Final stuff lecture 1-20 Flashcards
transfusion related acute lung injury
- onset of acute lung injury within 6 hrs transfusion
- donor plasma contains whit cell antibodies leading to aggultination and sequestion of recipient nuetrophils in pulmonary vasculature
What does protein C inhibit? what is it activated by?
inhibits factor 5, 8 , activated by thrombin
What does antithrombin inhibit
-switches of activated 10, 9, 11, and prothrombin
How does heparin work?
How does dabigatran work?
-what revereses this?
how can you tell between then?
Heparin
- up regulates antithrombin - so will mean clotting will slow down
- (antithrombin - blocks thrombin, 10, 9, 11)
- bleeding history
- long APPT, 1+ 1 and TCT
Dabigatran
- directly inhibits thrombin
- very sensitive to TCT
- reversible by - idarucizumab
Protamine will reverse heparin
3 reasons why
What does it mean when there is a prolonged APTT and a prolonged 1 + 1?
- lupus anticoagulant - (no bleeding), but can alter APPT lab test
- Autoimmune disease- (bleeding) can make antibodies against some clotting factors
- Drugs - slow down clotting e.g heparin, dabigatran
Multiple factor deficiencies cause
- vit K/ warfarin
- blood loss - missing all and missing platelets
- DIC - disseminated intravascular coagulation -widespread activation of coagulation which causes thrombin followed by bleeding as clotting factors and platelets are used up
- Liver disease - makes clotting components
What is most sensitive test for liver disease?
Liver disease - lack of production of coagulation factors and inhibitors (except 8) - all are made in liver except 8
-prothrombin assay most sensitive to liver disease, because vit K factors get used up first and billary system is most common in this disease
Prolonged PT causes
- extrinsic pathway
- wafarin - 2,7,9,10
- vit K deficiencey
- liver disease
- low factor 7 (but this is only if APPT is normal)
How to monitor wafarin
- Using PT ratio
- use INR - international normalised ratio
- this standardises the prothrombin ratio, so that if you measure the INR in any lab it will be the same
- APPT also prolonged with warfarin, but not to the same extent and dont routinely measure it
What does wafarin do?
- when is it used?
- how to reverse?
- inhibits recycling of vit K
- cannot get coagulation factors to stick onto platelets
- if give a big dose of Vit K - can overcome wafarin
- used in atrial fibrillation, venous thromboembolism, other thrombotic disorders
risks VT
-trauma, surgical manipulation, prior thrombosis, atherosclerosis
immobility - post op, plane
Pressure - (blockages) catheter, tumour obstruction
Increased viscosity - polycthaemia, dehydration, EPO
Inherited Thrombophilia
-abnormal inhibitor function - resistance to activated protein C (factor 5 leiden)
-Deficeincey of inhibitors - antithrombin , protien C, protien S
Increased factor levels - prothrobin gene mutation, elveated factor VIII APCR gene
APCR - heteroyzgous - increased risk
-homozygous - very large increased risk
Absolute risk - most important
To learn for exam
changes of DVT being spontaneous vs provoked
- 30-40% spontenous (50% of these are inherited)
- rest are provoked
Risk factors for VTE
Heriditary thrombophilia - treat with anticoagulation
Need to know the effect of the drugs on the clotting tests
direct acting oral anticoagulants
low molecular weight heparin
-will reverse 10a - no effect on APPT
Streptococcus pyogenes
2 virulence factors
2 diseases
Treatment
- adhesion factors - can adhere to ecm to further infect cells
- capsule - hyuloronidase to prvent opsonisation and phagocytosis
- M protein - binds to factor H , prevents opsonisation by c3b
- streptokinase - anticoagulant can break down clot - degreades fibrin and can further get out
disease
- rheumatic fever
- SSTI
- septic arthritis
- pharyngitis
treatment - penicillin, flucoxacyllin, amoxycillin (beta lacatamse resistant) ,
Staphylococcus aureus
2 virulence factors
2 diseases
Treatment
- slime layer - makes polysacharide layer to build up layers of bacteria underneath and protect them (prevent opsoinsaiton and phagocytosis)
- clumping factor - can bind fibrinogen, get a clot around it so that it can avoid phagocytosis and opsonisation
Disease
- Osteomyelitis
- toxic shock syndrome
- septic arthritis
- methicilin - cannot be destoryed by b-lactamase
- penicilin combined with b-lactamase inhibitor
- or amoxicilin + claulanic aice
- however can get menicillin resistant staph - give vancomycin
How to test these skin infections
- take a pus swab from area
- take to lab
- if in hospital - also take a blood sample
enzyme penicillin works on
transpeptidase
Risk factors for osteomylitis
- chicken pox can lead to SSTI can get osteomylitis
- surgery, trauma ect.
What is signal 2 for an antigen presenting cell
ICAM 3 - on APC, matches with LFA -1 on t helper cell
Main points about septic arthritis
- needs to be diagnosed quickly as early treatment prevents complications such as irreversible damage from growth plate disruption
- ealry diagnosis is hard to see
- knee, hip and ankle most common joints
- 2 most common - staph aureus and streptococcus pyogens
- drainage and wash out of septic joint is often needed for diagnosis and treatment
- IV antibiotics are needed initially and total corse is likley to be 2-3 weeks
Staphylococcus pyogenes - lab test
lab -head smear bacteria
- gram stain (positive)
- grow on horse blood agar (beta haemolysis - clear)
- bacitracin sensitivity - sensitive - is s.pyogenes
- confirm with streptococcus grouping test
Staphylococcus pyogenes - lab test
lab -head smear bacteria
- gram stain (positive)
- look at shape of bacteria on slide (coccus)
- catalyse test - negative
- grow on horse blood agar (beta haemolysis - clear)
- bacitracin sensitivity - sensitive - is s.pyogenes
- confirm with streptococcus grouping test
Staph aureus - lab test
lab - heat smear bacteria
- gram stain (positive)
- look at shape of bacteria - coccus
- catalase test (positive)
- coagulase test (positive)
- then is staph aureus
(if grown on MAC plate - turns it yellow)
(if grown on blood agar - beta haemolysis)
