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231 Cards in this Set
- Front
- Back
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what is the central nervous system?
what ion hyperpolarizes it what cell are in it? |
>>brain/spinal cord
>>Cl- in hyperpolarizes >>Oligodendrocytes |
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what is the Peripheral nervous system?
what ion depolarizes it and what cells are in it? |
>>everything else
>>K + out depolarizes >>Schwann cells |
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what is the Autonomic nervous system?
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automatic stuff
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what is Somatic nervous system?
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moving your muscles
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Parasympathetic vs. Sympathetic: function
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Parasympathetic: Rest-and-Digest => slows stuff down
Sympathetic: Fight-or-Flight => speed stuff up |
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sympathetic vs. parasympathetic. 2nd Messenger:
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sympathetic: cAMP
parasympathetic: cGMP |
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sympathetic vs. parasympathetic:
Control Craniosacral / thoracolumbar |
parasympathetic: Craniosacral: brain + below the belt.
sympathetic: Thoracolumbar: above the belt |
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sympathetic vs. parasympathetic:
Preganglionic NT: preganglionic receptor: long/short fibers: exceptions |
sympathetic: ACh (nicotinic receptor): except sweat
Short fibers parasympathetic: ACh (nicotinic receptor) Long fibers |
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sympathetic vs. parasympathetic:
Postgangiolic NT: postganglionic receptor: long/short fibers; exceptions |
sympathetic: NE (α or βreceptor): except sweat
glands Long fibers parasympathetic: ACh (muscarinic receptor): except skeletal mm, ganglia Short fibers |
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parasympathetic: side effects
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"DUMBBELS":
Diarrhea Urination Miosis "constrict" Bradycardia Bronchoconstrict Erection ''point" Lacrimation Salivation |
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8 sympathetic effects:
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Opposite of Parasympathetics:
Constipation Urinary retention Mydriasis "eyes wide with fright" Tachycardia Bronchodilate Ejaculation "shoot" Xerophthalmia (dry eyes) Xerostomia (dry mouth) |
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what are the 4 Stimulatory NT that depolarizes?
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acetylcholine
5-HIAA MOA and COMT |
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acetylcholine
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AcetylCoA +Choline ⇨ (Choline Acetyltransferase) ⇨ ACh ⇨ (AChase) ⇨ Acetate + Choline
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5-HIAA
when is 5HT high? when is 5HT low? |
Trp ⇨ (Trp OHase) ⇨ 5-HT (High: sleepy, Low: depression) ⇨ 5-HIAA
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MOA and COMT
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Tyr ⇨ (Tyr OHase) ⇨ DOPA ⇨ DA ⇨ NE ⇨ MAO (pre-synaptic)+ COMT (post-synaptic)
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what are the Inhibitory NT of the Spinal cord and Brain
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Spinal cord: Gly
Brain: GABA |
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which of the Catecholamines is a NT? hormone?
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NE:NT
Epi: Hormone |
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what are the COMT Inhibitors?
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tolcapone
entacapone |
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what are the Seratonin Agonists?
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Cisapride
Methysergide Sumatriptan Elatriptan |
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Cisapride
class tx complications |
Seratonin Agonists.
tx GERD not used due to Torsade |
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Methysergide
class tx complications |
Seratonin Agonists.
tx headaches, die of MI, off market due to kidney filiariasis |
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Sumatriptan
class tx |
Seratonin Agonists. tx acute migraines
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what receptor gives you sympathetic response?
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adrenergic and nicotinic
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what receptor gives you parasympathetic response?
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muscarinic
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what is the effect of α1 receptors?
what 2 second messanger pathway does it use? |
vasocontriction
Ca2+, IP3/DAG pathway |
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what happens when an alpha agonist drug is applied to
Sphincters? Arteries? eyes? |
Sphincters => tighten
Arteries => vasoconstrict Eye radial muscles=> mydriasis w/o cyclopegia (freeze iris via radial muscles) |
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what are the 3 α1 Agonists drugs?
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"Promote Enlarged Pupils"
Phenylephrine Ephedrine Pseudoephedrine |
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Phenylephrine
class tx |
α1 Agonists. tx neurogenic shock
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Ephedrine
class uses |
α1 Agonists. OTC cold remedies
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Pseudoephedrine
class usage |
α1 Agonists.
