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105 Cards in this Set
- Front
- Back
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THE BAND OF SKIN INNERVATED BY THE SENSORY ROOT OF A SINGLE SPINAL NERVE
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DERMATOME
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USEFULNESS OF DERMATOMES
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AID IN LOCALIZING LESIONS
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WHAT ARE NEURONS?
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INDIVIDUAL CELLS BUNDLED INSIDE PERINEURIUM TO MAKE A NERVE
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WHERE DO NERVES GET THERE BLOOD SUPPLY?
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FROM VASO NERVORUM
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THESE ARE VERY SMALL BLOOD VESSELS THAT BECOME THE TARGET OF MANY SYSTEMIC ILLNESSES SUCH AS DIABETES
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VASO NERVORUM
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COMPARE NERVES TO WIRES.
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THEY TRANSMIT ELECTRICAL IMPULSES, HOWEVER UNLIKE WIRES THEY ALSO HAVE ION CHANNELS AND ION PUMPS THAT ALSO CREATE A MEMBRANE POTENTIAL
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DESCRIBE RESTING ACTION POTENTIAL OF A NERVE.
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NA IS OUTSIDE CELL; K INSIDE CELL; GATED CHANNELS PREVENT MOVEMENT; MEMBRANE POTENTIAL AT -70 MV
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DESCRIBE DEPOLARIZATION.
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INFLUX OF NA INTO CELL; MEMBRANE POTENTIAL BECOMES +30 MV
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WHAT ARE THE EFFECTS OF LIDOCAINE AND MARCAINE ON DEPOLARIZATION?
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THEY ARE NA CHANNEL BLOCKERS; BLOCK INFLUX OF NA INTO CELLS (TRANSIENT)
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WHAT HAPPENS DURING REPOLARIZATION?
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K CHANNELS OPEN (TRIGGERED BY MEMBRANE POTENTIAL); K MOVES OUT OF THE CELL
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WHAT IS HYPERPOLARIZATION?
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MEMBRANE POTENTIAL SWEEPS BELOW -70 MV; PREVENTS REPEATED STIMULI UNTIL RESTING MEMBRANE POTENTIAL IS RESTORED AS NA CHANNELS CLOSE
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WHEN CELLS DIE, WHAT HAPPENS TO THE MEMBRANE POTENTIAL?
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CELL LOOSES ITS ABILITY TO MAINTAIN THE MEMBRANE POTENTIAL
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WHAT IS SELF PROPOGATION?
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ONCE AN ELECTRICAL IMPULSE BEGINS, IT IS SELF SUSTAINED UNTIL IT REACHES THE NERVE TERMINAL
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WHAT DOES MYELIN SHEATH DO TO THE SPEED OF TRANSMISSION AND ENERGY REQUIREMENT?
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INCREASE SPEED OF TRANSMISSION AND DECREASES ENERGY REQUIREMENT
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WHAT DO ALL DEMYELINATING CONDITIONS CAUSE?
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SLOW NEURAL TRANSMISSION
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WHERE ARE THE NA CHANNELS IN MYELINATED NERVES?
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ONLY AT THE NODES OF RANVIER INSTEAD OF THROUGHOUT
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BECAUSE OF THE NODES OF RANVIER, HOW DOES THE MEMBRANE POTENTIAL MOVE DOWN AN MYELINATED AXON?
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MORE OR LESS LEAP FROGS FROM ONE NODE TO THE NEXT ALL THE WAY DOWN
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IN DEMYELINATING CONDITIONS, WILL IMPULSES STILL PROPAGATE DOWN THE AXON?
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THEY CAN BE SLOWED OR STOPPED INITIALLY, BUT MAY LATER CARRY INFORMATION ONLY SLOWER
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WHAT CELLS MYELINATE AXONS IN THE CNS?
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OLIGODENDROCYTES
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WHAT CELLS MYELINATE AXONS IN THE PNS?
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SCHWANN CELLS
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EXPLAIN HOW NERVE DIAMETER AFFECTS CONDUCTION.
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THE BIGGER THE NERVE, THE FASTER THE CONDUCTION
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EXPLAIN WHAT HAPPENS AT THE SYNAPSE.
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NERVE IMPULSE ARRIVES CAUSING AN INFLUX OF CALCIUM; CALCIUM CAUSES RELEASE OF NT; NT DIFFUSE ACROSS THE SYNAPSE; NT BIND TO MEMBRANE PROTEIN CAUSES VOLTAGE ON POSTSYNAPTIC MEMBRANE; THEN NT IS BROKEN DOWN TO END STIMULATION
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WHAT IS SUMMATION?
