PHYSIOLOGY Flashcards

1
Q

where are bone marrow biopsy/aspirates taken from

A

PSIS

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2
Q

bone marrow hyperplasia definition

A

increased bone marrow production

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3
Q

bone marrow dysplasia definition

A

disordered bone marrow production

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4
Q

bone marrow hypoplasia definition

A

decreased bone marrow production

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5
Q

bone marrow aplasia definition

A

no bone marrow production

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6
Q

hypercellular bone marrow definition

A

increased cell production (eg RBCs) from bone marrow

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7
Q

hypocellular bone marrow definition

A

decreased cell production (eg RBCs) from bone marrow

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8
Q

what is in yellow marrow

A

fat

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9
Q

what is in red marrow

A

the haemopoietically active bit

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10
Q

whats the normal ratio of red to yellow marrow

A

50:50

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11
Q

what does yellow>red marrow mean

is it hypo or hypercellular

A

bone marrow suppression

hypocellular (the red bit is the active bit)

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12
Q

causes of hypocellular bone marrow

A

drug induced aplasia

aplastic anaemia

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13
Q

what does red>yellow marrow mean

is it hypo or hypercellular

A

bone marrow over activation

hypercellular (the red bit is the active bit)

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14
Q

causes of hypercellular bone marrow

A

peripheral destruction of cells eg hypersplenism, autoimmune haemolytic anaemia

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15
Q

what is immunophenotyping of cells used for

A

to tell which lineage a cell has come from

by looking at antigen expression

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16
Q

what does -cytosis mean

A

high …

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17
Q

what does -philia mean

A

high …

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18
Q

what does -penia mean

A

low …

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19
Q

which cells have the ability to self renew

A

stem cells

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20
Q

which hormone produced by the kidney regulates the production of RBCs

A

EPO (erythropoietin)

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21
Q

which hormone regulates production of platelets

A

thrombopoietin

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22
Q

where does haematopoiesis start in the fetus

A

yolk sac

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23
Q

which bones does haematopoiesis occur in in the fetus

A

all bones

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24
Q

which bones does haematopoiesis occur in in the adult

A
skull 
ribs 
sternum 
proximal humerus 
pelvis 
proximal femur
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25
Q

where do you get bone marrow samples from in children

A

tibia

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26
Q

how long do RBCs live for

A

3-4 months

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27
Q

what is the process of making RBCs called

A

erythropoiesis

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28
Q

another name for RBCs

A

erythrocytes

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29
Q

what is the function of RBCs

A

to carry oxygen in the blood to tissues

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30
Q

how is most oxygen transported in the blood

what % is bound to haemoglobin

A

60% dissolved as bicarbonate
30% transported by binding to haemoglobin
10% dissolved in solution

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31
Q

apart from directly binding O2 to hemoglobin, what other function does RBCs have in transporting O2 in the blood

A

RBCs are need to make bicarbonate (which is how 60% of O2 is transported)

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32
Q

what are the RBC precursors (in order) (4 precursors)

A

stem cells
common myeloid progenitor cell
erythroblast/normoblast
reticulocyte

then erythrocyte (RBC)

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33
Q

what genetic material does an erythroblast contain

A

has a nucleus

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34
Q

what genetic material does a reticulocyte contain

A

has RNA

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35
Q

what genetic material does an erythrocyte contain

A

none!

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36
Q

what do reticulocytes look like in comparison to RBCs

A

bigger

more purple

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37
Q

as RBCs develop during erythropoiesis, what is added to each of the cell types to form the next

what is taken away, by what process

A

haemoglobin is added

genetic material is removed = enucleation

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38
Q

when is EPO produced by the kidneys

A

hypoxia (occurs with anaemia)

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39
Q

what happens to RBC production in kidney failure

A

decreased = anaemia

bc kidneys cant sense hypoxia = cant produce EPO = no negative feedback to compensate for anaemia

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40
Q

what does EPO (erythropoietin) directly do

A

causes erythroid hyperplasia = increased RBC production in bone marrow

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41
Q

what shape are RBCs

A

biconcave

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42
Q

do RBCs have a nucleus

A

no - no DNA, enucleation occurs to produce RBCs

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43
Q

do RBCs have mitochondria

A

no

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44
Q

the nucleus of what cell type should be the same size as a RBC

A

nucleus of lymphocyte = same size as RBC

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45
Q

in the mitochondria, what 2 things combine to make a haem group

A

Fe2+ and photoporphyrin ring

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46
Q

what do haem groups bind with to make haemoglobin

where does this happen

A

globin

in the cytoplasm

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47
Q

in adults (HbA) what are the 4 haemoglobin subunits

A

2 alpha

2 beta

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48
Q

in fetus (HbF) what are the 4 haemoglobin subunits

A

2 alpha

2 gamma

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49
Q

which state must iron be in for O2 to bind to

A

Fe2+

if Fe3+ needs to be reduced

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50
Q

where is iron absorbed

A

duodenum

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51
Q

is haem iron or non-haem iron better absorbed

A

haem iron

non-haem iron is in plants (veggie diet)

