Genitourinary COPY Flashcards

1
Q

What are the major functions of the Kidney?

A
  • Filter or secrete waste/excess substances
  • Retain albumin and circulating cells
  • Reabsorb glucose, amino acids and bicarbonates (Acid-base regulation)
  • Control BP, fluid status and electrolytes
  • Activates 25-hydroxy vitamin D (by hydroxylating it to form 1,25 dihydroxy
    vitamin D)
  • Synthesis erythropoietin
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2
Q

Explain the Renal Blood Flow

A

Renal artery 🡪 interlobar artery 🡪 arcuate artery 🡪 interlobular artery 🡪 afferent arteriole 🡪 glomerular capillary 🡪 efferent arteriole 🡪 peritubular capillary around tubules

The peritubular artery is important in that secretion and reabsorption to/from filtrate is often active and requires energy and oxygen. Therefore, blood supply is crucial.

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3
Q

What is the Glomerular Filtrate rate?

A

The volume of fluid filtered from the glomeruli into Bowman’s space per unit
time (minutes)

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4
Q

Why is Creatinine a good marker for GFR?

A

Creatinine used as a marker of GFR because:
Freely filtered
Not metabolised
Not secreted
Not reabsorbed

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5
Q

What factors favour and oppose filtration in the glomerulus?

A

Favouring filtration = hydrostatic pressure from glomerular capillary

Opposing filtration = hydrostatic pressure from Bowman’s capsule and oncotic pressure from glomerular capillaries

Forward action favoured – so hydrostatic pressure from the glomerular capillary is the biggest

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6
Q

What is the normal GFR?

A

120ml/min

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7
Q

What mechanisms control renal perfusion and function?

A

Autoregulation:
Increase blood flow in afferent arteriole 🡪 stretch of wall 🡪 smooth muscle contract 🡪 arteriolar constriction
Systemic circulation BP doesn’t affect renal circulation

Tubuloglomerular feedback:
Macula densa (in DCT) detect levels of NaCl
Low levels of NaCl🡪 release prostaglandins 🡪 granular cells release renin which activates RAAS system
High levels of NaCl 🡪 sends signal to afferent arteriole causing vasoconstriction which will decrease GFR and lower BP

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8
Q

Give an example of a Loop Diuretic, its MOA and Side effects?

A

Furosemide:
Moa - Ascending limb, inhibits NKCl2 transporter

SE - Dehydration, hypotension, hypokalaemia, metabolic alkalosis (can cause ototoxicity)

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9
Q

Give an example of a K+ sparring Diuretic, its MOA and SE?

A

Amiloride/Spironolactone:
MOA - Act on DCT, inhibit ENaC channels to reduce sodium reuptake and therefore water

SE - GI upset, HYPERkalaemia, metabolic acidosis, gynaecomastia

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10
Q

Give an Example of a Thiazide Diuretic, its MOA and SE?

A

Bendroflumethiazide
MOA - Act on Na/Cl transporter in DCT

SE - HYPOkalaemia, Metabolic alkalosis, Hypovolaemia, Hyponatraemia, Hyperglycaemia in DM

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11
Q

What is Nephrolithiasis?

A

Renal Stones (calculi) commonly made from Calcium Oxalate (90%) which form in the CD and can be deposited anywhere from the renal pelvis to the urethra.

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12
Q

What are some other types of renal stone compared to calcium oxalate?

A

Calcium phosphate/oxalate (80%)
Uric Acid (10%)
Cysteine Stones
Struvite (infection often from proteus)

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13
Q

What are the 3 main narrowing’s where renal stones may be found?

A
  • Pelviureteric junction (PUJ)
  • Pelvic brim
  • Vesicoureteric junction (VUJ)
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14
Q

What is the epidemiology of Renal Stones?

A

10-15% lifetime risk
More common in males
Peak age 20-40 yrs
Increasing Incidence

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15
Q

What are the risk factors for renal stones?

A

Anatomical abnormalities
Hypercalciuria
Hypercalcaemia
Hyperparathyroidism
Family history / PMHx of Renal Stones
Hypertension
Gout
Immobilisation
Dehydration
Low urine output
Primary kidney disease

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16
Q

What are the main causes for renal stones?

A

Anatomical:
Congenital - horseshoe kidney
Acquired - Obstruction, trauma, reflux

Urinary Factors:
Metastable urine
Increased Calcium oxalate, urate, cystine
Infection induced - Proteus leads to Struvite stones
Dehydration

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17
Q

What is the pathophysiology of renal stones?

A

Excess solute in the collecting duct

Supersaturated urine - favours crystallisation

Stones cause regular outflow obstruction - lead to hydronephrosis

Subsequent dilation of the renal pelvis will lead to lasting kidney damage

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18
Q

What are the 2 key complications of renal stones?

A

Obstruction - leading to AKI

Infection - causing obstructive pyelonephritis

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19
Q

What is the presentation of Renal Stones?

A

Maybe ASx and never cause issue

Renal colic is presenting complaint in Symptomatic kidney stones:

Loin to groin pain that is colicky (peristaltic waves leading to fluctuations in severity)

LUTS symptoms (dysuria, strangury Urgency, Frequency)

Px cant lie still

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20
Q

What are the signs of renal stones?

A

Features of acute pyelonephritis or gram-negative septicaemia if there is infection associated in an obstructed urinary system

Bladder stones – urinary frequency and haematuria

Urethral stones – cause bladder outflow obstruction, resulting in anuria and painful bladder distension

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21
Q

What is Colicky Pain?

A

Pain that fluctuates in severity often due to peristalsis causing contaction of gallstones/renal stones which then settles when the contraction stops

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22
Q

What are the symptoms of Renal Colic?

A

Loin to groin pain
Px cannot lie still

Haematuria/dysuria
Nausea or vomiting
Reduced urine output (LUTS)
Symptoms of sepsis, if infection is present

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23
Q

What are the primary investigations for Renal stones?

A

1st Line - KUB (kidney, Ureter, Bladder) XR - 80% specific

Gold Standard - NCCT (non-contrast CT) KUB - 99% specific (diagnostic)

Bloods:
FBC
U&Es - raised creatinine in AKI

Urinalysis -Microscopic haematouria

Pregnancy test

Urine dipstick - UTI

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24
Q

What investigation would be used for hydronephrosis from a suspected renal stone for a Px who is pregnant?

