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M1 > week 10 > Flashcards

week 10 Flashcards

1
Q

Where does haemopoeisis occur in the embryo 2

A

yolk sac
liver

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2
Q

where does haemopoeisis occur in the foetus

A

liver
spleen

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3
Q

where does haemopoeisis occur in a developed feotus

A

bone marrow

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4
Q

where does haemopoesis occur in an adult 5

A

bone marrow of skull ribs and sternum
tibula and femur

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5
Q

what type of cell is the haematopoetic stem cell (multipotent., pleuripotent, unipotent)?

A

Pleuripotent

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6
Q

why is a HSC pluripotent 3

A

self renewing
ability to make any blood cell
can also make non haematopoetic stem cells

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7
Q

what does cytosis or philia mean

A

over production

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8
Q

what does penia mean

A

underproduction

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9
Q

what do colony stimulating factors stimulate

A

they stimulate different stafes of haematpetic stem cell differentiation

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10
Q

what are the colony stimulating factors 3

A

M-CSF
GM-CSF
G-CSF

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11
Q

what does M-CSF do

A

HSC into monocytes and macrophages

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12
Q

what does GM-CSF do

A

HSC into granulocytes and macrophages

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13
Q

what does G-CSF do

A

stimulates neutrophil release from the bone marrow

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14
Q

what does thrombopoeitin do

A

increase the production and maturation of platelets from megakaryocytes

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15
Q

structure of red blood cells

A

biconcave disc
lack of nucleus

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16
Q

where does haem synthesis begin

A

in the mitochondria

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17
Q

process of haem synthesis 3

A

amino acids converted into immediates known as porforins

porforins and iron bound together = produces haem

haem bound with haemoglobin protein chains

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18
Q

structure of haemoglobin

A

4 protein chains; two alpha and two beta

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19
Q

haemoglobin F 2

A

foetal haemoglobin dominant till birth

contains alpha and gamma chains

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20
Q

what has a higher affinity for oxygen Haemoglobin F or Haemoglobin A

A

Haemoglobin F

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21
Q

What happens morphologically to erythroblasts as they mature 4

A

cell size and nucleus decreases

cytoplasmic ratio increases

cytoplasmic staining changes from blue to pink

nucleus eventually disappears

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22
Q

where is erythropoetin released from

A

by the JG cells of the juxtamedullary apparatus in the kidneys

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23
Q

EPO production and stimulation of erythrocyte production

A

oxygen assessed at kidneys

if insufficient EPO released

stimulates the bone marrow

increases RBCs

increases haemoglobin oxygen

detected by kidneys

stop releasing EPO

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24
Q

where is the spleen located

A

left upper hypochondriac abodominal quadrant beneath ribs 9-11

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25
Q

where is thymus located

A

bilobed organ located under the sternum, above the heart

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26
Q

function of spleen4

A

immune response
removes old/dysfunctional RBCs
iron recycling
haemoptosis in foetus

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27
Q

white pulp key function

A

immune response

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28
Q

function of red pulp

A

filter and remove bad RBCs

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29
Q

marginal sinus of the spleen

A

plexus of veins located between the white pulp and red pulp

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30
Q

what is the marginal zone of the spleen

A

areas surrounding the marginal sinus containing specialised macrophages and b cells

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31
Q

what do periarteriolar lymphoid sheats (PALS) contain in the spleen

A

T cells and DCs

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32
Q

marginal sinus of the lymph node

A

channels through which lymph travels through the lymph node

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33
Q

movement of lymph through a lymph node 7

A

afferent lymph vessels
marginal sinus
cortex
paracortex
medulla
medullary sinus
efferent lymphatic vessels

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34
Q

which follicle, primary or secondary, in the lymph nodes is the germinal centre for b cells

