Urinary diseases Flashcards

1
Q

How does a UTI present?

A

Dysuria (pain on micturition), frequency and smelly urine.

  • If very young = unwell, failure to thrive
  • Very old = incontinence, off their feet
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2
Q

What is a UTI?

A

Urinary tract infection

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3
Q

What are the bacteriostatic properties of a normal urinary tract?

A
  • Free flow of urine through normal anatomy - assume drinking enough fluids.
  • Low pH, high osmolarity, and high ammonia content of normal urine
  • Prostatic secretions are bacteriostatic
  • anti-bacterial antibodies
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4
Q

Is a normal renal tract sterile?

A

Urinary tract sterile except for terminal urethra which contains perineal and gut flora.

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5
Q

Why do we want a Mid Stream Specimen of urine?

A

Urethra flora diminished but always present.

Patients void and stop mid stream, discarding urine then collects next volume.

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6
Q

How can we tell contamination is from real infection?

A

MSSU - microbiology for culture under set conditions.
Can count the number of bacteria - 10 to power 5 = usually infection. (99% accuracy)
10 to power 3-4 = infections sometimes ( if symptoms) more likely.
Less than 10 to 3 = usually no infection.

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7
Q

What are the main micro-organisms that cause UTI?

A

Gut flora - especially E.coli

Viral infection rare.

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8
Q

What is the route of infection?

A

Almost always ascending: Infection in kidneys usually infection has spread up from bladder. Upper UTI = more serious.

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9
Q

What is:

  1. Urethritis
  2. Cystitis
  3. Ureteritis
  4. Acute/chronic pyelonephritis?
A
  1. Inflammation of urethra
  2. Inflammation of bladder
  3. Inflammation of ureter
  4. Inflammation of kidney / If recurrent to prolonged chronic inflammation.
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10
Q

What are the predisposing factors to UTI?

A
  1. Stasis of urine
  2. Pushing bacteria up urethra from below
  3. Generalised predisposition to infection
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11
Q

What can cause stasis of urine?

A
  1. Obstruction, congenital or acquired

2. Loss of feeling of full bladder - spinal cord/brain injury

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12
Q

What can cause pushing bacteria up urethra from below?

A
  1. sexual activity in females

2. Catheterisation (other urological procedures)

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13
Q

What are the consequences of obstruction?

A
  1. Proximal dilatation
  2. slowed urine flow - cannot flush out bacteria - infection
  3. Slowed urine flow - sediments form calculous (stone) formation - obstruction
  4. Triad - infection - calculi - obstruction.
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14
Q

What are the common causes of obstruction in adults?

A

Men - benign prostatic hyperplasia of prostate - functional and anatomical obstruction.
Women - uterine prolapse
Both sexes - tumours and calculi.

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15
Q

What can causes obstruction in children?

A

Numerous renal tract abnormalities

Most important example = vesicoureteric reflux.

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16
Q

What is vesicoureteric reflux?

A

Decreased angulation - bladder - ureter reflux.

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17
Q

How does sexual activity in females cause UTI?

A

Tends to move lower urethral flora up the tract (back wall of urethra is just in front of vagina)

  • Short urethra
  • Lack of prostatic bacteriostatic secretion
  • Closeness of urethral orifice to rectum
  • pregnancy - pressure on ureters and bladder.
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18
Q

What are some of the generalised predisposition to infection that cause UTI’s?

A

Glucose in urine - diabetes

Poor function of WBC

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19
Q

What are the complications of UTI?

  1. Acute
  2. Chronic
A
  1. Severe sepsis and septic shock (bacteria get into blood)
  2. Chronic damage to kidneys if repeated infections - lead to hypertension, chronic renal failure
    - Calculi - obstruction - hydroneophrosis.
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20
Q

What is contained in the filter barrier of the glomerulus?

A

Membrane:

Endothelial cell cytoplasm, basal lamina (connective tissue) and podocyte.

