Renal and GU conditions Flashcards

(53 cards)

1
Q

Causes of acute kidney injury

A

3 causes:

Pre-renal (most common) - reduced kidney perfusion
(Liver failure and heart failure)
Hypovolaemia
Sepsis
Dehydration
Heart failure
(tachycardic and hypotensive)

Renal - intrinsic disease of the kidney - PCT is the most commonly affected
ACUTE TUBULAR NECROSIS (most common intrinsic cause) - can occur from surgery e.g. CABG, nephrotoxic drug

Acute Glomerulonephritis - inflammation of glomerulus
Acute Interstitial nephritis - inflammation of nephrons (type 1 or 4 hypersensitivity) -
(Nephrotoxic drugs: aminoglycosides, amphotericin B, cisplatin, NSAIDS, diuretics) + contrast and radioactive dyes)
(Diffuse cortical nephrosis - both kidneys stop working)

Post-renal - mechanical obstruction of the urinary outflow tract (obstructive uropathy)
Kidney stones
Tumour
Benign prostatic hyperplasia
Strictures of ureters/urethra
Catheter
(Hydronephrosis)

(can be due to NSAIDS and gentamicin)

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2
Q

Acute kidney injury

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

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

COULD BE AN OLDER PATIENT that present with heart condition, undergoes surgery (CABG), then can’t pee and starts vomiting

RF - Older age (>65 years), sepsis, CKD, heart failure, diabetes, medications (NSAIDS, diuretics, ACE inhibitors)

Because of AKI, there is now an accumulation of substances (that are usually excreted.)
Potassium
Urea
Fluid
H+

Acute tubular necrosis (due to prolonged ischaemia or a toxic event) – MOST COMMON FORM OF AKI → Hypoxaemia results in cellular dysfunction and death. → has muddy brown casts on urinalysis

SYMPTOMS
Typically asymptomatic
Hypotension (reduced perfusion)
Palpable bladder or enlarged prostate (obstructive cause)
Kidney insults (sepsis or other acute illness, nephrotoxins (NSAID, gentamycin) - pre-renal
Oliguria - reduced urine output

INVESTIGATIONS
1st - Urinalysis
Establish cause via urea:creatinine ratio (pre-renal, renal, post-renal) + diagnose with KDIGO classification (stage 1,2,3):
Reduced urine output - <0.5ml/kg/hr for at least 6 consecutive hours)
Serum creatinine - an increase >26 micromol/L within 48 hours or an increase >1.5 times baseline in 7 days

Urea:creatinine
>100:1 - Pre-renal (due to increased absorption of BUN due to reduced perfusion)
40:1 Post renal
<40:1 - Intra renal

U and E → K+, H+, urea, creatinine
FBC and CRP - check for infection

Ultrasound - to assess for obstruction (post-renal cause)
Biopsy - to confirm intra-renal cause

TREATMENT
Treat complications and underlying cause.
COMPLICATIONS
Hyperkalemia - Calcium gluconate
Fluid overload - diuretics
Hypovolemic patients - IV fluids

UNDERLYING CAUSE
Stop nephrotoxic medication e.g. gentamicin, NSAIDS

Last resort: Renal replacement therapy (haemodialysis) (depending on haemodynamic stability, severity of electrolyte imbalance)

In post-renal AKI - relieve obstruction (catheter)

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3
Q

What are the compensatory mechanisms for pre renal causes of AKI

A
  • Due to reduced renal perfusion

Sympathetic stimulation (via baroreceptor reflex)
Vasoconstriction of efferent arteriole and vasodilation of afferent arteriole
Activation of RAAS
Hypothalamus stimulates ADH release

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4
Q

Nephrolithiasis
-Investigations

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

The presence of crystalline stones within the urinary system (kidneys and ureter)

RF - Dehydration, high salt intake, white ancestry, male sex

PATHOLOGY

Crystals form in the renal pelvis response to elevated levels of urinary solute e.g. calcium, uric acid. (Uric acid can cause gout) (Struvite stones - magnesium, phosphate and ammonia - coffin lid (post infection stones) and cystine stones exist - hexagonal)
(Most are calcium oxalate stones - envelope shaped) (followed by calcium phosphate - wedged shape prism)
These crystals can be passed out with urine or be retained in the kidney where they can grow and form stones

Renal colic - the pain caused by the body trying to pass out a kidney stone.
Causes obstruction and dilation proximal to the obstruction.

SYMPTOMS
Severe, acute flank pain (radiating to the ipsilateral groin) - loin to groin
COLICKY pain which means experiencing the pain in waves (and fluctuating in severity)
Patients may be restless due to pain
Costovertebral angle tenderness
(haematuria - red cast, dysuria)

INVESTIGATIONS
First line - Urinalysis - haematuria,
Urine dipstick
Ultrasound KUB (but this is GS for children and pregnant women)

GS
(Suspected kidney stones) → within 24 hours perform Non-contrast CT scan (KUB) of the kidney, ureters and bladder - NCCT KUB
CONTRAINDICATED in children and pregnant women

X-ray may show calcium based stones but does not show uric acid stones.

