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Phase 2a > Genitourinary COPY > Flashcards

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
Q

How can a kidney be drained if infected?

A

Ureteric stent
Nephrostomy

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26
Q

What is the Treatment for Ureteric Stones?

A

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

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27
Q

What is the Treatment for Kidney Stones?

A

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%

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28
Q

What is a key complication of kidney stones?

A

Pyonephrosis
- Pus filled fluid caused by infection and obstruction together.
- Tx with septic six

Hydronephrosis

Abscess/fistulae

Xanthogranulomatous Pyelonephritis

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29
Q

What Treatment is used if a stone is too large to pass spontaneously?

A

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

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30
Q

What is a big issue once you have had one renal stone?

A

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

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31
Q

What are some differential Diagnoses for Loin pain other than Renal Colic?

A

Vascular accident - Ruptured AAA
Bowel Pathology - diverticulitis, appendicitis
Gynae - Ectopic pregnancy
Pyelonephritis
Pancreatitis
Testicular torsion
MSK pain

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32
Q

What is the treatment for bladder stones?

A

Conservative - asymptomatic
Endoscopic + Bladder Outlet Obstruction (BOO) Tx
Open Laparoscopic surgery - for large stones

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33
Q

What is Acute Kidney Injury (AKI)?

A

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.

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34
Q

What is the mortality rate for AKI?

A

25-30%

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35
Q

What are the NICE criteria for AKI

A

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

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36
Q

What is stage 1 AKI?

A

Increase Serum Creatinine by 1.5-1.9x Baseline

Decrease Urine output <0.5mg/kg/hr for 6-12hrs

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37
Q

What is Stage 2 AKI?

A

Increase Serum Creatinine by 2-2.9x Baseline

Decrease Urine output <0.5mg/kg/hr for >12hrs

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38
Q

What is Stage 3 AKI?

A

Increase Serum Creatinine by 3x Baseline

Decrease Urine output <3.5mg/kg/hr for >12hrs or during RRT

Anuria for >12 hours

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39
Q

What system is used to classify the stage of AKI?

A

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

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40
Q

What is the old staging classification system for AKI?

A

RIFLE:
* Risk
* Injury
* Failure
* Loss
* End-stage renal disease

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41
Q

What is the epidemiology of AKI?

A

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

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42
Q

What is AKI associated with?

A

Associated with
Diarrhoea
Haematuria
Haemoptysis
Hypotension
Urine retention

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43
Q

What are the risk factors for AKI?

A

Age - >75 years
Diabetes Mellitus
Sepsis
Peripheral vascular disease
Family history
Nephrotoxic Drugs
Poor fluid intake/fluid loss
Liver disease
Organ failure - HF

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44
Q

What are the different groups of causes of AKI?

A

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

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45
Q

What are the commonest causes of AKI?

A

Cardiogenic shock

Major Surgery

Nephrotoxins

Sepsis

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46
Q

Give some Pre-renal causes of AKI?

A

Dehydration
Hypotension (shock, Sepsis, Anaphylaxis)
Heart failure

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47
Q

Give some Renal Causes of AKI?

A

Glomerulonephritis
Interstitial nephritis - T1 or T IV hypersensitivity to NSAIDs, Penicillin’s, Diuretics
Acute tubular necrosis
Nephrotoxic Drugs (DAMN)

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48
Q

What are the DAMN drugs that cause nephrotoxicity?

A

Diuretics
ACEis/ARBs
Metformin
NSAIDs

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49
Q

Give some Post renal Causes of AKI?

A

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

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50
Q

Give some examples of drugs that are nephrotoxic

A

DAMN:
Diuretics
ACEi/ARBs/Aminoglycosides (gentamicin)
Metformin/Methotrexate
NSAIDs

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51
Q

What is the pathophysiology of AKI?

A

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

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52
Q

What substances will accumulate in AKI?

A

K+ - hyperkalaemia - arrythmias

Urea - Hyperuraemia - Pruritis and confusion

Fluid - oedema - pulmonary and peripheral

H+ - acidosis

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53
Q

What are the symptoms of AKI?

A

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

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54
Q

What are some clinical signs of AKI?

A

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

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55
Q

What are the primary investigations for AKI?

A
  • 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
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56
Q

What is a good way to establish whether AKI is caused by pre/renal/post renal cause?

A

Urea:Creatine Ratio
U:Cr > 100:1 = pre-renal

U:Cr < 40:1 = renal

U:Cr 40-100:1 = Post renal

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57
Q

What is the treatment for AKI?

A

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)

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58
Q

How would you treat pre-renal, Renal and Post renal causes of AKI?

A

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

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59
Q

What are the indications for RRT?

A

Acidosis (pH < 7.1)
Fluid overload (oedema)
Uremia that is symptomatic
Hyperkalaemia >6.5 or ECG changes

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60
Q

What are some potential complications of RRT?

A

CVD - MI
Infection

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61
Q

What are the major complications of AKI?

A

Hyperkalaemia - leads to cardiac arrest
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis

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62
Q

What is Chronic Kidney Disease (CKD)?

A

Progressive decline in renal Function where GFR <60ml/Min for more than 3 months

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63
Q

What is the Epidemiology of CKD?

A

Between 6-11% of people can be defined as having CKD
Risk increases with age
F>M

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64
Q

What are the common causes of CKD?

