RENAL Flashcards
1
Q
Vertebral levels of the kidney?
A
T12 to L3
2
Q
Order of renal blood flow from renal atery to renal vein?
A
Renal artery
Segmental artery
Interlobar
Arcuate
Cortical
Afferent
Glomerular capillaries
Efferent
Peritubular capillaries
Cortical
Arcuate
Interlobar
Renal vein
3
Q
Where do Loop, thiazide and spironolactone?
A
Loop - ascending loop
Thiazide - distal convoluted tubule
spironolactone - distal convoluted tubule and cortical collecting
4
Q
Layers of renal surfaces?
A
Renal fascia - attach
Adipose Capsule - shock
Renal Capsule-shape
5
Q
Glomerular filtration barrier?
A
Endothelium
Basement Membrane
Podocyte
6
Q
GFR calculation?
A
GFR = net ultrafilteration pressure X filtration rate
7
Q
Juxtaglomerular complex?
A
Juxtaglomerular cells - Renin - on the walls of afferent
Macula densa cells - Adenosine - DCT
Extraglomerular mesangial cells - supportive - macrophages and signalling
8
Q
Endocrine functions?
A
Renin
EPO
Vitamin D
9
Q
Autocrine function?
A
Prostaglandin
EPO
Renal natriuretic peptide
10
Q
Renal blood
A
P.RA - PRV / RESISTANCE IN ARTERIOLES
11
Q
Factors that increase arteriolar resistance and decrease blood flow?
A
Adrenaline
- Alpha 1 receptors on blood vessels
- Blood flow away from kidneys to vital organs
Angiotensin 2
- Binds to receptors of efferent and afferent arterioles constrictions
12
Q
Factors that decrease arteriolar resistance and increase blood flow?
A
ANP + BNP - Decrease cardiac workload
Prostaglandins E2, I2
Dopamine - binds to dopamine receptors - constricts capillaries of skin and muscle and dilates small vessels of the heart and kidney
13
Q
Autoregulation of the kidney?
A
- Myogenic mechanism - smooth muscle contracts when there is very high systemic pressure
- Tubularglomerula mechanism - Macula densa of DCT detect the high sodium and chloride so release adenosine to afferent arteriole to constrict (increase resistance and increase GFR)
14
Q
Measuring blood flow?
A
Fick principle - the amount of blood that flows into an organ is the same that flows out of an organ - if the organ doesn’t produce or breakdown products
Para-aminohippuric acid - used to measure renal blood flow
EFFECTIVE RENAL PLASMA FLOW = UPAH X URF / PLASMA CONC OF PAH FROM PERIPHERAL VEIN
RENAL BLOOD FLOW = RENAL PLASMA FLOW / 1 - HAEMATOCRIT
15
Q
Symptoms of renal disease?
A
Oliguria - low urine output over several hours (AKI and stones) - hypotension and hypovolaemia
Anuria - Exclude obstruction - no urine but strongly want to urinate - palpate mass and insert catheter/ Asses hypovolaemia - BP, JVP, Pulses and electrolytes / Management of AKI
Haematuria
Dysuria - Pain on micturition (Inflammation of urethra or bladder , LUTS, Inflammation of vagina or glans penis
Polyuria - DI or CKD
Nocturia - BPH
Pain - infection, stone cyctic renal disease
16
Q
Proteinuria?
A
Albumin >200mg/l due to increase permeability, decreased reabsorption, excess plasma proteins and physiological
17
Q
Microalbuminaemia?
A
Increase in urinary albumin undetectable by conventional methods
18
Q
Haematuria?
A
Blood in urine
Start - urethra
End- bladder or prostate
Throughout - above the bladder
19
Q
UM: white cells?
A
UTI
20
Q
UM: Sterile pyuria?
A
Pus cells without bacteria
UTI
21
Q
UM: red cells
A
Haematuria
22
Q
UM: Hyaline casts?
A
Precipitation of materials in renal tubules and they can also become incorporated in cells
23
Q
Muddy brown casts?
A
Acute tubular necrosis
24
Q
UM: Red cell casts?
A
Glomerulonephritis
25
UM: White cell casts?
Acute pyelonephritis
26
UM : Granular casts?
The disintegration of cellular debris
Chronic kidney disease
27
Ultrasonography?
Mass or cyst
28
Antegrade pyelography?
Identify the level of obstruction - pelvis, calyx + ureter
29
Retrograde pyelography?
