Haemodynamic And Cell/ Immunity Flashcards
Prothrombin time
Extrinsic pathway
VII X V
II(thrombin) and fibrinogen
PTT
Intrinsic pathways
XII XI IX VIII X V II(thrombin) and fibrinogen
Platelet alpha granules
P selectin
vWF, fibrinogen, V, XI, XII
Platelet factor 4, fibronectin, PDGF,
VEGF
Platelet dense granules
Serotonin
ADP ATP
calcium
Adrenaline
Haptoglobin
Carries hb releases from damaged red cells in circulation
Glial cell production
Ectodermal tissue embryo, not bone marrow
Agammaglobulinaemia
X linked primary immunodeficiency
B cells don’t mature
Recurrent resp infections
GPIIB/IIIA
integrin on plt
vwf and fibrinogen receptor
plt activation
main job fibrinogen -> coag
Blocker - tirofiban
Thrombomodulin
from endothelium - anticoag
activated protein C which inhibits tPA inhibitors -> inc plasmin
Virchows triad
hypercoagulable
stasis
injury
petichiae vs purpura
petichiae - 1-2mm, inc intravasc pressure, dec plt
purpura 3mm - fragile vessels, vasclitis, amyloid
causes non thrombocytopenic purpura
meningococcal, HSP, telangelactasia, CMV
cause of vasoconstriction at injury
endothelin
hyperaemia vs congestion
hyperaemia due to inc blood flow ACTIVE
inflammation, arteriolar dilation
Etythema,haemosiderrin laden macrophages
congestion stasis e.g. pulm oedema CCF
Cyanosis
Thrombi morphology
lines of zahn if blood flow
if post mortem red bottom white top
thrombi location art vs venous
art coronary > cerebral > femoral
venous 90% leg
PE
95% from dvt upper leg
60-80% silent
>60% occlusion bad
risk pulm haemorrhage rather than infarct due to dual blood
Morphology infarcts
red infarct venous/ dual circulation
white infarct solid organ
ischaemic coagulative necrosis takes 4-12 h to appear
Metabolic abnormalities in sepsis
insulin resistance and inc BSL
dec insulin secretion, dec GLUT4
lactic acidosis
late stage dec BSL due to adrenal insufficiency
cells in innate and adaptive immunity
macrophages and dendritic (APCs)
IgM
pentamer, 1st response by B cells, produced by foetus, doesn’t cross placenta
complement activation
IgG
2nd response, crosses placenta, opsonises
80% of Igs
BCell CD 40 and 21
40 - for activation by T helper
21 - binds EBV
T cells
60-70% of lymphocytes
helper 60% - activate B, + phagocytes, secrete cytokines
CD8 cytotoxic kill (30%)
regulatory T supress immune response
NK cells
CD16 - Fc receptor for IgG
CD56
Inhibitory receptor for MHCI - don’t kill self
early defence without prior exposure
Location lymphocytes secondary lymph organs
Lymph nodes - B cortical in follicles, T paracortical
spleen - B follicles, T periarteriolar
MHCI
on all nucleated cells + platelets
HLA ABC
viral + tumour antigens (endogenous) –> ER then expressed
CD8
MHC II
on phagocytes
HLA D
endocytosed, proteolysis
exogenous antigens e.g. microbes
CD4
HLA
A - inherited errors metabolism - haemochromatosis
B - inflammatory B27 ank spond
D - autoimmune, sjorgens, arthritis
Costimulators
+ APC -> naive t cell stiulation
B7 proteins (CD80+86)
recognised by CD28 on t cell
CD4 activation B cells and macrophages
secretes IL2 - more t cells activated
expressed CD40 ligand which binds CD40 on B cells and macrophages
Th1
Activated macrophages and IgG
defence against intracellular
secrete IFNy
Th2
Activate IgE, mast and eosinophils
Allergy and humoral immunity
Secrete IL4,5,13
Th17
Activate neutrophils and monocytes
against extra cellular bacteria
