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Phase 2a > renal + GU > Flashcards

renal + GU Flashcards

1
Q

Which drugs can cause prerenal damage?

A

drugs that cause excessive GI loss (d+v) or volume depletion
NSAIDs (renal underperfusion)
ACEi in patients with compromised renal perfusion

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2
Q

Why should you be cautious when prescribing an NSAID with and ACEi?

A

in combo can cause an acute deterioration in renal function

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3
Q

What issues can renal impairment cause in prescribing?

A

Failure to excrete a drug or its metabolites.
Many side-effects being poorly tolerated by patients with renal impairment.
Some drugs ceasing to be effective when renal function is reduced

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4
Q

What are the risk factors for AKI?

A

Advanced age
Underlying kidney disease
Toxin exposure
DM
Excessive fluid loss
Drug overdose
Surgery
Haemorrhage
Pancreatitis
Cardiac arrest
Sepsis

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5
Q

What is an acute kidney injury?

A

an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output

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6
Q

What is stage 1 of an AKI?

A

Creatinine rise of 26 micromol or more within 48 hours
OR
Creatinine rise of 1.50–1.99 x baseline within 7 days
OR
Urine output less than 0.5 mL/kg/hour for more than 6 hours

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7
Q

What is stage 2 of an AKI?

A
  • (2.00–2.99 x baseline) creatinine rise from baseline within 7 days
  • Urine output less than 0.5 mL/kg/hour for more than 12 hours
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8
Q

What is stage 3 of AKI?

A
  • Serum creatinine levels: 3-fold higher than baseline
  • Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days or
  • Urine output less than 0.3 mL/kg/hour for 24 hours or anuria for 12 hours
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9
Q

What are the 3 categories of aetiology for AKI?

A

Pre-kidney
Intrinsic
Post-kidney

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10
Q

What are the pre-kidney causes of AKI?

A

Reduced kidney perfusion:
- hypovolaemia
- haemorrhage
- sepsis
- overdiuresis
- hepatorenal syndrome

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11
Q

What are intrinsic causes of AKI?

A
  • Acute tubular necrosis
  • Rapidly progressive glomerulonephritis
  • Interstitial nephritis
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12
Q

What are post-kidney causes of AKI?

A

mechanical obstruction of the urinary outflow tract:
- Retroperitoneal fibrosis
- lymphoma
- stones
- tumour
- prostate hyperplasia
- strictures
- ascending urinary infection
- urinary retention

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13
Q

What is pre-kidney AKI?

A

injury due to impaired kidney perfusion

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14
Q

What is intrinsic AKI?

A

direct injury to the kidney parenchyma.

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15
Q

What is post-kidney AKI?

A

injury due to urinary outflow obstruction

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16
Q

Presentation of an AKI

A

Reduced urine output
Often asymptomatic, look at risk factors

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17
Q

What is the pathophysiology of pre-renal AKI?

A

Reduction in blood flow leads to reduction in GFR
More urea and creatinine in the blood as less is filtered out and more reabsorbed.
Sodium and water also reabsorbed.
Low GFR leads to low NaCl conc, macula densa cells sense and stimulate renin release.
RAAS stimulated. Increase in aldosterone and ADH leads to even more water and sodium reabsorption

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18
Q

What is the urine like in pre-renal AKI?

A

lower urea, sodium and water
Osmolality high, very concentrated

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19
Q

What is the urine like in an intrarenal AKI?

A

More water, sodium and urea
Lower osmolality than pre-renal, less concentrated

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20
Q

What is seen in the blood in a pre-renal AKI?

A

More urea than creatinine in blood

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21
Q

What is seen in the blood in an intra-renal AKI?

A

More creatinine than urea

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22
Q

What is the pathophysiology of intra-renal AKI?

A

Some form of kidney tubule injury, dysfunction of excretion and reabsorption.
Kidney tubule cells die and flake off, forming clumps and casts.
Casts block tubule and cause backlog, pressure rises within tubular system.
Less filtration, accumulation of urea and creatinine.
Creatinine also can’t be excreted so blood creatinine increases

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23
Q

What is the pathophysiology of an early stage post-renal AKI?

A

Obstruction of flow.
Lower GFR, increase in urea and creatinine as less filtered. Urea can be reabsorbed and creatinine excreted still as no damage to kidney cells.
Sodium and water also reabsorbed.
RAAS stimulated by low GFR

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24
Q

What is the urine like in an early stage post-renal AKI?

A

low sodium, water and urea

similar to pre-renal in early stages

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25
Q

What is the urine like in the later stages of a post-renal AKI?

A

High water, sodium and urea

resembles intrinsic

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26
Q

What is the pathophysiology of a later stage post-renal AKI?

A

Pressure continues to increase, blood vessels compressed and blood flow reduced.
Low GFR, kidney cells damaged.
Urea can’t be reabsorbed or creatinine excreted.
Reduced sodium and water reabsorption

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27
Q

What is the key investigation for AKI?

A

U&Es, creatinine + bicarb

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28
Q

What investigations would be done for AKI?

A

U&Es
Urinalysis: dipstick + osmolality
FBC

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29
Q

When is urine osmolality increased in AKI?

A

Above 500 in pre-renal and early stage post-renal

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30
Q

When is urine osmolality low in AKI?

A

Intrinsic (intra-renal) and late stage post-renal

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31
Q

What are the main presentations of an AKI?

A

Reduced urine output
May be symptomatic: check for risk factors, can also show as nausea, vomiting and dehydration

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32
Q

What are the differentials of AKI?

A

CKD
Drug side effects

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33
Q

How do you manage an AKI?