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WHEN MULTIPLE STIMULI ARE ADDED TOGETHER TO PRODUCE AN ACTION POTENTIAL
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NEUROTRANSMITTERS THAT ARE EXCITATORY DO WHAT?
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PRODUCE AN ACTION POTENTIAL
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NEUROTRANSMITTERS THAT ARE INHIBITORY SO WHAT?
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TURN OFF THE NEXT NEURON
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WHAT IS THE RESULT OF SUB THRESHOLD STIMULI?
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SMALL ACTION POTENTIALS
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IF THE TRIGGER REGION REACHES _______ MV, AN IMPULSE OCCURS.
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-55
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HOW DOES EMG (ELECTROMYOGRAPHY) TEST NERVE FUNCTION/WEAKNESS?
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RECORDS INTRINSIC ELECTRICAL ACTIVITY WITHIN A MUSCLE; TESTS HOW WELL A MUSCLE CONTRACTS WHEN STIMULATED BY ELECTRICITY
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HOW DOES NCV (NERVE CONDUCTION) TEST NERVE FUNCTION?
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NERVE IS STIMULATED AT ONE POINT AND RESPONSE IS RECORDED; USED IN THE EVALUATION OF NEUROMUSCULAR DISORDER, PERIPHERAL NEUROPATHY, OR ENTRAPMENT
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A GENERIC TERM FOR NERVE DISORDERS OF ANY TYPE
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PERIPHERAL NEUROPATHY
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REFERS TO A DISEASE AFFECTING ONE NERVE
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MONONEUROPATHY
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REFERS TO A DISEASE AFFECTING MANY NERVES
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POLYNEUROPATHY
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EXAMPLES OF POLYNEUROPATHIES
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METABOLIC DISORDERS (ETOH AND B12 DEF.); INFECTIOUS (LEPROSY, POLIO); INFLAMMATORY (MS, GUILLAIN-BARRE, DIABETIC PERIPHERAL NEUROPATHY)
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TYPE OF METABOLIC DISORDERS THAT ARE POLYNEUROPATHIES
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B12 DEFICIENCY, ALCOHOL
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TYPE OF INFECTIOUS CONDITIONS THAT ARE POLYNEUROPATHIES
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LEPROSY, POLIO
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TYPE OF INFLAMMATORY CONDITIONS THAT ARE POLYNEUROPATHIES
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MS, GUILLAIN-BARRE, DIABETIC PERIPHERAL NEUROPATHY
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WHAT IS THE MOA OF ISOLATED PERIPHERAL NEUROPATHIES (MONONEUROPATHY)?
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COMPRESSION TYPICALLY AFFECTS VASCULAR SUPPLY- START WITH TINGLING; SENSORY NEURONS ARE AFFECTED BEFORE MOTOR
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WHAT IS BELL'S PALSY?
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COMPRESSION OF CN VII (FACIAL) AS IT TRAVELS THROUGH THE BONY CANAL OF THE SKULL
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WHAT IS THE RESULT OF BELL'S PALSY?
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UNILATERAL FACIAL WEAKNESS
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WHAT IS THE RESULT OF COMPRESSION OF THE RADIAL NERVE (C5-C8)?
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COMPRESSED AS IT SPIRALS AROUND HUMERUS- DUE TO COMPRESSION, INJURY, OR FRACTURE OF THE ARM; RESULT IS WRIST DROP
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WHAT IS WRIST DROP?
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RESULT OF COMPRESSION OF RADIAL NERVE- UNABLE TO EXTEND ELBOW AND WRIST, NUMBNESS OF THE BACK OF THE HAND AND WRIST; LOSS OF TRICEPS REFLEX
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SATURDAY NIGHT PALSY
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DRUNK PEOPLE- COMPRESSION OF RADIAL NERVE WHEN FALL ASLEEP WITH THE BACK OF ARMS COMPRESSED BY BAR
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WHAT IS THE RESULT OF MEDIAN NERVE COMPRESSION (C6-T1)?
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IMPAIRED WRIST AND FINGER FLEXION AND RADIAL DEVIATION OF THE HAND; ATROPHY OF THENAR EMINENCE; LOSS OF SENSATION OVER PALMAR ASPECT OF INDEX AND MIDDLE FINGERS
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HOW DOES MEDIAL NERVE COMPRESSION PRESENT?