Ureter to bladder - more invasive and risk of infection
30
2 types of renal scintigraphy?
measure perfusion and excretion - anatomical + functional abnormalities or kidneys and ureters
Dynamic - renal blood flow
Static - assess size and position of kidneys and parenchymal affects
31
What can cause bleeding of the urinary tract?
Bleeding disorder
Trauma
Cysts
Tuberculosis
Glomerulonephritis
Carcinoma
Infarct
Papillary necrosis
Stone
-------
Uteric neoplasm or stone
-------
Parasites
Infection
Stone
Carcinoma or papilloma
-------
Prostatic enlargement
-------
Urethral - trauma, infection or tumour
32
Glomerulonephritis?
Inflammation
33
Glomerulonephropathy?
The disease of the kidney without inflammation
34
Focal?
some of the glomeruli not all
35
Segmental?
A section of individual glomeruli
36
Diffuse?
\>75% / most of the glomeruli
37
Global?
All of the glomeruli involved
38
Proliferative?
Increase in cell numbers due to hyperplasia of 1 or more resident glomerular cells +/- inflammation
39
Membrane alteration?
Thickening of the capillary wall due to deposition of immune deposits in the BM
40
Crescent formation?
Epithelial cell proliferation with mononuclear cell infiltration in Bowmans space - rapidly progressive glomerulonephritis
41
Nephrotic syndrome?
Haematuria
Proteinuria
Hypoalbuminemia
Hyperlipidaemia - increase hepatic lipogenesis and decreased clearance
Lipidura
Oedema - decreased oncotic and osmotic pressure
42
Acute glomerulonephritis?
Abrupt onset of haematuria of haematuria with cysts, dystrophic red cells, non-nephrotic range proteinuria, oedema, hypertension and transient renal impairment
43
Rapidly progressive glomerulonephritis?
Features of acute nephritis
Focal necrosis
Crescent formation
Rapidly progressive renal failure over weeks
44
Asymptomatic haematuria or proteinuria?
Incidental finding on urine dipstick or early indicator of renal disease
45
Types of nephrotic syndrome?
Structural and functional abnormalities of podocytes which increases the filtration of macromolecules
- Membranous nephropathy
- Focal segmental glomerulosclerosis
- Minimal change disease
- IgA nephropathy
- Mesangial proliferative glomerulonephritis
- Good pasture
- Post-strep glomerulonephritis
46
Membranous glomeronephropathy?
Subepithelial deposits which also activate the alternate complement pathways - damage of podocyts and mesangium
47
Antibodies found in membranous glomerulonephropathy?
AUTOANTIBODIES TO GBM -
**M type phospholipase A2 receptor**
**Neutral endopeptidase**
COMPLEXES OUTSIDE OF KIDNEY THAT GET DEPOSITED -
**Cationic bovine serum albumin**
48
EM and immunofluorescence of membranous glomerulonephropathies?
EM - spike and dome + effacement of podocytes
IM - granular casts
49
Management of membranous glomerulonephropathy?
Idiopathic - steroids
Secondary - treat underlying disease or infection or drugs
50
Focal segmental glomeruloscelrosis (FSG)?
Segmental sclerosis and hyalinosis
**Primary** - podocytes are damaged and allow proteins and lipids to be filtered out - trapped in glomeruli = hyalinosis which leads to sclerosis
believed to be a continuation of minimal change disease
**Secondary** - sickle cell, HIV, heparin or renal hyperperfusion
51
Histo, EM and IM of FSG?
**Histo** - segmental sclerosis and hyalinsis
**EM** - podocyte effacement
**IM** - non-specific focal deposits of IgM and complement
52
Minimal change disease?
mostly affects children - a common cause of nephrotic syndrome in boys
Damage to the podocytes which leads to **selective proteinuria** without haematuria - T cells release cytokines that damage the for processes of podocytes
EM - podocytes effacement
IM - No immunoglobulins
Treated with corticosteroids
53
Type 1 mesangial proliferative glomerulonephritis?
1a - Circulating immune complexes due to chronic infection deposit in glomeruli and activate complement
1b - inappropriate activation of the alternate complement pathway by a nephritic factor (IgG that stabilized C3 convertase)
- Deposit in **subendothelial space -** inflammation of the wall and it thickens - mesangial interposition through the BM = **tram track appearance on LM and granular appearance on IM**
54
Type 2 mesangial proliferative glomerulonephritis?