Abused on street to make methamphetamine |
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what are the 4 α1 Blockers?
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"Decrease Prostate/ Tame Tension"
Doxazosin Prazosin Terazosin Tamsulosin |
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Doxazosin
class tx |
α1 Blockers. tx BPH/ HTN
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Prazosin
class tx SE (2) |
α1 Blockers.
tx HTN only priapism,1st dose syncope "Pass out" |
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Terazosin
class tx |
α1 Blockers
tx BPH/ HTN |
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Tamsulosin
class tx advantage |
α1 Blockers.
only works on bladder/ prostate less side effects |
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α2 receptors effects (3)
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Decrease NE release
>>Decrease sympathetics >>Pancreas β cells (⇩ insulin) |
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α2 Agonists:
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"Can greatly ameliorate HTN"
Clonidine Guanabenz α-Me-DOPA |
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Clonidine
class tx complication |
α2 Agonists
tx HTN rebound HTN if stopped quickly |
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Guanabenz
class tx |
α2 Agonists
tx HTN |
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α-Me-DOPA
class tx |
α2 Agonists:
tx HTN in pregnant women and hemolytic anemia |
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what are the α2 blockers
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"treat your impotence"
Tolazoline Yohimbine |
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Tolazoline
class tx |
α2 blockers, tx premie RDS
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Yohimbine
class tx |
α2 blockers , tx impotence
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what are used for α-ns blockers used for?
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used for Epi reversal
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what are the α-ns blockers?
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Phentolamine
Phenoxybenzamine |
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Phentolamine
class tx usage duration |
class: α-ns Blockers
usage: diagnose pheochromocytoma duration: short-acting tx: cocaine HTN |
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Phenoxybenzamine
class tx duration |
α-ns Blockers: (irreversible)
tx carcinoid and pheochromocytoma long-acting |
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β1 receptors effects to the ff. organs:
CNS SA node • JG • Pancreas α cells • Sympathetic |
"Revs up the heart" ⇧cAMP
CNS => ⇧ activity >>SA node =>⇧ HR and contractility >>JG => ⇧ renin => ⇧BP >>Pancreas α cells => glucagon realease >>Sympathetic=>vasoconstriction |
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what is the only β1 Agonist drug?
what is the effect on HR, contraction and BP? What is the Tx for? |
Dobutamine
(⇧HR/⇧contraction; no effect on BP) tx CHF |
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what are the β1 Blockers:
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" ABEAM"
Atenolol (long acting) Butexolol Esmolol Acebutolol Metoprolol |
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Butexolol
class tx |
β1 Blockers
tx glaucoma |
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Esmolol
class duration tx |
β1 Blockers: (short acting)
tx thyroid storm |
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Atenolol
class duration |
β1 Blockers: (long acting)
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β2 receptors: how does it affect these:
CNS Ventricle Lungs Pancreas β cells Uterus Bladder Parasympathetic |
"bronchodilate"
CNS: ⇧ activity Ventricle: ⇧contractility (not rate) Lungs: dilation Pancreas β cells: ⇧insulin Uterus: relax Bladder: relax Parasympathetic: vasodilation |
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β2 Agonists: what should be checked?
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hypokalemia ⇨ check serum K
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what are the β2 Agonists?
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"FARTS"
Formoterol Albuterol Ritodrine Terbutaline Salmeterol |
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Salmeterol:
class how often it is given |
β2 Agonists, use q12h
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Terbutaline:
class what is it used for? |
β2 Agonists
relax uterus and bronchodilator (inhaler, use q4h) |
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Formoterol
class usage |
β2 Agonists, use q12h
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Albuterol
class tx and usage |
β2 Agonists
tx asthma (inhaler, use q4h) |
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what are the βns agonist:
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"Manage Inflated Lungs"
(β2 > β1) • Metaproterenol • Isoproterenol • Levoproterenol |
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Metaproterenol
class usage |
βns agonist (β2 > β1), used as bronchodilator
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Isoproterenol
class tx |
βns agonist (β2 > β1)
tx heart block and bradycardia |
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βns Blockers:
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" TPN"
Timolol Propanolol Nadolol |
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Timolol:
class Tx |
βns Blockers, tx glaucoma
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Propanolol
class tx (2) CI |
βns Blockers:
tx tremor and panic attack don't give with asthma |
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Nadolol
class tx |
βns Blockers
tx glucomas |
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what are the 3 α and β direct agonist?