A

treat underlying cause where possible
monitor fluid and electrolyte balance closely
optimise haemodynamic status with appropriate fluid therapy

Screen for and treat sepsis

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34
Q

Complications of AKI

A

Uraemia
Hyperkalaemia
Hyperphosphataemia
CKD

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35
Q

What is the definition of CKD?

A

GFR of less than 60mL/minute/1.73 m² or presence of kidney damage for 3 months or more

progressive, irreversible condition, reduced kidney function/damage, >3 months

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36
Q

What is glomerulonephritis?

A

Broad term that refers to a group of parenchymal kidney disease – inflammation and damage to glomeruli

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37
Q

What syndromes can glomerulonephritis present with?

A

Nephritic
Nephrotic

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38
Q

What is nephritic syndrome?

A

Clinical manifestations that occur within nephritis

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39
Q

What can cause nephritic syndrome?

A

Post-strep
IgA nephropathy
SLE
Rapidly progressive (crescentic) GN
Goodpasture’s disease (anti-glomerular basement membrane antibodies)

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40
Q

What are the main features of nephritic syndrome?

A

Haematuria
RBC casts in urine from glomerular bleeding
Sub-nephrotic proteinuria
Hypertension and fluid retention
Oliguria
Sterile pyuria (WBC without bacteria)

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41
Q

What are the symptoms of fluid retention/overload in nephritic syndrome?

A
  • Hypertension
  • Pulmonary oedema/effusions
  • Peripheral oedema
  • Raised JVP
  • Orthopnea and SOB
  • Increase in weight
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42
Q

What can cause glomerulonephritis

A
  • Infections, e.g. Hep B/C, HIV, Strep, Malaria
  • Systemic inflammatory conditions: SLE, Goodpasture’s, rheumatoid arthritis
  • Drugs
  • Metabolic disorders (DM, hypertension)
  • Malignancy
  • Hereditary disorders (Alport’s)
  • Deposition disorders (amyloidosis)
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43
Q

What is bacteriuria?

A

presence of bacteria in the urine

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44
Q

What is an asymptomatic bacteriuria UTI?

A

presence of significant levels of bacteria in the urine in a person without signs or symptoms of UTI

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45
Q

What is an uncomplicated UTI?

A

infection of the urinary tract by a usual pathogen in a person with a normal urinary tract and with normal kidney function

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46
Q

What is a complicated UTI?

A

UTI with increased likelihood of complications such as persistent infection, treatment failure and recurrent infection

anatomical, functional, or pharmacological factors predispose

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47
Q

What are some complications of long-term catheterisation?

A

UTI/Pyelonephritis
Stones
Obstruction
Chronic inflammation

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48
Q

What is pyuria?

A

Presence of leucocytes in the urine

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49
Q

What are the upper UTIs?

A

pyelitis
pyelonephritis

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50
Q

What are lower UTIs generally?

A

infection of the bladder (cystitis)

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51
Q

What are the different classifications of UTIs?

A

Lower/ upper

Asymptomatic bacteriuria
Complicated
Uncomplicated

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52
Q

What are the most common pathogens causing UTIs?

A

E.coli (more than 50%)
proteus (10-15%)
klebsiella (catheter associated)
enterococci
Staph.saprophyticus

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53
Q

What is incontinence?

A

lack of voluntary control over urination or defecation

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54
Q

What is stress incontinence?

A

Loss of urine with exertion/sneezing/coughing

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55
Q

What is urgency incontinence?

A

leakage accompanied by/ or immediately preceded by urinary urgency

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56
Q

What is mixed incontinence?

A

Loss of urine associated with urgency, also exertion, effort, sneezing or coughing

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57
Q

What is lower urinary tract dysfunction?

A

Failure to store/ void
- bladder or outlet issue

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58
Q

What is total incontinence?

A

Continuous urine leakage
Normally anatomical problems

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59
Q

Risk factors for incontinence in women

A

Increasing age
Obesity
Pregnancy
High exertion
Dementia and CNS disorders

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60
Q

Whar does the cough stress test for incontinence consist of?

A

filling the patient’s bladder to 300 mL
having the subject perform a series of forceful coughs in upright position or dorsal lithotomy position

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61
Q

Management for incontinence in women

A

Behavioural and lifestyle changes
e.g. pelvic floor exercises, weight reduction if obese, caffeine reduction

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62
Q

How are NSAIDs nephrotoxic?

A

disrupt the compensatory vasodilation response of renal prostaglandins to vasoconstrictor hormones released by the body

hypoperfusion of kidney and decrease in GFR

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63
Q

Which drugs should be stopped in AKI?

stop the damn drugs

A

Diuretics
ACEi/ARBs
Metoformin
NSAIDs

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64
Q

What are voiding LUTS?

A
  • Hesitancy : a longer than usual wait for urine flow to begin
  • Weak stream
  • Intermittency : urine flow that stops and starts
  • Terminal dribbling : weak urine flow continues after an attempt is made to stop
  • Straining : the need to increase abdominal pressure in order to urinate
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65
Q

What is benign prostate hyperplasia?

A

increase in size of the prostate gland without malignancy present

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66
Q

What are storage LUTS?

A
  • Dysuria : pain or burning on urination
  • Frequency : the passing of small volumes of urine at frequent intervals
  • Urgency : a sudden urge to pass urine
  • Urge incontinence : urgency leading to involuntary loss of urine
  • Nocturia : waking at night to pass urine
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67
Q

What can be used to assess the severity of lower urinary tract symptoms?

A

international prostate symptom score (IPSS)

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68
Q

What’s the epidemiology of BPH?

A

Commonly affects men
prevalence increasing with age
(40% of men age 50-60, 82% of men age 70-80)

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69
Q

What does 5-alpha reductase do and what condition is this relevant for?

