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Phase 2a Gold Standard > Renal/Genitourinary > Flashcards

Renal/Genitourinary Flashcards

1
Q

Functions of the kidney

A

AWETBED
Acid-base homeostasis
Water balance
Electrolyte balance
Toxin/waste product removal
Blood pressure control
Ertyhropoietin
D (vitamin D activation)

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2
Q

Define Acute Kidney Injury

A

A sudden decline in kidney function leading to a rise in serum creatinine and fall in urine output.

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3
Q

What can renal dysfunction cause

A

Dysregulation of
- Fluid balance
- Acid-base homeostasis
- Electrolyte imbalance

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4
Q

Drugs to stop in acute kidney injury

A

DAAMN
D - Diuretics
A - ACEi/ARB
A - Aminoglycosides
M - Metformin
N - NSAIDs

ACEi/ARB protective in Chronic

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5
Q

6 pre renal causes of AKI

A

Hypoperfusion

  • Hypovolaemia (bleeding, reduced cardiac output (CHF), cardiogenic shock)
  • Liver failure (hypoalbuminaemia)
  • Renal artery blockage/stenosis
  • ACEi & NSAID
  • Sepsis causing systemic vasodilation
  • Dehydration
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6
Q

4 intrarenal causes of AKI

A

Intrinsic disease of kidney

  • Acute tubular necrosis
  • Acute interstitial nephritis (these 2 can be drug induced)
  • Glomerulonephritis
  • Small vessel vasculitis
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7
Q

4 post renal causes of AKI

A

Obstruction to urinary outflow, causing back pressure into kidney. (Obstructive uropathy)
- BPH
- Urolithiasis
- Cervical and prostate cancer
- Bladder neck stricture

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8
Q

Risk factors of AKI

A
  • Age >65
  • Heart failure
  • Diabetes
  • Poor fluid intake
  • Hypovolaemia
  • Nephrotoxic meds (NSAID, ACEi)
  • Contrast medium usage in imaging
  • Prostate cancer
  • BPH
  • Sepsis
  • Liver disease
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9
Q

Electrolyte consequences of AKI

A

Hyperkalaemia and azotaemia (increased blood creatinine and urea)
Metabolic acidosis

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10
Q

Symptoms of pre renal AKI

A

Hypotension
Reduced capillary refill
Dry mucus membranes
Reduced skin turgor
Cool extremities

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11
Q

Intra renal AKI symptoms

A

Infection/ signs of underlying disease (vasculitis, glomerulonephritis etc)

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12
Q

Post renal AKI symptoms

A

Loin to groin pain
Haematuria
Palpable bladder/prostate
Prostatic urinary issues (dysuria, terminal dribbling, hesitancy)

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13
Q

Causes of Acute tubular necrosis

A

Ischaemia - Pre renal disease
Nephrotoxicity - (aminoglycosides, chemotherapy), contrast in CT, myoglobin, multiple myeloma

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14
Q

Pathophysiology of acute tubular necrosis

A

Nephrotoxins (aminoglycosides, NSAIDs, uric acid) can kill epithelial cells. When cells die, they block tubules increasing pressure. Less filtration occurs, causing azotaemia, hyperkalaemia and metabolic acidosis.

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15
Q

Pathophysiology of prerenal AKI

A

Less blood into kidney usually due to hypovolaemia causes activation of RAAS system
Na+ and urea reabsorbed, leading to oliguria
Causes less urine output which is more concentrated

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16
Q

Diagnostic criteria for AKI (stage 1)

A
  • Rise in creatinine > 26μmol/L within 48 hours
  • Rise in creatinine >1.5 x baseline (i.e. before the AKI) within 7 days.
  • Urine output <0.5ml/kg/hour for >6 consecutive days.
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17
Q

Investigations in AKI

A

Check for hypo/hypervolaemia and urine output
FBC, U&E, ABG, Creatinine Kinase, Urine output should all be checked.
Urinalysis
Imaging
- Ultrasound - urinary tract to look for obstruction
- CXR - Signs of volume overload (cardiomegaly, pulmonary oedema)
- ECG - Hyperkalaemic changes
- CTKUB check obstruction

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18
Q

What urinalysis is conducted in AKI

A

Urine osmolality and electrolytes checked
Dipsticks - Leucocytes and nitrites = infection
Protein/ blood = acute nephritis
Glucose suggests diabetes

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19
Q

Treatment of AKI

A

Prerenal: IV fluids and treatment of sepsis
Intrarenal: Stop nephrotoxic drugs, treatment specific to condition
Post renal: Catheter in BPH

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20
Q

Treatment of AKI complications

A

Hyperkalaemia
- Calcium gluconate (protect myocardium)
- Insulin/dextrose (drive K+ into cells)
- Stop K+ sparing medication

Acidosis
- Sodium bicarbonate

Pulmonary oedema/hypervolaemia
- Diuretics

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21
Q

Complications of AKI

A
  • Hyperkalaemia
  • Fluid overload from treatment
  • Metabolic acidosis
  • Uraemia (encephalopathy/pericarditis)
  • CKD
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22
Q

Classification systems in AKI

A

KDIGO (Kidney Disease: Improving Global Outcomes)
RIFLE (Risk Injury Failure Loss Endstage renal disease)

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23
Q

Staging of AKI

A

KDIGO criteria
Stage 1
- Creatinine >26 or 1.5-1.9x baseline in <48hr
- Urine output <0.5ml/kg/hr for 6-12 hours
Stage 2
- >2-2.9x baseline creatinine
- Urine output <0.5ml/kg/hr for >12 hours
Stage 3
>353 or 3x reference creatinine
<0.3ml/kg/hr for >24 hours or anuria for >12

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24
Q

Define CKD

A

Progressive deterioration in renal function over at least 3 months characterised by eGFR of <60ml/min/1.73m²

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25
Q

What 2 tests are considered in CKD classification

A

eGFR and albumin:creatinine ratio

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26
Q

How is eGFR used to stage CKD

A

Stage 1 - >90 (normal)
Stage 2 - 60-89 (mild reduction, only CKD if symptoms)
Stage 3a - 45-59 (mild-moderate reduction)
Stage 3b - 30-44 (moderate-severe reduction)
Stage 4 - 15-29 (severe reduction)
Stage 5 <15 (End stage kidney failure)

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27
Q

How is albumin:creatinine ratio used to stage CKD

A

Checks proteinuria to give A score
A1 - <3mg/mmol
A2 - 3-30mg/mmol
A3 - >30mg/mmol

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28
Q

What can be used as evidence of renal damage?

