Sc12 irene's incontinece

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Sc12 irene's incontinece

  1. 1. Irene’s Incontinence(refer to anatomy of the abdomen/pelvis)Imaging of the AbdominalViscera1.What techniques could be used forimaging of the abdominal viscera?12.Identify the labelled structures on thediagram23.What area of the abdomen would youexamine with a percutaneoustranshepatic cholangiogram or anendoscopic retrograde cholangio pancreatography?34. What two methods could you use to investigate a colonic polyp?4Physiology and Pharmacology of Urinary Incontinence1. What is the sympathetic input to the lower urinary tract?52. What is the parasympathetic input to the lower urinary tract?63. What is the somatic input to the lower urinary tract74. What is the function of Ad and C fibres in the detrusor?81 Plain and contrast X-ray (barium meal), endoscopy, nuclear medicine, ultrasound, CT, MRI, arteriograms,choleystogram (for examining gallbladder, where absorbtion of water concentrates the excreted contrastfrom the liver), fluoroscopy2 A = Liver, B = Aorta, C = Left Kidney, D = Right Kidney, E = Pancreas, F = Spleen3 Biliary tract4 Barium enema or colonoscopy5 Release of noradrenaline relaxes the detrusor muscle via B-3 receptors and constricts the urethra via A1receptors to inhibit urination6 Release of neurotransmitter acetylcholine contracts the detrusor muscle and nitric oxide relaxes the urethra7 Release of acetylcholine constricts the external urethral sphincter via nicotinic receptors8 Afferent (towards the CNS) fibres
  2. 2. 5. What happens when the pelvic nerve is stimulated by distention of the bladder96. What is the periadequacy grey (PAG)?107. Define the following terms:i) Lower unirary tract symptoms11ii)storage symptoms12iii)overactive bladder13iv)stress incontinence143. What are the three layers of cells lining the bladder lumen from inside out?154. What is the difference between neurogenic and idiopathic detrusor activity?165. How does the shape of umbrella cells change with bladder emptying?176. What is the function of uroplakin subunits in the bladder wall?189 Inhibits parasympathetic outflow to the detrusor, stimulates sympathetic outflow to the bladder, base andurethra which causes constriction of sphincters and relaxation of the detrusor. Stimulates motor (somatic)outflow to the external urethral sphincter, causing constriction. All referred to as guarding reflexes.10 The end CNS component of the bladder voiding pathway, works with the pontine micturition centre as theʻswitchʼ for micturition. The PAG is the inhibitory input which needs to be turned off for the detrusor muscle tocontract.11 Storage, voiding and post micturition symptoms (e.g. dribble, feeling of incomplete emptying.12 Increased daytime frequency, nocturia, urgency13 Urgency with or without urge incontinence. The urgency without incontinence itself is also a therapeutictarget.14 Involuntary loss of urine on effort, exertion, cough or sneezing. Occurs when the pelvic floor musclesbecome weakened (e.g. as a result of childbirth). Increased intra-abdominal pressure and force through theexternal urethral sphincter.15 largest inside = umbrella cells (lumenal), intermediate cells, basal cells16 In DO the bladder undergoes phasic contractions or contracts uncontrollably when full. Neurogenic = de-inhibition of pontine micturition centre (e.g. stroke, dementia) or other defect of CNS (e.g. MS). Idiopathic =arising for no apparent reason but possible reasons include (neurogenic, myogenic or urotheliogenic,increased afferent nerve firing)17 Lateral membrane unfolds and apical membrane refolds - the cell becomes more columnar18 Decrease permeability of membrane, the bladder wall is the least permeable membrane in the body.
  3. 3. 7. What are the effects of M3 receptors in the bladder198. What are the effects of M2 receptors in the bladder209. What is the role of B3 receptors2110.What happens when myosin light chain kinase combines with calmodulin?2211.Describe the use of muscarinic receptor antagonists in the treatment ofconditions involving overactive bladder2312.What is the most widely used muscarinic (parasympathetic/M3) receptorantagonist used for overactive bladder?2413.What would the predictable side effects be of a muscarinic (parasympathetic)antagonist?2514.Describe the use of botox in the treatment of overactive bladder, including themechanisms of action2615.B3 agonists can be used to stimulate relaxation of the detrusor muscle, allowingthe bladder to store urine longer, give an example of one of these drugs2719 M3 receptors are activated and cause contraction of the detrusor muscle by opening L-type Ca2+channels and inhibiting myosin phosphatase by increasing Rho kinase and myosin light chain kinasephosphatase, adding phosphate to myosin to initiate contraction.20 M2 receptors also facilitate contraction by inhibiting ongoing relaxation by cyclic AMP. M2 and M3 aremuscarinic acetylcholine receptors, so muscarinic receptor blockers are sometimes used to treat overactivebladder.21 Stimulate release of cAMP which decreases Ca2+ levels causing relaxation of the detrusor muscle.22 Increases Ca2+ levels and forms active myosin light chain kinase complex which phosphorylates myosininitiating the cross bridge cycle (contraction). Myosin phosphatase does the opposite (removing a phosphatefrom the myosin), using cyclicAMP23 Muscarinic receptor agonists block cholinergic stimulation of the detrusor. These are usually M3 selectivetherefore only block contraction).24 Oxybutinin (preferentially M3 selective)25 Blocks parasympathetic function (muscarinic receptors) so can lead to the usual dry mouth, constipation orblurred vision. Occasionally causes tachycardia.26 Botox is injected into the detrusor muscle at numerous sites through a urethral cytoscope. Produces a 10month improvement in bladder function. It works on nerve terminals to degrade the SNAP-25 proteininvolved in docking and fusion of (neurotransmitter) vesicles within the plasma membrane. Botox alsoinhibits Ach release from parasympathetic efferents, blocks ATP release (reduce signaling to bladderafferents), reduces P2X3 receptor expression and therefore afferent firing.27 Mirabegron is most commonly used (used if muscarinic receptor blockers innefective).
  4. 4. Hospitalisation and Stressful Procedures1. Describe the negative impacts of hospitalisation on patients282. What positive social impacts does hospitalisation have on recovery?293. How could issues of staff communication and attitude affect patients’ experienceof hospitalisation?304. What factors could affect distress in hospitalized children?315. Describe/list key stressful treatment environments326. What are the main sources of stress in post surgery recovery3328 Loss of identity and social role in impersonal environment, wearing hospital clothes etc. (R. Wilson 1963).Admission to hospital in and of itself. Pysical environment, cold/drab, invasion of personal space, change indaily routine.29 Kulik and Mahler on coronary bypass post-op recovery. Observed that people who shared a room had lessanxiety before surgery, walked more after surgery and did better than patients in own rooms.30 40-50% of patients critical of communication aspects of stay. Could be improved by not seeing demandingbehaviour as negative but rather an attempt to reduce helplessness. Some evidence that negative staffattitudes or seeing patientʼs behaviour as cause of health problem has a negative impact on recovery.31 Distress in hospitalized children decreases dramatically with age from 1-14 years. Distress in youngerchildren mainly due to separation from primary caretakers, emotional responses to illness, failure tounderstand situation, lack of preparation.32 Increased distress with increased number of different treatment environments. Particular treatment suchas ITU and renal dialysis increase distress. Intubation and associated communication issues. Stress inrelatives and staff. Hallucinations due to sensory depravation in ITU.33 Stresses before the operation (background stress), post op pain, anesthetic effects, infection, outcome orprocedural stress. Pre-op interventions improve post-op recovery.

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