A

Ultrasound as they cannot have CT

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25
How can a kidney be drained if infected?
Ureteric stent Nephrostomy
26
What is the Treatment for Ureteric Stones?
Sx management: Strong Analgesic - IV/PR Diclofenac for severe pain (opiates in poor renal function Px) Hydrate - oral or IV Anti-emetics - Metoclopramide (admit to hospital if signs of shock) Abx if infection present: Cefuroxime / IV Gentamicin Conservative - Stones normally pass spontaneously if small enough (<5mm) ESWL - Stones < 1cm Ureteroscopy
27
What is the Treatment for Kidney Stones?
Sx management: Strong Analgesic - IV/PR Diclofenac for severe pain (opiates in poor renal function Px) Hydrate - oral or IV Anti-emetics - Metoclopramide (admit to hospital if signs of shock) Abx if infection present: Cefuroxime / IV Gentamicin Extracorpeal Shock Wave Lithotripsy (ESWL) - stones 1-2cm Surgical Ureteroscopy Percutaneous Nephrolithotomy - good for larger stones Nephrectomy - if split function <10-15%
28
What is a key complication of kidney stones?
Pyonephrosis - Pus filled fluid caused by infection and obstruction together. - Tx with septic six Hydronephrosis Abscess/fistulae Xanthogranulomatous Pyelonephritis
29
What Treatment is used if a stone is too large to pass spontaneously?
ESWL: Extracorporeal shockwave lithotripsy - ultrasound that fragments the stones (does not clear the stone so Px still has to pass stone) Ureteroscopy - laser PCNL: Percutaneous nephrolithotomy - keyhole surgery to remove large/complex stones Nephrectomy - if kidney contributes to less than 15% renal function
30
What is a big issue once you have had one renal stone?
Recurrence is very common and therefore take steps to prevent it: Overhydration Low Ca dietary intake Low sodium diet Reduce BMI Active lifestyle Potassium Citrate and Thiazide diuretics may also help
31
What are some differential Diagnoses for Loin pain other than Renal Colic?
Vascular accident - Ruptured AAA Bowel Pathology - diverticulitis, appendicitis Gynae - Ectopic pregnancy Pyelonephritis Pancreatitis Testicular torsion MSK pain
32
What is the treatment for bladder stones?
Conservative - asymptomatic Endoscopic + Bladder Outlet Obstruction (BOO) Tx Open Laparoscopic surgery - for large stones
33
What is Acute Kidney Injury (AKI)?
Abrupt decline in kidney function that occurs within hrs to days due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis. It is usually (but not always) reversible.
34
What is the mortality rate for AKI?
25-30%
35
What are the NICE criteria for AKI
Rise in creatinine of ≥ 26 micromol/L in 48 hours Rise in creatinine of ≥ 50% in 7 days Urine output of < 0.5ml/kg/hour for > 6 hours
36
What is stage 1 AKI?
Increase Serum Creatinine by 1.5-1.9x Baseline Decrease Urine output <0.5mg/kg/hr for 6-12hrs
37
What is Stage 2 AKI?
Increase Serum Creatinine by 2-2.9x Baseline Decrease Urine output <0.5mg/kg/hr for >12hrs
38
What is Stage 3 AKI?
Increase Serum Creatinine by 3x Baseline Decrease Urine output <3.5mg/kg/hr for >12hrs or during RRT Anuria for >12 hours
39
What system is used to classify the stage of AKI?
KDIGO: Rise in creatinine of ≥ 26 micromol/L in 48 hours Rise in creatinine of ≥ 50% in 7 days Urine output of < 0.5ml/kg/hour for > 6 hours
40
What is the old staging classification system for AKI?
RIFLE: * Risk * Injury * Failure * Loss * End-stage renal disease
41
What is the epidemiology of AKI?
Common - affects 15% of all hospital admissions 25% of Px with sepsis and 50% of Px with septic shock will have AKI Common in elderly
42
What is AKI associated with?
Associated with Diarrhoea Haematuria Haemoptysis Hypotension Urine retention
43
What are the risk factors for AKI?
Age - >75 years Diabetes Mellitus Sepsis Peripheral vascular disease Family history Nephrotoxic Drugs Poor fluid intake/fluid loss Liver disease Organ failure - HF
44
What are the different groups of causes of AKI?
Pre-renal (most common) - due to inadequate blood supply reaching the kidneys reducing filtration of blood. Renal - where there is intrinsic disease within the kidney that leads to the reduced filtration of blood Post renal - caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy
45
What are the commonest causes of AKI?
Cardiogenic shock Major Surgery Nephrotoxins Sepsis
46
Give some Pre-renal causes of AKI?
Dehydration Hypotension (shock, Sepsis, Anaphylaxis) Heart failure
47
Give some Renal Causes of AKI?
Glomerulonephritis Interstitial nephritis - T1 or T IV hypersensitivity to NSAIDs, Penicillin's, Diuretics Acute tubular necrosis Nephrotoxic Drugs (DAMN)
48
What are the DAMN drugs that cause nephrotoxicity?
Diuretics ACEis/ARBs Metformin NSAIDs
49
Give some Post renal Causes of AKI?
Anything that causes obstruction to flow out of the kidney: Kidney stones Masses such as cancer in the abdomen or pelvis Ureter or uretral strictures Enlarged prostate or prostate cancer
50
Give some examples of drugs that are nephrotoxic
DAMN: Diuretics ACEi/ARBs/Aminoglycosides (gentamicin) Metformin/Methotrexate NSAIDs
51
What is the pathophysiology of AKI?
Impaired ability of the kidneys to filter the blood. This leads to accumulation of substances that are usually excreted Can lead to damage of the nephron and kidney
52
What substances will accumulate in AKI?
K+ - hyperkalaemia - arrythmias Urea - Hyperuraemia - Pruritis and confusion Fluid - oedema - pulmonary and peripheral H+ - acidosis
53
What are the symptoms of AKI?
Sx of underlying cause: Early stages often asymptomatic Oliguria – decreased urine output Anuria Dehydration Nausea and vomiting Confusion Fever (sepsis) Uraemia – weakness, tremor, fatigue, nausea, vomiting, mental confusion, seizures and coma Breathlessness – combination of anaemia and pulmonary oedema secondary to volume overload
54
What are some clinical signs of AKI?
Tachycardia Peripheral oedema Hypertension Poor tissue turgor Postural hypotension (dehydration) Fluid overload + ↑JVP, pulmonary oedema (CXR), Abdomen: large, painless bladder (chronic retention) Pallor, rash, bruising: petechiae, purpura and nosebleeds may suggest inflammatory/vascular disease, emboli DIC Pericarditis – occurs with severe untreated uraemia and may be complicated by pericardial effusion, tamponade or pericardial rub Arrhythmias due to hyperkalaemia Thirst
55
What are the primary investigations for AKI?
- Urine dipstick – blood, nitrites, leukocytes, glucose, protein - GN suggested by haematuria and proteinuria on dipstick and red cell casts on urine microscopy - Bloods – FBC, blood film, U&Es, creatinine, liver enzymes, clotting - Anaemia and high ESR may suggest myeloma or vasculitis as underlying cause - Serum calcium, phosphate and uric acid - Renal ultrasound – for obstruction - Gives assessment of renal size – very small indicates CKD - Monitor urine output - Non-contrast CT KUB - presence of stones - KUB XR - Urine and blood cultures to exclude infection - Autoantibodies – Anti-GBM, ANCA
56
What is a good way to establish whether AKI is caused by pre/renal/post renal cause?
Urea:Creatine Ratio U:Cr > 100:1 = pre-renal U:Cr < 40:1 = renal U:Cr 40-100:1 = Post renal
57
What is the treatment for AKI?
Tx underlying cause - STOP nephrotoxic drugs Regular Monitoring Tx complications: Hyperkalaemia - Calcium gluconate Metabolic acidosis- Sodium Bicarbonate Give IV fluids - if hypovolaemic Hypervolemic - Fluid Restriction and Diuretics Last resort - Renal Replacement Therapy (dialysis)
58
How would you treat pre-renal, Renal and Post renal causes of AKI?
Pre-renal: - Correct volume depletion with fluids - Treat sepsis with antibiotics Renal: – refer to nephrology if concern over tubulointerstitial or glomerular pathology Post-renal: -Catheterise and consider CT KUB -If signs of obstruction and hydronephrosis then think cystoscopy and retrograde stents or nephrostomy insertion
59
What are the indications for RRT?
Acidosis (pH < 7.1) Fluid overload (oedema) Uremia that is symptomatic Hyperkalaemia >6.5 or ECG changes
60
What are some potential complications of RRT?
CVD - MI Infection
61
What are the major complications of AKI?
Hyperkalaemia - leads to cardiac arrest Fluid overload, heart failure and pulmonary oedema Metabolic acidosis Uraemia (high urea) can lead to encephalopathy or pericarditis
62
What is Chronic Kidney Disease (CKD)?
Progressive decline in renal Function where GFR <60ml/Min for more than 3 months
63
What is the Epidemiology of CKD?
Between 6-11% of people can be defined as having CKD Risk increases with age F>M
64
What are the common causes of CKD?
Diabetes Hypertension Age-related decline Glomerulonephritis Polycystic kidney disease SLE Obstructive Uropathy Medications such as NSAIDS, proton pump inhibitors and lithium
65
Explain How Hypertension leads to CKD?
Walls thicken in order to withstand pressure 🡪 narrow lumen 🡪 less blood and O2 to kidney 🡪 ischaemic injury to glomerulus Immune cells (macrophages and foam cells) slip into damaged glomerulus and release TGF-B1 🡪 mesangial cells regress to immature mesangioblast and secrete extracellular matrix 🡪 glomerulosclerosis (hardening and scarring) Diminishes ability for nephron to filter blood
66
Explain How Diabetes Mellitus Leads to CKD?
