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Clinical Haematology Flashcards

(50 cards)

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1
Q

Blood Constituients

A

55% Plasma
45% Reds
Buffy coat (platelets, white cells) <1%
Also proteins

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2
Q

Diagnosing disease by looking at levels of blood constituents.

A

Separate based on density.

-too few reds= anemia
-too many whites= sepsis, leukaemia
-plasma changes= degradation or cancer (haemorrhage) (effects oxygenation)

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3
Q

Blood plasma characteristics

A

-95% water
-carries hormones, plasma proteins, inorganic ions, waste
-major co2 transporter (freely dissolved in plasma)
-prescribe when have low albumin (transporter)
- 70% of proteins in blood is albumin

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4
Q
A
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5
Q

What is haemopoiesis?

A

-Production of blood cells
- occurs in bone marrow of pelvis, femur
- from hematopoetic stem cells (from hemocytoblast)
-only see terminally differentiated stem cells in which peripheral blood

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6
Q

Myeloid cell lineage

A

Haematopoetic stem cell
Myeloid (mitosis one stem cell other differentiated)
Erythrocyte or myeloblast
Myeloblast -> other whites (immune cells)

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7
Q

Lymphoid cell lineage

A

Hematopoietic stem cell
Lymphoid (mitosis one stem cell other differentiated)
Lymphocytes
NK, B, T, Plasma cells

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8
Q

Changes in location of haematopoesis during ageing ?

A

-Prenatal = liver, spleen, yolk sac (if production here in adulthood = disease)
-veterbrae pelvis (all times)
-ribs, femur, tibia and sternum (decreased with age)

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9
Q

Diagnosing haematological disease

A

-sample from hematopoetic organs to see cells
-too much bones engaged in haematopoiesis can be bad thalassemia (e.g skull)

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10
Q

Haematopoeitic (bonemarrow) microenvironment

A

-Haematopoietic cells
-adipose tissue (energy)
-extra cellular matrix supports (C.T)

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11
Q

ECM Function in Haematopoietic Microenvironment

A
  • compartmentalises HP tissue
  • structural support
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12
Q

Haematopoietic Vascular Supply

A
  • Sinus lined with endothelial cells, controlling release of mature cells into peripheral blood.
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13
Q

How sinuses in HP microenvironment control which cells leave?

A
  • based on size, mature cells smaller able to fit (flexibility)
  • mature cells lose surface markers, P/E selectins that lock in bone marrow
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14
Q

Red blood cell general information

A

-most numerous blood cell (4.5 - 5.5 x 10^12 for male, female 3.8 -4.8)
-7um, biconcave disks (squeeze through 4um gaps)
-contain haemoglobin (26.7-32.5 pg / cell)
-no nucleus or major organelles, maximising oxygen capacity, allowing flexibility)

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15
Q

How is hematopoiesis cell differentiation regulated?

A

-erythropoietin (from kidneys, peritubular endothelial cells) (growth factor)
-thrombopoietin (from liver)
-granulocyte colony stimulating factor (GCSF) (innate immune system)

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16
Q

Erythrocyte cell lineage

A

-Normoblast (found in bone marrow)
-Reticulocyte
-Mature erythrocyte

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17
Q

Normoblast

A

-nucleated red blood cell precursor
-only enters peripheral blood in disease,
- much larger than RBC
- blue/purple cytoplasm, basophilic (more nucleic acid, no haemoglobin)

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18
Q

Reticulocyte

A

-commonly see in peripheral blood,
-semi mature RBC
-lost nucleus, organelles
-bit larger
-blue bodies in cytoplasm
=mRNA producing haemoglobin

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19
Q

Micronutrients RBCs require?

A

-Iron for haem
-Vitamin B12
-pholate

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20
Q

Iron Amounts in Body (forms haem for haemoglobin)

A

-4.5 grams in body
-required intake 1-2mg daily (excreted in bile, faeces)
-Average (healthy) intake 15mg
-absorption regulated by hepcidin
- deficiencies in Fe = haemoglobin deficiency

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21
Q

Hepcidin

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A

-acute phase reactant produced in liver
-increases in inflammation, anemia effects
-down regulates ferroportin when iron levels are high
-regulated by hypoxia and iron deficiency

22
Q

Absorption of iron

Study These Flashcards
A

-Stomach acid converts F2+ to Fe3+
-Enters duodenum where absorption occurs
-duodenal enterocytes have 2 transport channels one for haem (organic iron) other
-Divalent metal transporter (DMT) requires iron to be in Fe2+ form
-Enterocytes convert Fe3+ to Fe2+ for DMT absorption
-Ferroportin pumps out of duodenal enterocyte
-Hephaestin oxidises to Fe3+ again
-Stored in ferritin for future use

23
Q

Haemoglobin production

Study These Flashcards
A
  • (hetra) tetramer
  • 4 subunits (2a chains, 2B chains) (each has a haem group)
    -each haem binds O2 molecule
    -115-140 g/L in women
    -130-160 g/L in men
24
Q

Haem Synthesis

Study These Flashcards
A

-part of group of pigments called porphyrins
-mitochondria takes up iron puts into porphyrin compound (4 pyrrole groups)
-enzymatic process, lots of genetic conditions, porphyria’s (blistering) [can be life threatening]