A

Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
SLE
Obstructive Uropathy
Medications such as NSAIDS, proton pump inhibitors and lithium

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65
Q

Explain How Hypertension leads to CKD?

A

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

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66
Q

Explain How Diabetes Mellitus Leads to CKD?

A

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

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67
Q

What are the risk factors for CKD?

A

Older age
Hypertension (most common)
Diabetes (most common)
Smoking
Renal artery stenosis
PKD
Use of medications that affect the kidneys
Nephrotoxic Drugs

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68
Q

What are the stages of CKD?

A

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”)

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69
Q

What are the best readings to quantify CKD?

A

eGFR
Urine Albumin:Creatine Ratio (ACR)

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70
Q

What is the pathophysiology of CKD?

A
  • 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
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71
Q

What are the symptoms of CKD?

A

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

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72
Q

How does CKD lead to Bone Disease?

A

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

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73
Q

How does CKD lead to anaemia?

A

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

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74
Q

How can CKD lead to CVD?

A

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

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75
Q

What are the clinical signs of CKD?

A

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

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76
Q

What is the prognosis of CKD correlated with?

A

Poorly controlled HTN
Proteinuria
Degree of scarring on histology

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77
Q

What are the key complications of CKD?

A

Anaemia - due to reduced EPO
Renal bone disease (osteodystrophy due to lack of Vit D activation)
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems

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78
Q

What are the primary investigations in CKD?

A

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

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79
Q

What are the differences Ix findings between AKI and CKD?

A

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

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80
Q

What is the aim of management in CKD?

A

Slow the progression of the disease
Reduce the risk of cardiovascular disease
Reduce the risk of complications
Treating complications

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81
Q

What is the management of CKD?

A

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

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82
Q

What are the different types of Renal Replacement Therapy (RRT)?

A

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.

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83
Q

What are the indications for Dialysis?

A

Symptomatic uraemic including pericarditis or tamponade
Hyperkalaemia not controlled by conservative means
Metabolic acidosis
Fluid overload resistant to diuretics

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84
Q

How can CKD progression be slowed?

A

Optimise diabetic control
Optimise hypertensive control
Treat glomerulonephritis

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85
Q

What are the Major Complications of CKD?

A

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

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86
Q

How can the risk of CKD complications be reduced?

A

Exercise, maintain healthy weight, stop smoking

Special dietary advice (Vit D supplements, Na/K restriction)

Offer Atorvastatin for primary prevention of CVD

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87
Q

What is a Urinary Tract Infection (UTI)?

A

Inflammation of the urothelium in response to an infection that occurs anywhere along the Urinary Tract from the kidneys to the urethra

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88
Q

What is the clinical Definition of a UTI?

A

Pure growth of >10^5 organisms/ml of fresh mid-stream urine

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89
Q

What are the classifications of UTIs?

A

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

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90
Q

What are the organisms that generally cause UTIs?

A

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

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91
Q

What is the most common cause of a UTI?

A

UPEC:
Uropathogenic Escherichia coli (80% of uncomplicated UTIs)

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92
Q

Who are most affected by UTIs?

A

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

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93
Q

What are some pathological mechainisms of getting UTIs?

A

Catheterisation allowing colonisation

Bowel Flora from perineum (often females)

Reduced flow:
Obstruction (prostate, stones)
Low Urinary volume
Stasis during pregnancy

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94
Q

What are the Risk Factors for a UTI?

A

Female
Sexual intercourse
Menopause – less oestrogen 🡪 loss of protective vaginal flora
Catheterisation
Diabetes mellitus – hyperglycaemia stops diapedesis
Pregnancy
Urinary tract obstruction
Malformations
Immunosuppression

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95
Q

What are the Symptoms of an Upper UTI?

A
  • Systemic symptoms
  • Loin/abdominal pain
  • Tenderness
  • Nausea
  • Vomiting
  • Fever
  • Costovertebral angle pain
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96
Q

What are the Symptoms of a Lower UTI?

A

HD FUSS:

Haematuria
Dysuria
Frequency
Urgency
Suprapubic pain
Smelly urine

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97
Q

What are the general symptoms of a UTI?

A

Fever may be only Sx

Abdominal pain, particularly suprapubic pain/discomfort
Vomiting
Dysuria (painful urination)
Urinary frequency
Incontinence
Nocturia

Delirium/Confusion in elderly Px

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98
Q

How are UTIs Diagnosed / what would you find?

A

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

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99
Q

What are some alternative methods to take a Urine Sample?

A

Mid Stream Urine
Catheter Stream Urine
Clean Catch
Bag Urine
Supra Pubic Aspirate
Early morning urine - looks for TB

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100
Q

What would you look for on microscopy in a MC + S)?

A

WBC >10^4 wbc/ml (pyuria)
Bacteria >10^5 cfu/ul = infection
RBCs

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101
Q

What is the Treatment for Any complicated UTI?

A

MC+S and then adjust Abx as needed.
Longer Abx - 7 Days
Give Nitrofurantoin

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102
Q

What are some common Abx used to treat UTIs in the community?

A

Nitrofurantoin (now more commonly used)
Trimethoprim

+ Amoxicillin, Cefalexin

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103
Q

What are the side effects of Nitrofurantoin?

