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BDS2 bams > blood key points > Flashcards

blood key points Flashcards

1
Q

functions

A

transport of nutrients
removal of waste
transport of host defences

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2
Q

composition

A 
cells
plasma proteins - albumin and globulins
lipids
nutrients
water
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3
Q

RCC

A

estimate number of rbc/l of blood

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4
Q

HCT

A

% of rbc to total blood vol

cell/liquid ratio

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5
Q

anaemia

A

low Hb

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6
Q

polycythaemia

A

raised Hb

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7
Q

platelet number

A

FBC

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8
Q

platelet fct

A

bleeding time

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9
Q

DIC

A

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

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10
Q

clotting stages

A

vasoconstriction
platelet plug
coagulation

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11
Q

AT3

A

inhibits coagulation - neutralises enzymatic activity of thrombin

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12
Q

proteins C and S

A

anticoagulants

inactivate Va and VIIIa

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13
Q

thrombophilia

A

excessive tendency to clot - usually DVT

- life threatening due to PE

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14
Q

thrombophilia - thrombo-promoting actions

A 
smoking
immobility
pregnancy
surgery
OCP
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15
Q

thrombophilia common reasons

A

AT3 deficiency
protein C or S deficiency
factor V leiden variant

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16
Q

therapeutic coagulopathy

A

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

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17
Q

porphyria

A

abnormality of haem metabolism - deficiencies in enzymes
can’t produce enough haem
2 main types - hepatic and erythropoietic

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18
Q

clinically relevant porphyrias

A

variegate - Afrikaans descent
acute intermittent
hereditary coporphyria

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19
Q

clinical effects of porphyria

A 
photosensitive rash
neuropsychiatric disturbance in acute attacks
 - motor and sensory changes, seizures
 - autonomic disturbances
hypertension and tachycardia
may be fatal
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20
Q

porphyria triggers

A 
poorly understood
many drugs
pregnancy
acute infections
alcohol
fasting
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21
Q

broad causes of anaemia

A

reduced production
increased losses
increased demand

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22
Q

dental aspect of porphyria

A

drug administration - be vvvvvv cautious

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23
Q

microcytic anaemia

A

Fe deficiency, thalassaemia

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24
Q

macrocytic anaemia

A

B12/folate deficiency

reticulocytosis

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25
Q

anaemia - reduced production

A 
reduced normal red cells - marrow failure
 - aplastic anaemia
normal red cells, reduced Hb
 - deficiency states
 - abnormal globin chains
 - chronic inflammatory disease
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26
Q

iron absorption

A

duodenum

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27
Q

diseases reducing iron absorption

A

achlorhydria - lack of stomach acid - no conversion of non-haem iron
coeliac disease

28
Q

iron loss

A 
gastric erosion and ulcers
IBD: Crohns, UC
bowel cancer
haemorrhoids
internal bleeding
29
Q

sources of vit B12

A

animal/fortified foods

30
Q

absorption of vit B12

A

terminal ileum

- combines with intrinsic factor

31
Q

fct of vit B12

A

DNA synthesis

32
Q

vit B12 deficiency

A

lack of intake - strict vegans
lack of intrinsic factor - pernicious anaemia
disease of terminal ileum e.g. crohns

33
Q

folic acid deficiency

A

lack of intake (odd diet)
absorption failure
- jejunal disease e.g. coeliac
- usually seen codeficient with iron

34
Q

consequence of folic acid deficiency

A

can lead to neural tube defects in foetus - spina bifida

35
Q

anaemia - increased losses

A 
RCC and HCT
normal red cells - bleeding
 - chronic GI bleed, menstrual
abnormal red cells
 - AI, hereditary - sickle, G6PD, spherocytosis
36
Q

anaemia - increased demand

A

pregnancy

malignant disease

37
Q

thalassaemia

A

normal haem production
genetic mutation of globin chains
- a and B

38
Q

clinical effects of thalassaemia

A 
chronic anaemia
marrow hyperplasia (skeletal deformities)
splenomegaly
cirrhosis (liver affected by extra Fe)
gallstones
39
Q

management of thalassaemia

A

blood transfusions

prevent iron overload

40
Q

reticulocytosis

A

almost mature rbcs
released early into circulation to replace losses
will raise MCV

41
Q

sickle cell anaemia

A

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

42
Q

sickle cell trait

A

heterozygous
one abnormal gene
carrier

43
Q

anaemia diagnosis

A

Hb - degree of anaemia?
RCC and HCT - cell or Hb formation deficiency?
MCV - deficiency?

44
Q

anaemia investigations

A 
history
FBC
FOB
endoscopy/colonoscopy
renal fct
bone marrow examination
45
Q

anaemia tx

A 
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
46
Q

anaemia dental aspects

A

GA - O2 capacity

haematinic deficiency - oral infections, ROU, BMS

47
Q

myelooid cells

A 
erythrocytes
megakaryocytes
neutrophils
basophils
eosinophils
monocytes
48
Q

lymphoid cells

A

B
T
NK

49
Q

leukaemia and lymphoma types

A 
acute lymphoblastic leukaemia
acute myeloid leukaemia
chronic lymphocytic leukaemia
HL
NHL
multiple myeloma
chronic myeloid leukaemia
myeloproliferative disorders
50
Q

clinical presentation of leukaemia

A 
anaemia
neutropenia
thrombocytopenia
lymphadenopathy
splenomegaly/hepatomegaly
51
Q

acute lymphoblastic leukaemia

A

peak age 4yrs
catabolic state - fever, sweats, malaise
lymphadenopathy and tissue infiltration common

52
Q

acute myeloid leukaemia

A

more common elderly
similar presentation clinically to ALL
poor prognosis

53
Q

chronic lymphocytic leukaemia

A

elderly
mostly asymptomatic and discovered on routine blood tests
commonest leukaemia
slow progression, may not require tx

54
Q

chronic myeloid leukaemia

A

increase in neutrophils and their precursors

lots have philadelphia chromosome

55
Q

is HL or NHL more common?

A

NHL

56
Q

HL

A 
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
57
Q

symptoms of HL

A 
painless cervical lymphadenopathy
fever
night sweats
weight loss
itching
infection
58
Q

NHL

A

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

59
Q

NHL presentation

A

lymphadenopathy
extra-nodal disease more common - oropharyngeal involvement - Waldeyer’s ring (noisy breathing and sore throat)
symptoms of marrow failure
constitutional symptoms less common

60
Q

NHL prognosis

A

poor

61
Q

multiple myeloma

A

malignant proliferation of plasma cells - release lots of paraprotein (an antibody)
often elderly

62
Q

multiple myeloma features

A

monoclonal paraprotein in blood and urine
lytic bone lesions - pain and fracture
excess plasma cells in bone marrow - marrow failure

63
Q

multiple myeloma symptoms

A

infection
bone pain
renal failure
amyloidosis

64
Q

multiple myeloma management

A

bisphosphonates

65
Q

myeloproliferative disorders

A

make lots more cells

blood becomes more viscous - harder to move around body

66
Q

tx of haematological malignancies concepts

A 
induction
remission
maintenance and consolidation
relapse
 - often repeat this cycle several times before a cure is reached

BDS2 bams (6 decks)

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