blood key points Flashcards
functions
transport of nutrients
removal of waste
transport of host defences
composition
cells plasma proteins - albumin and globulins lipids nutrients water
RCC
estimate number of rbc/l of blood
HCT
% of rbc to total blood vol
cell/liquid ratio
anaemia
low Hb
polycythaemia
raised Hb
platelet number
FBC
platelet fct
bleeding time
DIC
atherosclerosis - inflamed endothelium releases tissue factor - initiate clotting (also sepsis)
blood clots form throughout body, blocking small blood vessels
depletes platelets and CFs - excessive bleeding
clotting stages
vasoconstriction
platelet plug
coagulation
AT3
inhibits coagulation - neutralises enzymatic activity of thrombin
proteins C and S
anticoagulants
inactivate Va and VIIIa
thrombophilia
excessive tendency to clot - usually DVT
- life threatening due to PE
thrombophilia - thrombo-promoting actions
smoking immobility pregnancy surgery OCP
thrombophilia common reasons
AT3 deficiency
protein C or S deficiency
factor V leiden variant
therapeutic coagulopathy
where coagulation cascade is manipulated by medicine to make clotting less likely
reduce platelet adhesion and function - usually prevent arterial thrombosis
reduce activity in coagulation cascade - usually prevent venous thrombosis
porphyria
abnormality of haem metabolism - deficiencies in enzymes
can’t produce enough haem
2 main types - hepatic and erythropoietic
clinically relevant porphyrias
variegate - Afrikaans descent
acute intermittent
hereditary coporphyria
clinical effects of porphyria
photosensitive rash neuropsychiatric disturbance in acute attacks - motor and sensory changes, seizures - autonomic disturbances hypertension and tachycardia may be fatal
porphyria triggers
poorly understood many drugs pregnancy acute infections alcohol fasting
broad causes of anaemia
reduced production
increased losses
increased demand
dental aspect of porphyria
drug administration - be vvvvvv cautious
microcytic anaemia
Fe deficiency, thalassaemia
macrocytic anaemia
B12/folate deficiency
reticulocytosis
anaemia - reduced production
reduced normal red cells - marrow failure - aplastic anaemia normal red cells, reduced Hb - deficiency states - abnormal globin chains - chronic inflammatory disease
iron absorption
duodenum
diseases reducing iron absorption
achlorhydria - lack of stomach acid - no conversion of non-haem iron
coeliac disease
iron loss
gastric erosion and ulcers IBD: Crohns, UC bowel cancer haemorrhoids internal bleeding
sources of vit B12
animal/fortified foods
absorption of vit B12
terminal ileum
- combines with intrinsic factor
fct of vit B12
DNA synthesis
vit B12 deficiency
lack of intake - strict vegans
lack of intrinsic factor - pernicious anaemia
disease of terminal ileum e.g. crohns
folic acid deficiency
lack of intake (odd diet)
absorption failure
- jejunal disease e.g. coeliac
- usually seen codeficient with iron
consequence of folic acid deficiency
can lead to neural tube defects in foetus - spina bifida
anaemia - increased losses
RCC and HCT normal red cells - bleeding - chronic GI bleed, menstrual abnormal red cells - AI, hereditary - sickle, G6PD, spherocytosis
anaemia - increased demand
pregnancy
malignant disease
thalassaemia
normal haem production
genetic mutation of globin chains
- a and B
clinical effects of thalassaemia
chronic anaemia marrow hyperplasia (skeletal deformities) splenomegaly cirrhosis (liver affected by extra Fe) gallstones
management of thalassaemia
blood transfusions
prevent iron overload
reticulocytosis
almost mature rbcs
released early into circulation to replace losses
will raise MCV
sickle cell anaemia
less common than thalassaemia
abnormal globin chains - a different genetic mutation to thalassaemia
change shape in low O2 env
- prevent rbc from passing through capillaries
- stick and block capillaries
- tissue ischaemia - pain and necrosis
sickle cell trait
heterozygous
one abnormal gene
carrier
anaemia diagnosis
Hb - degree of anaemia?
RCC and HCT - cell or Hb formation deficiency?
MCV - deficiency?
anaemia investigations
history FBC FOB endoscopy/colonoscopy renal fct bone marrow examination
anaemia tx
tx cause replace haematinics - FeSO4 200mg tds 3m - 1mg IM vitB12 x6 then 1mg/2m - 5mg folic acid daily transfusions - production failure erythropoietin - production failure - renal disease - made by kidneys, induces rbc formation
anaemia dental aspects
GA - O2 capacity
haematinic deficiency - oral infections, ROU, BMS
myelooid cells
erythrocytes megakaryocytes neutrophils basophils eosinophils monocytes
lymphoid cells
B
T
NK
leukaemia and lymphoma types
acute lymphoblastic leukaemia acute myeloid leukaemia chronic lymphocytic leukaemia HL NHL multiple myeloma chronic myeloid leukaemia myeloproliferative disorders
clinical presentation of leukaemia
anaemia neutropenia thrombocytopenia lymphadenopathy splenomegaly/hepatomegaly
acute lymphoblastic leukaemia
peak age 4yrs
catabolic state - fever, sweats, malaise
lymphadenopathy and tissue infiltration common
acute myeloid leukaemia
more common elderly
similar presentation clinically to ALL
poor prognosis
chronic lymphocytic leukaemia
elderly
mostly asymptomatic and discovered on routine blood tests
commonest leukaemia
slow progression, may not require tx
chronic myeloid leukaemia
increase in neutrophils and their precursors
lots have philadelphia chromosome
is HL or NHL more common?
NHL
HL
peak 15-40yrs mutation in DNA of B lymphocytes risk factors - weakened immune system e.g. HIV - immunosuppressant meds - (EBV) - had NHL Reed-Sternberg cells microscopically older peiple do less well
symptoms of HL
painless cervical lymphadenopathy fever night sweats weight loss itching infection
NHL
mutation in lymphocyte DNA - multiply uncontrollably
B cell (85%) or T cell (15%) types
any age - more indolent elderly
aetiology
- microbial factors strongly indicated: EBV, HTLV-1, h
pylori
- AI disease - SS, RA
- immunosuppression - AIDS, post-transplant
NHL presentation
lymphadenopathy
extra-nodal disease more common - oropharyngeal involvement - Waldeyer’s ring (noisy breathing and sore throat)
symptoms of marrow failure
constitutional symptoms less common
NHL prognosis
poor
multiple myeloma
malignant proliferation of plasma cells - release lots of paraprotein (an antibody)
often elderly
multiple myeloma features
monoclonal paraprotein in blood and urine
lytic bone lesions - pain and fracture
excess plasma cells in bone marrow - marrow failure
multiple myeloma symptoms
infection
bone pain
renal failure
amyloidosis
multiple myeloma management
bisphosphonates
myeloproliferative disorders
make lots more cells
blood becomes more viscous - harder to move around body
tx of haematological malignancies concepts
induction remission maintenance and consolidation relapse - often repeat this cycle several times before a cure is reached
