Pharmacology of Stroke: A Case Study
Added on 2023-06-11
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PHARMACOLGY OF STROKE 1
PHARMACOLOGY OF STROKE: A CASE STUDY
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PHARMACOLOGY OF STROKE: A CASE STUDY
By (Student’s name)
Course
Institutional affiliation
Date
PHARMACOLGY OF STROKE 2
PHARMACOLOGY OF STROKE: A CASE STUDY
Introduction
The current paper is a discussion of the pharmacologic management of stroke with reference to
the case study of Greta Balodis. Greta’s case study is a classic presentation of hemorrhagic stroke. She is
a 75-year-old widow, lived alone in Adelaide when she presented with a headache, dizziness, nausea,
and drooping of her left side of the face and mouth. She was diagnosed with a right cerebral vascular
accident with atrial fibrillation. After initial stabilization in the acute setting, and stroke rehabilitation at
a peripheral rehabilitation facility she was discharged and currently has mild residual hemiplegia with
resolving dysphagia. She is mobilizing with the use of a three-pronged walking stick. On discharge, her
outpatient medication was Aspirin PO 100mg daily, Clopidogrel PO 75mg daily and digoxin 125mcg PO
daily. This patient case will guide the discussion of the management of stroke. The linkage between
disease process, clinical manifestation, and the pharmacology will be provided. Furthermore, the signs
or symptoms that show improvement with pharmacotherapy will be discussed with clear rationales as
to the reason for improvement.
Stroke
The presentation of stroke is varied depending on the specific neurologic niche affected.
However, the pathology remains the same. Stroke can either be an ischemic or hemorrhagic type
(Walker and Colledge 2013, p. 1237). Ischemic stroke is caused by the blockage or restriction of blood
supply to either the entire brain or to focal areas causing brain hypoxia, that if not corrected end up
leading to brain ischemia and liquefactive necrosis (Walker and Colledge 2013, p. 1237). A transient
ischemic attack (TIA) occurs when the blockage, usually an embolic or thrombotic, occurs only for a
short period and resolves. Although it may be termed a “mini-stroke” and does not produce much
PHARMACOLOGY OF STROKE: A CASE STUDY
Introduction
The current paper is a discussion of the pharmacologic management of stroke with reference to
the case study of Greta Balodis. Greta’s case study is a classic presentation of hemorrhagic stroke. She is
a 75-year-old widow, lived alone in Adelaide when she presented with a headache, dizziness, nausea,
and drooping of her left side of the face and mouth. She was diagnosed with a right cerebral vascular
accident with atrial fibrillation. After initial stabilization in the acute setting, and stroke rehabilitation at
a peripheral rehabilitation facility she was discharged and currently has mild residual hemiplegia with
resolving dysphagia. She is mobilizing with the use of a three-pronged walking stick. On discharge, her
outpatient medication was Aspirin PO 100mg daily, Clopidogrel PO 75mg daily and digoxin 125mcg PO
daily. This patient case will guide the discussion of the management of stroke. The linkage between
disease process, clinical manifestation, and the pharmacology will be provided. Furthermore, the signs
or symptoms that show improvement with pharmacotherapy will be discussed with clear rationales as
to the reason for improvement.
Stroke
The presentation of stroke is varied depending on the specific neurologic niche affected.
However, the pathology remains the same. Stroke can either be an ischemic or hemorrhagic type
(Walker and Colledge 2013, p. 1237). Ischemic stroke is caused by the blockage or restriction of blood
supply to either the entire brain or to focal areas causing brain hypoxia, that if not corrected end up
leading to brain ischemia and liquefactive necrosis (Walker and Colledge 2013, p. 1237). A transient
ischemic attack (TIA) occurs when the blockage, usually an embolic or thrombotic, occurs only for a
short period and resolves. Although it may be termed a “mini-stroke” and does not produce much
PHARMACOLGY OF STROKE 3
neurologic damage, it is an indicator of existing risk of a CVA and should be taken seriously. Greta has a
past history of a similar presentation.
Hemorrhagic stroke is due to vascular compromise with the bursting of blood vessels in the
brain (Walker and Colledge 2013, p. 1237). The vessels are usually weakened, especially as a
consequence of hypertension like in Greta’s case since she was also hypertensive. The weakened
segments are either aneurysms or arteriovenous malformations. Bleeding occurs directly into the brain
parenchyma. As blood accumulates, the manifestations of the stroke with include focal neurological
symptoms related to that site of bleeding and sign of increased intracranial pressure usually due to
blood pooling in a confined cranium (Mohr et al. 2011)
Greta experienced a CVA, most likely an ischemic stroke. This type of stroke is commonest with
85% of cases being attributed to it (Walker and Colledge 2013, p. 1237). Like in TIA it is caused by
thrombi or emboli occluding the vascular supply to the brain, but in this case, the blockage lasts longer,
leading to focal ischemia and neurological deficits.
The most likely source of emboli in Greta’s case is the heart. This is evidenced by the diagnosis
of atrial fibrillation. Atrial fibrillation is the most common cardiac arrhythmia (Hart and Halperin 2001).
In the elderly, the erratic electrical activity disturbs normal cardiac contraction with stasis and flow
abnormalities predisposing the patient to thrombus formation, especially left atrial appendage thrombi
(Mattle, Schwerzmann, and Seiler 2003).