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epi
NE dopamine |
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Epinephrine
class effects on high and low dose tx |
α and β direct agonist:
α1/α2 (high dose) β1/β2 (low dose) tx bronchospasm and anaphylaxis=>⇧pulse pressure |
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NE:
class effects what receptors? complication |
α and β direct agonist:
α1/α2/ β1 NE does NOT do β2=> blue digits (powerful vasoconstrictor) |
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DA:
class effects on low dose, intermidiate and high doses what is high dose equivalent to? |
α and β direct agonist:
Low Dose: D2 ⇨ perfuse kidney Int. Dose: β1 ⇨ ⇧contractility High Dose: α1⇨ vasoconstrict, ⇧ afterload (high dose = 10 μg/kg/ min) |
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blue injection site
what was injected Tx: |
injected norepinephrine
tx. phentolamine |
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Anaphylaxis management
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Epinephrine Tx: for anaphylaxis:
1:1,000 (0.5mL q15min x 3doses ⇨ then 50mg Benadryl IV) |
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Cardiac Arrest management
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Epinephrine Tx for Cardiac Arrest: 1:10,000
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Direct Blockers (α1+β1)
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"double treatment of HTN"
Labetalol Carvedilol |
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Labetalol
class tx |
Direct Blockers (α1+ β1)
tx A Fib, most α properties |
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Carvedilol
class tx (2) |
Direct Blockers (alpha1 + beta1 receptors)
tx HTN crisis and chronic CHF |
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Cholinergic Receptors: effects
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Only anti-cholinergic, nonsympathetic effect = hot, dry skin
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Muscarinic receptor effects?
name the 4 muscarinic drugs? |
>>think parasmpathetic
"Can Promote Bladder movement" Carbachol Pilocarpine Bethanechol Methacholine |
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Carbachol:
class tx |
>>Muscarinic Agonists:
>>tx post-op urinary retention |
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Pilocarpine:
class usage |
>>Muscarinic Agonists:
>>CF sweat test |
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Bethanechol:
class tx |
>>Muscarinic Agonists:
tx post-op urinary retention |
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Methacholine:
usage class |
>>formerly used to diagnose reversible airway disease (asthma)
>>Muscarinic Agonists: |
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Indirect Muscarinic Agonists:
what do they inhibit name all |
inhibit AcetylCholinesterase:
Parathion Physostigmine Neostigmine Pyridostigmine Edrophonium |
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Parathion
class usage antidote |
(indirect muscarinic agonist)
organophosphate, irreversible "nerve gas" (Tx: Pralidoxime "2-PAM") |
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Neostigmine
class tx |
(Indirect Muscarinic Agonist)
tx myasthenia gravis |
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Pyridostigmine
class tx |
(Indirect Muscarinic Agonists)
tx myasthenia gravis |
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Edrophonium
class usage |
(Indirect Muscarinic Agonists)
diagnose myasthenia gravis |
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Muscarinic Blockers:
effects and name all |
>>think sympathetic actions
>>"Do Block Gmp; Almost Totaly Imitating Sympathetics" Dicyclomine Benztropine Glycopyrrolate Atropine Trihexyphenidyl lpratropium Scopolamine |
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Dicyclomine:
class tx |
Muscarinic Blockers
tx IBD sx (blocks Ach) |
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Benztropine:
class Tx |
muscarinic blocker:
tx dystonia/ torticollis |
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Glycopyrrolate:
class Tx |
muscarinic blocker
⇩pre-op pulmonary secretions |
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Atropine:
class Tx |
muscarinic blocker:
tx heart block and cholinergic crisis |
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Trihexyphenidyl:
class MOA Tx |
muscarinic blocker:
blocks cGMP tx Parkinson's tremor |
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lpratropium:
class MOA Tx |
muscarinic blocker that ⇩cGMP
tx asthma |
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Scopolamine:
class tx |
muscarinic blocker:
tx: motion sickness (patch) |
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Nicotinic receptors effects
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think sympathetic
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the only Nicotinic receptor Agonist:
what is it used for? |
Varenicline- used for smoking cessation
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name all 4 Nicotinic Blockers:
|
"Have Near Sympathetic Tendencies"
Hexamethonium Nicotine Succinylcholine Tubocurarine |
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Nicotine:
class MOA |
Nicotinic blocker
stimulates ganglia, then blocks (persistent depolarization) |
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Succinylcholine:
class effects tx |
Nicotinic Blockers:
flaccid paralysis (the only depolarzing agent) tx malignant hyperthermia |
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Tubocurarine:
SE |
Nicotinic Blockers:
histamine release (flushing, hypotension) |
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Malignant Hyperthermia
tx how does it work? complication |
Tx: Dantrolene ⇨inhibits Ca release ⇨ MetHb/Cyanosis
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Malignant Hyperthermia: Tx for MetHb/Cyanosis
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Methylene blue
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Malignant Hyperthermia: next surgery what anesthetic to be used
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use NO as anesthetic
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what ions is use by all muscles to depolarize? except
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Muscle Physiology:
All muscles use Na+ to depolarize (except the atrium: Ca2+) • |
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what ions are use to contract?
