Epilepsy Definition and Causes

- define epilepsy→**Recurrent episodes of abnormal excessive depolarization of groups of cerebral neurons.** - List potential causes of Epilepsy.→Neurological disease, Brain damage, Heredity, Metabolic disorders (e.g., hypoglycemia), Sudden alcohol withdrawal, Intoxication with loca...

- define epilepsy→**Recurrent episodes of abnormal excessive depolarization of groups of cerebral neurons.** - List potential causes of Epilepsy.→Neurological disease, Brain damage, Heredity, Metabolic disorders (e.g., hypoglycemia), Sudden alcohol withdrawal, Intoxication with local anesthetics - What are the major categories of epileptic seizures? - Partial seizures (Simple & Complex) - Generalized seizures (Absence & Tonic-clonic) - Status epilepticus - Describe simple partial seizures.→Motor seizures causing repetitive jerking of a specific muscle group without impairment of consciousness. - Describe complex partial seizures.→Characterized by repetitive actions, confusion, and possible impairment of consciousness. - Describe absence (petit mal) seizures.→Characterized by abrupt onset and cessation, with maintained posture; patient appears distracted for a few seconds. - Describe tonic-clonic (grand mal) seizures.→Brief strong muscle contraction followed by irregular jerking of multiple muscle groups, with impaired consciousness. - Define status epilepticus.→A life-threatening condition involving prolonged, uncontrollable seizures. - What is the purpose of EEG in epilepsy?→Records electrical activity of the brain to help diagnose epilepsy and localize seizure activity. - Mechanism of action of Phenytoin in epilepsy treatment.→Blocks voltage-dependent Na+ channels to prevent repetitive neuronal discharges. - Common side effects of Phenytoin.→Anemia, cognitive impairment, developmental abnormalities in fetuses, increased risk of heart disease. - Mechanism of action of Carbamazepine in epilepsy treatment.→Blocks voltage-dependent Na+ channels, similar to Phenytoin. - Side effects of Carbamazepine.→Dizziness, blurred vision, risk of spina bifida in fetuses. - Mechanism of action of Vigabatrin.→Inhibits GABA transaminase to increase GABA levels in the brain, aiding in seizure control. - Side effect of Vigabatrin.→Sedation. - Define neurodegenerative disorders.→Chronic, progressive diseases resulting from neuron death, leading to symptoms based on affected cell types. - Characteristic symptoms of Parkinson's Disease (PD).→Muscle rigidity, bradykinesia, akinesia, and other CNS disturbances. - Mechanism of action of Levodopa in PD.→A dopamine precursor that crosses the blood-brain barrier and is converted to dopamine. - Side effects of prolonged Levodopa use.→Nausea, anxiety, confusion, hypotension, and involuntary movements with long-term use. - What are the pathological hallmarks of Alzheimer\'s Disease (AD)?→Amyloid plaques, tau protein tangles, synaptic and neuronal loss, inflammation, oxidative stress. - Mechanism of action of Donepezil in AD treatment.→Acetylcholine esterase inhibitor that reduces acetylcholine breakdown to mitigate memory loss. - Side effects of Donepezil.→Vomiting, salivation, bradycardia, respiratory depression. - Mechanism of action of Memantine in AD treatment.→NMDA receptor antagonist that reduces neuronal excitotoxicity. - Define Motor Neuron Disease (MND).→A progressive neurodegenerative disease affecting motor neurons, leading to movement, speech, and breathing difficulties. - Treatment option for ALS in MND.→Riluzole, which may inhibit glutamate neurotransmission, extending survival by 2-3 months. - Define Vertigo.→A sensation of spinning or dizziness, often accompanied by nausea, blurred vision, and balance issues. - Medications used in Vertigo treatment - Prochlorperazine (dopamine receptor antagonist for vomiting relief) - Betahistine (vasodilator for improved inner ear blood flow) - **Mechanism of action of Phenytoin in treating epilepsy.**→Phenytoin blocks voltage-dependent Na+ channels in the axonal membrane, preventing initiation and spread of repetitive neuronal discharges. - Mechanism of action of Carbamazepine in treating epilepsy.→Similar to Phenytoin, Carbamazepine blocks voltage-dependent Na+ channels, stabilizing the neuronal membrane and reducing seizure activity. - Mechanism of action of Vigabatrin in treating epilepsy.→Vigabatrin is structurally related to GABA and inhibits GABA transaminase, leading to increased GABA concentrations in the brain, which helps control seizures. - Mechanism of action of Tiagabine in epilepsy treatment.→Tiagabine inhibits GABA reuptake, increasing extracellular GABA levels and enhancing inhibitory effects in the CNS. - Mechanism of action of Valproate in epilepsy treatment.→Valproate weakly inhibits GABA transaminase and affects Na+ channels, helping to control neuronal excitability and reduce seizures. - Mechanism of action of Levodopa in treating Parkinson's Disease.