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31 Cards in this Set
- Front
- Back
Parkinson's disease
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anything that damages the substantia nigra
- idiopathic (aging, genetics, environment) - secondary parkinsonism (same symptoms but from other causes) - feature of other syndromes - dopamine deficiency due to damage to substantia nigra - lewy bodies (inclusion bodies) |
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Dopamine receptors
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D1 family (+) adenyl cyclase
D2 family (-) adenyl cyclase, SN neurons |
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Triad of Parkinsonism
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before seeing symptoms, loss 70% of dopamine
- TRAP (tremor, rigidity, akinesia, posture) - dementia - autonomic |
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Clinical presentation
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-Early complaints - aches pains numbness coldness
-Tremors - initially unilateral, occurs at rest, absent during sleep, not symmetrical -Postural changes - stooped -Dementia -Rigidity - cogwheeling catch/release -Bradykinesia - slow movement, unsteady gait, disease of inertia -autonomic disturbances-orthostatic HTN -other manifestations - drooling, constipation, speech diff |
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Why does handwriting sample get smaller and smaller?
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B/c of loss of dopamine, cant replenish it enough to continue functioning so writing gets smaller
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5 stages of parkinsons
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Stage 1. unilateral - aches and pain
Stage 2. bilateral, some tremor, normal posture Stage 3. bilateral, slightly abnormal posture, independent Stage 4. bilateral, posture instability, pt requires help (very little dopamine left) Stage 5. severe, fully developed, pt restricted to bed or chair (immobilized) |
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Dopamine Agonist
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directly stimulate dopamine receptors
D1 (+) adenyl cyclase D2 (-) adenyl cyclase monotherapy early, adj later AR: impulsive behaviors, sleep attks, naus, vom, orthostatic HTN |
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Carbidopa/Levodopa
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Carbidopa prevents peripheral LDopa metabolism by DOPA decarboxylase
LDopa - dopamine replacement stimulation of D1 and D2 receptors Standard Therapy, replaced dopamine-Ldopa (gold standard) AR: nas, vom, anorexia, orthostasis, psychotic sx at higher doses, dyskinesias w/ prolonged use |
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MAO Inhibitors
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MOA: only work in CNS to inhibit metabolism of L-dopa
Adj to L-dopa, rarely used for monotherapy, tends to be used later in disease as more dopamine required AR: dizziness, confusion, vivid dreams, nightmares, hallucination, dyskinesias |
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COMT inhibitors
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MOA: inhibit Ldopa metabolism in PNS by COMT so more Ldopa can enter the CNS
Adj to levodopa in later disease AR: nas, dry mouth, hypotension, dystonia, muscle cramps |
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Anticholinergic Agents
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MOA: restore cholinergic/dopamine balance by reducing levels of ACh
Early disease thearpy (tremor and sialorrhea) AE: peripheral anticholinergic effects (dry mouth, constipation), central effects at higher doses (paranoia, hallucinations), not well tolerated w/ age |
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Adaptation
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response to continued stress injury
- hypertrophy - hyperplasia - atrophy - metaplasia |
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Irreversible cell injury
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- necrosis by ATP depletion
- necrosis by free radicals |
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Hypoxia and ATP depletion
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- reversible injury by reintroduction of oxygen
- low oxygen, low ATP - Na, K pump stops --> cell swells, more permeable, Ca gets in and destroys mitochondria - anaerobic glycolysis increases --> lactic acid accumulation --> dec pH - ribosomes disassemble from rough ER --> dec protein synthesis --> lysosomal membrane breaks down, releasing digestive enzymes that digest the cell |
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Free radical generation
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- hydroxyl radical, hydrogen peroxide, superoxide
- free radical scavengers - vit E, SOD SOD: superoxide --> H2O2 --> H2O + O2 via catalase or H2O2 --> hydroxyl radical via fenton rxn |
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Tissue Changes in Response to Injury
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Acute Inflammation --> chronic infl, pain, organization
Chronic Inflammation |
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Acute Inflammation - Blood Vessels
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Injured vessel becomes inflammed through direct damage, chemical mediators, nervous system reflex
Dilated vessel - inflammation - congestion, redness, heat, swelling |
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Acute Inflammation - Arteries and Capillaries
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Swelling reaction (endothelial cells) - two types of fluid will leak from inflamed vessel
- transudate (plasma, water, protein) - exudate (plasma, water, protein, formed elements) - edema (fluid suck in tissue due to inflammation) - formed elements (inflammatory cells) - ability to actively move through endothelial cells and smooth muscle tissue to get into the CT |
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Triggers of Leakage
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- physical stress
- chemical mediators - histamine (produced by mast cells, when stimulated release histamine --> inflammation and swelling) binds to receptors on endothelial cells and makes them contract, opening spaces between them and stuff will leak out |
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Sympathomimetic nervous system
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- constricts smooth muscle
- pseudoephedrine - contracts smooth muscle so vessel constricts, less flow (adrenergic receptors of sympathomimetic) |
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Antihistamines
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H1 antagonist
- prevents endothelial shrinkage, prevents leakage - relaxes smooth muscle (bronchodilation) H2 antagonist - prevents vasodilation |
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Other mediators of acute inflammation
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Derived from membrane lipids by phospholipase to Arachidonic Acid
1. Lipoxygenase: AA --> leukotrienes (chemotaxis for immune cells, increased permeability) 2. COX: AA --> prostaglandins (vasodilators, pain) |
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Role of steroids
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- blocks cascade of infl mediator production at first step
- inhibits phospholipase from breaking down membrane lipids into arachidonic acid, needed to form other chemical mediators (leukotrienes, prostaglandins) - but also prevents wound healing |
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Role of NSAIDs and aspirin
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target COX needed to convert arachidonic acid to prostaglandins (vasodilators, pain)
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Acute inflammation can lead to Organization (via excess pus)
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- growth of new blood vessels in area
- invasion of macrophages - proliferation of connective tissue cells (collagen) --> scarring |
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Pus
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Abcess of exudates - cells (neutrophils and macrophages), collagen, new blood vessels
Acute inflammation - neutrophils actively kill bacteria via phagocytosis and cytotoxic substances (free radicals) - recruited by chemicals (chemotaxis) - monocytes recruited --> macrophage clean up |
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Scarring - organization following acute inflammation
- clean cut/suture |
clean cut/suture - heals via reformation of blood vessels, collagen, nice epithelium cover
- scab --> CT vascular --> nice epithelial layer --> less vascular CT to normal CT |
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Scarring - organization following acute inflammation
- jagged wound |
jagged wound - filled by connective tissue (granulation tissue), epithelium growing, uneven and not so nice
- CT over sides --> epithelium layer --> CT growing under and pushing up --> uneven healing |
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Ulceration
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surface necrosis and replacement by inflammatory tissue
- immune cells fill in crater initially for surface necrosis Surface necrosis --> crater (acute infl) --> crate (chronic infl) |
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Chronic Inflammation
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Involvement of Immune Cells (humoral response)
- lymphocytes, plasma cells (secrete antibodies), macrophages (no neutrophils) - chemotaxis - recruitment of other cells to areas of inflammation (neurophils, lymphocytes, monocytes) reinforcement of immune response at multiple levels - complement system |
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Complement System
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collection of proteins that work together in response to antigen-antibody complex and starts another effector pathway for inflammation
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