seminar stroke.4th rotation medicine
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By
Siti Nur Shafiqah Binti FazilMohammad Hazim Fikri Bin Adnan
Mohd. Amirul Hafifi Bin KhairulzamanNor Akma Binti Sulaiman
Norashikin Binti Naim
Zafirah Hani Binti RamliAtika Azura Binti Abdul Rashed
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Public: weakness, usually permanent on oneside, often with loss of speech.
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Stroke is a clinical syndrome characterized by
rapidly developing clinical symptoms and/or signs of
focal, and at times global, loss of cerebral function,
with symptoms lasting more than 24 hours or leading
to death, with no apparent cause other than that of
vascular origin.
~ Academy of Medicine, Malaysia
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Ischemic Hemorrhage
- Sudden loss of fx dt loss of bloodsupply to an area that controls thatfx.
- Usually caused bypartial/complete blockage of anartery that supplies the brain.
- results from a weakenedvessel that ruptures andbleeds into the surroundingbrain.
- blood accumulates andcompresses the surrounding
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HemorrhagicIschemic
Corticol
Lacunar
Brainstem
(85%) (15%)
h ertension - Em olism- atheroma
Large vessel
- Throm osis- Em olism
- Su arachnoidhemorrhage
- Intracere ralhemorrhage
- Mesothelioma
Anteriorcirculation
Posteriorcirculation
Smallarteries
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NON-MODIFIABLE MODIFIABLE
Age Hypertension (systolic and diastolic)
Sex Cigarette smoking
Ethnicity/race Diabetes Mellitus
Family history of stroke Atrial fibrillation
Coronary heart disease
Hyperlipidemia
Obesity and physical inactivity
Raised homocysteine levelHigh dietary salt intake
Heavy alcohol consumption
Previous stroke
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Three main causes of ischaemic stroke are:
1. Atherothromboembolism (50%)
2. Intracranial small vessel disease (penetrating arterydisease) (25%)
3. Cardiogenic embolism (20%)
Other causes:
Arterial dissection
Trauma
Vasculitis
Metabolic disorder
Congenital disorder
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Caused by :
Extracranial embolism
Intracranial thrombosis
Decreased cerebral blood
flow
Necrosis of brain tissue
Cerebral infarction
Stroke
Initiate ischaemic cascade
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1- Embolism
May arise from the heart or extracranial arteries
Sources of cardiogenic emboli : Valvular thrombi (MS, IE, prosthetic valve)
Mural thrombi ( MI, AF)
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2- Thrombosis
Large vessels (including carotid artery system) Small vessels (comprising intracerebral arteries,
including the Circle of Willis & posterior circulation)
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3- Flow disturbances
Inadequate cerebral blood flow due to :
Decreased cerebral perfusion pressure
Hematologic hyperviscosity ( sickle cell disease,multiple myeloma, polycythemia vera)
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Less common cause :
polycythemia, sickle cell anemia, protein C deficiency,fibromuscular dysplasia of the cerebral arteries, andprolonged vasoconstriction from migraine headachedisorders.
Any process that causes dissection of the cerebral arteries(trauma, thoracic aortic dissection, arteritis)
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Loss of perfusion to a portion of the brain
unleashed the ischemic cascade
On cellular level :
Ischemic neurons become depolarized (ATP depleted)
Membrane ion-transport systems fail
Calcium influx release neurotransmitters (including
glutamate)
Activates N-methyl-D-Aspartate (NMDA) & otherexcitatory receptors on other neurons
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Neurons become depolarized
Further calcium influx
Further glutamate release
Local amplification of initial ischemic insult
+ Massive calcium influx activates various degradative
enzymes
destruction of the cell membrane and otheressential neuronal structures
+ Free radicals, arachidonic acid, and nitric oxide aregenerated by this process further neuronal damage
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Intracerebral and subarachnoid hemorrhage
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Blood vessel ruptures
Explosive entry of blood into the brain parenchyma.
The extravasation forms a roughly circular or oval massthat disrupts the tissue and grows in volume as the
bleeding continues.
Swelling of brain tissue (cerebral edema)
Adjacent brain tissue is distorted and compressed.
