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Medicine year 2 semester 2 > Case 20- Pharmacology 2 > Flashcards

Case 20- Pharmacology 2 Flashcards

1
Q

Newer anticoagulants (NOACs)

A

NOACs interrupt part of the coagulation cascade and are as effective as warfarin. The main difference are that NOACs are less influenced by diet and other medication so don’t require frequent blood tests and monitoring.

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2
Q

Direct thrombin inhibitors

A

Parenteral forms
• Hirudins- polypeptides which act as direct thrombin inhibitors
• Lepirudin- recombinant hirudin that binds irreversibly to both fibrin binding and catalytic sites on thrombin and is used for thromboembolic disease in patients with type II HIIT
• Other example Bivaliruding and argatroban
Orally active direct thrombin inhibitors= Dabigatran

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3
Q

Direct inhibitors of factor XA- Rivaroxaban, Apixaban, Edoxaban

A
  • Only oral dosage forms. They directly bind to and inhibit both free and bound factor Xa.
  • They are administered orally for prevention of venous thromboembolism following hip or knee surgery and prevention of stroke in patients with atrial fibrillation.
  • Has a rapid onset of action and a shorter half life than warfarin.
  • It is metabolised in the liver but can be used in liver disease if there is no coagulopathy. Renal excretion is minimal
  • Does not require routine oral anticoagulant monitoring.
  • The Antidote is Andexanet alfa or Prothrombin complex concentrate (PCC
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4
Q

Direct thrombin (factor IIa) inhibitors- i.e. dabigatran (oral), bivalirudin and argatroban (parenteral)

A
  • Competitive reversible inhibitor of thrombin
  • Used for prophylaxis of venous thromboembolism after hip or knee replacement surgery. Treatment for DVT and PE. Prevention of stroke and embolism in patients with atrial fibrillation
  • Has a rapid onset of action, given on a fixed dose
  • Does not require routine oral anticoagulant monitoring
  • Avoid in severe hepatic impairment and if CrCl <30ml/min
  • Antidote- Idarucizumab
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5
Q

Use of Antiplatelet drugs

A

Platelets provide the initial haemostatic plug at sites of vascular injury. Inhibition of platelet function is a useful prophylactic and therapeutic strategy against MI and stroke caused by thrombosis.

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6
Q

What triggers platelet aggregation

A

Prostaglandins, TXA2 (Thromboxin A2), ADP, thrombin and fibrin

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7
Q

Substances which increase intracellular cAMP inhibit platelet aggregation

A

cAMP, prostacyclin (PGI), adenosine. Adenosine acts through adenosine A2 receptors to increase platelet cAMP and inhibit aggregation.

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8
Q

Anti-platelet drugs examples

A
  1. COX inhibitor (inhibits PG and TXA)- Aspirin
  2. ADP receptor pathway inhibitor- Ticlopidine, Clopidogrel
  3. Glycoprotein IIb/IIIa inhibitors- Abciximab, Tirofiban and Eptifibatide
  4. Phosphodiesterase inhibitor (increase cAMP)- Dipyridamole, Cilostazol
    Platelet derived thromboxane A2 (TXA2) promotes aggregation
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9
Q

Anti-platelet drugs i.e. Aspirin

A
  • Aspirin irreversibly inhibits COX-1 therefore inhibiting the synthesis of TXA2
  • Because platelets do not contain DNA or RNA they cannot synthesise new COX-1
  • The inhibition is irreversible and is effective for the life of the circulation platelet (7-10 days)
  • Clinical use- used prophylactically to prevent arterial thrombosis leading to transient ischaemic attack, stroke and myocardial infarction
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10
Q

What happens when an atherosclerotic plaque ruptures

A

It stimulates platelets to bind to it which release cytokines stimulating the synthesis of thromboxin and stimulates expression of Glycoprotein IIa/IIIb receptors which platelets bind to each other with.