A
  • Albuminuria (ACR>3)
  • Electrolyte abnormalities
  • Histological abnormalities
  • Structural abnormalities on imaging
  • Kidney transplant history
  • Urine sediment abnormalities
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29
Q

At what eGFR is metformin contraindicated

A

<30ml/min/1.73² (stage 3b)

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30
Q

Causes of CKD

A

Most common: Diabetes and HTN

Nephrotoxic drugs
Glomerulonephritis
Systemic disease e.g. rheumatoid arthritis/SLE

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31
Q

How does CKD lead to its complications

A

low eGFR = azotaemia (which can cause encephalopathy and pericarditis)
Urea affects platelet function (bleeding)
Uremic frost (urea crystals in skin)
Kidneys normally activate vit D. No activation = hypocalcaemia = PTH secretion = bone resorption (renal osteodystrophy)
Low fluid to kidney = RAAS activation = HTN
HTN causing increased intraglomerular pressure - causing shearing and loss of selective permeability (protein/haematuria)
Kidneys produce less EPO = Anaemia

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32
Q

Signs/symptoms of CKD

A

Asymptomatic at first

Uraemic frost (tiny yellow white urea crystals on skin)
Uraemia swallow (pale/brown colour on skin)
Pallor
Fatigue
Lethargy
Frothy urine
Swollen ankles/oedema
Increased bleeding

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33
Q

What does anaemia, with low calcium and low phosphate imply

A

CKD

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34
Q

Investigations in CKD

A

Urine dipstick
- Haematuria, glycosuria
eGFR and urine albumin:creatinine ratio
U&E
FBC
- Normocytic normochromic anaemia
Bone profile/PTH
- Ca2+ low, phosphate high, PTH high, ALP high

Renal ultrasound
Bilateral kidney atrophy (small kidneys)

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35
Q

Complications of CKD

A

Anaemia (EPO reduced)
Osteodystrophy (decreased vit D activation)
Neuropathy/encephalopathy
Pericarditis

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36
Q

Treatment of CKD

A

No cure except transplant, can only treat symptoms
Anaemia - EPO + Iron
Osteodystrophy - Vit D supplementation
CVD - ACEi + statins
Oedema - Diuretics

(ACEi help in CKD but harm in AKI)

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37
Q

What is RRT and what are its indications

A

Renal replacement therapy - Persistent severe complications (electrolyte, oedema, uraemia) or Stage 5 CKD
AEIOU
Acidosis > 7.2 - Acidosis not helped by sodium bicarbonate
Electrolytes K+>7mmol/L
Intoxication - Stage 5 CKD
Oedema
Uraemic pathology - Encephalopathy, pericarditis etc

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38
Q

What are the types of RRT

A

Haemodialysis (most common)
- Blood taken from artery, filtered and returned into vein at AV fistula.
- 3x4 hours a week
- Complications: hypotension, nausea, chest pain, infected catheter (sepsis)

Peritoneal dialysis
- Peritoneal catheterisation, exchange of solutes across peritoneal membrane
- Done at home
- Complications: Peritonitis, abdominal wall hernia

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39
Q

Causes of CKD-mineral bone disease

A

Reduced 1-alpha hydroxylase activity (reduced vit D activation)

Reduced renal excretion of phosphate (phosphate stimulates bone resorption)

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40
Q

Treatment of CKD mineral bone disease

A

Reduced dietary phosphate (fish, meat, poultry)
Vit D replacement (calcitriol is already 1-alpha-hydroxylated)
Phosphate binders
Bisphosphonates

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41
Q

BP Targets in CKD

A

140/90 or 130/80 if coexisting diabetes

ACEi used (reduce filtration pressure, less proteinuria)

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42
Q

Define renal colic

A

AKA Nephrolithiasis

Formation of renal stones in urinary system

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43
Q

Pathophysiology of Nephrolithiasis

A

When solvent (water) too low, or solute too high, solutes can precipitate and crystallise, forming a nidus. More solutes precipitate around this, forming kidney stone.

Mg and Citrate inhibit crystal growth

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44
Q

What are the types of kidney stone, how do they form and how do they show?

A

Calcium oxalate (most common)
- Black/dark brown, radiopaque on X ray
- Form in acidic urine

Calcium phosphate stones
- Dirty white, Radiopaque
- Form in alkaline urine

Struvite stones (magnesium, ammonium. phosphate)
- Dirty white, radiopaque
- AKA infection stones, form during UTI (UTI organisms hydrolyse urea into CO2 and ammonia)

Uric acid stones
- Red-brown, radiolucent (transparent to X ray)
- High purine diet, dehydration, acidic urine

Cystine stones
- Yellow/light pink, radiopaque
- Cystinuria, autosomal recessive condition causing decreased cystine absorption

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45
Q

Renal stone appears dirty white and radiopaque, which 2 could it be?