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AS CARPAL TUNNEL SYNDROME
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WHAT IS THE RESULT OF ULNAR (C8-T1) NERVE COMPRESSION?
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CAN'T PERFORM ULNAR DEVIATION OF THE HAND, LOSS OF SENSATION OVER PINKY FINGER
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WHERE DOES THE ULNAR NERVE BECOME COMPRESSED?
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AT THE GROOVE B/W OLECRANON PROCESS AND MEDIAL HUMERAL EPICONDYLE
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TYPE OF NEUROPATHY (POLY OR MONO USUALLY ASSOCIATED WITH SYSTEMIC AND METABOLIC DISORDERS?
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POLYNEUROPATHY
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HOW DOES B12 DEFICIENCY USUALLY PRESENT?
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DISTAL, SYMMETRIC SENSORIMOTOR POLYNEUROPATHY; ALSO INVOLVES DESTRUCTION OF SPINAL CORD
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MOST COMMON WORLDWIDE CAUSE OF TREATABLE NEUROPATHY THAT IS AN INFECTION OF THE PERIPHERAL SENSORY NEURONS
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LEPROSY
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EARLY SIGNS OF LEPROSY
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DISCOLORED OR LIGHT PATCHES OF SKIN WITH LOSS OF FEELING;
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WHEN NERVE TRUNKS IN ARMS ARE AFFECTED IN LEPROSY, WHAT HAPENS?
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PART OF THE HAND BECOMES NUMB AND SMALL MUSCLES BECOME PARALYZED, LEADING TO CURLING OF THE FINGERS AND THUMB
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WHAT HAPPENS WHEN LEPROSY ATTACKS NERVES IN LEGS?
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IT INTERRUPTS COMMUNICATION OF SENSATION IN THE FEET; FEET ERODE THROUGH UNTENDED WOUNDS AND INFECTION
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IF THE FACIAL NERVE IS AFFECTED IN LEPROSY, WHAT HAPPENS?
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LOSE BLINKING REFLEX, DRYNESS, ULCERATION, AND BLINDNESS; BACILLI ENTERING MUCOUS LINING OF NOSE CAUSE NOSE COLLAPSE
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AKA ACUTE INFLAMMATORY POLYRADICULONEUROPATHY
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GUILLAIN-BARRE SYNDROME
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THIS POLYNEUROPATHY MAY FOLLOW AN ILLNESS OR VACCINATION
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GUILLAIN-BARRE SYNDROME
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GUILLAIN-BARRE HAS AN ASSOCIATION WITH PREVIOUS INFECTION OF THIS
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CAMPYLOBACTER JEJUNI ENTERITIS
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MAIN COMPLAINT IN GUILLAIN-BARRE
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VARIABLE WEAKNESS USUALLY IN LEGSM AND ASCENDS; NO PAIN B/C IT AFFECTS MOTOR NEURONS, NOT SENSORY
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WHY IS GUILLIAN-BARRE POTENTIALLY FATAL?
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IT MAY PROGRESS TO MUSCLES OF RESPIRATION
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AUTONOMIC DYSFUNCTIONS PRESENT IN GUILLIAN-BARRE?
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TACHYCARDIA, ARRHYTHMIAS, SWEATING, LABILE BP
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EVALUATION OF GUILLAIN-BARRE
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CSF- WILL HAVE HIGH PROTEIN, NORMAL CELL COUNT; NCV- SLOWING OF MOTOR AND SENSORY CONDUCTION (DEMYELINATION PATTERN)
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TREATMENT FOR GUILLAIN-BARRE
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ADMIT TO ICU; INTUBATION (OFTEN DONE IN ANTICIPATION); IV IMMUNOGLOBULIN (TARGETS MYELIN DESTROYING IGG); PLASMAPHERESIS; STEROIDS NOT HELPFUL
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PROGNOSIS FOR GUILLIAN-BARRE
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REVERSIBLE; SELF-LIMITING; FULL RECOVERY W/IN FEW MTHS TO YEAR; MINOR FINDINGS MAY PERSIST LIKE AREFLEXIA; DEATH RATE 2-3%
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AREFLEXIA
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ABSENCE OF NEUROLOGIC REFLEXES LIKE KNEE JERK REACTION
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THIS IS NERVE DEATH RELATED TO LONG-STANDING HYPERGLYCEMIA
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DIABETIC PERIPHERAL NEUROPATHY
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POPULATION THAT DIABETIC PERIPHERAL NEUROPATHY IS MOST OFTEN SEEN IN
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NONCOMPLIANT PATIENTS
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DIABETIC PERIPHERAL NEUROPATHY IS ________ IN NATURE.