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11
Q

Abciximab

A

A monoclonal antibody to receptors for glycoprotein IIb/IIIa

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12
Q

Fibrinolytic (thrombolytic) drugs i.e. streptokinase, alteplase

A
  • Thromboses are dynamic- there is balance between break down (fibrinolysis) and formation
  • Thrombolytic drugs potential the effects of the fibrinolytic system
  • MoA: they activate conversion of plasminogen to plasmin which breaks down fibrin thus dissolving the clot
  • Endogenous forms of plasminogen activator- Alteplase
  • Protein synthesised by Streptococci which is Streptokinase
  • Derived from neonatal kidney cells- Urokinase
  • Administered IV- immediate
  • Short half life
  • Main hazard is bleeding such as cerebral haemorrhage
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13
Q

Clinical use Fibrinolytic drugs

A

Restoring catheter and shunt function by lysing clots causing occlusion. They are principally used to reopen occluded arteries in patients with stoke or acute myocardial infarction

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14
Q

Clinical use of Anticoagulants and Antiplatelet agents

A

Anticoagulants are principally indicated for the prevention of recurrent thrombosis in patients with venous thromboembolism (VTE), which includes deep venous thrombosis and pulmonary embolism, and ischemic stroke.
Antiplatelet agents are used prophylactically to prevent arterial thrombosis leading to transient ischemic attack, stroke, and myocardial infarction

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15
Q

Stroke imaging process

A
  • Assess history- for example, are they in the thrombolysis window/ PMH
  • Non contrast CT head and/or intracranial CT angiogram- to assess for intracranial haemorrhage
  • MRI head or angiopathy- for clarification, angiopathy to remove a clot
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16
Q

Attenuation on CT

A

High attenuation on CT= Hyperdense, white. For example, bone and acute haemorrhage
Low attenuation on CT= Hypodense, black. For example, CSF, water, air
Isodense on CT- Grey, same colour as surrounding brain parenchyma- reference density

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17
Q

Effacement and contrast enhancement

A

Effacement- compression of CSF spaces i.e. ventricles or sulci. Effacement of ventricles leads to Hydrocephalus
Contrast enhancement- increased attenuation post-contrast administration. Increases visibility of vessels and lesions

18
Q

CT head

A
  • Can see mass effect- localised swelling and displacement of surrounding structures
  • Effacement- compression of CSF spaces
  • Contrast enhancement
19
Q

MRI vs CT- MRI facts

A
  • Pro’s- better soft tissue definition, better availability to age infarcts (tells us if its hyperacute, acute or subacute) and haemorrhage, problem solving (in CT uncertainty)
  • Cons- limited availability, slower than CT, contraindications (pacemakers), limited bone definition
20
Q

Primary parenchymal haemorrhage

A
  • Most common type of haemorrhage
  • Most common in adults in mid-late age
  • Most are due to rupture of small intraparenchymal vessels such as the striate arteries
  • Hypertension is the leading cause
  • Variable severity- can range from small and clinically silent to devastating
  • Typically occurs in the basal ganglia, pons and cerebellum
21
Q

Anterior choroidal artery

A
  • Very prone to haemorrhage- especially in hypertension
  • It gives branches to the optic tract and radiation and the lateral geniculate body- visual field defects
  • Also gives branches to the posterior part of the internal capsule- motor and sensory defecits
22
Q

Haemorrhagic stroke on ct

A
  • Fresh blood within brain parenchyma- white
  • Surrounding oedema and mass effect which will compress vessels and ventricles- darker with less definition (visible gyri)
  • Can rupture into ventricles/CSF spaces and form a subarachnoid haemorrhage
  • Attenuation decreases as haemorrhage gets older
23
Q

Small hypertensive haemorrhagic infarct

A

Small rounded focus of increased attenuation at the posterior limb of the left internal capsule. No oedema, less severe.

24
Q

Small hypertensive haemorrhagic infarct on CT

A

On CT blood will become isodense with the brain at 1-2 weeks depending on clot size it will then become hypodense with the brain at about 2-3 weeks.