A

nausea, vomiting, liver problems, weakness

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104
Q

Why is Trimethoprim used less to treat UTIs these days?

A

Due to much higher levels of antibiotic resistance

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105
Q

What is the treatment for someone who is >65yrs + and has asymptomatic bacteriuria?

A

Do NOT treat

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106
Q

What is the treatment for someone who is pregnant and has asymptomatic bacteriuria?

A

Give treatment (Nitro/Trim depending on trimester) as 20-40% will go on to develop pyelonephritis

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107
Q

What is Pyelonephritis?

A

Upper UTI of the renal parenchyma and upper ureter at the renal pelvis

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108
Q

When would you avoid treating a UTI with Trimethoprim?

A

First trimester of pregnancy as it interferes with folic acid synthesis

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109
Q

When would you avoid treating a UTI with Nitrofurantoin?

A

Third trimester of pregnancy as there is a risk of Neonatal Haemolysis

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110
Q

What do UTIs during pregnancy increase the risk of?

A

Pyelonephritis
Premature rupture of membranes
Pre-term Labour

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111
Q

How can you prevent UTIs?

A

Drink plenty of fluids
Urination after sex
Good hygiene
Prophylactic antibiotic

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112
Q

What is a major risk of catheterisation?

A

Become colonised with bacteria within a few days.
Can cause serious UTIs

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113
Q

What are some complications of long term cathetisation?

A

UTIs/Pyelonephritis
Stones
Obstruction
Chronic Inflammation

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114
Q

What are risk factors for Pyelonephritis?

A

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

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115
Q

What is the most common causative organism of Pyelonephritis?

A

E.coli (+KEEPS)

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116
Q

What is the Epidemiology of Pyelonephritis?

A

Predominantly females <35
Associated with significant sepsis and systemic upset

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117
Q

What is the pathophysiology of Pyelonephritis?

A
  • 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

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118
Q

What is the classical presentation of Pyelonephritis?

A

Triad:
Loin Pain
Fever
Pyuria - pus in pee

+ nausea/vomiting
Anorexia
Haematuria
Renal angle Tenderness

Signs - Usually Unilateral

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119
Q

What is the primary investigation for Pyelonephritis?

A

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

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120
Q

What is the management of pyelonephritis?

A

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)

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121
Q

What are some complications for Pyelonephritis?

A

Renal Abscesses (common in diabetics)
Emphysematous Pyelonephritis

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122
Q

What are some Differential Diagnoses for Pyelonephritis?

A

Diverticulitis
Abdominal aortic aneurysms
Kidney stones
Cystitis
Prostatitis

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123
Q

What are the main symptoms of lower UTI?

A

Dysuria
Frequency

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124
Q

What is Cystitis?

A

Urinary infection of the bladder
Commonly due to UPEC

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125
Q

Who is affected by Cystitis?

A

More common in women
Can occur in children

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126
Q

What are the risk factors for Cystitis?

A
  • Urinary obstruction resulting in urinary stasis
  • Previous damage to bladder epithelium
  • Bladder stones
  • Poor bladder emptying
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127
Q

What is a classical presentation of Cystitis?

A

Suprapubic tenderness + discomfort
Dysuria
Nocturia
Fever
Increased frequency
Increase urgency
Visible Haematuria

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128
Q

What is the primary Investigations to diagnose Cystitis?

A

1st Line: Urine Dipstick
- Positive for Leukocytes, Blood, Nitrites

Gold Standard: Urine MC+S

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129
Q

What is the treatment for Cystitis?

A

First line:
Nitrofurantoin (1st Trimester)/ Trimethoprim (3rd Trimester)
Cefalexin

Second Line:
Co-amoxiclav/Ciprofloxacin

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130
Q

What is Urethritis?

A

Inflammation in the urethra due to infection

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131
Q

What is the most common cause of Urethritis?

A

Sexually acquired condition:

Non-Gonococcal (Chlamydia) - More common
Gonococcal - Less common

Non infective - trauma

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132
Q

What are the risk factors for Urethritis?

A

Male Gay sex
Unprotected sex

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133
Q

What is the presentation of Urethritis?

A

Maybe ASx
Dysuria +/- urethral discharge (blood/pus)
Penile Discomfort
Urethral pain

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134
Q

What is the diagnostic test for Urethritis?

A

NAAT (Nucleic Acid Amplification Test) - detects STI pathogen (NG/CT)

Urine Dipstick + Urine MC+S if UTI

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135
Q

What is the treatment for urethritis?

A

N.G - IM Ceftriaxone + Oral Azithromycin

C.T - Oral Azithromycin (or Doxycycline) for 1 week

Patient Education and Contact Tracing

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136
Q

What is Epididymo-Orchitis?

A

Inflammation of the epididymus which extends to the testes often secondary to urethritis (STI) or Cystitis.

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137
Q

What is the Eidemiology of Epididymo-Orchitis?

A

Most common in 15-30 and >60

138
Q

What are the symptoms of Epididymo-Orchitis?

A

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
Q

What diagnostic investigations are done for Epididymo-Orchitis?

A

NAAT
Urine Dipstick
Urine MC+S
USS to rule out abscesses

140
Q

What is the treatment for Epididymo-Orchitis?

A

Depends on underlying cause:

STI/UTI to determine Abx

141
Q

What is an uncomplicated UTI?

