Drug induced parkinsonism
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Certain drugs like reserpine, tetrabenazine, haloperidol, and metoclopramide can deplete dopamine or block dopamine receptors, leading to a parkinsonian syndrome within 3 months. The syndrome is symmetric with mild tremor and usually resolves after withdrawing the causative drug. For treatment, antimuscarinic agents are preferred over levodopa, which may worsen symptoms if the neuroleptic drug is continued. MPTP, through its metabolite MPP+, can selectively damage cells in the substantia nigra by inhibiting mitochondrial complex I, leading to parkinsonism through striatal dopamine depletion. MPTP parkinsonism was discovered in individuals who self-administered M
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Parkinsonism
1. Parkinsonism is a progressive neurodegenerative disorder caused by loss of dopamine-producing neurons in the substantia nigra, leading to motor symptoms like bradykinesia, rigidity, resting tremor, and impaired balance.
2. Treatment aims to restore dopamine levels through levodopa or dopamine agonists to improve motor symptoms, and anticholinergics to reduce acetylcholine activity in the striatum.
3. Levodopa is most effective but side effects emerge with long term use, so combinations with carbidopa are used to sustain dopamine levels and minimize side effects.
Antiparkinsonian Drugs
This document provides information on drugs used to treat Parkinson's disease. It begins with a brief history of Parkinson's disease and then discusses the pathophysiology involving the loss of dopamine-producing neurons in the substantia nigra. The main classes of antiparkinsonian drugs described are those affecting the brain's dopaminergic and cholinergic systems. Key drugs discussed in depth include levodopa, peripheral decarboxylase inhibitors like carbidopa, dopamine agonists like pramipexole and ropinirole, MAO-B inhibitors like selegiline and rasagiline, and COMT inhibitors like entacapone and tolcapone. Adverse effects and considerations for each drug class are
Pharmacological management of depression
This document provides an overview of the pharmacological management of depression. It discusses general considerations for antidepressant treatment, types of antidepressants including SSRIs, SNRIs, TCAs and others. It covers treating refractory depression, antidepressant use in special populations like children/adolescents and during pregnancy, and a symptom-based approach. Key points include recommending SSRIs as first-line treatment for moderate-severe depression and continuing medication for 6-9 months after symptom resolution to prevent relapse.
Drugs used in Parkinsons Disease ( anti- Parkinson drugs)
1) Parkinson's disease is a progressive disorder causing tremors, rigidity, slow movement, and impaired balance. It results from loss of dopamine-producing neurons in the brain.
2) Common drug treatments include levodopa to replace dopamine, COMT inhibitors like carbidopa to increase levodopa's effects, MAO-B inhibitors like selegiline to prolong dopamine activity, and amantadine to stimulate dopamine release.
3) While effective initially, long term levodopa use can cause dyskinesias and fluctuations; combining it with carbidopa or selegiline can improve outcomes.
Antipsychotics agents
Pharmacology of anti psychotic agents including classification, pharmacokinetics, adverse effects and use cum indication of antipyschotics agents
Parkinsons disease
Dopamine and tyrosine are not used directly for Parkinson's disease therapy because:
1. Dopamine does not cross the blood-brain barrier, so administering it systemically would not increase dopamine levels in the brain where it is needed.
2. Tyrosine is the amino acid precursor to dopamine, but giving large amounts of tyrosine would decrease the activity of the rate-limiting enzyme tyrosine hydroxylase in dopamine synthesis. This enzyme's activity is tightly regulated, and excess tyrosine would inhibit its activity, reducing dopamine production rather than increasing it.
So instead, drugs are used to either increase dopamine levels in the brain indirectly by increasing its precursors (levodopa) or prolonging its actions once synthesized
Parkinsonism_2.pptx
Parkinsonism is a progressive neurological disorder characterized by bradykinesia, muscular rigidity, resting tremor, and impaired balance. It is caused by the loss of dopamine-producing neurons in the substantia nigra. Treatment aims to enhance the dopaminergic pathway and inhibit the cholinergic pathway. Levodopa is the most effective drug as it is converted to dopamine in the brain, but it causes side effects when taken alone. Co-administering it with carbidopa limits peripheral conversion and side effects. Other treatment options include dopamine agonists, MAO-B inhibitors like selegiline, COMT inhibitors, amantadine, and antimuscarinic drugs, each with their own
dr. Ike - update on opioid pharmacology
dr. Ike - update on opioid pharmacologyDepartment of Anesthesiology, Faculty of Medicine Hasanuddin University
Opioid --> are important drugs used in the pain management.
Employ appropriate pharmacological choice by knowing the pharmacology of the drugs --> both pharmaco dynamic and pharmaco kinetics.