25
Q

Subarachnoid haemorrhage

A
  • Most common non traumatic cause is rupture of berry aneurysm but it normally caused by trauma.
  • Thunderclap headache with altered neurological state
  • Blood covers the brain surface filling the subarachnoid space and mixes with CSF. So, in order to be seen it needs to be a significant bleed
  • Mortality up to 50% one third have complications
  • Hypodense (white) around the brain and in the ventricles
26
Q

Prognostic values of subarachnoid haemorrhage

A
  • > 65 years
  • Volume of blood on CT
  • Lower GCS on admission
27
Q

Difference between haemorrhage and haematoma

A

A haemorrhage is the leaking of blood from a blood vessel due to the lack of integrity in the vessel wall or clotting mechanism whereas haematoma is the accumulation of leaked blood inside the body within the tissue planes

28
Q

Subdural haemorrhage

A
  • Venous bleeding in potential space between dura and arachnoid mater
  • More chronic and slow
  • Tearing or shearing of bridging veins
  • Can cross suture lines
  • Most often caused by blunt trauma though can occur spontaneously in people who are anticoagulated
  • Risk factors: Elderly / Alcoholics / Anticoagulation
  • Bleeds into a potential space, blood is venous so low pressure, hence the clot slowly grows
  • Half moon hypodense area along the side, oedema secondary to the bleed compressing structures
29
Q

Reasons for tearing/shearing of bridging veins

A
  • Trauma
  • Old age- atrophy of the brain
  • Involution- as everything shrinks, veins have increased tension so increased risk of bleeding
30
Q

Extradural haematoma

A
  • Occurs in 1-2% of all head trauma
  • Arterial bleeds between bone and dura
  • Usually caused by fracture- tempo parietal bones often affected
  • Normally caused by a focused blow to the head i.e. hammer
  • Many have lucid intervals following trauma and then get delayed neurological deterioration
  • Biconcave/convex/lens shaped on CT head- hyperdense (white)
  • Wont cross suture lines
  • Overtime gets less dense and becomes hypodense
  • Can be fatal, rapidly deteriorating patient
31
Q

Pterion

A

Joining of parietal, temporal, frontal and sphenoid bone. Area of weakness. Site of middle meningeal artery. Common location of extradural haemorrhage

32
Q

Haematoma on CT

A
  • Initially near isodense
  • Realistically wont scan immediately so they only see it when its very bright/dense
  • Overtime gets more hypodense until its very dark – chronic
33
Q

Ischaemic stroke on CT

A

Infarctions can be seen as early as 2-3 hours but most are not clearly evident on CT until 12-24 hours following the event. Urgent CT scans are often completely normal

34
Q

Acute ischaemia stroke- CT

A
  • Early- lots of grey-white matter differentiation
  • Oedema- dark (hypodense) area of parenchyma
  • Mass effect- effacement of sulci and ventricles
  • Attenuation decreases as stroke gets older, starts dark gets brighter then goes darker
35
Q

Infarct

A

Has to contain grey matter and extends into the cortex

36
Q

Anterior cerebral artery infarct

A

Wedge shape abnormality, very sharp cut off at peripheral lateral border. Near the middle extends upwards

37
Q

Middle cerebral artery infarct

A

Pretty much supplies most of the brain. Midline shift with squashing of ventricles. On the side

38
Q

Posterior cerebral artery infarct

A

Posteriorly, dark wedge shaped infarct

39
Q

Hyperdense artery

A

Early signs of infarct. Clot or thrombus in artery- brighter than normal blood. Early sign of a stroke

40
Q

Embolic stroke

A

Typically infective in nature i.e. due to a heart deformity/defect. The clot goes to the brain. Geographically well defined areas- typically peripheral. More circular

41
Q

Ischaemic lesions on an MRI

A

Scattered bright lesions in an ageing brain, can be normal

42
Q

Acute cerebral infarction on an MRI

A
  • High signal- hyperintense (white)
  • Intermediate signal – isotense (grey)
  • Low signal – hypointense (black)

Medicine year 2 semester 2 (47 decks)

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