A

Calcium phosphate
Struvite

(struvite forms during UTI)

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46
Q

Risk factors for renal stone development (7)

A

Dehydration
Low urine output
Hypercalcaemia, Hypercalciuria Hyperparathyroid
Previous kidney stones
Foods high in oxalate, phosphate or calcium (spinach, tea, rhubarb, chocolate)
Gout
Renal tubular acidosis

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47
Q

Signs/symptoms of nephrolithiasis

A

Severe, colicky loin to groin pain
- Lasts minutes to hours and fluctuates in severity
- Caused by peristalsis against stone (dilation, stretching and spasm due to obstruction of ureter)
Flank/renal-angle tenderness
Fever
Nausea/vomiting
Haematuria

(Hypotension and tachycardia if sepsis)

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48
Q

2 most common renal stone sites

A
  1. Ureteropelvic junction
  2. Renal pelvis (staghorn calculi form here)
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49
Q

Investigations in nephrolithiasis

A

Urine dipstick - haematuria (+ leucocytes and nitrites if infection)
Abdominal X ray - calcium based stones
USS KUB - Pregnant or under 16, only radiopaque

NCCT-KUB (Non Contrast CT of Kidney, Ureter, Bladder) - Stones seen in renal collecting system or ureter

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50
Q

Management of Nephrolithiasis

A

Hydration
IV diclofenac for renal colic
Antibiotics for UTI

Surgery if stones too big
- Extracorporeal shockwave lithotripsy (CI in pregnant)
- Percutaneous Nephrolithotomy (PCNL)

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51
Q

Kidney stone recurrence prevention

A

Citrus e.g. lemon juice (citric acid binds to urinary calcium)
Avoid cola drinks
Potassium citrate
Cystine binder if cystine stone
Thiazide diuretics (increase Ca2+ excretion)

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52
Q

What are the upper and lower UTIs

A

Upper - Pyelonephritis (renal parenchyma and renal pelvis)

Lower
- Urethritis (Urethral inflammation usually due to STI)
- Cystitis (Infection of bladder)
- Prostatitis (acute/chronic infection of prostate)
- Epididymis-Orchitis (epididymis, extends to testes, usually 2° to urethritis or cystitis)

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53
Q

How do you know if a UTI is complicated? (7)

A

If it affects:
a man
a pregnant lady
a baby
the immunocompromised
it is recurrent
people with abnormal urinary tracts (e.g. stones)
Catheterised

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54
Q

General UTI causing microbes

A

KEEPS
K- Klebsiella
E- E Coli (UPEC) (80% of cases)
E- Enterococci
P- Proteus spp
S- Staphylococcus

(Most common E Coli strain is UPEC (UroPathogenic E Coli))

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55
Q

Why are women more affected by UTIs

A

They have a shorter urethra, which is closer to the anus, allowing for easier microbial colonisation

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56
Q

Investigations in uncomplicated UTI

A

Midstream urine dipstick (leukocytes, nitrites, may or may not have haematuria)
Midstream urinary culture (MC and S - Microscopy, culture and sensitivity)

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57
Q

Treatment of uncomplicated UTI

A

Nitrofurantoin and trimethoprim (teratogenic) 3 days, while waiting for culture

Do not treat >65 years if asymptomatic

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58
Q

Define Pyelonephritis with risk factors

A

Infection of renal parenchyma and upper ureter, which can be direct or haematogenous
- Vesico-ureteral reflux
- Unprotected sex
- Female
- Pregnancy
- Urinary tract obstruction
- Indwelling catheter
- Ascending lower UTI

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59
Q

Signs/symptoms of pyelonephritis

A

TRIAD:
Fever, loin/back pain, pyuria (WBC in urine)

Renal angle tenderness, nausea/vomiting, haematuria

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60
Q

Abdo exam and Investigations in pyelonephritis

A

Abdominal exam
- Tender loin
- Renal angle tenderness
Midstream urine disptick
- Blood, protein, leukocyte, nitrites, foul smell
CT scan first line imaging

GOLD: Midstream urine MC+S

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61
Q

Management of pyelonephritis

A

IV fluids and broad spectrum antibiotics (Co-amoxiclav 14 days)
Drain obstructed kidney and remove catheter

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62
Q

Complications of pyelonephritis

A

Renal abscess
Emphysematous pyelonephritis (gas accumulation in tissues, life threatening)
Chronic pyelonephritis

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63
Q

How should catheterised UTI be investigated

A

DONT use urine dipstick.
Culture should come from catheter

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64
Q

Define cystitis

A

Usually UPEC infection of bladder

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65
Q

Signs and symptoms of cystitis

A

Suprapubic pain/tenderness, Dysuria (pain/burning when urinating), frequency, urgency, cloudy/smelly urine

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66
Q

How to diagnose cystitis

A

Abdominal exam
Urine dipstick and MC+S

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67
Q

Define urethritis

A

Urethral infection and inflammation, usually sexually acquired

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68
Q

Causes of urethritis

A

Infective
- Gonococcal (Neisseria gonorrhoea)
- Non gonococcal (chlamydia tractomatis)

Non infective
Trauma
Reactive arthritis

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69
Q

Signs/symptoms of urethritis

A

Urethral discharge (blood/pus), itching, irritation
Dysuria, frequency, urgency

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70
Q

Investigations in urethritis

A

1st - NAAT (Nucleic acid amplification test)
Females - vulvovaginal swab
Males - First void urine (first in morning)

Urethral discharge gram stain (Gram negative diplococci = N gonorrhoeae)

Urine dipstick and culture

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71
Q

Treatment of urethritis

A

N gonorrhoea
- Single dose of IM Ceftriaxone (1g) or oral ciprofloxacin (500mg)

Chlamydia
- Doxycycline 2x a day for 7 days

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72
Q

What should be looked at after pharmacological treatment in urethritis

A

Sexual abstinence
Safeguarding issues in children
Contact tracing

Disseminated Gonococcal Infection most common complication (skin and joints affected)

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73
Q

Define Epididymo-Orchitis

A

Inflammation of epididymis, extending to testes, usually secondary to urethritis (STI pathology) or Cystitis (Mostly UPEC)

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74
Q

Signs/symptoms and treatment of Epididymo-Orchitis

A

Unilateral scrotal pain and swelling.
Pain relieved with elevation of testes
cremaster reflex intact

Treatment will be identical to cystitis or urethritis depending on cause.