Excess glucose in blood stick to proteins (particularly affects efferent arteriole making it stiff and narrow Creates obstruction for blood to leave glomerulus 🡪 hyperfiltration 🡪 supportive mesangial cells secrete more structural matrix increasing size of glomerulus Glomerulosclerosis 🡪 CKD
67
What are the risk factors for CKD?
Older age Hypertension (most common) Diabetes (most common) Smoking Renal artery stenosis PKD Use of medications that affect the kidneys Nephrotoxic Drugs
68
What are the stages of CKD?
Classified based on eGFR: G1 = eGFR >90 w/Renal signs G2 = eGFR 60-89 w/ Renal signs G3a = eGFR 45-59 G3b = eGFR 30-44 G4 = eGFR 15-29 G5 = eGFR <15 (known as “end-stage renal failure”)
69
What are the best readings to quantify CKD?
eGFR Urine Albumin:Creatine Ratio (ACR)
70
What is the pathophysiology of CKD?
- Many nephrons are damaged in CKD which reduces GFR - Increased burden on remaining functional nephrons - Functioning (remnant) nephrons experience hyperfiltration (increased flow per nephron as blood flow remains the same), and adapt with glomerular hypertrophy, and reduced arteriolar resistance - This leads to shearing and loss of basement membrane selective permeability leading to proteinurea (loss of filtration ability) - Angiotensin II upregulates TGF-B and PAI-1 which leads to increased scarring of functional nephrons
71
What are the symptoms of CKD?
Early - ASx due to lots of nephrons in reserve Non-Specific Sx: Nausea, Malaise, Anorexia, Itching, Vomiting, Lethargy Urinary Sx: Oligouria, Haematuria, Proteinuria, Nocturia, polyuria Normochromic, normocytic anaemia Bone disease – osteomalacia, osteoporosis HTN Cardiac Arrythmias - Due to Hyperkalaemia Fluid overload – oedema CVD – cardiomyopathy
72
How does CKD lead to Bone Disease?
Renal phosphate retention and impaired production of 1, 25-dihydroxyvitamin D lead to a fall in serum calcium and a compensatory increase in PTH secretion Excess PTH causes skeletal decalcification (loss of calcium) and classic radiological signs can be seen e.g. pseudofractures, pepperpot skulls and subperiosteal erosions
73
How does CKD lead to anaemia?
Anaemia – pallor, lethargy, exertional breathlessness, bruising Reduced erythropoietin production --> less stem cells stimulated to become RBCs 🡪 Anaemia Liver produces hepcidin which kidney normally excretes When kidney function decreases, hepcidin builds up and inhibits iron absorption in duodenum This causes low iron levels 🡪Anaemia
74
How can CKD lead to CVD?
Highest mortality in CKD due to MI, heart failure, sudden cardiac death and strokes (proteinuria is a risk factor for IHD as more prone to atherosclerosis) This occurs due to an increased frequency of hypertension, dyslipidaemia and vascular calcification Lower than normal fluid filtration causes release of renin which increases BP In CKD, falling GFR 🡪 more renin release 🡪 hypertension (a cause of CKD) Creates a vicious cycle Renal disease also results in a form of cardiomyopathy with both systolic and diastolic function Pericarditis and pericardial effusion occur in situations of severe uraemia (pericardium becomes inflamed) Bleeding as urea stops platelets binding together
75
What are the clinical signs of CKD?
Hypertension Pallor Bilaterally small kidneys on USS Increased Skin Pigmentation (excoriation yellow tinge) Fluid Overload/Peripheral Oedema Postural Hypertension PVD Pleural Effusions Evidence of underlying aetiology
76
What is the prognosis of CKD correlated with?
Poorly controlled HTN Proteinuria Degree of scarring on histology
77
What are the key complications of CKD?
Anaemia - due to reduced EPO Renal bone disease (osteodystrophy due to lack of Vit D activation) Cardiovascular disease Peripheral neuropathy Dialysis related problems
78
What are the primary investigations in CKD?
FBC: - Anaemia - Normocytic U&Es: - Raised creatinine and urea, (ACR >3 is significant) - Decreased Ca2+, raised phosphate, PTH, K+ and renin Urine and blood cultures to exclude infection - White cells – bacterial UTI - Eosinophilia – allergic tubulointerstitial nephritis - Granular casts – active renal disease - Blood - glomerulonephritis Urinalysis: - Dipstick - Haematuria and proteinuria suggest GN - Leukocytes and nitrites suggest infection - Mid-stream urine sent for microscopy and sensitivity - Albumin to creatinine ratio (ACR) or protein to creatinine ratio (PCR) Renal ultrasound: - excludes obstruction - Bilateral Small Kidneys CT – useful for diagnosis of retroperitoneal fibrosis and other causes of urinary obstruction Biopsy – immunofluorescence, histology - Look for GN Cystoscopy ECG – for hyperkalaemia
79
What are the differences Ix findings between AKI and CKD?
Hx: AKI shorter Sx onset CKD - 3 month Hx AKI - Serum Creatine Inc : Urine output Dec CKD - Decreased eGFR AKI - no Anaemia CKD - Anaemia due to EPO AKI USS - normal CKD USS - Bilateral atrophied kidneys
80
What is the aim of management in CKD?
Slow the progression of the disease Reduce the risk of cardiovascular disease Reduce the risk of complications Treating complications
81
What is the management of CKD?
Tx underlying cause to prevent further deterioration: - Antibiotics for sepsis - Correct volume depletion with fluids - Immunosuppressive agents for vasculitis - Blood Pressure (BCD (NO ACEi as they are nephrotoxic) - Tight metabolic control in diabetes - Stop nephrotoxic drugs Tx complications: Oral sodium bicarbonate to treat metabolic acidosis Iron supplementation and erythropoietin to treat anaemia Vitamin D to treat renal bone disease Dialysis in end stage renal failure Renal transplant in end stage renal failure
82
What are the different types of Renal Replacement Therapy (RRT)?
Dialysis – the removal or “uraemic toxins” from the blood by diffusion across a semi-permeable membrane towards low concentrations present in dialysis fluid Haemodialysis: - Surgical construction of AV fistula in forearm – join an artery and vein to make large vessel - Two needles places in different places and blood flows through special tubing (contains heparin to stop clotting) into an artificial kidney Peritoneal dialysis: - Involves infusing a sugary solution into the abdomen which draws off toxins - Water moves across from circulation into PD fluid by diffusion - Sugary solution diffuses across from PD fluid into circulation and is consumed until there is no sugar left (loses osmotic gradient) - Water then diffuses back across.
83
What are the indications for Dialysis?
Symptomatic uraemic including pericarditis or tamponade Hyperkalaemia not controlled by conservative means Metabolic acidosis Fluid overload resistant to diuretics
84
How can CKD progression be slowed?
Optimise diabetic control Optimise hypertensive control Treat glomerulonephritis
85
What are the Major Complications of CKD?
Electrolyte disturbances - hyperkalaemia Osteoporosis – GFR <30 – give bisphosphonates Vitamin D deficiency – give cholecalciferol Anaemia Metabolic acidosis Pruritis – due to nitrogenous waste products of urea Pericarditis Hypertension
86
How can the risk of CKD complications be reduced?
Exercise, maintain healthy weight, stop smoking Special dietary advice (Vit D supplements, Na/K restriction) Offer Atorvastatin for primary prevention of CVD
87
What is a Urinary Tract Infection (UTI)?
Inflammation of the urothelium in response to an infection that occurs anywhere along the Urinary Tract from the kidneys to the urethra
88
What is the clinical Definition of a UTI?
Pure growth of >10^5 organisms/ml of fresh mid-stream urine
89
What are the classifications of UTIs?
Upper UTI: Often Descending Infection Kidneys - Pyelonephritis Ureter - Ureteritis Lower UTI: Often Ascending Infection Bladder - Cystitis Prostate - Prostatitis Epidiymo-Orchiditis Urethra - Urethritis Uncomplicated Vs Complicated
90
What are the organisms that generally cause UTIs?
KEEPS: Klebsiella (10% - catheter associated) E.coli - (UPEC) most common > 50% Enterobacter Proteus 10-15% - Associated with Renal Stone Formation (Struvite) S.Saprophyticus P. aeruginosa - recurrent UTI/underlying pathology
91
What is the most common cause of a UTI?
UPEC: Uropathogenic Escherichia coli (80% of uncomplicated UTIs)
92
Who are most affected by UTIs?
Women - Due to a shorter urethra and closer to the anus therefore it is easier for bacteria to colonise and cause and infection Post-menopause - Absence of Oestrogen increases risk
93
What are some pathological mechainisms of getting UTIs?
Catheterisation allowing colonisation Bowel Flora from perineum (often females) Reduced flow: Obstruction (prostate, stones) Low Urinary volume Stasis during pregnancy
94
What are the Risk Factors for a UTI?
Female Sexual intercourse Menopause – less oestrogen 🡪 loss of protective vaginal flora Catheterisation Diabetes mellitus – hyperglycaemia stops diapedesis Pregnancy Urinary tract obstruction Malformations Immunosuppression
95
What are the Symptoms of an Upper UTI?
- Systemic symptoms - Loin/abdominal pain - Tenderness - Nausea - Vomiting - Fever - Costovertebral angle pain
96
What are the Symptoms of a Lower UTI?
HD FUSS: Haematuria Dysuria Frequency Urgency Suprapubic pain Smelly urine
97
What are the general symptoms of a UTI?
Fever may be only Sx Abdominal pain, particularly suprapubic pain/discomfort Vomiting Dysuria (painful urination) Urinary frequency Incontinence Nocturia Delirium/Confusion in elderly Px
