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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