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75
Q

Define prostatitis

A

Severe prostate infection usually due to KEEPS pathology

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76
Q

Signs/symptoms of prostatitis

A

Tender hot swollen prostate on DRE
Pelvic pain
LUTS (Dysuria, frequency, hesitancy, urgency etc)
Pain with bowel movements

Infection symptoms (Tachycardia, fever, nausea, rigors etc)

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77
Q

Investigations of prostatitis

A

Digital rectal exam (DRE)
Urine dipstick and MSU (midstream urine sample) with culture
Blood culture
STI screen (NAAT)

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78
Q

Differentials of prostatitis (5)

A

BPH
UTI
Prostate cancer
Bladder cancer
Epididymo-orchitis

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79
Q

Management of prostatitis

A

Acute
- 14 day ciprofloxacin
analgesia and laxatives if pain

Chronic
- Alpha blockers (tamsulosin)
- 4-6 week doxycycline or trimethoprim

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80
Q

Complications of prostatitis

A

Main: Prostate abscess (especially if indwelling catheter)
Sepsis
Progression to chronic

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81
Q

Define Benign Prostatic Hyperplasia

A

Non malignant growth of the prostate gland, causing compression of the prostatic urethra causing Lower Urinary Tract Symptoms (LUTS). Usually affects transitional zone

82
Q

What are some causes of fluid overload

A

Heart or kidney conditions
Pregnancy
Too much salt in diet/too much water intake
Liver failure (hypoalbuminaemia)
Conns

83
Q

Pathophysiology of BPH

A

Luteinising hormone acts on leydig cells to produce testosterone
5a-reductase converts testosterone to dihydrotestosterone (DHT)
Androgens bind to androgen receptors, preventing apoptosis and allowing glandular epithelial cells and stromal cells (connective tissue) to grow.
With age, testosterone decreases but 5a-reductase activity increases leading to excess DHT, causing excess hyperplasia of the prostate.
This compresses prostatic urethra, causing build up of urine and difficulty voiding. This also causes bladder hypertrophy.

84
Q

Signs/symptoms of BPH

A

LUTS Symptoms
Voiding: Hesitancy, weak stream, straining, dysuria, incomplete emptying, terminal dribbling.
Storage: Urgency, frequency, nocturia, incontinence

85
Q

DRE findings in BPH

A

Smooth, enlarged, non tender prostate

86
Q

Investigations in BPH

A

Digital rectal exam - Smooth, enlarged, non tender bladder
PSA Testing - raised in prostate cancer but can also be raised in BPH
IPSS score (international prostate symptom score) used

Urinary frequency volume chart

87
Q

Pharmacological management of BPH with side effects.

A

1) Alpha-1-blockers - Tamsulosin (relaxes muscles in bladder to reduce resistance to bladder flow) (SE: Postural hypotension)

2) 5-alpha-reductase-inhibitors - finasteride (inhibit conversion of testosterone to dihydrotestosterone to reduce prostate size) SE: Sexual dysfunction

88
Q

Surgical management of BPH with main side effect

A

Transurethral resection of the prostate (TURP)

Main side effect: Retrograde ejaculation, erectile dysfunction

89
Q

Define prostate cancer with 4 risk factors

A

Adenocarcinoma of the prostate gland (usually peripheral zone).

Associated with BRCA1 and BRCA2
Age
Afro Caribbean
Family history

90
Q

Signs/symptoms of prostate cancer

A

LUTS- Voiding: Hesitancy, weak stream, straining, dysuria, incomplete emptying, terminal dribbling.
Storage: Urgency, frequency, nocturia, incontinence

  • Bone pain (if metastasised to bone)
  • Wight loss, fatigue, night sweats
91
Q

Investigations of prostate cancer

A

DRE: Hard, asymmetrical, nodule, irregular prostate with loss of median sulcus
PSA
Transrectal ultrasound
Prostate Biopsy - GOLD. Used with Gleason score.

Bone scan to check for bone metastasis (Lesions)

92
Q

What scoring system is used in prostate cancer

A

Gleason scoring - Uses biopsy to grade prostate cancer
1-5
1 - Well differentiated cancer
5 - Anaplastic (Extremely poorly differentiated)

1st and 2nd most prevalent histological patterns graded and added together to give score out of 10.

93
Q

Management of prostate cancer

A

Local - prostatectomy
Active surveillance if >70 or not severe

If metastatic
- Radiotherapy
- Hormone therapy (GnRH e.g. Goserelin) or bilateral orchidectomy (remove testicles) - reduce testosterone
- Androgen receptor blocker

94
Q

Other causes of raised PSA

A

BPH
Prostatitis
UTI
Vigorous exercise
Recent ejaculation

95
Q

Define Bladder cancer with 4 main risk factors

A

Transitional cell carcinoma of the bladder most common.
- Aromatic amines (Dyes/rubber)
- Polycyclic aromatic hydrocarbons (aluminium, coal)
- Bladder stones causing chronic inflammation

96
Q

Signs and symptoms of bladder cancer

A

Painless haematuria
Weight loss
Palpable suprapubic mass
History of working in atrisk industries

97
Q

Investigations of bladder cancer

A

Urinalysis - haematuria
CT Urogram - staging
Cystoscopy and biopsy GOLD

98
Q

Management of bladder cancer

A

Chemo/Radio
TURBT (Transurethral resection of bladder tumour)

99
Q

Define renal cell carcinoma

A

Clear cell Adenocarcinoma of proximal convoluted tubule most common

Kidney cancer of under 5s usually Wilms’ tumour

100
Q

Main risk factor for RCC

A

von Hippel-Lindau. Autosomal dominant tumour suppressor gene loss.

