Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MELS302 > Red Cells > Flashcards

Red Cells Flashcards

1
Q

RBC lifecycle

A

EPO released by kidneys when it senses low oxygen tension
Stimulates RBC production in bone marrow
120 life span
Must pass through the sinusoids of MPS (mononuclear phagocyte system) where it is trapped and phagocytosed if deformed from ageing
RBC broken into haem (bilirubin/iron) and Globin (amino acids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does RBC breakdown into

A

Haem - bilirubin and iron
Globin - amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is an erythrocyte made and order of development

A

Pluripotent stem cell stimulated by specific IL to “pick” the erythroblasts lineage. This happens after EPO binds to stem cells to stimulate the process
BFU-E then CFU-E
Pro erythroblasts, erythroblasts, reticulocyte, erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Order of expansion from haemopoietic stem cells to erythrocytes

A

Haemopoietic stem cells
Proerythroblasts
Basophilic erythroblasts
Polychromatic erythroblasts
Reticulocytes - 7-10 days to get here
Erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do the erythroblasts do in the bone marrow

A

Proliferate
Iron uptake from macrophages
Hb production
Removal of organelles via macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an erythroid island

A

Erythroblasts surround a macrophage in the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is haem and Globin produced

A

Globin produced on polyribosomes
Haem produced in mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the MPS

A

Mononuclear phagocyte system also known as the reticuloendothelial system where monocyte derived cells phagocytose bacteria, present antigens and make cytokines and find old RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens to RBC as they age

A

Membrane lipids and proteins are damaged and lost
Enzymes decrease
CD47 decrease
CD55/59 decrease
Increased phosphatidylserine
Increase rigidity and surface changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is CD47

A

An adhesion molecule which stops phagocytosis of cells
Decreases as RBC age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is CD55/59

A

Decay acceleration factor which degrades activated complement proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where are RBC phagocytosed

A

Splenic cords, marrow and liver sinusoids through the MPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does the splenic cords remove old RBC

A

old RBC are rigid with cell surface changes so they cannot pass through the endothelial cells in the splenic sinuses and are macrophages by RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hb triangle

A

Hb
MCH RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ht triangle

A

Ht
MCV RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MCH triangle

A

MHC
MCHC MVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 most important RBC indices

A
  1. Hb
  2. MCV
  3. MHC
    Then RBC for disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define anisocytosis

A

Abnormal cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define ansiochromia

A

Variation in colour between cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Poikilocytosis

A

Variation in cell shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Polychromasia

A

More blue colour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Conditions relating to hypochromic microcytic

A

Iron deficiency
Thalassaemia
HbE
Anaemia of chronic disease
Lead poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Conditions for normochromic normocytic

A

Renal disease
Anaemia of chronic disease and lead poisoning (tendency for microcytic)
Blood loss
BM failure
Haemoglobinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Conditions for macrocytic anaemia

A

Megaloblastic: B12/folate deficiency
Non-Megaloblastic: liver disease, drugs, alcohol, reticulocytosis, aplastic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Most common cause of anaemia

A

Iron deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of iron deficiency

A

Chronic blood loss (period, GI bleeding from tumour or ulcerations)
Increased demand in pregnancy/children/recovering from blood loss
Dietary deficiency
Malabsorption disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Iron cycle

A

Most goes to the bone marrow to make erythrocytes, this is recycled using transferrin
Iron lost chronic blood loss/urine/poo/hair/skin/nails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How to diagnosis iron deficiency anaemia

A

Blood film - microcytic hypochromic, pencil and targeting so poikilocytosis also o along with increased central pallor
Check ferritin levels - should be increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

False ferritin elevation seen when

A

In inflammation - recent or current
Cancers maybe
Acute liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Anaemia of chronic disease appears like what on blood film

A

Normochromic with a tendency to be microcytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What happens widely in anaemia of chronic disease

A
  1. Hepcidin is up-regulated in the liver so iron sequestered in macrophage so less for RBC production
  2. Inhibits EPO release in kidneys so less stimulation in BM
  3. Inhibits erythroid production
  4. Augments hemophagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Is normal RBC breakdown extravascular or intravascular

A

Extravascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where does normal RBC breakdown happen

A

Phagocytosis of old/damaged RBC in the splenic cords/marrow/liver sinusoids. This is the mononuclear phagocyte system. If the RBC cannot pass through the narrow endothelium it is phagocytosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does RBC breakdown into

A

Globin - amino acids
Iron - binds to transferrin
Protoporphyrin - bilirubin then liver into faeces/urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Extravascular haemolysis