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21
Q

What are mesangial cells>

A

“tree like” group of cells which support capillaries

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22
Q

What is Glomerulonephritis?

A

Disease of glomerulus
Inflammatory or non-inflammatory
Primary or secondary.

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23
Q

Causes of Glomerulonephritis

A

Immunoglobulin depostition

Some are diseases with no immunoglobulin deposition e.g. diabetic glomerular disease.

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24
Q

What are the 4 common presentations of Glomerulonephritis?

A
  1. Haematuria (blood in urine)
  2. Heavy proteinuria (nephrotic syndrome)
  3. Slowly increasing proteinuria
  4. Acute renal failure
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25
Q

What are the main causes of Haematuria?

A

UTI
UT stone
UT tumour
Glomerulonephritis

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26
Q

Causes of IgA glomerulonephritis? (GN)

A

Unknown - could be excess antibody produced?

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27
Q

What happens in IgA GN?

A

Mesangium becomes clogged with antibody. Red blood cells then escape into urine. Causes proliferation and production of more matrix.

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28
Q

What is prognosis of IgA nephropathy?

A

Usually self-limiting, i.e. return to normal

Small percent go onto chronic renal failure.

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29
Q

What happens in Membranous glomerulonephritis?

A

Thickened glomerular basement membrane
IgG stuck in membrane - between basal lamina dn podocyte.
IgG too big to be filtered into urine. But activates complement which punches holes in filter.

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30
Q

What does the leaky filter cause?

A

Albumin to be filtered into urine - nephrotic syndrome

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31
Q

Prognosis of Membranous GN?

A

1/4 chronic renal failure within 10 years.

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32
Q

Diabetic nephropathy prognosis

A

Inevitable decline if established or continued poor diabetic control.

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33
Q

What is Crescentic GN?

A

Granulomatosis with polyangiitis - form of vasculitis (inflammation in vessels)
Antiglomerular basement membrane disease.

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34
Q

Wegener’s prognosis

A

Fatal if left untreated.

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35
Q

When thinking of what could be the cause of symptoms and presentation what should we think about?
Surgical sieve

A
Infection 
Inflammation 
Iatrogenic 
Neoplasia 
Trauma 
Degenerative 
Congenital 
Genetic/Hereditary 
Vascular 
Endocrine 
Failure 
Idiopathic
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36
Q

Nature of renal diseases what are we looking for?

A

Infection - pyelonephritis
Inflammation - glomerulonephritis
Iatrogenic - nephrotoxicity, PCNL
Neoplasia - renal tumours, collecting system tumours
Trauma - blunt
Vascular - atherosclerosis, hypertension, diabetes
Hereditary - polycystic kidney disease, nephrotic syndrome

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37
Q

Presentation of renal diseases

A
Pain
Pyrexia
Haematuria 
Proteinuria 
Pyuria (leukocytes)
Mass on palpation 
Renal failure
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38
Q

Define proteinuria

A

Urinary protein excretion > 150mg/day

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39
Q

How many types of haematuria are there?

A

3 - microscopic, macroscopic and dip stick

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40
Q

What is the definition of microscopic haematuria?

A

> 3 or equal to 3 red blood cells per high power field.

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41
Q

Define the following:

  1. Oliguria
  2. Anuria
  3. Polyuria
  4. Nocturia
  5. Nocturnal polyuria
A
  1. Urine output < 0.5 ml/kg/hour
  2. Absolute anuria = no urine output; relative = <100ml/24hr
  3. Urine output > 3l/24hr
  4. Waking up at night are than 1 occasion to pee
  5. Nocturnal urine output > 1/3 of total urine output in 24 hr (frequency volume chart)
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42
Q

Acute kidney injury:

What is the RIFLE staging criteria?