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ISCHEMIC
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WHAT NERVES ARE MOST AFFECTED BY DIABETIC PER. NEUROPATHY?
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PRIMARILY SENSORY AND AUTONOMIC
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AGE RANGES FOR DIABETIC PERIPHERAL NEUROPATHY
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TYPE I- 20S TO 40S; TYPE II- GREATER THAN 50 YEARS
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SENSORY NEUROPATHY IN DIAB. PERI. NEUROPATHY MOST OFTEN ASSOCIATED WITH WHAT SYMPTOM
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TERRIBLE PAIN
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MOTOR NEUROPATHY IN DIAB. PERI. NEURO INVOLVES WHAT SYMPTOMS
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WEAKNESS OF MUSCLES
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MOTOR NEUROPATHY OF DPN MANIFESTS IN WHAT MUSCLES
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THOSE THAT ARE INNERVATED BY THE FEMORAL AND OBTURATOR NERVES- ILIOPSOAS, QUAD. FEMORIS, AND ADDUCTOR MAGNUS---CAUSES IPSILATERAL LOSS OF KNEE JERK
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TX FOR DIABETIC NEUROPATHY
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TIGHT GLYCEMIC CONTROL; ANALGESICS; NARCOTICS; CAPSAICIN CREAM; AMITRIPTYLINE (ANTIDEPRESSANT); CARBAMAZEPINE (ANTICONVULSANT); GABAPENTIN (ANTICONVULSIVE); DULOXETINE (ANALGESIC PROPERTIES- ANTIDEPRESSANT); TRAMADOL (OPIATE LIKE RECEPTOR AGONIST)
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RISK OF TRAMADOL USE
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ABUSED; ALSO LOWERS THE SEIZURE THRESHOLD SIGNIFICANTLY
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PREVENTIVE MEASURES FOR DIABETIC NEUROPATHY
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PROPER FOOT CARE, FOOT WEAR, CHECK FEET DAILY, ANNUAL FOOT EXAM W/ MONOFILAMENT TESTING, ANNUAL DILATED EYE EXAM
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WHAT SPORE CAUSES TETANUS?
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CLOSTRIDIUM TETANI
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MOA OF CLOSTRIDIUM TETANI IN CAUSING TETANUS
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TOXIN EXPOSURE F/ CONTAMINATE WOUND; TOXIN IS TRANSPORTED THROUGH MOTOR NERVES/BLOOD STREAM; TOXIN BINDS IRREVERSIBLY TO RECEPTORS IN THE BRAIN AND SPINAL COLUMN, BLOCKS RELEASE OF GABA (INHIBITORY NT) SO THERE ARE UNCHECKED EXCITATORY IMPULSES
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WHAT DO THE UNCHECKED EXCITATORY IMPULSES IN TETANUS CAUSE?
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INCREASED MUSCLE TONE, SPASMS, AND RIGIDITY- LOCK JAW
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ASSOCIATE LOCK JAW WITH WHAT
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TETANUS
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TX FOR TETANUS
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HYPERIMMUNE GLOBULIN (HYPERTET); HOSPITALIZE AS FATALITY RATE IS 60%
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SYNDROME ASSOCIATED WITH INGESTION OF TOXIN DERIVED FROM THE SPORE FORMING CLOSTRIDIUM BOTULINUM FOUND IN HONEY AND GREEN BEANS
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BOTULISM
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HOW DOES BOTULISM WORK?
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BY PREVENTING RELEASE OF ACETYLCHOLINE AT THE NMJ AND AUTONOMIC SYNAPSES
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RESLUT OF BOTULISM TOXIN
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SHUTS DOWN COMMUNICATION B/W NERVOUS SYSTEM AND THE MUSCLE, WEAKNESS OCCURS
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WHERE IS WEAKNESS SEEN FIRST WITH BOTULISM?
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IN THE MOST COMMONLY USED MUSCLES WHEN SYSTEMICALLY INGESTED
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HOW IS BOTULISM USED THERAPEUTICALLY?