25
Iron Deficiency (anemia)
-effects 1/3rd of world pop. -gradually develops -latent iron deficiency is common - caused by decreased Fe supply or increased Fe demand -mensurating women (loss of iron stores) or limiting diets (vegans) put people at risk
26
Iron Deficiency Effect on Blood
-decreased haem, haemoglobin, O2 transportation -microcytosis (shrunken RBCs) -hypochromia (pale RBCs) -Poikilocytosis (RBCs vary in shape (tennis racket, eliptical) -Reticulocytopenia (decreased presence of reticulocytes) -Target cells present (cell with red blotch)
27
General Effects of Iron Deficiency
glossitis (smooth tongue) koilonychia (spooning fingernails) Angular stomatitis (lesions of mouth corners) -Pica (abnormal appetite, dirt, ice)
28
Treatment for Anemia
-Dietary change, supplements -Vitamin C increases absorption (pregnant women) -blood transfusion? -Tea can decrease absorption -Citric juices increase absorption
29
Vitamin B12 General
-cobalamins (cobalt ion central) -corrin nucleus -used in conversion of L-methylmalonyl CoA to succinyl CoA -methylation of homocysteine to methionine (for DNA nucleotide production)
30
Vitamin B12 Dietary Info
-only available through diet -typically intake 5-30mg a day -typically loss 1-4mg a day (faecal) -average stores 4mg (lots destroyed by stomach acid)
31
Absorption of B12
-terminal ileum -forms complex with intrinsic factor (IF is from parietal cells) - binds cubam receptors of - 2ug per meal -IF:B12 complex dissociates in cell
32
Pernicious anemia
- Vitamin B12 deficiency leads to decrease in RBCs - Caused by parietal cells not producing intrinsic factor
33
Transcobalamins
-B12 transporters - 1 or (haptocorrin) produced by saliavary glands and protects VB12 from acid digestion -2, from ileal enterocytes transports B12 into tissues (prevents denaturation by blood)
34
Folate General Information
-folic acid -tetrahydrofolates or dihydrofolates -single carbon group attached to N5 or N10 nitrogen (methyl group) -conjugated with a bunch of glutamate residues e.g N-5,10-methyleneTHF or N-5-methyleneTHF
35
Folate Dietary Info
-10mg stored in body mainly liver -daily loss 100ug -daily intake 700ug, heat labile (destruction) spina bifidia if deficiency present during pregnancy
36
Folate Role in Body?
-single carbon donor/acceptor -synthesis of methionine -histidine catabolism -converts serine to glycine -Purine synthesis -pyrimidine synthesis (all nucleotides^=) [conversion of dUMP to dTMP rate limited by presence of N-5-methylTHF
37
Folate Absorption
-Upper jejunum -Before absorption polyglutamates converted to monoglutamates by enzymes -Jejunal enterocytes convert various folic acids to N-5-methyleneTHF (circulates freely in blood) -Folate receptors absorb into developing cells [jejunum inflammation prevents absorption]
38
Folate and VB12 in DNA Synthesis
1. Folate absorbed in cells as N-5-methyltetrahydrofolate 2. Donates methyl group to homocysteine [methylcobalamin co-enzyme] converting to tetrahydrofolate 3.THF converted to N-5,10-methyleneTHF in the process serine is converted to glycine. 4. N-5,10-methyleneTHF cofactor for DTMP synthase converting dUMP to dTMP [B12 or folate deficiency leads to RBCs not producing enough nucleotides causing swelling]
39
Haematinic Deficiencies (B12 and Folate) causes?
-Inadequate dietary intake - malabsorption through lack of intrinsic factor, G.I disease (inflammation), drug induced malabsorption (metabolism) -Increase requirements -failure of utilisation (congenital defect in transcobalamin)
40
What is megaloblastic anemia?
Vit B12 or folate anemia
41
Megoblastic anemia signs and symptoms?
-Weak muscles, appetite loss, weight loss, irritability, fatigue, diarrhea, tachycardia, stomatitis, glossitis, jaundice -altered sensation (numbness) myelin breakdown=nerve pain [diarrhea epithelial barrier cannot regenerate without DNA]
42
Clinical Findings in Megaloblastic anemia?
Decreased Hb Increased red blood cell size Less Hb per cell Less WBC Less platelets Reduced B12 or folate Can be anti intrinsic factors (b12 supplements won't work with out it) Microcytic, pale centre RBC -Neutrophils become hyper lobulated (too many nucleus)[due to too much uracil fragmentation stayed in circulation too long)
43
Globin Genes
8 genes, alpha, beta, g-gamma, a-gamma, delta, epsilon, zeta only 7 chains
44
Foetal haemoglobin
2 alpha and 2 gamma chains
45
Haemoglobinopathies
-effect synthesis of Hb -Structural (Hb synthesis is wrong) errors or rate of synthesis errors (Hb can't be made fast enough) -Each chromosome 2 alpha globin gene (4 total) -Only 1 beta globin gene per chromosome (2 total)
46
Sickle cell anemia (structural error haemoglobinopathy)
- Point mutation in (E6V) beta-globin gene -haemoglobin polymerises in hypoxic conditions=sickle cell crisis (sickle shapes, crescent) -shapes clog up blood vessels, ischemia, necrosis
47
Thalassemia (rate of synthesis error haemoglobinopathy)
-alpha or beta effected -reduced or absent synthesis of one or more globin chain type -alpha globin production reduction prevents production of mature Hb (same for beta respectively)
48
Thalassemia Classification alpha
Alpha= 4 genes = normal 3 genes = silent (asymptomatic) carrier 2 genes = alpha thalassemia trait 1 gene= Hb H Ds 0 genes= (death) Hb Barts / hydrops fatalis
49
Thalassemia Classification Beta
B/B+, B/B0 silent (minor) B+,B+, B+,B0 moderate (intermediate) B0, B0 severe (major)
50
Management of Haemoglobinopathies
Depends on severity -no cure just management -blood transfusions (top up Hb, rejection risk, iron over deposited) -antibiotics -painkillers

Clinical Physiology (8 decks)

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