→Levodopa, a dopamine precursor, crosses the blood-brain barrier and is converted into dopamine, which helps restore dopaminergic activity in the brain. - Mechanism of action of Carbidopa when combined with Levodopa for Parkinson's Disease.→Carbidopa inhibits peripheral dopa-decarboxylase, preventing the breakdown of Levodopa outside the brain and allowing more to reach the CNS. - Mechanism of action of Donepezil in Alzheimer's Disease treatment.→Donepezil is an acetylcholine esterase inhibitor that reduces the breakdown of acetylcholine, enhancing cholinergic transmission and potentially improving memory and cognition. - Mechanism of action of Memantine in treating Alzheimer's Disease.→Memantine acts as an NMDA receptor antagonist, blocking excessive glutamate activity to prevent excitotoxicity and reduce neuronal damage. - Mechanism of action of Riluzole in treating ALS (Amyotrophic Lateral Sclerosis).→Riluzole may inhibit glutamate release and inactivate voltage-dependent sodium channels, reducing excitotoxicity and prolonging neuron survival. - Mechanism of action of Prochlorperazine in Vertigo treatment.→Prochlorperazine is a dopamine (D2) receptor antagonist that acts on the chemoreceptor trigger zone to suppress nausea and vomiting. - Mechanism of action of Betahistine in Vertigo treatment.→Betahistine acts as a vasodilator, improving blood flow to the inner ear, which may reduce vertigo symptoms associated with vestibular disorders. - What is the pathophysiology of Epilepsy?→Epilepsy involves recurrent, excessive depolarization of groups of cerebral neurons, leading to sudden bursts of electrical discharges in the brain. This abnormal neuronal activity disrupts normal brain function, resulting in seizures. - What is the primary pathophysiological mechanism in Parkinson's Disease?→Parkinson's Disease is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra of the midbrain. This leads to a significant reduction in dopamine levels, disrupting the balance between dopamine and acetylcholine in the brain, which impairs movement control. - How does dopamine depletion affect motor function in PD? - **uscle Rigidity:** Increased muscle tone and resistance to movement. - **Bradykinesia:** Slowness of movement. - **Akinesia:** Difficulty initiating movements. - **Tremors:** Involuntary shaking, typically at rest. - What imbalance occurs in the neurotransmitter systems in PD?→There is an imbalance between dopamine and acetylcholine, where decreased dopamine levels result in relative excess of acetylcholine activity, contributing to motor dysfunction. - What are the pathological hallmarks of Alzheimer's Disease? - **Amyloid-beta Plaques:** Accumulation and aggregation of misfolded amyloid-beta peptides disrupt neuron function. - **Neurofibrillary Tangles:** Hyperphosphorylated tau proteins form tangles that interfere with neuronal transport. - **Synaptic and Neuronal Loss:** Significant loss of synapses and neurons, especially in the hippocampus and cortical areas. - **Inflammation and Oxidative Stress:** These processes exacerbate neuronal damage and accelerate disease progression. - How do amyloid-beta plaques contribute to AD?→Amyloid-beta plaques disrupt neuron-to-neuron communication, induce inflammation, and trigger oxidative stress, all of which contribute to neuronal death and cognitive decline. - What role do neurofibrillary tangles play in AD?→Neurofibrillary tangles, formed by hyperphosphorylated tau proteins, disrupt the transport systems within neurons, leading to cell death and impaired neuronal function. - What is the primary mechanism of neuron degeneration in ALS?→ALS involves the progressive degeneration of motor neurons in the brain and spinal cord, leading to muscle wasting and loss of voluntary movement. - How does excitotoxicity contribute to ALS?→Excessive glutamate activity leads to overstimulation of neurons, causing calcium overload and triggering pathways that result in neuron death. - What is the pathophysiology of Vertigo?→Vertigo arises from disturbances in the vestibular system, which includes the inner ear structures and their connections to the brain. These disturbances disrupt balance and spatial orientation, leading to the sensation of spinning or dizziness. - What is cancer?→Inappropriate and uncontrolled proliferation of the host's own cells. - What are the main treatment methods for cancer? - **Surgery** - Curative for localized, non-metastasized tumors. - **Radiation** - Used for localized malignancy, often delivers photons (gamma radiation). - **Chemotherapy** - Used for systemic cancers and adjunct to surgery/radiation. - What is chemotherapy, and how does it generally work?→Chemotherapy uses cytotoxic agents to target rapidly dividing cells by interfering with DNA synthesis or mitosis. - What is the mechanism of action for alkylating agents?→Form chemical bonds with DNA, causing cross-links and chain breakage, impairing replication and transcription. - Give an example of an alkylating agent and its adverse effects.