Usmle 1 Neuromuscular Junction

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  1. Blocked
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    • At the synaptic terminal needs Ca influx for NT to be released into cleft


    • • If blocked = Neuropathy
    •  
    •     Ca channel blockers
    •       – Verapamil (Most potent; constipation)
    •       – Diltiazam (Good for atrial arrhythmia)
    •       – Nimodipine (Stops vasospasm after subarachnoid hemorrhage)
    •       – Nifedipine
    •       – Nicaradapine
    •       – Amalodopine
    •       – Fenlodipine
    •  
    •    • EDTA
    •     Penicillamine
    •     Gentamycin and aminoglycosides
    •     Botulinum toxin inhibits presynaptic release of ACH.
    •       – All block Ca presynaptically and cause neuropathy.
    •     Black widow spider venom causes increased release of ACH leading to tetany and death
  2. Enzymes
    • AChesterase Breaksdown ACh

    • • MAO
    •  
    •   – Presynaptic
    •   – Breaksdown Catecholamines

    • •COMT
    •  
    •   – Postsynaptic
    •   – Breaksdown
    •   – Catecholamines

    • • Reserpine
    •    
    •    – Impairs vesicles
    •    – Can’t store Norepi

    • • Guanethidine
    •  
    •    – Displaces Norepi out of the vesicle
    •    – MAO will break this down
    •    – SE: Retrograde Ejaculation
  3. MUSCLE CONTRACTION SEQUENCE
    • • Ca binds Troponin-C
    • • Troponin C releases Troponin-I (arrives 2 hrs. peaks 2 days, gone by 7 days)
    • • Troponin I releases Tropomyosin
    • • Tropomyosin uncovers Actin binding sites
    • • Myosin heads bind Actin
    • Contraction – No energy required
    • • Myosin heads release ADP (from previous cycle)
    • • Myosin heads bind new ATP
    • • Myosin heads hydrolyze ATP à ADP +Pi (releasing 7300 cal)
    • Release occurs → Requires ATP
    • • Myosin returns to start position
    • • Tropomyosin covers actin
    • • Troponin I covers tropomyosin
    • • Troponin C covers Troponin I
    • • Ca2+ -ATPase pumps Ca2+ into the SR
    • • Protein called phospholambin inhibits Ca-ATPase when its done
  4. Muscle and ATP
    • Get tight muscle contraction without ATP → Cramp = “Rub it out” → inflaming the skin will bring more blood = ↑ O2 = ↑ ATP → Relaxation

    • If don’t have ATP, muscle is stuck unreleased, in full contraction.

    •    – Swimming after a meal → drown b/c most of the energy is digesting food
    •         Can’t scream either!!!
    •    – Death → rigor mortis

    • Any Ca2+ left over in the cytoplasm (by Ca2+-ATPase) will be excreted by Na+/Ca2+ exchange.

    •    – Without Phospholambin, Ca2+-ATPase activity will increase and pump intracellular Ca2+ back into SR
    •    – Cytoplasmic Ca2+ will decrease → Muscle weakness
    •    – There won’t be enough Ca2+ to cause contraction → Will die of respiratory failure
  5. Diagnosis of a Myocardial Infarction (MI)
    EKG: Na-K pump stops > peaked T-wave > STwave depression > ST-wave elevation > T-wave depression, then inversion > Q-wave

    Troponin I: rises at 2 hours > peaks in 2days > positive up to 7 days

    CK-mb: rises in 6 hours > peaks in 12 hours > gone in 24 to 36 hours

    LDH 1: rises in 24 hours > peaks in 48hours > gone in 72 hours
  6. Management of an MI
    • • 24 hour hospitalization
    • • Check EKG Q6
    • • Check CIE’s Q6
    • • Monitor for arrythmias
    • • Discharge after 24 hours IF asymptomatic
    • • Re-evaluate in 6 weeks
  7. Management of an MI after 6 wks
    • Exercise stress test
    •    – Positive IF: chest pain is reproduced; ST-wave changes; drop in BP

    • Stress Thallium test
    •    – A perfusion test; looking for a COLD spot

    • Dobutamine or Dipyridamole stress test
    •    – Use when patient unable to exercise

