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Irene’s Incontinence
(refer to anatomy of the abdomen/pelvis)
Imaging of the Abdominal
Viscera
1.What techniques could be used for
imaging of the abdominal viscera?1
2.Identify the labelled structures on the
diagram2
3.What area of the abdomen would you
examine with a percutaneous
transhepatic cholangiogram or an
endoscopic retrograde cholangio pancreatography?3
4. What two methods could you use to investigate a colonic polyp?4
Physiology and Pharmacology of Urinary Incontinence
1. What is the sympathetic input to the lower urinary tract?5
2. What is the parasympathetic input to the lower urinary tract?6
3. What is the somatic input to the lower urinary tract7
4. What is the function of Ad and C fibres in the detrusor?8
1 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 contrast
from the liver), fluoroscopy
2 A = Liver, B = Aorta, C = Left Kidney, D = Right Kidney, E = Pancreas, F = Spleen
3 Biliary tract
4 Barium enema or colonoscopy
5 Release of noradrenaline relaxes the detrusor muscle via B-3 receptors and constricts the urethra via A1
receptors to inhibit urination
6 Release of neurotransmitter acetylcholine contracts the detrusor muscle and nitric oxide relaxes the urethra
7 Release of acetylcholine constricts the external urethral sphincter via nicotinic receptors
8 Afferent (towards the CNS) fibres
5. What happens when the pelvic nerve is stimulated by distention of the bladder9
6. What is the periadequacy grey (PAG)?10
7. Define the following terms:
i) Lower unirary tract symptoms11
ii)storage symptoms12
iii)overactive bladder13
iv)stress incontinence14
3. What are the three layers of cells lining the bladder lumen from inside out?15
4. What is the difference between neurogenic and idiopathic detrusor activity?16
5. How does the shape of umbrella cells change with bladder emptying?17
6. What is the function of uroplakin subunits in the bladder wall?18
9 Inhibits parasympathetic outflow to the detrusor, stimulates sympathetic outflow to the bladder, base and
urethra 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 the
ʻswitchʼ for micturition. The PAG is the inhibitory input which needs to be turned off for the detrusor muscle to
contract.
11 Storage, voiding and post micturition symptoms (e.g. dribble, feeling of incomplete emptying.
12 Increased daytime frequency, nocturia, urgency
13 Urgency with or without urge incontinence. The urgency without incontinence itself is also a therapeutic
target.
14 Involuntary loss of urine on effort, exertion, cough or sneezing. Occurs when the pelvic floor muscles
become weakened (e.g. as a result of childbirth). Increased intra-abdominal pressure and force through the
external urethral sphincter.
15 largest inside = umbrella cells (lumenal), intermediate cells, basal cells
16 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 columnar
18 Decrease permeability of membrane, the bladder wall is the least permeable membrane in the body.
7. What are the effects of M3 receptors in the bladder19
8. What are the effects of M2 receptors in the bladder20
9. What is the role of B3 receptors21
10.What happens when myosin light chain kinase combines with calmodulin?22
11.Describe the use of muscarinic receptor antagonists in the treatment of
conditions involving overactive bladder23
12.What is the most widely used muscarinic (parasympathetic/M3) receptor
antagonist used for overactive bladder?24
13.What would the predictable side effects be of a muscarinic (parasympathetic)
antagonist?25
14.Describe the use of botox in the treatment of overactive bladder, including the
mechanisms of action26
15.B3 agonists can be used to stimulate relaxation of the detrusor muscle, allowing
the bladder to store urine longer, give an example of one of these drugs27
19 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 kinase
phosphatase, adding phosphate to myosin to initiate contraction.
20 M2 receptors also facilitate contraction by inhibiting ongoing relaxation by cyclic AMP. M2 and M3 are
muscarinic acetylcholine receptors, so muscarinic receptor blockers are sometimes used to treat overactive
bladder.
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 myosin
initiating the cross bridge cycle (contraction). Myosin phosphatase does the opposite (removing a phosphate
from the myosin), using cyclicAMP
23 Muscarinic receptor agonists block cholinergic stimulation of the detrusor. These are usually M3 selective
therefore only block contraction).