A

Converts testosterone into dihydrotestosterone.
Prostate cells respond to DHT and continue growing into BPH

Therefore 5-alpha reductase is inhibited in treatment of BPH

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70
Q

How does BPH cause LUTS?

A

prostatic hyperplasia can result in bladder outlet obstruction

increased stromal:epithelial ratio

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71
Q

How does BPH present?

A

Voiding symptoms: hesitancy, intermittency, weak stream, straining, incomplete emptying, and post-void dribbling
Storage symptoms: urinary frequency, nocturia, and urgency

older men

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72
Q

What are the risk factors for BPH?

A

Men age over 50
Family hx of BPH

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73
Q

How can BPH be investigated?

A

Digital rectal examination
Frequency/volume chart voiding diary for 3 days by patient
Prostate specific antigen- unreliable (lots of false +/-ves)
Urinalysis (dipstick)

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74
Q

What are the possible differentials of BPH?

A

Overactive bladder
Prostatitis
Prostate cancer
Urinary tract infection (UTI)
Bladder cancer

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75
Q

Why is the prostate specific antigen test not ideal?

A

unreliable
with a high rate of false positives (75%) and false negatives (15%)

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76
Q

What are some common causes of a raised PSA?

A

Prostate cancer
Benign prostatic hyperplasia
Prostatitis
Urinary tract infections
Vigorous exercise (notably cycling)
Recent ejaculation or prostate stimulation

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77
Q

What are the medical therapies for BPH?

A

Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate

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78
Q

What’s an important side effect of tamsulosin for patients needing to undergo cataract surgery?

A

intra-operative floppy iris syndrome

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79
Q

What’s the most common surgical therapy for BPH?

A

Transurethral resection of the prostate

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80
Q

What are the complications of BPH?

A

UTI
Bladder stones
Urinary retention

Tamsulosin can cause ejaculatory dysfunction

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81
Q

What is nephrolithiasis?

A

Nephrolithiasis refers to the presence of crystalline stones (calculi) within the urinary system (kidneys and ureter)

kidney stones

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82
Q

What are renal stones?

A

crystalline mineral depositions that form from microscopic crystals in the loop of Henle, distal tubules, or the collecting duct

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83
Q

What typically causes renal stones to form?

A

elevated levels of urinary solutes such as calcium, uric acid, oxalate, and sodium
decreased levels of stone inhibitors such as citrate and magnesium
Low urinary volume
abnormally low or high urinary pH

all can lead to urine supersaturation

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84
Q

What is the basic pathophysiology of renal stones?

A

Urine becomes super saturated by concentrated solutes
These solutes are precipitated, form crystals and act as a nidus for more crystal formation

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85
Q

What are the different types of kidney stone?

composition

A

Calcium (80%)
Uric acid
Cystine
Struvite

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86
Q

What are the 2 types of calcium kidney stone?

A

Calcium oxalate
Calcium phosphate

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87
Q

What are the risk factors for developing a calcium oxalate kidney stone?

A

low urine volume
hypercalciuria
hyperuricosuria
hyperoxaluria
hypocitraturia

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88
Q

What are the risk factors for a calcium phosphate kidney stone?

A

low urine volume
hypercalciuria
hypocitraturia
high urine pH
primary hyperparathyroidism
renal tubular acidosis

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89
Q

What causes uric acid stones?

A

urinary pH <5.5
hyperuricosuria can also contribute

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90
Q

What causes cystine urine stones?

A

cystinuria

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91
Q

What does staghorn calculi mean in kidney stones?

A

the stone forms in the shape of the renal pelvis, giving it a similar appearance to the antlers of a deer stag

most commonly occurs with struvite stones

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92
Q

What are struvite kidney stones?

A

infection stones, e.g. Proteus, Pseudomonas, and Klebsiella
composed of magnesium, ammonium, and phosphate
They frequently present as staghorn calculi

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93
Q

What is the cardinal symptom of kidney stones?

A

severe, acute flank pain

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94
Q

Apart from severe, acute flank pain, what other symptoms may be present with kidney stones?

A

Haematuria
Nausea or vomiting
Reduced urine output

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95
Q

What investigations should be run for kidney stones?

A

Non-contrast CT within 24 hours of presentation
Urinalysis: haematuria
FBC
Serum chemistry (calcium, electrolytes, serum urea/creatinine, phosphorus, and uric acid)

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96
Q

What are the differentials for kidney stones?

A

Acute appendicitis
Ectopic pregnancy
Ovarian cyst
Diverticular disease
Bowel obstruction
Acute pancreatitis

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97
Q

What are the management options for kidney stones?

A

Maintain adequate hydration
NSAIDs for pain relief, e.g. IM diclofenac
asymptomatic renal stone <5 mm: watchful waiting
stones ≥10 mm or smaller intolerable stones: surgical treatment
- 5-10mm shockwave lithotripsy
- 10-20 mm shockwave lithotripsy OR ureteroscopy
- > 20 mm percutaneous nephrolithotomy

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98
Q

What are the 2 ways of categorising chronic kidney disease?

A

glomerular filtration rate category (G1-5)
albuminuria category (A1-3)

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99
Q

What are the different G stages for CKD?

A

G1- Over 90
G2- 60-89
G3a - 45-59
G3b- 30-44
G4- 15-29
G5- Under 15

Below 60 is reduced GFR, G5 is need for renal replacement therapy (end stage)

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100
Q

What are the 3 different A stages for CKD based off albumin-creatinine ratio? (ACR)

A

A1 Under 3 mg/mmol
A2 3-30 mg/mmol
A3 Above 30 mg/mmol

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101
Q

What can cause chronic kidney disease?