    • Calcium Pyrophosphate scan
    •    – Taken up by DEAD tissue; looking for HOT spot

    • 2-D echo
    •    – Evaluates anatomy of heart; measures SV and CO
  8. Myocardial Infarction (Congestive Heart Failure after)
    • AT LEAST 40% of myocardium lost

    • EJECTION FRACTION is less than 45%

    • Due to left coronary artery infarcts 90% of time
  9. Congestive Heart Failure
    • Over 50% mortality in 5 years

    • Most common medicare diagnosis

    • Muscle fibers are overstretched

    • Dilated ventricle

    • Increased EDV and ESV

    • Decrea
  10. Smooth Muscle
    • Has No troponin

    •    – Actin and Myosin are always bound è Latching
    •       After you eat  → release Muscles and burn more ATP in the GI
    •    – Sounds created by latching called Boborygmi (gut sounds)

    • Has no ATPase activity

    •    – uses MLCK = myosin light chain kinase
    •    – And MLCP = myosin light chain phosphatase

    • Employs Basal bodies

    •    – They are more mobile
    •    – Moves Glucose from one place to another
  11. Skeletal Muscle (Fxn of the Sarcomere)
    • Sarcomere = from 1 Z line to the other Z line.
    • Distance will decrease during contraction
    • Light chain = actin
    • Heavy chain = myosin
    • A band = length of myosin
    • Contains both Myosin and actin
    • No change in length during contraction
    • I band =
    • Has only actin in it
    • No overlap à will shrink during muscle contraction
    • H band =
    • Has only myosin
    • No overlap à will shrink during muscle contraction
    • T-tubules of:
    • Cardiac muscle – is found in the z –line
    • Skeletal muscle – is found in AI junction
    • m-line:
    • Where you will find CK-MB
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  12. Actions of Sarcomere during contraction
    • Sarcomeres get smaller 

    • H & I bands get smaller (HI)

    • Distance b/w Z lines gets smaller

    • A band no change

    • Force and Tension ↑ as length ↓

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  13. Pre load
    • Pre load = tension on a muscle before work is done

    •    – As increase preload, you increase the time it takes for cross bridging.
    •    – Too much stress on a muscle will cause the tension to release
  14. Golgi Tendon Organ
    • Senses maximum overlap → max tension in muscle

    • It holds for 1 sec and GTO fires and releases tension

    • • Protects from destruction (Think about a weight lifter)
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  15. Recruitment of more motor units
    • 1 motor unit = 1 nerve and all the muscle fibers it innervates

    • – 1 nerve innervates several muscle fibers
    • – 1 muscle fiber is stimulated by only one nerve

    • Muscle cells hypertrophy by increasing the size of the cell to create more cross bridges to handle increased pre-load.

       – Preload = tension put on a muscle before any distance moved

    • ↑ Stress = ↑ Hypertrophy = ↑ Cross bridges

    • – Muscles will anticipate stress = Hypertrophy
    • – That’s why weight lifting gets easier with time as muscles hypertrophy due to increased pre-load.
  16. Frank - Sterling Curve
    • As EDV rises (heart dilates) get more CO up to a certain point until Heart stops completely è sudden death

    • – ↑ Amt. of Bloof flow = ↓ contractility = ↑ ability to hold more blood
    • – It’s the same principle as preload and muscle tension
    •     Once you reach a certain point the tension releases and lose contractility


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  17. Treatment for CHF
    • Increase contractility 

    •    – Diuretic
    •    – Digitalis
    •    – Dobutamine
    •    – Dopamine

    • Decrease volume

    •    – Restrict sodium intake
    •    – Restrict volume intake

    • • ACE inhibitors 
    •  
    •    – Vasodilatation and vasodilatation  = balanced dilatation and ↓ preload and afterload
  18. Myositis
    • • Myositis = one muscle hurts, caused by
    •  
    •   – Drugs:  “RIPS” Muscle
    •       Rifampin
    •      • INH
    •       Prednisone
    •       Statins 

    • Disease/Infection that can cause it

    •    – Hypothyroidism
    •    – Cushing’s
    •    – Trichinella spirallis
  19. Myopathies (All have)
    • • High ESR
    • • High WBC count
    • • Myoglobinemia
    • • High AST, ALT and Aldolase