→Cyclophosphamide; adverse effects include pulmonary fibrosis, blisters, liver damage, and renal failure. - What is the mechanism of cytotoxic antibiotics?→Bind to DNA to prevent RNA and protein synthesis and may degrade DNA, creating free radicals. - Give an example and adverse reactions of cytotoxic antibiotics.→Bleomycin; adverse reactions include bone marrow suppression and gastrointestinal upset. - What phase do antimetabolites target, and how do they work?→Active in the S phase; they insert themselves into the DNA structure, disrupting replication. - Name three types of antimetabolites and examples. - **Folate antagonists** - e.g., Methotrexate. - **Pyrimidine analogues** - e.g., Fluorouracil. - **Purine analogues** - e.g., Pentostatin. - How do mitotic poisons work?→Bind to tubulin, preventing mitosis and arresting cells at metaphase. - Give examples of mitotic poisons and associated adverse effects.→Vincristine, vinblastine; adverse effects include myelosuppression, leukocyte dysfunction, and sensory changes (paraesthesia). - How do hormonal agents work in cancer treatment?→They either block hormone receptors on cancer cells or reduce hormone levels, slowing hormone-dependent cancer growth. - Provide examples of hormonal agents and their cancer targets. - **Tamoxifen** - Estrogen receptor antagonist for breast cancer. - **Flutamide** - Androgen receptor antagonist for prostate cancer. - Why is combination therapy used in chemotherapy? - Increases cancer cell cytotoxicity without excessive general toxicity. - Reduces resistance by targeting multiple pathways. - Allows for treatment intervals for bone marrow recovery. - What are major side effects of chemotherapy? - **Emesis (nausea/vomiting)** - Managed with anti-emetics and anti-diarrheals. - **Bone marrow suppression** - Managed with stem cell harvest and re-infusion, or drugs to stimulate blood cell recovery. - What is chemotherapy resistance?→Cancer cells adapt to become less susceptible to chemotherapy drugs, often by increasing drug exclusion or deactivation mechanisms. - List some mechanisms of chemotherapy resistance. - **Drug efflux pumps** (e.g., P-glycoprotein). - **Altered target enzymes** (e.g., DNA topoisomerase isoforms). - **Increased drug inactivation** (e.g., Glutathione conjugation). - **Reduced drug entry** via lowered active transport. - Describe the stages of the cell cycle targeted by chemotherapy drugs. - **G1 phase:** RNA synthesis - **S phase:** DNA synthesis and replication. - **G2 phase:** Protein production and completion of RNA synthesis. - **M phase:** Nuclear and cytoplasmic division. - **G0 phase:** Resting phase. - Why are cells in certain cell cycle phases more susceptible to chemotherapy?→Chemotherapy drugs target rapidly dividing cells, as these cells are often actively synthesizing DNA or dividing, which are processes interrupted by cytotoxic drugs. - What is an anesthetic?→A drug used to cause loss of sensation (local anesthetic) or both sensation and consciousness (general anesthetic). - Difference between local and general anesthetics?→Local anesthetics cause reversible loss of sensation in a specific area, while general anesthetics cause loss of sensation and consciousness throughout the body. - What is the mechanism of action for local anesthetics?→They block sodium channels, preventing sodium ion flux and thus blocking nerve depolarization and transmission. - Order of sensation loss with local anesthetics?→Loss of pain, temperature, touch, and then motor function. Recovery follows the reverse order. - Types of local anesthetics?→Ester group (e.g., cocaine) and amide group (e.g., lidocaine, bupivacaine). - Why add vasoconstrictors like adrenaline to local anesthetics?→They localize the drug, increase contact time, prolong duration, and reduce systemic toxicity. - What are the desirable properties of an anesthetic?→Quick onset, sufficient duration, low systemic toxicity, and reversibility. - Key effects achieved by general anesthesia?→Analgesia, amnesia, loss of consciousness, inhibition of reflexes, and muscle relaxation. - Stages of general anesthesia?→Stage I (Analgesia), Stage II (Excitement), Stage III (Surgical anesthesia), and Stage IV (Medullary paralysis). - Examples of inhalational agents and their use?→Nitrous oxide (analgesic with rapid induction but low potency), methoxyflurane (used as analgesic), mainly for maintaining anesthesia. - Examples of intravenous anesthetics and use?→Thiopentone, propofol, ketamine -- primarily used for induction due to rapid onset. - Mechanisms of action for general anesthetics?→They may interact with lipid cell membranes, block synaptic transmission, increase inhibitory (GABA) or decrease excitatory (glutamate) neurotransmitters. - How does solubility affect general anesthetic pharmacokinetics?→Lipid-soluble agents are more potent; low aqueous solubility leads to fast induction and recovery (e.g., nitrous oxide). - Thiopentone's mechanism and disadvantages?