A
  1. Risk - increase in serum creatinine level (1.5x) or decrease in GFR by 25%. UO <0.5ml for 6 hr
  2. Injury - increase in serum creatinine level (2x) or decrease in GFR by 50%. UO<0.5ml for 12 hr
  3. Failure - Increase serum creatinine level (3x), decrease in GFR by 75% or UO < 0.3 for 24hr or Anuria for 12 hr
  4. Loss - persistent ARF or complete loss of kidney function > 4 weeks
  5. End stage kidney disease - completely loss of kidney function > 3 months
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43
Q

Chronic renal failure:

Presentation

A
Asymptomatic (found on blood and urine testing)
Tiredness
Anemia 
Oedema 
High Blood pressure 
Bone pain due to renal bone disease 
Pruritus (in advanced and all below) 
Nausea/vomiting
Dyspnoea 
Pericarditis 
Neuropathy 
Coma
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44
Q

Presentation of ureteric diseases

A
Pain (renal colic 10/10) 
Pyrexia 
Haematuria
Palpable mass
Renal failure (only if bilateral obstruction or single functioning kidney)
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45
Q

What are the different natures of ureteric disease?

A
  1. Infection - ureterirtis
  2. Trauma/Iatrogenic - hysterectomy or inadvertently cut.
  3. Neoplasia - TCC of ureter or bladder obstructing VUJ, prostate cancer. (transitional cell carcinoma)
  4. Hereditary - PUJ obstruction, VUJ reflux
  5. Obstruction
    - intra-luminal (stone, blood clot)
    - intra-mural (scar tissue, TCC)
    - Extra-luminal (pelvic mass, lymph nodes)
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46
Q

Natures of bladder disease

A
  1. Infection - cystitis
  2. Inflammation - interstitial cystitis, colonic diverticulitis
  3. Iatrogenic/trauma - Bladder rupture, bladder injury from hysterectomy
  4. Neoplasia - TCC of bladder, SCC of bladder
  5. Idiopathic - overactive bladder syndrome
  6. Degenerative - Chronic urinary retention
  7. Neurological - neurogenic bladder dysfunction
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47
Q

Presentation of bladder disease

A

Pain (suprapubic)
Pyrexia
Haematuria
LUTS:
- storage - frequency, nocturne, urgency, urge
- Voiding - poor flow, intermittency, terminal dribbling - underachieve bladder
- Incontinence - stress, urge, mixed,overflow

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48
Q

Nature of bladder outflow tract diseases

A

Infection/inflammation - prostates, balanitis
Iatrogenic/trauma - pelvic floor damage, urethral injury
Neoplasia - prostate cancer, penile cancer
Idiopathic - chronic pelvic pain syndrome
OBSTRUCTION - primary bladder neck obstruction, benign prostatic enlargement, urethral stricture, metal stenosis.

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49
Q

Presentation of bladder outflow tract diseases

A
Pain 
Pyrexia 
Haematuria 
Lower urinary tract symptoms
Recurrent UTIs
Acute urinary retention 
Chronic urinary retention
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50
Q

Define acute urinary retention

A

Painful inability to void with a palpable and percusible bladder.
- BPO

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51
Q

Define Chronic urinary retention

A

Painless, palpable and permissible bladder after voiding.

- detrusor under activity

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52
Q

What types of organisms can be seen in a UTI?

A
E.coli
Staph saprophyticus
Klebsiella proteus
Pseudomonas
Staph aureus
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53
Q

Complications of UTI

A
Infective sepsis
Renal failure 
Bladder malignancy 
Acute urinary retention 
Bladder/renal stones
frank haematuria
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54
Q

Treatment for UTI

A

Appropriate oral antibiotic therapy

Treat complications and cause.

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55
Q

Investigations for UTI

A

Urine dipstick
Urine microscopy
Culture and sensitivity

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56
Q

How do we assess for kidney disease?

A

Filtration (excretory) function - remove
Filtration (barrier) function - retain
Anatomy - structural abnormality

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57
Q

How do we measure excretory Renal function?

A

Isotope GFR used if someone is donating a kidney.

