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Medicine > Urinary > Flashcards

Urinary Flashcards

1
Q

What are symptoms of end stage renal disease?

A

N+V, Fatigue, Anorexia, Weight loss, Muscle cramps, Pruritis, Lower extremities uncomfortable and swollen, Dry cough, SOB

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2
Q

What is the main reason why patients have symptoms during end stage renal disease?

A

Hyperuricaemia
Loss of fluid, electrolyte and pH homeostasis
Loss of endocrine functions of kidneys

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3
Q

What are signs of end stage renal disease?

A 
Tachypnoea 
Tachycardia
HTN
Dry skin - uraemic frost
Petechia
Moist rales posterior lung bases
S3 on cardiac exam
Abdominal exam - benign
Pitting oedema
MSK pain
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4
Q

What are the stages of CKD?

A

1 -4

5 is ESRD

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5
Q

What is a long term problem with the endocrine function in ESRD?

A

Anaemia
90% of EPO made by interstitial peri-tubular cells
Response to cellular hypoxia
Vit D deficiency
Proximal tubule cells - produce 25-hydroxyvitamin D-1 alpha-hydroxylase -> Activates Vit D -> Functionally Vit D deficient

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6
Q

What are common symptoms of diabetes?

A 
Polyuria
Polydipsia
Pruritis
Weight loss
FMHx of DM
Diet, smoking, eye symptoms (retinopathy)
Fungal infections
Poor wound healing
Sensation in feet - peripheral neuropathy
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7
Q

Where are the kidneys located and what is their approximate size?

A 
Located retroperitoneal
Long axis parallel to psoas muscle
Bean shaped
Height of 3 vertebral bodies
Between T11-T12 is their mid point so sits below the ribs and in the abdomen
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8
Q

At what time in development do the kidneys ascend to their final position?

A

Week 8

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9
Q

Why can patients get a horse-shoe kidney?

A

Gets caught on the aorta and the bottoms fuse to prevent it moving further up

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10
Q

What imaging modalities can be used for the kidneys?

A 
Ultrasound, x-ray, CT, MRI
Renal doppler
Renal scintigraphy (gamma scanner)
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11
Q

What size urolithiasis would require intervention?

A

> 6mm

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12
Q

What are 2 methods of treating a urolithiasis?

A 
Extracorporeal Shock-Wave Lithotripsy (ESWL)
Percutaneous nephrolithotomy (PCNL)
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13
Q

What stone size would deem extracorporeal shock-wave lithotripsy unsuitable?

A

> 2cm
Lower pole calyx
Radiolucent
Body habitus/ weight

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14
Q

What can cause a PUJ obstruction?

A

Idiopathic - congenital
Retroperitoneal fibrosis
Secondary to trauma or infection

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15
Q

If someone presents with pain after alcohol consumption in the flank what could that indicate?

A

PUJ obstruction

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16
Q

When do you use DMSA and MAG3?

A

DMSA - renal function test - accumulates in renal cortical tubules and cortex
MAG3 - renal function and structure

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17
Q

What is TNM staging for urothelial carcinoma?

A

T1 - through lamina propria
T2 - through lamina propria + into the inner muscle layer
T3a - through above + into the outer muscle layer
T3b - through above + outer muscle layer
T4a - through all bladder layers and to nearby structures - pelvis etc
T4b - through all bladder layers + through prostate gland

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18
Q

What are indications for a nephrostomy?

A

Relieve urinary tract obstruction especially if urosepsis
Urinary diversion
PCNL access or access for alkanisation of stones
Delivery of chemo

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19
Q

Through which embryonic layer does the kidney develop from?

A

Intermediate mesoderm

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20
Q

What two structures make up the embryonic kidney?

A

Mesonephric tubules and mesonephric duct

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21
Q

What structure drives the development of the true kidney in the embryo?

A

Ureteric bud

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22
Q

If the ureteric bud fails to interact with the intermediate mesoderm what is the potential result?

A

Renal agenesis

Can have unilateral but bilateral is not compatible with life

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23
Q

What is the urachus and what is a potential problem at birth?

A

Urachus connects foetal bladder to the umbilicus called the allantois. If it is patent after birth then the urine can still keep coming out of the umbilicus

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24
Q

What does the urorectal septum become after development?

A

Perineum at the base -> pouch of douglas/ rectovesicle pouch

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25
Q

What does the urogenital sinus develop into?

A

Superior parts -> umbilicus
Majority -> urinary bladder
Inferior parts -> urethra

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26
Q

What 4 parts is the urethra divided into?

A

Pre-prostatic (bladder to prostate)
Prostatic
Membranous
Spongy

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27
Q

What is hypospadias?

A

Defect in the fusion of the urethral folds

Urethra opens onto the ventral surface rather than at the end of the glans penis

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28
Q

Define GFR?

A

GFR - glomerular filtration rate

Amount of filtrate that is produced from the blood flow per unit time

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29
Q

What is the normal GFR?

A

90-120mls/min/1.73m2

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30
Q

What is the normal total glomerular filtrate per day?

A

140-180litres/day

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31
Q

What does GFR depend on?

A 
Age
Gender
Size of individual
Size of kidneys
Pregnancy
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32
Q

What is the GFR at birth?

A

~20ml/min/1.73m2

Normalises by ~18months

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33
Q

How does GFR change with age?

A

> 30 years of age - GFR declines 6-7ml/min/ decade

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34
Q

How does GFR change in pregnancy?

A

GFR increases to 130-180ml/min

Kidney size increases too ~1cm growth

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35
Q

What 2 reasons in simple terms would point to a decrease in GFR

A

Decline in number of nephrons

Decline of GFR within individual nephrons (GN, diabetes, HTN)

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36
Q

How do you measure clearance through the kidneys?

A

Clearance (ml/min) = Amount of substance eliminated per unit time (mg/min) / Plasma conc of substance (mg/ml)
Alternatively:
Renal clearance = excretion rate / plasma conc
Excretion rate = amount in urine X urine flow rate

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37
Q

What 4 factors would lead to the best substance to measure for renal clearance calculation?

A

1 - produced at a constant rate
2 - freely filtered across glomerulus
3 - not reabsorbed in the nephron
4 - not secreted into the nephron

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38
Q

What 3 exogenous substance can be used to determine renal clearance?

A

1 - Inulin clearance
2 - 51 Cr-EDTA = radio active labelled marker
3 - Iohexol - contract agent

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39
Q

What endogenous substance can be used to determine renal clearance?

A

Creatinine

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40
Q

What is the problem with creatinine being used as a marker for renal clearance?

A

It is secreted into the renal tubule so shows a 10%-20% overestimation of the renal clearance
Cumbersome as 24hour clearance measurement

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41
Q

What is the normal serum creatinine level?