→Enhances GABA activity with rapid onset; causes cardiovascular/respiratory depression and potential bronchospasm. - Propofol's action and common side effects?→Enhances GABA activity, blocks Na+ channels; side effects include injection site pain and hypotension. - Ketamine's unique properties and disadvantage?→Produces dissociative anesthesia with catatonia, analgesia, and amnesia; may cause cardiovascular stimulation and hallucinations. - Purpose of pre- and post-anesthesia medications?→To reduce anxiety, pain, secretion reflexes, and need for deep anesthesia. - Examples of pre- and post-anesthesia medications?→Atropine (reduces secretions), diazepam (sedation/anxiolytic), morphine (analgesia), and suxamethonium (muscle relaxation). - How does pH influence local anesthetic action?→At physiological pH, local anesthetics partially exist in an uncharged form that can cross the neuronal membrane and a charged form that blocks the sodium channel from within. - How are ester and amide local anesthetics metabolized?→Esters are rapidly hydrolyzed by plasma/liver esterases; amides are slowly metabolized by liver enzymes. - How does vasoconstriction affect local anesthetics?→Vasoconstrictors like adrenaline prolong the duration of anesthetics by increasing contact time with nerves, slowing absorption, and reducing systemic toxicity. - What are the different types of administration for local anesthetics?→Surface/topical, infiltration, nerve block, epidural, and spinal injections. - What factors affect the rate of absorption of local anesthetics?→Vascularity and blood flow at the injection site; for example, rapid absorption occurs intercostally, whereas subcutaneous or spinal injection results in delayed absorption. - How is acute toxicity from local anesthetics managed?→By maintaining the airway (oxygen administration), using diazepam for seizures, and adrenaline for hypotension. - What is diabetes?→A chronic metabolic disease characterized by high blood glucose, which can lead to damage in the heart, blood vessels, eyes, kidneys, and nerves. - What are the prevalence statistics of diabetes in Australia?→About 1.8 million Australians have diabetes, with 280 new diagnoses daily. It is Australia's fastest-growing chronic condition, costing \$14.6 billion annually. - What hormone controls blood glucose in the fed state, and where is it produced?→Insulin, produced by β-cells in the pancreas, is the hormone of the fed state, lowering blood glucose. - What role does glucagon play in blood glucose control?→Produced by α-cells in the pancreas, glucagon increases blood glucose by promoting glycogen breakdown (glycogenolysis), particularly during fasting or hypoglycemia. - What characterizes Type 1 Diabetes?→Autoimmune destruction of pancreatic β-cells, leading to an absolute insulin deficiency. - How is Type 1 diabetes managed?→Through lifelong insulin injections or pumps, blood glucose monitoring, and a healthy lifestyle with diet and exercise. - What is fast-acting insulin?→It works within 1 to 20 minutes, peaks in about 1 hour, and lasts 3 to 5 hours. - Describe the action profile of long-acting insulin.→It has no pronounced peak and lasts up to 24 hours, often used in combination with shorter-acting insulins for blood glucose control. - Why are multiple insulin types often used together?→To better match blood glucose changes throughout the day, minimizing risks like hypoglycemia and managing food-related blood glucose increases. - What causes Type 2 Diabetes?→Insulin resistance due to genetic factors, lifestyle influences (e.g., obesity, inactivity), often leading to high blood glucose levels. - How is Type 2 diabetes managed?→Primarily with lifestyle changes (diet, exercise) and medications, including several classes of oral hypoglycemics. - What is the mechanism of action of biguanides like Metformin?→It decreases glucose production by the liver, slows glucose absorption, reduces appetite, and increases insulin sensitivity. - What are common side effects of Metformin?→GI effects such as nausea, vomiting, diarrhea, and a reduced appetite; it rarely causes hypoglycemia unless combined with other agents. - When should Metformin be avoided?→In cases of severe renal impairment, conditions prone to lactic acidosis, and before procedures using contrast dyes. - How do sulphonylureas like Gliclazide work?→They stimulate the pancreas to increase insulin production, enhancing glucose uptake in cells. - What are the main side effects of sulphonylureas?→Hypoglycemia, weight gain, and increased appetite, with contraindications in severe renal or liver disease. - Why are sulphonylureas not recommended during pregnancy or breastfeeding?→Due to potential risks to the fetus and infant, as well as risk of hypoglycemia. - What is the main difference in insulin dependency between Type 1 and Type 2 diabetes?→Type 1 diabetics are dependent on insulin due to lack of production, while Type 2 diabetics are generally not dependent but may need it as their condition progresses. - Which form of diabetes is commonly diagnosed in children, and why?