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All muscles contract b/c of intracellular Ca2+
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what ions are use to contract the ventricle and SM
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Ventricles/SM depend on extracellular Ca2+ to trigger contraction
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what is a motor unit?
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Each neuron ⇨ multiple muscle fibers (1 motor unit)
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how many nerves innervate a muscle?
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Each muscle ⇦ 1 nerve (only want 1 action)
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describe the Skeletal Muscle
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Skeletal Muscle:
• Has motor units, uses recruitment (increase preload on muscle ⇨ increase recruitment) • Electrochemically coupled=> dependant on nerve for life and fxn • T-tubule invaginations: depolarize ⇨ DHP ⇨ ranodine stimulation ⇨ SR Ca2+ release • Use intracellular calcium for contraction |
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what is Rhabdomyolysis? Tx
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⇧serum K+, Urine: 3+ blood/0 RBCs (b/c Mb is detected as Hb)
>>Tx: Bicarbonate (alkalinize urine to prevent precipitation |
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describe the features of the Cardiac Muscle:
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Cardiac Muscle:
• Uses intracellular calcium for contraction • Uses extracellular calcium to trigger intracellular release • Acts as a syncsitium => holds onto contraction until everyone contracts (need gap jxns) • Has autonomies => don't need your permission to beat • "Wall motion abnormalities": part of heart has died, and those cells won't contract |
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decribe the feature of the Smooth Muscle:
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• Needs extracellular Ca2+ via Calmodulin for 2nd messenger system
• Uses intracellular Ca for contraction • Has autonomies • Acts as a partial syncitium, has autonomies (Ex: gut peristalsis) • No sarcomeres =>why it is smooth • No troponin = > actin and myosin are always bound= "latching"=> bowel sounds • No ATPase activity • Has MLC kinase to phosphorylate; MLC phosphorylase to chop off |
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what are the 3 things responsible for Neuromuscular Transmission:
|
Soma - makes and transports all proteins, NT
kinesin - anterograde transport Dynein - retrograde transport |
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what are the type of peripheral Nerve Injuries
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>Neuropraxia: no axon injury (temporary loss of function)
>Axonotmesis: loss of axon (grows 1mm/day) >Neurotmesis: loss of entire nerve |
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Black widow:
describe the spider MOA of venom presentation Tx |
red hourglass
Ach release abd/ back/ thorax pain (Tx: Ca gluconate) |
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Brown recluse:
describe how it looks like what does it release presentation of bite Tx |
>>violin-shaped band, Ca release, tissue necrosis
>>(Tx: Dapsone) |
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Don't Swim 30min After Meal, why?
