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Stroke ppt

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FARAZULHODA

Stroke is a disease that affects the arteries within the brain. It is the 5th cause of death and a leading cause of disability in the United States. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts (or ruptures). When that happens, part of the brain cannot get the blood (and oxygen) it needs,and brain cells die.

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2 Submitted by: FARAZUL HODA M. Pharm Pharmacy Practice (IInd Semester) Department of Pharmacology SPER,Jamia Hamdard
3 Content:- Definition 4 Epidiemiology 6 Pathophysiology 9 Risk Factor 14 Clinical presentation 18 Diagnosis 20 Treatment 23 Pharmacological Treatment 25
Stroke is a disease that affects the arteries within the brain. It is the 5th cause of death and a leading cause of disability in the United States. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts (or ruptures). When that happens, part of the brain cannot get the blood (and oxygen) it needs,and brain cells die. 4
Stroke involves abrupt onset of focal neurologic deficit that lasts at least 24 hours and is presumed to be of vascular origin. Stroke can be either ischemic or hemorrhagic. Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours and usually less than 30 minutes. 5
6 EPIDEMIOLOGY
7 The point prevalence of stroke in America is nearly 7 million Americans. Stroke is the fifth leading cause of death in the US. The incidence of stroke is around 800.000 people annually. The incidence of stroke has declined, but the morbidity has increased.
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12 ISCHEMIC STROKE Ischemic strokes (87% of all strokes) are due either to local thrombus formation or emboli occluding a cerebral artery. Cerebral atherosclerosis is a cause in most cases, but 30% are of unknown etiology. Emboli arise either from intra- or extracranial arteries. Twenty percent of ischemic strokes arise from the heart. Carotid atherosclerotic plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or dislodge and travel distally, eventually occluding a cerebral vessel. In cardiogenic embolism, stasis of blood flow in the atria or ventricles leads to formation of local clots that can dislodge and travel through the aorta to the cerebral circulation. Thrombus formation and embolism result in arterial occlusion, decreasing cerebral blood flow and causing ischemia. PATHOPHYSIOLOGY
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14 HEMORRHAGIC STROKE Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH), intracerebral hemorrhage, and subdural hematomas. SAH may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation (AVM). Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain causes a hematoma. Subdural hematomas are usually caused by trauma. Blood in the brain parenchyma damages surrounding tissue through a mass effect and the neurotoxicity of blood components and their degradation products. Hemorrhagic stroke can result in abrupt increased intracranial pressure leading to herniation and death.
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16 Nonmodifiable risk factors or risk markers Risk Factors Age Gender Race Family history of stroke Low birth weight
17 Hypertension single most important risk factor for ischemic stroke Atrial fibrillation most important and treatable cardiac cause of stroke Other cardiac diseases Diabetes independent risk factor Dyslipidemia Cigarette smoking Alcohol Sickle cell disease Asymptomatic carotid stenosis Postmenopausal hormone therapy Lifestyle factors associated with stroke risk Obesity Physical inactivity Diet Modifiable, well documented
18 Oral contraceptives Migraine Drug and alcohol abuse Hemostatic and inflammatory factors- fibrinogen linked to increased risk Homocysteine Sleep-disordered breathing Potentially modifiable, less well documented
19 CLINICAL PRESENTATION OF STROKE
20 The patient may complain of weakness on one side of the body Inability to speak Loss of vision, Vertigo, or falling. Ischemic stroke is not usually painful, but patients may complain of headache, and with hemorrhagic stroke, it can be very severe. Symptoms
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22 Patients usually have multiple signs of neurologic dysfunction, and the specific deficits are determined by the area of the brain involved. Hemi- or monoparesis occurs commonly, as does a hemisensory deficit. Patients with vertigo and double vision are likely to have posterior circulation involvement. Aphasia is seen commonly in patients with anterior circulation strokes. Patients may also suffer from dysarthria, visual field defects,and altered levels of consciousness. Signs
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24 DIAGNOSIS Laboratory tests for hypercoagulable states should be done only when the cause cannot be determined based on presence of risk factors. Protein C, protein S, and antithrombin III are best measured in steady state rather than in the acute stage. Computed tomography (CT) and magnetic resonance imaging (MRI) head scans can reveal areas of hemorrhage and infarction. Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) studies can each provide valuable diagnostic information.
25 25
26 TREATMENT Goals of Treatment: The goals are to (1) reduce ongoing neurologic injury and decrease mortality and long-term disability, (2) prevent complications secondary to immobility and neurologic dysfunction, and (3) prevent stroke recurrence.