Used all the time is serum creatinine to measure eGFR.

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58
Q

What is the problem with using creatinine?

A

generated from breakdown of muscle and not everyone has same muscle mass - depends on age, ethnicity, gender, weight.
Also It will not be raised above normal range until 60% of total kidney function is lost.

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59
Q

How do we assess kidney filtering function?

A

Urinalysis - dipstick for blood and protein.

PCR - protein creatinine ratio

60
Q

Definition of CDK

A

Chronic kidney disease - presence of kidney damage (abnormal blood, urine, or x-ray) or GFR<60 this is present for > 3 months.

61
Q

Causes of CDK

A
Diabetes
Genetic disorders - Polycystic kidney disease 
Glomerulonephritis 
Systemic disease - high BP
Reno vascular disease
62
Q

Symptoms of CKD

A
Risk factors present
Fatigue 
Peripheral oedema 
Nausea and vomiting 
Anorexia 
Pruritis (itch and cramps)
63
Q

What to look for in 1. History and 2. Examination

A
  1. Previous renal disease, sam history, systemic diseases, drug exposure, pre/post renal factors, uraemia symptoms
  2. Vital signs, VOLUME STATUS, obstruction
64
Q

What tests should be carried out for CKD?

A

Blood tests - FBC, U&Es
Urine tests - dip, PCR and ACR (24hr collection)
Histology - Renal biopsy (specifically in glomerulus)
Radiology - US, CT

65
Q

How can you slow rate of renal decline?

A

BP control
Control proteinuria (particularly ACE inhibitors)
Treat underlying cause

66
Q

Complications of CDK

A
Acidosis - bicarb 
Anaemia - EPO and iron 
Bone disease - diet and phosphate binders 
CV risk - BP - aspirin, exercise 
Electrolytes - diet and consider drug 
Fluid overload - salt and fluid restriction 
Gout - optimise plus/minus meds. 
Hypertension - weight, diet, drugs
67
Q

Glomerulonephritis features

A

Haematuria - cola coloured, nephritic > nephrotic, dysmorphic RBC.
Proteinuria - Persistent, proteinuria of more than 1 gram.
Hypertension
Renal insufficiency

68
Q

What is a nephritic state?

A

Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
hypertension
renal impairment

69
Q

What presentation occurs with nephrotic syndrome?

A
Oedema 
Proteinuria > 3.5 g/day
Hypoalbuminemia 
Hyperlipidemia 
Can be caused by primary or secondary glomerular diseases.
70
Q

Causes of glomerulonephritis

A

Autoimmune, infection, malignancy, drugs

71
Q

Treatment for post-infective glomerulonephritis

A

Antibiotics for infection
Loop diuretics such as frusemide for oedema
Vasodilator drugs for hypertension (amlodipine)

72
Q

IgA nephropathy (most common) presentation

A

Microscopic haematuria and proteinuria
Nephrotic syndrome
IgA crescentic glomerulonephritis

73
Q

Treatment for crescentic GN

A

High dose steroids, cyclophosphamide, plasma exchange, B cell therapy.

74
Q

Anti - GBM disease presentation and treatment

A

Nephritis + lung haemorrhage.

Treatment - aggressive immunosuppression: steroid, plasma exchange, cyclophosphamide

75
Q

Proliferative GN summary

A

Nephritic syndrome
Blood on dipstick
Rapid decline in renal function can be seen
Early diagnosis and treatment needed.

76
Q

What shows with proliferative GN?

A

Excessive numbers of cells in glomeruli. Infiltrating leucocytes.

77
Q

What shows in Non-proliferative GN?

A

Glomeruli look normal and have areas of scaring. Normal number of cells.

78
Q

Nephrotic syndrome-management

A

General measures:

treat oedema, hypertension, reduce risk of thrombosis, reduced risk of infection.

79
Q

What is minimal change nephrotic syndrome?