→Type 1 diabetes, often due to autoimmune β-cell destruction, is common in younger individuals. - How does lifestyle influence Type 2 diabetes?→Inactivity, obesity, and poor diet are major contributors to insulin resistance and the development of Type 2 diabetes. - Why is matching insulin to food intake important for Type 1 diabetics?→To prevent hypoglycemia, which can occur if insulin action does not match carbohydrate intake. - What are the primary complications of unmanaged diabetes?→Long-term damage to blood vessels, heart, kidneys, nerves, and eyes due to chronic high blood glucose levels. - What are antimicrobials?→Drugs that stop the spread and multiplication of harmful bacteria, viruses, or fungi in the body. - Name the three main types of antimicrobials.→Antibiotics, Antivirals, Antifungals. - How do antibiotics aid in infection treatment?→They either kill bacteria (bactericidal) or slow bacterial growth (bacteriostatic), allowing the immune system to clear the infection. - Why is narrow-spectrum antibiotic use preferable?→Narrow-spectrum antibiotics target fewer species, reducing the impact on beneficial bacteria and lowering resistance risk. - Name the primary mechanisms by which antibiotics act on bacteria. - Inhibit cell wall synthesis (e.g., Penicillins - Bactericidal) - Disrupt cell membrane (e.g., Antifungals - Fungistatic) - Inhibit protein synthesis (e.g., Tetracyclines, Macrolides) - Inhibit metabolism (e.g., Trimethoprim - Bacteriostatic) - List the major classes of antibiotics.→β-lactams (Penicillins, Cephalosporins), Aminoglycosides, Macrolides, Vancomycin, Tetracyclines. - What is the mechanism of β-lactams like Penicillins?→They inhibit bacterial cell wall synthesis, causing bacterial cell death. - Describe the spectrum and pharmacokinetics of Penicillins. - Narrow spectrum (e.g., Benzylpenicillin for Gram-positive bacteria) - Oral bioavailability ranges from 15% to 80% (amoxicillin). - Primarily cleared by kidneys. - What are some common side effects of Penicillins?→GI disturbances (diarrhea, nausea), allergic reactions (e.g., rash, anaphylaxis) - What is Benzylpenicillin commonly used for?→Bacterial endocarditis, meningitis, community-acquired pneumonia. It is not acid stable and must be given by injection. - What is Amoxicillin commonly used for?→Community-acquired pneumonia, bronchitis, otitis media, sinusitis, UTI. It is effective against some Gram-negative bacteria. - What is antibiotic resistance?→The ability of bacteria to resist the effects of an antibiotic, making infections harder to treat. It is a global health issue causing 700,000 deaths annually. - List mechanisms of bacterial resistance. - Blocking antibiotic entry (e.g., efflux pumps in Pseudomonas) - Producing enzymes that destroy the drug (e.g., β-lactamase) - Altering the drug's binding site - What are the challenges of developing antivirals?→Viruses are intracellular parasites, making it hard to target them without also affecting host cells. - Name viral infections treatable with current antivirals.→Herpes (HSV), Influenza, HIV/AIDS, Hepatitis B and C. - Name three guanine analogue antivirals and their use.→Famciclovir, Aciclovir, Valaciclovir - used for treating and preventing HSV and shingles - What are some side effects of guanine analogue antivirals?→GI issues (nausea, vomiting), CNS effects (confusion, dizziness, seizure), and crystalluria with dehydration (Aciclovir, Valaciclovir). - What is the mechanism of action of Azole antifungals?→They inhibit fungal cytochrome P450, which is necessary for ergosterol synthesis, disrupting cell membrane permeability. - Give examples of common Azole antifungals.→Fluconazole, Miconazole, Clotrimazole. - For which conditions is Fluconazole used?→Vulvovaginal candidiasis (single dose) and dermal candidiasis (once daily). - What are potential side effects of Fluconazole?→Rash, headache, dizziness, GI upset, and liver toxicity. It also interacts with drugs by inhibiting CYP450. - Name common GI adverse effects of antimicrobials.→Nausea, vomiting, diarrhea, which can lead to superinfection by allowing other pathogens to grow. - What is antibiotic-associated colitis?→Inflammation of the colon wall caused by antibiotics, leading to severe diarrhea. - Which populations are especially vulnerable to antimicrobial adverse effects?→Elderly patients and those with weakened immune systems. - What makes alcohol and other drugs psychoactive?→Drugs are psychoactive because they affect the brain\'s neurochemistry, primarily by activating or inhibiting neurotransmitter systems, which leads to changes in mood, cognition, perception, and behavior. - What is the mesolimbic dopamine pathway, and why is it important in drug use?→The mesolimbic dopamine pathway, also known as the reward system, is activated by drugs of abuse, leading to an increased release of dopamine. This pathway is crucial for the reinforcing effects of drugs, resulting in positive reinforcement and addiction. - What changes occur in the brain with continued drug use?