TREATMENT
For stones <5mm
1st line - Watch and wait as they may be passed spontaneously

Symptomatic
Hydrate + give nsaid (DICLOFENAC) IM

If UTI confirmed –> Antibiotics e.g. Gentamycin

For larger stones
Surgical intervention
Extracorporeal shock wave lithotripsy (ESWL) - where shock waves are directed at the stones to break them into smaller pieces
Percutaneous nephrolithotomy (PCNL) - keyhole removal of stones - through the patient’s back.
Ureteroscopy

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5
Q

Chronic kidney disease
-Most common cause

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Having a glomerular filtration rate <60ml/min/1.73m^2 for > 3 months. (or presence of markers of kidney damage for more than 3 months)

RF - DM, hypertension, >50 years

PATHOLOGY
Most common cause: DIABETES
Other causes:
Hypertension
Polycystic kidney disease
Obstructive uropathy
Glomerulonephritis

1) Due to the causes mentioned nephrons are damaged resulting in reduced GFR
2) RAAS tried to compensate and increase GFR but the increase in trans glomerular pressure leads to a loss of basement membrane selective permeability
3) Increased angiotensin 2 production causes an upregulation of transforming growth factor beta (TGF- beta)
4) An increase in glomerular permeability to macromolecules like TGF-beta can lead to mesangial fibrosis and scarring → reduced GFR

SYMPTOMS
FOPPA
Fatigue
Oedema
Proteinuria (haematuria)
Pruritus
Anorexia
(Trouble sleeping?)

INVESTIGATIONS
1st line
Urine dipstick - proteinuria

FBC - Anaemia of chronic disease
Ultrasound - bilateral renal atrophy

GS
eGFR - <60

And eGFR function staging (G score 1-5)
G1 >90
G2 60-89
G3 30-59
G4 15-29
G5 <15

Serum creatinine - elevated

Diagnosis made when eGFR is sustained <60 over 3 months

TREATMENT
First line - really managing the complications
eGFR stage 1-4 →Ace inhibitors - Ramipril, (Angiotensin 2 receptor 2 blocker - telmisartan) + statins (to protect patients from cardioascular complications)

eGFR stage 5 → Dialysis

If End stage renal failure → Renal transplant

(For managing complications:
Anaemia → iron and erythropoietin
Renal osteodystrophy → vitamin D
Oedema → diuretics
Cardiovascular → ace inhibitors and statins

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6
Q

Complications of CKD

A

Anaemia - Due to decreased EPO

Osteodystrophy - Due to decreased vitamin D activation

Neuropathy + Encephalopathy - Due to accumulation of uremic toxins

Cardiovascular disease

Oedema - hypoalbuminemia

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7
Q

Differences between AKI and CKD

A

Definition
AKI - Increased serum creatinine and decreased urine output
CKD - Decreased eGFR

Symptom onset
AKI - Shorter symptom onset
CKD - Symptoms for more than 3 months

Anaemia
AKI - No anaemia
CKD - Anaemia of chronic disease

Ultrasound findings
AKI - Normal
CKD - bilateral atrophied kidneys

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8
Q

Benign Prostatic Hyperplasia

Last resort treatment
Which part of the prostate does it occur

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Benign prostatic hyperplasia involving smooth muscle hyperplasia and prostatic enlargement. (and bladder dysfunction)

RF - >50 years, family history of BPH, smoking, african caribbean

PATHOLOGY
Hyperplasia of the (epithelial and stromal cells) in the transitional zone of the prostate → can lead to bladder outlet obstruction (via narrowing of urethra).
(BPH - transitional zone, malignancies -periphery)

5 alpha reductase synthesises dihydrotestosterone from testosterone → which causes prostate growth.

SYMPTOMS
LUTS (FUNI SHID)
Hesitancy
Weak, intermittent flow
Terminal dribbling
Incomplete emptying of the bladder
Straining
Urgency
Frequency
Nocturia

International prostate symptom score (IPSS) - used to assess severity of LUT

INVESTIGATIONS
1st and GS
Digital rectal examination (to assess size, shape and characteristics of the prostate - SMOOTH AND ENLARGED, soft) - hard, irregular and enlarged could be prostate cancer

Urine dipstick - to assess for infection (leukocytes and nitrites)

Prostate specific antigen (PSA) test for prostate cancer
(may ask them to do a bladder diary)

TREATMENT
Lifestyle - decreasing caffeine (may need catheter acutely)

1st line - Alpha blockers (tamsulosin) - reduce muscle tone in bladder neck (but is CI in patients with postural hypotension)

2nd line - 5 alpha reductase inhibitor (finasteride) - blocks the synthesis of dihydrotestosterone from testosterone - which usually can lead to prostate growth
Can lead to sexual dysfunction

Last resort - Surgery (TURP) - Transurethral resection of the prostate (complication - retrograde ejaculation

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9
Q

Name upper and lower UTIs

What are the main causative organisms?