Provide optimal effect and minimize side effectsANTIDEPRESSANTS
Depression is a treatable mental illness characterized by changes in mood and loss of interest. Antidepressants work by increasing levels of neurotransmitters like serotonin, dopamine, and norepinephrine in the brain. There are several classes of antidepressants including tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and atypical antidepressants. Each class has different mechanisms of action, side effects, and prescribing considerations. Antidepressants generally take 4-6 weeks to take effect and should be tapered gradually rather than stopped abruptly.
Antiparkinson's Drugs
Parkinson's disease is a progressive nervous system disorder that causes a loss of dopamine-producing brain cells, leading to motor symptoms like tremors and rigidity. It occurs due to degeneration of the substantia nigra, decreasing dopamine levels in the basal ganglia. The document discusses the causes, symptoms, diagnosis, treatment and management of Parkinson's disease with a focus on increasing dopamine levels through drugs like L-DOPA, COMT inhibitors, and dopamine receptor agonists.
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Drugs used in Parkinsons Disease ( anti- Parkinson drugs)
Drugs used in Parkinsons Disease ( anti- Parkinson drugs)
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ECG S
1) The Sgarbossa criteria provide guidelines for diagnosing acute myocardial infarction in patients with left bundle branch block (LBB) or ventricular paced rhythm on electrocardiogram (ECG), as these conditions can obscure ECG changes.
2) The original Sgarbossa criteria included three criteria involving concordant or discordant ST segment changes greater than 1mm. The modified criteria expanded this to include proportionally excessive discordant ST elevation.
3) Different types of STEMI are described based on the location of maximal ST elevation, including anterior, inferior, lateral, posterior, and right ventricular STEMI, each with characteristic ECG patterns.
ECG I
This document discusses interventricular conduction delay and raised intracranial pressure as seen on electrocardiograms (ECGs). It defines interventricular conduction delay and lists various causes including fascicular blocks, bundle branch blocks, ventricular hypertrophy, dilatation, electrolyte abnormalities, toxins, pre-excitation, and arrhythmogenic cardiac conditions. It then discusses raised intracranial pressure and the associated ECG findings of widespread T-wave inversions, QT prolongation, and bradycardia as part of the Cushing reflex, indicating imminent brainstem herniation. Massive intracranial hemorrhages such as subarachnoid hemorrhage are the most common causes
ECG H
The document discusses various electrolyte abnormalities and their ECG manifestations, including hypercalcemia, hypocalcemia, hyperkalemia, hypokalemia, hypomagnesia, hyperthyroidism, hypothyroidism, and hypothermia. For each condition, it provides the normal and abnormal ranges for the electrolyte levels and describes the associated ECG changes such as peaked T waves, QT prolongation, low QRS voltage, bradycardia, and arrhythmias. The document serves as a reference for clinicians to recognize ECG patterns caused by electrolyte and endocrine abnormalities.
ECG F
1) Fascicular ventricular tachycardia is the most common form of idiopathic ventricular tachycardia originating from the left ventricle. It typically presents in young patients without structural heart disease.
2) It has characteristic ECG features including a monomorphic ventricular rhythm with fusion complexes and AV dissociation. The QRS duration is between 100-140 ms with a short RS interval of 60-80 ms. It also shows a right bundle branch block pattern and axis deviation.
3) Posterior fascicular ventricular tachycardia, which arises near the left posterior fascicle, shows a right bundle branch block pattern with left axis deviation. Anterior fascicular ventricular tachycardia arises
ECG E
The document discusses several electrocardiogram (ECG) findings and rhythms including ectopic atrial tachycardia, atrial tachycardia, electrical alternans seen in massive pericardial effusion which produces low QRS voltage, electrical alternans and tachycardia, escape rhythms like junctional escape rhythms where the pacemaker rate decreases down the conducting system, and ventricular escape rhythms. It also discusses the terminology of junctional rhythms and includes literature references.
ECG D
The document discusses De Winter's T waves, which are characterized by three key findings on ECG: upsloping ST depression in precordial leads, tall symmetric T waves in precordial leads, and ST elevation in aVR. It also summarizes the ECG patterns seen in dextrocardia, including right axis deviation, positive complexes in aVR, and dominant S waves in precordial leads. Finally, it outlines the ECG features of digoxin effect and toxicity, such as biphasic T waves, shortened QT, and the dysrhythmia of supraventricular tachycardia with a slow ventricular response seen in digoxin toxicity.
ECG C
Massive carbamazepine overdose of more than 50 mg/kg can cause cardiotoxicity due to sodium channel blockade, which may be detectable on ECG as subtle QRS widening or first-degree AV block. Dilated cardiomyopathy is characterized by ventricular dilatation and reduced ejection fraction below 40%, commonly presenting with symptoms of biventricular failure. Chronic obstructive pulmonary disease can cause prominent P waves in inferior leads, exaggerated ST segments, low QRS voltage especially in V4-V6, and may show an SV1-SV2-SV3 pattern.