A

Diabetes – most common
Hypertension – second most common
Glomerular kidney disease, e.g. glomerulonephritis
Medications (e.g., NSAIDs or lithium)
Polycystic kidney disease

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102
Q

What is the basic pathophysiology of CKD?

A

Renal damage/injury, e.g. from high blood pressure causing arteriosclerosis
Inflammatory cell recruitment
Fibroblasts activated
Fibrosis and glomerulosclerosis
Decrease in GFR

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103
Q

What is the epidemiology of CKD?

A

Increases with age, higher incidence of DM and HTN
Associated with socioeconomic desparities

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104
Q

What are the risk factors for CKD?

A

diabetes mellitus
hypertension
age >50 years
childhood kidney disease
smoking
obesity

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105
Q

How might a patient with CKD present?

A

Haematuria
Foamy urine (proteinuria)
fatigue
oedema
nausea with/without vomiting
pruritus
restless legs
anorexia
HTN

patients can be asymptomatic + symptoms are non-specific

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106
Q

What investigations should be done for CKD?

A
  • Serum creatinine: elevated
  • eGFR: <60 mL/minute/1.73 m²
  • Urinalysis: looking for haematuria + proteinuria
  • Albumin excretion rate (AER) or albumin to creatinine ratio (ACR): increased
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107
Q

What is accelerated progression in CKD?

A

a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2

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108
Q

What are some differentials of CKD?

A

Diabetic kidney disease
Hypertensive nephrosclerosis
Ischaemic nephropathy
Obstructive uropathy
Nephrotic syndrome
Glomerulonephritis

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109
Q

What’s the management for a patient with CKD with a G score between G1-4?

A
  • ACEi/ARB to reduce BP
  • SGLT2 inhibitors, e.g. dapagliflozin
  • Statin

+ lifestyle modifications

110
Q

What lifestyle modifications are recommended for patients with CKD?

A

smoking cessation
low salt + protein diets
weight management

111
Q

What is the management for G5 CKD?

A

Renal replacement therapy:
- dialysis
- transplant

112
Q

What are the complications of CKD?

A

anaemia
renal osteodystrophy
cardiovascular disease
protein malnutrition
metabolic acidosis
hyperkalaemia
pulmonary oedema

113
Q

What is a UTI?

A

an infection of the kidneys, bladder, or urethra

114
Q

What’s the most common pathogen causing UTI?

115
Q

When are UTIs considered recurrent?

A

two episodes within 6 months or three or more episodes within 12 months

116
Q

What’s the epidemiology of UTIs?

A

occur more frequently in women
increase with age, men rarely affected before age 50
very common, lifetime incidence of UTIs is 50% to 60% in adult women

117
Q

Which pathogen is most associated catheter related UTIs?

A

Klebsiella

118
Q

How can UTIs develop in catheterised patients?

A

Insertion may carry organisms into the bladder, also allow formation of biofilm which make it harder for antibiotics to penetrate and bacteria are protected.
Cause incomplete voiding
leftover urine in bladder helps bacteria to grow

119
Q

Why are UTIs more common in women?

A

urethra is much shorter, making it easier for bacteria to get into the bladder

120
Q

How do lower UTIs tend to present?

A

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Haematuria
Cloudy or foul-smelling urine
Confusion is commonly the only symptom in older and frail patients

121
Q

What are the key symptoms of a UTI in a women under 65?

A

dysuria
new nocturia
cloudy-looking urine

122
Q

What are some symptoms a UTI may present with?

A

dysuria, frequency, urgency, suprapubic pain, costovertebral angle pain

123
Q

What investigations should be done for a suspected UTI?

A

Urine dipstick + urinalysis: positive for nitrite and leukocytes
Urine microscopy: leukocytes and bacteria
Urine culture: ≥10² colony-forming units

124
Q

What are some differentials for UTIs in women?

A
  • Over-active bladder
  • Urothelial carcinoma of the bladder or upper urinary tract
  • Non-infectious urethritis
  • Vaginitis
  • Bacterial vaginosis and cervicitis
  • Interstitial cystitis (painful bladder syndrome)
125
Q

What are some differentials for UTIs in men?

A
  • BPH
  • Bladder cancer
  • Prostate cancer
  • Renal cancer
  • Epididymitis
126
Q

What are the antibiotic options for treating UTIs?

A
  • Nitrofurantoin
  • trimethoprim
127
Q

What are the risk factors in women for developing a UTI?

A
  • History of UTI
  • Pregnant
  • Sexual activity
  • Oestrogen deficiency
  • Incontinence
  • Catheter
128
Q

What is pyelonephritis?

A

inflammation of the kidney resulting from bacterial infection

129
Q

What can cause pyelonephritis?

A

Acute infection: E.Coli, Proteus, enteric bacteria
Haematogenous spread

130
Q

Who does pyelonephritis tend to affect?

A

Acute uncomplicated pyelonephritis occurs primarily in younger women.
Complicated acute pyelonephritis tends to occur in men, older people, pregnant women, and those with underlying anatomical or physiological abnormalities

131
Q

What are the risk factors for pyelonephritis?

A

UTI
DM
Stress incontinence
Foreign body in urinary tract (e.g., calculus, catheter)
Anatomical/functional urinary abnormality
Immunosuppressed
Pregnancy
Frequent sexual intercourse

132
Q

What triad of symptoms are present in pyelonephritis?

alongside typical UTI symptoms

A

Fever, flank pain, nausea / vomiting

133
Q

What are the first line investigations for pyelonephritis?