A

A UTI in a healthy NON-PREGNANT women with a normally functioning urinary tract

142
Q

What is a complicated UTI?

A

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
Q

What is significant about complicated UTIs?

A

Treatment failure is more likely

Complications are more likely:
Renal papillary necrosis
Renal Abscesses

144
Q

What is Benign Prostatic Hyperplasia (BPH)?

A

Benign proliferation of musculofibrous/glandular tissue of the transitional (inner) zone of the prostate that results in lower urinary tract symptoms

145
Q

What are the risk factors for BPH?

A

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
Q

What is the pathophysiology of BPH?

A

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
Q

What is Responsible for the growth of the Prostate in BPH?

A

Dihydrotestosterone is responsible for prostatic growth

148
Q

What are the typical Symptoms that occur in BPH?

A

Lower Urinary Tract Symptoms (LUTS):
o Storage:
- Frequency
- Urgency
- Nocturia
- Incontinence
o Voiding:
- Straining/ Stream Poor
- Hesitancy
- Incomplete Emptying
- Terminal Dribbling

149
Q

What are symptoms of Urinary Storage?

A

Fequency
Urgency
Nocturia (>30%)
Incontinence

150
Q

What are symptoms of urinary Voiding?

A

Straining/ Stream Poor
Hesitancy
Incomplete Emptying
Terminal Dribbling

151
Q

What are the signs of PBH?

A

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
Q

What complications may arise in BPH if the urethra is completely occluded?

A

Auria - no urination

Retention
Hydronephrosis
UTI
Stones

153
Q

What is PSA?

A

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
Q

What are the Diagnostic investigations of BPH?

A

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
Q

What is the treatment for PBH?

A

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
Q

What is the mechanism of action of Tamsulosin?

A

Alpha blocker that will relax the bladder neck increasing urinary flow rate and improving obstructive Sx of BPH

157
Q

What is a side effect of Tamsulosin?

A

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
Q

What is the mechanism of action of Finasteride?

A

5-alpha reductase inhibitor that will block conversion of testosterone to dihydrotestosterone to reduce prostatic growth

159
Q

What are the Side Effects of Finasteride?

A

Fatigue, lethargy and degree of ED and libido loss

160
Q

What is a common complication of transurethral resection of prostate surgery?

A

Retrograde ejaculation.

161
Q

What is Glomerular Disease?

A

Glomerulonephritis refers to groups of parenchymal kidney diseases that all result in the inflammation of glomeruli and nephrons

162
Q

Explain the Structure of the glomerulus?

A

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
Q

What are the classifications of Glomerulonephritis?

A

Nephrotic Syndrome
Nephritic Syndrome (acute GN)
Rapidly Progressive GN

164
Q

What is Nephritic syndrome?

A

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
Q

What are the features of a patient with Nephritic Syndrome?

A

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
Q

Give some conditions that present with a clinical picture of nephritic syndrome?

A

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
Q

What are the investigations for nephritic syndrome?

A
  • 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
Q

What is the general management for Nephritic Syndrome?

A
  • Immunosuppression (e.g. steroids)
  • Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
169
Q

What is the most common cause of Nephritic Syndrome?

A

IgA Nephropathy

170
Q

What is IgA Nephropathy?

A

(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
Q

What is Glomerulonephritis?

A

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
Q

What is Nephrotic Syndrome?

A

Inflammation of Podocytes leads to protein leaking out of kidneys.
Nephrotic syndrome has a set criteria to fit to be classified as NEPHROTIC.

173
Q

What are the features of Nephrotic Syndrome?

A

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
Q

What is the criteria for Nephrotic syndrome?

A

A Px must Fulfil:

Peripheral oedema - due to 3rd spacing
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia

175
Q

What is the main Difference between Nephritic and Nephrotic syndrome?

A

In Nephritic syndrome - Haematuria predominates

In Nephrotic Syndrome - Proteinuria Predominates

176
Q

What is the characteristic Presentation Nephritic Syndrome?

A

Visible Haematuria
(Ribena/coke coloured Pee)

Arterial HTN

Peripheral Oedema

Oligouria

177
Q

What are the primary investigations for IgA nephropathy?

A

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
Q

What is the Treatment for IgA nephropathy?

A

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
Q

What is Post strep Glomerulonephritits (PSGN)?

A

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
Q

How long does it take to develop PSGN after infection?

A

2 weeks after pharyngitis from S. pyogenes

181
Q

How is PSGN Diagnosed?

A
  • 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
Q

What is the treatment of PSGN?

A

Only Sx management - Self limiting usually

Abx for strep infection - Amoxicillin/Flucloxacillin
Could Use furosemide for HTN

May progress to rapidly progressive GN

183
Q

How can SLE cause Nephropathy?

A

Cause Lupus nephritis secondary to SLE

Deposition of Antigen-antibody complexes and ANA in the kidneys leads to nephritis and a nephritic picture

184
Q

How is Lupus Nephritis diagnosed?

A

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
Q

What is the most common form of Lupus Nephritis?

A

Diffuse proliferative glomerulonephritis

186
Q

How is Lupus Nephritis treated?

A

Lifestyle - stop smoking, exercise, dietary advice

Medication:
Corticosteroids -
Immunosuppressive agents - Azathioprine

Hydroxychloroquine

187
Q

What is good Pasture’s Syndrome?