98
How are UTIs Diagnosed / what would you find?
1st Line: Urine Dipstick +tve Leukocytes +tve Nitrites (bacterial breakdown product) +/- Haematuria Gold Standard: Mid-stream Urine Microscopy, Culture and Sensitivity (MC+S) This confirms UTI and IDs pathogen
99
What are some alternative methods to take a Urine Sample?
Mid Stream Urine Catheter Stream Urine Clean Catch Bag Urine Supra Pubic Aspirate Early morning urine - looks for TB
100
What would you look for on microscopy in a MC + S)?
WBC >10^4 wbc/ml (pyuria) Bacteria >10^5 cfu/ul = infection RBCs
101
What is the Treatment for Any complicated UTI?
MC+S and then adjust Abx as needed. Longer Abx - 7 Days Give Nitrofurantoin
102
What are some common Abx used to treat UTIs in the community?
Nitrofurantoin (now more commonly used) Trimethoprim + Amoxicillin, Cefalexin
103
What are the side effects of Nitrofurantoin?
nausea, vomiting, liver problems, weakness
104
Why is Trimethoprim used less to treat UTIs these days?
Due to much higher levels of antibiotic resistance
105
What is the treatment for someone who is >65yrs + and has asymptomatic bacteriuria?
Do NOT treat
106
What is the treatment for someone who is pregnant and has asymptomatic bacteriuria?
Give treatment (Nitro/Trim depending on trimester) as 20-40% will go on to develop pyelonephritis
107
What is Pyelonephritis?
Upper UTI of the renal parenchyma and upper ureter at the renal pelvis
108
When would you avoid treating a UTI with Trimethoprim?
First trimester of pregnancy as it interferes with folic acid synthesis
109
When would you avoid treating a UTI with Nitrofurantoin?
Third trimester of pregnancy as there is a risk of Neonatal Haemolysis
110
What do UTIs during pregnancy increase the risk of?
Pyelonephritis Premature rupture of membranes Pre-term Labour
111
How can you prevent UTIs?
Drink plenty of fluids Urination after sex Good hygiene Prophylactic antibiotic
112
What is a major risk of catheterisation?
Become colonised with bacteria within a few days. Can cause serious UTIs
113
What are some complications of long term cathetisation?
UTIs/Pyelonephritis Stones Obstruction Chronic Inflammation
114
What are risk factors for Pyelonephritis?
Female sex <35yrs Urine stasis (due to stones) Catheters Structural urological abnormalities Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children) Diabetes
115
What is the most common causative organism of Pyelonephritis?
E.coli (+KEEPS)
116
What is the Epidemiology of Pyelonephritis?
Predominantly females <35 Associated with significant sepsis and systemic upset
117
What is the pathophysiology of Pyelonephritis?
- Infection is mostly due to bacteria (primarily E.coli) from own patients bowel flora - Most common via the ascending transurethral route Other causes can be via Haematogenous/lymphatic spread
118
What is the classical presentation of Pyelonephritis?
Triad: Loin Pain Fever Pyuria - pus in pee + nausea/vomiting Anorexia Haematuria Renal angle Tenderness Signs - Usually Unilateral
119
What is the primary investigation for Pyelonephritis?
1st Line: Urine Dipstick Gold Standard: Urine MC+S Abdominal Exam - Tender loin, Renal Angle tenderness Bloods + Cultures - Raised WCC, CRP/ESR USS - rule out obstructions
120
What is the management of pyelonephritis?
1st Line: Hydration/fluid replacement IV antibiotics – broad spectrum e.g. Co-amoxiclav ± Gentamicin Ciprofloxacin Other Considerations: Pregnancy - Cefalexin Drain obstructed kidney Catheter Analgesia Complete 7-14 days (depending on choice of antibiotic)
121
What are some complications for Pyelonephritis?
Renal Abscesses (common in diabetics) Emphysematous Pyelonephritis
122
What are some Differential Diagnoses for Pyelonephritis?
Diverticulitis Abdominal aortic aneurysms Kidney stones Cystitis Prostatitis
123
What are the main symptoms of lower UTI?
Dysuria Frequency
124
What is Cystitis?
Urinary infection of the bladder Commonly due to UPEC
125
Who is affected by Cystitis?
More common in women Can occur in children
126
What are the risk factors for Cystitis?
- Urinary obstruction resulting in urinary stasis - Previous damage to bladder epithelium - Bladder stones - Poor bladder emptying
127
What is a classical presentation of Cystitis?
Suprapubic tenderness + discomfort Dysuria Nocturia Fever Increased frequency Increase urgency Visible Haematuria
128
What is the primary Investigations to diagnose Cystitis?
1st Line: Urine Dipstick - Positive for Leukocytes, Blood, Nitrites Gold Standard: Urine MC+S
129
What is the treatment for Cystitis?
First line: Nitrofurantoin (1st Trimester)/ Trimethoprim (3rd Trimester) Cefalexin Second Line: Co-amoxiclav/Ciprofloxacin
130
What is Urethritis?
Inflammation in the urethra due to infection
131
What is the most common cause of Urethritis?
Sexually acquired condition: Non-Gonococcal (Chlamydia) - More common Gonococcal - Less common Non infective - trauma
132
What are the risk factors for Urethritis?
Male Gay sex Unprotected sex
133
What is the presentation of Urethritis?
Maybe ASx Dysuria +/- urethral discharge (blood/pus) Penile Discomfort Urethral pain
134
What is the diagnostic test for Urethritis?
NAAT (Nucleic Acid Amplification Test) - detects STI pathogen (NG/CT) Urine Dipstick + Urine MC+S if UTI
135
What is the treatment for urethritis?
N.G - IM Ceftriaxone + Oral Azithromycin C.T - Oral Azithromycin (or Doxycycline) for 1 week Patient Education and Contact Tracing
136
What is Epididymo-Orchitis?
Inflammation of the epididymus which extends to the testes often secondary to urethritis (STI) or Cystitis.
137
What is the Eidemiology of Epididymo-Orchitis?
Most common in 15-30 and >60
138
What are the symptoms of Epididymo-Orchitis?
Unilateral scrotal pain and swelling Pain relieved when elevating testes STI Cause - Urethritis/Urethral Discharge (DDx - testicular Torsion which is much more acute and N+v)
139
What diagnostic investigations are done for Epididymo-Orchitis?
NAAT Urine Dipstick Urine MC+S USS to rule out abscesses
140
What is the treatment for Epididymo-Orchitis?
Depends on underlying cause: STI/UTI to determine Abx
141
What is an uncomplicated UTI?
A UTI in a healthy NON-PREGNANT women with a normally functioning urinary tract
142
What is a complicated UTI?
Most other UTIs (not in non-preggo women) A UTI in a man A Px who has abnormal urinary tract (eg. stones) Systemic disease involving the kidney
143
What is significant about complicated UTIs?
Treatment failure is more likely Complications are more likely: Renal papillary necrosis Renal Abscesses
144
What is Benign Prostatic Hyperplasia (BPH)?
Benign proliferation of musculofibrous/glandular tissue of the transitional (inner) zone of the prostate that results in lower urinary tract symptoms
145
What are the risk factors for BPH?
Increased age: o Histologically seen in: - 23% of men 41-50 - 42% of men 51-60 - 71% of men aged 61-70 - 82% of men 71-80 Afro-Caribbean (increased testosterone) Castration is protective
146
What is the pathophysiology of BPH?
Benign proliferation of the transitional zone of the prostate (in contrast to peripheral layer expansion seen in prostate carcinoma) After 30, men produce ~1% less testosterone each year but 5a-reductase increases with age 🡪 increased dihydrotestosterone levels Prostate cells respond by living longer and growing 🡪 hypertrophy As the prostate gets bigger, it may squeeze or partly block: - The bladder 🡪 urine retention 🡪 bladder dilation and hypertrophy 🡪 urine stasis 🡪 bacterial growth 🡪 UTIs - The urethra 🡪 urination problems
147
What is Responsible for the growth of the Prostate in BPH?
Dihydrotestosterone is responsible for prostatic growth
148
What are the typical Symptoms that occur in BPH?
Lower Urinary Tract Symptoms (LUTS): o Storage: - Frequency - Urgency - Nocturia - Incontinence o Voiding: - Straining/ Stream Poor - Hesitancy - Incomplete Emptying - Terminal Dribbling
149
What are symptoms of Urinary Storage?
Fequency Urgency Nocturia (>30%) Incontinence
150
What are symptoms of urinary Voiding?
Straining/ Stream Poor Hesitancy Incomplete Emptying Terminal Dribbling
151
What are the signs of PBH?
DRE - Smooth enlarged Lower abdominal Tenderness Palpable Bladder o Red flags - Dysuria – painful or difficult urination - Haematuria – blood in the urine - Painless haematuria always suspected as malignancy until proven otherwise
152
What complications may arise in BPH if the urethra is completely occluded?
Auria - no urination Retention Hydronephrosis UTI Stones
153
What is PSA?
Prostate Specific Antigen serine protease responsible for liquefaction of semen Prostate specific but not condition specific (essentially any condition affecting the prostate will cause a rise in PSA)
154
What are the Diagnostic investigations of BPH?
IPSS (International Prostate Symptom Score) DRE - Digital Rectal exam: Smooth and enlarged (hard/irregular = cancer) PSA - may be raised but also raised in cancer Trans-rectal USS Biopsy Abdo Exam - enlarged bladder Urine Dipstick - assess for other pathology
155
What is the treatment for PBH?
If Sx minimal - Watch and Wait Lifestyle advice: Reduce caffeine Relax when voiding Medication: 1st Line - alpha blocker - Tamsulosin 2nd Line - 5-alpha Reductase inhibitors - Finasteride Surgery (last resort) Transurethral resection of prostate