A

Commonest form in children
sudden onset of oedema - days
complete loss of proteinuria with steroids
2/3 patients relapse

80
Q

Treatment for minimal change disease

A

Prednisolone 1mg/kg for up to 16 weeks.

Many relapses treated with cyclophosphamide, cyclosporin

81
Q

What is focal and segmental glomerulonephritis?

A

Not a single disease, rather a syndrome with multiple causes
presents with nephrotic syndrome.
Pathology reveals focal and segmental sclerosis with distinctive patterns

82
Q

Treatment for focal and segmental glomerulosclerosis

A

General measures
Trail of steroids
Alternative - cyclosporin

83
Q

Membranous nephropathy what is it?

A

Commonest cause in adults.

Serological markers

84
Q

Summary of non-proliferative GN

A

Present with nephrotic syndrome.
Renal biopsy is key investigation
General measures important
Specific treatment as appropriate.

85
Q

Where is a transplanted kidney placed?

A

Iliac fossa and anastomosed to iliac vessels.

86
Q

What would be indications for native nephrectomy?

A

Size (polycystic kidneys) and infection (chronic pyelonephritis)

87
Q

What are possible surgical complications of transplant?

A

Vascular complications:
Bleeding:
- usually anastomotic sites
- perirenal haematoma can be arterial or venous

Arterial thrombosis
Venous thrombosis
Lymphocele

Uteric
- Urine leak

Infections

88
Q

What is the protocol for immunosiuppresions for people after surgery?

A

Induction - Depleting agent e.g. (Basiliximab)
Maintenance - Calcineurin inhibitors (tacrolimus) + Anti-proliefratives (mycophenolate) + corticosteroids
Steroid free is possible
Others: CNI-free using Costimulatory signal blocker (belatacept)

89
Q

What are the side effects of

  1. Corticosteroids
  2. Tacrolimus
  3. Cyclosporin
  4. Belatacept
  5. Mycophenolate mofetil
A
  1. Hypertension, hyperglycaemia, infections, bone loss, GI bleeding.
  2. Hyperglycaemia, AKI, tremor
  3. Hirsutism (men body hair on women), Hypertension, AKI, gout
  4. Infections, malignancy
  5. Cytopenia, GI upset.
90
Q

What are the types of kidney donors?

A
  1. Deceased donors
    - Donation after brain death/ DBD
    - Donation after cardiac death / DCD
    * both standard / extended criteria
  2. Living Donors
    - Living related donor
    - Living unrelated donors
    Spousal, altruistic, paired/pooled
91
Q

What is the standard brain death criteria?

What is the Extended criteria?

A

Standard:

  1. Coma, unresponsive to stimuli
  2. Apnoea off ventilator
  3. Absence of cephalic reflexes
  4. Body temp above 34
  5. Absence of drug intoxication

Extended:

  1. Donor aged over 60yr
  2. Donar aged 50-59 and history of hypertension, death from cerebrovascular accident or terminal creatinine of over 132.
92
Q

Complications after renal transplantation

A

Rejection:

  • cell mediated
  • Humoral (Ab mediated)

Infective:

  • bacterial
  • fungal
  • viral

Cardiovascular:

  • underlying renal disease
  • CRF (chronic renal failure)
  • Hypertension
  • Hyperlipidaemia
  • PT diabetes

Malignancy:

  • skin
  • lymphoma
  • Solid cancers
93
Q

What is Cytomegalovirus?

What tissue invasive disease can come with it?

A

Most important transplant-related infection:
- Affects around 8% of transplant recipients, despite prophylaxis therapy.
- High mortality and morbidity if untreated
- Recipient affected via:
Transmission from donor tissue
Reactivation of latent virus

Tissue invasive disease:
Pneumonitis
hepatitis 
Retinitis 
Gastroenteritis 
Colitis
Nephritis
94
Q

What is acute rejection?