RF of UTIs

A

Upper - Pyelonephritis

Lower (bladder onwards) - Cystitis, prostatitis, urethritis, epididymo orchitis

KEEPS - Klebsiella species, Enterobacter, E.coli, proteus mirabilis, S.saprophyticus
(Most common cause is E.COLI)

RF - Frequent sexual intercourse, catheter, diabetes

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10
Q

Are females or males more susceptible to UTIs?

A

Females as they have a short urethra –> shorter distance for bacteria to travel to the bladder

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11
Q

Pyelonephritis
-Symptoms
- Investigations

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Inflammation of the kidney resulting from bacterial infection. → affects the renal pelvis and parenchyma (UTI)

RF - Females, diabetes, catheter, stress incontinence, obstruction (renal stones)

PATHOLOGY
Most common cause → E.coli
Other causes: Klebsiella.pneumoniae, enterococcus, S.saprophyticus, P. aeruginosa

Most develop as a result of ascending UTI. (Pathogens first colonise the distal urethra and then ascend via the bladder and ureters to the kidney)

SYMPTOMS
Quad of :
Flank pain
Fever
Nausea+vomiting
Costovertebral angle tenderness

Systemic - hypertension, tachycardia
(Also pyuria but more investigation)

INVESTIGATIONS
First line - Urine dipstick (positive for leukocytes and nitrites) - pyuria

FBC - increased WBC
(There would also be gas in the renal parenchyma)

GS - Midstream urine culture and sensitivity test

TREATMENT
1st line - Empirical antibiotics
Ciprofloxacin/co-amoxiclav, CEFALEXIN if pregnant

For pain management - Paracetamol (Analgesia)

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12
Q

What can chronic pyelonephritis lead to?

A

Chronic pyelonephritis presents with recurrent episodes of infection in the kidneys. Recurrent infections lead to scarring of the renal parenchyma, leading to chronic kidney disease (CKD). It can progress to end-stage renal failure.

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13
Q

What is sepsis 6?

A

3 tests and 3 treatments

Tests (out)
- Lactate measurements (blood)
- Blood cultures
- Urine output

Treatments (in)
- Oxygen (to maintain oxygen saturation)
- Empirical broad spectrum IV antibiotics
- IV fluids

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14
Q

Cystitis
-Treatment

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

A lower UTI affecting the bladder.

RF - Frequent sexual intercourse, history of UTI (diabetes), urine stasis, catheter

PATHOLOGY
Most common in young, sexually active women.

Usually due to E.coli being introduced into the urethra during sexual intercourse
(Can either be complicated or uncomplicated based on the presence/absence anatomical/functional abnormalities within the urinary tract.

SYMPTOMS
Suprapubic tenderness (pain)
Urgency
Frequency
Dysuria
(Visible haematuria)

INVESTIGATIONS
First line - midstream urine dipstick

FBC - mostly normal WBC (only increased if WBC spread to upper urinary tract)

GS - Midstream urine culture and sensitivity test

TREATMENT
Antibiotics –> Trimethoprim or nitrofurantoin
(Amoxicillin if pregnant)

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15
Q

Urethritis

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Urethral inflammation - usually a SEXUALLY acquired condition

RF - Age 15-24, females, new/multiple sex partners, male-male sex, unprotected sex

PATHOLOGY
Usually a sexually acquired condition

Infective cause is either gonococcal or non gonococcal

Gonococcal → Neisseria gonorrhoeae
Gram negative diplococcus

Non gonococcal → Chlamydia trachomatis (more common) - obligate gram negative aerobe bacillus

Spread by:
Unprotected sex
Can be transmitted to neonates by infectious exudates in the birth canal

SYMPTOMS
Dysuria
Urethral discharge (blood/pus)
Urethral itching/irritation

INVESTIGATIONS

1st -
Nucleic acid amplification test (NAAT) → may detect N.gonorrhoeae or C.trachomatis

Urine dipstick + Urine culture and sensitivity test - to identify the pathogen in the case of a UTI

TREATMENT
Neisseria gonorrhoea - IM Ceftriaxone

Chlamydia trachomatis - Doxycycline (Azithromycin - for pregnant women)

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16
Q

Epididymo orchitis
-Symptoms

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Inflammation of the epididymis extending to the testes (on one side)

RF - Unprotected sex, bladder outflow obstruction, catheter

PATHOLOGY
Caused by:
In men <35
Chlamydia trachomatis
Neisseria gonorrhoea

In men >35, infection may be non STI, due to uropathogens like : E.coli and proteus

SYMPTOMS
- Gradual onset of unilateral scrotal pain and swelling
- Pain is relieved with elevating testis (Positive prehn’s sign)
- Tenderness on palpation
- Possible urethral discharge (in the case of chlamydia or gonorrhoea)

  • May check the cremasteric reflex is intact to rule out testicular torsion which is a urological emergency.