A

secondary follicles

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35
Q

what doe the medullary cords of lymph nodes contain 1

A

plasma cells whcih produce antibodies which then rapidly enter the blood stream

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36
Q

progression of lymph vessel structure

A

lymph capillary->lymphatc vessels->lymphatic trunk->lymphatic duct

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37
Q

right sided lymphatic drainage

A

drains via right lymphatic duct->right subclavian

equates to drainage of 1/3rd of body

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38
Q

left sided lymphatic drainage

A

drains via large thoracic duct->left subclavian vein

equates to drainage of 2/3rds of body

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39
Q

important lymph nodes in the head 2

A

auricular and occipital

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40
Q

important lymph nodes in the neck

A

cervical chains

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41
Q

important lymph nodes in the upper limbs

A

axillary

42
Q

important lymph nodes in the upper chest

A

mediastinal

43
Q

important lymph nodes in the abdomen

A

coeliac

44
Q

important lymph nodes in the pelvis 3

A

external iliac
common illiac
inguinal

45
Q

important lymph nodes in the lower limbs

A

popliteal

46
Q

what is the plant version of iron and what is its 2 property

A

Fe3+ it has high soluability but low oxygen affinity

47
Q

what is the animal product of iron and what is its two properties

A

Fe2+ it has low soluability and high oxygen affinity

48
Q

what transporter transports iron from the intestinal lumen into the enterocyte

A

DNMT-1 transporter

49
Q

what transporter tranports iron from the enterocyte into the bloodstream

A

ferroportin

50
Q

what transporter transports the iron around the body via the the bloodstream

A

transferrin

51
Q

process of iron absorption 3 chunky

A
  1. Fe3+ converted to Fe2+ by DNMT1 transporters as all iron transporter from intestinal lumen into enterocytes
  2. All Fe2+ in enterocyte transported into bloodstream via ferroportin
  3. All fe2+ changed to Fe3+ by transporter transferrin and then transported arouond the body
52
Q

what facttors influence iron absoption 4

A

hypoxia
erythropoeitin
inflammation
haemochromatosis

53
Q

how does hypoxia influence iron absorption 2

A

increases DNMT1
decreases hepacidin
=
increased iron absorption

54
Q

how does erythropoeitin influence iron absorption

A

decreases hepacidin

55
Q

how does inflammation influence iron absorption

A

increases hepacidin

56
Q

how does haemochromatosis influence iron absorption

A

decreases hepicidin

57
Q

ferritin

A

globular protein taht stores iron

58
Q

apoferritin

A

stores iron in organs such as the liver

59
Q

transferrin role

A

transports iron around the blood
it regulates iron levles

60
Q

hepacidin (function, were produced, when produced)

A

binds to ferroportin and degrades it preventing the release of iron into the blood stream

released during inflammation, infection and when iron stores are high

produced by the liver

61
Q

types of microcytic anaemia
(TAILS)

A

thalassemia
chronic disease anaemia
iron deficiency anaemia
lead poisoninig
sideroblastic anaemia

62
Q

types of macrocytic anaemia
(FATRBC)

A

Folate deficiency
Alcoholic liver disease
Hypothyroidism
Reticulocytosis
B12 deficiency
Cirrhosis

63
Q

2 ways that anaemia is classified

A

size via mean cell volume
reticulocyte count

64
Q

low reticulocyte count anaemia causes (MARBL)

A

myelofibrosis
aplastic anameia
renal failure
bone marrow failure
leukaemia

65
Q

high reticulocyte count anaemia causes 1

A

sickel cell disease

66
Q

thalassemia

A

reduction/absence of a globin chain (Haemoglobin) resulting in the imabalance of alpha and beta chains

67
Q

alpha thalassemia

A

deletions in the globin alpha locus causing impaired/absent production of alpha chains

results in excessive beta chains

68
Q

beta thalassemia

A

mutations in the haemoglobin beta locus resulting in impaired/absent production of beta globin chains

69
Q

genetic differences between alpha thalassemia and beta thalassemia 2each

A

alpha:
due to deletions
affects chromosome 16

beta:
due to mutations
affects chromosme 11

70
Q

thalassemia minor

A

individual has one normal and one mutated/deleted gene

71
Q

thalassemia major

A

both gense for the loci are affected

72
Q

what is the consequence of thalassemia (3 steps)

A

abnormal haemoglobin molecules

cuases structural changes to RBCS

RBCS have shorter lifespans and reduced oxygen carrying capacity

73
Q

majore consequence of beta thalassemia major

A

iron overloading which results in iron deposition in organ tissues

74
Q

complications of iron overloading (heart, liver, endocrine, bone marrow, immune system)

A

heart = heart failure
liver = cirrhosis and fibrosis
endocrine = diabeters and hypothyroidism
bone marrow suppression leading to reduced erythropoeisis
immune system weakened

75
Q

causes of iron deficiency anaemia 5

A

increased demand without supply - kids and pregnancy
dietary lack
malabsorption due to GIT issues
bleeding incl menstruation GI malignancy
impaired iron recycling

76
Q

which population groups are most at risk to becoming anaemic 4

A

pregnant women
non pregnant women
children
elderly

77
Q

4 mechanisms for anaemia pathogenesis in chronic inflammatory diseases

A

mech 1: inflammation->cytokines->increases hepcidin->degrades ferroportin->iron not released from enterocytes

mech 2:inflammation->cytokines->haemopoesis bias to myeloid cell production->inhibits erythropoeis

mech 3: inflammation->cytokines->activate macrophages to initiate erythropoeisis

mech 4: inflammation->cytokines->reduces erythropoeitin

78
Q

food pairing to increase iron (one to do two to avoid)

A

vitamin c w high iron meals
avoid: caffeine+dairy w high iron meals

79
Q

what decreases iron absorption 4

A

caffeine
dairy
reduced stomach acids
antacid usage

80
Q

what increases iron absorption 4

A

stomach acid
vitamin c
meat factor protein
high demand for RBCs

81
Q

where does vitaminb12 absorption occur

A

in the ileum of the small intestine

82
Q

where is folate absorbed

A

in the duodenum and jejunum

83
Q

why are b12 and folate important in erythropoeisis

A

help in RBC production, formation and maturation

84
Q

what can macroyctic anaemia be further subdivided into 2

A

magaloblastic or non megaloblastic

85
Q

the 2 causes of megaloblastic anaemia

A

b12 deficinecy
folate deficiency

86
Q

megaloblastic def

A

erythroblasts have delayed nucleus maturation due to defective DNA synthesis

87
Q

causes of b12 deficiency (think Joe 2)

A

veganism
crohn’s disease

88
Q

causes of folate deficiency 6

A

povery
old age
pregnancy
cancer
liver disease
alcoholism

89
Q

autoimmune causes of b12 deficiency mech 3

A
  1. autoimmune destruction of the stomach’s gastric mucosa
  2. lack of intrinsic factor seceretion
  3. prevents b12 absorption
90
Q

anticonvulsants and associated anaemia

A

causes folate deficiency

91
Q

3 key characteristics of haemolytic anaemia

A

increased red cell breakdown
increased red cell production
damaged red cells

92
Q

intrinsic haemolytic anaemia def 2

A

hereditary red blood cell defects due to gene mutations and G6PD deficiency

93
Q

extrinsic haemolytic anaemia (3 examples of causes)

A

acquired red blood cell defects which can be due to:
- drugs
- autoimmune
- infection

94
Q

intravascular haemolytic anaemia 2

A

occurs within blood vessels

indication is fragemnetd RBCs present in blood

95
Q

extravascular haemolytic anaemia

A

occurs outside of blood vessels in locations such as the spleen and liver

96
Q

sickle cell disease 2

A

due to amino acid swap in beta globulin gene

autosomal recessive

sickle cell disease = homoxygous
sickle cell trait = heteroxygous

97
Q

results of sickle cell disease 5

A
  • redcued oxygen carrying capacuty due to morphology
    -tissue damage due to morphology
    -shorter lifespan
    -more prone to ruptue
    -increase blood viscosisty
98
Q

general organ tests when suspecting anaemia 3

A

thyroid function
renal function
liver functino

99
Q

specific blood tests 6

A

CBE
blood film
iron studies
vitaminb12 and follate assay
Hb electrophoresis
bone marrow biopsy

100
Q

indications of haemolysis

A

high bilirubin
high reticulocyte count
high LDH

101
Q

anaemia management (case dependent but…)

A

vitamin b12/folate injection
iron replacement
transfusion

102
Q
A

M1 (13 decks)

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