→Chronic drug use causes neurobiological changes that lead to tolerance, loss of control, compulsive use, and withdrawal symptoms. These include changes in the stress axis, memory, attention, decision-making, and connectivity of brain regions, especially the prefrontal cortex. - What is the difference between positive and negative reinforcement in the context of addiction?→Positive reinforcement occurs when drug use leads to pleasurable effects (dopamine release), encouraging repeated use. Negative reinforcement happens when drug use relieves discomfort or pain, reinforcing the behavior to avoid withdrawal symptoms or negative emotions. - What is tolerance, and how does it develop?→Tolerance occurs when repeated drug use leads to a down-regulation of receptor systems, meaning the same dose no longer produces the same effect. This requires the person to take higher doses to achieve the same effect. - What causes withdrawal symptoms?→Withdrawal symptoms arise when the body attempts to restore balance after drug use stops. This includes dysregulation of neurotransmitters and systems that had adapted to the presence of the drug, resulting in symptoms such as anxiety, irritability, tremors, and other physical signs. - What are common symptoms of alcohol withdrawal?→Symptoms include hypersensitivity to stimulation, depressed mood, anxiety, tremor, perspiration, increased pulse, increased blood pressure, restlessness, insomnia, and difficulty concentrating. - What neurobiological changes are associated with addiction?→Addiction involves changes in brain pathways that lead to compulsive behavior, loss of control, and tolerance. The brain\'s reward system and areas responsible for decision-making, memory, and emotional regulation are altered. - What criteria are used to diagnose substance use disorder according to the DSM-5?→The DSM-5 diagnosis includes impaired control (e.g., using longer or more than intended), social impairment (e.g., neglecting obligations), risky use (e.g., using in dangerous situations), and physical indicators (tolerance and withdrawal). A diagnosis requires at least two criteria to be met. - How does addiction differ from risky use?→Addiction is characterized by compulsive use, loss of control, withdrawal symptoms, and continued use despite negative consequences. Risky use refers to behavior that may lead to addiction or harm but does not yet meet the criteria for addiction. - What factors influence the risk of developing addiction?→Factors include genetics, mental health disorders, gender, early age of drug use, social environment, education, availability, and the type of drug used. These risk and protective factors interact to determine an individual\'s susceptibility to addiction. - What is the biopsychosocial model of addiction?→The biopsychosocial model posits that addiction results from a complex interplay of biological, psychological, and social factors, where genetic predispositions, mental health, social environments, and drug characteristics contribute to the development of addiction. - What are the key risk factors for addiction?→Risk factors include genetics, age of first drug use, social skills, mental disorders, environmental factors (e.g., availability of drugs), and the type of drug or substance used (e.g., nicotine, opioids, alcohol). - How does alcohol affect pain and medication?→Alcohol has analgesic effects but develops tolerance over time, requiring more alcohol for pain relief. It also interacts dangerously with medications like acetaminophen (increasing liver failure risk) and opioids (increasing overdose risk). - How does marijuana affect pain and medications?→Marijuana is often used for self-medication for pain, with medicinal cannabis becoming more common. However, it interacts with medications like warfarin (increases bleeding risk) and hydrocortisone (affects glucocorticoid clearance), and has potential drug interaction risks. - What are the risks of combining alcohol with opioids?→Alcohol enhances the reinforcing, sedative, and analgesic effects of opioids, increasing the risk of misuse, overdose, and liver toxicity when combined with medications like acetaminophen or aspirin. - Why might athletes use performance-enhancing drugs? - political/social pressures and desire to win - Wealth, fame, and faster injury recovery - Social use in non-professional sports for performance/appearance - Why are performance-enhancing drugs banned? - Create unfair advantages not from training/skill - Pose substantial health risks, especially with hormones - What are the main categories of substances banned at all times? - S0: Non-approved substances (not for human use) - S1: Anabolic agents (e.g., testosterone, stanozol) - S2: Peptide hormones and growth factors (e.g., EPO, HGH) - S3: Beta-2-agonists (permissible for asthma within limits) - What are the main categories of substances banned in-competition only? - S6: Stimulants (e.g., cocaine, pseudoephedrine) - S7: Narcotics (e.g., opioids) - S8: Cannabinoids (e.g., marijuana) - S9: Glucocorticosteroids (anti-inflammatory drugs) - How do anabolic steroids work in the body? - Mimic testosterone, promoting protein synthesis for muscle growth - Block catabolic processes, allowing more muscle accumulation - Affect the hypothalamus, reducing testosterone and sperm production - What are the side effects of anabolic steroids in athletes? - Short-term: acne, hair loss, stunted growth - Long-term: cardiovascular disease, organ damage, shorter lifespan - Males: testicular shrinkage, impotence - Females: masculinization, voice deepening - How are athletes tested for anabolic steroids? - Sample collection (urine) - Gas chromatography and mass spectrometry - What is EPO and its effect on performance? - A glycoprotein hormone that stimulates red blood cell production - Increases hematocrit, enhancing oxygen capacity and endurance - What are the risks and detection methods for blood doping? - Risks: polycythemia (too thick blood), cardiovascular issues - Detection: gel electrophoresis for synthetic EPO, blood tests for high hematocrit - What are some banned doping methods? - M1: Manipulation of blood products (blood transfusions) - M2: Chemical/physical manipulation (urine tampering, injections) - M3: Gene doping/therapy (transfer of nucleic acids or modified cells) - What is gene doping, and why is it banned? - Involves transfer of genetic material to enhance performance - Difficult to detect, introduces ethical and health concerns - How do anti-doping tests work? - Two samples (A and B) are collected; both must confirm a positive result - Gas chromatography, mass spectrometry, and blood analysis are common - What is the Athlete Biological Passport (ABP)? - Tracks an athlete's biological markers over time - Detects abnormal changes rather than one-time positives - What is a Therapeutic Use Exemption (TUE)? - Allows athletes with legitimate medical needs to use prohibited substances - Must demonstrate no competitive advantage from the medication - What is Complementary and Alternative Medicine (CAM)?→CAM refers to therapies and procedures outside the standard health system, including traditional medicines, herbal supplements, vitamins, homeopathy, and acupuncture. CAM can be used alongside (complementary) or instead of (alternative) conventional treatments. - Define \"complementary\" vs. \"alternative\" medicine.→Complementary medicine is used alongside standard treatments and often has some scientific basis (e.g., herbal therapy, massage). Alternative medicine replaces standard treatments and typically lacks robust evidence (e.g., homeopathy, magnets). - Why do people use CAM?→Reasons include health maintenance, dissatisfaction with conventional treatments, autonomy over health choices, and alignment with personal beliefs. CAM is often used for chronic issues like cancer, arthritis, and pain where conventional treatments are limited. - Describe the demographic that most frequently uses CAM in Australia.→Primarily young to middle-aged women (30-50 years), with good educational and economic backgrounds, who often use CAM for general health. - What are the main CAM therapies for arthritis?→Common therapies include herbal supplements (e.g., chondroitin, glucosamine), Green-lipped mussel extract, massage, Tai Chi, meditation, yoga, and acupuncture. - What are some common adverse effects and drug interactions associated with CAM?→CAM can lead to adverse reactions like anaphylaxis (bee products), allergic reactions (Echinacea), warfarin interactions (Ginkgo biloba), caffeine overdose (Guarana), and serotonin syndrome (St John's Wort with SSRIs). - Why is the perception that \"natural = safe\" problematic with CAM?→Natural does not equate to safety. Some CAM products are toxic, contaminated with heavy metals or pharmaceuticals, or even deadly. Examples include hepatotoxicity from Kava, kidney damage from Aristolochic acid, and strokes from ma huang. - How does the Therapeutic Goods Administration (TGA) regulate CAM in Australia?→The TGA ensures the quality, safety, and efficacy of medicines. CAM must meet certain quality and safety standards and is categorized as either \"Listed\" (AUST L) with safety review or \"Registered\" (AUST R) with full evaluation for quality, safety, and efficacy. - What is the difference between "Listed" and "Registered" CAM products in Australia?→Registered products (AUST R) undergo full evaluation, including efficacy, while Listed products (AUST L) are only reviewed for quality and safety but not efficacy. - How does the TGA manage CAM advertising and labeling?→CAM products must follow guidelines for labeling and advertising, including adherence to Good Manufacturing Process standards to avoid contamination (e.g., with heavy metals in Ayurvedic products). - What are some of the limitations of TGA regulation for CAM products?