Also
- Polycystic kidneys
- Renal failure

101
Q

Signs/symptoms of RCC

A

Classic triad
- Haematuria
- Flank pain
- Weight loss

Left sided varicocele possible

102
Q

Investigations and treatment of RCC

A

1st - USS
GOLD - CT Chest, abdomen, pelvis

Staging with Robson staging, TNM if metastatic

Treated with Nephrectomy

103
Q

Define testicular cancer

A

Most common cancer in young men
Can be germ cell (Seminoma, Yolk sac tumour (Children) Teratoma) (90%) or non germ cell (Leydig cell, Sertoli cell) (10%).
Non hodgkin lymphoma also possible

Seminomas secrete b-hCG (make pregnancy test positive)

104
Q

Signs/symptoms of testicular cancer

A
  • Firm non-tender testicular mass that does NOT transilluminate.
  • Supraclavicular lymphadenopathy
105
Q

Signs of testicular cancer

A
  • Firm non-tender testicular mass that does NOT transilluminate.
  • Supraclavicular lymphadenopathy
106
Q

Symptoms of testicular cancer with B-hCG pathology

A
  • Hyperthyroid (B-hCG mimics TSH)
  • Gynaecomastia
  • Loss of libido
  • Erectile dysfunction
  • Testicular atrophy
107
Q

What tells you its choriocarcinoma vs seminoma?

A

Choriocarcinoma presents younger and has a greater increase in bHCG

108
Q

Investigation and tumour markers in testicular cancer

A

Testicular doppler ultrasound GOLD

B-hCG - Choriocarcinoma and Seminoma
AFP - Yolk sac tumour, Teratoma, Embryonal carcinoma

109
Q

Management of testicular cancer (seminoma as MC)

A

Localised - Radical orchiectomy

Metastatic - Add chemo and radiotherapy (Just combination chemo if non seminoma)

110
Q

Define autosomal recessive polycystic kidney disease with 3 signs and main investigation

A

Rare PKHD1 mutation which codes for fibrocystin. Disease of infancy.
Causes renal failure before birth.
- Clubbed feed
- Flat nasal bridge
- Underdeveloped lungs and ears

Prenatal ultrasound will show bilaterally large kidneys with cysts and oligohydramnios (low amniotic fluid).

111
Q

Define autosomal dominant PKD

A

Mutations in PKD1 (C16) and PKD2 (C4), which code for polycystin 1 and 2. This causes cyst formation all over the kidney, making it appear larger

PKD1 more severe and earlier onset.

112
Q

What do PKD1 and 2 code for, and what happens in their absence

A

In primary cilium, urinary filtrate passage cause cilium to bend. Polycystin 1 and 2 allow calcium influx, which activate pathways that inhibit cell proliferation.

In mutation, cells proliferate abnormally, and proteins attract water into lumen. This causes cyst growth which press on vessels causing ischaemia.

Hypoperfused kidneys cause activation of RAAS, leading to fluid retention and HTN.

Cysts can also press on collecting duct causing urinary stasis and kidney stones.

Eventually, enough renal damage occurs, leading to renal failure

113
Q

What is the second hit mutation in PKD

A

In heterozygous ADPKD, enough polycystin 1 or 2 is produced to prevent PKD. In life, a “second hit” mutation causes the mutation to become homozygous, causing PKD

114
Q

Extra renal cyst formations in PKD (5)

A

Polycystins found in other places, can cause cysts all over:
- Liver (polycystic liver)
- Aortic root (aortic regurgitation/heart failure)
- Berry aneurysm of cerebral artery/circle of willis, which can rupture causing subarachnoid haemorrhage
- Pancreas
- Seminal vesicles

115
Q

Signs and symptoms of PKD

A

Signs:
Bilateral flank masses with flank pain
HTN

Symptoms:
Haematuria
Renal colic
Polyuria, polydipsia, nocturia (kidneys non responsive to ADH)

116
Q

Investigations in PKD

A

Ultrasound - bilateral renal cysts

If positive family history >= 3 cysts diagnostic.

117
Q

Management of PKD

A

Mainly targets symptoms/complications
HTN - ACEi
If severe, tolvaptan (Vasopressin 2 (V2) receptor antagonist) slows cyst development

Analgesia, dialysis, transplant

118
Q

Complications of PKD (5)

A

Cyst rupture
Haemorrhagic cyst rupture/ haemorrhagic stroke!
Infection
Renal stones
HTN

119
Q

Define Testicular Torsion

A

Emergency caused by twisting of the testicle on its spermatic cord, causing ischaemia and eventual necrosis.

6 hour window after onset until ischaemic damage is irreversible

120
Q

4 risk factors for testicular torsion

A

Adolescent
Bell clapper deformity (high riding testicles with horizontal lie, due to failure to attach to tunica vaginalis)
Cryptorchidism (undescended testis)
Trauma

121
Q

Signs and symptoms of testicular torsion

A
  • Hard, swollen, high riding, tender testicle with horizontal lie.
  • Absent cremasteric reflex
  • Prehn’s negative - pain not relieved on lifting testicle (unlike epididymitis)

Sudden onset excruciating pain, may have nausea/vomit

TWIST score

122
Q

What is the cremasteric reflex

A

Stroking of the inner thigh causes cremaster muscle to contract and pull ipsilateral testicle up towards the inguinal canal.

