oxygen transport

232
Q

why is pregnancy a vulnerable stage of life to iron dependency

A

Increased iron demand to support the growing foetus and prevent maternal iron
deficiency anaemia.

233
Q

why is menstruation a vulnerable stage of life to iron dependency

A

Monthly blood loss through menstruation necessitates adequate iron intake to
prevent iron-deficiency anaemia

234
Q

list some sources of dietary iron

A

red meat
seafood
fortified cereals
legumes
dark leafy greens
poultry

235
Q

how does Fe2+ and Fe3+ effect the bioavailability of iron

A

Heme iron (animal based) is more readily absorbed (15-35% absorption) compared to non heme iron (found in plant-based sources), which is less efficiently absorbed (2-20% absorption)

236
Q

how does vitamin C effect the bioavailability of of iron

A

Vitamin C (ascorbic acid) enhances the absorption of non-haeme iron. Consuming
vitamin C-rich foods with iron-rich meals can improve iron absorption

237
Q

how does calcium effect the bioavailability of iron

A

Calcium can inhibit the absorption of both heme and non-heme iron. Avoiding high-
calcium foods with iron-rich meals may help improve iron absorption.

238
Q

how do tannins effect the bioavailability of iron

A

Tannins in tea and coffee can interfere with iron absorption. It’s advisable to consume
these beverages separately from iron-rich meals.

239
Q

how do GI disorders effect the bioavailability of iron

A

Conditions such as celiac disease and inflammatory bowel disease can affect iron absorption due to damage to GI tract

240
Q

how does cooking method effect the bioavailability of iron

A

Cooking in iron cookware can increase the iron content of food. Conversely,
overcooking, or excessive heat, can reduce iron content

241
Q

outline food pairing to maximise iron absorption

A

combining foods in a way that enhances the body’s ability to absorb non heme iron eg steak and broccoli

242
Q

common causes of folate deficiency

A

-Old age, poverty, famine, institutions
-Gluten-induced enteropathy
-anticonvulsants
-liver disease, alcoholism

243
Q

common causes of b12 deficiency

A

Veganism
Pernicious Anaemia
Gastrectomy
Ileal resection
Crohn’s disease
Atrophic gastritis

244
Q

what is packed cell volume

A

a measurement of the proportion of blood that is made up of cells

245
Q

what is red blood cell distribution width

A

blood test measures how varied your red blood cells are in size and volume

246
Q

why are reticulocytes tested

A

Tested as an assessment of the function of the bone marrow, more reticulocytes means increased risk of clotting, less reticulocytes means more risk of anaemia

247
Q

what is haemoglobin electrophoresis

A

-Hemoglobin electrophoresis is a test that measures the different types of hemoglobin in the blood. It also checks for hemoglobinopathy disorders involving abnormal types of hemoglobin
-Uses electric current to seperate proteins based on charge
Mainly used to dx sickle cell disease, anaemia

248
Q

what is haptoglobin

A

Binds to and gets rid of Hb outside red blood cells (in the blood)

249
Q

how are direct coombs test interpreted

A

Determines if RBC circulating in the bloodstream are covered with antibodies
-can mean autoimmune, chronic leukaemia, blood disease

250
Q
A

Medical Studies 1 (15 decks)

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