A

70-150micromol/litre

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42
Q

What 2 main factors affect creatinine levels in an individual?

A 
Protein intake
Muscle mass
Age
Gender
Race - black higher creatinine, hispanic/ indo-asian lower
Drugs - trimethoprim
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43
Q

What are the variables used in the MDRD GFR calculator

A

Serum creatinine
Age
Sex
Caucasian or black

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44
Q

When is MDRD GFR inaccurate?

A 
People without kidney disease
Children
Pregnancy
Old age
Other ethnicities
When true GFR changes quickly - AKI
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45
Q

Why is eGFR less accurate with mild kidney disease?

A

1 - reduction in GFR
2 - rescued nephron number -> nephron hypertrophy -> GFR same
3 - Increased serum creatinine -> increased secretion into the tubule

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46
Q

What does nephrogenic autoregulation mean?

A

Controlling the GFR within physiological blood pressure limits by the myogenic response and the tubuloglomerular feedback systems.

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47
Q

Which nephrons undergo autoregulation?

A

Cortical nephrons

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48
Q

Which nephrons have AA>EA and which have AA=EA?

A 
AA>EA= Cortical
AA=EA = Juxtamedullary
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49
Q

Which nephrons have a higher concentration of renin?

A

Cortical
Much higher as they have a higher response to RBC due to their differing arteriolar sizes they can control BP more effectively with the release of renin

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50
Q

What cells create the filtration barrier?

A

Podocytes
Acellular gelatinous layer of glycoproteins that are negatively charged - aka basement membrane
Slits allows fluid to leave through the capillary membrane

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51
Q

How does charge affect the filtration of substances in the kidney?

A

Basement membrane is negatively charged
Small but negatively charged molecules - not cleared
Large but positively charged molecules can still get through

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52
Q

What causes the ultra filtrate to be produced?

A

Hydrostatic pressure within blood > oncotic pressure within blood
Oncotic pressure within blood = Hydrostatic pressure within the bowman’s capsule

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53
Q

What is the myogenic response in the kidneys?

A

Arterial smooth muscle responses to increases and decreases in vascular wall tension - property of preglomerular resistance vessels

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54
Q

What is tubuloglomerular feedback?

A

[Na] + [Cl] at macula densa linked with control of renal arterial resistance
Control of tubular resorption = control of distal solute delivery
Afferent arteriole resistance
Efferent arteriolar feedback (hormonal)

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55
Q

What is released from the granular cells of the kidney?

A

Renin

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56
Q

What is released from the juxtaglomerular cells of the kidney?

A

Renin

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57
Q

Where are the macula densa cells found in the kidney?

A

Next to the glomerulus in the DCT

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58
Q

What is the process of tubuloglomerular feedback if GFR increases?

A

Inc GFR -> Inc NaCl delivery to DCT lumen -> Inc in NKCC2 transport of MD cells -> Inc intracellular [NaCl] -> ATP released extracellularly -> ADP -> AMP -> Adenosine -> binds to A1 receptor on extraglomerular mesangial cells in AA -> Gq receptor -> PLC -> DAG and IP3 -> Calcium released from SER in mesangial cells -> gap junctions -> smooth muscle cells -> smooth muscle contraction -> decreased lumen of AA -> decreased pressure distal -> dec GFR

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59
Q

What causes renin to be released from the kidney?

A

Low blood pressure hence reduced renal blood flow - detected by baroreceptors in JGA
Decreased NaCl delivery from the DCT to the juxtaglomerular cells
Direct sympathetic stimulation of the JGA

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60
Q

What is the immediate response of a decreased in GFR?

A

Sensed in AA =>Prostaglandin release (PGI2 and PGE2) from the MD cells -> vasodilation -> inc blood flow -> GFR inc
Sensed in EA => Angiotensin 2 + Norepinephrine released

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61
Q

Are there and if so where are baro-receptors in the kidneys?

A

Yes

Found in the Juxtaglomerular apparatus

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62
Q

What chemical neurotransmitter acts to cause sympathetic stimulation of the JGA?

A

Dopamine

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63
Q

What does renin do?

A

Angiotensiongen -> Ang1

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64
Q

What is the action of angiotensin converting enzyme?

A

Convert ANG1 -> ANG2

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65
Q

What are the effects of Angiotensin 2?

A

1 - Increase sympathetic activity
2 - Increase Na,Cl,K reabsorption from the DCT -> H2O retention
3 - Stimulate pituitary to secrete ADH -> H2O reabsorption increases
4 - Stimulate adrenals -> aldosterone secretion -> increase Na,Cl,K reabsorption
5 - Arteriolar vascoconstriction

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66
Q

What are the 3 layers of the adrenal cortex gland?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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67
Q

From which part of the kidney is aldosterone released from?

A

Cortex

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68
Q

What are the effects of aldosterone?

A

1 - Upregulate Na/K pump on basolateral membrane of DCT
2 - Upregulates Na channels on CD (and colon)
3 - Stimulates secretion of K into tubule
4 - Stimulates Na and H2O reabsorption in GI, Saliva, Sweat glands
5 - Stimulates H+ secretion in CD
6 - Upregulats Na/Cl cotransporter in DCT

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69
Q

How does glucose get reabsorbed in the kidneys?

A

SGLUT symporter

Na/K sets up gradient for Na to flow down into the cell along with glucose on the apical membrane

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70
Q

What is the pressure-natriuresis curve?

A

As MAP inc the amount of Na excretion when arterial pressure to the kidneys rises would also increase to compensate.
If HTN then the amount of sodium excreted would want to remain the same as if the BP was normal in order to maintain normal blood volume. Therefore if the sodium levels rise then the BP would have to accommodate by also increasing to remove the excess sodium but this would occur at a higher BP than normal

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71
Q

What could be a renal cause of HTN seen in a CT angiogram of the kidneys?

A

Renal arterial stenosis

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72
Q

What sodium transporters are found in the Proximal tubule?

A 
Na-H antiporter
NaHCO3 - cotransporter
Na/Glucose symporter
Na/AA - cotransporter
Na-Pi
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73
Q

What sodium transporters are found in the loop of Henle?

A

NaKCC (symporter)

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74
Q

What sodium transporters are found in the early DT?

A

NaCl - symporter

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75
Q

What sodium transporters are found in the late DT and CD?

A

ENaC (Epithelial Na Channels)

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76
Q

What is the relationship between glucose filtration, reabsorption and excretion to the plasma glucose concentration?

A

As plasma glucose concentration rises so the the amount of glucose filtered out of the ultra filtrate in the kidneys. This occurs up to a threshold limit of approximately 300mg/100ml or 11mmol/litre.
Above 11mmol/litre the amount reabsorbed tails off and the amount excreted increases

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77
Q

How does amiloride affect renal function?

