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Neurophys
| Question | Answer |
|---|---|
| The most common signs of ANS impairment are ... | a drop in blood pressure when a person is standing or stands up suddenly (orthostatic hypotension) or a drop in blood pressure within one hour of eating a meal (postprandial hypotension). |
| Catecholamine (NE/EPI) disorders | Synthesis – (Biosynthetic pathway) Packaging (Vesicular monoamine transporter Type 2 – VMAT2) Clearance – NE transporter |
| Tetrahydrobiopterin Deficiency | enzymes defects. required for catecholomines synth->neurotransm deficiency Symptoms begin 2-8 months of age;unstable body temp, swallowing difficulties, hypersalivation, pinpoint pupils, ptosis of the eyelids, decreased mobility, drowsiness, and irritabi |
| Aromatic L- Amino Acid Decarboxylase (AAAD) Deficiency: | catalyzes the decarboxylation of aromatic amino acids, dopa to dopamine, tryptophan to tryptamine, hydroxytryptophan to serotonin. |
| Aromatic L- Amino Acid Decarboxylase (AAAD) Deficiency: | Symptoms;thermoregulatory diffic, drooping eyelids, hypersalivation, distal chorea,dysphagia,drowsiness, irritability, truncal hypotonia, pinpoint pupils |
| Dopamine-β-Hydroxalase (DBH) Deficiency – | caused by absence of DBH, the enzyme involved in the conversion of dopamine to norepinephrine. congenital, nonhereditary form of severe orthostatic hypotension |
| Dopamine-β-Hydroxalase (DBH) Deficiency – | sympathetic noradrenergic denervation and adrenomedullary failure, but intact vagal and sympathetic cholinergic function. |
| Dopamine-β-Hydroxalase (DBH) Deficiency – | In the upright position, systolic blood pressure always falls below 80 mm Hg, However, opposite of other forms of autonomic failure, the compensatory rise in heart rate is completely preserved. |
| Pheochromocytoma | tumor (up to 3.5 kg, usually benign) made up of chromaffin tissue of the adrenal medulla or sympathetic paraganglia. |
| Pheochromocytoma | increased secretion of epinephrine and norepinephrine, is persistent or intermittent hypertension. |
| Effects of hyperkalemia on resting membrane potential and action potentials | Reduction in electrical potential Brings nerve or heart muscle closer to depolarization threshold value and initiates the action potential |
| Effects of hyperkalemia on resting membrane potential and action potentials | Nerve conduction and muscle contraction are more easily initiated. Clinical sequelae include parethesias and weakness and eventually paralysis |
| Multiple sclerosis disease | multiple regions of demyelination and inflammation along axonal pathways monocular blindness, motor weakness paralysis, abnormal somatic sensations, double vision, dizziness |
| Genetic diseases: “channelopathies | Altered ion channel proteins Some skeletal muscle diseases, channel defects in heart, inner ear, kidney, and familial hemiplegic migraine |
| Four causes of acquired hearing loss | Acoustical trauma Infection of inner ear Ototoxic drugs Prebyacusis |
| parkinson's disease | hypokinetic |
| huntington's disease | hyperkinetic |
| cerebellar lesions | same side quite specific lack of coordination of ongoing movements difficulty in performing rapid alternating movements;inability to perform smooth, directed movements Tremors: action or intention |
| Amyotropic lateral sclerosis ALS Lou Gehrig’s disease | Loss of alpha motor neuronsProgressive weakness and wasting of skeletal muscles, usually death within 5 years No effective therapy |
| Amyotropic lateral sclerosis ALS Lou Gehrig’s disease | Gene mutation: encodes cytosolic antioxidant enzyme copper/zinc superoxide dismutase (SOD1) cause defect in slow and fast axonal transport. Mutation dynactin which bins microtubles |
| Lower motor neuron syndrome | Paralysis/ loss in movement Paresis/weakness Areflexia/ loss motor limb of sensory motor reflex arcs |
| Lower motor neuron syndrome | Loss in tone/ interrupt monosynaptic reflex arc in muscle spindle Muscle atrophy due to de-nervation and disuse/ exhibit fibrillations and fasciculation/ spontaneous twitches |
Created by:
lovisa2014
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