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101 Cards in this Set

  • Front
  • Back
What is Virchow's triad?
The three factors that contribute to thrombosis:
- Hypercoagulability
- Static blood / abnormal flow
- Endothelial damage
What is the difference in colour between arterial and venous thromboses and why is this?
Arterial thrombus = full of platelets -> white
Venous thrombus = more rich in RBCs -> red
What is THE main thing that activates platelets?
Thrombin (II)
What is clopidogrel?
An ADP receptor antagonist _. inhibits platelet function
What is the GPIIa-IIIa complex?
GP = glycoprotein
It's on the surface of platelets
Involved in lots of things, namely:
- Platelet aggregation
- Fibrinogen binding (its the receptor to which fibrinogen binds)
- Platelet activation
Which is more likely to result in a PE, distal or proximal DVT?
Obviously proximal
What are some of the mechanisms by which tumours promote venous clotting?
- They might be blocking the vessel to some extent -> blood stasis
- They can result in higher conc of proteins and WBCs in blood -> more viscous blood
- Can invade BVs -> endo damage
- The tumour cells can release pro-coagulant that's able to directly activate X without VII
What does lupus anticoagulant do to the APTT?
It prolongs the APTT -> suggests that it would increase bleeding in the body but it's actually the opposite ie it increases thrombosis (it's a misnomer!)
Who would we recommend to take LMWH before a flight of longer than 5 hours duration?
Anyone who's have a thrombus previously
Pregnant woman
Someone who's had recent trauma or surgery
What does thrombophilia mean?
Tendency to clot
By how many times does heparin potentiate anti-thrombin's effects?
1000 fold!
What three major groups of inherited abnormalities can we have that increase thrombosis? and some egs in each group
- Reduction in inhibitors eg decreased ATIII, decreased prot C and/or S
- Increase in procoagulants eg factor V Leiden, prothrombin mutation
- Increased homocysteine
What are some acquired causes of thrombophilia?
Surgery = definitely the most common / main one
Lupus anticoagulant and anti-cardiolipin antibody
What is the difference in oral bioavailabilities of unfractionated and LMW heparins?
Unfractionated -> very low oral bioavailability
LMWH -> much higher
Which has better dose-response predictability: unfractionated heparin or LMWH?
LMWH - this means that we don't need to do so much monitoring because we can much more effectively predict their response based on weight etc
What test do we use to monitor warfarin levels / effects?
INR ie the PT
Which factor is the INR / PT most sensitive to?
Factor VII
With warfarin therapy, what INR are we aiming for?
About 2.5 usually (might be higher in some cases)
How many days do we need cross-over between heparin and warfarin therapy?
Must cross-over for at least FOUR DAYS!
This is even if the INR gets up to the therapeutic range in that time
Someone in hospital on heparin and you want to switch them to warfarin. Monitoring INR - after 2 days it reaches therapeutic range. Are we now safe to take them off the heparin?

must have cross-over for 4 days regardless of what the INR is saying
Which type of BVs are called the 'capacitance vessels' and why?
The veins
Because they usually store about 60% of the circulating blood
What are the three major venous pathways in the leg?
Deep veins - in the muscle compartments (ie venae commitantes)
Superficial veins - in the subcutaneous tissue
Communicating veins
What direction does blood flow in the communicating veins?
from superficial to deep
Which blood vessels have more 'sluggish flow'?
The veins
What are the three main consequences of a DVT in the leg?
1. Local venous congestion
2. Organisation - ingrowth of endo cells and fibrous tissue - could result in the formation of a new little channel in the vessel so blood can flow through still
3. Embolism = the most severe
What are the effects of a DVT on the local area?
Limb become oedematous and painful
There's an increase risk of infections if there's a little trauma and increase risk of ulcers forming
Other than location and size of the PE, what impacts its severity?
The ability of the systemic bronchial artery to compensate for the blockage
What is factor V Leiden
a gene defect -> V is less susceptible to cleavage by activated protein C -> hypercoagulability
How much does factor V Leiden increase your risk of clotting? give values for both homos and heterozygotes
hetero - increases 7-8 times
homo - about 50 times
What would we consider 'abnormal sites' for thrombosis?
In the cerebral or mesenteric vessels
In a patient who was moderate-high risk of a thrombosis during surgery, what would we do in terms of prophylaxis?
Would give them HEPARIN prophylactially - it decreases the risk of DVT and PE by 75%
What are the three main clinical signs of DVT?
Painful calf
Leg swelling
Positive Homan's test (but this isn't very sensitive or specific)
What are our two main options for imaging a suspected DVT?
- Venogram (x-ray the veins after injecting contrast)
- Ultrasound
What are the disadvantages associated with a venogram?
Radiation dose
Invasive (need to inject contrast)
Potential for an allergic reaction to contrast
Because of these, we prefer to do an US of the suspected DVT rather than venogram
What is a duplex ultrasound?
Implies that we have a combination of doppler information (on the speed of the blood flow) and structural info
By how much does plasma volume increase in pregnancy?
By how much does red cell volume increase during pregnancy?