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All blood in gut and Skeletal mm. ran out of ATP
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why is massage good for the muscle?
|
Massage:
• Induces skin inflammation • Brings O₂/ATP to muscles |
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Sequence of Events for Muscle Contraction
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>Depolarize
>Extracellular Ca2+ flows into T-tubule >Ca2+ binds Troponin-C=>Troponin C releases Troponin T >Troponin T releases Tropomyosin >Tropomyosin releases Actin binding sites >Myosin head binds Actin >CONTRACTION: no ATP used (Ex: rigor mortis) >Myosin heads release ADP (from previous cycle) >Myosin heads bind new ATP >Myosin heads hydrolyze ATP => ADP +Pi (releasing 7300 cal) >RELEASE |
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continuation of Sequence of Events for Muscle Contraction
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>Myosin head returns to start position
>Tropomyosin binds Actin >Troponin T binds Tropomyosin >Troponin C binds Troponin T >Ca-ATPase pumps Ca into the SR >Phospholambin inhibits Ca-ATPase when it's done |
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Subendocardial Infarct: how it happens and mangement
I |
Subendocardial Infarct:
Ischemia blocks Na/K pump ⇨ K+ leaks out ⇨ cell becomes negatively charged ⇨ ST depression (70% stenosis) ⇨ subendocardial damage Tx: Dilate to ⇧ blood flow) |
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Transmural Infarct: how it happens and management
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Na + rushes in ⇨ cell becomes positively charged ⇨ ST elevation (90% stenosis) ⇨ more likely to
depolarize ⇨ transmural infarct (Tx-: Thrombolytics) |
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Ventricular Fibrillation: how it happens
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Ventricular Fibrillation:
Na + drives all Ca2+ into cells ⇨ extracellular Ca2+ ⇨ no p waves ⇨ SA node stops ⇨ vessels dilate, bladder and gut stop ⇨ ventricle can't contract but can depolarize ⇨ V Fib |
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how does ischemia lead to dead heart cells?
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Ischemia (decreased blood flow) ⇨ Injury (hurt cells) ⇨ Infarct (dead cells)
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what EKG wave would you see on a ischemia?
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1)T wave peak
2) ST depression inversion |
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what EKG wave would you see on a injury (hurt cells)
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3) ST elevation
4) T wave |
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what EKG wave would you see on a infarct dead cells?
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5) Q waves
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what is the order of the cardiac enzymes?
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Cardiac enzymes: (rise ⇨ peak ⇨ last)
"TICAL" troponin I, CPK-MB, AST |
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what happens during a myocardial Infarction
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decreased O₂ ⇨ myocardial cell death
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signs and symptoms of an MI
|
• Chest pressure or pain radiating to left arm, shoulder, jaw
• Epigastric pain radiating to back, scapula • Sweating • Sense of "impending doom" |
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what does nausea mean when there is an inferior MI
|
Nausea => inferior MI
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what should we look out for in patients with DM and MI?
|
Silent MI => DM
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What are the CAD risk factors
|
CAD Risk Factors:
• Age (>45 male, >55 female) • Fam Hx (Dad <55, Mom <65) • Obese • Smoker • HTN • DM • Dyslipidemia |
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Post-MI Complications: name all 5
|
Post-MI Complications:
1. 2nd MI 2. Arrhythmias (most common cause of death) 3. IV/ pulmonary rupture 4. Aneurysm, heart failure 5. Dressler syndrome: Pericarditis 2-10wk post-MI => neck and pleuritic chest pain |
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treatment for dressler syndrome
|
(Tx: Steroids, NSAIDs)
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most common cause of death in post MI.
|
Arrhythmias (most common cause of death)
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Angina Workup:
|
Angina Workup:
Hospitalize for 24-hr observation Serial EKGs and cardiac enzymes Follow-up in 6 weeks |
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Angina Workup: what test should be done after 6 weeks?
|
Follow-up in 6 weeks
Ca-Pyrophosphate scan: Treadmill stress test: Thallium stress test: Dobutamine stress test: 2-D Echo: |
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Ca-Pyrophosphate scan:
|
hot spot shows dead calcified cells
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Treadmill stress test:
|
positive stress test if pain, change inEKG, or ⇩BP
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Thallium stress test:
|
cold spot shows ischemia
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Dobutamine stress test
|
use dipyridamole to dilate vessel during test
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2-D Echo
|
evaluates anatomy of heart
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what are the 3 Platelet ADP Receptor Blockers:
describe each |
Platelet ADP Receptor Blockers:
Dipyridamole - also dilates vessels Ticlopidine - agranulocytosis, seizures Clopidogrel- decreases clotting in high risk patients |
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Dipyridamole
class function |
Platelet ADP Receptor Blockers: also dilates vessels
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Ticlopidine
class SE |
Platelet ADP Receptor Blockers: agranulocytosis, seizures
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Clopidogrel
class function |
Platelet ADP Receptor Blockers: decreases clotting in high risk patients
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Sarcomere
location what happens to it during contraction? |
between Z lines, decreases during contraction
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Light chain
|
actin
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Heavy chain
|
myosin
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A band
define length change |
length of myosin (will include some actin), no change length
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I band
define what happens during contraction |
actin only, decreases during contraction
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H band
describe what happens during contraction |
myosin only, decreases during contraction
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where are the t-tubles located in the cardiac and skeletal muscle?
