Haemostasis and bleeding disorders Flashcards
What is causes bleeding in mouth?
what does can it be a sign of?
common, esp orally (flossing, plaque)
- inflamaed gums, gingivitis, irritation
- damage/ rupture of blood vessels and expulsion of blood
- red is Hb
- = sign of Leukaemia
What are platelets?
where to they bud off from?
what is process of making platelets?
- what can they do with their shape?
what can platelets release?
what causes platelets to release?
bud from megakaryocytes
- shape change is to cluster and form plug
- release granules when activated by triggers like vasoconstrictor
- ADP causes aggregration
NOTE should be ADP!
what is haemostasis?
what are the main steps?
do the steps happen individually?
what happens in second step?
what could happen to vessels with HBP?
what is needed for blood flow/ BP?
3 major steps
Vasoconstriction: reduction narrow of BV wall, local response, factors in area released nearby to trigger it
Formation of platelet plug
Coagulation
ALL happen together, triggered by damage.
- need BP to deliver blood to brain (fainting is way to do that?
SECOND STEP
- clot
- image: LHS= normal, endothelial prod vasodilators to inhibit platelet adhesion (saying “ im ok, no need for plateletes to stick to me), person who has HBP, coudl damage endothelial layer= clot formation happens. block= heart attack
- need factors to vasodilate.
- damage= expose underlying collagen, exposing factor that triggers platelets to come. granules come, attracts more platelets to side. get positive feedback loop. more ps coming, more granules rls, more ps come to damaged area = form PLUG
Factors involved in platelet function
- vWF role
complicated p function
chem factors
- exposure of collagen basically expose ps to the site to trigger plug to cokllagen
- vWF: activated when collagen exposed= provides bond to stick ps
- other bunch of factors: cont for ps to stick together and remain in site until clot no longer needed.
What is 3rd step of H
is plug stable?
what pw involved in coag pw?
- plug not stable
- coag pathway= heaps of steps, 2 sep pw that can trigger to form clot 1. intrinsic, and extrinsic = feeds to common pw when forming clot
- heaps of enzymes, precursors, all Calcium derived (ca trigger inactive precursor to become active)
- coag cascade
how many pw in coag?
which pathway is longer?
what happens in extrinsic pw?
what is take home message in terms of what it activates?
- 2 pw
- intrinsic = longer more step, ex= 1 step, exposure of collagen. damage internally like blood vessel due to stress or HBP
- extrinsic= external, like cut.
- extrinsic: damage, tissure factor 3 exposed, once activated, feeds into intrinsic pw, there to activate factor 9 (2nd bunch of enzymes)
- in intrinsic pw: bunch of enzymes F12, F11. Ca activates.
- BOTH PATHWAYS HAVE SEP TRIGGERS BUT ACTIVATES FACTOR 9
both pw feed to common pw
what is common pw to form clot caused by?
what happens when F10 is activated?
what positive feedback occurs?
how is mesh formed?
how is mesh strengthened?
Factor 9
- F9 goes in common pw activate F10= key enzyme activated, activates prothrombin into THROMBIN
- prothrombin goes back in extrinsic pw and positive feedback to clotting
- thrombrin activated: turns fibrinogen->; to fibrin
- fibrin= mesh trapping blood + F13 cross links it, making it stronger
take home message for coag cascasde pw?
what pw caused from triggers of cut on skin vs HBP damage to BV?
- 2 pathways: I= 1 exposure collagen E= cell injury,
- Factor 9 -> F10: prothrom to throm= fibrinogen + fibrin + F13= strong mesh
know how to draw from scratch
cut ourselves
= F3 + extrinsic pathway
if HBP and damage to BV= intrinsic pathway
How is clot removed?
what is process called?
what is involved in positive feedback of clot and also breakdown?
fibrinolysis= breakdown fibrin
- trigger= prod of thrombin
- plasminogen= key protein in activated, activated to plasmin breaks down to fibrin
thrombin feeds in pw to POSITIVE reinforce clot AND also trigger breakdown
summarise hemostasis
back and forth process in middle
how clot is formed and broken down
Bleeding disorders
- where can bleeding disorders come from?
- what is found in inherited vs aq. do + eg. of inherited blood do?
- inherit or acquired
- inherit = removal of some clotting factors
- aquired= BM do, vit do
- what are some p DO?
- causes?
- thrombocytopenia= lower ps, inhibitors present
- drugs impairing platelet f.
What are some Hereditary Coagulation disorders?
2 types of Haemophilia?
problem with it?
clinical presentation?
Haemophilia= x link recessive= female carriers but affect males
2 types
A= less F8 in coag pw
B= less F9
Def in factors in clot cascade= lots of bleeding, can’t clot properly. probs can do plug but can’t clot.
see bruises, takes time to stop bleeding.
Haemophilia= iNTERNAL BLEEDING
Queen Victoria was carrier of Haemophilia= royals mainly males got it (black)
Hereditary Coagulation disorders
VW disease
types
symptoms
tx
- lots undx unless ppl exp lots of trauma and you see not clotting properly,
- low level of VW factor
- type 1= not enough of Factor, some ability to clot= gen undx.
- type 2= normal, not working properly
- t3: little or no VW F= severe bleeding, cannot cope well
tx: avoid certain drugs that thin blood like aspirin,
Acquired Coagulation disorders
list
- most common one
- damage to liver might cause what?
- most common= Vit K: important in coagcascade (in extrinsic pw), newborns, young ones, susceptible bc low Vit K, but can supp.
- liver disease: if bdown of liver= Factors involved in clotting impacted
- drugs
summarise bleeding disorders
congenital, haemophilia, genetic, aquired, vascular DO, platelet DO,
what are oral manifestation of bleeding do?
gums bleed
bleeding manifest after sig. surgery, see not clotting, e.g. after exo.
platelet disorder (image lil dots roof of mouth)
keep an eye on after exo, is clotting ok?
take home messages
- importance of p activation
- ext and intr pw
- how clot formed and broken
- coag DO
LO