27 NONPHARMACOLOGIC THERAPY Acute ischemic stroke: Surgical decompression is sometimes necessary to reduce intracranial pressure. An interprofessional team approach that includes early rehabilitation can reduce long-term disability. In secondary prevention, carotid endarterectomy and stenting may be effective in reducing stroke incidence and recurrence in appropriate patients. Hemorrhagic stroke: In SAH, surgical intervention to clip or ablate the vascular abnormality reduces mortality from rebleeding. After primary intracerebral hemorrhage, surgical evacuation may be beneficial in some situations. Insertion of an external ventricular drain with monitoring of intracranial pressure is commonly performed in these patients.
28 PHARMACOLOGICAL THERAPY OF ISCHEMIC STROKE Evidence-based recommendations for pharmacotherapy of ischemic stroke are given in Table 1. Alteplase (t-PA, tissue plasminogen activator) initiated within 4.5 hours of symptom onset reduces disability from ischemic stroke. Adherence to a strict protocol is essential to achieving positive outcomes: (1) activate the stroke team (2) treat as early as possible within 4.5 hours of onset (3) obtain CT scan to rule out hemorrhage (4) meet all inclusion and no exclusion criteria (5) administer alteplase 0.9 mg/kg (maximum 90 mg) infused IV over 1 hour, with 10% given as initial bolus over 1 minute (6) avoid anticoagulant and antiplatelet therapy for 24 hours; and (7) monitor the patient closely for elevated BP, response, and hemorrhage.
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30 Aspirin 160 to 325 mg/day started between 24 and 48 hours after completion of alteplase also reduces long-term death and disability. Secondary prevention of ischemic stroke: Use antiplatelet therapy in noncardioembolic stroke. Aspirin, clopidogrel, and extended-release dipyridamole plus aspirin are all first-line agents . Cilostazol is also a first-line agent, but its use has been limited by lack of data. Limit the combination of clopidogrel and ASA to select patients with a recent MI history or intracranial stenosis and only with ultralow-dose ASA to minimize bleeding risk. Oral anticoagulation is recommended for atrial fibrillation and a presumed cardiac source of embolism. A vitamin K antagonist (warfarin) is first line, but other oral anticoagulants (eg, dabigatran) may be recommended for some patients.
31 Treatment of elevated BP after ischemic stroke reduces risk of stroke recurrence. Treatment guidelines recommend BP reduction in patients with stroke or TIA after the acute period (first 7 days). Statins reduce risk of stroke by approximately 30% in patients with coronary artery disease and elevated plasma lipids. Treat ischemic stroke patients, regardless of baseline cholesterol, with high-intensity statin therapy to achieve a reduction of at least 50% in LDL for secondary stroke prevention. Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin (5000 units three times daily) is recommended for prevention of deep vein thrombosis in hospitalized patients with decreased mobility due to stroke and should be used in all but the most minor strokes.
32 PHARMACOLOGICAL THERAPY OF HEMORRHAGIC STROKE There are no standard pharmacologic strategies for treating intracerebral hemorrhage. Follow medical guidelines for managing BP, increased intracranial pressure, and other medical complications in acutely ill patients in neurointensive care units. SAH due to aneurysm rupture is often associated with delayed cerebral ischemia in the 2 weeks after the bleeding episode. Vasospasm of the cerebral vasculature is thought to be responsible for the delayed ischemia and occurs between 4 and 21 days after the bleed. The calcium channel blocker nimodipine 60 mg every 4 hours for 21 days, along with maintenance of intravascular volume with pressor therapy, is recommended to reduce the incidence and severity of neurologic deficits resulting from delayed ischemia.
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34 EVALUATION OF THERAPEUTIC OUTCOMES Monitor patients with acute stroke intensely for development of neurologic worsening (recurrence or extension), complications (thromboembolism, infection), and adverse treatment effects. The most common reasons for clinical deterioration in stroke patients include: (1) extension of the original lesion in the brain, (2) development of cerebral edema and raised intracranial pressure, (3) hypertensive emergency, (4) infection (eg, urinary and respiratory tract), (5) venous thromboembolism, (6) electrolyte abnormalities and rhythm disturbances, and (7) recurrent stroke. The approach to monitoring stroke patients is summarized in Table 3.
35
36 1.Khaku AS, Dulebohn SC. Stroke. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan 2.Pharmacotherapy A Pathophysiologic Approach Eighth Edition chp-27 Stroke(page no.353-364) Joseph T. DiPiro 3.Pharmacotherapy Handbook Ninth Edition chp- 13 Stroke(page no.120-124) Joseph T. DiPiro 4. Kamalakannan S,et al.Incidence & prevalence of stroke in India: A systematic review. Indian J Med Res. 2017 Aug; 146(2): 175185.