INVESTIGATIONS
First line - Urine dipstick

GS - Urine Culture, microscopy and sensitivity test

Nucleic acid amplification test (NAAT) - for C.trachomatis and N.gonorrhoeae.

Treatment
Neisseria gonorrhoea - IM Ceftriaxone (if chlamydia not ruled out)

Chlamydia trachomatis - Doxycycline (azithromycin if pregnant)

If its a UTI cause
Ciprofloxacin (wide spec)

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17
Q

Nephrotic syndrome
Causes?

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

A syndrome defined as the presence of PROTEINURIA, HYPOALBUMINEMIA, and PERIPHERAL OEDEMA.

PATHOLOGY - overall, basement membrane becomes highly permeable to protein

(Primary)
Minimal change disease –> Most common cause in young children
- It results in podocyte effacement –> thus increasing permeability of membrane and proteinuria
Can occur secondary to: NSAID use and hodgkin lymphoma.

Focal segmental glomerulosclerosis –> Most common cause in adults
- Also results in podocyte effacement

Membranous nephropathy (seen mainly in adults) - due to infection (Hep B), malignancy, drugs
- Leads to thickening of glomerular BM due to immune complex deposition (no haematuria, more proteinuria) - differentiating from nephritic syndrome.

(Secondary) - Diabetic nephropathy secondary to long standing diabetes

SYMPTOMS
- Frothy urine - due to protein and lipid loss
- Generalised oedema e.g. puffy face
- Hyperlipidemia and weight gain - liver increases production of lipoproteins to compensate for loss of albumin
- Pallor

INVESTIGATIONS
First line - urinalysis → proteinuria
For young patients (minimal change disease)
Biopsy + electron microscopy → podocyte effacement (and fusion)
No changes on light microscopy

In adults (focal segmental glomerulosclerosis)
Biopsy + light microscopy → Segmented sclerosis in <50% of the glomeruli (scarring of glomeruli - resulting in proteinuria)

In adults (membranous nephropathy)
Biopsy + light microscopy - thickened glomerular basement membrane
Biopsy + electron microscopy - Spike + dome appearance and subepithelial immune complex deposition (on thickened basement membrane)

TREATMENT
Steroids - Prednisolone

Minimal change - responds well
FSG and MN - responds less well

(Diuretics for oedema)
(Albumin infusion for severe hypoalbuminemia)

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18
Q

Nephritic syndrome

What conditions does it encompass and what are the typical presentations.

A

A clinical syndrome that presents with haematuria, hypertension, decreased urine output and oedema. (inflammation within the nephrons of the kidney)

PATHOLOGY
Encompasses 4 main conditions
1) IgA nephropathy (Berger’s disease)
2) Post strep glomerulonephritis
3) SLE nephropathy
4) Goodpasture’s syndrome
Goodpastures - Type 2 hypersensitivity the rest is type 3.

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19
Q

IgA nephropathy (Berger’s disease)- treatment

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

MOST COMMON form of glomeruloNEPHRITIS defined by the presence of mesangial IgA deposits in the mesangium of the GBM. (under nephritic syndrome)

RF - Family history, asian/whites, 20-30 males, HIV

PATHOLOGY
Type 3 sensitivity

Occurs due to mesangial IgA immune deposits. (IgA immune complexes deposit at mesangium of glomerular BM)

Closely related to Henoch schonlein purpura - IgA vasculitis

SYMPTOMS
- Haematuria (cola coloured)
- Hypertension
- Oedema
- Usually preceded by a viral infection (URTI/gastrointestinal) within a few days

INVESTIGATIONS
First line - Urine dipstick and urinalysis - haematuria and possible albuminemia

GS - Kidney biopsy with immunofluorescence microscopy - shows mesangial IgA deposition

TREATMENT
Non curative (30% progress to ESRF)
But supportive treatment for hypertension with ACE-I –> RAMIPRIL

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20
Q

Post strep glomerulonephritis
- treatment
RF

Pathophysiology
Symptoms
Investigations
Treatment

A

Glomerulonephritis that occurs 2-4 weeks after beta haemolytic streptococcus infection (s.pyogenes) e.g. recent presentation of tonsilitis/pharyngitis