A

Urine dipstick: signs of infection, including nitrites, leukocytes and blood.
Midstream urine (MSU): microscopy, culture and sensitivity
FBC: leukocytosis
ESR and CRP: elevated

134
Q

What are the differentials for pyelonephritis?

A

Lower urinary tract infection
Cystitis
Acute prostatitis
Urethritis
Chronic pyelonephritis
Pelvic inflammatory disease

135
Q

What is the treatment for pyelonephritis?

A

Cefalexin for 7 to 10 days
Amoxicillin or trimethoprim (if culture results are available due to high resistance rates)

oral antibiotics

136
Q

How does urethritis typically present?

A

acute urethral discharge following unprotected sex

137
Q

What is cystitis?

A

Infection of urinary bladder
Lower UTI

138
Q

Who tends to be affected by cystitis and what is the most common cause?

A

most commonly seen in young, sexually active women
E.Coli

139
Q

What investigations would be run for cystitis?

A

Mid stream:
* urinalysis
* urine microscopy
* urine culture with sensitivity

140
Q

What are the differentials of cystitis?

A

Pyelonephritis
Vaginitis
Interstitial cystitis
Chlamydia urethritis

141
Q

What’s the treatment of cystitis?

A

Oral antibiotics: nitrofurantoin for 3-5 days

142
Q

What is acute prostatitis?

A

painful inflammation within the prostate that is usually accompanied by evidence of recent or ongoing bacterial infection

143
Q

How does acute prostatitis typically present?

A

acute onset of LUTS (e.g., dysuria, urinary frequency, perineal discomfort) accompanied by variable systemic signs of fever, chills, and malaise

144
Q

What is the first line treatment for acute bacterial prostatitis?

A

oral fluoroquinolone antibiotic: e.g. ciprofloxacin

145
Q

What are the extra-renal manifestations of ADPKD?

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurgitation
Colonic diverticula

146
Q

What is polycystic kidney disease?

A

Condition characterised by the development of multiple cysts within the renal tubules of kidney
Most common hereditary renal disease

147
Q

What are the 2 types of PKD?

A

Autosomal dominant: most common
Autosomal recessive

148
Q

Which mutations occur in ADPKD?

A
  • PKD1 on chromosome 16, coding for protein polycystin 1
  • PKD2 on chromosome 4, coding for polycystin 2
149
Q

What mutation is typically present in ARPKD?

A

PKHD1 gene on chromosome 6, coding for fibrocystin

150
Q

What is ADPKD?

A

typically adult-onset disorder
characterised by gradually growing renal cysts with progressive fibrocystic renal disease

151
Q

What is ARPKD?

A

a rarer and often more severe form of cystic disease
usually presents in children
phenotypically highly variable
involving the kidneys and biliary tract

152
Q

What’s the pathophysiology of PKD?

A

Renal tubules develop into fluid-filled cysts.
Cannot carry out normal filtering function
number of working nephrons decreases
As cysts grow, nearby nephrons are compressed
Remaining nephrons may increase function to maintain GFR so initially no clinical impact

As disease progresses and more nephrons are affected, overall renal function deteriorates and eventually reaches end stage renal disease

153
Q

What are the symptoms of PKD?

A

Pain
Fullness
Polyuria
Increased risk of UTI and renal stones
abdominal/flank pain
palpable kidneys/abdominal mass
headaches
dysuria
suprapubic pain
fever

154
Q

What may be present in ADPKD?

A

HTN: activation of RAAS
Haematuria: vessel damage
Renal cysts
Cardiac murmur
Hepatomegaly

155
Q

What investigations should be done for PKD?

A

Renal ultrasound
Urinalysis
U&Es
FBC: possible excess erythropoietin and therefore Hb

Consider genetic testing to help confirm

156
Q

What are some of the differentials for PKD?

A

Acquired cystic kidney disease
Simple cyst
Tuberous sclerosis complex
von Hippel-Lindau syndrome(VHL)

157
Q

What’s the criteria for a diagnosis of ADPKD?

A

Age 15-29, 3 or more cysts (unilateral or bilateral)
Age 30-39, 3 or more cysts (unilateral or bilateral)
Age 40-59, 2 or more cysts in each kidney)

158
Q

In ADPKD, what does tolvaptan do and when is it indicated?

A

slows decline in kidney function
indicated in adults at risk of rapidly progressing ADPKD

159
Q

What are the management options for end stage renal disease caused by ADPKD?

A

Renal transplant
Dialysis

160
Q

How is ADPKD typically managed?

A

Healthy lifestyle moderations
Treatment of HTN
Tolvaptan: a vasopressin V2 receptor antagonist, slows kidney function decline, good for use in rapidly prgressing disease

161
Q

What are the complications of ADPKD?

A

cardiac complications: LV hypertrophy, cerebral aneurysm
gastro-oesophageal reflux disease (GORD)
ruptured intracranial aneurysm
sepsis
complications during pregnancy

162
Q

What are the differences in how the kidneys are affected in ADPKD vs ARPKD?

A

ADPKD: normal size kidneys, larger cysts
ARPKD: larger kidneys with lots of smaller cysts

163
Q

In nephritic syndrome, what can a decrease in GFR lead to?

A

Activation of RAAS causing Na retention and HTN
Reduced urine output

164
Q

What is the pathology behind the features of nephritic syndrome?

A

Injury and inflammation to glomerular filtration barrier allows some protein and RBCs to leak through
RBCs can also clump together and form casts (suggestive of GN)
Injury also means that WBCs are recruited and pass into urine
GFR falls causing RAAS activation (HTN) and oliguria

165
Q

What can crescentic GN (rapidly progressive glomerulonephritis) be subdivided into?