    • – Myositis
    • – Polymyositis
    • – Dermatomyositis
    • – Fibrositis
    • – Fibromyalgia
    • – Polymyalgia rheumatica
  20. Polymyositis
    • Polymyositis = more than one muscle hurting

    •    – Elevated enzymes:
    •       – CK
    •       – LDH

    •    – Inflammatory cells found:
    •       – T-cell
    •       – macrophages
  21. Dermatomyositis
    • Dermatomyositis = myositis + rash

    •    – Heliotropic rash
    •       – violatious rash on eye lids
    •       – Look for Colon CA in the patient → must rule out INTERNAL MALIGNANCY
  22. Fibrositis
    • Fibrositis = inflammation in tendon insertions

       – pain only with movement
  23. Fibromyalgia
    • Fibromyalgia = tendon insertions and muscles hurt all the time

    • – multiple tender trigger points
    • – Amytriptyline is the treatment → because of ↑↑↑ incidence of depression
  24. Polymyalgia rheumatica
    • Polymyalgia rheumatica = when the shoulder girdle is the weakest

    •    – Pain in the shoulder girdle (actions of waving, combing hair)
    •    – Tender trigger pointsvery high incidence of Temporal Arteritis (Giant cell)temporal headache
    •    – very high ESR
    •    – Rule of 60’s
    •       age>60 years old
    •       ESR >60 sed rate
    •       Need more than 60mg of Prednisone to treat it.

    • Diagnose with temporal artery biopsy (MUST DO)

    • Complications – blindness due to involvement of ophthalmic artery.
  25. Duchene/Becker Muscular Dystrophie
    • X-linked recessive → Nonsense/frameshift mutation (trinucleotide repeat)

    • – Dystrophin gene
    • – Recall inheritance is that the maternal father and grandfather also had disease

    • Dystrophin protein

    • Gower sign – patient uses hands to walk up their own legs

    • They have pseudohypertrophy of the calf due to fat deposition = Cankle’s

        – Also seen in Gaucher’s

    • Waddling gait- due to transferring torso on the hips

    • Onset of Duchene before age 5

    • – Ex. 6 year old with Sx for 3 yrs.
    • – Frame shift, nonsense mutation

    • • Becker’s has symptoms. after age 5.
    •    
    •    – missense mutation → late onset
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  26. Myotonic Dystrophy
    • • Face looks like a birds beak
    •    – Facial muscles are worn

    • • Increased muscle tone
    •    – Can’t let go of hand when shaking it.
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  27. Guillian Barre
    • • Ascending paralysis (starts in feet)
    • • 2 wks after a URI → Viral prodrome
    • • Inflammation around peripheral nerves
    • • polyrediculoneuropathy – many dermatomes involved
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  28. Syphilis
    Many ripping, stabbing, lancenating neuropathy
  29. DM
    • • glove and stocking distribution
    •    – Always symmetrical and bilateral
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  30. Myasthenia Gravis
    Middle age female with ptosis (drooping of eye lids)

    • Gets weaker as the day goes by, strongest in the morning

    Anti ACH Antibodies is the problem

    • Associated with Thymoma (40%)

    •    – Do a CT scan of the neck
    •    – Removal of the thymoma will be curative
  31. Myasthenic Syndrome (Eaton Lambert)
    • • Associated with small cell CA (malignant)
    • • Gets stronger as the day goes by
    • • Ca2+ is slow in returning into the SR
    •    – muscle contractions become stronger
  32. Multiple Sclerosis
    • • Middle age woman with vision problem
    •  
    •     – Optic neuritis
    •         inflammation of the optic nerve
    •     – halo vision
    •        • can see things off to the periphery
    •        • can’t see things if looking right at them

    • • Internuclear opthalmoplegia
    •    
    •    – MLF = medial Longitudinal fasciculus is taken out
    •       connect CN III and CN VI
    •    – the connection between the two CNs is destroyed but each CN is functional

    • • Associated with Anti-myelin Antibody
    •  
    •           – Presents 2 wks after infection