ECG B
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- Beta-blocker and calcium channel blocker toxicity can cause prolonged PR interval and bradycardia. Propranolol toxicity specifically causes QRS widening and positive R' wave in aVR. Sotalol toxicity causes QT prolongation and risk of Torsades de Pointes.
- Bifascicular block is a combination of right bundle branch block with either left anterior or posterior fascicular block, and can be caused by ischemia, hypertension or other
ECG A: AVNRT, AVRT
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ECG A: AV blocks
This document summarizes different types of atrioventricular (AV) blocks seen on electrocardiograms (ECGs). It describes first-degree AV block as a PR interval over 200ms. Second-degree AV block, Mobitz type I (Wenckebach phenomenon) shows progressive PR prolongation until a blocked pulse. Mobitz type II shows intermittent non-conducted pulses without PR prolongation. High-grade second-degree AV block has a P:QRS ratio of 3:1 or higher, with an extremely slow ventricular rate. Third-degree or complete heart block shows no relationship between atrial and ventricular rates. Causes include myocardial infarction, drugs, and conduction system disease. Treatment ranges from
ECG A: first part.
This document provides an overview of several cardiac arrhythmias and conditions including:
1. Accelerated idioventricular rhythm (AIVR), which results when an ectopic ventricular pacemaker exceeds the sinus node rate. AIVR is seen post-myocardial infarction and features a regular rhythm between 50-110 bpm with three or more QRS complexes.
2. Atrial flutter, a supraventricular tachycardia caused by a reentry circuit in the right atrium with a rate of around 300 bpm. The ventricular rate is determined by AV conduction.
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Cardiorenal syndrome
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Categorization of risks and benefits (food additives)
The document discusses various categories of risks associated with food, including foodborne hazards of microbial origin, nutritional hazards, environmental contaminants, naturally occurring toxicants, and food additives. It notes that foodborne diseases of microbial origin pose the greatest risks. Nutritional hazards can arise from deficiencies or excesses. Environmental contaminants can enter the food supply from industrial or natural sources. Naturally occurring toxicants are found in some foods. Food additives present minimal risks when consumed within permitted levels. The document also outlines categories of potential benefits from foods, including health benefits, supply benefits, hedonic benefits, and convenience benefits.
Benefits and risks of additives
This document discusses the benefits and risks of food additives. The benefits include making foods safer, more nutritious, and longer lasting through the use of preservatives and antioxidants. Additives also provide greater variety of foods and lower prices. However, there are also risks. There is a lack of data on the long term health effects of combinations of additives. Some additives are associated with "junk foods" that are low in nutrients. While direct toxic effects are unlikely at legal levels, some individuals may have hypersensitivity reactions. Some animal studies also indicate potential cancer and reproductive issues, but no direct evidence in humans. The risks must be weighed against the benefits on a case by case basis.
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T cell stimulation by drugs
1. Small molecule drugs can become immunogenic by undergoing bioactivation into chemically reactive metabolites that covalently bind to proteins, forming hapten-carrier complexes.
2. These complexes are then processed and presented by antigen presenting cells to T cells, stimulating an adaptive immune response.
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Drug induced parkinsonism
- 1. Drug induced parkinsonism Domina Petric, MD
- 2. Drug induced parkinsonism • Reserpine and the related drug tetrabenazine deplete biogenic monoamines from their storage sites. • Haloperidol, metoclopramide and the phenothiazines block dopamine receptors. • These drugs may produce a parkinsonian syndrome, usually within 3 months after introduction.
- 3. Drug induced parkinsonism • The disorder tends to be symmetric with inconspicuous tremor. • The syndrome is related to high dosage and clears over several weeks or months after withdrawal. • If treatment is necessary, antimuscarinic agents are preferred. • Levodopa is of no help if neuroleptic drugs are continued and may aggravate the mental disorder.
- 4. MPTP and parkinsonism • MPTP is a protoxin that is converted by monoamine oxidase B to N-methyl-4- phenylpyridinum (MPP+). • MPP+ is selectively taken up by cells in the substantia nigra through an active mechanism normally responsible for dopamine reuptake. • MPP+ inhibits mitochondrial complex I: inhibits oxidative phosphorylation.
- 5. MPTP and parkinsonism • The interaction of MPP+ with complex I probably leads to cell death and thus to striatal dopamine depletion and parkinsonism. • In 1983, MPTP-parkinsonism was discovered in individuals who attempted to synthesize and use a narcotic drug related to meperidine, but actually synthesized and self-administered MPTP.
- 6. Literature • Katzung, Masters, Trevor. Basic and clinical pharmacology.