A

Hyper acute rejection - pre-existing alloreactivity to donor.
Acute rejection:
- T cell mediated (TCMR) Lymphocytic infiltrate.
- Acute antibody mediated rejection (ABMR)
Microvascular inflammation
Donor specific antibodies
Positive C4d

95
Q

What is the definition of acute renal failure?

A

Increase in SCreatinine by > 26.5 within 48hr or more than 1.5 times baseline.
Urine volume <0.5 ml/kg/h for 6 hours

96
Q

What are the different stages of acute renal failure?

A

AKI 1 = serum creatinine = 1.5-1.9 times baseline or more than 26.5 increase.
Urine output = <0.5 ml/kg/h for 6-12 hours.

AKI 2 = serum creatinine = 2.0-2.9 times baseline
Urine output <0.5 for > 12 hours.

AKI 3 = serum creatinine = 3 times baseline or increase to 354 and above.
Urine output < 0.3 for > 24hr or anuria for > 12 hours

97
Q

Incidence of Acute renal injury

A

Hospital admissions = 1 in 5

ITU admissions = more than half.

98
Q

What are the immediately dangerous consequences of AKI?

A

Dependent on cause to an extent at least in the first few hours.

Acidosis (cause cardiac arrest)
Electrolyte imbalance 
Intoxication TOXINS (cause resp arrest)
Overload (cardiac arrest)
Uraemic complications
99
Q

Outcomes of AKI even if “not that bad”

A
Short term (in hospital) 
- Death, dialysis, length of stay

Intermediate / Long term (post-discharge)
- Death, CKD, Dialysis, CKD released CV events.

100
Q

Causes of Acute renal injury

A

Pre-renal
- Blood flow to kidney:
Sepsis, hypotension, hypovolaemia, haemorrhage, Cardiac failure

Renal
- Damage to renal parenchyma:
Acute tubular necrosis, glomerulonephritis, toxin-related, acute interstitial nephritis, intra renal vascular obstruction.

Post-renal
- obstruction to urine exit:
Kidney stones, tumours, Intraluminal (clot) , Intramural (malignancy), Extramural (Malignancy)

101
Q

What is the most common cause of AKI?

A

Poor perfusion leading to established tubule damage.

102
Q

What is Radiocontrats nephropathy?

A

AKI following administered iodine as contrast agent.
Common contributor to hospital acquired AKI.
Usually resolved after 72hr
May lead to permanent loss of function.

103
Q

Risk factors for RCN

A
Diabetes mellitus 
Renovascular disease 
Impaired renal function 
Paraprotein 
High volume of radio contrast
104
Q

What renal failure can be seen in myeloma?

A
Cast nephropahy "myeloma kidney" 
Light chain nephropathy 
Amyloidosis 
Hypercalcaemia 
Hyperuricaemia
105
Q

Investigations for AKI

A
History
Examination (fluid status)
Drugs
Insults 
Renal function 
Urine dipstick, PCR, ACR
FBC, U&amp;E, Bicarb
USS 
Blood gas
106
Q

Prevention of AKI

A
Avoid dehydration 
Avoid nephrotoxic drugs
Review clinical status in those in risk and act on findings:
Sepsis
Toxins
Optimise BP and vol status
Prevent harm
107
Q

Management of AKI

A
  1. Maintain fluid balance
  2. Optimise blood pressure - give fluid/vasopressors
  3. Stop nephrotoxic drugs (NSAIDS, ahminoglycosides)
108
Q

How do we spot hyperkalaemia on ECG?

A

Peaked T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear

109
Q

How to treat hyperkalamia?

A
Stabilise (myocardium)
- calcium glutinate 
Shift (K intracellularly) 
- salbutamol
- insulin-dextrose 
Remove 
- diuresis 
- dialysis
- anion exchange resins
110
Q

What is Benign prostatic hyperplasia?

A

Characterised by fibromuscular and glandular hyperplasia. Predominately affects transition zone. LUTS caused by bladder outlet obstruction due to BPH.