A

Anti-glomerular basement membrane: goodpastures
Immune complex mediated: Post strep, IgA nephropathy
Pauci immune: ANCA vasculitis

generally have poor prognosis

these don’t always cause RPGN

166
Q

What is Goodpasture’s?

Subtype of nephritic GN

A

defined by the presence of autoantibodies to the alpha-3 chain of type IV collagen

Can cause RPGN and pulmonary haemorrhage

167
Q

How common is Goodpasture’s as a cause for GN?

A

causes 1% to 2% of GN cases
10%-20% of all crescentic GN

168
Q

What is the pathophysiology of Goodpasture’s disease?

A

Glomerular injury is the result of autoimmunity directed against the alpha-3 chain of type IV collagen.
Alpha-3 type IV collagen most commonly in alveoli and glomerular basement membranes

169
Q

What are the symptoms of Goodpasture’s disease?

A

Reduced urine output/ dark urine
Haemoptysis
Oedema
Cough
SOB
Fatigue
Malaise

pulmonary-renal syndrome

170
Q

What investigations should be run for suspected goodpasture’s causing RPGN?

A

Renal biopsy
Renal function: abnormal
Anti-GBM serology: positive
Hepatitis panel

171
Q

How is goodpasture’s disease treated?

A

high-dose oral prednisolone
plasma exchange
oral cyclophosphamide

172
Q

What are the complications of goodpasture’s disease?

A

Pulmonary haemorrhage
CKD

173
Q

What is IgA nephropathy?

aka Berger’s

A

Subtype of nephritic syndrome
defined by prescence of mesangial IgA immune deposits

174
Q

How common is IgA nephropathy in GN and what’s its outlook?

A

commonest pattern of glomerulonephritis
it accounts for approximately 10% to 50% of biopsy-proven primary glomerular diseases

used be considered benign but can slowly progress to CKD in some patients

175
Q

What is the pathophysiology of IgA nephropathy?

A

Excessive production of galactose deficient IgA
These are then targeted by other IgA and IgG
Formation of immune complexes that are deposited in mesangium of kidney

176
Q

How does IgA nephropathy present?

A

Haematuria
Sub-nephrotic levels proteinuria

177
Q

What is seen on a renal biopsy for IgA nephropathy?

A

diffuse mesangial IgA deposition

178
Q

What’s the management for IgA nephropathy?

A

Observe or supportive therapy
RAAS inhibitors: ACEi, ARBs
In high risk of progression consider prednisolone

179
Q

What are the possible complications of IgA nephropathy?

A

CKD
End stage kidney disease

180
Q

What is the most common cause of acute GN in children?

A

post-streptococcal glomerulonephritis

181
Q

What is the pathophysiology of post-strep GN?

A

IgG and IgM antibodies form immune complexes with bacterial antigens, most commonly M-type virulence factors.
Deposited in subepithelial glomerular basement membrane

182
Q

When does post-strep GN tend to occur?

A

2-3 weeks following Group A strep infection

183
Q

What would be found in post-strep GN?

A

High or rising antistreptolysin O antibody

184
Q

What are the different causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Diabetic nephropathy
Amyloidosis

185
Q

How is fluid overload treated?

A

Diuretics (loop): furosemide

186
Q

What are the treatment options for nephritic syndrome?

A

Corticosteroids
Immunosuppressants: cyclosporine
ACEi/ARBs
Antibiotics for infections
Diuretics for fluid overload

187
Q

What are the treatment options for nephrotic syndrome?

A

Supportive treatment:
- Control fluid state – diuretics, ACEi/ARBs, spironolactone
- Statins
- Anticoagulation: especially in membranous or amyloid where albumin <20g/l
- Prevent infections – prophylactic antibiotics in children
Steroids
Immunosuppressants: cyclophosphamide

188
Q

What are the differentials for GN?

A

Nephrolithiasis
Bladder cancer
Renal cancer
Pre or post acute kidney injury

189
Q

What are some risk factors for GN?

A

Infection
Hepatitis
HIV
SLE
Some cancers: lung, NHL, colorectal, leukaemia
Drugs: lithium, NSAIDs

190
Q

What investigations should be run for GN?

A

Urinalysis + urine microscopy first line
FBC
Renal biopsy/Antibodies

191
Q

What’s the most common form of nephrotic syndrome in children?

A

Minimal change disease

192
Q

What are the risk factors for minimal change disease?

A

2-8 years
Hodgkin’s lymphoma
leukemia
recent viral illness

193
Q

How does minimal change disease present?

A

Nephrotic syndrome
Oedema
Proteinuria
Often children age 2-8years

194
Q

What lab findings would be present for minimal change disease?

A

Urinalysis: high protein, hyaline casts
Electron microscopy: podocyte effacement
Hypoalbuminaemia

195
Q

What’s the treatment for minimal change disease?

A

Corticosteroids: prednisolone

196
Q

How does focal segmental glomerulosclerosis manifest?

A

manifests initially with proteinuria
progresses to nephrotic syndrome
ultimately to end-stage renal failure

197
Q

What pathologically causes focal segmental glomerulosclerosis?

A

injury to podocytes in the renal glomeruli

198
Q

What are the aetiological causes of focal segmental glomerulosclerosis?

A

Primary idiopathic
Secondary: HIV, obesity, heroin, lithium

199
Q

What investigations should be done for focal segmental glomerulosclerosis?

A

Urinalysis and microscopy: oval fat bodies and fatty casts
Serum albumin: low
Urea and creatinine: high

200
Q

What’s the first line therapy for FSG?

A

corticosteroids

ciclosporin if resistant

201
Q

What are the risk factors for FSGS?

A

male sex
black race
family history of FSGS
heroin abuse
use of known causative medications
chronic viral infection

202
Q

Possible complications of FSG?

