Pharmacology Exam 3 Study Guide PDF

Chronic and Degenerative Neurologic Disorders: Basic Neurological Concepts: 1.​ Central Nervous System: brain and spinal cord 2.​ Peripheral Nervous System: a.​ Somatic nerves (motor and sensory) b.​ Autonomic Nervous System 3.​ Neurons: help conduct electrical signals...

Chronic and Degenerative Neurologic Disorders: Basic Neurological Concepts: 1.​ Central Nervous System: brain and spinal cord 2.​ Peripheral Nervous System: a.​ Somatic nerves (motor and sensory) b.​ Autonomic Nervous System 3.​ Neurons: help conduct electrical signals that the brain is sending a.​ Three basic types - motor, sensory, and interneurons 4.​ Glial Cells: Provide structural support for neurons Neurotransmitters: Know what they are responsible for 1.​ Acetylcholine (ACh): Muscle movement, memory, learning 2.​ Serotonin: Mood regulation, appetite, sleep 3.​ Dopamine: Movement, memory, behavior 4.​ GABA: Calms the brain down so that it isn’t anxious or helps it to prevent it to convulse 5.​ Norepinephrine: Alertness and stress response (BP and HR) 6.​ Glutamate: Learning and memory Nerve Conduction: pg 823 1.​ Resting state: The inside of the neuron is more negative than the outside, maintained by the sodium-potassium pump (pumps 3 Na⁺ out, 2 K⁺ in). 2.​ Depolarization: When a stimulus triggers the neuron, sodium (Na⁺) channels open, allowing Na⁺ to rush into the cell. This makes the inside less negative (more positive). 3.​ Repolarization: After the peak of depolarization, potassium (K⁺) channels open, allowing K⁺ to flow out of the cell, restoring the negative charge inside.  4.​ Hyperpolarization: The cell briefly becomes more negative than its resting state due to excess K⁺ leaving. 5.​ Return to resting state: The sodium-potassium pump restores the original ion balance, preparing the neuron for the next signal 6.​ This process allows nerve signals to travel down the axon efficiently. 7.​ Refractory Period: A rest time to return to base line, a healthy body needs this Myelin Sheath: Protective layer around the axon -​ White matter -​ Insulator -​ Helps nerve conduction move quicker -​ Degeneration of the Myelin Sheath: MS, ALS (nerve impulse cannot travel through as well) Brain: a.​ Frontal Lobe: Reasoning b.​ Parietal Lobe: Spatial understanding c.​ Temporal Lobe: Memory, language d.​ Brainstem: Communicates to rest of body, HR, BP e.​ Occipital Lobe: Vision f.​ Cerebellum: Balance Substantia Nigra: Synthesis of dopamine (Behavior, Movement, Memory) Ion Channel Disorders: Channelopathies Epilepsy: Recurrent Seizures -​ Disrupted channel activation -​ Repetitive synchronous firing of neuronal action potentials Seizures: Sudden, abnormal, disorderly discharge of neurons within the brain -​ Traditional Diagnosis: Two unprovoked seizures at least 24 hours apart -​ “Every person gets one seizure in their life” -​ Move objects out of their way -​ Nothing in their mouth and NO restraints -​ Place on side and turn head - aspiration risk -​ Epileptogenesis: Usually caused by head trauma, stroke, or infection that changes the brain, the part of the brain is hyperexcitable in that area Etiology: a.​ Head trauma (most common) b.​ Stroke: Bleeding from stroke c.​ Brain neoplasm (cancer) d.​ Alzheimer's disease e.​ Genetic f.​ Congenital g.​ Infections h.​ Electrolyte imbalance i.​ Detox Types: a.​ Focal: ONE hemisphere i.​ Can see it on an EEG b.​ Generalized: BOTH hemispheres Terminology: a.​ Motor, nonmotor, or both b.​ Clonic: sustained rhythmic jerking c.​ Atonic: Weak or limp muscles d.