PATHOLOGY
S pyogenes - has M protein virulence factor (molecular mimicry)

Immune complexes get stuck in the glomerular basement membrane, causing inflammation. (IgG, IgM and complement proteins)

SYMPTOMS
Cola/tea coloured urine (haematuria), oedema (swelling hands and feet) and hypertension

INVESTIGATIONS
1st - urinalysis - haematuria, proteinuria

GS -
Kidney biopsy + light microscope (hypercellular glomeruli)
+ electron microscope+ immunofluorescence (hump shaped subepithelial immune complex deposits) –> shows starry sky appearance

Serology for S pyogenes (as self limiting)

TREATMENT
Usually self limiting
Supportive treatment for hypertension with Ace-inhibitor (ramipril)

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21
Q

Goodpasture’s syndrome
-Investigations

RF

Pathophysiology
Symptoms
Investigations
Treatment

A

A type 2 hypersensitivity reaction affecting type 4 collagen.

RF - 20-30/60-70 male, HLA DR15

PATHOLOGY
Causes pulmonary-renal syndrome (consisting of glomerulonephritis and pulmonary haemorrhage)

Associated with Anti glomerular basement membrane antibodies - Anti GBM

SYMPTOMS
- Reduced urine output
- Haemoptysis
- Oedema
(Other non specific symptoms –> cough, fever, nausea, dyspnoea)

INVESTIGATIONS
First line - Anti GBM antibodies
GS - Renal biopsy which shows damage and immunoglobulin deposition. (Necrosis with epithelial cell crescents)

Treatment
Prednisolone + plasma exchange (to remove pathogenic antibody)

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22
Q

Lupus nephritis

A

Glomerulonephritis occurring secondary to SLE.

Antinuclear antibody deposits in the subepithelium of GBM

Symptoms (usual few) - Oliguria, haematuria, hypertension, oedema

INVESTIGATIONS
Serology for ANA and anti double stranded DNA antibodies

Presents with WIRE LOOP glomerulonephritis - on biopsy

TREATMENT
Prednisolone, hydroxychloroquine

Methotrexate (immunosuppressant)

23
Q

What is rapidly progressing glomerulonephritis?

What are its causes?

How would you diagnose it?

A

A subtype of glomerulonephritis that progresses to End Stage Renal Failure very fast

Caused by: Wegener’s granulomatosis (C-ANCA positive), Microscopic polyangitis (P-ANCA positive + autoantibodies against myeloperoxidase90), Good pastures (Anti GBM antibodise)

INVESTIGATION
Biopsy would show inflammatory crescents in Bowman’s space.

24
Q

Comparison in the characteristics of nephrotic and nephritic syndrome

A

Nephrotic
(Increased permeability to protein e.g. albumin)
Occurs when glomeruli do not properly filter the protein albumin –> prOteinuria
hypOalbuminaemia
Oedema

Nephritic
(Inflammation and damage to the glomeruli, increasing its permeability)
Occurs when inflamed glomeruli do not properly filter red blood cells –> Haematuria
Reduced urine output
Oedema (due to fluid overload)
Hypertension

