Exocytosis/Endocytosis Flashcards
Botulism
Defect: Inhibits SNARE/exocytosis
Mode of Inheritance: Acquired from Clostridium botulinum toxin (foodborne, wound, infants eating off floor)
Mechanism: Cleaves synaptobrevin (V SNARE) of vesicles carrying ACh (stimulatory NT) ! unable to interact with syntaxin!inhibits exocytosis/release of NT at NMJ
Characteristics: Paralysis of respiratory and skeletal muscles (potentially fatal) because stimulatory NT is not released to elicit muscle contraction ! flaccid paralysis; “floppy baby syndrome” – hypotonia, hyporeflexia
Key Words: flaccid paralysis, synaptobrevin cleaved, ACh-stimulatory
Tetanus
Defect: Inhibits SNARE/exocytosis
Mode of Inheritance: Acquired from Clostridium tetani (wound contamination) Mechanism: Cleaves synaptobrevin of vesicles carrying GABA & glycine (inhibitory NTs)! unable to interact with syntaxin!inhibits exocytosis/release of NT
Characteristics: Prolonged contraction of skeletal muscles (potentially fatal)!violent spastic paralysis; 1st sign – trismus (lock jaw), neck stiffness, dysphagia, pectoral & calf muscle rigity, muscle rigity & spasms; spatula test
Key Words: spastic paralysis, synaptobrevin cleaved, GABA&glycine-inhibitory, trismus, spatula test
Familial Hypercholesterolemia
Defect: Endocytosis
Mode of Inheritance: Autosomal dominant
Mechanism: LDL-R does not cluster in the membrane so endocytosis is not effective - CLASS IV
Characteristics: increased plasma cholesterol levels; increased LDL synthesis; major risk factor for CHD, premature atherosclerosis, Xanthomata, corneal arcus, Xanthelasmata Key Words: LDL-R, CHD (CAD), plasma cholesterol, Xanthomata, Xanthelasmata