Neurological deficit
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1- Intracranial hemorrhage
Common : chronic high BP Weakens the arteries burst
2- Subarachnoid hemorrhage
Common : ruptured
aneurysm
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Presentation of patient of stroke varies frommild confusion to altered level ofconsciousness, coma and death.
The presentation are dependant on whatportion of the brain is damage.
The areas of the brain affected by the strokedepend on the particular artery that is affected.
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Ischemic stroke
Cortical
Lacunar
Brainstem
Hemorrhagic stroke
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Anterior (carotid) artery circulation
Middle cerebral arteryAphasia
Hemiparesis / plegia
Hemianopia
Anterior cerebral artery
personality changes
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Symptoms:
Dizziness
Diplopia
Dysarthria
Dysphagia
Dystaxia
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Aphasia
Agnosia
Apraxia hemineglect
Loss of consciousness
Drowsy
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Definition:
strokes caused by the occlusion of a small branch ofa larger blood vessel. Because of the way bloodvessels divide in the brain, lacunar strokes tend tooccur in areas located away from the surface of thebrain, where many of the smaller blood vesselbranches are located.
Alert
Normal cognitive function (absence of cortical signs)
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Pure motor stroke
Pure Sensory
Sensorimotor
Ataxic Hemiparesis
Dysarthria Clumsy-Hand Syndrome
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- dangerous: small portion but have many functions.
: most patient die.
Wallenberg's syndrome Horners syndrome Hemiparesis : corticospinal tract Diplopia: occulomotor Facial numbness and weakness: 5th and 7th cranial
nerve Nystagmus and vertigo: vestibular Dysphagia and dysartria: 9th and 10th
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Dangerous within 24 hours.
Clinical manifestation is almost the same, but usuallypatient with hemorrhagic stroke present with severe
headache which sometimes preceed with vomitting.
Differences between intracerebral and subarachnoidcan only be found radiologically. However, in severe
hemorrhage, its difficult to distinguish between thetwo.
Definite differences between hemorrhagic and
infarction can only be seen radiologically.
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Metabolic/toxic encephalopathy Epileptic seizures ( Todds palsy) Hemiplegic migrain Structural intracranial lesion ( subdural
hematoma, brain tumor, AVM) Encephalitis Head injury Relapsing multiple sclerosis
Conversion disorder Hyperviscosity syndrome Peripheral nerves lesion ( guillaine barre
syndrome)
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FBC, ESR, serumelectrolytes, serumcreatinine,liverfunctiontest, bloodglucose, lipidprofile,coagulationprofile, ABG
- to detect common vascular risk factor and
markers of rarer causes such as atherosclerosis,diabetis mellitus or blood clotting problem
ECG, echocardiography, chest X-ray
- should be considered if cardiac embolism is
suspected Ctbrain
-should be done as soon as possible in all patient
to exclude or confirm hemorrhage
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MRI brainandMRA
- should be considered if CT is negative (CT scan
unable to differentiate ischemic andhemorrhagic stroke especially perfomed >10
days after stroke)
DopplerorDuplexultrasoundscan
- this is used to find out whether there has beena narrowing of the blood vessels in the neck (the
carotid arteries), which supply blood to the
brain.