A

ischaemic stroke
ACS
renal failure
hyperlipidaemia
hypertension

203
Q

What is membranous nephropathy?

A

chronic, immunologically mediated disease of the glomerular basement membrane

cause of nephrotic syndrome

204
Q

What are the most common causes of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis
Membranous nephropathy

205
Q

What are the aetiological causes of membranous nephropathy?

A

Most cases are idiopathic
Secondary causes can be infection, autoimmune, malignancy, certain drugs: lithium, nsaids

206
Q

How does membranous nephropathy present?

A

Nephrotic syndrome
Xanthelasma
Muehrcke’s lines
Oedema

207
Q

What investigations should be run for membranous nephropathy?

A

Urinalysis
Serum albumin
Urea
Creatinine
Lipid profile

208
Q

What’s the treatment for membranous nephropathy?

A

Supportive: low salt diet, ACEi
Furosemide to treat oedema
Statins
Corticosteroids + immunosuppressants if at moderate/high risk of progressing, e.g. pred + cyclophosphamide

209
Q

What are the possible complications of membranous nephropathy?

A

Hypovolaemia due to oedema
Elevated cholesterol
CKD
Hypercoaguability

210
Q

What would be seen on a renal biopsy for membranous nephropathy?

A

Microscopic analysis: shows thickened glomerular basement membrane
Immunofluorescence: shows diffuse uptake of IgG

211
Q

What is membranoproliferative GN?

A

a group of immune-mediated disorders characterised histologically by glomerular basement membrane (GBM) thickening and proliferative changes on light microscopy

Can cause nephritic or nephrotic syndrome

212
Q

What would be seen on a renal biopsy for membranoproliferative GN?

A

Thickened basement membrane
Thickened mesangium
“Tram tracking” appearance

213
Q

What is diffuse proliferative GN?

A

histopathologic classification of glomerulonephritis (GN) commonly associated with autoimmune diseases
characterized by an increased cellular proliferation affecting > 50% of the glomeruli.

can be nephritic or nephrotic

214
Q

What’s the difference between visible and non-visible haematuria?

A

visible: blood is visible in the urine
non-visible: blood is present in the urine on urinalysis, but not visible

215
Q

What can cause haematuria?

A

UTI
renal cancer
bladder cancer
renal stones
prostate cancer
BPH
GN

216
Q

What is prostate cancer?

A

A malignant tumour of glandular origin, situated in the prostate

217
Q

What’s the epidemiology of prostate cancer?

A

Most commonly reported in men aged over 50 years
median age at diagnosis 67 years
Most common cancer in males

218
Q

Where does advanced prostate cancer tend to spread to?

A

lymph nodes
bones

219
Q

What are some possible causes for prostate cancer?

A

Exact aetiology unclear but may involve genetic mutations such as BRCA1/2
High fat diet

220
Q

What’s the most common form of prostate cancer?

A

Most commonly an adenocarcinoma growing in peripheral zone of prostate

221
Q

What are the risk factors for prostate cancer?

A

age over 50 years
black ethnicity
family hx of prostate cancer
High fat diet

222
Q

How can prostate cancer present?

A

Often asymptomatic following PSA or DRE

LUTS
Weight loss
Lethargy
Bone pain and painful lymph nodes – mets
Haematuria

223
Q

What investigations should be run for suspected prostate cancer?

A

prebiopsy multiparametric MRI
PSA
DRE
Prostate biopsy – should be offered based on results of other investigations, not just a positive PSA

224
Q

Why is a PSA test not always appropriate?

A

unreliable - high rate of false positives (75%) and false negatives (15%)
can increase risks of over-diagnosing and overtreating clinically insignificant prostate cancer

225
Q

What are the possible differentials for prostate cancer?

A

BPH
Chronic prostatitis

226
Q

On a DRE how would a benign and cancerous prostate present?

A

Benign: smooth, symmetrical, may be enlarged, central sulcus
Cancerous: firm, hard, loss of central sulcus, asymmetrical

227
Q

What’s the gleason grading score for prostate biopsies?

A

6 is considered low risk
7 is intermediate risk (3 + 4 is lower risk than 4 + 3)
8 or above is deemed to be high risk

228
Q

What are the treatment options for prostate cancer?

A

Watchful waiting - regular PSA (6 months) and DRE (12mon)
androgen deprivation therapy (ADT)
external beam radiotherapy (EBRT)
brachytherapy
radical prostatectomy

EBRT, brachytherapy, prostatectomy should be curative in non-metastatic

229
Q

What’s the most common histological type of bladder cancer?

A

urothelial carcinoma

accounts for over 90%

230
Q

Epidemiology of bladder cancer

A

10th most common cancer in the world
More common in men than women, but women have worse prognosis
Increases with age and typically affects people over the age of 65

231
Q

What typically causes bladder cells to become malignant?

A

Carcinogens are concentrated and excreted in urine so cells lining urinary tract are exposed and exposure in bladder is prolonged

232
Q

What are the risk factors for bladder cancer?

A

tobacco exposure
exposure to chemical carcinogens
age >65 years
pelvic radiation, e.g. treatment of prostate cancer
systemic chemotherapy
Schistosoma infection
male sex
chronic bladder inflammation
genetic predisposition

233
Q

What is the typical presentation of bladder cancer?

A

Painless haematuria

234
Q

What investigations should be run for suspected bladder cancer?

A

Urinalysis: haematuria
Cystoscopy: visualises bladder tumours and enables pathological diagnosis

235
Q

What are the 2 main distinctions of bladder cancer?