By how many g/L does Hb change in pregancy?
It decreases ie being diluted out by the increased BV
Decreases by 10-20g/L
How much more iron do we need each day during pregnancy?
800-1000mg MORE than the normal (normal is 1-1.5g -> need about 2-2.5g)
Why do we need extra iron during pregnancy? ie what's it used for?
1/3 goes to the placenta and 2/3 is needed for the increased red cell mass
What happens to iron absorption during pregnancy?
It increases. But this often isn't enough to prevent iron deficiency anaemia - the mum's often start at borderline low iron levels then increased Fe needs in pregnancy will tip them into being deficient
By how much do folate requirements change in pregnancy?
They double
What evidence is there for the benefits of folate and iron supplementation in pregnancy?
Folate - definitely beneficial
Iron supplementation hasn't been shown to be beneficial to mum or baby
What happens to transferrin levels in pregancy?
They are increased
What happens to serum iron and serum folate levels in pregnancy?
They are decreased even in the case of no deficiency
Which of these should and shouldn't we look at when looking for iron and folate deficiencies in pregnancy?
Serum iron, serum folate, red cell folate, serum ferritin, serum transferrin
serum iron and serum folate - fall in pregnancy naturally -> not good indices
transferrin - increased -> not good index
serum ferritin - good index for iron!
red cell folate = good for folate
What happens to coagulability in pregnancy?
You become hyper-coagulable!
Which clotting factors' levels change during pregnancy
Fibrinogen - rises 2-3 fold
II, VII, X, VIII and vWF
Why do mothers with vWD not have frequent and serious bleeds during pregnancy / birth?
Both vWF and VIII increase during pregancy, but VIII increases the most out of the two
70kg man has how much iron (in grams) in his body?
What form is all the iron in your body in?
1/2 is contained in haemoglobin
1/3 is stored as ferritin and haemosiderin
Remainder is in myoglobin and other enzymes etc
How much iron is in the average person's diet each day? How much of this gets absorbed?
10-15mg p/day
But you only absorb about 10% of this ie 1-1.5mg p/day approx
Where in the GIT does iron get absorbed?
The duodenum
what are the two types of iron in our diet?
what's difference in absorbance?
haem iron - from animal sources. Better absorbed (fe2+ form)
non-haem iron - from veggies, eggs etc. Not as well absorbed (fe3+ form)
What increases and what decreases non-haem iron absorption?
Increased by: acidic pH, vitamin C
Decreased by: tannates, alkaline conditions in the stomach
How do we absorb non-haem iron?
It's in 3+ form -> needs to be reduced to 2+ this is done b duodenal cytochrome B (DcytB) on apical mem of enterocyte
Then the 2+ form can bind to DMT1 (divalent metal transporter 1) transporter and get taken into enterocyte
Ferroportin takes iron across basal membrane
What is DcytB and what's its role in Fe absorption?
duodenal cytochrome B
It's a reductase that converts 3+ heam to 2+ so it can get absorbed
On apical mem of enterocytes
What is DMT1 and what's its role in Fe absorption?
divalent metal transporter 1
Carries Fe2+ across apical mem of enterocytes
What's ferroportin and what's its role in Fe absorption?
On the basement membrane of teh enterocytes - transports Fe out of the enterocyte and into the blood
What transporter takes a) haem and b)non-heam iron into the enterocyte
Non-haem crosses apical membrane via DMT1 (divalent metal transporter1)
we're not sure what receptor takes haem iron across
What form of iron does transferrin bind?
Fe3+ ie once Fe2+ is transported out of the enterocyte via ferroportin, it needs to be converted to Fe3+
Where is hepcidin produced?
The liver
What does hepicidin do?
Controls release of iron from enterocytes AND release from RES macros.
Negative regulator ie up hepcidin -> down release of Fe
(we have lots of hepcidin if the body stores of iron are increased)
How does hypoxia affect iron absorption?
Hypoxia -> hypoxia inducible factor 1 -> upregulation of DcytB and DMT1
What happens to serum ferritin, transferrin and transferrin saturation in Fe deficiency?
Ferritin low
Transferrin high
Saturation low
What happens to serum ferritin, transferrin and transferrin saturation in chronic disease?
Ferritin low
Transferrin low
Saturation - normal
What happens to serum ferritin and transferrin saturation in iron overload
ferritin high
saturation high
What is the thing we have to be aware of when we're looking at a person's ferritin levels?
It's an acute phase reactant! -> levels will be elevated in inflammation, infection or neoplasia. Will also be increased if Fe is released from its stores (eg liver damage)
What is the relationship between synthesis of transferrin + body iron stores?
They're inversely proportional
Low stores -> icnreased transferin
What happens to transferrin receptor levels in a) Fe deficiency and b) chronic disease?
fe deficiency -> increased receptor levels
chronic disease -> they're not increased (because transferrin isn't increased in chronic disease -> cells aren't increasing their expression of the receptor)
What is the Perl's stain?