|
T-tubules:
o Cardiac muscle: Z line o Skeletal muscle: A-I junction |
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Z-line
|
actin only
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M-line
describe what is another thing located in here? |
myosin only, CPK located here
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Length-tension curve:
max over lap what are touching |
max overlap in sarcomere = 2.2 μm (I bands are touching)
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Dx: distal weakness+ Fasciculations
|
Neurogenic muscular diseases
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Dx: proximal weakness + pain
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Myopathic muscular disease
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how do we read the length tension curve during contraction?
|
Read from right to contract
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what is preload
|
Preload = tension on a muscle before work = > increased time to cross bridge
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how does a muscle hyperthropies
|
⇧ number of cross bridges to handle increased preload
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function of the golgi tendon
|
Muscle will hold max weight for 1 sec => Golgi tendon lets go
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Isotonic muscles: how does it tone muscles?
|
low weight, burns ATP when you release
"tones muscles" |
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Isometric muscles: how does it build muscles?
|
build muscles => compresses arteries =>⇧ TPR => HTN
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how can a rise of EDV cause sudden Death:
|
Sudden Death: EDV rises => increase CO => heart stops
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neuromuscular diseases most common cause of death?
|
respiratory failure (heart has autonomics)
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myositis definition and labs
|
>> one muscle hurts
>>⇧ESR, ⇧WBC, ⇧ AST, ⇧ALT, ⇧ Aldolase, Myoglobinemia |
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Drug-induced myositis
|
Rifampin, INH, Prednisone, Statins "RIPS"
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Bug-induced myositis
|
Trichinella spiralis
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Endocrine disease myositis
|
Hypothyroidism, Cushing's
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Anti-Phospholipid Ab Syndrome:
presentation what are its 3 types |
recurrent thrombosis, abortions
Type 1: False(+) syphilis Type 2: Lupus anticoagulant (⇧aPTT) Type 3: Anti-cardiolipin Ab |
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define Polymyositis:
Elevated enzymes (2) 2 Inflammatory cells involved EMG how is it Diagnosed? what can this lead to? |
>1 muscle weak (hard to walk stairs, kneel)
>Elevated enzymes: CK, LDH >Inflammatory cells: T-cell, MP > low EMG >Dx: Muscle biopsy=> inflammation |
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Dermatomyositis: clues, signs, symptoms and Tx
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>myositis + rash
>Dysphagia of solids/liquids >Heliotrope rash: purple periorbital edema >Gottron's sign: scaly purple patches on MCP / PIP joints Tx: Steroids or Methotrexate |
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Fibrositis
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pain w/ muscle movement
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what is Fibromuscular Dysplasia?
presentation test |
renal artery stenosis, child diastolic HTN
• cv bruit • Angiogram "string of beads" |
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Fibromyalgia
describe what should be ruled out? tx |
Def: 11 tender trigger points + axial skeletal pain, sleep disturbance, hurt all the time
Rule out hypothyroidism Tx: Amitriptyline+ Water aerobics |
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fibromyalgia: what needs to be ruled out? and Tx
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Rule out hypothyroidism
Tx: Amitriptyline+ Water aerobics |
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Polymyalgia Rheumatica: define and Tx:
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stiff, weak shoulders, pelvic girdle pain (can't comb hair/wave)
tx: Prednisone (only disease where low-dose predisone improves sx < 1 wk) |
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Temporal Arteritis:
Define and presentation criteria tx |
"Giant cell arteritis": unilateral HA, blindess, thoracic aortic aneurysm
o Age >60 o ESR >60 o Tx: Prednisone: 60mg now, then temporal artery biopsy (if sx) |
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Becker's: who gets it?