Dense deposit disease
Only complement deposits in the basement membrane (nephritic factor) - causing inflammation and decreased C3
55
Type 3 mesangial proliferative glomerulonephritis?
Immune complexes and complement in subendothelial and subepithelial space
56
IgA nephropathy (berger's syndrome)?
**Galactose deficient IgA** and **anti-glycan IgA antibodies** form complexes - get trapped in the mesangium and causes activation of complement pathway and inflammation
57
IgA nephropathy clinical features?
present in childhood or during infection of the mucosal lining
Increase galactose deficient IgA and anti-glycan IgG
Hypertension
58
IgA nephropathy management?
Control BP
Prevent immune complexes - corticosteroids
59
Good pasture syndrome?
Haematuria and Haemoptosis
Autoantibodies to alpha 3 chain of type 4 collagen - once they nine to type 3 they activate complement (type 2 ) - which attracts neutrophils which release enzymes that increase free O2 radicals that damage BM, endothelium and the organ
60
Risk factors of good pastures syndrome?
**HLA-DR5**
**The environmental damage** that exposes alpha 3 chain - infection, smoking, hydrocarbon-based solvents, oxidative stress
61
Investigations and management of good pastures syndrome?
Kidney biposy - inflammation of BM
Immunofluorescence - anti-BM autoantibodies
Management - corticosteroids, immunosuppressants or plasmapheresis (filter plasma)
62
Post-strep glomerulonephritis?
Caused by Lancefield A beta-haemolytic streptococci - specific antigens, streptolysin (RBC) and nephritogenic - **M protein virulence factor**
Immune deposits in the subendothelial space and GBM - activate complement and inflammation
63
Clinical features of post-strep glomerulonephritis?
Haematuria + proteinuria - dark cola urine
Oliguria
Fluid retention - peripheral and periorbital oedema
Inflammation
64
Investigations and management of post-strep glomerulonephritis?
**LM** - enlarged and hypercellular glomeruli
**EM** - subepithelial deposition
**IM** - stary sky and granular appearance
**Blood** - decreased C3 and anti-DNaseB (antigen against step)
**Management** - supportive but some children - renal failure and 1/4 of adults rapidly progressive glomerulonephritis
65
Acute glomerular nephritis?
Bacterial antigens become trapped in the glomeruli resulting in inflammation
Haematuria, proteinuria, Hypertension oedema, oliguria and uraemia
**Investigations** - Baseline (GFR, Urinary proteins, Serum albumin, U+E), Culture, Urine microscopy, Serum antibodies, Cryoglobulins
**Management** - Supportive management, monitor fluid balance, fluid restriction if oliguric and immunosuppressants if SLE or vasculitis
66
What can cause rapidly progressive glomerulonephritis?
Acute nephrotic syndrome
Good pasture
Anti-neutrophilic cytoplasmic antibodies - vasculitis
67
Pathogenesis of UTI?
Bacteria from patients own bowel flora travels up the urethra - E.coli is the biggest baddie
68
Risk factors of UTI?
Post menopausal women
Sexual activity
Catheter or instruments of urinary tract
UT stones or stasis
DM or immunosuppressants
69
Clinical features of LUTS?
Frequency, urgency, dysuria - smelly urine, tenderness and even haematuria
70
Clinical features of acute pyelonephritis?
Loin pain, tenderness, vomiting and fever
71
Investigations to confirm UTI?
- History of infection or UT instrument use
- Dysuria, frequency or urgency
- culture of midstream urine + sterile pyuria
- Dipstick - leukocyte elastase and nitrites
Renal imagining or CT needed for recurrent infection or if symptoms persist after medication
72
Management of UTI?
Trimethoprim- Sulfamethoxazole - Nitrofurantoin
Amoxicilin - Trimethoprim - Cephalosporin
singe shot
Lots of fluid
IV antibiotics
First time acutely ill - renal ultrasound
73
single shot management of UTI?
Amoxicillin or co-trimethoprim
Bladder symptoms lasting more than 36 hours
74
Difference between relapse and Reinfection UTI?
Relapse - same organisms bacturia within 7 days of treatment - associated with renal tract abnormality
Reinfection - same or different organisms 2 weeks after stopping treatment
75
Acute pyelonephritis?
Neutrophil infiltration in the parenchyma - small cortical abscess and streaks of pus in the medulla - acute deterioration of the kidneys
76
Difference between acute and chronic tubulointerstitial nephritis?