Lumbarpuncture- should be done if subarachnoid hemorrhage is
suspected and CT brain is negative
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Acute management
Long-term management
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Airway check the patient can protect can protect his/her airway andswallow w/o evidence of aspiration
Breathing check that the patient is breathing adequately; check O2
saturation and give O2 if saturation < 95%Circulation check peripheral perfusion, pulse, and blood pressure
adequate and treat w fluid replacement, anti-arrhythmics drugand inotropic drug as appropriate
Hydration screen for sign of dehydration and give fluids parenterally orby nasogastric tube if necessary
Nutrition assess nutritional status and provide nutritional supplementsif necessary; if dysphagia persist for a day or two, start feedingvia a nasogastric tube
Medication if the patient is dysphagic, consider alternative routes foressential medications
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BP unless there is heart failure or renal failure, evidence ofhypertensive encephalopathy or aortic dissection, do not lowerthe blood pressure in the fist few week since the cerebrelperfusion may decrease. BP often returns towards the patientsnormal level within the first few days
Bloodglucose
check blood glucose and treat w insulin when levels are > 11.1mmol/L. monitor closely to avoid hypoglycemia
Temperature check for pyrexia and investigate and treat underlying cause ;
give antipyretics since raised brain temperature may increaseinfarct volume
Pressuresarea
check pressure areas and introduce measures to reduce the riskfor bedsores : treat infection, maintain nutrition, provide apressure-relieving mattress, turn immobile patient regularly
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Incontinence
check for constipation and urinary retention and treatappropriately; avoid urinary catheterization unless the patient isin acute urinary retention or incontinence is threatening pressureareas
Investigation
CT/MRI, blood glucose, urea n electrolyte, FBC, INR, ESR, ECG
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Medical therapy Risk factor should be identified and addressed Risk factor are :
HPT treat and monitor
Smoking stop Lifestyle more active (exercise) Alcohol moderate intake/stop High cholesterol statins, diet Raised hematocrit reduce Atrial fibrillation anticoagulate
Obesity weight reduction Diabetes good control Severe carotid stenosis - surgery Sleep apnoea - treat
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Antihypertensive therapy Recognition and good control of high BP is the major factor in both 1st and
2nd stroke prevention. Transient HPT often seen following stroke usuallydoes not require treatment provided diastolic pressure does not rise > 100mmHg. Sustained severe HPT needs treatment. BP should be loweredslowly to avoid any sudden fall in perfusion.
Antiplatelet therapy Long-term soluble aspirin(75 mg daily) reduces substantially the incidence
of further infarction following thromboembolic TIA or stroke. Clopidogrel and dipyrimadole are also used Combined aspirin 75 mg daily and dipytidamole 200 mg twice daily
possibly provide optimal prophylaxis against further thromboembolic
stroke or TIA.
Anticoagulants Heparin and warfarin shoud be given when there is atrial fibrillation
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Other measures Polycythaemia and any clotting abnormalities should be
treated. Statin therapy should be given for all
Surgical approaches Internal carotid endarterectomy
Surgery is recommended in TIA or stroke patient with internalcarotid stenosis >70%.
Successful surgery reduces the risk of further TIA/stroke byaround 75%.
Endarterectomy has a mortality around 3% and a similar risk of
stroke. Percutanous transluminal angioplasty (stenting) is an
alternative. The value of surgery for asymtomatic carotid stenosis is
debatable.
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Rehabilitation after stroke
Optimal care is on a stroke rehabilitation unit that
provides multidisciplinary services, coordinatesdisability-related medical care and trains caregivers.
Physiotherapy*
Speech therapy*
Occupational therapy*
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Is particularly useful in the few weeks inreducing spasticity, relieving contractures andteaching patients to use walking aids.
The benefits of physiotherapy for longer-termoutcome are still inadequately researched.
Baclofen and/or botulinum toxin aresometimes helpful in the management ofsevere spasticity.
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Speech therapists have a vital understanding ofaphasic patients problem and frustration.
Return of speech is hastened by conversation
generally. If swallowing is unsafe because of the risk of
aspiration, either nasogastric feeding orpercutanous gastrostomy will be needed.
Video-fluoroscopy while attempting toswallow is helpful.
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Following recovery, the occupational therapistsplay a valuable role in assessing therequirement for and arranging the provision of
various aids and modifications in the home,such as stair rails, hoists or wheelchairs.