A

ENaC inhibitor in DCT

Blocks Na/H+ anti porter in PCT

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78
Q

What ions are transported through the PCT 2nd and 3rd sections?

A

Na/K sets up Na conc gradient
Na/H anti-porter
Anion/Cl anti porter with chloride entering the cell

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79
Q

In the PCT what is the driving force of reabsorption?

A

Osmotic gradient established by solute absorption
Hydrostatic force in interstitium
Increased Oncotic force in peritubular capillary

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80
Q

What occurs in the descending limb of the Loop of Henle in terms of solute/ water movement?

A

Water is reabsorbed by paracellular and transcellular routes

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81
Q

What type of transport is Na moving through in the thin ascending limb of LoH?

A

Passive movement as the water leaving has created a gradient

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82
Q

What transport occurs in the thick ascending limb of LoH?

A

-NKCC2 channel - all reabsorbed into the cell -> blood
Na/K channel sets up some of the driving force
-K/Cl channel allows them to move into the blood
-K leaves the apical membrane down conc gradient into the lumen through the ROMK channel

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83
Q

What channel do potassium sparing diuretics effect?

A

ROMK channels on apical renal tubule surface

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84
Q

What is the DCT permeable to?

A

Early DCT - not water permeable, Na reabsorption occurs

Late DCT - water permeability is variable depending on ADH

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85
Q

How is Na reuptaken by the DCT?

A

Hypo-osmotic fluid enters DCT
Active transport of Na by NCCT (Na/Cl co-transporter) and ENaC
Water permeability is low
DCT 1 - NaCl enters across apical membrane + Na/K sets up gradient, K/Cl leaves together on the basolateral membrane

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86
Q

What channel is sensitive to thiazide diuretics?

A

NCCT on the apical membrane

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87
Q

In the late DCT the movement of Na through ENaC is not electroneutral, what ion does it allow paracellular transport with?

A

Chloride

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88
Q

How is calcium reabsorbed through the kidney?

A

In the DCT
Apical Ca transport
Ca bound to calbindin which shuttles calcium to the basolateral aspect of the DCT
Transported out by NCX and Ca ATPase

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89
Q

What 2 types of cells are found in the cortical collecting ducts?

A

Principal cells and Intercalated cells

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90
Q

What is the function of principal cells?

A

Reabsorption of Na via ENaC on apical membrane
Na/K ATPase driving force of gradient
ROMK allows K to leave the cell on apical surface
Cl uptakes via paracellular route
Variable H2O uptake through AQP channels dependent on ADH

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91
Q

What is the function of intercalated cells?

A

3 types of intercalated cells A-IC, B-IC and Type B
Type B-IC Secrete HCO3
Type A-IC Secrete H+
In cortical and outer medullary CD:
Type A-IC = express H+ ATPase and H/K ATPase at the apical membrane
Express Cl/HCO3 exchanger at basolateral membrane

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92
Q

Where in the kidneys is most of the water re-absorbed?

A

Proximal tubule and descending thin limb of LoH

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93
Q

Where in the kidneys is most of the sodium re-absorbed?

A

PT -> Ascending thin and thick limb of LoH

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94
Q

What is normal plasma osmolality?

A

280-300 mOsm/Kg

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95
Q

How many of the nephrons are cortical and how many are juxtamedullary?

A

85-90% Cortical

10-15% Juxtamedullary

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96
Q

Which of the nephron types are responsible for making concentrated urine?

A

Juxtamedullary

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97
Q

What is the vertical osmolality gradient and how is it formed?

A

Large vertical osmotic gradient established in the interstitial fluid of the medulla
Isotonic at corticomedullary border 300mOsm/Kg
Hyperosmotic at medullary interstitium 1200 mOsm/Kg
Active NaCl transport in thick ascending limb - recycling of urea (effective osmole)
Ascending limb LoH -> NaCl active transport into interstitium
Descending limb LoH -> H2O passive moves out
As more NaCl is transported out more H2O moves out passively behind it.
Concentrates the filtrate even more

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98
Q

How is urea removed from the PT?

A

Urea/Na co-transporter
Urea passively moves into blood on basolateral side
Na/K ATPase maintains Na gradient

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99
Q

What is urea recycling in the kidneys?

A

Urea reabsorbed from medullary CD
Under influence of ADH fractional excretion of urea decreased and urea re-cycling increases i.e. more ADH = more urea re-absorbed through AQP1 channels

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100
Q

How do the vasa recta in the kidneys help the counter current?

A

Concentration gradient produced by the loop of Henle acting as a counter current, opposite direction to the flow of the ultrafiltrate and direction of travel in the LoH
Slow flow prevents wash out and allows equilibrium at each stratification level

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101
Q

Where are osmoreceptors found?

A

Hypothalamus

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102
Q

What are the 2 responses for high plasma osmolarity?

A

1 - ADH release to increase AQP and water reabsorption

2 - Changing behaviour to drink more water - thirst

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103
Q

How does BP alter response to changes in osmolarity?

A

At lower plasma osmolality e.g. 260 mOsm/Kg a decrease in volume/ BP will have a greater impact on the release of ADH than if there was a higher plasma osmolality e.g. 300 mOsm/Kg.
Volume is more important than osmolality if volume crashes

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104
Q

What is the condition where too little ADH is produced?

A

Diabetes insipidus

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105
Q

What happens in diabetes insipidus?

A

Too little ADH produced
Damage to hypothalamus or pituitary gland
Water is inadequately reabsorbed from CD therefore large amount of urine produced

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106
Q

What is the condition when the kidneys are insensitive to ADH?

A

Nephrogenic diabetes insipidus

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107
Q

What happens in nephrogenic diabetes insipidus?

A

Acquired insensitivity of kidney to ADH
Water is inadequately reabsorbed from CD -> large volume urine produced
Tx - ADH injections/ spray

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108
Q

What is the condition called when there is too much ADH produced?

A

Syndrome of inappropriate ADH

SIADH

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109
Q

What happens in SIADH?

A

Excessive release of ADH from posterior pituitary or other source
Dilutional hyponatraemia - too much fluid not enough sodium

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110
Q

What blood test results would be seen in SIADH in terms of serum osmolality, urine osmolality, urine sodium?

A

SIADH - excess ADH produced therefore water reabsorbed in larger amounts
Serum osmolarity - low
Urine osmolarity - high
Urine sodium - high

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111
Q

How do you treat SIADH?

A 
Fluid restriction
Low Na diet
Hypertonic saline
Diuretics
If drug induced change the drug
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112
Q

What are common symptoms of hyponatraemia?

A 
Aggitation
Nausea
Focal neurology
Coma
Seizures
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113
Q

Name 4 causes of true Na loss

A

D+V
Diuretics/ Renal failure
Peritonitis
Burns/ CF

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114
Q

If you correct hyponatraemia too quickly what is the condition that results called?

A

Central pontine myelinolysis
Osmotic demyelination syndrome
Fluid shifting into CNS which normally compensates well

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115
Q

How do you calculate osmolarity?

A

2Na + Glucose + Urea all in mmol/L

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116
Q

What causes hypovolaemic hyponatraemia?

A

Non-renal losses:
GI losses - D+V, Fistulas
Excessive sweating
Third spacing of fluids- ascites, peritonitis, burns
Cerebral salt-wasting syndrome: traumatic brain injury/ intracranial surgery etc can lead to sodium losses

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117
Q

If urine sodium is low but hypovolaemic what could be the cause?

A

GI/Skin losses

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118
Q

If urine sodium is low but hypervolaemic what could be the diagnosis?

A

CCF
Nephrotic syndrome
Liver failure

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119
Q

If urine sodium is high + hypovolaemic what could be the diagnosis?

A

Renal loss

120
Q

If urine sodium is high + hypervolaemic what could be the diagnosis?

A

Renal failure

121
Q

If urine sodium is high + euvolaemic what could be the diagnosis?

A

SIADH

122
Q

What are potential side effects of hyper or hypokalaemia?

A

Nerve dysfunction and cardiac arrest

123
Q

How long does insulin roughly reduce potassium for?

A

6 hours

124
Q

Why is most of the potassium inside the cell?

A

Na/K ATPase

125
Q

What are the ECG findings in hypokalaemia?

A

Depressed ST wave
Diphasic T wave
Prominent U wave

126
Q

What are the ECG findings in hyperkalaemia?

A

Tall tented T waves
Long PR interval
Wide QRS duration

> 9mEq/L - Absent P waves + Sinusoidal wave

127
Q

What are symptoms of hypokalaemia?

A 
AF
Muscle weakness
Muscle cramps
Constipation
<2.5= cardiac conduction abnormalities, cardiac arrest
128
Q

Where is most of the potassium excreted from?

A

Renally

129
Q

Which part of the nephron is potassium reabsorbed from?

A

PCT - 67%
Ascending thick limb LoH - NKCC2 channel - 20-25%
DCT - K+ and other cations

130
Q

How does aldosterone affect potassium?

A

Stimulates potassium secretion into the lumen therefore antagonists -> hyperkalaemia

131
Q

Which part of the nephron does aldosterone affect?

A

DCT/ CD

132
Q

What drug affects potassium reabsorption in the PCT?

A

Acetazolamide

133
Q

Where do thiazide diuretics work in the nephron?

A

DCT

Na/Cl channels

134
Q

What problems can cause poor renal potassium excretion?

A

AKI, CKD
Potassium sparing diuretics
ACE-I, ARBS
Aldosterone deficiency

135
Q

What problems can cause increased potassium release from cells?

A

Acidosis

Cellular breakdown - ischaemia, toxins, chemo, rhabdomyolysis

136
Q

What methods can cause increased potassium to be administered?

A

Potassium in IV fluid

Blood transfusions

137
Q

What are the immediate treatments for hyperkalaemia?

A

Insulin
Salbutamol
Calcium - stabilises cardiac membrane potential

138
Q

What are the longer term treatments for hyperkalaemia?

A 
Low potassium diet
Calcium resonium binds GI K+
Stop meds
Furosemide - enhances K+ loss
Dialysis
139
Q

What are potential causes of hypokalaemia?

A

Insulin, alkalosis, beta-2 agonists
Extra renal cause - diarrhoea, laxatives
Decreased intake
Renal losses- diuretics, renal tubular acidosis, DKA

140
Q

What 3 things mainly increase Na/K ATPase activity?

A

[K+] in plasma
Insulin
Noradrenaline on B2-adrenoceptors

141
Q

What drug inhibits Na/K ATPase to an extent that causes hyperkalaemia?

A

Digoxin (Digitalis)

142
Q

What is Liddle’s syndrome?

A

ENaC channels increase therefore more Sodium is reabsorbed and less potassium is reabsorbed

143
Q

By what 4 methods causes hypokalaemia with increased urine loss?

A
  • inc aldosterone - volume depletion, primary hyperaldosteronism, secondary hyperaldosteronism
  • Inc urine flow
  • Renal tubular acidosis
  • Magnesium deficiency
144
Q

How much glucose is generally required in a hospitalised non-diabetic patient to avoid starvation ketosis?

A

50-100grams

145
Q

How much sodium, potassium and chloride is required per day as maintenance (orally/ IV)?

A

1mmol/Kg/day

146
Q

How much water is generally required per day?

A

30ml/kg/day

147
Q

What IV fluid is given to a patient on variable rate insulin?

A

Dextrose and potassium bag

0.45% saline with 5% glucose and 0.15% potassium chloride

148
Q

What nerves supply the detrusor muscle?

A

Parasympathetic S2,3,4 (pelvic nerves)

149
Q

What nerve roots supply the external urethral sphincter?

A

Pudendal nerve - S2,3,4

150
Q

What side effect does having a weakened pelvic floor in women lead to?

A

Urinary incontinence

151
Q

What are the 2 phases of normal bladder function?

A

Filling phase - storage. Receptive relaxation, sensation of bladder filling, no detrusor contraction
Voiding phase - voluntary initiation, complete emptying

152
Q

What does a lower motor neurone lesion cause in terms of urinary continence/ incontinence?

A

Low detrusor pressure -> large residual urine +/- overflow incontinence

153
Q

What does a upper motor neurone lesion cause in terms of urinary continence/ incontinence?

A

Dilated ureters, thickened detrusor muscle -> High pressure detrusor contractions -> Poor coordination with external sphincters -> detrusor sphincter dyssynergia

154
Q

What are the categories of Lower Urinary Tract Symptoms?

A

Storage
Voiding
Post-micturition

155
Q

What are Storage LUTS?

A

Increased frequency
Incontinence
Nocturia
Urgency

156
Q

What are voiding LUTS?

A 
Slow stream
Splitting or spraying
Intermittency
Hesitancy
Straining
Terminal dribble
157
Q

What are post-micturition LUTS?

A

Post-micturition dribble

Feeling of incomplete emptying

158
Q

Define urinary incontinence

A

Complaint of any involuntary leakage of urine

159
Q

What are the 4 types of incontinence?

A

Stress urinary incontinence
Urgency urinary incontinence
Mixed urinary incontinence
Overflow incontinence

160
Q

Define stress incontinence?

A

Complaint of involuntary leakage on effort or exertion, or on sneezing or coughing

161
Q

Define urgency urinary incontinence

A

Leakage or urine accompanied by or immediately preceded by urgency

162
Q

Define mixed urinary incontinence

A

involuntary leakage of urine associated with urgency and also with exertion, effort, sneezing or coughing

163
Q

Define overflow incontinence

A

chronic painless retention e.g. lower motor neurone causes

164
Q

What are risk factors for urinary incontinence?

A 
Pregnancy/ childbirth
Pelvic surgery
Pelvic prolapse
Race, FMHx, Anatomical abnormalities, neurological abnormalities
Co-morbidities, obesity, age
Inc intra-abdo pressure
Cognitive impairment
UTI, drug menopause
165
Q

What examinations would be done if a patient complains of urinary incontinence?

A

BMI
Abdo exam to exclude palpable bladder
Digital rectal exam - prostate in males specifically
Females - external genitalia stress test - cough and see if collection, vaginal exam

166
Q

What are investigations done if a patient complains of urinary incontinence?

A

Urine dipstick - UTI, haematuria, proteinuria, glucosuria
Urodynamics - frquency-volume chart, bladder diary, post-micturition residual volume
Cystoscopy

167
Q

What are conservative managements of urinary incontinence?

A 
Modify fluid intake
weight loss
stop smoking
decreased caffeine intake
avoid constipation
timed voiding - fixed schedule - normally for 4 hourly to keep healthy
168
Q

How could you contain the incontinence?

A

Indwelling catheter
Sheath device - condom attached to catheter tubing and bag
Incontinence pads

169
Q

How do you manage stress incontinence?

A

1 - Pelvic floor muscle training - 8 contractions/ day TDS -
3/12 duration of treatment
2 - Duloxetine - SNRI/ SSRI - inc activity of striatal muscle of EUS
3 - Surgery - Females= retropubic suspension procedure/ intramural bulking. Males = artificial urinary sphincter, male sling

170
Q

What is a retropubic suspension procedure?

A

Tightening up of the levator ani muscle with a sling that goes around the ureter and up the abdominal wall

171
Q

How do intramural bulking agents work?

A

Improve ability of urethra to resist abdo pressure

Inject - fat, silicone, collagen into the urethra

172
Q

How does bladder training work?

A

void every hour - not in between, wait

Intervals of no voiding increased by 30mins-1hour until interval of 2-3hours reached

173
Q

What are pharmacological treatment options of urgency urinary incontinence?

A

Anticholinergic Act on M2,M3 receptors - Oxybutynin, solifenacin
B3- adrenoceptor agonist - Mirabegron
Intravesical injection of Botox - neurotoxin - inhibits release of ACh - flaccid paralysis

174
Q

Define enuresis

A

Bedwetting = involuntary wetting during sleep at least 2x/ week in children aged >5 years with no CNS defects

175
Q

What is primary enuresis?

A

Never achieving sustained continence at night

176
Q

What is secondary enuresis?

A

Enuresis restarted having been dry at night for 6+months

177
Q

How do you manage enuresis in children?

A

Primary enuresis - primary care, reassurance, alarms with positive reward system, desmopressin
Secondary enuresis - treat underlying cause, e.g. UTI, constipation, diabetes, psychological problems, family problems etc

178
Q

What are two main types of nephron pathologies?

A

Nephritis - Blockage - renal failure therefore dec. GFR

Nephrotic - Leakage - proteinuria, haematuria

179
Q

What are common primary causes of nephrotic syndrome?

A

Podocyte/ sub epithelial damage/ glomerular basement membrane
Primary causes: Minimal change glomerulonephritis, focal segmental glomerulosclerosis, membranous glomerulonephritis

180
Q

What are common secondary causes of nephrotic syndrome?

A

Diabetes mellitus

Connective tissue diseases e.g. SLE

181
Q

What is minimal change glomerulonephritis?

A 
Childhood or adolescent
Due to unknown circulating factor damaging podocytes - immunologic origin as responds to steroids - but no immune complex deposition
Heavy proteinuria or nephrotic syndrome
Responds to steroids
May recur
Usually no progression to renal failure
182
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Similar to Minimal change glomerulonephritis
Nephrotic
Less responsive to steroids
Glomerulosclerosis
Circulating factor damages podocytes - even in transplant patients they get FSGS in that kidney
Progression to renal failure

183
Q

What is membranous glomerulonephritis?

A

Commonest cause of primary nephrotic syndrome in adults
Rules of thirds on recovery- 1/3 recover fully, 1/3 recover partially, 1/3 never recover and progress to renal failure
Immune complex deposits cause damage
May be secondary - e.g. associated with lymphoma

184
Q

How do sub epithelial deposits in the glomerulus cause problems?

A

1 - Immune complexes can’t get through the podocytes

2 - Antigen on the podocytes attracted by antibodies that are against these antigens causing immune reaction -> damage

185
Q

What could haematuria be a sign of in terms of renal deposition pathology?

A

IgA nephropathy
Commonly after URTI
Thin glomerular basement membrane

186
Q

How does good pasture’s syndrome present and how is it treated?

A

Nephritic syndrome
Haemoptysis, cough,
Anti-GBM disease
Tx - steroids, plasmapheresis

187
Q

What is IgA nephropathy?

A 
Glomerulonephritis
Visible/ invisible haematuria
Relationship with mucosal infection hence IgA
\+/- proteinuria
-> renal failure
188
Q

What is vasculitis?

A

Group of systemic disorders - inflammation of blood vessels including glomeruli
No immune complex deposition
Associated with Anti Neutrophil Cytoplasmic Antibody (ANCA)
Nephritic presentation - rapidly progressing GN
Treatable - immunosuppression

189
Q

What is the difference between nephrotic and nephritic in terms of area affected?

A

Nephritic - Inflammation disrupting GBM

Nephrotic - Podocyte damage leading to glomerular charge - barrier disruption

190
Q

What is the nephrotic triad?

A

Proteinuria >3.5g/24hours
Hypoalbuminaemia
Oedema
(accompanied by hypercholesterolaemia)

191
Q

What secondary causes are there of nephrotic syndrome?

A

Diabetes
SLE
Amyloid

192
Q

How do you manage nephrotic syndrome?

A

Oedema - fluid/salt restrict + loop diuretics
ACE-I = anti-proteinuric
Hypercholesterolaemia = statin
Tx underlying condition

193
Q

What is the triad of nephritic syndrome?

A

Haematuria
Reduction in GFR
HTN
(some proteinuria, rapid onset)

194
Q

How do you manage nephritic syndrome?

A

BP control - ACE-I/ ARB + salt restriction
Oedema - loop diuretics + fluid restrict
Disease specific - steroids, immunosuppressants
CVS risk - statins, modifiable risk factors
Dialysis - short term if required

195
Q

What happens to the GBM in diabetes?

A

It gets thicker with mesangial expansion

This decreases the ability to filter effectively

196
Q

What are the pathological changes in diabetic nephropathy?

A 
1 - hyper filtration/ capillary HTN
2 - GBM thickening + lipoprotein deposition
3 - Mesangial expansion
4 - Podocyte injury
5 - Glomerulosclerosis/ arteriosclerosis
197
Q

How is glucose re-uptaken in the renal cells?

A

Apical membrane = SGLT2 transporter - symporter with Na+

Basolateral side = passive facilitated through GLUT-2 transporters

198
Q

Why in diabetes is there hyper filtration in the glomerulus?

A

Inc glucose delivery to nephron -> more glucose reabsorbed + Na+ -> less Na/Cl delivery to macula densa cells -> release of renin -> inc BP -> HTN

199
Q

What is the relationship between proteinuria and GFR in diabetes?

A

Initially -> Increased GFR -> very slight inc proteinuria
5-10 years = dec GFR -> increasing proteinuria
20 year mark = GFR < proteinuria (damage is done and is enough to now cause a rapid decline in GFR)

200
Q

What are the 5 stages of diabetic nephropathy?

A 
1 - hyper filtration and hypertrophy
2 - latent stage
3 - microalbuminuria
4 - overt proteinuria
5 - ESRD
201
Q

Describe what is seen in microalbuminuria due to diabetes

A 
GBM thickening
Mesangial expansion
Albuminuria
30-300mg/day
Potentially still reversible here
202
Q

Describe what is seen in overt proteinuria due to diabetes

A

GFR normal initially -> drops in linear fashion
Mesangial expansion / sclerosis - reduced surface area for filtration
Proteinuria >30mg/mmol
Worsening systemic HTN
Microvascular changes - tissue ischaemia
ESRD - 3-7years reached
Irreversible damage

203
Q

How do you manage microalbuminuria and proteinuria?

A 
Inhibit RAAS
Tight BP control
Statins
CV risk management
Moderate protein intake
Tight glucose control
204
Q

How would SGLUT2 inhibitors help with diabetic nephropathy?

A

Blocking Na/Glucose reabsorption -> more sodium delivery to macula densa -> reduced feedback to increase BP -> normalised GFR -> reduced hyperfiltration

205
Q

What is classed as an Upper UTI and a Lower UTI?

A

Upper UTI Bladder and above

Lower UTI Bladder and below

206
Q

What is the pathophysiology of a UTI?

A

Urinary tract normally sterile and resistant to bacterial colonisation
Ascending colonisation of bacteria from urethra

207
Q

What are the major defences for getting a UTI?

A

Emptying of bladder (micturition), vescio-urethral valves, immunological factors (IgA), mucosal barriers, urine acidity

208
Q

What is the term used to describe a bladder infection and a kidney infection?

A

Cystitis

Pyelonephritis

209
Q

What age ranges do UTIs peak?

A

Infants and pre-school <5 years
20-25 Honeymoon cystitis + pyelitis of pregnancy
>65 years - prostatism

210
Q

What are 6 risk factors for UTI and why?

A

Female - short UTI
Neurological condition - MS, strokes
Pregnancy - enlarged uterus, hormone effects
Abnormal renal tract - vesicle-ureteric reflux in children, indwelling catheter
Impaired host defence - DM, immunosuppression

211
Q

What is the most common bacterium causing a UTI

A

Coliforms (found in colon)
E. coli
Gram negative

Then: Proteus -> Enterococci

212
Q

Why is E. coli so good at causing UTIs?

A

Flagellar, pili - help move and stick
Capsule polysaccharide - colonisation
Haemolysin, toxins - damage host defence and membranes

213
Q

What are 7 symptoms and signs of cystitis?

A 
Dysuria
Cloudy urine
Nocturia/ increased frequency
Urgency
Suprapubic tenderness
Haematuria
Pyrexia
214
Q

What are 3 signs and symptoms of pyelonephritis (excluding cystitis signs and symptoms)?

A

High fever +/- rigors
Loin pain and tenderness
N+V
+/- symptoms of cystitis

215
Q

Define uncomplicated UTI

A

Infection by a usual organism in a patient with a normal urinary tract and normal urinary function

216
Q

Define complicated UTI

A

≥1 factor that predisposes to persistent infection, recurrent infection or treatment failure:

  • Abnormal urinary tract
  • Virulent organism
  • Impaired host defence
  • Impaired renal function
217
Q

What investigations would be done for a patient presenting with a complicated UTI?

A

Urine culture
MSU - mid-stream urine collection
Urine dipstick - leucocyte esterase, nitrites, blood, pH, protein

218
Q

Why are urine dipsticks not useful in >65yrs?

A

Asymptomatic infection is common in upto half of the population

219
Q

What is sterile pyuria?

A

Raised white cells in the urine but no growth of bacteria

220
Q

What could cause sterile pyuria?

A 
Prior antibiotics
Urethritis (chlamydia/ gonococci)
Vaginal infection/ inflammation
TB
Appendicitis
221
Q

What is asymptomatic bacteriuria?

A

Significant levels of bacteria in urine with UTI symptoms
High prevalence in elderly, indwelling catheters
Screened for and treated only in pregnancy

222
Q

What is the treatment of UTIs?

A 
Increase fluid intake
Regular analgesia
Address underlying disorders
3 day course for uncomplicated UTI
5-7 day course for complicated lower UTI
223
Q

What medications can be used to treat simple cystitis?

A 
Nitrofurantoin
Trimethoprim
Pivmecillinam
Fosfomycin
Treatment duration = 3 days
224
Q

What medications can be used to treat complicated lower UTI?

A 
Nitrofurantoin
Trimethoprim
Pivmecillinam
Fosfomycin
Cefalexin 
Treatment duration = 5-7 day course
225
Q

What medications would be used to treat pyelonephritis?

A

IV ABx - co-amoxiclav, ciprofloxacin, gentamicin

Treatment duration = 7-10days

226
Q

When would UTI prophylaxis be used?

A

No treatable underlying condition despite behavioural and personal hygiene measures
If ≥3 UTI episodes/ year

227
Q

What causes urolithiasis?

A 
Metabolic - secondary to hypercalcuria
UTI - proteus, pseudomonas, klebsiella
Diet - high in salt, obesity
Medication - furosemide
Genetic - primary hyperoxaluria, cystinuria
228
Q

How are urate stones treated?

A

Alkanisation

229
Q

Define CKD

A

Progressive loss of renal function over a period of months or years
Symptoms of worsening kidney function are unspecific

230
Q

Define AKI

A

A abrupt decrease in renal function within 48hours
If baseline serum Cr = ≥1.5 times baseline
OR
Urine volume <0.5ml/kg/hour for 6 hours
OR
Inc in serum Cr >26.5micromol/L within 48hours

231
Q

What are the CKD stages and renal functions?

A

CKD 1: eGFR >90 with proteinuria/haematuria
CKD 2: eGFR >60 with proteinuria/ haematuria
CKD 3: eGFR 30-60
CKD 4: eGFR 15-30
CKD 5: eGFR <15
End stage renal failure

232
Q

What are 6 causes of CKD?

A 
20% diabetes nephropathy
HTN
Glomerulonephritis
UTI
Polycystic kidney disease
Renal vascular disease
233
Q

What are the 3 stages of AKI?

A 
Stage 1: 
Serum creatinine 1.5-1.9x baseline OR
Urine output <0.5ml/kg/hour for 6 hours
Stage 2:
Serum creatinine 2.0-2.9x baseline OR
Urine output <0.5ml/kg/hour for ≥12 hours
Stage 3:
Serum creatinine 3.0x baseline OR
Urine output <0.3ml/kg/hour for ≥24hours or Anuria ≥12hours
234
Q

What are AKI causes split up into?

A

Pre-renal
Renal
Post-renal

235
Q

What are renal causes of AKI?

A 
Drugs: antibiotics, NSAIDs, ACE-I
Sepsis
Rhabomyolysis
Myeloma
Tubulointersitital disease
GN
236
Q

What are pre-renal causes of Aki?

A

Renal artery stenosis

Hypoperfusion: Septic shock, hypovolaemic shock, cardiogenic shock

237
Q

How do you treat AKI?

A

Fluid replacement
Dialysis
Electrolyte replacement/ management

238
Q

What is adult polycystic kidney disease?

A

Autosomal dominant condition
Mutation in polycystic kidney disease gene
Cysts grow with age - present in adulthood
Diagnosed with ultrasound

239
Q

In adult polycystic kidney disease what are secondary complications?

A 
Pain
Bleeding into cyst
Infection
Renal stones
HTN
240
Q

How do you treat adult polycystic kidney disease?

A

Inhibit RAAS
Diet - drink plenty of fluid, low salt, normal protein
Tolvaptan
Somatostatin analogues

241
Q

What blood tests would be helpful in CKD management?

A

U+Es, Bone biochemistry, LFT, FBC, CRP
+/- iron levels (ferritin, iron, reticulocyte Hb)
+/- PTH

242
Q

What blood tests would be helpful in diagnosing the cause of CKD?

A

Auto-antibody screen (auto-immune)
Complement levels (auto-immune)
Anti-neutrophil cytoplasmic antibody (vasculitis)
Serum immunoglobulin screen (myeloma)
Protein electrophoresis and serum free light chain measurement (myeloma)

243
Q

How do you manage CKD?

A

Modifiable risk factors

Control DM, HTN, Proteinuria (with ACE-I), Lipids

244
Q

How does CKD effect water/ salt handling by the kidneys?

A

Lose ability to maximally dilute and concentrate urine
Small glomerular filtrate but same solute load causes osmotic diuresis
Low volume of filtrate reduces maximum ability to excrete urine therefore maximum urine volume is much smaller

245
Q

How do you treat acidosis in CKD?

A

Sodium bicarbonate capsules

246
Q

How do you treat anaemia in CKD?

A

Hb low -> Iron levels first -> replace if low -> Hb recheck -> if low start Epo

247
Q

How do you manage CKD- bone mineral density?

A

Reduce phosphate intake
Phosphate binders
Vit D

248
Q

In the prostate where are most cancers found?

A

Peripheral zone

249
Q

What are the main risk factors for prostate cancers?

A

Older age
FMHx - 4x risk. BRCA2 gene mutation
Ethnicity - Black>white>asian

250
Q

What are some issues with PSA screening?

A

Over diagnosis -> over treatment
Quality of life would be reduced
Cost-effectiveness

251
Q

Apart from prostate cancer what are reasons for a raised PSA?

A

Urinary Infection
Prostate inflammation
Large prostate
Urinary retention

252
Q

What are common presentations of prostate cancer?

A 
Urinary symptoms
Bone pain
PSA checked -> biopsied
DRE for another reason
Incidental finding at transurethral resection of prostate for urinary retention/ urinary symptoms
253
Q

What is the tumour staging of the prostate?

A

T1 - local in peripheral zone
T2 - local in peripheral zone but much larger than T1 and also starting to affect the outer margins of the prostate
T3 - locally advanced -> very nodular and also spreading to local sites i.e. seminal vesicles etc.
T4 - Advanced - spread to more than the urinary system e.g. bone, colon and having a mass effect

254
Q

What is the scoring system for prostate cancers?

A

Gleason score
Score from 1-5 given to the type of cells in the largest area
Score from 1-5 given to the type of cells in the second largest area
Scores tallied up and final score is the Gleason score
1 - healthier tissue 5 - most abnormal tissue
Score of ≥7 means risk of cancer likely

255
Q

What is the treatment for a locally advanced prostate cancer?

A

Surveillance
Hormones
Hormones + radiotherapy

256
Q

What is the treatment for a local prostate cancer?

A

Surveillance
Robotic radial prostatectomy
Radiotherapy - external beam, brachytherapy

257
Q

Where is a common place for prostate cancers to metastasise to and what type of met are they?

A

Bone

Bone mets are sclerotic

258
Q

What treatments are for metastatic prostate cancer?

A

Hormones (+/- chemotherapy):
Surgical castration
Medical castration - decrease testosterone enough to castration levels. -> LHRH agonists.
Palliation

259
Q

Where do TCC and RCC originate from?

A

TCC - Kidney + Ureter + Bladder + Urethra

RCC - Kidney parenchyma only

260
Q

How does RCC present?

A

Haematuria
Incidental finding on imaging - US/ CT
Rare - palpable mass

If advanced - Large varicocele may be present, PE, tumour embolus, loss of weight/ appetite, hyper calcaemia

261
Q

How does TCC present?

A

Haematuria
Incidental finding on imaging

If advanced - loss of weight, appetite
DVT
Lymphoedema

262
Q

What are the 3 classes of haematuria?

A

Visible
Dipstick
Microscopic

263
Q

What are differential diagnosis for haematuria?

A

Cancer - RCC, TCC, metastatic prostate carcinoma
Other - stones, infection, inflammation, BPH
Nephrological - glomerular cause

264
Q

What are risk factors for developing RCC?

A

Smoking
Obesity
Dialysis

265
Q

What are the 3 ways that RCC spreads?