A

Destruction via macrophages in organs
Due to RBC abnormality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Intravascular haemolysis

A

Lysis of cells in blood vessels
Accompanied by extravascular haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens to Hb in intravascular haemolysis - oxidation route

A

Excess is oxidised to Fe3+ where the Globin chain is recycled
Methaem and albumin make methaemalbuminaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Intravascular haemolysis - haptoglobin route

A

Hb binds with haptoglobin and is cleared by macrophages in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Intravascular haemolysis- kidney route

A

Filtered by glomeruli
Reabsorbed by renal tubules until saturated = haemoglobinuria
Iron from breakdown is absorbed by renal tubules and stored as Haemosiderin = haemosiderinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does increased haemolysis lead too

A

Haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Hereditary causes of haemolytic anaemia

A

Membrane abnormalities
Some Haemoglobinopathies
Enzymopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Acquired causes of haemolytic anaemia

A

Antibodies directed at self RBC
Infections like malaria
Secondary to severe renal/liver disease
Mechanical/chemical/physical agents
Microangiopathic (TTP/HUS/DIC)
PNH - cells missing CD55/59

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does chronic haemolysis present as

A

Jaundice - as more RBC breakdown = more bilirubin
RBC production increases as there is never enough (6-8 times increase)
Erythroid hyperplasia
But mild haemolysis may be asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Clinical features of haemolytic anaemia

A

Pallor
Jaundice = icteric sclera (yellow eyes), increase risk of gallstones
Splenomegaly (cell trapping)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chronic hereditary haemolytic anaemia effect

A

Aplastic crisis
Infection with parvovirus B19, Hb will rapidly decline as erythropoiesis stops but haemolysis continues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lab features in haemolytic anaemia

A

Increased unconjugated bilirubin, LDH, urinary urobilinogen
Haptoglobins are absent as Hb binds and then is cleared
Haemoglobinuria, Haemosiderin, methaemalbuminaemia

Reticulocytosis
Low folate levels
Erythroid hyperplasia (myeloid:erythroid ratio decreases)

Poikilocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are RBC membranes made of (%)

A

52% protein for protection and structure
40% lipids for elasticity and strength
8% carbs for protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name two RBC surface proteins

A

CD55 and CD59

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does CD55 do

A

Degrades complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does CD59 do

A

Inhibits lysis
MAC inhibitory protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What do RBC membrane lipids do

A

Confers elasticity and cholesterol confers tensile strength
Phospholipids redistribute when membrane is disrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What do integral proteins do on RBC membrane

A

Transport and osmotic tension
Adhesion and receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

List skeletal proteins in inner RBC membrane

A

Ankyrin, protein 4.1/4.2, actin, alpha and beta spectrum form a horizontal scaffold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What do skeletal proteins do

A

Interact with integral proteins for lateral structure and to maintain biconcave shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What happens during RBC deformation (skeletal proteins)

A

Spectrin helices and bonds open and close during RBC deformation
Abnormalities cause poikilocytosis which decreases lifespan and deformability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the RBC membrane permeable too

A

water, HCO3-, Cl-
GLUT1 transports glucose
Ca2+ ATPase pumps out Ca2+
Na and K pumps

57
Q

List RBC membrane disorders

A

Hereditary spherocytosis/eliptocytosis/stomatocytosis/ovalocytosis

58
Q

What is HS

A

Hereditary spherocytosis
Mutated gene caused by deficiency of skeletal proteins like ankyrin/spectrin/protein 4.2, band 3

59
Q

What happens to the RBC in HS

A

Loss of skeletal proteins
Loss of membrane as underlying connection is broken
Less SA:V ratio
Decreased deformability so cells get trapped in the spleen

60
Q

HS signs

A

Jaundice
Splenomegaly
Can be asymptomatic or severe anaemia

61
Q

HS blood film

A

Spherocytosis
High bilirubin
Low haptoglobin or none
Reticulocytosis
Polychromatic cells
Poikilocytosis
Anisocytosis

62
Q

DAT for HS

A

Negative for IgG on RBC

63
Q

What is an EMA and when is it used

A

Eosin 5 maleimide assay
Fluorescent dye binds to skeletal proteins in RBC so low fluorescence in HS as they are deficient in these proteins

64
Q

What is an SDS-PAGE and why is it not good

A

Genetic test for HS
identifies primary gene defect
BUT difficult as many proteins can be affected and expensive

65
Q

What is a historical test for HS

A

Increased RBC osmotic fragility
Measures haemolysis in increasing conc of saline
Doesn’t confirm

