W5 NeuroDis

Question 1

3 parts of the net spy system responsible for the perception of pain

Answer 1

1) peripheral- afferent and efferent

2) CNS- where the pain is interpreted brain stem midbrain diencephalon, the cortex

Question 2

Nociceptor pains

Answer 2

Special receptors diffused throughout the body

1) thermal TRPU1 TRPM8
2) mechanical TRPA1 external pressure laceration or puncture
3) chemical stimuli- higher threshold

Question 3

Acute pain pathway

Answer 3

1) peripheral nociceptor
-prostaglandin E 2/ I2, bradykinins will polarize
-substance P- neurotoxin a propagate pain
GABE endorphins enkephalins
Within an individual pain may vary

Question 4

Onset of pain

Answer 4

Endorphins and encephalitis interfere with pain signal.

Pain-tachycardia techipnia, diamanté’s pupils

Somatic pain- superficial pain, laceration
Visceral- injury of hollow organs, difficult to localize
Refered pain- shares spinal nerve segment area of the body. Shoulder pain with a splenic injury
Kehrs sign- irritation of phrenic nerve/diaphragm, lay supine, pain at top of the shoulder bc spine and phrenic nerve

Question 5

Neuropathy

Answer 5

Damage or injury to pain pathway
Mononeuropathy- one nerve or nerves bundle is injured. Damage to carpel tunnel nerve bundle. Most common mechanism of injury is overuse. Pain, sensory loss weakness
Failen sign (pray sign) helps to diagnose carpel tunnel.

Question 6

Mononeuritis multiplex

Answer 6

Simultaneous involvement of several non cont Usps nerve trunks, Acura subacute of nerves. Nerve bundles don’t join each other and aren’t in same pathway. Can accur in many body parts. De-symmetrical- asymmetrical
Achy pain that’s deep and worse at night
DM, HIV, jellyfish stings (poring laminators chemical serotonin)
Wagners gramulocitosis, inflammation of bloodcells, when Ancka is overactivated, neutrophils activates, inflammation of vascular endothelial
Conjunctivitis, damages gascularture that supply these vessel
Pathological processes of nerve stimulation

Question 7

Polyneurpathy

Answer 7

Result of damage to vasa-nervorum- arteries hat supply blood to peripheral nerves.
Sustained elevation in blood glucose levels.
DM is one of the most common. Involves a sustained elevation in blood glucose levels. Glucose residues binding to nerve proteins alter function. Activate enzymes involved in vasoconstriction, produces ROS in blood vessels in the nerve
Nerve cell death exceeds repair and neuropathy ensues. < sensation to feet and lower extremities.
Treatment is prevention through glucose control

Question 8

Fixed Dementia

CNS Disease

Answer 8

Loss of global cognitive ability
Can be static (TBI, stroke, wernikies encephalopay, ) or progressing AD)
Depression common early on, eventually completely abnormal feelings

Question 9

wernikies encephalopathy triad

Answer 9

Thiamine cannot he absorbed bc of alcohol disease
Thiamine cannot be replaced
Excitatory amines destroy the myelin
Ataxia
Stagnis (shaking of the eye)
Dementia- fabricate their short term memory bc they can’t remember.

Question 10

Alzheimer’s dementia

Answer 10

Generic causes are very rare. No diagnostic tests but psych test. H
Patho involves protein misfolding
Amyloid precursor proteins- transmembrane protein critical to neuronal growth and survival.
APP breaks down into beta amyloid and they accumulate into plaques. Apoptosis of neighboring healthy neurons
Tao proteins form tangled around nerves making it nonfunctional
Frontal cortex most affected along with cingulate gyrus

Question 11

Lewy Body Demetia

Answer 11

Alpha sinuclein clump 
Loss of neurons that produce Ach and Da
More acute onset. Parkinson’s-like
Fluctuating days
Reduplicative paraamnesia.
A place has been ducplicated.
Park11 connection?

Question 12

Creutzfeldt- Jakob Disease

Answer 12

Debated
Prions from viruses, protein misfolding
Amyloids insoluble fibrous inappropriately folded, create holes in Nervous tissues (spongy brain)
Ingestion of prions from contaminated meat
Dementia, hallucinations, ataxia

Question 13

Parkinson’s Disease

Answer 13

Substantia Nigra-produces Da
Parkinson’s is Da death
SNCA-gene, mutation create lewy body’s 
Limbo system degenerated 
Acts as inhibitory NT in motor circuit 
Change in balance of neurotory transmitter Da and excitatory NT Ach
Tremor, pillroll, bradykinesia, rigidity (cogwheel-stiff), orthostatic hypotension, loss of emotions, inappropriate emotions, 
Levopoda, Mao-inhibitors

Question 14

Huntington’s Disease

Answer 14

Gene mutation leads to three nucleotide protein. > 35 repeates HD ensues
Mutated HD protein will form more abnormal bonds to itself & other. Aggregates of proteins will be cleaved to form NIIs Neuronal Intranuclear Inclusions. Help dispurse large aggregates, inhibit function. Reach saturation point that prevents hormonal activity
Chaperone proteins help fold normal proteins, remove abnormally folded ones. HD interrupts. Also overexcited glutamate
CREB- antiaptotic. HD makes it unavailable.
Signs & symptoms: abnormal facial expressions, cognitive disfunction
Genetic diagnosis. Symptomatic treatment.
No cure

Question 15

Myasthenia Gravis

Answer 15

Autoimmune neuromuscular
Directed against Ach Nicotinic. Antibodies destroy these receptors & MUSC- muscle specific kinase. Enzyme that’s required for this Ach receptor
Signs: muscle fatigue that improves with rest, droopy eyes, depression to the point of respiratory failure. Tosis- dropping of the lids,
Diplopia-double vision Dyshpagia
Need Ach for activation of muscular contraction
Thymoma- tumor of thyroid gland.
Look for levels of antibodies