Both are injury to renal tubules and interstitium that results in decreased renal function
**ACUTE** - cellular infiltrate and variable tubular necrosis
allergic drug reaction of penicillin family or NSAIDS - fever, eosinophilia and mild proteinuria
**CHRONIC** - prolonged use of analgesics - tubular damage to the medullary area so difficulty concentrating urine - polyuria, proteinuria and uraemia
77
Accelerated hypertension?
Fibrinoid necrosis in afferent arterioles and fibrin deposits in arteriole walls causing hypertension
Increase arteriolar lesions - renal damage - increased renin released - increase BP - progressive uraemia
78
What can cause renal artery stenosis?
Atheroma
PVD or CAD
Fibromuscular hyperplasia
All-cause decreased renal perfusion causing ischaemia
79
Most common causes of urinary tract obstruction?
Prostatic enlargement
Caliculi
Gynae tumour
80
Hydronephrosis?
Dilation of renal pelvis - compression and thinning of renal parenchyma and decreased size of the kidney
81
Clinical features of UT obstruction?
Dull ache pain in flank or loin made worse by increase urine volume
Anuria or polyuria (full or partial obstruction that may have caused tubular damage)
Obstruction of bladder outlet - hesitancy, poor stream, dribble, incomplete emptying -- urinary retention
82
Investigations of UT obstructions?
Pelvic exam or rectal exam
Ultrasound and excretion urography
Radionuclide studies - long standing obstruction
Retrograde and anterograde pyelography
83
Management of UT obstruction?
Surgery
Insert catheter
Stent
Management of prostatic enarlgement, cancer or caliculi
84
Pathophysiology of kidney stones?
supersaturation of solutes - precipitate out and forms nidus which crystallises and causes obstruction of the urinary tract
85
What inhibits crystallisation of kidney stones?
Magnesium
Citrate
86
Calcium oxalate?
Black/ dark brown
Radiopaque
Acidic urine
87
Calcium phosphate?
Dirty white
Radiopaque
Alkaline urine - renal tubular acidosis causes failure to reabsorb bicarbonate
88
Uric acid stones?
Red/ Brown
Radiolucent
Monosodium urate crystals associated with gout
89
Struvite stones?
Dirty white
Radiopaque
Magnesium, ammonium and phosphate
Bacteria causes urea to break apart into CO2 and ammonia causing urine to be more alkaline
Staghorn crystals - branch out of different calyx
90
Bacteria associated with struvite stones?
Klebsiella
Proteus Mirabilis
Pseudomonas
91
Cystine stones?
Yellow/ pink stones
Excessive excretion of cystine
Radiopaque
92
Xanthine stone?
Red/ Brown
Excessive purine breakdown
Radiolucent
93
Clinical features of kidney stones?
Dull, localised flank pain
Renal colic - sharp and consistent pain that lasts hours
Haematuria
UTI
Urinary infrequency
Outflow obstruction
Painful bladder distention
94
Management of renal stones?
\<5mm - pass through urine
High fluid intake
Pain relief
Reduce stone formation - potassium citrate
Help stone pass - Alpha-adrenergic receptor or a calcium channel blocker
Shockwave lithotripsy - high-intensity acoustic pulses to break apart the stone
Surgery for massive stones
95
Management of uric acid or Xanthine stones?
Allopurinol - makes more soluble hypoxanthine and inhibits xanthine oxidase
96
Management of cystine stones?
V high water intake
D penicillamine - chelates cysteine forming a more soluble complex
97
Causes of hyperoxaluria?
Genetic defect causing increased oxalate excretion
Increase oxalate containing food - rhubarb, spinach, nuts
Decreased calcium
98
AKI?
Abrupt disruption in renal function over hours or days which is seen by decreased urine output and increased serum urea and creatinine
99
Criteria used to indicate the degree of renal damage and have a predictive value of mortality?
RIF (U+C) LE
Risk
Injury
Failure
Loss \> 4 weeks
End-stage renal failure \> 3 months
100
Causes of pre-renal, renal and post-renal AKI?
Pre-renal - Hypovolaemia, hypotension, low CO, NSAIDs or ACEi
Renal - Acute tubular necrosis, acute tubulointerstitial nephritis or pyelonephritis
Post-renal - obstruction
101
Clinical features of AKI?
