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31 Cards in this Set

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Parkinson's disease
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)
Dopamine receptors
D1 family (+) adenyl cyclase
D2 family (-) adenyl cyclase, SN neurons
Triad of Parkinsonism
before seeing symptoms, loss 70% of dopamine
- TRAP (tremor, rigidity, akinesia, posture)
- dementia
- autonomic
Clinical presentation
-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
Why does handwriting sample get smaller and smaller?
B/c of loss of dopamine, cant replenish it enough to continue functioning so writing gets smaller
5 stages of parkinsons
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)
Dopamine Agonist
directly stimulate dopamine receptors
D1 (+) adenyl cyclase
D2 (-) adenyl cyclase

monotherapy early, adj later

AR: impulsive behaviors, sleep attks, naus, vom, orthostatic HTN
Carbidopa/Levodopa
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
MAO Inhibitors
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
COMT inhibitors
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
Anticholinergic Agents
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
Adaptation
response to continued stress injury
- hypertrophy
- hyperplasia
- atrophy
- metaplasia
Irreversible cell injury
- necrosis by ATP depletion
- necrosis by free radicals
Hypoxia and ATP depletion
- 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
Free radical generation
- 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
Tissue Changes in Response to Injury
Acute Inflammation --> chronic infl, pain, organization

Chronic Inflammation
Acute Inflammation - Blood Vessels
Injured vessel becomes inflammed through direct damage, chemical mediators, nervous system reflex

Dilated vessel - inflammation
- congestion, redness, heat, swelling
Acute Inflammation - Arteries and Capillaries
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
Triggers of Leakage
- 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
Sympathomimetic nervous system
- constricts smooth muscle
- pseudoephedrine - contracts smooth muscle so vessel constricts, less flow (adrenergic receptors of sympathomimetic)
Antihistamines
H1 antagonist
- prevents endothelial shrinkage, prevents leakage
- relaxes smooth muscle (bronchodilation)

H2 antagonist
- prevents vasodilation
Other mediators of acute inflammation
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)
Role of steroids
- 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
Role of NSAIDs and aspirin
target COX needed to convert arachidonic acid to prostaglandins (vasodilators, pain)
Acute inflammation can lead to Organization (via excess pus)
- growth of new blood vessels in area
- invasion of macrophages
- proliferation of connective tissue cells (collagen)
--> scarring
Pus
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
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
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
Ulceration
surface necrosis and replacement by inflammatory tissue
- immune cells fill in crater initially for surface necrosis

Surface necrosis --> crater (acute infl) --> crate (chronic infl)
Chronic Inflammation
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
Complement System
collection of proteins that work together in response to antigen-antibody complex and starts another effector pathway for inflammation