    • • Diagnosis
    •    
    • – MRI can see demyelinated plaques → bilateral asymmetric distribution
    • – LP will show myelin baic protein in CSF
  33. Metachromatic Leukodystrophy
    • MS equivalent in a child

    • Arylsulfatase deficiency
  34. Cerebellar problems can present as three diseases: (Child 5-10 years old)
    • Ataxia – telangiectasia

    • – Telangiectasia all over skin
    • – lady with spider veins
    • Have IgA deficiencies
    •    • diarrhea, respiratory illness

    • Fredriechs Ataxia

    • – Retinitis pigmentosa (pigments on the retina)
    • – Scoliosis (5-10%)
    •  
    • • Adrenoleukodystropy

    • –  adrenal gland is knocked out
    •     electrolyte problems
    • – Long chain fatty acids accumulation in the mitochondria (transferred by carnitine)
    •     • Involvement of Cortex early on
    •        – spasticity
    •        – babinsky
  35. Lower Motor Neurons
    • Fasciculations = LMN deficit

    • – ALS
    •     Fasciculations in middle age male
    •     Descending paralysis
    •     No sensory involvement, all motor nerves

    • – Werdnig Hoffman
    •     Fasciculations in a newborn
    •     born with no anterior horns = no motor neurons
    •     will die of respiratory failure

    • – Polio
    •    • Occurs in children < 2 years old
    •    • anterovirus
    •    • Will present 2 weeks after diarrhea first
    •    • Develop into asymmetrical fasciculations and paralysis
  36. Cerebral Palsy
    • Permanent neurological damage suffered before age 21.

    • – Not just at birth
    • – Ex. 18yr old breaking back and get paralyzed

    • Spastic diplegia

    • – UMN
    •    • Cortex is involved
    •    • Legs are worse than arms
    •    • Midline cortical problem because legs are medial in the brain
    •       – Hydrocephalus can cause this

    • Spastic Hemiplegia

    • – Cortex involved → lesion on one side
    • – One side of the body is affected more than the other → Contralateral symptoms
    •    • Ex. herpes likes temporal lobe, toxoplasmosis loves parietal lobe

    • Choreoathetosis

    • – dance-like movements
    • – ringing of the hands and quivering voice
    • – Problem in the basal ganglia
    • – MCC =  kernicturus (bilirubin)

    • Atonic cerebral palsy

    • – no muscle tone
    • Frontal lobe tumor/stroke/AVM

    • Pancreatic CA

         – Trousseau Syndrome
  37. DIAGNOSIS
    • To differentiate the two:

    • – Do an EMG (electro myogram)
    •    • increased contraction will cause stronger amplitude of contraction

    • – Medication
    •    • MG is diagnosed using Endrophonium (ACH breakdown inhibitor, short acting)
    •       – MG patients stronger
    •       – Myasthenic Syndrome will get weaker.

    • – Treatment:
    •    • MG: 
    •       – Neostigmine, (#1 choice)
    •       – Pyridostigmine
    •       – Don’t like Physostigmine – because can cross BBB = CNS side effects.
    •       – SE = parasympathetic side effects.

    • To differentiate between worsening MG and cholinergic crisis need to do an Edrophonium test again:

    •    – if get stronger → MG got worse
    •       • need to increase neostigmine dose
    •    – if get weaker → cholinergic crisis
    •       • need to treat with atropine
    •       • Need to decrease neostigmine dose
  38. Pharmacology
    • Organophosphates

    •    – MOA:
    •         IRREVERSIBLE AChesterase inhibitors (non-competitive)

    •    – Examples:
    •        • Pesticides
    •          – “… phates
    •          – “…thions
    •    – Antidote:
    •        • Atropine
    •        • Scopolamine

    • Other notable anti – cholinergic drugs

    •    – Glyropyrolate and Atropine
    •         Dries up secretions before surgery
    •    – Benztropine
    •         Stimulates 2PAM → inhibits toxins
    •         Used for dystonia
    •    – Scopolamine
    •         Motion sickness

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Author:
docbrito
ID:
332744
Filename:
Usmle 1 Neuromuscular Junction
Updated:
2017-07-18 19:31:55
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Neuromuscular Junction
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Neuromuscular Junction
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