156
What is the mechanism of action of Tamsulosin?
Alpha blocker that will relax the bladder neck increasing urinary flow rate and improving obstructive Sx of BPH
157
What is a side effect of Tamsulosin?
Postural hypotension so patient should take at night in bed, so they can’t faint Retrograde ejaculation – bladder neck relaxes so sperm travels back into bladder
158
What is the mechanism of action of Finasteride?
5-alpha reductase inhibitor that will block conversion of testosterone to dihydrotestosterone to reduce prostatic growth
159
What are the Side Effects of Finasteride?
Fatigue, lethargy and degree of ED and libido loss
160
What is a common complication of transurethral resection of prostate surgery?
Retrograde ejaculation.
161
What is Glomerular Disease?
Glomerulonephritis refers to groups of parenchymal kidney diseases that all result in the inflammation of glomeruli and nephrons
162
Explain the Structure of the glomerulus?
Tuft of capillaries that has 3 components: Epithelium – composed of podocytes which only makes contact with GBM via foot processes Glomerular BM Fenestrated endothelium – lining of capillaries Mesangial cells holding it all together
163
What are the classifications of Glomerulonephritis?
Nephrotic Syndrome Nephritic Syndrome (acute GN) Rapidly Progressive GN
164
What is Nephritic syndrome?
inflammation of the blood vessels of the glomerulus that damages the basement membrane leading to blood leaking out but Px does not have a specific underlying cause.
165
What are the features of a patient with Nephritic Syndrome?
Haematuria Proteinuria - <3g/24 Oliguria Oedema - due to Fluid overload Hypertension Reduced GFR - (hypercellular glomeruli 🡪 decreased blood flow and leaky BM 🡪 reduced filtration rate)
166
Give some conditions that present with a clinical picture of nephritic syndrome?
Primary - IgA Nephropathy Secondary: Post Strep Glomerulonephritis Good Pasture's Syndrome (Type II Hypersensitivity) SLE Nephropathy Haemolytic Uremic Syndrome These are all examples of TYPE 3 Hypersensitivity reactions (except good pasture's Syndrome). They are the result of immune complex deposition
167
What are the investigations for nephritic syndrome?
- **Bloods:** increased creatinine and BUN (blood urea nitrogen) - **Urinalysis:** haematuria, red blood cell casts, proteinuria (but less than 3.5g per day) - **Renal biopsy** if necessary
168
What is the general management for Nephritic Syndrome?
- **Immunosuppression** (e.g. steroids) - **Blood pressure control** by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
169
What is the most common cause of Nephritic Syndrome?
IgA Nephropathy
170
What is IgA Nephropathy?
(also called Berger's Disease) Commonest cause of glomerulonephritis worldwide IgA levels rise 1-2 days after a viral infection (tonsilitis, gastroenteritis etc). These IgA deposit in the mesangium (part of glomerulus) activating C3. A Type 3 hypersensitivity Rxn occurs and this causes Glomerulonephritis. Presents with Nephritic Syndrome
171
What is Glomerulonephritis?
umbrella term used to describe inflammation of the Glomerulus/nephrons of the kidney. Conditions causing glomerulonephritis typically present with either a nephritic or Nephrotic syndrome picture which are a group of symptoms.
172
What is Nephrotic Syndrome?
Inflammation of Podocytes leads to protein leaking out of kidneys. Nephrotic syndrome has a set criteria to fit to be classified as NEPHROTIC.
173
What are the features of Nephrotic Syndrome?
Proteinuria (>3.5g/day) – damaged glomerulus more permeable 🡪 more protein come across from blood into nephron 🡪 proteinuria Hypoalbuminaemia – albumin leaves blood Oedema (periorbital and arms) – oncotic pressure falls due to less protein in blood 🡪 lower osmotic pressure 🡪 water driven out of vessels into tissues Hyperlipidaemia and lipiduria – loss of protein = less lipid synthesis 🡪 more lipids in blood 🡪 more in urine
174
What is the criteria for Nephrotic syndrome?
A Px must Fulfil: Peripheral oedema - due to 3rd spacing Proteinuria more than 3g / 24 hours Serum albumin less than 25g / L Hypercholesterolaemia
175
What is the main Difference between Nephritic and Nephrotic syndrome?
In Nephritic syndrome - Haematuria predominates In Nephrotic Syndrome - Proteinuria Predominates
176
What is the characteristic Presentation Nephritic Syndrome?
Visible Haematuria (Ribena/coke coloured Pee) Arterial HTN Peripheral Oedema Oligouria
177
What are the primary investigations for IgA nephropathy?
Urine Dipstick: Blood and protein (<3g/dl) U&Es - assess renal function C3/4 levels: C3 - low or normal due to activation of the complement pathway by IgA C4 - normal - not involved in IgA Complement activation Renal Biopsy (diagnostic) - Mesangial Cell proliferation - Immunofluorescence - IgA immune complexes in mesangium
178
What is the Treatment for IgA nephropathy?
Rapid progression of condition with approx 30% developing ESRF. ACEi/ARB to control BP and reduce the damage to kidneys. Corticosteroids - Can be trialled but not always effective Statins - Lower Cholesterol
179
What is Post strep Glomerulonephritits (PSGN)?
Immunologically-mediated delayed consequence of pharyngitis or skin infections caused by streptococcus pyogenes that leads to glomerulonephritis and consequential Nephritic Syndrome Occurs Via M-Protein molecular mimicry leading to a Type 3 Hypersensitivity reaction
180
How long does it take to develop PSGN after infection?
2 weeks after pharyngitis from S. pyogenes
181
How is PSGN Diagnosed?
- **Bloods:** low levels of C3 and CH50 - **Positive streptozyme test** confirms recent group A streptococcal infection - **Kidney biopsy:** isn’t always necessary, but can provide specific clues - **On light microscopy:** the glomeruli are enlarged and hypercellular. - **On immunofluorescence:** IgG, IgM and C3 deposits along the glomerular basement membrane and the mesangium, which create a “starry sky” appearance. - **On electron microscopy:** subepithelial deposits which appear as “humps”.
182
What is the treatment of PSGN?
Only Sx management - Self limiting usually Abx for strep infection - Amoxicillin/Flucloxacillin Could Use furosemide for HTN May progress to rapidly progressive GN
183
How can SLE cause Nephropathy?
Cause Lupus nephritis secondary to SLE Deposition of Antigen-antibody complexes and ANA in the kidneys leads to nephritis and a nephritic picture
184
How is Lupus Nephritis diagnosed?
Urinalysis - Haematuria and Proteinuria PMHx of SLE + (GS) renal Biopsy: - showing diffuse proliferative glomerulonephritis - **On light microscopy:** immune complexes create an overall thickening of the capillary wall, which gives a “wire loop” appearance. - **On immunofluorescence:** granular immune complexes. - **On electron microscopy:** sub-endothelial immune complexes.
185
What is the most common form of Lupus Nephritis?
Diffuse proliferative glomerulonephritis
186
How is Lupus Nephritis treated?
Lifestyle - stop smoking, exercise, dietary advice Medication: Corticosteroids - Immunosuppressive agents - Azathioprine Hydroxychloroquine
187
What is good Pasture's Syndrome?
Autoimmune disease where there are anti-GBM Antibodies against Type IV Collagen that target the lungs and the kidneys causing pulmonary haemorrhage and glomerulonephritis
188
What is the diagnosis of good pasture's Syndrome?
Serology - Anti-GBM Abs Renal Biopsy: - Light microscopy may show crescentic glomerulonephritis - Immunofluorescence staining shows linear deposition of IgG along glomerular capillaries
189
What is the treatment for Goodpasture's Syndrome?
plasmapheresis, steroids and cyclophosphamide.
190
What is the pathology of Nephrotic Syndrome?
Underlying pathology that leads to direct sclerosis of podocytes on the glomerulus leading to the clinical features of nephrotic syndrome
191
What conditions lead to a nephrotic syndrome clinical picture?
Primary: Minimal Change Disease (Most common cause in Children) Focal Segmental Glomerulosclerosis (most common cause in adults) Membranous Nephropathy (most common cause in the elderly) Secondary: Diabetic Nephropathy Amyloidosis Infections Drugs
192
What are the investigations for Nephrotic Syndrome?
Urinalysis - Proteinuria predominates ACR - Raised due to protein U&Es - Monitor eGFR to assess renal function Lipid Profile - Hypercholesterolaemia and Hyperlipidaemia Renal Biopsy: Different changes depending on underlying cause.
193
What would be seen on Light and Electron microscopy in Nephrotic Syndromes: Minimal Change Focal Segmental Glomerulosclerosis Membranous Nephropathy Diabetes
- **Minimal change disease** - **Light microscopy**: normal glomeruli on light microscopy - **Electron microscopy (EM)**: effacement of foot processes - **Focal segmental glomerulosclerosis** - **Light microscopy**: focal and segmental glomerular sclerosis - **EM**: effacement of foot processes - **Membranous nephropathy** - **Light microscopy**: thick glomerular basement membrane - **EM**: subepithelial immune complex deposition (spike and dome pattern) - **Diabetes** - **Light microscopy:** mesangial sclerosis and Kimmelstiel-Wilson nodules
194
What is the general treatment of Nephrotic Syndromes?