→The TGA does not cover all CAM products. Some homeopathic products, low-risk supplements, and international internet sales are not regulated, allowing potentially unsafe products to enter the market. - Explain the controversy of using CAM for serious conditions like cancer.→CAM may be used to limit disease progression or relieve symptoms. However, some treatments lack evidence and may delay conventional therapies, reducing effectiveness and potentially harming patients. - What is the pathophysiology of herbal toxicity associated with CAM?→Herbs can contain hepatotoxic or nephrotoxic compounds (e.g., Kava, Aristolochic acid) that can cause liver or kidney damage, often due to contaminants, fillers, or active toxic ingredients not declared on labels. - Why is it important for CAM users to inform their healthcare providers?→CAM can interact with prescription drugs (e.g., warfarin, SSRIs), leading to adverse effects or reduced efficacy of conventional treatments. Over 50% of CAM users do not disclose their usage to doctors, increasing health risks. - What adverse events are associated with specific CAMs like St John's Wort?→St John's Wort can lead to serotonin syndrome if used with SSRIs or cause dangerous increases in drug levels when stopped suddenly, due to its impact on liver enzymes that metabolize medications. - Define an Adverse Drug Reaction (ADR).→An ADR is any noxious, unintended response to a drug that occurs at normally prescribed doses for disease prevention, diagnosis, or treatment (WHO, 1984). It does not include overdose, withdrawal, abuse, or administration errors. - Why are ADRs important in healthcare?→ADRs contribute to patient harm, are the second most common cause of hospital harm, can cause hospital admissions, are often preventable, and contribute to around 30% of medication noncompliance. - What is a Type A (Augmented) ADR?→Type A reactions are dose-dependent, predictable, and related to the drug's pharmacological action, often mild and preventable. Examples include hypoglycemia with insulin and bleeding with anticoagulants. - Describe a Type B (Bizarre) ADR.→Type B reactions are not dose-related, unpredictable, and often immunologic or idiosyncratic. Examples include anaphylaxis with penicillin and hepatotoxicity. These reactions are typically severe. - What characterizes a Type C (Chronic) ADR?→Type C reactions are dose and time-related, usually occurring with long-term use. They are uncommon but can include tolerance to opioids or adrenal suppression with corticosteroids. - Explain a Type D (Delayed) ADR.→Type D reactions appear long after drug exposure and are often due to cumulative dosing. Examples include cancer with long-term immunosuppressants or phocomelia with thalidomide exposure in the 1950s. - What is a Type E (End of Use) ADR?→Type E reactions are withdrawal symptoms that occur after stopping a drug, often as the reverse of its pharmacological action. Examples include withdrawal symptoms from opioids, benzodiazepines, and SSRIs. - Define a Type F (Failure) ADR.→Type F reactions represent an unexpected failure of therapy, often due to drug interactions. This is increasingly common as medications interact, impacting efficacy. - How prevalent are ADRs in the community?→ADRs are common, with 10% of patients experiencing an ADR in the past six months. Over 1.5 million people are affected yearly, causing at least 190,000 hospital admissions. - Which medications are commonly implicated in ADRs?→Common drugs associated with ADRs include antineoplastics, anticoagulants, analgesics, anti-inflammatories, cardiovascular drugs, corticosteroids, CNS drugs, and antibiotics. - What are some risk factors for developing ADRs?→Risk factors include extremes of age, female gender, organ failure (renal, hepatic, cardiac), frailty, high exposure (dose, duration), genetic factors, and enzyme deficiencies. - Why are the elderly at higher risk for ADRs?→Elderly patients have decreased renal function, less efficient homeostasis, higher sensitivity to drugs, lower lean body mass, and are often prescribed drugs with a narrow therapeutic index. - How are children more sensitive to ADRs?→Children, particularly infants, have immature hepatic enzymes and renal clearance, making them more vulnerable to central nervous system ADRs and certain drug toxicities - What are some preventable causes of ADRs?→Preventable causes include polypharmacy, lack of drug selectivity, prescribing errors, dispensing errors, and administration errors. - What steps can be taken to prevent ADRs?→Prevention includes using drugs only when necessary, minimizing the number of drugs, using the lowest effective doses, checking patient history for sensitivities, monitoring therapy, and avoiding the quick adoption of new drugs. - How are ADRs monitored in Australia?→The Therapeutic Goods Administration (TGA) monitors ADRs, particularly for new medicines, drug interactions, unexpected reactions, and serious reactions causing death, hospitalization, increased investigations, or birth defects