A

Non-muscle-invasive bladder cancer (not invading the muscle layer of the bladder)
Muscle-invasive bladder cancer (invading the muscle and beyond)

236
Q

What are the differentials for bladder cancer?

A

BPH
Haemorrhagic cystitis
Prostatitis
UTI
Nephrolithiasis
Other cancers incl. renal cell carcinoma + gynaecological cancers

237
Q

What’s the standard management for muscle invasive bladder cancer?

A

chemo, radical cystectomy and node dissection

cannot be reliably resected and risks mets

238
Q

What is the recommended management of non-muscle invasive bladder cancer?

A

Transurethral resection of a bladder tumour
intravesical chemo
+ BCG immunotherapy in higher risk

239
Q

What factors are associated with a poor prognosis of bladder cancer?

A

older age
female sex
smoking
higher stage at diagnosis
muscle invasion

240
Q

What do testicular cancers arise from and what are they further classified into?

A

More than 95% of testicular cancers arise from germ cells

seminoma or non-seminoma

241
Q

What’s the epidemiology of testicular cancer?

A

overall a rare cancer
more common in younger men, with the highest incidence between 15 and 35 years

242
Q

What are the risk factors for testicular cancer?

A

Undescended testicle
Family hx of testicular cancer
White ethnicity
Testicular atrophy
HIV infection

243
Q

What’s the typical presentation for testicular cancer?

A

young adult male with lump/mass on testicle
often painless

244
Q

What investigations should be run for testicular cancer?

A

Ultrasound of testis
Tumour markers:
- Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas)
- Beta-hCG – may be raised in both teratomas and seminomas
- Lactate dehydrogenase (LDH)

245
Q

What are the differential diagnoses for testicular cancer?

A

Testicular torsion
Epididymo-orchitis
Scrotal hernia
Hydrocele
Benign cyst

246
Q

What are common areas for testicular cancer to metastasize to?

A

Lymphatics
Lungs
Liver
Brain

247
Q

What are the management options for testicular cancer?

A

Surgery to remove the affected testicle (radical orchidectomy)
Chemotherapy
Radiotherapy

sperm banking due to infertility risk

248
Q

What is renal cell carcinoma?

& who does it affect

A

adenocarcinoma arising from the renal parenchyma/cortex
most common tumour of the kidneys, (80-90%)

tends to affect men more than women

median age 65 years

249
Q

How does RCC typically present?

A

Asymptomatic, symptoms can suggest worse prognosis and only present in <10% cases

flank pain, haematuria, and palpable abdominal mass

250
Q

What’s commonly seen if RCC metastasizes to lungs?

A

Cannonball metastases in the lungs

251
Q

What are the risk factors for RCC?

A

Hypertension
Smoking
Obesity
Male sex
Over 55 years
Family hx of renal cancer
Hereditary: von hippel lindau

252
Q

How is RCC often diagnosed and managed?

A

Ultrasound
Surgery to remove tumour< can involve partial or radical nephrectomy

253
Q

What is a varicocele?

A

an abnormal dilation of the internal spermatic veins and pampiniform plexus that drain blood from the testis

254
Q

What are the key causes of scrotal lumps?

A

Hydrocele
Varicocele
Epididymal cyst
Testicular cancer
Epididymo-orchitis
Inguinal hernia
Testicular torsion

255
Q

What causes varicoceles and which side do they typically affect?

A

Increased resistance from incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus

left sided much more common, can be a sign of RCC

256
Q

How does a varicocele typically present and what investigations can be done?

A

Asymptomatic, can be painless unilateral mass (bag of worms), infertility

typically a clinical diagnosis but ultrasound can also be used

257
Q

How is a varicocele treated?

A

Reassurance
Surgical treatment if >20% size difference

258
Q

What is testicular torsion & who does it tend to affect?

A

urological emergency caused by the twisting of the testicle on the spermatic cord leading to constriction of the vascular supply

affects adolescent boys most

259
Q

What are the typical causes of testicular torsion?

A

A bell-clapper deformity - fixation between the testicle and the tunica vaginalis is absent, hangs more horizontally
Trauma - far less common

260
Q

What’s the typical hx for a patient with testicular torsion?

A

sudden-onset severe scrotal pain, often with associated nausea and vomiting

no pain relief on elevation

261
Q

What’s the management for testicular torsion?

A

Immediate surgical exploration
- Orchiopexy (correcting the position of the testicles and fixing them in place)
- Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis

262
Q

What are the possible complications of testicular torsion?

A

Infarction
Infertility
Recurrent torsion

263
Q

What is obstructive uropathy?

A

blockage of urinary flow, which can occur at any level in the urinary tract

264
Q

What does obstruction in the urinary tract cause?

A

Obstruction leads to back-pressure in the urinary system, causing areas proximal to the site of obstruction to become swollen with urine
Prevents urinary flow
Decreases renal blood flow and GFR
Leads to kidney damage

265
Q

What can cause obstructive uropathy?

A

Unilateral obstruction
- Renal stones
- Nearby malignancy
Bilateral obstruction
- BPH
- Urethral strictures

266
Q

What are the 2 types of hydrocele?

A

communicating: caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum. common in newborn males
non-communicating: caused by excessive fluid production within the tunica vaginalis

267
Q

What’s a hydrocele?

A

collection of serous fluid between the layers of the membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord

tends to affect infants and children

268
Q

What are the key features of a hydrocele?

A

Scrotal swelling which enlarges with an increase in intra-abdo pressure, e.g. coughing or straining
Transillumination

269
Q

What’s the management for a hydrocele?

A

Often observation and they resolve spontaneously
Surgery may be used in children over age of 2

typically resolve within first 2 years of life

Phase 2a (14 decks)

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