More Related Content

Stroke ppt

  • 1. 2 2
  • 2. 2 Submitted by: FARAZUL HODA M. Pharm Pharmacy Practice (IInd Semester) Department of Pharmacology SPER,Jamia Hamdard
  • 3. 3 Content:- Definition 4 Epidiemiology 6 Pathophysiology 9 Risk Factor 14 Clinical presentation 18 Diagnosis 20 Treatment 23 Pharmacological Treatment 25
  • 4. Stroke is a disease that affects the arteries within the brain. It is the 5th cause of death and a leading cause of disability in the United States. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts (or ruptures). When that happens, part of the brain cannot get the blood (and oxygen) it needs,and brain cells die. 4
  • 5. Stroke involves abrupt onset of focal neurologic deficit that lasts at least 24 hours and is presumed to be of vascular origin. Stroke can be either ischemic or hemorrhagic. Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours and usually less than 30 minutes. 5
  • 7. 7 The point prevalence of stroke in America is nearly 7 million Americans. Stroke is the fifth leading cause of death in the US. The incidence of stroke is around 800.000 people annually. The incidence of stroke has declined, but the morbidity has increased.
  • 8. 8
  • 9. 9 8
  • 10. 10 9
  • 11. 11
  • 12. 12 ISCHEMIC STROKE Ischemic strokes (87% of all strokes) are due either to local thrombus formation or emboli occluding a cerebral artery. Cerebral atherosclerosis is a cause in most cases, but 30% are of unknown etiology. Emboli arise either from intra- or extracranial arteries. Twenty percent of ischemic strokes arise from the heart. Carotid atherosclerotic plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or dislodge and travel distally, eventually occluding a cerebral vessel. In cardiogenic embolism, stasis of blood flow in the atria or ventricles leads to formation of local clots that can dislodge and travel through the aorta to the cerebral circulation. Thrombus formation and embolism result in arterial occlusion, decreasing cerebral blood flow and causing ischemia. PATHOPHYSIOLOGY
  • 13. 13
  • 14. 14 HEMORRHAGIC STROKE Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH), intracerebral hemorrhage, and subdural hematomas. SAH may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation (AVM). Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain causes a hematoma. Subdural hematomas are usually caused by trauma. Blood in the brain parenchyma damages surrounding tissue through a mass effect and the neurotoxicity of blood components and their degradation products. Hemorrhagic stroke can result in abrupt increased intracranial pressure leading to herniation and death.
  • 15. 15
  • 16. 16 Nonmodifiable risk factors or risk markers Risk Factors Age Gender Race Family history of stroke Low birth weight
  • 17. 17 Hypertension single most important risk factor for ischemic stroke Atrial fibrillation most important and treatable cardiac cause of stroke Other cardiac diseases Diabetes independent risk factor Dyslipidemia Cigarette smoking Alcohol Sickle cell disease Asymptomatic carotid stenosis Postmenopausal hormone therapy Lifestyle factors associated with stroke risk Obesity Physical inactivity Diet Modifiable, well documented
  • 18. 18 Oral contraceptives Migraine Drug and alcohol abuse Hemostatic and inflammatory factors- fibrinogen linked to increased risk Homocysteine Sleep-disordered breathing Potentially modifiable, less well documented
  • 20. 20 The patient may complain of weakness on one side of the body Inability to speak Loss of vision, Vertigo, or falling. Ischemic stroke is not usually painful, but patients may complain of headache, and with hemorrhagic stroke, it can be very severe. Symptoms
  • 21. 21 21
  • 22. 22 Patients usually have multiple signs of neurologic dysfunction, and the specific deficits are determined by the area of the brain involved. Hemi- or monoparesis occurs commonly, as does a hemisensory deficit. Patients with vertigo and double vision are likely to have posterior circulation involvement. Aphasia is seen commonly in patients with anterior circulation strokes. Patients may also suffer from dysarthria, visual field defects,and altered levels of consciousness. Signs
  • 23. 23 23
  • 24. 24 DIAGNOSIS Laboratory tests for hypercoagulable states should be done only when the cause cannot be determined based on presence of risk factors. Protein C, protein S, and antithrombin III are best measured in steady state rather than in the acute stage. Computed tomography (CT) and magnetic resonance imaging (MRI) head scans can reveal areas of hemorrhage and infarction. Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) studies can each provide valuable diagnostic information.
  • 25. 25 25
  • 26. 26 TREATMENT Goals of Treatment: The goals are to (1) reduce ongoing neurologic injury and decrease mortality and long-term disability, (2) prevent complications secondary to immobility and neurologic dysfunction, and (3) prevent stroke recurrence.