A

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
Q

What is the diagnosis of good pasture’s Syndrome?

A

Serology - Anti-GBM Abs

Renal Biopsy:

  • Light microscopy may show crescentic glomerulonephritis
  • Immunofluorescence staining shows linear deposition of IgG along glomerular capillaries
189
Q

What is the treatment for Goodpasture’s Syndrome?

A

plasmapheresis,
steroids and cyclophosphamide.

190
Q

What is the pathology of Nephrotic Syndrome?

A

Underlying pathology that leads to direct sclerosis of podocytes on the glomerulus leading to the clinical features of nephrotic syndrome

191
Q

What conditions lead to a nephrotic syndrome clinical picture?

A

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
Q

What are the investigations for Nephrotic Syndrome?

A

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
Q

What would be seen on Light and Electron microscopy in Nephrotic Syndromes:
Minimal Change
Focal Segmental Glomerulosclerosis
Membranous Nephropathy
Diabetes

A
  • 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
Q

What is the general treatment of Nephrotic Syndromes?

A

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
Q

What is Minimal Change disease?

A

Most common cause of nephrotic syndrome in children:

often due to a benign excessive response to steroids

196
Q

What is the Pathology of Minimal Change Disease?

A

Cytokines attack foot processes of podocytes
Shrinkage/blunting of podocytes 🡪 protein leakage

197
Q

What is the diagnostic findings for Minimal change disease?

A

Renal Biopsy

Light microscopy - normal/no change

Electron Microscopy - Podocyte effacement + fusion

198
Q

What is Focal Segmental Glomerulonephritis (FSG)?

A

Most common cause of Glomerulonephritis and nephrotic syndrome in adults:

Associated with HIV, heroin use, sickle cell

199
Q

What are the diagnostic findings for focal segmental glomerulonephritis?

A

Renal Biopsy and Light Microscopy

  • Segmental sclerosis and hyalinosis
  • Focal so only part of the glomerulus is affected
200
Q

What is Membranous Nephropathy?

A

The most common cause of nephrotic syndrome in the elderly:

Associated with malignancy, hepatitis B, NSAIDs, SLE

201
Q

What are the diagnostic Findings of Membranous Nephropathy?

A

Light microscopy

  • Thickened Glomerular BM

Electron Microscopy

  • Sub epithelial immune complex deposition
    Spike + Dome appearance.
202
Q

What is the characteristic clinical picture of Nephrotic syndrome?

A

Frothy urine (proteinuria)

Hypalbuminaemia

Facial and peripheral oedema

Predisposition to thromboembolic disease

Recurrent Infections

Hypertension

203
Q

What conditions can cause both a Nephritic and Nephrotic syndrome clinical picture?

A

Diffuse Proliferative glomerulonephritis

Membranoproliferative Glomerulonephritis:
Tram Tracks on light Microsco

204
Q

What is obstructive uropathy?

A

Blockage of urine flow that can affect one or both kidneys depending on the level/site of the blockage

205
Q

What conditions can cause obstructive uropathy?

A

BPH, Malignancy and stones

206
Q

What is the pathogenesis of obstructive uropathy?

A

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
Q

What is the treatment of obstructive uropathy?

A

Relieve kidney pressure:
Catheterise / ureteral stent

Tx of cause of obstruction
BPH - Tamsulosin
Stones - ESWL/PCNL

208
Q

What are the main types of GU cancer?

A

Renal Cell Carcinoma
Bladder Cancer
Prostate Cancer
Testicular Cancer

209
Q

What is Renal cell Carcinoma?

A

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
Q

What is Wilms Tumour?

A

A specific renal mesenchymal stem cell tumour that affects children typically under 5 years old

(A.K.A Nephroblastoma)

211
Q

What are the main subtypes of Renal cell carcinoma?

A

Clear cell (80%)

Papillary (15%)

Chromophobe (5%)

212
Q

What are the risk factors for Renal cell carcinoma?

A

Smoking
Obesity
Hypertension
End-stage renal failure
Von Hippel-Lindau Disease
PCKD
Tuberous sclerosis

213
Q

What is the Pathology of RCC?

A

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
Q

How does Renal cell carcinoma typically present?

A

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
Q

What are the primary investigations for renal cell carcinoma?

A

1st Line: USS
Gold Standard: CT CAP - Diagnostic

Bloods:
U&Es - renal dysfunction
LFTs - liver mets
LDH - if increased = poor prognosis

216
Q

What is the treatment for Renal Cell carcinoma?

A

25% have Mets at Presentation

Partial/Full Nephrectomy

217
Q

What is the the most common type of kidney cancer in adults?

A

Renal Cell Carcinoma

218
Q

What are the complications of RCC?

A

Paraneoplastic Syndromes - Production of Hormones:
EPO – more RBCs 🡪 polycythaemia
PTHrP – hypercalcaemia
ACTH – more cortisol 🡪 Cushing’s

219
Q

What is bladder cancer?

A

Often a transitional cell carcinoma of the bladder due to the transitional epithelium (urothelium) that lines the renal pelvis, bladder, ureter and urethra

220
Q

What is the Epidemiology of Bladder Cancer?