25
Renal cell carcinoma -What staging do you use? - What syndrome is associated? RF Pathophysiology Symptoms Investigations Treatment
A renal adenocarcinoma arising from the renal cortex (or tubules). RF - Smoking, males, >55 years PATHOLOGY Accounts for 80-90% of renal cancers 3 most common types: Clear cell carcinoma (80% of RCC) Papillary Chromophobe Associated with Von-hippel lindau syndrome — Caused by autosomal dominant mutation in the VHL gene, a tumour suppressor gene- increasing risk of renal and pancreas cysts SYMPTOMS Triad of: haematuria, flank pain and palpable mass + weight loss (possible anaemia due to reduced production of EPO - or can even lead to polycythaemia, depends on tumour's features) (Causes left sided varicocele in men- varicose veins in spermatic cord) INVESTIGATIONS 1st line - Ultrasound (abnormal renal mass/cyst) GS - Contrast CT scan of chest/abdomen/pelvis (Use robson staging or TNM staging) TREATMENT 1st line - surgery --> Nephrectomy
26
What is Wilm's tumour?
Most common paediatric renal cancer - Tumour of renal tubules and mesenchymal cells - Also called nephroblastoma - Seen in children under 5
27
Complications of RCC and paraneoplastic syndromes caused by it
Complication RCC can lead to a cannonball metastases in the lungs (by spreading to the renal vein --> IVC --> and lungs Paraneoplastic syndromes for renal cell carcinoma: When a tumour secretes things that cause syndromes Renal cell carcinoma releases: EPO - polycythaemia Renin - hypertension PTH like protein - hypercalcemia ACTH - Cushing's
28
Bladder cancer RF Pathophysiology Symptoms Investigations Treatment
Urothelial carcinoma of the urinary bladder (transitional cell carcinoma)- accounts for >90% of bladder cancers. RF- Smoking, occupational exposure to dues/paints/rubber - painter, hairdresser, mechanic working with tyres, >65 year old man (Aromatic amines - e.g. naphthylamine) PATHOLOGY SMOKING is the biggest risk factor for bladder cancer Although most bladder cancers are transitional cell carcinomas, But if a patient has schistosomiasis (parasitic disease), they are more likely to have squamous cell carcinoma (10%) Caused by chronic irritation of the bladder (cuboidal and columnar epithelium changes to squamous (metaplasia) → dysplasia and cancer) SYMPTOMS Painless haematuria Exposure to Aromatic amines - 2-naphtylamine retired dye factory worker/painter/hairdresser presenting with painless haematuria INVESTIGATIONS (urinalysis to confirm for presence of haematuria) GS - Flexible Cystoscopy - visualises bladder tumours (with possible biopsy) TREATMENT 1st line - Transurethral resection of bladder tumour with [possible] intravesical chemotherapy (gemcitabine) - to reduce risk of recurrence Medical - chemotherapy/radiotherapy
29
Prostate cancer - Investigations+ scoring system RF Pathophysiology Symptoms Investigations Treatment
Adenocarcinoma (malignant tumour) situated in the peripheral zone of the prostate RF - >50 years, BRCA2, HOXBI3, black ethnicity, family history PATHOLOGY Most common cancer in males It relies on androgen hormones to grow (e.g. testosterone) Most commonly spreads to lymph nodes and bones (lumbar back pain) - haematogenous (can spread to liver, lung and brain also) SYMPTOMS LUTS Nocturia, urinary frequency, hesitancy, dysuria, haematuria + Systemic cancer symptoms - weight loss, fatigue, night pain + Bone pain (lumbar back pain) INVESTIGATIONS First line - Digital rectal examination Serum PSA levels (elevated) (Cancerous tumour feels hard, irregular, asymmetrical) GS - GS - transrectal ultrasound + biopsy Also grade tumour based on gleason score TREATMENT First line - Radical prostatectomy (for local cancer) For metastatic cancer --> 1) Hormone therapy (to deprive androgens) with either - Bilateral orchidectomy (Surgical removal of testes) - Goserelin (GnRH agonist) - it desensitises GnRH receptors eventually so they produce less LH and FSH 2) Radiotherapy (External beam radiotherapy)
30
How reliable is PSA testing?
PSA testing is unreliable with 75% false positives and 15% false negatives
31
Testicular cancer -Painful or painless? RF Pathophysiology Symptoms Investigations Treatment
RF - Cryptorchidism (undescended testis), family history, infertility, 20-34 years PATHOLOGY 95% arise from germ cells 5% is non germ cell tumour: Germ cell tumours: (cells producing gametes) Seminoma - (most common) or non seminoma (teratoma, yolk sac tumour - common in children under 3) Non germ cell tumours: leydig and sertoli cell tumours Common places for testicular cancer to metastasise to are: lymphatics, lungs, liver and the brain. (hematogenously) SYMPTOMS Painless lump in testicles, which does NOT transilluminate (patient may also have hydrocele?) INVESTIGATIONS First line - Doppler ultrasound test → testicular mass (90% diagnostic) Blood tests Serum alpha feto-protein - elevated in teratoma, yolk sac tumour Beta hcg - elevated in both seminoma an non seminoma (Lactate dehydrogenase) GS - biopsy and microscopy Seminoma- fried egg (large central nuclei surrounded by clear cytoplasm) (Staging CT scan to look for areas of spread and to stage the cancer) TREATMENT 1st line Radical (inguinal) orchidectomy (surgery to remove the affected testicle) (offer sperm storage) Adjuvant therapy (post surgery) Chemotherapy Radiation therapy
32
Common places for testicular cancer to metastasise to
lymphatics, lungs, liver and the brain. (hematogenously)
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Common places for prostate cancer to metastasise to
Most commonly spreads to lymph nodes and bones (lumbar back pain) - haematogenous (can spread to liver, lung and brain also)
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Obstructive uropathy - Investigation RF Pathophysiology Symptoms Investigations Treatment
Blockage of urinary flow RF - BPH, urolithiasis (renal stones), medications e.g. alpha receptor agonists PATHOLOGY Obstructive uropathy can cause: 1) Urinary retention 2) Increased kidney, ureter and bladder pressure 3) Hydronephrosis - can lead to renal tubular atrophy, a dilated renal pelvis and also increases risk of infection --> ADDITIONALLY reduced renal function can lead to hyperkalemia which leads to arrhythmias and possible death. SYMPTOMS - LUTS - Distended bladder - Inability to urinate - Costovertebral angle tenderness (kidney stones/obstruction) - Haematuria INVESTIGATIONS First line - Renal ultrasound GS maybe Magnetic Resonance Urography? - shows obstruction and anatomical abnormalities e.g. stones/tumours TREATMENT First line - Relieve kidney pressure --> Insert catheter, insert ureteral stent Then treat underlying cause e.g. BPH, stones, infection
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Polycystic kidney disease -Which chromosome affected? RF Pathophysiology Symptoms Investigations Treatment
A genetic condition characterised by development of multiple cysts within the renal tubules. (leads to bilateral enlargement and damage) RF- Family history of ADPKD, family history of cerebrovascular event PATHOLOGY There are 2 types: Autosomal dominant (more common) and autosomal recessive ADPKD Most commonly affected genes: PKD1 on CHROMOSOME 16 (more common-85%), PKD2 on chromosome 4. PKD1 and 2 code for polycystin, a protein found in the cilia of renal epithelial cells involved in cellular interaction and coding for voltage gated calcium channels, Mutation would result in abnormal signalling and formation of fluid filled cysts. SYMPTOMS Bilateral flank/back/abdominal pain Hypertension Haematuria Abnormal polycystine Can lead to extra renal manifestations: Circle of willis - Berry aneurysm (which can rupture → subarachnoid haemorrhage) Hepatomegaly - liver cysts INVESTIGATIONS 1st line - Renal ultrasound (enlarged kidneys with cysts) Genetic testing - PKD1/2 mutation TREATMENT No curative treatment 1st - Lifestyle modification - smoking cessation, regular exercise 1st line drug treatment --> Tolvaptan for slowing down development of cysts and progression of renal failure If patient is hypertensive - Ace inhibitors If patient reaches end stage renal disease → Renal transplant first. (If cannot, dialysis)
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What are the extra renal manifestations of abnormal polycystin protein
Abnormal polycystin Can lead to extra renal manifestations: Circle of willis - Berry aneurysm (which can rupture → subarachnoid haemorrhage) Hepatomegaly - liver cysts Pancreatic cysts
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Varicocele RF Pathophysiology Symptoms Investigations Treatment
Abnormal dilation of the internal testicular veins and pampiniform plexus (that drains blood from the testis) PATHOLOGY Pampiniform plexus drains into the testicular vein. It plays a role in regulating the temperature of blood entering the testes by absorbing heat and cooling blood in the testicular artery. Main causes: Which results in blood flowing back from the testicular vein into the pampiniform plexus. - Increased hydrostatic pressure in the left renal vein - as left pampiniform plexus inserts into the left renal vein at a right angle (rather right pampiniform plexus which joins the IVC) - Incompetent/congenitally absent valves (incompetent valves within the left testicular vein) SYMPTOMS Painless scrotal mass described like a bag of worms (More prominent on standing) INVESTIGATIONS Clinical diagnosis In patients with a small scrotum/obese patients --> Doppler ultrasound can be used TREATMENT No treatment--> reassure patient Surgery only required if varicocele is severe
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Epididymal cysts RF Pathophysiology Symptoms Investigations Treatment
Cysts that occur at the head of the epididymis (Extratesticular cyst - above and behind testis) Cyst - Abnormal sacs of fluid SYMPTOMS Scrotal mass is not transilluminated (because of fluid) - but the CYST itself is transuilluminated (Soft round lump, typically at the top of the testicle) INVESTIGATION 1st line + GS - Scrotal ultrasound TREATMENT Conservative treatment - no treatment needed, reassurance If they cause pain, discomfort or infertility then consider surgical removal
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What is the "get above the lump" test?
It helps to differentiate between a hernial swelling and a true scrotal swelling. If you can get above the lump/swelling on squeezing --> true scrotal swelling If unable to get above --> hernia
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Hydrocele RF Pathophysiology Symptoms Investigations Treatment
A collection of fluid within the tunica vaginalis RF - Infants <6 months, infants whose testes descend late PATHOLOGY The tunica vaginalis is a sealed pouch of membrane surrounding the testes (and is part of the peritoneal membrane → during development of the fetus, it is separated from the peritoneal membrane and remains in the scrotum partially covering each testicle) Can be idiopathic or can be secondary to: Testicular torsion Trauma Epididymo Orchitis SYMPTOMS Scrotal mass that may enlarge with activity due to increased abdominal pressure --> fluid flows into scrotal sac TRANSILLUMINATION (because of fluid) INVESTIGATIONS GS - Scrotal ultrasound Serum HCG to exclude testicular cancer TREATMENT Mostly observation, only if hydrocele gets large and uncomfortable then surgical repair is definitive treatment
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Testicular torsion RF Pathophysiology Symptoms Investigations Treatment
A urological emergency caused by the twisting of the testicle on the spermatic cord leading to constriction of the vascular supply, time sensitive ischaemia, and necrosis of testicular tissue. RF - <25 years, neonate, trauma, bell clapper deformity PATHOLOGY Causes: -- Bell clapper deformity - most common anatomical defect (testicle is freely mobile within the tunica vaginalis) - testes are lying horizontally instead of vertically -- Can be triggered by activity e.g. sport, trauma SYMPTOMS Rapid onset unilateral testicular pain Abdominal pain Nausea and vomiting NO PAIN RELIEF WITH ELEVATING TESTES Loss of cremasteric reflex INVESTIGATIONS 1st Ultrasound to check testicular blood flow (if there is increased risk - do a surgical exploration rather than ultrasound) TREATMENT (Surgical exploration) then Urgent surgery (within 6 hours) - Testicular detorsion
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Urinary incontinence RF Pathophysiology Symptoms Investigations Treatment
The involuntary loss of urine RF - Obesity, increasing age, pregnancy (mostly females) PATHOLOGY and SYMPTOMS 2 types 1) Stress incontinence - Due to weakness of the pelvic floor and sphincter muscles. Therefore urine leaks at times of increased intra abdominal/bladder pressure. Caused by: sneezing, laughing, coughing (increases abdominal pressure), pregnancy and obesity, 2) Urgency incontinence - Due to overactivity of the detrusor muscle of the bladder - urgency to pass urine and have to rush to the bathroom, sometimes not arriving before urination occurs. INVESTIGATIONS Cough stress test? To see if it is stress incontinence TREATMENT Stress incontinence 1st line - Lifestyle modifications --> Avoid caffeine, supervised PELVIC FLOOR EXERCISES Last resort - Surgery Urgency incontinence 1st line- Lifestyle modifications- Limit caffeine and alcohol 1st line drug treatment - Anticholinergic medication - oxybutynin (blocks muscarinic receptors on the detrusor muscle)
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Urinary retention --> leading to overflow incontinence (treatment?) RF Pathophysiology Symptoms Investigations Treatment
Chronic urinary retention due to obstruction to the outflow of urine RF- MEN PATHOLOGY Loss of ability to pass urine even when bladder is full (500ml). --> Result in an overflow of urine. Can be due to: - Benign prostatic hyperplasia - Renal stones - Neurological conditions - multiple sclerosis, diabetic neuropathy - Pelvic tumours (Anti cholinergic medication) TREATMENT - Catheterisation
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Acute prostatitis RF Pathophysiology Symptoms Investigations Treatment
Painful inflammation within the prostate (Chronic is symptoms lasting more than 3 months) RF - UTI, BPH PATHOLOGY Commonly caused by organisms entering the prostate from urinary tract infections. Especially E.coli SYMPTOMS Chronic prostatitis - presents with at least 3 months of Pelvic pain - which can affect the perineum, testicles and scrotum LUTS - FUNI SHID Sexual dysfunction Acute is above + Fever Chills Myalgia Malaise Warm, soft boggy prostate gland INVESTIGATIONS 1st - Urinalysis/urine dipstick - leukocytes Urine microscopy, culture and sensitivity - for bacteria (mostly E.coli) Digital rectal examination - Prostate is warm, boggy (wet and mushy to the touch) TREATMENTS Acute Without sepsis Oral antibiotics - Ciprofloxacin Consider: NSAIDS - Ibuprofen for pain relief Chronic prostatitis - Alpha blockers (tamsulosin)
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What are the LUTS symptoms? Separate into voiding and storage symptoms
FUNI SHID Storage (FUNI) - Frequency - Urgency - Nocturia - Incontinence Voiding (SHID) - Weak, intermittent stream - Hesitancy - Incomplete emptying of bladder - Terminal dribbling
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Which antibiotic is used for UTI in pregnant women?
Cefalexcin
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Common places of kidney stones
Ureteropelvic junction Ureterovesical junction Pelvic brim (when ureter crosses over iliac vessels)
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When is NCCT or Contrast CT scan used?
NCCT - Kidney stones, trauma, strokes Contrast CT - blood vessels, organs or tissues with increased vascularity/perfusion.
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Most common form of glomerulonephritis
IgA nephropathy
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Alport syndrome
Genetic defect in type 4 collagen (X-linked most common) Triad of Hereditary nephritis, sensorineural deafness, ocular abnormalities (cataracts, etc)
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How would you test for a recent streptococcus infection?
Antistreptolysin O Titre and low C3
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Human papillomavirus that most commonly cause cervical cancer
HPV 16 and 18
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What drugs should be withheld in AKI?
Stop the DAMN drugs - Diuretics (and digoxin) - Ace inhibitor/ARB - Metformin and methotrexate - NSAIDs