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Anti-platelet- aspirin, clopidogrel, ticlopidine
Anticoagulants-heparin, warfarin
Thrombolytics-streptokinase, urokinase,t-PA
Antihypertensiveagents
ACE inhibitors
Beta-blockers
Hydralazine Lipidloweringdrugs
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ANTIPLATELETS
Inhibition of prostaglandin mechanism
Aspirin
Inhibition of ADP-induced platelet aggregation Ticlodipine, clopidogrel
Blockade of GP llb/llla receptors on platelets
Abciximab, integrelin
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irreversibly inactivates platelet cyclooxygenase1 (through acetylation)and suppresses theproduction of thromboxane A2
Interfere with platelet aggregation
Anuclear platelet cannot synthesize newenzyme during its 10 day lifetime
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Irreversibly inhibit binding of ADP to itsreceptors on platelets
Thus, inhibit activation of GP llb/IIIa receptors
required for platelets to bind to fibrinogen andto each other
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ANTICOAGULANTS
Heparin
serve as a calatytic template to accelerate the
antithrombin reaction antithrombin inhibits clotting factor proteases by
forming stable complexes with them
it interacts with activated factors (thrombin)IIa,
IXa,Xa, providing anticoagulant effect withinminutes
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Warfarin
Antagonist of vitamin K
inhibit the synthesis of Vitamin K dependent clotting
factors: factor II
factor VII
factor IX
factor X
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THROMBOLYTICS
Streptokinase
Combines with ciculating plasminogen to form an
activator complex: convert plasminogenplasmin t-PA (Alteplase, Reteplase)
Preferentially activate plasminogen bound to fibrin confines fibrinolysis to the formed thrombus and
avoids systemic activation
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ANTIHYPERTESIVE AGENTS
IV betablockers
hydralazine are recommended
ACE inhibitors
limited effect on cerebral circulation
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angiotensinogen
Angiotensin 1
Angiotensin 2
Angiotensin 2 receptor
vasoconstriction Aldosterone secretion
Increase peripheral
vascular resistanceIncreased sodium,
Increase water retention
Increased blood pressure
ACE inhibitors
Captopril, enapril, lisinopril, ramipril
Inhibit peptidyl dipeptidase enzymeDecreased formation of angiotensin 2
Decreased breakdown of bradykinin
Angiotension
receptor blocker
Losartan, valsartan, irbesartan,candesarta
Block angiotensin 2 receptorDo not have effect on bradykinin
Similar benefits like ACE inhibitor
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Labetalol
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This drug causes direct vasodilation, actingprimarily on arteries and arterioles.
This results in a decreased peripheral
resistance, which in turn prompts a reflexelevation in heart rate and cardiac output.
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LIPID LOWERING DRUGS
HMG CoA Reductase Inhibitor Bile acids binding resin
Nicotinic acid
Fibric acid derivatives
Cholesterol absorption inhibitors
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HMG CoA reductase inhibitor
Lovastatin, simvastatin, pravastatin, fluvastatin
MOA: - analogs of 3-hydroxy-3-methylglutarate-competitive inhibitors of 3-H-3-M coenzyme A (HMG
CoA reductase) which catalyze mevalonate biosynthesis
HMG CoA mevalonate
HMG CoA re uctase ihibitor
Decreased de novo synthesis of cholesterol
Increase LDL receptor number
Increased LDL uptake by hepatocytes
Decreased plasma LDL
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Bileacidbindingresin(cholestyramine,cholestipol,colesevelam)
Nicotinic acid(niacin)
Fibrates (clofibrate,benzafibrate,gemfibrozil)
Cholesterolabsoprtioninhibitor(ezetimibe)
MOA: binds to bileacid in the intestineand preventsreabsorbtion ;
Enterohepaticcycling interuptedMore cholesterolneede to form bileacidOutcome:
Increased de novesynthesis ofcholesterolIncreased LDL
MOA: -decreasedintracellular lipaseactivityIncreased
lipoprotein lipaseactivityDecrease catabolicrate of HDL
MOA: - activateperoxixomeproliferator-activated receptor
-Increasedexpression oflipoprotein lipase-Increasedcatabolism of VLDL
MOA: inhibitintestinal absorptionof dietry and biliarycholesterol
-reduce hepaticcholesterol stores-increase hepaticuptake of LDL fromplasma.
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Phychosocial Financial
Sexual relationships changed.
Most of the females lost interest intheir appearance, regardless of their
age.
felt unable to prevent outbursts andthis compounded their feelings ofguilt, low-esteem and despair.
increase anger and feelings offrustration.
Loss of self esteem makes depressioncommon
Need to buy some equipment for thepatients for example, wheel chair, airbed, medication, pampers.
The fees for physiotherapy andspeech therapist treatment.
Many become unemployable, loseindependence and are financiallyembarrassed
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Family members must be educated about howto take care of stroke patient
Both the family and stroke patient must go for
counseling in order to over come the problem Physiotherapy and speech therapy have an
important psychological role, as it will increaseconfidence of stroke patients to live their life.
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