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Where are the muscarinic Ach receptors and what makes them different from Nicotinic?
- Sympathethic post synaptic (post ganglia) of sweat glands and some blood vessels
- Parasympathetic post ganglion/synamptic Heart smooth muscle and glands
- Muscarinic are G-protein linked while nicotinic are ion channels
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What are the ligands of nicotinic Ach receptors?
Usually quarternary ammonium compounds (CATIONS)
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Describe the nicotinic receptor action of muscle.
- Heteropentameric ligand gated ion channel with 2 alpha subunits which both must be bound. All or none 70% must be blocked and 90% for full paralysis
- Most receptors in muscles of respiration then for coarse movement
- Least occurs in the facial expression and eyes
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What are the problems with curare?
- Blocks ganglia (no BP control)
- Affects muscarinic ( no parasymp to heart-> tachycardia)
- Releases histamine (bronchoconstriction & hypotension)
- 30 minute long duration
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What are the major features of nondepolarizing neuromuscular blockers?
- Competitive antagonist (70% for effect, 90% for full)
- Vercuronium
- Rocuronium- most popular
- Cistacurium- Hoffman elimination (good for medically compromised)
- Onium = aminosteriod
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Explain how the depolarizing neuromuscular blocker works.
- Succinylcholine
- Rapidly stimulates and leaves Na channel inactive to prevent repolarization and is not broken down by Achesterase (plasma cholinesterase must break down)
- Phase 1 block for short 5 minute duration (except with plasma cholinesterase defficincies)
- Could lead to bradycardia and Hyperkalemia and malignant hyperthermia
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Why can succinylcholine lead to malignant hyperthermia?
Variation in RYANODINE receptor in the sarcoplasmic reticulum can result in uncontrolled Ca2+ rls and a hypermetabolic response when triggered by succinylcholine and some volatile inhaled anesthetics like sevofluorane
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Therapeutic uses of NMBs?
Surgery, intubation, tetnus (non), join, bone maniupulation, electroconvulsant (dep) and laryngospasm (dep)
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Describe other agents that affect NMJ.
- GABA (valium, lioresal)
- Alpha 2 agonist (zanaflex)
- Tricyclic (flexeril)
- Ach rls blocker (botox)
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Bulla
- Raised lesion > .5 cm wit water, no pus
- Sometimes autoimmune
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Comedne
- Plug of sebaceous and dead skin in opening of hair follicle
- Open=blackhead
- Closed = whitehead
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Fomite
Inanimate disease carrying object
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What is the most common skin cancer dentists observe?
Basal cell carcinoma
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Macule
- Change in skin color
- Flat not palpated
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Papule and nodule
- Elevated small, no depth
- Nodule= papule w depth/elevation
- Pustule = pus-filled papule
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Vesicles
Fluid-filled lesions less than .5 cm (sun blisters)
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Urticaria/Hives
- Blood plasma leaks
- Allergic degranulation of mast cells
- Wheals=circumscribed rounded, slightly elevated lesions of hives
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What are the different types of muscle fibers?
- Type I: slow, mitochondria/lipid rich (acid)
- Type II: fast, glycogen (alkaline)
- What types of stains used to observe mitochondria in muscles?
- OXIDATIVE found in inner mitochondrial membrane
- 1. NADH (more mit, darker)
- 2. SDH (complex II)
- 3. COX2
- Gmori will have purple spots if ragged red
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What types of stains are used to discover neuropathic muscle problems?
- HYDROLYTIC
- 1. NSE non-specific esterase: shows NMJ, dark = not well innervated
- 2. Alkaline phosphatase: regenerated, dermatomyositis (dark perimyosium
- 3. Acid phosphatase: lysosomal activity: macrophages
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What are the exceptions for not biopsying muscle tissue?
- Genetic tests available: dystrophinopathies,
- Myasthenia gravis:Abs blocking Ach receptors and NMJ
- Endocrine myopathies
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When do you want to do a biopsy of muscle tissue?
- Neuromuscular disease: myopathy, neuropathic
- Ststemic disorders: dermatomyositis
- Repeat or treatment related
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Neurogenic process
- Fiber size variation
- ANGULAR atrophy
- Nuclear clumps
- Loss of mosaic pattern
- Eg diabetes, ALS, spinal muscular atrophy
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Myopathic
- Random myofiber size
- ROUND atrophy
- Nuclear/cytoplasmic changes: regeneration/degeneration (bluer and mononucleated)
- Inflammatory cells: myositis
- Eg. Dystrophy
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What are the dental manifestations of muscular dystrophy?
- Facial, head, neck muscles
- Teeth don’t meet
- Problems with TMJ checwing, headaches tenderness
- OH problems
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Dermatomyositis
- Non-infective inflammatory myopathy CD4 & MAC expression
- Rash, periorbital edema, proximal muscle weakness
- High serum creatine kinase
- PERIFASICULAR ATROPHY: (black) regenerated myofibers along edge of fascicle
- Often seen w alkaline phosphatase rxn
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