111
Q

How common is BPH?

A

Part of waging process in men:
50% of men at 60
90% of men at 85

112
Q

Assessment of LUTS

Frequency volume charts.

A
Symptom scoring system:
Voiding (obstruction):
- Hesitancy 
- Poor stream 
- Terminal dribbling 
- Incomplete emptying

Storage (Irritative)

  • Frequency
  • Nocturia
  • Urgency +/- urge incontinence
113
Q

What physical examination take place for BPH?

A

Abdomen:
- palpable bladder?

Penis:

  • External urethral metal stricture?
  • Phimosis?

Digital rectal examination:

  • assess prostate size
  • Suspicious nodules or firmness

Urinalysis:

  • Blood?
  • Signs of UTI
114
Q

What investigations could you do for BPH?

A
MSSU
Flow rate study 
Bloods: 
- PSA
- Urea and creatinine (if chronic retention) 
Ultrasound renal
115
Q

Treatment for uncomplicated Benign prostatic obstruction

A

Watchful waiting
Medical therapy:
- alpha bockers (smooth muscle relaxation)
- 5 alpha reductase inhibitors (reduce prostate size and reduces risk of progression)

Surgical

  • TURP (prostate size <100cc)
  • Open retropubic or transvesical prostatectomy
116
Q

Complications of Bladder outflow obstruction

A
Progression of LUTS 
Acute/chronic urinary retention
Urinary incontinence 
UTI 
Bladder stone 
Renal failure
117
Q

Treatment for complicated BOO

A

Medical therapy:
Surgery.
Long term urethral or suprapubic cathertirisation.

118
Q

Define acute urinary retention

A

Painful inability to void with a palpable and perusable bladder.

119
Q
  1. What is treatment for AUR?

2. Complications?

A
  1. Catheterisation.

2. UTI, post-decompression haematuria, pathological diuresis, renal failure.

120
Q

Define chronic urinary retention

A

Painless, palpable and percussible bladder after voiding. Main cause is detrusor under activity.

121
Q

Treatment for CUR?

A

Catheterisation.

Manage with IV fluids.

122
Q

What are the types of Urinary tract Obstruction?

A

Upper tract (supra-vesical)

  • PUJ
  • ureter
  • VUJ

Lower tract (bladder outflow obstruction)

  • Bladder neck
  • prostate
  • urethra
  • urethral meatus
  • foreskin
123
Q

Causes of upper tract obstruction

A

Pelvic-ureteric junction:
Intrinsic:
- stone, Ureteric tumour (TCC), Blood clot, fungal ball.

Extrinsic:
-Lymph nodes (tumour), Abdominal mass (tumour)

Ureter:
Intrinsic:
- Stone, Ureteric tumour, scar tissue, blood clot, fungal ball.

Extrinsic:
-Lymph nodes (tumour), Iatrogenic, abdominal/ pelvic mass (tumour)

Visio-ureteric junction (VUJ):
Intrinsic:
- Stone, bladder tumour, ureteric tumour

Extrinsic:
- cervical tumour, prostate cancer

124
Q

Presentation of upper tract obstruction

A

Symptoms:
- pain, frank haematuria, symptoms of complications.

Signs:
- palpable mass, microscopic haematuria, signs of complications

Complications:
- infection and sepsis, renal failure

125
Q

What is used for emergency treatment of obstruction?

A

Percutaneous nephrostomy insertion (usually under LA with US guidance) or retrograde stent insertion (silicone, polyurethane, nickel titanium)

126
Q

Chronic retention:

High pressure and low pressure presentation

A
High pressure:
Painless
Incontinent 
Raised cr
Bilateral hydro-nephrosis
Low pressure:
Painless
Dry
Normal cr
Normal kidneys
127
Q

Complications of chronic retention

A

Decompression haematuria

Post obstructive diuresis.