Pharmacology of stroke
Greta was on aspirin, Clopidogrel, and digoxin. Aspirin and Clopidogrel are related to stroke
management while digoxin is a cardiac glycoside that was to manage her comorbid atrial fibrillation.
neurologic damage, it is an indicator of existing risk of a CVA and should be taken seriously. Greta has a
past history of a similar presentation.
Hemorrhagic stroke is due to vascular compromise with the bursting of blood vessels in the
brain (Walker and Colledge 2013, p. 1237). The vessels are usually weakened, especially as a
consequence of hypertension like in Greta’s case since she was also hypertensive. The weakened
segments are either aneurysms or arteriovenous malformations. Bleeding occurs directly into the brain
parenchyma. As blood accumulates, the manifestations of the stroke with include focal neurological
symptoms related to that site of bleeding and sign of increased intracranial pressure usually due to
blood pooling in a confined cranium (Mohr et al. 2011)
Greta experienced a CVA, most likely an ischemic stroke. This type of stroke is commonest with
85% of cases being attributed to it (Walker and Colledge 2013, p. 1237). Like in TIA it is caused by
thrombi or emboli occluding the vascular supply to the brain, but in this case, the blockage lasts longer,
leading to focal ischemia and neurological deficits.
The most likely source of emboli in Greta’s case is the heart. This is evidenced by the diagnosis
of atrial fibrillation. Atrial fibrillation is the most common cardiac arrhythmia (Hart and Halperin 2001).
In the elderly, the erratic electrical activity disturbs normal cardiac contraction with stasis and flow
abnormalities predisposing the patient to thrombus formation, especially left atrial appendage thrombi
(Mattle, Schwerzmann, and Seiler 2003).
Pharmacology of stroke
Greta was on aspirin, Clopidogrel, and digoxin. Aspirin and Clopidogrel are related to stroke
management while digoxin is a cardiac glycoside that was to manage her comorbid atrial fibrillation.
PHARMACOLGY OF STROKE 4
Treatment for stroke can be divided into stroke specific therapy and stroke preventive therapy. Stroke
specific therapy is the acute management of a stroke episode and is dependent on the type of stroke. In
Greta’s case, the mainstay of acute stroke management is the lysis of the occluding thrombus or emboli
in order to restore blood flow to the affected areas.
Stroke specific therapy
Stroke specific therapy for ischemic stroke is in the acute care setting and is aimed at
thrombolysis and antithrombotic therapy (Gorin et al. 2010).
Tissue plasminogen activator (t-PA)
Tissue plasminogen activator is the approved first-line drug for ischemic stroke (Hacke et al.
2008). It is a fibrinolytic agent that activates plasminogen which is bound to fibrin. It is different from
other fibrinolytic agents because it reduces bleeding by lysing only the formed thrombi and since it binds
to plasminogen on the fibrin avoiding free plasminogen in the blood (Katzung, Masters, and Trevor
2010). The human form is the drug Alteplase. Plasminogen is activated to plasmin which is the active
fibrinolytic enzyme and lyses the fibrin clot, restoring the integrity of the blood vessel and restoring
circulation. According to Stroke Foundation of Australia (2018), Alteplase is only recommended for the
treatment of acute stroke within 4.5 hours of the stroke. The case study, however, does not show
whether Greta benefited from this thrombolytic agent.
Aspirin
Aspirin is an antiplatelet drug that inhibits platelet aggregation and thus clot formation, by
inhibiting the synthesis of thromboxane A2 (Katzung, Masters, and Trevor 2010). In the background of
stroke, it is a recommended therapy and is useful in preventing a repeat episode of CVA (Site 2006).
According to the Stroke Foundation of Australia (2018), it should be started as soon as a diagnosis of
Treatment for stroke can be divided into stroke specific therapy and stroke preventive therapy. Stroke
specific therapy is the acute management of a stroke episode and is dependent on the type of stroke. In
Greta’s case, the mainstay of acute stroke management is the lysis of the occluding thrombus or emboli
in order to restore blood flow to the affected areas.
Stroke specific therapy
Stroke specific therapy for ischemic stroke is in the acute care setting and is aimed at
thrombolysis and antithrombotic therapy (Gorin et al. 2010).
Tissue plasminogen activator (t-PA)
Tissue plasminogen activator is the approved first-line drug for ischemic stroke (Hacke et al.
2008). It is a fibrinolytic agent that activates plasminogen which is bound to fibrin. It is different from
other fibrinolytic agents because it reduces bleeding by lysing only the formed thrombi and since it binds
to plasminogen on the fibrin avoiding free plasminogen in the blood (Katzung, Masters, and Trevor
2010). The human form is the drug Alteplase. Plasminogen is activated to plasmin which is the active
fibrinolytic enzyme and lyses the fibrin clot, restoring the integrity of the blood vessel and restoring
circulation. According to Stroke Foundation of Australia (2018), Alteplase is only recommended for the
treatment of acute stroke within 4.5 hours of the stroke. The case study, however, does not show
whether Greta benefited from this thrombolytic agent.
Aspirin
Aspirin is an antiplatelet drug that inhibits platelet aggregation and thus clot formation, by
inhibiting the synthesis of thromboxane A2 (Katzung, Masters, and Trevor 2010). In the background of
stroke, it is a recommended therapy and is useful in preventing a repeat episode of CVA (Site 2006).
According to the Stroke Foundation of Australia (2018), it should be started as soon as a diagnosis of
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