A

4th most common cancer in men
8th most common cancer in women

221
Q

When is a patient more likely to have squamous cell carcinoma of the bladder?

A

If they have Schistosomiasis infection

222
Q

What is the most common type of bladder cancer?

A

Transitional urothelium cancer (bladder cancer)

This lines the renal pelvis and bladder

223
Q

What are the risk factors for Bladder cancer?

A

Age >40yrs
Male
Smoking
Occupational Exposure - Dyes/paints/rubber
Aromatic Amines
FHx

224
Q

What are the signs and symptoms of Bladder cancer?

A
  • 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
Q

What are the primary investigations for bladder cancer?

A

Gold Standard:
Flexible Cytoscopy + biopsy

CT AP - for staging

226
Q

What is the treatment of bladder cancer?

A

Conservative - support
Surgical:
Transurethral Resection of Bladder Tumour (TURBT)
Cystectomy - last resort

Medical:
Chemotherapy
Radiotherapy

227
Q

What is the most common cancer in males?

A

Prostate cancer

228
Q

What is the most common type of prostate cancer?

A

Adenocarcinoma that arises from the peripheral zone of the prostate.

These are often neoplastic and malignant which spread to bones

229
Q

What are the types of Prostate Cancer?

A

Adenocarcinomas – most common, arise from peripheral zone

Transitional cell carcinomas – arise from transitional zone

Small cell prostate cancer – arise from neuroendocrine cells

230
Q

What are the risk factors for prostate cancer?

A

Environmental
Genetics
High fat/low Fibre diet
Increasing age
Afro-Caribbean ethnicity
FHx - accounts for 8% of cases

231
Q

Why is there an increase in the prevalence of prostate cancer?

A

Ageing population
Increased detection

232
Q

What genetic factors increase a patients risk of prostate cancer?

A

BRCA1/2 Mutations
HOXB13

233
Q

What is the presentation of prostate cancer?

A

LUTs (Frequency, Hesitancy, terminal dribbling)

Systemic Cancer Sx (weight loss, fatigue night pain)

Bone pain - suggests metastasised to bone (typically lumbar back pain)

234
Q

What are the investigations for prostate cancer?

A

DRE + PSA in community

New First Line:
Multiparametric MRI

Previously Gold Standard:
Transrectal USS + biopsy - Diagnostic

235
Q

What is the grading system used for prostate cancer?

A

Gleason Score
High = worse prognosis

236
Q

What area of the prostate is commonly affected by prostate cancer?

A

Peripheral zone

237
Q

What are the common metastatic sites for prostate cancer?

A

Bones - sclerotic lesions
Brain
Liver
Lungs

238
Q

What are the primary prevention methods for Prostate cancer?

A

Screening? - PSA test (benefits dont necessarily outweigh harms of screening)

Chemoprevention - 5 alpha reductase inhibitors

Diet and Supplements

Exercise and weight control

239
Q

What is the treatment for Prostate cancer?

A

Local - Watchful waiting/Prostatectomy/radiotherapy

Advanced- Hormone therapy (GnRH agonists)

Metastatic - surgical/medical castration (orchidectomy)

240
Q

What is the purpose of Hormone Therapy in prostate cancer?

A

Reduce testosterone - reduce cancer growth

241
Q

What are some options for hormone therapy for prostate cancer?

A

Surgical:
Bilateral Orchidectomy - Testicular removal (castration)

Medical:
GnRH receptor agonists - Goserelin
Androgen Receptor Blockers - Enzalutamide

242
Q

How do GnRH receptor agonists work?

A

Goserelin:
Agonist GnRH and therefore these increase LH and FSH

but this leads to exogenous suppression of the HPG axis

243
Q

What is the treatment for metastatic prostate cancer?

A

Surgical Castration
Medical castration (GnRH agonists)
Palliative care

244
Q

What is the most hormone sensitive cancer?

A

Prostate cancer

245
Q

What are the differential Diagnoses for Prostate Cancer?

A

BPH
Prostatitis
Bladder tumour

246
Q

What are the two classes of testicaular tumour?

A

Germ cell (90%):
Seminoma - most common
Teratoma

Non-Germ Cell (10%):
Sertoli
Leydig
Sarcoma

247
Q

What is the most common cancer in young men (20-40yrs)

A

Testicular Cancer

248
Q

What are the risk factors for testicular cancer?

A

Cryptorchidism - undescended teste
Infertility
FHx

249
Q

What is the presentation of Testicular Cancer?

A

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
Q

What are the signs for Testicular cancer?

A

Hydrocele
Abdominal/Testicular Mass

251
Q

What are the primary investigations for testicular cancer?

A

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
Q

What is the treatment of Testicular cancer?

A

ALWAYS 1ST LINE:
Urgent orchidectomy
offer sperm storage

Adjuvant chemotherapy/radiotherapy

253
Q

What is Polycystic Kidney Disease (PKD)?

A

Cyst formation throughout the renal parenchyma often leading to bilateral enlargement and damage

254
Q

Why may a patient have left sided varicocele in renal cell carcinoma?
(and not Right sided)

A

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
Q

What are the causes of PKD?

A

Simple – develop over time
Acquired – CKD
Drugs – lithium (used for treating depression)
Autosomal dominant/recessive – genetic cause
Syndromic disease – tuberous sclerosis

256
Q

What are the types of Inherited PKD?