mutation symptoms |
(XL) males get it, females carry it
• Dystrophin missense mutation • Symptoms > 5 y/o, normal lifespan |
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Duchenne's (XL): pathology and lab
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dystrophin frameshift mutation => truncated protein, increase CPK
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Duchenne's (XL):
pressentation (3) life expentancy tx |
Pseudohyper trophy of calf (fat deposition)
Gower sign - pt walks up legs to stand up Waddling gait- due to transferring torso on hips, toe stepping Die by age 30 Tx: Prednisone |
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Myotonic Dystrophy (AD): presentation and mode of inheritance
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: bird's beak face, ⇧muscle tone => can't let go of hand
• Triple repeat |
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describe Guillain-Barre
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ascending paralysis "Ground-to-Butt"
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Guillain-Barre:
onset Ab pathogenesis presentation tx |
2 wks after URI or C. jejunii infection
• Anti-ganglioside Ab • No reflexes • MP eat myelin off nerve axons ⇨ ⇧CSF protein, segmental demyelination, ⇩conduction velocity • Polyradiculopathy- many dermatomes involved • Same presentation as tick bites, resolves spontaneously like MS • Tx: Intubate if needed, IV Ig/Plasmapheresis |
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what is Transverse Myelitis:
onset/pathogenesis Dx |
>>Guillain-Barre symptoms + back pain
>>URI ⇨rapid myelopathy, urine retention, back pain >>post viral • Dx: MRI |
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describe Diabetic neuropathy
what is this due to? |
sorbitol
glove & stocking neuopathy. |
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3° Syphilis:
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Tabes dorsalis, Argyll-Roberston pupil, shooting/lancinating pain
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Charcot-Marie-Tooth
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fat muscle atrophy, stocking glove neuropathy, high arch foot
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Myasthenia Gravis:
Ab define and clues as presentation associations management |
post-synaptic Achr Ab => can't make an end-plate potential
• Middle aged female with ptosis, diplopia • Gets weaker as day goes by • Associated with thymomas -=> get CT chest |
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Myasthenia Gravis,
what 2 test should be ordered to diagnose MG? how do we test for cholinergic crisis vs MG is getting worse |
1)Repetitive stimulation EMG ⇨ weaker
2) Edrophonium "Tensilon": inhibits Achase ⇨ stronger Cholinergic crisis vs MG is getting worse: Repeat Edrophonium "Tensilon" test after tx If get weaker ⇨ cholinergic crisis If get stronger ⇨ MG is worse |
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Myasthenia Gravis Tx (3)
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Tx:
• Anti -cholinesterases: Neostigmine, Pyridostigmine • Immnnosuppression: prednisone • Thymectomy |
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Myasthenic Syndrome define
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"Lambert-Eaton": pre-synaptic Ca2+ channel Ab => ⇩Ach release
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Myasthenic Syndrome:
presentation associated cancer |
>>Muscle contraction gets stronger as the day goes by
>>Associate with small cell CA |
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Myasthenic Syndrome: test and treatment
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Test: Repetitive stimulation EMG => stronger
• Tx: Immunosuppression |
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Multiple Sclerosis:
ab presentation (3) LP: management |
anti-myelin Ab, symptoms come and go
o MLF lesion (connects CN 3 and CN 6) o Bilateral trigeminal neuralgia • LP: myelin basic proteins, MRI (q3 mo): plaques |
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Multiple Sclerosis:
presentation (2) good prognosis |
Middle aged woman with vision problems
• Optic neuritis =>halo vision (can't see directly) • Optic neuritis presentation => good prognosis • Internuclear ophthalmoplegia: opposite eye won't go past midline |
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Multiple Sclerosis:
what is Internuclear ophthalmoplegia? what other problem she might have? |
opposite eye won't go past midlline
>>MLF lesion (connects CN 3 and CN 6) Bilateral trigeminal neuralgia |
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Multiple Sclerosis:
what is seen on an LP? management |
LP: myelin basic proteins, MRI (q3 mo): plaques
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Multiple Sclerosis: Acute Tx and chronic Tx
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Acute Tx: Methylprednisolone IV
Chronic Tx: INF β (can cause suicidal ideation), Glatiramer acetate |
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metachromic leukodystrophy