mucosal immunity
Secrete IL17 and 22
Mast cell activators
IgE, C3a+C5a, IL8, codeine, morphine, adenosine
IgE coated mast calls are ‘sensitise’
IL5
activates eosinophils
T1 hypersensitivity summary
sensitisation - B cell produces IgE which coats mast cell
re exposure - degranulation
IL4 activates Th2 (secretes more IL4)
IL5 activates eosinophils
IL13
TII hypersensitivity summary
antibody mediated
reaction to antigen on cell surface
complement activation
+ IgG and M - recognised on NK cells - perforins and granzymes
TIII hypersensitivity summary
antibody/ antigen complex
soluble complex in blood
deposited in tissue
inflammation and tissue injury
complement (lots of it)
cause fibrinoid necrosis
TIV hypersensitivity summary
cell mediated
CD4 and 8
IL12–>Th1 (IFNy–>macrophage)
IL1+6–>Th17 (neutrophil)
CD4 presents peptide
secretes IL2 in autocrine manner
CD8 - perforins and granzymes
T II examples
transfusion, haemolytic anaemia, thrombocytopenia purpura
goodpastures, rheumatic fever, ANCA
MG, insulin resistance diabetes
T III examples
SLE
serum sickness, arthurs reaction
post strep glomerulonephritis
polyarteritis nodosa
reactive arthritis
farmers lung
Henoch schonlein
T IV examples
contact dermatitis
mantoux test
TB
MS
T1DM
Central tolerance
in BM and thymus
T cell negative selection and deletion
B cell apoptosis or receptor editing
Peripheral tolerance
Anergy - made so won’t be activated by costimulator
suppression by regulatory T
deletion by apoptosis
Hyperacute rejection
avoided by cross matching blood
pre formed antibodies
Ischaemic + thrombotic
IgG+ complement, fibrin + plt
Acute rejection
antidonor ABs produced post transplant
T cells - tubulitis + vasculitis
B cell - complement
Chronic rejection
Progressive renal failure, no ABs in graft
Arterioscleosis, parenchymal fibrosis
RNA genome contains
gag, pol, env genes
HIV viral glycoproteins
GP120 - binds CD4 allowing CCR5 to bind
GP41 - fusion virus to cell
Seroconversion HIV
3-7 weeks
Assoc viral like illness
HIV defining cancers
Kaposi - HHV8 most common, can have normal CD4
Non hodgkins CNS lymphoma - assoc EBV, low CD4
Cervical invasive
HIV defining viruses
HSV, VZV, CMV, PML
HIV defining bacterial infections
atypical mycobacteria
nocardiosis
disseminated salmonella
HIV defining Fungal + protozoal
pneumocytis, cryptococcus, histoplasmosis
cryptosporidiosis, toxoplasmosis (CNS/ pneum)
Spherocytosis tx
tx with splenectomy or folate or blood transfusions
Megaloblastic anaemia
oval shaped macrocytosis with large hypersegmented neutrophils and abnormal megakaryocytes
Hyperchromic
anisocytosis and poikilocytosis
reticulocyte count is low
cause reticulocytosis
haemolytic anaemia (which also causes inc bilirubin and ldh)
Trousseau syndrome
migratory thrombophlebitis due to hypercoagulable state
Types vWD
1 - autosomal dominant, deficiency (mild)
2 - autosomal dominant dysfunction (mild)
3 - autosomal recessive, complete deficiency
Traumatic haemolysis (exercise/ heart valve)
red cell fragments (schistocytes), burr cells, helmet cells, and triangle cells
Methaemoglobin
Hb containing Fe3 ferric
Steps haemostasis
- vasoconstriction
- PRIMARY - plt actovation
- SECONDARY - clotting cascade
- Clot stabilisation
Platelet activation stages
- vWF binds GB1b and binds collagen
- Plt changes shape
- Granules secreted e.g. ADP to recruit more plt, TXA2 aggregates
- GPIIbIIIa binds fibrinogen