A

Autosomal Dominant PKD (ADPKD)

Autosomal Recessive PKD (ARPKD)

257
Q

When does ADPKD typically present?

A

Often presents in later life/adults

258
Q

When does ARPKD typically present?

A

Often presents in neonates and is found on antenatal uss

259
Q

Which is more common ADPKD or ARPKD?

A

ADPKD is more common

260
Q

What are the genetic factors leading to ADPDK?

A

Mutated PKD1 (85%) or PKD2 (15%) on chromosome 16 and chromosome 4 respectively

261
Q

Who is typically affected by ADPKD?

A

More males

262
Q

What are some facts about ARPKD?

A

Much less common that ADPKD
A disease of infancy/prebirth
High mortality rate
Many congenital abnormalities

263
Q

What are the genetic factors leading to ARPKD?

A

Mutation in PKHD1 on chromosome 6

264
Q

What is the pathogenesis of ARPKD?

A

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
Q

What are some consequential features of ARPKD?

A

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
Q

What is the pathophysiology of ADPKD?

A

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
Q

What is the presentation of ADPKD?

A

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
Q

What are the symptoms of ADPKD?

A

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
Q

What are the signs of ADPKD?

A

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
Q

What is the diagnostic investigation of PKD?

A

Kidney Uss - Enlarged bilateral kidneys with multiple cysts

Genetic testing for PKD1/2 mutations
FHx of PKD

271
Q

What are the diagnostic findings on ultrasound for ADPKD?

A

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
Q

What is the management of PKD?

A

Non-curative

Manage Sx:
HTN - ACEi
ESRF - RRT

273
Q

What are some differential Diagnoses of ADPKD?

A

Acquired and simple cysts of kidneys
Autosomal recessive PKD
Medullary sponge kidney
Tuberous sclerosis

274
Q

What are some ongoing problems throughout life that Px with PKD may have?

A

Liver failure due to liver fibrosis
Portal hypertension leading to oesophageal varices
Progressive renal failure
Hypertension due to renal failure
Chronic lung disease

275
Q

What are the common STIs?

A

Chlamydia F>M
Gonorrhoea M>F
Syphilis

276
Q

What is Chlamydia?

A

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
Q

What are risk factors for Chlamydia?

A

Age < 25
Multiple Sexual partners
Unprotected Sex
Sharing unwashed sex toys

278
Q

What are the sites of infection for Chlamydia and Gonorrhoea?

A

Adult – both infect non-squamous epithelia
Urethra
Endocervical canal
Rectum
Pharynx
Conjuctiva

Neonate:
Conjuctiva
Atypical pneumonia also in neonatal chlamydia

279
Q

What are the symptoms of Chlamydia?

A

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)

280
Q

What is the primary investigation for chlamydia?

A

NAAT
looks for DNA/RNA of chlamydia

Females - self collected vaginal swap
Males - First Void Urine

281
Q

What is the treatment for Chlamydia?

A

doxycycline 100mg twice a day for 7 days.

282
Q

What are some complications of Chlamydia?

A

Pelvic inflammatory disease
Chronic pelvic pain
Infertility
Ectopic pregnancy
Epididymo-orchitis
Conjunctivitis
Lymphogranuloma venereum
Reactive arthritis

283
Q

What is Gonorrhoea?

A

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

284
Q

What are the risk factors for Gonorrhoea?

A

Frequent uprotected sex
MSM (men who have sex with men)
multiple sexual partners

285
Q

What are the symptoms of Gonorrhoea?

A

More commonly Symptomatic (90% males and 50% females)

Odourless purulent discharge, possibly green or yellow
Dysuria
Pelvic pain
Testicular pain or swelling (epididymo-orchitis)

286
Q

What are the primary investigations for gonorrhoea?

A

NAAT

Charcoal endocervical swab and microscopy and culture
Male - From Urethra
Female - Endocervix

287
Q

What is the treatment for gonorrhoea?

A

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

288
Q

What is Syphilis?

A

An STI caused by the bacteria Treponema Pallidum.

This can get into the mucous membranes and then disseminate throughout the body

289
Q

How can Syphilis be contracted?

A

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

290
Q

What are the stages of syphilis infection?

A

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

291
Q

What are gummas?

A

granulomatous lesions that can affect the skin, organs and bones secondary to syphilis

292
Q

What are the primary diagnostic investigations of syphilis?

A

Treponemal Antibody testing - positive if ulcer present for >2 weeks

Early Moist Lesions - Dark Field Microscopy

PCR

293
Q

What is the treatment for Syphilis

A

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

294
Q

What are some non-cancerous scrotal diseases?

A

Varicocele
Testicular Torsion
Epididymal Cyst
Hydrocele

295
Q

What is a Hydrocele?

A

A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes

296
Q

What are the Examination findings of a Hydrocele?

A

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)

297
Q

What is the definitive diagnostic Ix for Hydrocele?

A

USS scrotum
Serum AFP/HCG to exclude tumours

298
Q

What is the management of Hydrocele?

A

Exclude serious causes
Many Resolve Spontaneously

Surgery/aspiration to remove fluid

299
Q

What are some causes of Hydrocele?

A

Idiopathic
Testicular cancer
Testicular torsion
Epididymo-orchitis
Trauma

300
Q

What is an Epididymal Cyst?