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52
Q

iron transporter between duodenal epithelium and blood stream (for iron to be transported in blood)

A

ferroportin

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53
Q

how is free iron transported round the body in the blood

A

as transferrin

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54
Q

where is the majority of the bodys iron

where else is it

A

70% in haemoglobin

rest; liver, bone marrow, macrophages etc

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55
Q

why must Fe2+ be bound (ie to oxygen or transferrin)

A

otherwise free radical production

56
Q

in what form is iron stored in the liver

A

ferritin (also small amount in blood as ferritin)

57
Q

which parts of the body have transferrin receptors (hence transferrin can transport iron there)

A

liver

bone marrow

58
Q

marker of circulating iron

A

transferrin

59
Q

marker of iron stores

A

serum ferritin - small amount of ferritin in blood is representative of the ferritin stores in liver/macrophages

60
Q

excretion of iron

A

doesn’t happen naturally

need iron chelating drugs to excrete in urine/faeces

61
Q

how many oxygens bind to 1 haemoglobin subgroup

how many oxygens bind to 1 RBC

A

1 O2 per subgroup

4 O2 per RBC (bc 4 subgroups)

62
Q

how does oxygen bind to RBCs

what does this mean

what shape of curve does this produce on a graph

A

by cooperative binding

once one O2 has bound, there is increased affinity for the next O2 to bind = allosteric effect

sigmoidal curve

63
Q

does fetal Hb saturate more or less at the same pO2 compared to adult Hb

A

saturates more at same pO2 = bc needs to take O2 from maternal circulation

64
Q

methods of shifting O2-Hb curve to the right (ie increasing O2 binding when higher O2 demands)

A

increase temp
increase CO2
increase DPG
DEcrease pH - rest are increase!

65
Q

what shunt generates DPG

what is this important for

A

rapapoport-lubering shunt

shifts the O2-Hb curve to the right = increases O2 binding

66
Q

how much O2 does 1g of saturated Hb bind

A

1.34ml O2

67
Q

where are RBCs destructed

A

spleen

68
Q

what cells remove old RBCs from circulation and take them to the spleen for destruction

A

macrophages

69
Q

in RBC destruction, what are globin chains broken down into

A

amino acids

70
Q

in RBC destruction, what are the haem groups broken down to

A

porphyrin ring and Fe2+

71
Q

in RBC destruction, after haem has broken down into porphyrin ring and Fe2+, what is the porphyrin ring broken down into

then what

A

haem
then porphyrin ring (+ Fe2+)
then biliverdin
then bilirubin

72
Q

after RBC destruction, where is bilirubin taken to, what happens to it

A

bilirubin taken to liver

liver conjugates bilirubin = excreted in bile (urine and faeces)

73
Q

if there is no mitochondria in RBC, where do they get their energy from

A

glycolysis (needs glucose)

74
Q

what chemical prevents the oxidation of Fe2+ to Fe3+by free radicals

A

NADH

75
Q

what chemical prevents the formation of free radical forming (which is important to prevent oxidative damage to RBCs)

what is this chemical made form

what is the rate limiting enzyme involved in its formation

A

glutathione (GSH)

made from NADPH

G6PD is the rate limiting enzyme

76
Q

function of WBCs

A

fight infection

77
Q

3 categories of WBCs

A

monocytes
lymphocytes
granulocytes (3)

78
Q

3 types of granulocytes

A

neutrophils
basophils
eosinophils

79
Q

where do you find monocytes

A

in circulation

in the tissues they are called macrophages

80
Q

where do you find macrophages

A

in tissues

in the circulation they are called monocytes

81
Q

WBC

larger horseshoe shaped nucleus

A

monocyte

82
Q

what does a monocyte look like

how many nuclei

A

large single horseshoe shaped nucleus

mono= one nucleus

83
Q

function of monocytes/macrophages

A

phagocytosis

84
Q

types of lymphocyte

A

NK cells
T cells
B cells
dendritic cells

85
Q

where are T cells made

A

thymus

T cells = Thymus

86
Q

where are B cells made

A

bone marrow

B cells = Bone marrow

87
Q

what do mature lymphocytes look like

what do activated lymphocytes look like

A

mature lymphocytes - small, condensed nucleus, rim of cytoplasm
activated lymphocyte - large, ‘open’ nucleus, lots of cytoplasm

88
Q

when are lymphocytes ‘activated’

A

viral infection

89
Q

lymphocytes with lots of cytoplasm and an ‘open’ nucleus

A

activated lymphocytes = viral infection

90
Q

what should the lymphocyte nucleus be the same size as

A

RBC

91
Q

when do you get lymphocytosis (high lymphocytes)