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BY ADMINISTERING IT INTO DESIRED MUSCLE AND CAUSING PARALYSIS
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ACHALSIA
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ESOPHAGEAL ADMINISTRATION OF BOTULISM
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WEAKNESS IN BOTULISM BEGINS IN WHAT TIME FRAME
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12 TO 72 HOURS AFTER INGESTION
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SYMPTOMS OF BOTULISM
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DIPLOPIA, PTOSIS, FACIAL WEAKNESS, DYSPAGHIA, NASAL SPEECH; RESP. DIFFICULTIES LATER; WEAKNESS IN LIMBS LAST
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THE __________ ARE PRESERVED IN BOTULISM.
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DEEP TENDON REFLEXES B/C THERE IS NO SENSORY INVOLVEMENT
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TX FOR BOTULISM
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SEVERE CASES WITH RESPIRATORY INVOLVEMENT, ELDERLY, AND KIDS---HOSPITALIZATION AND TRIVALENT ANTITOXIN (FROM HORSE SERUM0; GUANIDINE HYDROCHLORIDE TO FACILITATE RELEASE OF ACH
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FUNDAMENTAL DEFECT IN MYASTHENIA GRAVIS
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NMJ WEAKNESS- DECREASES ACH RECEPTORS AT THE POSTSYNAPTIC MUSCLE MEMBRANE
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HOW ARE THE ACH RECEPTORS DESTROYED IN MYASTHENIA GRAVIS?
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BY IGG MEDIATED PROCESS
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SYMPTOMS IN MYASTHENIA GRAVIS
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FLUCTUATING WEAKNESS- VOLUNTARY MUSCLES FATIGUE EASILY; EOM'S AFFECTED FIRST W/ DIPLOPIA AND PTOSIS; GENERALIZED WEAKNESS WORSE TOWARDS END OF DAY
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EXAM OF MYASTHENIA GRAVIS WILL SHOW WHAT
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ASYMMETRIC OCULAR PALSY AND PTOSIS; CANNOT SUSTAIN UPWARD GAZE OR BLINKING; VARIABLE PARESIS; NORMAL SENSATION AND REFLEX; MUSCLE ATROPHY LATE
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LABS FOR MYASTHENIA GRAVIS
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ANT-ACHR IN 85%; VIRTUALLY DIAGNOSTIC ALTHOUGH NEGATIVE DOESN'T RULE OUT DISEASE
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WHAT HAPENS IN NERVE STIMULATION TESTS IN MYASTHENIA GRAVIS?
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RAPID REDUCTION IN THE AMPLITUDE OF EVOKED RESPONSES
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CT SCAN ON MYASTHENIA GRAVIS
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MAY REVEAL THYMOMA
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THYMOMA
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tumor originating from the epithelial cells of the thymus
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TEST TO VERIFY DIAGNOSIS OF MYASTHENIA GRAVIS
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EDROPHONIUM 2 MG IV- CALLED TENSILON TEST- TRANSIENTLY IMPROVES WEAKNESS BY INHIBITING ACH BREAKDOWN AT THE NMJ
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TX FOR MYASTHENIA GRAVIS
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ANTICHOLINESTERASE DRUGS- PYRIDOSTIGMINE FOR SYMPTOMS; THYMECTOMY FOR THOSE LESS THAN 60S; STEROIDS- FOR FLARES; PLASMAPHERESIS IF RESPIRATORY INVOLVEMENT
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HOW DO NERVE AGENTS WORK?
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INHIBIT ACETYLCHOLINE ESTERASE SO ACH IS NOT DESTROYED- CONTINUED OVERSTIMULATION OF ORGANS
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NERVE AGENT PRETREATMENT
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PYRIDOSTIGMINE BROMIDE- HIDES OR PROTECTS A FRACTION OF ACHE- INCREASES THE AMT OF NERVE GAS A PERSON CAN BE EXPOSED TO AND SURVIVE
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WHAT IS PRALIDOXINE
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IRREVERSIBLY BINDS TO NERVE AGENT AND PREVENTS ACETYLCHOLINESTERASE FROM DEGRADATION
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PRALIDOXINE AKA
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2 PAM CHLORIDE OR MARK I AUTO INJECTOR
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MOST COMMON DIABETIC AUTONOMIC NEUROPATHY
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SWEATING DISTURBANCE
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VASOMOTOR DISTURBANCE OF THE LIMBS, OH, SWEATING DISTURBANCE, EXERCISE INTOLERANCE, DIZZINESS, HYPOGLYCEMIA UNAWARENESS, GASTROPARESIS, AND BLADDER DYSFUNCTION- WHAT ARE THESE?
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AUTONOMIC NEUROPATHIES THAT ARE DIABETIC IN NATURE
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