Oliguria
Biochem - Increase K, Decrease Na, Ca and phosphate - metabolic acidosis
symptoms - weakness, fever, fatigue, nausea, confusion, pruritus and bruising
Breathless - anaemia and pulmonary oedema
Impaired platelet function
Inffection
102
Investigations of uraemic emergency?
1. Acute or chronic
2. Degree of renal damage - Urea and creatine and urine output
3. Pre-renal, renal or post-renal
103
Investigations of AKI?
Blood - Anaemia and increased ESR
Urine and blood cultures
Urine dipstick and microscopy - red cell casts, haematuria and proteinuria
Urinary and serum electrolytes
Renal ultrasound - mass or obstruction?
CT - renal scarring
Histology
Serum antibodies
104
Management of AKI?
Optomise fluid balance and volume expansion
Monitor weight, fluid and bP
Remove nephrotoxins
EMERGENCY - prevent high potassium and pulmonary oedema, prevent further renal damage, consult nephrologist and adjust dose of drugs
105
Management of hyperkalaemia?
Calcium gluconate
Salbutamol
Insulin
106
CKD?
GFR \<90ml/min/1.7m2 for greater than 3 months
107
Causes of CKD?
**Hypertension** - ischaemia injury due to walls of arterioles becoming thicker = **TGFB1** causes mesangial cells to go back to mesangioblasts - secrete more extracellular matrix = **GLOMERULOSCELROSIS**
**Diabetes** - non-enzymatic glycations of the efferent arteriole - backflow and hyperfiltration - mesangial cells secrete more extracellular matrix - expanding the size of the glomerulus = **HYALINATERIOSCLEROSIS**
**Tubulointerstitial disease**
**Congenital kidney disease**
**UT obstruction**
**Systemic disease**
**Prolonged medication**
**Infection**
108
Clinical features of CKD?
**Azotemia** - Decreased appetite, nausea, encephalopathy (asterixis), pericarditis, bleeding because platelets don't stick as well, uremic frost (uric acid crystals in the skin)
**Electrolytes** - increased potassium and decreased sodium, calcium and phosphate
**Anaemia** - decreased EPO
**Hypertension** - increased renin
109
Investigations of CKD?
Changes in GFR over time \<90 and if really bad \<60
Renal biopsy - glomerulosclerosis
110
Management of CKD?
Renoprotective - good BP control and monitoring, ACEi or ARB, Diuretics and calcium channel blockers
Reduce cardiovascular risk - statins, no smoke, control diabetes, control bP
Decrease potassium - Dietary restriction, stop drugs that retain potassium, ion exchange resins so less potassium absorbed in the GI
Anaemia - recombinant EPO
Acidosis - sodium bicarbonate
111
ADPKD?
AD condition where multiple cysts develop on both kidneys causing an increase in size as the cysts fill up with fluid
Develop in both cortex and medulla and obstruct blood flow of neighbouring nephron which causing decreased blood flow and activates renin - hypertension
Also compresses collecting duct - urinary stasis
Also prone to getting cysts on other places of the body
112
Aetiology of ADPKD?
mutation of PKD1 or PKD2 - polycystin protein of tubules and vasculature - abnormal sp they don't allow calcium to enter so water flows in and you get uncontrolled cell proliferation
113
Clinical features of ADPKD?
Hypertension
Acute loin pain
Abdo discomfort
Progressive renal impairment
Liver cyst
Subarachnoid haemorrhage
Mitral valve prolapse
114
Investigations of ADPKD?
Hypertension
Enlarged kidneys
Family history
Maybe hepatomegaly
115
Management of ADPKD?
Nothing can slow down progression
Monitor BP and serum creatinine
Dialysis or transplant
Children given early ultrasonography
116
ARPKD?
mostly in infancy
mutation of PKHD1 - fibrocystin which is associated with polysytin - renal failure before birth
OLIGOHYDROAMNIOS - decreased urine in the amniotic fluid which leads to potters sequence - uterine walls crush the baby and cause deformities - respiratory insufficiency
Also prone to congenital hepatic fibrosis - portal hypertension and it affects the intrahepatic ducts and common bile duct
117
Medullary sponge kidney?
Dilated collecting ducts and cysts on the collecting ducts
Congenital abnormality of the induction of the urteric bud and metanephric blastoma
Increased excretion of calcium, phosphate and oxalate = nephrolithiasis
increased risk of UTI and infection
Metabolic acidosis
118
Symptoms of medullary sponge?
Stones - pain and haematuria
UTI - fever and pain
119
Investigations of Medullary sponge?