A

viral infection
childrens infection
CLL

92
Q

are granulocytes in the myeloid or lymphoid lineage

A

myeloid

93
Q

are platelets in the myeloid or lymphoid lineage

A

myeloid

94
Q

are RBCs in the myeloid or lymphoid lineage

A

myeloid

95
Q

are lymphocytes (NK cells, B cells, T cells, dendrites) in the myeloid or lymphoid lineage

A

lymphoid

96
Q

eosinophil appearance

granule stain
nucleus shape

A

granules stain red

bi lobed nucleus

97
Q

neutrophil appearance

granule stain
nucleus shape

A
neutral stain (don't colour) 
segmented nucleus (hence polymorph)
98
Q

basophil appearance

granule stain
nucleus shape

A

granules stain dark blue (Basophils = Blue)

nucleus is obscured by granules

99
Q

eosinophil function

A

parasitic infection

hypersensitivity IgE reaction (allergy)

100
Q

basophil function

A

hypersensitivity IgE reactions (contains histamine)

RARE in circulation

101
Q

neutrophil function

A

phagocytosis
chemoattraction of other immune cells
margination (stick to vessel walls)

102
Q

which type of granulocyte is least common in circulation

A

basophils

103
Q

what is the circulating version of a mast cell

A

basophils

104
Q

another name for neutrophils

A

polymorphs

105
Q

which type of granulocyte is most common in circulation

A

neutrophil

106
Q

how long is the life span of a neutrophil

clinical significance of this

A

7-8 hours

in pancytopaenia (bone marrow failure), neutropenia is the first symptom (RBCs last 3 months)

107
Q

how do steroid cause neutrophilia (high neutrophils)

A

inhibit margination of neutrophils to vessel walls = more in circulation (not actually ore made)

108
Q

neutrophilia aetiology

A

infection
trauma
steroids

109
Q

life span of platelets

clinical significance of this

A

7-10 days

need to stop anti platelet (aspirin) 1 week before surgery

110
Q

function of platelets

A

stop bleeding via primary haemostasis

111
Q

platelet precursor

A

megakaryocyte

112
Q

how are platelets made from megakaryocytes

A

‘budding’ cytoplasm ‘buds off’ = platelet

rest of cell remains in bone marrow

113
Q

what are plasma cells

A

mature B cells that have returned to bone marrow

114
Q

where are lymphoid cells made

A

primary lymphoid tissues - thymus and bone marrow

115
Q

primary lymphoid tissues

A

thymus and bone marrow

116
Q

after production in primary lymphoid tissues (thymus and bone marrow) where do lymphoid cells go

A

secondary lymphoid organs - lymph nodes, spleen, tonsils

117
Q

what does the lymph node filter

A

lymphatic fluid

118
Q

what does the spleen filter

A

blood

119
Q

where does lymph from L torso and arms drain

A

between L subclavian and jugular veins

120
Q

where does lymph from R torso and arms and lower limbs drain

A

thoracic duct (between the R subclavian and jugular veins)

121
Q

causes of enlarged lymph nodes (4)

A

local infection
systemic inflammation - TB, autoimmune
malignancy
other stuff - sarcoidosis, SLE

122
Q

enlarged cervical lymph nodes with atypical lymphocytes

A

local infection
EBV (glandular fever)

atypical lymphocytes = viral infection

123
Q

are lymph nodes painful in local infection

A

yes

bc fast growing

124
Q

types of malignancy that can present as enlarged lymph nodes

A

haematological - lymphoma, leukaemia

metastatic

125
Q

most common cause of enlarged lymph nodes

A

local infection (though always consider malignancy)

126
Q

are lymph nodes painful if malignancy cause

A

no

bc slow growing

127
Q

consistency of lymph nodes in lymphoma

A

soft/rubbery

other causes = hard

128
Q

what aetiology of enlarged lymph nodes causes irregular consistency of hard lymph nodes

A

metastatic cancer

129
Q

lymph node biopsy; predominantly B cells

A

autoimmune condition

infection

130
Q

lymph node biopsy; predominantly T cells

A

viral infection

drugs - phenytoin

131
Q

lymph node biopsy; predominantly phagocytes

A

tumour

132
Q

what is accumulation of lymph fluid in the peritoneal cavity called

what causes it

A

chylous ascites

caused by trauma/obstruction of lymphatic system

133
Q

causes of splenomegaly

A

infection eg EBV
portal congestion
haemotological disease eg lymphoma, leukaemia, haemolytic anaemia
inflammatory conditions

134
Q

how can splenomegaly present on the skin

how does it occur

A

jaundice

hypersplenism = increased function of spleen =increased destruction of RBCs = increased RBC degradation products (bilirubin) = liver cant cope = accumulation of bilirubin = jaundice

135
Q

how does hyposplenism present on histology

what are they
how do they occur

A

Howell joly bodies

RBCs with small fragments of DNA
they are normal RBCs but are usually removed by the spleen, so hyposplenism = underactive spleen = doesn’t remove them