​ Myoclonus: Muscle twitching e.​ Nonmotor Symptoms: Staring spells with no movement f.​ Aura: Sensation before a seizure  g.​ Ictal Period: Time of seizure h.​ Postictal: After seizure has ended i.​ Interictal: Time between multiple seizures Testing: a.​ CBC b.​ Serum Chem (Electrolyte imbalance check) c.​ MRI/CT (Cancer, stroke, trauma) d.​ EEG Treatment: a.​ Antiepileptic b.​ Ketogenic diet c.​ CBD d.​ Vagus nerve stimulation: Lower BP, stimulates PNS - sloowwwss down Status Epilepticus (SE) -​ Seizure > 5 minutes OR -​ > 1 seizure within 5 minutes (without returning to normal LOC) -​ ABCs! -​ First line treatment: Benzodiazepines Sudden Unexpected Death in Epilepsy (SUDEP): -​ Unsure why - mostly when they are sleeping -​ 20-40 years of age -​ Have seizure and they stop breathing and their heart stops Upper vs Lower Motor Neuron a.​ Upper Motor Neuron: BRAIN b.​ Lower Motor Neuron: SPINAL CORD Headaches: Primary Headaches: Not due to any other medical illness or traumatic case 1.​ Tension Type: -​ Most common -​ Does NOT worsen with movement -​ NO N/V -​ Bilateral -​ Pain relievers 2.​ Migraine -​ Comes in four stages -​ Serotonin decreases and calcitonin gene-related peptide (CRGP) increases a.​ S/S: -​ Periodic, throbbing -​ Photophobia and phonophobia -​ Worsens with movement -​ Nausea -​ Aura may be present -​ 75% of those affected are women -​ Treatment: -​ NSAIDs (ibuprofen) -​ SSRIs (Triptans) -​ Dopamine receptor antagonists -​ Prevent triggers -​ Botox injections 3. Trigeminal autonomic cephalgia (TAC) -​ Cluster headache most common -​ Only one side -​ Orbital (has to do with eyes) -​ Bloodshot eyes, pupil constriction, eyelid edema  a.​ S/S -​ Excruciating, unilateral pain (on one side) -​ Cluster headache most common -​ Males 25-50 most affected b.​ Treatment: -​ 100% O2 inhalation -​ Anti-CGRP monoclonal antibodies Secondary Headaches: Caused by another primary condition 1.​ Head injury 2.​ Vascular problems 3.​ Medication SE 4.​ Sinus disease -​ Fever -​ Pain worsens with bending -​ Tender over face -​ antibiotics 5.​ Tumors -​ Dull and constant pain -​ 50% of tumors cause headaches 6.​ Trigeminal Neuralgia: -​ CN V irritation -​ Triggered by contact with face (shaving, talking, wind, etc) Parkinson’s Disease: Progressive loss of dopamine producing cells in Substantia Nigra -​ Unknown etiology -​ Movement affected a.​ Dopamine imbalance: acetylcholine stimulates muscle movement while dopamine is inhibitory  b.​ Alpha-synuclein (abnormal protein) accumulating in the brain = neurodegeneration c.​ Tremors, uncoordinated movements -​ Treatment: Carbidopa-levodopa (DOPA - replace dopamine) -​ Diminishing returns with levodopa usage (have to keep increasing it) -​ Triad: Bradykinesia (slow movement), tremor (pill-rolling), muscle rigidity -​ Postural instability, nonmotor, neuropsychiatric T- Tremor at rest​ R- Rigidity​ A- Akinesia or Bradykinrsia​ P- Postural/gait instability Amyotrophic Lateral Sclerosis (ALS) - Lou Gehrig’s Disease -​ Painless muscle weakness and atrophy -​ Death of motor neurons in the brain and spinal cord -​ Secondary death of myelin sheath, since the neurons are dying -​ UMN (brain): muscle tone increase, slow movement, hyperreflexia, babinski (toes spread apart) -​ LMN (lower): decreased strength, weakness -​ Clumsiness, gait disturbances, difficulty chewing, swallowing, and speaking -​ No cure Multiple Sclerosis (MS): Autoimmune -​ Chronic demyelinating disorder (myelin sheath is going away) -​ Affects brain, spinal cord, and optic nerves -​ Weakness, numbness, balance problems, abstract reasoning, attention -​ Can see depression in some patients Treatment:  -​ Want to decrease inflammation to prevent t-cells from continually attacking the myelin sheath -​ Stem cell transplant Huntington's Disease (HD): -​ Mutated gene which keeps producing an abnormal repetition of DNA bases -​ Disrupts protein “huntingtin” -​ Collects in the brain and is damaging the brain S/S: -​ Involuntary motor symptoms: Dyskinesia, chorea (dancelike movements), Athetosis (twisting and writhing) -​ Cognitive decline: apathy, slowed thought process -​ Emotional and behavioral symptoms: MDD Treatment: -​ Symptom management -​ Antipsychotic and Antidepressants Guillain-Barré Syndrome (GBS): Postinfectious disease -​ Acute inflammatory demyelination -​ Following respiratory illness or gastroenteritis -​ Recovery over a long period of time -​ Symmetrical ascending muscular weakness -​ Diminished deep tendon reflexes & sensory loss Treatment: -​ IVIG (immunoglobulins) and Plasmapheresis Myasthenia Gravis (MG): Autoimmune Disease -​ Antibodies (B-Cells and T-Cells attacks Ach receptors)  -​ Muscle weakness and fatigue -​ Extraocular muscles often attacked first -​ “True muscle fatigue” -​ Rest improves muscle function Treatment: -​ Physostigmine: Acetylcholinesterase inhibitor -​ Sambuterol -​ Corticosteroid Dementia: -​ Decline in reasoning, memory, judgement, and other cognitive functions -​ Difficulty with ADLs -​ NEED daily routine and reorientation -​ Main causes: 1.​ Alzheimer’s disease 2.​ Lewy body dementia S/S: -​ Anomia (forgetting names of persons or things) -​ Amnesia (short-term memory deficit) -​ Anxiety (worry or concern) -​ Agnosia (forgetting the purpose of familiar items) -​ Apraxia (forgetting how to perform activities) -​ Apathy (lack of concern for losses) -​ Aphasia (mute) -​ Sundowning (symptoms during late day into night) Treatment: Can't reverse but try to slow down progression -​ Cholinesterase inhibitors -​ Antidepressant/mood stabilizers -​ Monoclonal antibodies  Alzheimer’s Disease: Main form of dementia -​ Progressive neurological degeneration of brain -​ Accumulation of neurofibrillary tangles, Ach deficiency -​ Usually family history -​ Mental & physical stimulation reduces risk Vascular Dementia: -​ Multi-infarct -​ Small strokes causing lack of blood flow Lewy Body Dementia: -​ Abnormal deposits of protein in the body Parkinsons: Classification Therapeutic MOA Adverse Effects Examples Use Dopamine Reduce tremors Promote dopamine CNS effects Levodopa/Carbidopa Agonist & muscle synthesis & Peripheral effects (Duopa) Pramipexole (Dopaminergics) rigidity prevent breakdown Bone marrow depression (Mirapex) Hepatic dysfunction Help to restore balance between inhibitory and stimulating neurotransmitters Anticholinergic Reduce tremors Blocks effect of CNS effects Benztropine & muscle Ach to enhance Peripheral anticholinergic (Cogentin) rigidity dopamine/Ach effects balance Tachyardia Extrapyramidal Palpitations side effects of Have greater Hypotension some psych affinity for Urianry retention or medications receptor sites in hesitancy CNS than those in PNS  Alzeimer’s Disease & Myasthenia Gravis: Classification Therapeutic MOA Adverse Effects Examples Use Indirect-Acting Slow memory loss Blocks Ach at the synaptic Related to stimulation Donepezil Cholinergic and cognitive cleft of PNS (Aricept) Agonists decline in early stages of Allows accumulation of GI effects Pyridostigmine Alzheimers Ach released from nerve CV effects (Mestinon, endings Urinary tract effects Regional) Myasthenia Cholinergic effects Gravis Leads to increased and prolonged stimulation of Ach Migraines: Classification Therapeutic Use MOA Adverse Effects Examples Ergot Vascular, cluster, Block alpha-adrenergic CNS effects Ergotamine Derivatives and migraine and serotonin receptor CC effects (Ergomar) headache pain sites in the brain GI effects relief Ergotism Sumatriptan (constriction of cranial (Imitrex) vessels, decrease in cranial artery pulsation, decrease in hyperperfusion) Triptans Bind to selective CNS effects GI Almotriptan, serotonin receptor sites effects CV effects eletriptan to cause vasoconstriction Almotriptan reported (Relpax) of cranial vessels to have fewer side effects than other triptans Calcitonin CGRP inhibitors: Inhibit Lasmiditan: Eptinezumab- Gene-Related CGRP, a potent dizziness, fatigue, jjmr (Vyepti) Peptide vasodilator chemical paresthesia, sedation (CGRP) released during migraine Lasmiditan Inhibitors & headache attacks CGRP inhibitors: (Reyvow) Serotonin risk of Agonist Serotonin agonist: Has hypersensitivity selective action on a reactions specific serotonin receptor Gepant substances: nausea Monoclonal antibodies: injection site reactions Seizures: Classification Therapeutic MOA Adverse Effects Examples Use Hydantoins Epilepsy Stabilize nerve membranes Severe liver toxicity, Phenytoin throughout CNS by bone marrow (Dilantin) decreasing excitability and suppression, gingival hyperexcitability to hyperplasia, Fosphenytoin stimulation potentially serious (Cerebyx, dermatological Sesquient) Reduce tonic–clonic, reactions, frank muscular, and emotional malignant lymphoma responses to stimulation Barbiturates Inhibit impulse conduction Most common relate Phenobarbital in ascending RAS to CNS depression (Solfoton, Luminal) Depress cerebral cortex Phenobarbital May be  Alter cerebellar function associated with physical dependence Depress motor nerve and withdrawal output syndrome Stabilize nerve membranes Linked to severe throughout the CNS dermatological directly and decrease reactions and excitability and development of drug hyperexcitability to tolerance stimulation Benzodiazepin Anxiety, Enhances GABA CNS depression Alprazolam es sedation (Xanax) May be associated Antiepileptic with physical dependence and withdrawal syndrome, especially with rapid reduction in dose Drugs that Cross use for Valproic acid: reduces All: CNS effects Valproic Acid modulate the seizure abnormal electrical activity (Depakote) inhibitory disorders or in the brain; may increase Valproic acid and neurotransmitt for bipolar GABA activity at divalproex: Carbamazepi er GABA disorders inhibitory receptors Liver toxicity ne (Tegretol) Hyperammonemia Divalproex: action thought Thrombocytopenia to be related to increased Pancreatitis GABA levels in brain Acetazolamide and Acetazolamide: alters zonisamide: electrolyte movement Rash Dermatological Zonisamide: inhibits changes voltage sensitive sodium and calcium channels Zonisamide:  Bone marrow suppression Renal calculi development GI upset Mechanism of action not Dizziness Levetiraceta completely understood; Weakness m (Keppra) may be related to Fatigue suppression of rapid action Agitation potentials Anxiety Depression Suicidal ideation (rare) Things She Mentioned In Class: Dilantin: Liver enzyme levels, formed blood components, BP, skin signs Status Epilepticus: critical situation, one seizure longer than 5 minutes or multiple in the span of 5 minutes; PHENOBARBITAL (SOLFOTON) first line drug!