Management varies due to different responsiveness: Lifestyle - Low salt, protein and fat diet, improve CVD RFs Corticosteroids: Minimal Change - very responsive FSGS - variable response (ciclosporin used in resistance) MN - Corticosteroids + Cyclophosphamide
195
What is Minimal Change disease?
Most common cause of nephrotic syndrome in children: often due to a benign excessive response to steroids
196
What is the Pathology of Minimal Change Disease?
Cytokines attack foot processes of podocytes Shrinkage/blunting of podocytes 🡪 protein leakage
197
What is the diagnostic findings for Minimal change disease?
Renal Biopsy Light microscopy - normal/no change Electron Microscopy - Podocyte effacement + fusion
198
What is Focal Segmental Glomerulonephritis (FSG)?
Most common cause of Glomerulonephritis and nephrotic syndrome in adults: Associated with HIV, heroin use, sickle cell
199
What are the diagnostic findings for focal segmental glomerulonephritis?
Renal Biopsy and Light Microscopy - Segmental sclerosis and hyalinosis - Focal so only part of the glomerulus is affected
200
What is Membranous Nephropathy?
The most common cause of nephrotic syndrome in the elderly: Associated with malignancy, hepatitis B, NSAIDs, SLE
201
What are the diagnostic Findings of Membranous Nephropathy?
Light microscopy - Thickened Glomerular BM Electron Microscopy - Sub epithelial immune complex deposition Spike + Dome appearance.
202
What is the characteristic clinical picture of Nephrotic syndrome?
Frothy urine (proteinuria) Hypalbuminaemia Facial and peripheral oedema Predisposition to thromboembolic disease Recurrent Infections Hypertension
203
What conditions can cause both a Nephritic and Nephrotic syndrome clinical picture?
Diffuse Proliferative glomerulonephritis Membranoproliferative Glomerulonephritis: Tram Tracks on light Microsco
204
What is obstructive uropathy?
Blockage of urine flow that can affect one or both kidneys depending on the level/site of the blockage
205
What conditions can cause obstructive uropathy?
BPH, Malignancy and stones
206
What is the pathogenesis of obstructive uropathy?
Obstruction causes retention of urine. This increases KUB pressure leading to reflux of backlogged urine into the renal pelvis. This will lead to hydronephrosis which is more prone to infection
207
What is the treatment of obstructive uropathy?
Relieve kidney pressure: Catheterise / ureteral stent Tx of cause of obstruction BPH - Tamsulosin Stones - ESWL/PCNL
208
What are the main types of GU cancer?
Renal Cell Carcinoma Bladder Cancer Prostate Cancer Testicular Cancer
209
What is Renal cell Carcinoma?
Renal cell carcinoma (RCC) is the most common type of kidney tumour. It is a type of adenocarcinoma that commonly arises from the epithelium of the PCT
210
What is Wilms Tumour?
A specific renal mesenchymal stem cell tumour that affects children typically under 5 years old (A.K.A Nephroblastoma)
211
What are the main subtypes of Renal cell carcinoma?
Clear cell (80%) Papillary (15%) Chromophobe (5%)
212
What are the risk factors for Renal cell carcinoma?
Smoking Obesity Hypertension End-stage renal failure Von Hippel-Lindau Disease PCKD Tuberous sclerosis
213
What is the Pathology of RCC?
Malignant cancer of proximal tubular epithelium and may be solitary, multiple and occasionally bilateral Spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung) Metastasise Bone Liver Lungs – “cannon ball” mets
214
How does Renal cell carcinoma typically present?
Often ASx - 25% metastasised at Dx Typical Triad of Sx: Flank pain Haematuria Abdominal palpable mass Cancer Sx - Weight loss, anorexia, Night sweats Fever and Anaemia
215
What are the primary investigations for renal cell carcinoma?
1st Line: USS Gold Standard: CT CAP - Diagnostic Bloods: U&Es - renal dysfunction LFTs - liver mets LDH - if increased = poor prognosis
216
What is the treatment for Renal Cell carcinoma?
25% have Mets at Presentation Partial/Full Nephrectomy
217
What is the the most common type of kidney cancer in adults?
Renal Cell Carcinoma
218
What are the complications of RCC?
Paraneoplastic Syndromes - Production of Hormones: EPO – more RBCs 🡪 polycythaemia PTHrP – hypercalcaemia ACTH – more cortisol 🡪 Cushing’s
219
What is bladder cancer?
Often a transitional cell carcinoma of the bladder due to the transitional epithelium (urothelium) that lines the renal pelvis, bladder, ureter and urethra
220
What is the Epidemiology of Bladder Cancer?
4th most common cancer in men 8th most common cancer in women
221
When is a patient more likely to have squamous cell carcinoma of the bladder?
If they have Schistosomiasis infection
222
What is the most common type of bladder cancer?
Transitional urothelium cancer (bladder cancer) This lines the renal pelvis and bladder
223
What are the risk factors for Bladder cancer?
Age >40yrs Male Smoking Occupational Exposure - Dyes/paints/rubber Aromatic Amines FHx
224
What are the signs and symptoms of Bladder cancer?
- Signs - **Palpable suprapubic mass** in advanced cases - **Anaemia** e.g. pallor, if chronic bleeding present - Symptoms - **‘Painless’ haematuria**: microscopic or macroscopic - **Dysuria** (pain when urinating) can occur - **Frequency** - Constitutional symptoms e.g. **weight loss**
225
What are the primary investigations for bladder cancer?
Gold Standard: Flexible Cytoscopy + biopsy CT AP - for staging
226
What is the treatment of bladder cancer?
Conservative - support Surgical: Transurethral Resection of Bladder Tumour (TURBT) Cystectomy - last resort Medical: Chemotherapy Radiotherapy
227
What is the most common cancer in males?
Prostate cancer
228
What is the most common type of prostate cancer?
Adenocarcinoma that arises from the peripheral zone of the prostate. These are often neoplastic and malignant which spread to bones
229
What are the types of Prostate Cancer?
Adenocarcinomas – most common, arise from peripheral zone Transitional cell carcinomas – arise from transitional zone Small cell prostate cancer – arise from neuroendocrine cells
230
What are the risk factors for prostate cancer?
Environmental Genetics High fat/low Fibre diet Increasing age Afro-Caribbean ethnicity FHx - accounts for 8% of cases
231
Why is there an increase in the prevalence of prostate cancer?
Ageing population Increased detection
232
What genetic factors increase a patients risk of prostate cancer?
BRCA1/2 Mutations HOXB13
233
What is the presentation of prostate cancer?
LUTs (Frequency, Hesitancy, terminal dribbling) Systemic Cancer Sx (weight loss, fatigue night pain) Bone pain - suggests metastasised to bone (typically lumbar back pain)
234
What are the investigations for prostate cancer?
DRE + PSA in community New First Line: Multiparametric MRI Previously Gold Standard: Transrectal USS + biopsy - Diagnostic
235
What is the grading system used for prostate cancer?
Gleason Score High = worse prognosis
236
What area of the prostate is commonly affected by prostate cancer?
Peripheral zone
237
What are the common metastatic sites for prostate cancer?
Bones - sclerotic lesions Brain Liver Lungs
238
What are the primary prevention methods for Prostate cancer?
Screening? - PSA test (benefits dont necessarily outweigh harms of screening) Chemoprevention - 5 alpha reductase inhibitors Diet and Supplements Exercise and weight control
239
What is the treatment for Prostate cancer?
Local - Watchful waiting/Prostatectomy/radiotherapy Advanced- Hormone therapy (GnRH agonists) Metastatic - surgical/medical castration (orchidectomy)
240
What is the purpose of Hormone Therapy in prostate cancer?
Reduce testosterone - reduce cancer growth
241
What are some options for hormone therapy for prostate cancer?
Surgical: Bilateral Orchidectomy - Testicular removal (castration) Medical: GnRH receptor agonists - Goserelin Androgen Receptor Blockers - Enzalutamide
242
How do GnRH receptor agonists work?
Goserelin: Agonist GnRH and therefore these increase LH and FSH but this leads to exogenous suppression of the HPG axis
243
What is the treatment for metastatic prostate cancer?
Surgical Castration Medical castration (GnRH agonists) Palliative care
244
What is the most hormone sensitive cancer?
Prostate cancer
245
What are the differential Diagnoses for Prostate Cancer?
BPH Prostatitis Bladder tumour
246
What are the two classes of testicaular tumour?
Germ cell (90%): Seminoma - most common Teratoma Non-Germ Cell (10%): Sertoli Leydig Sarcoma
247
What is the most common cancer in young men (20-40yrs)
Testicular Cancer
248
What are the risk factors for testicular cancer?
Cryptorchidism - undescended teste Infertility FHx
249
What is the presentation of Testicular Cancer?
Painless lump in testicle which does NOT transilluminate May also have: Sx of hyperthyroidism - BhCG mimics TSH Bone pain - if bone Mets Breathlessness - if Lung Mets
250
What are the signs for Testicular cancer?
Hydrocele Abdominal/Testicular Mass
251
What are the primary investigations for testicular cancer?
Urgent (doppler) USS testes (90% diagnostic) Raised tumour markers: AFP BhCG LDH (Raised non-specifically in tumours) CXR and CT to assess tumour staging
252
What is the treatment of Testicular cancer?
ALWAYS 1ST LINE: Urgent orchidectomy offer sperm storage Adjuvant chemotherapy/radiotherapy
253
What is Polycystic Kidney Disease (PKD)?