128
Q

Presentation of Lower tract obstruction

A
Acute/chronic urinary retention
Recurrent UTI and sepsis
Frank haematuria 
Bladder stones 
Renal failure
129
Q

What is the relative incidence of stone types

A
Calcium oxalate - 45%
Calcium oxalate and phosphate - 25%
Triple phosphate (infective) - 20%
Calcium phosphate - 3%
Uric acid - 5%
Cystine - 3%
130
Q

Symptoms and signs of stones

A
Renal pain (fixed in loin)
Ureteric colic (radiating to groin) 
Dysuria/haematuria/testicular or vulva pain
Urinary infection 
Loin tenderness 
Pyrexia
131
Q

Investigations for stones

A
Blood tests - FBP, U&amp;E, Creatinine 
Calcium, Albumin, Urate 
Parathormone 
Urine analysis and culture 
24hr urine collections 
KUB
US
IVU (IV urogram) 
CT KUB
132
Q

What are the techniques for surgical treatment?

A

Open surgery
Endoscopic surgery
ESWL

133
Q
  1. Advantages and disadvantages of open surgery

2. What are the indications for open surgery?

A

+ Single procedure with least recurrence rate

  • Large scar, long hospital stay, general wound complications
    2. Non functioning infected kidney with large stones necessitating nephrectomy. Technical reasons cannot be managed by PCNL or ESWL.
134
Q

Indications for Percutaneous nephrolithotomy

A
Large stone burden 
Associated PUJ stenosis 
Infundibular stricture 
Calyceal diverticulum 
Morbid obesity or skeletal deformity 
ESWL resistant stones e.g. Cystine
135
Q

Contraindications for PCNL

A

Uncorrected coagulopathy
Active UTI
Obesity or unusual body habits unsuitable for X-ray tables
Relative contraindications include small kidneys and sever perirenal fibrosis.

136
Q

Complications of PCNL

A

Local complications - AV fistula

UT injury - Pelvic tera, Ureteral tear, Stricture of PUJ

137
Q

What is E.S.W.L?

When is it used?

A

Extracorporeal Shock Wave Lithotripsy
- Shock waves crush stones and smaller pieces pass out of body in urine.

Commonly used for renal and ureteric calculi as first line treatment. Day case. Repeated as often as required.

138
Q

Indications for open ureterolithotomy

A

Not suitable for laparoscopic approach.
Failed ESWL or ureteroscopy.
Severe obstruction, uncontrollable pain, persistant haematuria.

139
Q

What are bladder stones?

A
Suprapubic / groin/ penile pain. 
Dysuria, frequency, haematuria
UTI 
Usually secondary to outflow obstruction
Most treated endoscopically
140
Q

Prostate cancer: How common is it?

A
  • Commonest cancer diagnosed in men
  • 75% of new cases are aged > 65yrs
  • 11,300 deaths / year
  • 800 million/year
141
Q

Causes and risk factors of prostate cancer

A

Age
Race/ethnicity
Geography
Family history - first degree relative 2x risk.

142
Q

Diagnosis of prostate cancer

A

80% newly diagnosed prostate cancers are localised.
Mostly asymptomatic
Diagnosed through opportunistic PSA testing
Diagnostic triad of PSA, digital rectal examination and TRUS-guided prostate biopsies

143
Q

Presenting symptoms of localised prostate cancer

A
Locally invasive disease: 
Haeamaturia 
Perineal and suprapubic pain 
Impotence 
Incontinence 
Loin pain or anuria resulting from obstruction of the ureters 
Symptoms of renal failure 
Haemospermia 
Rectal symptoms including tenesmus
144
Q

Metastatic prostate cancer presenting symptoms

A

Distant:
Bone pain, paraplegia secondary to spinal cord compression, lymph node enlargement, lymphedema, loin pain.

Widespread:
Lethargy
Weight loss and cachexia

145
Q

Why do we not screen for prostate cancer?

A

Leads to over-diagnosis and over treatment of harmless cancers.