123
Q

Investigations and management in testicular torsion

A

Emergency surgical exploration (waiting longer than 6 hours, irreversible damage likely)

If testicle is viable, Bilateral detorsion and orchidopexy (testicle untwisted and fixed to scrotal sac)

If unviable, orchiectomy and orchidopexy of other testicle

124
Q

If testicular torsion surgery is delayed, what can be done in the meantime?

A

Manual detortion - temporary measure if surgery not possible in 6 hours.

125
Q

Define Varicocele with 2 main causes

A

Dilated testicular veins in pampiniform plexus, 90% occur on left side. Give a “bag of worms” appearance

  • Absent/defective valves
  • Increased pressure in left renal vein (left sided only)
126
Q

Normal blood supply of the testicles

A

Blood enters through testicular artery and leaves through the pampiniform plexus and then the testicular veins.

The left testicular vein drains into the left renal vein at right angle
The right testicular vein drains directly into the inferior vena cava

Pampiniform plexus helps manage temperature of testicles by absorbing heat through testicular artery

127
Q

Pathophysiology of varicocele

A

Dilatation of pampiniform plexus due to increased pressure in testicular veins. Mostly left sided due to LTV being longer and joining at right angle.

RCC can cause obstruction of left renal artery increasing resistance in LTV, causing left sided varicocele

128
Q

How are varicoceles graded

A

Subclinical - No clinical abnormality, but detectable by Doppler USS
Grade 1 (small) - Only palpable with Valsalva manoeuvre
Grade 2 (moderate) - Palpable without Valsalva
Grade 3 (Large) - Varicocele visible through skin

Valsalva manoeuvre - Exhale forcefully with mouth closed and nose pinched

129
Q

Signs/symptoms of varicoceles

A

Palpable scrotal veins (bag of worms appearance)
Dilatation increased with Valsalva manoeuvre
Scrotal mass greater when standing, disappears when lying down
Affected testicle may be lower and smaller

May have dull/throbbing pain which is worse on standing

130
Q

Investigations of varicoceles

A

Testicular examination standing and lying (bag of worms, worse standing, better lying, asymmetry of testicle size)
Doppler Ultrasound

Semen analysis may be done to check fertility

131
Q

When might a varicocele warrant referral

A
  • Sudden, painful onset
  • Doesn’t drain when lying down
  • Solitary on right side
132
Q

What are the 2 types of scrotal cyst?

A

Hydrocele - serous fluid between parietal and visceral layers of tunica vaginalis (goes around testical)

Epididymal cyst - Smooth, extra testicular, spherical sac of fluid in epididymis (top of testicle). Generally harmless.

133
Q

Two main types of hydrocele

A

Communicating (Primary) - failure of normal closure of processus vaginalis. Allows passage of peritoneal fluid into tunica vaginalis

Non communicating (Secondary)- No abnormal connection with peritoneal cavity. Fluid from mesothelial lining of t vaginalis. Can be secondary to:
- Testis tumours
- Trauma
- Infection (epididymo-orchitis)
- Testicular torsion
- TB

134
Q

How does hydrocele present (3 points) and main 3 investigations

A

Scrotal swelling
- Smooth, non reducible, non tender
- Transilluminates
- Communicating is soft and fluctuates in size, non communicating stays the same size

  • Pen torch illumination
  • Physical examination
  • Testicular ultrasound
135
Q

Management of hydrocele

A

Mostly self limiting

Late onset non communicating may need surgery
- aspiration
- Lord’s or Jaboulay procedure

136
Q

Define Epididymal cyst

A

Smooth, extra testicular sac of fluid at head of epididymis (top of testicle)

If it contains sperm it is called a spermatocele

137
Q

How does Epididymal cyst present and give its management

A

Soft round lump at top of testicle.
Well defined and transilluminates
Most are asymptomatic but larger cysts can be painful or cause heaviness

  • Usually self limit (10 days) and have no lasting effects.
  • Surgical excision can be done if needed
138
Q

Define Nephritic syndrome with its main symptoms

A

Non specific clinical picture of inflammation within the kidneys. Consists of;
- Haematuria
- Oliguria (low urine)
- HTN (Na+ retention) and oedema (fluid retention/overload)
- Slight Proteinuria BUT:
<3.5g of protein in 24 hours. (anymore = nephrotic)

139
Q

Define Nephrotic syndrome with its main triad

A

Issue with filtration barrier due to damage to glomeruli. Pathology affecting podocytes in primary disease.
Triad is:
- Proteinuria (>3.5g in 24 hours)
- Hypoalbuminaemia (loss of albumin in urine)
- Peripheral oedema (loss of oncotic pressure)

(haematuria may be present but is minor)

140
Q

Secondary causes of Nephrotic syndrome

A

Diabetes
Amyloidosis
Infection (Hep B/C, HIV)
Drugs (NSAID, gold, penicillamine)

141
Q

Main 5 protein/serum constituent features of Nephrotic syndromes

A

Proteinuria >3.5g
Hypoalbuminaemia
Hypercoagulability (loss of anti-thrombin III)
Hyperlipidaemia (causes frothy urine)
Susceptibility to infection (Loss of Ig in urine)

142
Q

Conditions involved in nephritic syndrome

A

PIGS
Post-strep glomerulonephritis
IgA nephropathy
Goodpasture’s
SLE nephropathy

143
Q

Conditions involved in nephrotic syndrome

A

MFM
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy

144
Q

Define IgA nephropathy

A

Type 3 hypersensitivity reaction (antigen-antibody deposition)
Abnormal IgA immune deposits accumulate in mesangium of kidney, inciting immune response causing inflammation.