Cyst formation throughout the renal parenchyma often leading to bilateral enlargement and damage
254
Why may a patient have left sided varicocele in renal cell carcinoma? (and not Right sided)
Left testicular vein drains into the left renal vein; a left RCC can invade the renal vein causing backpressure and varicocele formation Right testicular vein drains directly into the IVC, therefore a right RCC does not cause a varicocele
255
What are the causes of PKD?
Simple – develop over time Acquired – CKD Drugs – lithium (used for treating depression) Autosomal dominant/recessive – genetic cause Syndromic disease – tuberous sclerosis
256
What are the types of Inherited PKD?
Autosomal Dominant PKD (ADPKD) Autosomal Recessive PKD (ARPKD)
257
When does ADPKD typically present?
Often presents in later life/adults
258
When does ARPKD typically present?
Often presents in neonates and is found on antenatal uss
259
Which is more common ADPKD or ARPKD?
ADPKD is more common
260
What are the genetic factors leading to ADPDK?
Mutated PKD1 (85%) or PKD2 (15%) on chromosome 16 and chromosome 4 respectively
261
Who is typically affected by ADPKD?
More males
262
What are some facts about ARPKD?
Much less common that ADPKD A disease of infancy/prebirth High mortality rate Many congenital abnormalities
263
What are the genetic factors leading to ARPKD?
Mutation in PKHD1 on chromosome 6
264
What is the pathogenesis of ARPKD?
Mutation in PKHD1 on chromosome 6 Encodes for Fibrocystin/polyductin protein complex (FPC) which is responsible for the creation of tubules. Also responsible for maintenance of healthy kidneys liver and pancreas
265
What are some consequential features of ARPKD?
affects birth development leading to potters syndrome: Dysmorphic features such as a flattened nose and Clubbed feet Most Px with ARPKD develop ESRF before adulthood
266
What is the pathophysiology of ADPKD?
Mutation in PKD1/PKD2 which encode for polycystin Ca channel. In normal circumstances: Cilia move when filtrate passes and this causes polycystin to open and allows Ca influx to inhibit excessive growth. In ADPKD the mutation does not open polycystin so Ca cannot inhibit excessive growth leading to cyst formation
267
What is the presentation of ADPKD?
Bilateral flank pain and masses Back or Abdo pain +/- HTN and Haematuria Can also cause extra-renal cysts - berry aneurysms - Hepatomegaly - Pancreatic Cysts - Cardiac Valve Disease
268
What are the symptoms of ADPKD?
Acute loin pain due to cyst haemorrhage or infection, or urinary tract stone formation Abdominal discomfort caused by renal enlargement Nocturia Haematuria Renal colic due to clots
269
What are the signs of ADPKD?
Hypertension Bilateral kidney enlargement UTI and pyelonephritis Progressive renal failure Extra-renal manifestations Sub-arachnoid haemorrhage – intracranial aneurysms more common in ADPKD patients Liver cysts Mitral valve prolapse
270
What is the diagnostic investigation of PKD?
Kidney Uss - Enlarged bilateral kidneys with multiple cysts Genetic testing for PKD1/2 mutations FHx of PKD
271
What are the diagnostic findings on ultrasound for ADPKD?
Ultrasound – diagnostic if: With FHx - <30 at least 2 cysts 30-39 years > 3 cysts (uni/bilateral) 40-59 years > 2 cysts (each kidney) > 60 years > 4 cysts (each kidney)
272
What is the management of PKD?
Non-curative Manage Sx: HTN - ACEi ESRF - RRT
273
What are some differential Diagnoses of ADPKD?
Acquired and simple cysts of kidneys Autosomal recessive PKD Medullary sponge kidney Tuberous sclerosis
274
What are some ongoing problems throughout life that Px with PKD may have?
Liver failure due to liver fibrosis Portal hypertension leading to oesophageal varices Progressive renal failure Hypertension due to renal failure Chronic lung disease
275
What are the common STIs?
Chlamydia F>M Gonorrhoea M>F Syphilis
276
What is Chlamydia?
Chlamydia Trachomatis is a gram negative obligate intracellular parasite. It is responsible for the STI chlamydia which is the most common STI in the UK
277
What are risk factors for Chlamydia?
Age < 25 Multiple Sexual partners Unprotected Sex Sharing unwashed sex toys
278
What are the sites of infection for Chlamydia and Gonorrhoea?
Adult – both infect non-squamous epithelia Urethra Endocervical canal Rectum Pharynx Conjuctiva Neonate: Conjuctiva Atypical pneumonia also in neonatal chlamydia
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What are the symptoms of Chlamydia?
Commonly ASx (70% of women and 50% of men) Can present with: Abnormal vaginal discharge Pelvic pain Abnormal vaginal bleeding (intermenstrual or postcoital) Painful sex (dyspareunia) Painful urination (dysuria)
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What is the primary investigation for chlamydia?
NAAT looks for DNA/RNA of chlamydia Females - self collected vaginal swap Males - First Void Urine
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What is the treatment for Chlamydia?
doxycycline 100mg twice a day for 7 days.
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What are some complications of Chlamydia?
Pelvic inflammatory disease Chronic pelvic pain Infertility Ectopic pregnancy Epididymo-orchitis Conjunctivitis Lymphogranuloma venereum Reactive arthritis
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What is Gonorrhoea?
Caused by Neisseria Gonorrhoea (a gram -tve diplococci) it is the second most common STI in the UK. It infects columnar epithelium lined mucous membranes of the urethra, rectum, conjunctiva and pharynx and endocervix
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What are the risk factors for Gonorrhoea?
Frequent uprotected sex MSM (men who have sex with men) multiple sexual partners
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What are the symptoms of Gonorrhoea?
More commonly Symptomatic (90% males and 50% females) Odourless purulent discharge, possibly green or yellow Dysuria Pelvic pain Testicular pain or swelling (epididymo-orchitis)
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What are the primary investigations for gonorrhoea?
NAAT Charcoal endocervical swab and microscopy and culture Male - From Urethra Female - Endocervix
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What is the treatment for gonorrhoea?
High levels of Abx resistance - why culture is important: A single dose of intramuscular ceftriaxone 1g if the sensitivities are NOT known A single dose of oral ciprofloxacin 500mg if the sensitivities ARE known
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What is Syphilis?
An STI caused by the bacteria Treponema Pallidum. This can get into the mucous membranes and then disseminate throughout the body
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How can Syphilis be contracted?
Oral, vaginal or anal sex involving direct contact with an infected area Vertical transmission from mother to baby during pregnancy Intravenous drug use Blood transfusions and other transplants
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What are the stages of syphilis infection?
Primary: a painless ulcer called a chancre at the original site of infection (usually on the genitals). Secondary: Systemic Infection Fever, headaches, maculopapular skin rash and damage to mucous membranes Tertiary: Affects many organs of the body and develops gummas, CVD and neurological complications
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What are gummas?
granulomatous lesions that can affect the skin, organs and bones secondary to syphilis
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What are the primary diagnostic investigations of syphilis?
Treponemal Antibody testing - positive if ulcer present for >2 weeks Early Moist Lesions - Dark Field Microscopy PCR
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What is the treatment for Syphilis
A single deep intramuscular dose of benzathine benzylpenicillin (penicillin) is the standard treatment for syphilis. Full screening for other STIs Advice about avoiding sexual activity until treated Contact tracing Prevention of future infections
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What are some non-cancerous scrotal diseases?
Varicocele Testicular Torsion Epididymal Cyst Hydrocele
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What is a Hydrocele?
A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes
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What are the Examination findings of a Hydrocele?
The testicle is palpable within the hydrocele Soft, fluctuant and may be large Irreducible and has no bowel sounds (distinguishing it from a hernia) Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)
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What is the definitive diagnostic Ix for Hydrocele?
USS scrotum Serum AFP/HCG to exclude tumours
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What is the management of Hydrocele?
Exclude serious causes Many Resolve Spontaneously Surgery/aspiration to remove fluid
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What are some causes of Hydrocele?
Idiopathic Testicular cancer Testicular torsion Epididymo-orchitis Trauma
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What is an Epididymal Cyst?
An extra-testicular cyst found above and behind the testes that WILL transilluminate.