24 Oxybutinin (preferentially M3 selective)
25 Blocks parasympathetic function (muscarinic receptors) so can lead to the usual dry mouth, constipation or
blurred vision. Occasionally causes tachycardia.
26 Botox is injected into the detrusor muscle at numerous sites through a urethral cytoscope. Produces a 10
month improvement in bladder function. It works on nerve terminals to degrade the SNAP-25 protein
involved in docking and fusion of (neurotransmitter) vesicles within the plasma membrane. Botox also
inhibits Ach release from parasympathetic efferents, blocks ATP release (reduce signaling to bladder
afferents), reduces P2X3 receptor expression and therefore afferent firing.
27 Mirabegron is most commonly used (used if muscarinic receptor blockers innefective).
Hospitalisation and Stressful Procedures
1. Describe the negative impacts of hospitalisation on patients28
2. What positive social impacts does hospitalisation have on recovery?29
3. How could issues of staff communication and attitude affect patients’ experience
of hospitalisation?30
4. What factors could affect distress in hospitalized children?31
5. Describe/list key stressful treatment environments32
6. What are the main sources of stress in post surgery recovery33
28 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 in
daily routine.
29 Kulik and Mahler on coronary bypass post-op recovery. Observed that people who shared a room had less
anxiety 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 demanding
behaviour as negative but rather an attempt to reduce helplessness. Some evidence that negative staff
attitudes 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 younger
children mainly due to separation from primary caretakers, emotional responses to illness, failure to
understand situation, lack of preparation.
32 Increased distress with increased number of different treatment environments. Particular treatment such
as ITU and renal dialysis increase distress. Intubation and associated communication issues. Stress in
relatives and staff. Hallucinations due to sensory depravation in ITU.
33 Stresses before the operation (background stress), post op pain, anesthetic effects, infection, outcome or
procedural stress. Pre-op interventions improve post-op recovery.

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Sc12 irene's incontinece

  • 1. Irene’s Incontinence (refer to anatomy of the abdomen/pelvis) Imaging of the Abdominal Viscera 1.What techniques could be used for imaging of the abdominal viscera?1 2.Identify the labelled structures on the diagram2 3.What area of the abdomen would you examine with a percutaneous transhepatic cholangiogram or an endoscopic retrograde cholangio pancreatography?3 4. What two methods could you use to investigate a colonic polyp?4 Physiology and Pharmacology of Urinary Incontinence 1. What is the sympathetic input to the lower urinary tract?5 2. What is the parasympathetic input to the lower urinary tract?6 3. What is the somatic input to the lower urinary tract7 4. What is the function of Ad and C fibres in the detrusor?8 1 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 contrast from the liver), fluoroscopy 2 A = Liver, B = Aorta, C = Left Kidney, D = Right Kidney, E = Pancreas, F = Spleen 3 Biliary tract 4 Barium enema or colonoscopy 5 Release of noradrenaline relaxes the detrusor muscle via B-3 receptors and constricts the urethra via A1 receptors to inhibit urination 6 Release of neurotransmitter acetylcholine contracts the detrusor muscle and nitric oxide relaxes the urethra 7 Release of acetylcholine constricts the external urethral sphincter via nicotinic receptors 8 Afferent (towards the CNS) fibres
  • 2. 5. What happens when the pelvic nerve is stimulated by distention of the bladder9 6. What is the periadequacy grey (PAG)?10 7. Define the following terms: i) Lower unirary tract symptoms11 ii)storage symptoms12 iii)overactive bladder13 iv)stress incontinence14 3. What are the three layers of cells lining the bladder lumen from inside out?15 4. What is the difference between neurogenic and idiopathic detrusor activity?16 5. How does the shape of umbrella cells change with bladder emptying?17 6. What is the function of uroplakin subunits in the bladder wall?18 9 Inhibits parasympathetic outflow to the detrusor, stimulates sympathetic outflow to the bladder, base and urethra 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 the ʻswitchʼ for micturition. The PAG is the inhibitory input which needs to be turned off for the detrusor muscle to contract. 11 Storage, voiding and post micturition symptoms (e.g. dribble, feeling of incomplete emptying. 12 Increased daytime frequency, nocturia, urgency 13 Urgency with or without urge incontinence. The urgency without incontinence itself is also a therapeutic target. 14 Involuntary loss of urine on effort, exertion, cough or sneezing. Occurs when the pelvic floor muscles become weakened (e.g. as a result of childbirth). Increased intra-abdominal pressure and force through the external urethral sphincter. 15 largest inside = umbrella cells (lumenal), intermediate cells, basal cells 16 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 columnar 18 Decrease permeability of membrane, the bladder wall is the least permeable membrane in the body.