66
Q

Complications of HS

A

Haemolytic crisis
Megaloblastic crisis from folate deficiency
Gallstones
Aplastic crisis in parvovirus B19

67
Q

Treatment for mild HS

A

None needed

68
Q

Treated for severe HS

A

Splenectomy

69
Q

How does a splenectomy help HS

A

Cells survive longer
Less bilirubin and so lower risk of gallstones

70
Q

What are you at the risk of post splenectomy

A

Sepsis and strep pneumoniae infections so need vaccinations and prophylaxis

71
Q

Blood film after a splenectomy

A

Howell jolly bodies
Spherocytea
Target
Thrombocytosis
Pappenheimer bodies
Acanthrocytes

72
Q

What is G6PD deficiency

A

genetic decrease in G6PD leading to early death of RBC in spleen

73
Q

Genetical pattern of G6PD

A

X linked recessive
7.5% Africa as malaria resistance

74
Q

Class 1 and 2 G6PD

A

Severe
All RBC have less G6PD so chronic haemolysis

75
Q

Class 3 G6PD

A

Mild - African type
Young RBC have normal G6PD but it loses function
Oxidative stress = acrid haemolysis

76
Q

What type of haemolysis is seen in G6PD deficiency

A

Extravascular mainly by macrophages
Some intravascular

77
Q

How does G6PD deficiency cause Heinz bodies

A

Hb gets oxidised by radicals which damages RBC membrane and Hb is oxidised
The denatured Hb precipitates and sticks to inner membrane

78
Q

Blood film G6PD

A

If in haemolytic crisis - blister cells, bite cells, Heinz bodies, spherocytosis, fragments, poikilocytosis, reticulocytosis

79
Q

What makes G6PD WORSE

A

Oxidative stress from drugs, infections, fava beans

80
Q

Other lab finding of G6PD

A

Haemoglobinuria and retics

81
Q

How to treat or avoid G6PD crisis

A

Vaccination
Antibodies
Avoid fava beans and some drugs

Transfusion, dialysis, splenectomy if severe

82
Q

G6PD blood film in a haemolytic crisis

A

Normal
FBC normal too

83
Q

G6PD should be done when

A

After a crisis when reticulocytosis count and Hb are normal
120 days after as reticulocytes have increases G6PD

84
Q

Core four in G6PD crisis

A

Increased reticulocytes/LDH/bilirubin
Low or absent haptoglobin

85
Q

G6PD effect on neonates

A

Neonatal Hyperbilirubinaemia
2-3 days after birth = jaundice

86
Q

What is kernicterus

A

Bilirubin in Brain
Possible in neonatal Hyperbilirubinaemia

87
Q

4 types of AIHA

A

Warm
Cold
Paroxysmal cold haemoglobinuria
Mixed - rare

88
Q

What does a DAT do

A

Positive in AIHA
Detects IgG and Cd3 on RBC surface

89
Q

What type of haemolysis is happening in AIHA

A

Extravascular by macrophages
And/or intravascular complement mediated haemolysis

90
Q

What causes warm AIHA

A

IgG that reacts at 37
Idiopathic, secondary to autoimmune disorders/neoplasms/viral infections/immunodeficiency

91
Q

Treatment of warm AIHA

A

Splenectomy is chronic and refractive
Treat underlying (immunotherapy)

92
Q

Presentation of warm AIHA

A

fever
Jaundice
Hepatosplenomegaly
Mainly extravascular with spherocytea and polychromasia

93
Q

Cold AHIA cause by what antibody

A

IgM autoantibodies reacting at 4 degrees

94
Q

Pathogenic cold AHIA

A

High IgM autoantibody titres, reactive above 30C causing cold agglutin disease

95
Q

Non pathological cold AIHA

A

low titres of IgM autoantibodies, polyclonal antibodies, non reactive above 30C

96
Q

What causes acute cold agglutinin disease

A

Secondary to infection
EBV, mycoplasma pneumoniae
Self limiting, polyclonal with some anaemia

97
Q

What causes chronic cold agglutinin disease

A

Idiopathic
Secondary to LPD

98
Q

How to diagnosis CAD

A

High titres antibodies in blood tube but needs to be warmed to 37 for a blood film and analysis

99
Q

What should people with chronic CAD do

A

Avoid cold temps
Supportive therapy
Monoclonal Ab therapy (anti CD20)