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What is the Presentation, Diagnosis and Treatment of an Epididymal Cyst?
Sx - often asymptomatic - painful if large Dx - Scrotal Uss Tx - none (they are harmless). Removal considered if painful
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What is a varicocele?
A varicocele occurs where the veins in the pampiniform plexus become swollen. They are common, affecting around 15% of men
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What is the pathophysiology of a varicocele?
Varicoceles are the result of increased resistance in the testicular vein. Incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus.
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What may a left sided Varicocele suggest?
Renal Cell Carcinoma therefore check for this.
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What are the examination findings of a varicocele?
Sx - Dull ache, Heavy scrotum A scrotal mass that feels like a “bag of worms” More prominent on standing Disappears when lying down Asymmetry in testicular size if the varicocele has affected the growth of the testicle
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What is the diagnostic investigation for a varicocele?
Clinical Dx Colour Doppler USS of Scrotum
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What is the management of a Varicocele?
Conservative Mx Can be surgically treated if painful
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What are some potential complications of a Varicocele?
Testicular atrophy Infertility
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What is Testicular Torsion?
Twisting of the spermatic cord with rotation of the testicle. Can lead to occlusion of the testicular artery leading to ischaemia and necrosis of the testicle It is a urological emergency, and a delay in treatment increases the risk of ischaemia and necrosis of the testicle, leading to sub-fertility or infertility.
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Who is typically affected by Testicular Torsion?
Typical patient is a teenage boy but can occur at any age
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What are the causes of Testicular Torsion?
Adolescents and neonates Bell-clapper deformity – testis is inadequately affixed to scrotum allowing it to move freely on axis and more susceptible to twisting Adults Testicular malignancy
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What is the pathology of testicular Torsion?
Twisting of the spermatic cord which cuts of blood supply to the testes Leads to ischaemia, infarction and potential loss of the testis Germ cells are the most susceptible cell line to ischaemia
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What are the symptoms of Testicular Torsion?
Acute rapid onset unilateral testicular pain abdominal pain Nausea and vomiting
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What are the examination findings for testicular torsion?
Firm swollen testicle Elevated (retracted) testicle Absent cremasteric reflex Abnormal testicular lie (often horizontal) Rotation, so that epididymis is not in normal posterior position
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What are risk factors for testicular torsion?
Bell clapper deformity:
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what is a bell clapper deformity?
A bell-clapper deformity is where the fixation between the testicle and the tunica vaginalis is absent. the testicle can the rotate within the tunica vaginalis causing twisting of the spermatic cord
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What is the diagnostic Ix of testicular torsion?
if suspected the medical emergency and surgical exploration is always first line USS doppler can confirm diagnosis but this will delay treatment
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What is the treatment for Testicular torsion?
Surgical treatment within 6hrs: Viable testicle - orchioplexy (untwisting and fixing to scrotal sac) Unviable testicle - Orchiectomy
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What is a testicular appendage torsion?
Twisting of a vestigial appendage (remnant of Mullerian duct) that is located along the testicle. This appendage has no function, yet more than half of all boys are born with one. Torsion of this small bit of tissue can cause intense pain that mimics testicular torsion and characteristically causes a ‘blue-dot’ sign, but is often managed conservatively
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What are the classifications of lower urinary tract symptoms (LUTS)
Storage Symptoms: FUNI Frequency Urgency Nocturia Incontinence Voiding Symptoms: SHIT Stream poor Hesitancy Incomplete Emptying/Straining Terminal Dribbling Post Micturition: Sensation of incomplete voiding. Post micturition Dribbling
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When do storage symptoms and voiding symptoms occur
Storage Sx: Occur when bladder should be storing urine and therefore Px needs to pee Voiding Sx: Occur when bladder outlets obstructed and therefore its hard for Px to pee
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What is generally affected by incontinence?
Females
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Who is generally affected by Urine retention?
(overflow incontinence) Males
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What are the different types of Incontinence?
Stress (sphincter weakness from pregnancy/trauma) - pee leaks with increased abdo pressure Urge - detrusor muscle overactivity Spastic paralysis - UMN lesion
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What is the treatment for incontinence?
surgery Anticholinergic drugs
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What are the causes of urinary retention?
Obstruction: Stones BPH Neurological flaccid paralysis
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What is the treatment for Urinary retention?
Tx underlying cause Catheterise
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What are the Red flags LUTS?
Haematuria Proteinuria
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What is Detrusor overactivity
urodynamic observation characterized by involuntary detrusor contractions during the filling phase that may be spontaneous or provoked
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What drug class are used to treat overactive bladder?
Anti-Cholinergics (inhibit Detrusor contraction) Oxybutynin Solifenacin Mirabegron (beta 3 agonist that Activate relaxation of the detrusor muscle)
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What surgical procedure could be used for overactive detrusor muscle?
Cystoplasty
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What is the Neural control of the lower urinary tract?
Parasympathetic (cholinergic) S2-S4 Drives detrusor muscle contraction So, we pee when we are relaxed Sympathetic (noradrenergic) T10-T12 Sphincter/urethral contraction Inhibits detrusor contraction
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What are the 3 classifications for for neuro-urophysiological dysfunction?
Brain Problems Supra-sacral spinal problems Sacral Spinal Problems
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What are the 3 spinal reflexes involved in bladder function?
Reflex Bladder Contraction - Sacral micturition centre Guarding - Onuf's Nucleus Receptive relaxation (sympathetic)
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Where does co-ordination of voiding occur?
Pontine micturition centre Allows for completion of voiding. (However there is a Higher cortical control to decide when to void.) Peraquductal grey
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What is Detrusor Sphincter Dyssynergia?
When there is a supra-sacral spinal cord injury that means that the innervation to the detrusor muscle and external urethral sphincter is lost. This means the bladder with automatically contract when it fills. The sphincter will go into the guarding reflex which also leads to contraction of the sphincter This means that the bladder is contracting whilst the sphincter contracts which can lead to increased pressures and potential serious kidney damage.
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What are the aims of management of a neurogenic bladder
Prevent autonomic dysreflexia Bladder safety Continence and Sx control.
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What is autonomic dysreflexia?
Occurs lesions above T6 Overstimulation of sympathetic NS below level of lesion in response to noxious stimulus Sx are headache, Severe HTN, Flushing
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What is the most common cause of Autonomic Dysreflexia
A full Bladder
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How is Autonomic Dysreflexia treated?
Catheterise and the bladder will drain reducing the dysreflexia
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What is an Unsafe bladder?
A bladder that will damage the kidneys most commonly due to prolonged high bladder pressure.
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What is the target urine output for an adult?
0.5-1.5ml/kg/hr