A

Perinephric spread
Lymph node mets
IVC spread to right atrium

266
Q

How do you treat localised RCC?

A

Surveillance
Excision - radical/ partial
Ablation - cryoablation, radiofrequency

267
Q

How do you treat metastatic RCC?

A

Palliative - Tyrosine kinase inhibitors

268
Q

What is the most common type of bladder cancer?

A

TCC - 90%

269
Q

What are risk factors for bladder TCC?

A 
Smoking
Occupational exposure (20yr latent period) - rubber or plastic manufacture (arylamines), handling of carbon, crude oil, combustion, smelting (polyaromatic carbons),
Painters, mechanics, printers, hairdressers
270
Q

What are initial treatments of bladder TCC?

A

TURBT- TransUrethral Resection of Bladder Tumour

Local instillation of mitomycin C - local effects

271
Q

How is bladder TCC staged?

A

75%
Ta - into the bladder from the epithelium
T1 - epithelium + sub epithelial connective tissue
5%
Tis - Epithelium confined - carcinoma insitu
T2-4 = muscle-invasive

272
Q

What are risk factors for upper urinary tract TCC?

A

Smoking
Phenacetin abuse
Balkan’s nephropathy

273
Q

How do you investigate using imaging for upper urinary tract TCC?

A

Ultrasound - hydronephrosis
CT urogram - filling defect, ureteric stricture
Retrograde pyelogram
Ureteroscopy - biopsy, washings for cytology

274
Q

What are standard treatments for upper urinary tract TCC?

A

Nephro-ureterectomy

275
Q

How do you treat metastatic TCC?

A

Systemic chemotherapy - cisplatin based treatment

Biologics - programmed cell death receptor 1 drugs

276
Q

What can cause ureteric strictures?

A

Intraluminal - stones, sloughed off papilla, clots
Intramural - PUJ obstruction, TCC,
Benign - TB, surgery

277
Q

What can cause ureteric obstruction?

A

Extraluminal - retroperitoneal malignancy
Direct obstruction by a tumour - bladder cancer (obstruction at vesicoureteric junction), locally advanced prostate cancer
Retroperitoneal fibrosis

278
Q

What could cause an acute ureteric obstruction?

A

Calculus - stone
Blood clots
Sloughed papilla
Superadded infection-> pyonephritis or infected obstructed system

279
Q

What are problems with obstructive uropathy?

A

Renal impairment- bilateral ureteric obstruction, unilateral ureteric obstruction (solitary kidney), high pressure chronic retention

Post-renal AKI
Hyperkalaemia

280
Q

What is pyonephritis?

A

Infected, obstructed kidney - urological emergency

Failure to decompress - sepsis or permanent loss of renal function

281
Q

What are two causes of non-obstructive hydronephrosis?

A

Vesico-ureteric reflux

Pregnancy

282
Q

What imaging technique will be done to diagnose a upper urinary tract obstruction?

A

Diuretic renography with MAG3 = functional test

283
Q

What are options for treatment of an upper tract drainage?

A

JJ stent
Good for intraluminal not good for extraluminal
The JJ part - ring part - keeps it in place

Nephrostomy

284
Q

What is a clinical presentation of PUJ obstruction?

A

Loin pain
Worse after heavy fluid intake or alcohol
Definitive treatment is a pyeloplasty

285
Q

What are potential causes of retroperitoneal fibrosis

A 
Idiopathic
Malignant
Auto-immune
Drugs
AAA
286
Q

What are problems of infravesical obstruction?

A

Acute urinary retention - painful

Chronic urinary retention - high and low pressure - painless

287
Q

In urinary retention, what type of pain is felt and are patients still voiding?

A

Acute - painful, inability to void

Chronic - painless, may still be voiding

288
Q

What are causes of urinary retention?

A

Men: BPH, Prostate cancer

Both men and women: UTI, constipation, neurological dysfunction, recent surgery, drugs, urethral strictures, pelvic mass

289
Q

How do you treat acute urinary retention?

A 
Catheterise
Abdo, rectal, genital exam
Urine dip
Tx constipation
Alpha blocker
TWOC
TURP in Men
290
Q

What are problems with high and low pressure chronic urinary retention?

A

High - hydronephrosis - abnormal U+E’s

Low - no hydronephrosis - normal renal function

291
Q

How do you treat chronic urinary retention?

A

Catheterise
Urine dip
Bloods
Monitor for post-obstructive diuresis

292
Q

What is post-obstructive diuresis?

A

Physiological off-loading of accumulated salt and water during chronic retention
Excess/severe unloading - dehydration and electrolyte imbalane

293
Q

If the bladder is filling what is the neuronal reflex arc to store urine?

A

Bladder stretch -> detection by sensory afferent -> signals sent to CNS ->

(1) excitatory onto sympathetic pre-ganglionic neurone -> sympathetic postganglionic -> bladder wall (negatively stimulated) + EUS (positively stimulated)
(2) positive signal to parasympathetic neurone in CNS -> overall inhibitory signals to preganglionic parasympathetic neurone -> no signals sent to bladder to contract

294
Q

If the bladder is full what is the control arc of micturition?

A

Active conscious decision made to urinate -> M center in PONS ->

(1) Inhibitory signal to L (urination) centre in Pons -> (a) Less excitatory signal sent to pudendal nerve -> less innervation of EUS -> relaxation and increasing lumen of urethra. (b) inhibitory signal sent to sympathetic pre-ganglionic neurone -> less signals sent through postganglionic sympathetic neurone -> less inhibition of bladder to contract and less activation of the IUS to relax
(2) Excitatory signal to preganglionic parasympathetic nerve in CNS -> bladder wall -> postganglionic neurone bladder wall -> release of ACh on M3 receptors - bladder contraction

Sensory afferent in bladder wall -> preganglionic parasympathetic nerve in CNS -> bladder wall -> postganglionic neurone bladder wall -> release of ACh on M3 receptors -> bladder contraction

295
Q

If there is a spinal cord injury at the base of the spine in the L3-5 region what is the potential problem seen in bladder control and micturition?

A

Less inhibitory signals sent to the preganglionic parasympathetic nerve to the bladder. Small stretch will cause the parasympathetic to be over activated -> more ACh release onto bladder wall -> increase activity and contraction of bladder -> spinal micturition reflex over active

296
Q

If there is a spinal cord injury at the level of the sacral level S2-S4 (caudal equina) what could be the potential problem?

A

The sensory afferents to the parasympathetic nerve is not going to be received as the nerve is damaged -> no voiding via PNS. Excessive stretch signals sent to M centre -> sympathetic signals sent down to PNS preganglionic nerve -> no signals sent as this nerve is damaged -> no voiding

Medicine (15 decks)

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