100
Q

Presentation of chronic CAD

A

Monoclonal antibodies in middle aged and elderly
Variable anaemia and cyanosis

101
Q

What is paroxysmal cold haemoglobinuria

A

Acute intravascular haemolysis after cold exposure

102
Q

What triggers paroxysmal cold haemoglobinuria

A

Viruses and syphilus
Self limiting tho

103
Q

What do the antibodies do in paroxysmal cold haemoglobinuria

A

IgG antibody binds to P blood group antigens
Binds to RBC in cold but in warm lysis of RBC happen

104
Q

3 methods of drug induced immune haemolytic anaemia

A

1 Hapten mediated (antibody against drug membrane complex in penicillin)
2 complement mediated (Ab against drug-protein complex)
3 True AIHA (unclear drug does)

105
Q

What is microangiopathic haemolytic anaemia

A

Endothelial injury from shear stress causes micro thrombi formation
Fibrin damages RBC in small vessels
Two types : TTP and HUS

106
Q

What is microangiopathic haemolytic anaemia associated with

A

Gram nega septicaemia
DIC
malignant hypertension
Pre eclampsia
Some drugs

107
Q

Lab findings with microangiopathic haemolytic anaemia

A

Schistocytes
Severe - jaundice, reticulocytosis

108
Q

What is TTP Pentad

A

MAHA
thrombocytopenia
Neurological effects
Maybe fever and renal dysfunction

109
Q

HUS triad

A

MAHA
renal failure
Thrombocytopenia

110
Q

TTP and HUS is more common in who

A

TTP - women 30-40y
HUS - children 6m-4y

111
Q

TTP stands for

A

Thrombotic thrombocytopenic purpura

112
Q

HUS stand for

A

Haemolytic uraemic syndrome

113
Q

What happens in TTP

A

Autoantibody go ADAMTS13
Enzyme that cleaves vWF causing accumulation of lots of large vWF multimedia leading to thrombosis

114
Q

What happens to EPO in anaemia of renal disease

A

Low EPO also triggers neocytolysis
Less RBC made
So you get normocytic normochromic anaemia with Hb 50-80g/L

115
Q

What happens to RBC in anaemia of renal disease

A

RBC survival decreases to 70-90 days
Waste products build up in kidneys further impacts lifespan

116
Q

Anaemia of renal disease blood film

A

Burr cells

117
Q

What does lead poisoning interfere with

A

Porphyrin production and incorporation of iron

118
Q

How to treat lead poisoning

A

Remove lead by chelating using EDTA

119
Q

Leading poisoning symptoms in children and adults

A

Peripheral neuropathy
Vomiting
Abdomen cramps

120
Q

Leasing poisoning effects on infants

A

CNS effects
Impaired mental

121
Q

Lead poisoning blood film more

A

Normocytic to microcytic
Reticulocytosis
Basophilic stippling

122
Q

What is basophilic stippling

A

Undegraded ribosomes aggregates

123
Q

What happens to DNA synthesis in Megaloblastic anaemia

A

DNA synthesis and cell division is inhibited
Cells will die or grow without diving making them bigger but less are there

124
Q

Less common causes of Megaloblastic anaemia

A

MDS
myelosuppressive drugs
Congenital

125
Q

Most common cause of Megaloblastic anaemiA

A

B12 and folic acid deficiency

126
Q

Causes of B12 deficiency

A

Nutritional - vegetarian
Need intrinsic factors as hard to absorb

127
Q

Causes of folate deficiency

A

Nutritional
Malabsorption

128
Q

Main sources of B12

A

Animal and diary produxts

129
Q

Body stores for B12

A

2-4 years

130
Q

Where is B12 absorbed

A

Distal ileum

131
Q

Where is folate absorbed

A

Duodenum/jejunum

132
Q

Body stores for folate

A

3-4 months

133
Q

Where is folate found

A

Greens
Nuts
Eggs
Liver
Cereal

134
Q

Is folate destroyed in cooking

A

Yes

135
Q

Megaloblastic clincial features

A

Loss of epithelial cells as all cell division is effected so GI and skin problems
Jaundice
Neurological

136
Q

Blood film Megaloblastic anaemia

A

Low reticulocytes
Pancytopenia if severe
Oval cells
NRBC
Poikilocytosis -ani
Hypersegmented neutrophils
Howell jolly bodies
Basophilic stippling
Leftover spindle

137
Q

What happens to LDH and bilirubin in Megaloblastic anaemia

A

Increase LDH and bilirubin from ineffective erythropoiesis

138
Q

Non Megaloblastic causes

A

Liver disease
Alcohol
Hypothyroidism
Reticulocytosis
Aplastic anaemia
Normal in neonates
Drugs

MELS302 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions