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PBL SEM 2 > PBL 8 > Flashcards

PBL 8 Flashcards

1
Q

what is haemostasis?

A

a process to prevent and stop bleeding, meaning to keep blood within a damaged blood vessel (the opposite of haemostatis is haemorrhage)

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2
Q

what are some risk factors for DVT?

A
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3
Q

how can straining lead to DVT?

A

straining —> increased intrathoracic pressure

release —> lowered or normal pressure — leading to breaking of clots

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4
Q

PE cannot be ruled out if what are/is present?

A
  • age >_ 50
  • HR >_ 100
  • SaO2 on room air <95%
  • unilateral leg swelling
  • hemoptysis
  • recent trauma or surgery
  • prior ER or DVT
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5
Q

describe a V/Q scan

A
  • involves 2 isotopes
  • isotopes are difficult to get
  • gas used for ventilation is very rarely available
  • have moved away from V/Q scan
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6
Q

describe a CTPA

A
  • Computerised Tomography Pulmonary Angiogram
  • more readily available - isotope not needed
  • can also see tumour + PE
  • exposes patient to more radiation
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7
Q

V/Q scans and CTPA both use what?

A

injected radioactive material

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8
Q

what are all heparins made from?

A

pork

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9
Q

what is VTE?

A

= venous thromboembolism

= when DVT and PE occur together

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10
Q

symptoms of DVT

A
  • swelling in affected leg
  • pain in leg
  • red or discoloured leg
  • symptoms of PE
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11
Q

symptoms of PE

A
  • SOB
  • pleuritic chest pain (worse on inspiration)
  • feeling dizzy or fainting
  • tachycardia
  • dyspnoea
  • haemoptysis
  • low BP
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12
Q

how does a PE cause right sided HF and a decrease in BP?

A

pulmonary embolism —> increase pulmonary vascular pressure —> increase RV pressure —> right-sided HF —> decrease SV —> decrease CO —> decrease BP

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13
Q

what is chronic venous insufficiency?

A

when leg veins don’t allow blood to flow back up to your heart. causes leg and foot swelling, varicose veins and aching legs. can be due to faulty valves inside veins. can be due to DVT

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14
Q

what do intact blood vessels release?

A
  • prostacyclin (PGI2) is secreted to inhibit platelet activation
  • nitric oxide is secreted to inhibit platelet aggregation
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15
Q

extrinsic vs intrinsic pathways

A

extrinsic

  • quicker to respond and more direct
  • begins when damage occurs to the surrounding tissues
  • extrinsic tenase complex leads to activation of X, which activates the common pathway
  • events completed within a few seconds

intrinsic:

  • longer and more complex
  • factors involved are intrinsic (present within) the bloodstream
  • events completed within a few minutes
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16
Q

definition of obesity

A

BMI > 30 (>25 is overweight)

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17
Q

why is obesity a risk factor for DVT?

A

> obesity promotes chronic inflammation and impaired fibrinolysis (enzymatic breakdown of fibrin in a blood clot) — both lead to an increased risk of thrombosis
obesity leads to overproduction of plasminogen activator inhibitor-1 that comes from adipocytes or fat cells) — both lead to an increased risk of thrombosis
obesity leads to overproduction of plasminogen activator inhibitor-1 that comes from adipocytes or hepatocytes — leads to inhibition of clot break down or fibrinolysis promoting clot formation
more adipokines released from adipose tissue — activate platelets

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18
Q

name other risk factors for DVT

A
  • major surgery
  • compression
  • pregnancy
  • increasing age
  • obesity
  • malignancy
  • long distance flight
  • bed rest/hospitalisation
  • genetics eg. antithrombin III deficiency (autosomal dominant) (antithrombin inactivates Xa and
    thrombin)
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19
Q

what is not part of the wells criteria?

A

obesity

20
Q

how is DVT prevented in hospitalised patients?

A
  • hydration — if not able to drink doctor may arrange for fluids to be given by i.v drip
  • get out of bed and walk as soon as your condition allows — improve blood flow to veins
  • move feet (if possible and doctors says its ok)
  • compression stockings — should be removed 2x daily to clean and check the skin beneath
  • anticoagulants
  • heparin injections
21
Q

in who is DVT prophylaxis important?

A

cancer patients because cancer is a procoagulant state

22
Q

what med is not used prophylactically?

A

heparin

23
Q

describe ibuprofen

A

= NSAID

  • non-selective inhibitor of COX (enzyme involved in prostaglandin and thromboxane synthesis via the arachidonic acid pathway
  • inhibits both COX1 and COX2
  • lowers prostaglandin levels in teh body — reduces pain, inflammation, fever
  • anticoagulant effects come about due to reduced production of thromboxane A2
  • inhibiton of COX1 — pain and inflammation-reducing effects
  • inhibition of COX2 — blocks TXA2 production. causes gastric toxicity side effects
24
Q

vitamin K is used to make what clotting factors?

A

FII, FVII, FIX, FX, PC + PS

25
Q

how does vitamin K affect INR?

A

lowers INR — the lower the INR, the less time it takes for your blood to clot

26
Q

describe INR

A
27
Q

what are some side effects of anticoagulants?

A
  • excessive bleeding
  • passing blood in urine or faeces
  • severe bruising
  • prolonged nosebleeds
  • vomiting or coughing up blood
  • heavy periods
28
Q

describe von willebrand disease

A
  • autosomal dominant
  • either not enough vWB factor or they are enough but it doesn’t work properly
  • symptoms: spontaneous bleeding from mucous membranes, excessive bleeding from wounds, prolonged bleeding time in the presence of a normal platelet count
29
Q

what is vWF produced by?

A

endothelial cells, and to a lesser extent MK cells

30
Q

what does vWF stabilise?

A

FVIII, increasing its half-life

31
Q

what platelets use vWF to bind to the collagen, promoting platelet aggregation?

A

GP1b/IIb/IIIa

32
Q

what are the 2 most common bleeding disorders?

A

von WB disorder and haemophilia type A

33
Q

haemophilia A vs B vs C

A 
A = VIII deficiency 
B = IX deficiency 
C = XI deficiency
34
Q

who should not take DOACs?

A

people with severe kidney disease and people with mechanic heart valves

35
Q

where are DOACs excreted?

A

by the kidneys

36
Q

what number clotting factor is prothrombin?

A

II

37
Q

what is serum?

A

blood without clotting factors

38
Q

which protein causes platelet contraction?

A

thrombosthenin

39
Q

what is a normal INR value for someone not on warfarin?

A

0.9-1.3

40
Q

INR for someone on warfarin

A

around 2-3

41
Q

what is heparins mechanism of action?

A

binds to antithrombin III to increase its affinity for serine proteases

42
Q

what is a normal prothrombin time?

A

12-16 seconds

43
Q

what is the formula to calculate BMI?

A

Kg/m^2

44
Q

what coagulation factors does heparin activate?

A

II and X

45
Q

what do dense bodies of the platelet cytoplasmic granules contain?

A

serotonin

46
Q

what does TFPI inhibit?

A

FXa

47
Q

how long does it take for the heart attack risk of an ex-smoker to reach that of a non smoker?

A

15 years

PBL SEM 2 (44 decks)

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