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arylsulfatase deficinecy, MS in childhood
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Amyotrophic Lateral Sclerosis (ALS) = Lou Gehrig disease
presentation and Tx |
>>Descending paralysis, fasciculations in middle aged male
>>Only motor nerves are affected >>CS tract and ventral horn • Tx: Riluzole ( ⇩pre-synaptic Glu) |
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polio
presentation onset |
asymetric fasciculattions as a child
2 weeks after gastroenteritis |
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Werdnig-Hoffman
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fasciculations in a newborn, no anterior horns=> no motor neurons
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name 3 Lower Motor Neuron Diseases
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Amyotrophic Lateral Sclerosis
polio Werdnig-Hoffman |
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Cerebellar Disease:
presentation (3) name 3 diseases |
affects depth perception, has intention tremor, dysdiodokinesis
Adrenal Leukodystropy (XLR) Ataxia-Telangiectasia Friedreich's Ataxia |
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Adrenal Leukodystropy (XLR)
pathogenesis presentation (4) life expentancy |
> Long chain fatty acids are not transferred via carnitine shuttle, stuck in mitochondria
>Adrenal failure >Rapid central demyelination >Hyperpigmentation >Seizures death by age 12 |
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Ataxia-Telangiectasia
presentation pathogenesis |
>>spider veins, IgA deficiency
>>DNA endonuclease defect >>Sx: ataxia, telangiectasias of skin/ conjunctiva, recurrent sinus infxn, thymus hypoplasia |
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Friedreich's Ataxia
presentation associated with what syndrome mode of inheritance |
>>retinitis pigmentosa (brown pigment on retina), scoliosis
>> Spinal cord atrophy- affects gracilis and cuneatus (ipsilateral) >>Sick sinus syndrome >>Triple repeat, |
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Cerebral Palsies
pathogenesis give 4 examples |
permanent neuro damage <21y/o
Atonic cerebral palsy Choreoathetosis: Spastic Diplegia Spastic Hemiplegia |
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Atonic cerebral palsy
describe common causes |
>>no muscle tone=> floppy
>>Cause: frontal lobe tumor, stroke, AVM, anoxia |
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Choreoathetosis:
describe etiology example diseases |
dance-like movements, wringing of the hands, quivering voice
• Cause: kernicterus (bilirubin accumulating) => damage to basal ganglia • Ex: Wilson's: Cu deposition • Ex: Huntington's: caudate atrophy |
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Spastic Diplegia
pathogenesis presentation etiology |
midline cortical problem
leg problems CMV infection |
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Spastic Hemiplegia
pathogenesis etiology |
cortical problem on one side of the brain, herpes/toxoplasmosis infection
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Restless Leg Syndrome
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⇩Fe⇨⇩blood flow to legs ⇨ irresistible urge to move legs
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Clonazepam Tx for what diesease
SE |
Restless Leg Syndrome
SE: sleepiness |
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Pramipexole Tx for what disease
MOA |
Restless Leg Syndrome tx
DA agonist (contracts muscles to increase blood flow to legs) |
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Ropinirole "Requip":
class |
DA agonist
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Succinylcholine
MOA usage SE |
muscle relaxant: depolarizing blocker
use for intubation=> hyperkalemia |
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Tubocurarine
MOA usage releases what? |
non-depolarizing
(rvs w / Edrophonium,Neostigmine) => histamine release |
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Atracurium:
MOA who should use it? where does it degrade/ |
muscle relaxant, NM blocker, degrades in plasma
=> OK for kidney, liver failure pts |
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X-linked Recessive Deficiencies:
who had it? |
maternal uncle or grandpa had it
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X-linked Recessive Deficiencies: name all
|
''Lesch-nyhan went Hunting For Pirates and Gold Cookies"
LeschNyhan Hunter's Fabry's PDH def G-6PD def. CGU |
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LeschNyhan
deficiency presentation |
HGPRT def.- self mutilation, gout, neuropathy
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Hunter's
enzyme deficiency |
iduronidase def.
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Fabry's
enzyme deficiency presentation |
(α-galactosidase def.)
corneal clouding, attacks baby's kidneys |
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G-6PD def.
presentation |
get infxns, hemolytic anemia
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CGD
what it stands for? enzyme deficiency? |
chronic granulomatous disease
(NADPH oxidase clef.) |