  • 3. 7. What are the effects of M3 receptors in the bladder19 8. What are the effects of M2 receptors in the bladder20 9. What is the role of B3 receptors21 10.What happens when myosin light chain kinase combines with calmodulin?22 11.Describe the use of muscarinic receptor antagonists in the treatment of conditions involving overactive bladder23 12.What is the most widely used muscarinic (parasympathetic/M3) receptor antagonist used for overactive bladder?24 13.What would the predictable side effects be of a muscarinic (parasympathetic) antagonist?25 14.Describe the use of botox in the treatment of overactive bladder, including the mechanisms of action26 15.B3 agonists can be used to stimulate relaxation of the detrusor muscle, allowing the bladder to store urine longer, give an example of one of these drugs27 19 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 kinase phosphatase, adding phosphate to myosin to initiate contraction. 20 M2 receptors also facilitate contraction by inhibiting ongoing relaxation by cyclic AMP. M2 and M3 are muscarinic acetylcholine receptors, so muscarinic receptor blockers are sometimes used to treat overactive bladder. 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 myosin initiating the cross bridge cycle (contraction). Myosin phosphatase does the opposite (removing a phosphate from the myosin), using cyclicAMP 23 Muscarinic receptor agonists block cholinergic stimulation of the detrusor. These are usually M3 selective therefore only block contraction). 24 Oxybutinin (preferentially M3 selective) 25 Blocks parasympathetic function (muscarinic receptors) so can lead to the usual dry mouth, constipation or blurred vision. Occasionally causes tachycardia. 26 Botox is injected into the detrusor muscle at numerous sites through a urethral cytoscope. Produces a 10 month improvement in bladder function. It works on nerve terminals to degrade the SNAP-25 protein involved in docking and fusion of (neurotransmitter) vesicles within the plasma membrane. Botox also inhibits Ach release from parasympathetic efferents, blocks ATP release (reduce signaling to bladder afferents), reduces P2X3 receptor expression and therefore afferent firing. 27 Mirabegron is most commonly used (used if muscarinic receptor blockers innefective).
  • 4. Hospitalisation and Stressful Procedures 1. Describe the negative impacts of hospitalisation on patients28 2. What positive social impacts does hospitalisation have on recovery?29 3. How could issues of staff communication and attitude affect patients’ experience of hospitalisation?30 4. What factors could affect distress in hospitalized children?31 5. Describe/list key stressful treatment environments32 6. What are the main sources of stress in post surgery recovery33 28 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 in daily routine. 29 Kulik and Mahler on coronary bypass post-op recovery. Observed that people who shared a room had less anxiety 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 demanding behaviour as negative but rather an attempt to reduce helplessness. Some evidence that negative staff attitudes 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 younger children mainly due to separation from primary caretakers, emotional responses to illness, failure to understand situation, lack of preparation. 32 Increased distress with increased number of different treatment environments. Particular treatment such as ITU and renal dialysis increase distress. Intubation and associated communication issues. Stress in relatives and staff. Hallucinations due to sensory depravation in ITU. 33 Stresses before the operation (background stress), post op pain, anesthetic effects, infection, outcome or procedural stress. Pre-op interventions improve post-op recovery.