Lecture 22 - drugs for urinogenital disease Flashcards
Erectile dysfunction
inability to achieve or maintain erection sufficient for satisfactory penetration or sexual satisfaction
physiology of erection
parasympathetic - to get erection; release NO which causes vasodilation (blood flow into blood cavities in penis)
sympathetic - losing erection; vasoconstriction
physiology of erection
arousal -> activation of PSNS -> blood enters CC/CS -> following organism, ps nerves inhibited and sympathetic nerves activated
NO
not in vesicles, synthesised on demand. calcium dep, as ca goes up, NO produced
PDE5 inhibitors
enhance cyclic GMP - enhance relaxation - keep the erection
local treatments of EF
direct vasodilators or drugs inhibiting SNS (sympatholytics) directly in penis - can cause priapism (erection that won’t go away, treatment is to drain penis of blood)
urinary incontinence
involuntary loss of urine
stress incontinence - in absence of detrusor muscle contraction
urge incont. - due to detrusor muscle overactivity e.g. UTI
female bladder control
PSNS - contracts detrusor muscle, when you gotta pee
SNS - maintained bladder integrity, relaxes detrusor muscle
what does the opening of calcium channels lead to at the nitrergic neuroeffector junction
calcium entry and thus the entry of Nitric oxide synthase enzyme. Calcium activates the NOS enzyme which converts L-arginine into NO and citrulline
PDE5
destroys cyclic gmp
What is benign prostatic hyperplasia?
Enlargement of the prostate that occurs in the periurethral and transitional zones of the gland. It causes bladder outflow obstruction and reduced urine flow or conversely urge incontinence. you retain when youd rather empty tour bladder and thus urge incontinence as an increased likelihood of infection etc.
what is prostate contraction controlled by?
contraction controlled by sympathetic NS releasing NORADRENALINE and acting on receptor called the alpha1a (A1A) subtype receptor.