= How we assess iron levels in the BM
ie the perl's stain stains iron containing material blue. Absence or decrease in blue = iron deficiency
What are the three clinical features of DVT?
Painful calf
Leg swelling
+ve Homan's sign
What might make us suspicious that a person has inherited clotting disorders?
family Hx of DVT / PE
past history of thrombosis, particularly if it was in weird location, unexplained and/or at early age
What is our principle aim with treating a DVT?
Totally inhibit clot formation ASAP - this prevents further extension (hence decreases risk of embolus) and allows fibrinolysis and clot organisation to start occuring
What drug do we give to someone with a DVT?
HEPARIN immediately
Would probably start an oral anti-coagulant soon as well ie warfarin (this learning topic says you need 5 days overlap, others have said 4)
What does warfarin inhibit
protein C and S
ie the vitK dep factors
What is the time scale of warfarin's effects?
The inhibition of C and S is the net effect of warfarin in the first few days. This makes the person HYPER COAGULABLE -> need another anticoag drug over the top at this time
Which test do we use to monitor warfariN?
Aiming for 2-2.5
When is it safe to stop heparin after the combo of heparin and warfarin?
Must wait 4 days ie need four days of warfarin treatment WITH heparin before we can do warfarin alone
T/F: when we're administering heparin and warfarin, we stop the concurrent heparin once INR has reached therapeutic range
FALSE !!!! need to wait at least 4 days regardless of the INR is saying
Once we've had those 4 days, we need the INR to be in therapeutic range as well
Do we usually use fibrinolytic agents with DVTs?
Not usually. Benefits don't usually outweigh the risks (haemorrhage)
Because of the big rate of recurrence of DVTs and PEs, how do we treat someone in LT post a DVT? (hint: 2 diff groups of people will be treated differently)
- If there was a clear predisposing factor (eg post op / immobilisation) that's been removed, then we anti-coagulate for 6 weeks
- if there wasn't such a clear predisposing factor that we can remove, we anticoagulate for at least 3 months
During pregnancy, what is the time when you're most at risk of a clot?
The puerperium ie 6 week period post giving birth
What is coumadin?
What groups of people is warfarin contra-indicated in?
- The very old
- People who are confused / demented
- People on multiple meds (because it has lots of rxns)
- People with liver disease
- people with potential focal bleeding eg peptic ulcer
- pregnant women
If someone is suspected of having a DVT / PE, what tests would we run and in which order?
First do D-dimers - if it's above 500, we start on heparin immediately. Below -> they don't have either DVT or PE
Then for DVT do a lower limb ultrasound
For PE, do V/Q lung scan
If you have a PE, what will the V/Q scan show?
ventilation is normal
perfusion is abnormal
What does heparin act on?
Potentiates the actions of anti-thrombin III
- the unfractionated acts on both Xa and IIa (thrombin)
- LMWH only acts on Xa
What's the difference between unfractionated heparin and LMWH?
Unfractionated = big mix of polysacc chains that vary significantly in size - lots are long enough to interact with both ATIII and IIa -> can inhibit both Xa and IIa
Fractionated - much smaller chains -> most can't bind both ATIII and IIa -> only acts on Xa
What is the size range of molecules in unfractionated heparin?
What is the administration route of unfractionated heparin?
IV or deep SC - can't do intermuscular because would cause a big haematoma
What are the advs of LMWH over UFH? (5)
- no need for lab monitoring because response is much more predictable
- higher oral bioavailability
- longer plasma half life
- less inhibition of platelet function
- less chance of HITs though still possible!
What is the different in oral bioavailability of LMWH cf UFH?
LMWH = 90%
UFH = 30%
What is the pathogenesis of HITs?
PF4 (platelet factor 4) forms complex with heparin -> IgG antibodies against this complex bind and then activate the platelets --> thrombosis and thrombocytopenia
What do we monitor heparin with?
Why do we need to monitor someone on unfractionated heparin so regularly?
There isn't a very predictable dose-response relationship with UFH -> need to always do their APTT and adjust dosage as requried
What is the difference in the anti-Xa:IIa ration between UFH and LMWH?
LMWH - can't bind to IIa as well as ATIII --> higher action on Xa compared to IIa
UFH - more equal -> smaller ratio
How do we reverse the action of warfarin?
Give them plasma ie we're replacing all the factors - rapid response but short lasting
Vitamin K replacement - takes longer to get a response but then it lasts longer (1-2 weeks)
what are the effects of warfarin on baby in utero a) first trimester? b) 2nd and 3rd trimesters
first trimester -> 10% chance of mental retardation, nasal hypoplasia, stippled cartilage and small fingers and hands
Later on, there's no developmental risks, just increased risk of intracranial haemorrhage (particularly at time of birth)
Do we use warfarin during pregnancy and/or breast feeding?
No for pregnancy - particularly in first trimester because causes birth defects
Ok for breast feeding - inactive form only in the breast milk -> doesn't affect the baby
What does heparin bind to?
Anti-thrombin III
which then inhibits Xa and IIa (inhibition of IIa requires that IIa also binds to the heparin molecule - only possible with the big heparin molecules)