  • 27. 27 NONPHARMACOLOGIC THERAPY Acute ischemic stroke: Surgical decompression is sometimes necessary to reduce intracranial pressure. An interprofessional team approach that includes early rehabilitation can reduce long-term disability. In secondary prevention, carotid endarterectomy and stenting may be effective in reducing stroke incidence and recurrence in appropriate patients. Hemorrhagic stroke: In SAH, surgical intervention to clip or ablate the vascular abnormality reduces mortality from rebleeding. After primary intracerebral hemorrhage, surgical evacuation may be beneficial in some situations. Insertion of an external ventricular drain with monitoring of intracranial pressure is commonly performed in these patients.
  • 28. 28 PHARMACOLOGICAL THERAPY OF ISCHEMIC STROKE Evidence-based recommendations for pharmacotherapy of ischemic stroke are given in Table 1. Alteplase (t-PA, tissue plasminogen activator) initiated within 4.5 hours of symptom onset reduces disability from ischemic stroke. Adherence to a strict protocol is essential to achieving positive outcomes: (1) activate the stroke team (2) treat as early as possible within 4.5 hours of onset (3) obtain CT scan to rule out hemorrhage (4) meet all inclusion and no exclusion criteria (5) administer alteplase 0.9 mg/kg (maximum 90 mg) infused IV over 1 hour, with 10% given as initial bolus over 1 minute (6) avoid anticoagulant and antiplatelet therapy for 24 hours; and (7) monitor the patient closely for elevated BP, response, and hemorrhage.
  • 29. 29
  • 30. 30 Aspirin 160 to 325 mg/day started between 24 and 48 hours after completion of alteplase also reduces long-term death and disability. Secondary prevention of ischemic stroke: Use antiplatelet therapy in noncardioembolic stroke. Aspirin, clopidogrel, and extended-release dipyridamole plus aspirin are all first-line agents . Cilostazol is also a first-line agent, but its use has been limited by lack of data. Limit the combination of clopidogrel and ASA to select patients with a recent MI history or intracranial stenosis and only with ultralow-dose ASA to minimize bleeding risk. Oral anticoagulation is recommended for atrial fibrillation and a presumed cardiac source of embolism. A vitamin K antagonist (warfarin) is first line, but other oral anticoagulants (eg, dabigatran) may be recommended for some patients.
  • 31. 31 Treatment of elevated BP after ischemic stroke reduces risk of stroke recurrence. Treatment guidelines recommend BP reduction in patients with stroke or TIA after the acute period (first 7 days). Statins reduce risk of stroke by approximately 30% in patients with coronary artery disease and elevated plasma lipids. Treat ischemic stroke patients, regardless of baseline cholesterol, with high-intensity statin therapy to achieve a reduction of at least 50% in LDL for secondary stroke prevention. Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin (5000 units three times daily) is recommended for prevention of deep vein thrombosis in hospitalized patients with decreased mobility due to stroke and should be used in all but the most minor strokes.
  • 32. 32 PHARMACOLOGICAL THERAPY OF HEMORRHAGIC STROKE There are no standard pharmacologic strategies for treating intracerebral hemorrhage. Follow medical guidelines for managing BP, increased intracranial pressure, and other medical complications in acutely ill patients in neurointensive care units. SAH due to aneurysm rupture is often associated with delayed cerebral ischemia in the 2 weeks after the bleeding episode. Vasospasm of the cerebral vasculature is thought to be responsible for the delayed ischemia and occurs between 4 and 21 days after the bleed. The calcium channel blocker nimodipine 60 mg every 4 hours for 21 days, along with maintenance of intravascular volume with pressor therapy, is recommended to reduce the incidence and severity of neurologic deficits resulting from delayed ischemia.
  • 33. 33 33
  • 34. 34 EVALUATION OF THERAPEUTIC OUTCOMES Monitor patients with acute stroke intensely for development of neurologic worsening (recurrence or extension), complications (thromboembolism, infection), and adverse treatment effects. The most common reasons for clinical deterioration in stroke patients include: (1) extension of the original lesion in the brain, (2) development of cerebral edema and raised intracranial pressure, (3) hypertensive emergency, (4) infection (eg, urinary and respiratory tract), (5) venous thromboembolism, (6) electrolyte abnormalities and rhythm disturbances, and (7) recurrent stroke. The approach to monitoring stroke patients is summarized in Table 3.
  • 35. 35
  • 36. 36 1.Khaku AS, Dulebohn SC. Stroke. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan 2.Pharmacotherapy A Pathophysiologic Approach Eighth Edition chp-27 Stroke(page no.353-364) Joseph T. DiPiro 3.Pharmacotherapy Handbook Ninth Edition chp- 13 Stroke(page no.120-124) Joseph T. DiPiro 4. Kamalakannan S,et al.Incidence & prevalence of stroke in India: A systematic review. Indian J Med Res. 2017 Aug; 146(2): 175185.