A

An extra-testicular cyst found above and behind the testes that WILL transilluminate.

301
Q

What is the Presentation, Diagnosis and Treatment of an Epididymal Cyst?

A

Sx - often asymptomatic - painful if large

Dx - Scrotal Uss

Tx - none (they are harmless). Removal considered if painful

302
Q

What is a varicocele?

A

A varicocele occurs where the veins in the pampiniform plexus become swollen. They are common, affecting around 15% of men

303
Q

What is the pathophysiology of a varicocele?

A

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.

304
Q

What may a left sided Varicocele suggest?

A

Renal Cell Carcinoma
therefore check for this.

305
Q

What are the examination findings of a varicocele?

A

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

306
Q

What is the diagnostic investigation for a varicocele?

A

Clinical Dx

Colour Doppler USS of Scrotum

307
Q

What is the management of a Varicocele?

A

Conservative Mx

Can be surgically treated if painful

308
Q

What are some potential complications of a Varicocele?

A

Testicular atrophy
Infertility

309
Q

What is Testicular Torsion?

A

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.

310
Q

Who is typically affected by Testicular Torsion?

A

Typical patient is a teenage boy but can occur at any age

311
Q

What are the causes of Testicular Torsion?

A

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

312
Q

What is the pathology of testicular Torsion?

A

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

313
Q

What are the symptoms of Testicular Torsion?

A

Acute rapid onset unilateral testicular pain

abdominal pain

Nausea and vomiting

314
Q

What are the examination findings for testicular torsion?

A

Firm swollen testicle
Elevated (retracted) testicle
Absent cremasteric reflex
Abnormal testicular lie (often horizontal)
Rotation, so that epididymis is not in normal posterior position

315
Q

What are risk factors for testicular torsion?

A

Bell clapper deformity:

316
Q

what is a bell clapper deformity?

A

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

317
Q

What is the diagnostic Ix of testicular torsion?

A

if suspected the medical emergency and surgical exploration is always first line

USS doppler can confirm diagnosis but this will delay treatment

318
Q

What is the treatment for Testicular torsion?

A

Surgical treatment within 6hrs:

Viable testicle - orchioplexy (untwisting and fixing to scrotal sac)

Unviable testicle - Orchiectomy

319
Q

What is a testicular appendage torsion?

A

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

320
Q

What are the classifications of lower urinary tract symptoms (LUTS)

A

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

321
Q

When do storage symptoms and voiding symptoms occur

A

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

322
Q

What is generally affected by incontinence?

A

Females

323
Q

Who is generally affected by Urine retention?

A

(overflow incontinence)
Males

324
Q

What are the different types of Incontinence?

A

Stress (sphincter weakness from pregnancy/trauma) - pee leaks with increased abdo pressure

Urge - detrusor muscle overactivity

Spastic paralysis - UMN lesion

325
Q

What is the treatment for incontinence?

A

surgery
Anticholinergic drugs

326
Q

What are the causes of urinary retention?

A

Obstruction:
Stones
BPH
Neurological flaccid paralysis

327
Q

What is the treatment for Urinary retention?

A

Tx underlying cause
Catheterise

328
Q

What are the Red flags LUTS?

A

Haematuria
Proteinuria

329
Q

What is Detrusor overactivity

A

urodynamic observation characterized by involuntary detrusor contractions during the filling phase that may be spontaneous or provoked

330
Q

What drug class are used to treat overactive bladder?

A

Anti-Cholinergics (inhibit Detrusor contraction)
Oxybutynin
Solifenacin

Mirabegron (beta 3 agonist that Activate relaxation of the detrusor muscle)

331
Q

What surgical procedure could be used for overactive detrusor muscle?

A

Cystoplasty

332
Q

What is the Neural control of the lower urinary tract?

A

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

333
Q

What are the 3 classifications for for neuro-urophysiological dysfunction?

A

Brain Problems
Supra-sacral spinal problems
Sacral Spinal Problems

334
Q

What are the 3 spinal reflexes involved in bladder function?

A

Reflex Bladder Contraction - Sacral micturition centre
Guarding - Onuf’s Nucleus
Receptive relaxation (sympathetic)

335
Q

Where does co-ordination of voiding occur?

A

Pontine micturition centre
Allows for completion of voiding.
(However there is a Higher cortical control to decide when to void.)

Peraquductal grey

336
Q

What is Detrusor Sphincter Dyssynergia?

A

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.

337
Q

What are the aims of management of a neurogenic bladder

A

Prevent autonomic dysreflexia
Bladder safety
Continence and Sx control.

338
Q

What is autonomic dysreflexia?

A

Occurs lesions above T6
Overstimulation of sympathetic NS below level of lesion in response to noxious stimulus

Sx are headache, Severe HTN, Flushing

339
Q

What is the most common cause of Autonomic Dysreflexia

A

A full Bladder

340
Q

How is Autonomic Dysreflexia treated?

A

Catheterise and the bladder will drain reducing the dysreflexia

341
Q

What is an Unsafe bladder?

A

A bladder that will damage the kidneys most commonly due to prolonged high bladder pressure.

342
Q

What is the target urine output for an adult?

A

0.5-1.5ml/kg/hr

Phase 2a (24 decks)

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