Intravenous pyelogram - dilated collecting ducts and cysts
Excretion urography
120
Management of medullary sponge?
Prevent stones - stay hydrated, citrate or bicarbonate supplements to stop calcium leaving the bone
Small stones - pass or shockwave lithotripsy
infection - antibiotics
121
Horseshoe kidney?
Fusion of the inferior poles of the kidney - they end up low in the abdomen due to getting caught by the IMA
either by mechanical fusion or teratogenic cause - posterior nephrogenic cells migrate to the inferior poles can cause a parenchymal isthmus
More predisposed - hydronephrosis, stones, infection, chromosomal disorders, kidney cancer
122
PSA?
Prostate-specific antigen is a glycoprotein expressed by normal or neoplastic prostatic tissue and is detected in blood
123
Factors that can increase Exercise PSA?
BPH
Carcinoma
Mechanical manipulation of prostate
124
Which zone of the prostate increases the most in BPH?
Transitional zone
125
Clinical features of BPH?
Frequency
Nocturia
Hesitancy
Dribble
Urinary retention
Smooth lump on rectal exam
126
Investigations of BPH?
Serum PSA
Prostate biopsy
Rectal exam
Ultrasonography to rule out renal disease
127
Management of BPH?
**Tamsulosin** - relaxes bladder neck and prostate (selective alpha adrenoreceptor antagonist) - increase urine flow and decrease obstructive symptoms
**Finasteride** - 5 alpha-reductase inhibitor - inhibits the conversion of testosterone to dihydrotestosterone
**Urethral catheterization**
**Prostatectomy or permanent catheter**
128
Clinical features of prostatic cancer?
Hard irregular prostate - peripheral zone
PSA
Bladder outflow obstruction
Bone meets
129
Investigations of prostate cancer?
Transrectal ultrasound
Transrectal prostate biopsy
Serum PSA \> 16
Endorectal coil - stage
130
Management of prostatic carcinoma?
Watch and wait
Radical prostatectomy
Remove androgenic drive - orchidectomy, synthetic LH or antiandrogens
131
Testicular tumours?
Most common in younger men
Seminoma or Teratoma
CF: Painless lump on testes, lung mets (cough and dyspnoea) and para-aortic lymph nodules (back pain)
Investigations - ultrasound, serum tumour markers, CXR, CT
132
Serum tumour markers of testicular cancer?
Alpha-fetoprotein (AFP)
Beta subunit of human chorionic gonadotropin (B-HCG)
Teratoma - both high
Seminoma - Only B-HCG is high
133
Management of testicular tumour?
Orchidectomy
Radiotherapy - seminoma that mets below the diaphragm
Chemo - widespread teratoma
offer sperm banking to these people before treatment is started
134
Where do most kidney cancers arise?
Proximal tubular epithelium
135
Clinical features of kidney cancer?
Haematuria
Loin pain
Mass on flank
Fever, malaise and weight loss
Left scrotal varicocies
Mets - bone, liver and lung
136
Investigations of kidney cancer?
Ultrasonography
CT
MRI
137
Management of renal cancer?
Local - radical or partial nephrectomy or ablasive technique
meets - IL2 or interferon, **Termsirlimus** - inhibit vascular endothelial growth factor and mTOR
138
Urothelial tumours?
Bladder is the most common of urothelial tumours
RF: smoking, indi=ustrial chemicals, drugs and chronic inflammation
CF: painless haematuria and symptoms of UTI with not bacteria
Anyone over 40 years old with haematuria has a urethral tumour until proven otherwise
Management: Nephrouterectomy
Bladder - local diathermy, cystoscope resection, bladder resection, radio or chemo
139
2 factors that ensure continence?
Low intravesical pressure - a stretch of bladder wall and stability of detrusor
Sphincter mechanism
140
Types of incontinence?
**Stress** - post-prostatectomy or childbirth or urethral atrophy (cough, laugh or stand up)
**Urge** - strong desire to void but the patient can't hold in urine (Detrusor spasms, bladder retaining urine and bladder hypersensitivity)
**Overflow** - caused by an obstruction (leaks and distended bladder)
**Neurogenic** - Brainstem damage (incoordination of sphincter or detrusor), Reduced outflow pressure (alpha-adrenergic blockers) or autonomic neuropathy (distended atonic bladder, diabetes or decreased excitability of detrusor)
**Elderly** - immobile, dementia (antisocial incontinence), Diuretics