145
Q

Pathophysiology of IgA nephropathy

A

IgA released in response to infection of mucosal lining, e.g. gastroenteritis or upper resp tract infection. IgG bind to them and the complex deposits in mesangium of kidney (Bowman’s capsule) activating alternative complement system. Inflammation of glomeruli occurs, causing blood to seep into urine.

If untreated leads to end stage renal failure

146
Q

Signs/symptoms of IgA nephropathy

A

Haematuria
Oedema/Hypertension
Pink, red, “coke” coloured urine

Sore throat suggest URTI as recent trigger
Loose stools or abdominal discomfort suggests gastroenteritis
(usually within 2 days)

147
Q

Investigations of IgA nephropathy

A

Urine Dipstick/urinalysis: Blood (if protein, less than 3.5g)
C3/C4 - C4 normal (normal pathway not activated), C3 may be low

Renal biopsy GOLD
- Immunofluorescence - IgA complex
- Light microscopy - Mesangial proliferation
- Electron microscopy - Immune complexes

148
Q

Management of IgA nephropathy

A

ACEi/ARB
Corticosteroids if proteinuria present after 3-6 months

149
Q

Main differential of IgA nephropathy

A

IgA vasculitis/ Henoch-Schonlein purpura
- Systemic and can be nephrotic too.
- Arthritis, skin lesions, Bloody stools, abdominal pain

150
Q

Define post strep glomerulonephritis

A

Delayed complication of pharyngitis (sore throat) or skin infections caused by beta haemolytic Strep Pyogenes. (1-2 weeks after) (NB: IgA nephropathy is 1-2 days!)

151
Q

Pathophysiology of post strep glomerulonephritis

A

Group A streptococci (Strep pyogenes) carry M protein virulence factor which allows them to evade host defence. IgM or IgG form immune complexes with antigen which deposit in glomerular basement membrane causing activation of complement and inflammation.

Type 3 hypersensitivity reaction.

152
Q

Signs/symptoms of post strep glomerulonephritis

A

Haematuria
Oliguria
Peripheral oedema

Signs of recent infection / Sore throat history!!

153
Q

Investigations in post strep glomerulonephritis

A

Throat/skin swab - recent step pyogenes
Anti streptolysin antibody

Renal biopsy GOLD
Immunofluorescence - IgG, IgM, C3 deposits “starry sky”
Light microscopy - Enlarged hypercellular glomeruli
E- Microscopy - Subepithelial deposits (humps)

154
Q

Management of post strep glomerulonephritis

A

Penicillin (underlying strep)
ACEi/ARB for HTN
Furosemide if oedema

155
Q

Define Goodpasture’s syndrome

A

Type 2 hypersensitivity reaction

AKA Anti-GBM (Glomerular Basement Membrane) disease.
Autoantibodies target type 4 collagen in glomerular and alveolar membrane causing both haematuria and haemoptysis (pulmonary haemorrhage)

156
Q

Risk factors of Goodpasture’s

A

HLA-DR15
Smoking (haemorrhage more likely)
Oxidative stress

157
Q

Signs/symptoms of Goodpasture’s

A

Lungs (present first)
- Cough, SOB, HAEMOPTYSIS

Kidneys
- Haematuria, proteinuria, oliguria, HTN (nephritic syndrome signs)

Systemic (lethargy, fever, weight loss etc) may also present

158
Q

Investigations in Goodpastures

A

Anti-GBM positive, p-ANCA positive
Urinalysis
Protein:creatinine ratio to calculate eGFR
Chest CT

159
Q

Management of Goodpastures

A

Corticosteroids
Plasmapharesis

Intubation/dialysis if damage reaches endstage

160
Q

Define SLE Nephropathy with antibodies and treatment

A

Lupus nephritis secondary to SLE.

  • Anti dsDNA, ANA
  • Hydroxychloroquine, Prednisolone and immunosuppressant (azathioprine)
161
Q

Refresher card: Define Nephrotic with its classical triad

A

Issue with filtration barrier due to damage to glomeruli. Pathology affecting podocytes in primary disease.
Triad is:
- Proteinuria (>3.5g in 24 hours)
- Hypoalbuminaemia (loss of albumin in urine)
- Peripheral oedema (loss of oncotic pressure)

162
Q

Main 5 features of Nephrotic syndrome

A

Proteinuria >3.5g
Hypoalbuminaemia
Hypercoagulability (loss of anti-thrombin III)
Hyperlipidaemia (causes frothy urine)
Susceptibility to infection (Loss of Ig in urine)

163
Q

Signs/symptoms of nephrotic syndrome

A

Proteinuria
Hypoalbuminaemia
Oedema
Frothy urine
Recurrent infection
Thromboembolic predisposition

164
Q

Define Minimal change disease, age of onset and what makes it unique

A

Most common Nephrotic.
Aetiology unknown but associated with Hodgkin’s Lymphoma, leukaemia and NSAID use.
Usually occurs before the age of 8.

Immunoglobulins ARENT excreted in urine (Only Nephrotic with this feature)

165
Q

Investigations in Minimal change disease

A

Kidney biopsy
Light microscopy - Normal
E- Microscopy - Podocyte effacement

Urinalysis has protein but no blood

166
Q

Management of minimal change disease

A

High dose prednisolone

167
Q

Define focal segmental glomerulosclerosis with causes

A

Focal - Only some glomeruli affected
Segmental - Only part of affected glomeruli affected
Sclerosis - Scarring

Can be idiopathic or secondary to
- HIV
- Heroin
- Lithium
- Lymphoma

168
Q

Investigations in Focal Segmental Glomerulosclerosis

A

Light microscopy - sclerosis/hyalinosis

169
Q

Management of FSG

A

Prednisolone + ACEi/ARB

170
Q

Define Membranous nephropathy

A

Anti-PLA2R antibodies cause disease of glomerular basement membrane. GBM damage causes it to form expansions - “spike and dome” appearance.

Mostly affects white male adults.

171
Q

Investigations of Membranous nephropathy

A

Anti-PLA2R antibodies
Light microscopy - GBM thickening
Electron microscopy - Subepithelial spike and dome pattern

172
Q

Treatement of membranous nephropathy

A

Prednisolone + ACEi/ARB

173
Q

What 2 diseases can be both nephritic and nephrotic

A

Diffuse proliferative glomerulonephritis
Membranoproliferative glomerulonephritis

174
Q

What can be seen on microscopy in a patient with Nephrotic syndrome caused by diabetes

A

Light - Mesangial expansion, GBM thickening, Kimmelstiel-Wilson nodules

Caused by non enzymatic glycation

175
Q

What hypersensitivity reactions are all the Nephritic syndromes?

A

All type 3 except Goodpastures

Goodpastures is type 2

176
Q

Define diffuse proliferative glomerulonephritis with main investigation

A

Proliferation affecting >50% of the glomeruli, SLE Nephritis is an example of this. Presents with signs of both nephritic and nephrotic

Renal biopsy GOLD - “Wire loop” appearance due to immune complexes creating an overall thickening

177
Q

Define Membranoproliferative glomerulonephritis with main investigations

A

Deposits in kidney mesangium cause thickening of it. (Membranous glomerulonephritis doesnt have mesangial thickening!!)

Renal biopsy shows “tram track” appearance

178
Q

LUTS Symptoms to know!

A

Storage (FUNI)
- Frequency
- Urgency
- Nocturia
- Incontinence

Voiding (SHID)
- poor Stream
- Hesitancy
- Incomplete emptying
- terminal Dribbling

179
Q

What muscle wraps around the bladder and controls urination?

A

The detrusor muscle

180
Q

What allows the bladder to stretch and grow as it fills?

A

Umbrella cells in the transitional epithelium lining

181
Q

Define Urge incontinence with cause

A

Overactive bladder causes sudden urge then involuntary urination due to involuntary, uninhibited detrusor contraction.

Usually due to UTI (infection may trigger detrusor muscle)

182
Q

Define stress incontinence with causes

A

Acute increase in abdominal pressure overwhelms sphincter muscles.

Caused by pregnancy and exertion (sneezing, coughing, laughing)

183
Q

Define overflow incontinence with causes

A

Bladder doesn’t empty properly so when it fills back up, it overflows and urine leaks through sphincters.

Usually due to nerve damage;
- Diabetes
- MS
- Syphilis
- Brain/spinal cord injury
Can be due to urinary flow blockage e.g. prostate hypertrophy

184
Q

Define outlet incompetence with causes

A

Urethral hypermobility or intrinsic sphincter damage/deficiency means body cant stop urine passage

185
Q

Give some causes of an inability to pass urine

A

Obstruction
- Stones
- BPH
- Flaccid paralysis
- Hypotonia of detrusor

186
Q

2 types of drug which cause AKI through reduced renal perfusion

A

NSAID
ACEi

187
Q

4 types of drug which cause intrarenal injury (acute tubular necrosis, interstitial nephritis)

A

Penacillamine
Penicillin
Rifampicin
Cephalosporins (Ceftriaxone)

188
Q

4 drugs that cause obstructive post renal pathology of the kidney

A

Sulfonamides (trimethoprim)
Methotrexate
Tricyclic antidepressants
Alcohol

189
Q

Morphology of chlamydia causing bacteria

A

Gram negative coccoids (No peptidoglycan in cell wall)

190
Q

What is the most common STI and what bacteria causes this?

A

Chlamydia

Chlamydia trachomatis

191
Q

Presentation of chlamydia

A

Women
- Abnormal discharge
- Dysuria
- Intermenstrual bleeding
- Pain during sex

Men
- Urethral discharge
- Dysuria
- Epididymo-orchitis
- Reactive arthritis

Can also have effects on bowels (change in habit, bleeding, discharge)

192
Q

Investigations of chlamydia

A

Swab (women) or MSU (men)
+ Nucleic Acid Amplification Test (NAAT) diagnostic

193
Q

Management of chlamydia

A

Doxycycline for 7 days.

CI in pregnancy, so give Azithromycin 1mg STAT and 500mg for 2 days after.

194
Q

Causative bacteria of gonorrhoea with its morphology

A

Neisseria gonorrhoea - gram negative diplococcus

195
Q

How does gonorrhoea present

A

Odourless green/yellow discharge
Dysuria
Pelvic pain (epdidymo-orchitis in men)

196
Q

Investigations in gonorrhoea

A

NAAT

197
Q

Management of gonorrhoea

A

IM ceftriaxone single dose

198
Q

What else can chlamydia and gonorrhoea cause

A
  • Conjunctivitis
  • Prostatitis
  • Chronic pelvic pain/ inflammation
  • Urethral strictures
  • Rectal infection

Gonorrhoea can cause disseminated gonococcal infection

199
Q

What bacteria causes syphilis

A

Treponema pallidum - gram negative

200
Q

Disease course of syphilis

A

Incubation period - 21 days

Primary - Painless ulcer at site of infection

Secondary - Systemic symptoms for 3-12 weeks
- condylomata lata (grey wart like lesions on genitals)
- Maculopapular rash on palms, soles, trunk
- Fever
- Alopecia

Latent - 2 years

Tertiary
- Granulomatous lesions
- Aortic aneurysms
- can cause brain symptoms

201
Q

Treatment of syphilis

A

Single IM dose of benzathine penicillin or doxycycline

202
Q

How else can syphilis be passed?

A

From mother to child!

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