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CP1 > Renal medicine & urology > Flashcards

Renal medicine & urology Flashcards

1
Q

What is the function of the kidneys?

A
  • To regulate plasma concentrations, specifically decrease plasma creatinine, urea K+ and H+ concentration, thus kidney disease leads to an increase in these. Produces urine

Secondary functions:

  • Secretion of EPO (to stimulate erythropoiesis in the bone marrow)
  • Secretion of renin (to increase blood pressure)
  • 1-alpha-hydroxylation of calcidiol to form calcitriol (vitamin D)
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2
Q

Where are the kidney anatomically?

What are the structures which produce the urine in the kidney? - how?

A

Kidney sits at L1-3

  • Millions of nephrons in each kidney produces the urine:
    • Renal corpuscle: produces the glomerular filtrate
    • Proximal convoluted tubule (PCT): reabsorps water, ions and organic nutrients
    • Loop of henle: further reabsorption of water (descending limb), reabsorption of Na+/Cl- ions (ascending limb)
    • Distal convoluted tubule (DCT): secretion of ions, acids, drugs and toxins, variable reabsorption of water/sodium under the control of aldosterone
    • Collecting duct: variable reabsorption of water under control of ADH, variable solute reabsorption
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3
Q

How is renal failure causes classified?

A

Pre-renal

Renal

Post-renal

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4
Q

What is the pathology for pre-renal causes of renal failure?

What common diseases cause it?

A

Pre-renal (most common 75%)

  • Occurs when blood supply to kidney is interupted
  • The two main causes:
    • Shock:
      • Hypovolemic
      • Cardiogenic
      • Distributive
    • Renovascular obstruction:
      • embolus
      • aortic dissection
      • renal artery stenosis
      • thrombosis
      • ACEIs given in bilateral renal artery stenosis
  • Is the interuption in blood supply is prolonged, there will be acute tubular necrosis, where ischaemia leads to necrosis of the cells that line the renal tubules
  • This leads to porous tubular membranes (leading to loss of concentrating power) and also blockage of the tubules by necrosed cells
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5
Q

What is the pathology for renal causes of post-renal failure?

What common diseases cause it?

A
  • Occurs when there is obstruction to the outflow of the urinary tract
  • This leads to backflow of urine, damage to the kidney architecture and resultant organ failure
  • The blockage is often in the ureters:
    • stones
    • strictures
    • clots
    • external/internal malignancy
  • Bladder outlet obstruction can also cause post-renal failure e.g.:
    • prostatic enlargement
    • urethral strictures
    • Phimosis/paraphimosis (tight foreskin)
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6
Q

What is the pathology for renal causes of renal failure?

What common diseases cause it?

A
  • Can occur by 3 separate mechanisms/pathologies - acute tubular necrosis (85%), interstitial nephritis (10%), glomerular disease (5%)

Acute tubular necrosis (ATN)

  • Due to drugs or toxins damaging the tubular cells rather than ischaemia
  • Drugs: aminoglycosides, cephalosporins, radiological contrast mediums, NSAIDs
  • Toxins: heavy metal poisoning, myoglobinuria or haemolytic uraemic syndrome (HUS)
  • Myoglobinuria
    • Follows an episode of rhabdomyolysis (muscle breakdown from trauma, stenuous exerise or medications), releasing myoglobin, which is readily filtered by the glomerulus
  • Haemolytic uraemic syndrome (HUS)
    • Occurs in children following a diarrhoeal illness caused by verotoxin-producing E.coli O157, or following an URTI in adults
    • It leads to thrombocytopenia (can cause purpura), haemolysis and acute tubular necrosis

Interstitial nephritis:

  • Most commonly caused by drigs, however the damage is not limited to tubular cells (such as in ATN), and bypasses the basement membrane to cause damage to the interstitium
  • Antibiotic most common cause, other agents include diuretics, allopurinol and PPIs

Glomerular disease

  • Glomerulonephritis
    • damage to the tiny filters inside your kidneys (the glomeruli)
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7
Q

Describe the clinical & biochemical features of acute renal failure/injury

A

AKI = AKF

  • NICE specify that an AKI is present if either:
    • Urine output <0.5ml/kg/hr for 6 hours
    • >50% rise in creatinine over 7 days
    • >26 micromol rise in creatinine over 48 hours
  • The AKIN criteria can also be used to classify AKI in terms of serum creatinine and urine output

In severe AKI ther may be symptoms secondary to complications:

  • Uraemia (vomiting, pruritis, pericarditis, encephalitis)
  • Hyperkalaemia (Tall, peaked T waves on ECG, widened QRS complex, flattened P waves)
    • If left untreated, ventricular fibrilation/tachycardicia can develop
  • Hypernatremia
  • Metabolic acidosis
  • Pulmonary oedema due to fluid overload
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8
Q

List the common causes of AKI

A
  • Renal artery thrombosis
  • massive hypotension/haemorrhage
  • burns
  • D+V
  • pancreatitis
  • diuretics
  • MI
  • CCF
  • endotoxic shock
  • snake bite
  • globinaemias
  • liver failure
  • radiological contrasts
  • drugs
  • pregnancy (pre-eclampsia, eclampsia, abruption placentae
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9
Q

List the life threatening aspects of ARF

A
  • Prognosis is worst when AKI complicates non-renal organ failure, and sepsis related AKI
  • Uraemia will eventually cause fitting and coma.
  • Pulmonary oedema may be a feature of AKI
  • Hyperkalaemia is associated with cardiac arrhythmias
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10
Q

In AKF what abnormalities of serum urea and electrolyte results would you find?

A

hyperkalaemia and hyponatraemia, alongside raised creatinine and urea

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11
Q

Describe the clinical features (signs and symptoms) assoiciated with chronic renal failure

A

Symptoms:

  • Often asymptomatic until very advanced (vague fatigue and anorexia)
  • Polyuria/nocturia
  • Restless legs syndrome
  • Sexual dysfunction
  • Nausea & pruritis (early uraemia)
  • Yellow pigmentation, encephalopathy and pericarditis (severe uraemia)
  • Pedal oedema & pulmonary oedema (due to hypertension)

Signs:

  • Pallor due to anaemia
  • Excoriations due to pruritis (skin is scraped or abraded due to itching)
  • Hypertension/fluid overload signs
  • Pericardial rub (rare)
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12
Q

What systemic complications may develop in a patient with longstanding CKD?

A

Renal anaemia:

  • Kidney secretes EPO
  • Lose of EPO secretion in CKD leading to anaemia

Renal bone disease:

  • Kidneys produce 1-alpha-hydroxylase, which enables conversion of calcidol from the liver to calcitriol (activated vitamin D)
  • Low Vit D leads to hypocalcaemia and hyperphosphataemia and osteomalacia

Secondary hypertension:

  • Over activation of RAAS leading to hypertension
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13
Q

Describe the assessment of CKD

A

Is done using the eGFR and the 5 stages of CKD

  • CKD is diagnosed when any two tests three months apart show reduced eGFR, and can be staged 1-5 depending on the level of reduction
  • eGFR is just an estimate of GFR based on a plasma level creatinine
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14
Q

What are the common causes of chronic kidney disease?

A
  • Diabetes mellitus (20-40%)
  • Hypertension
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • Obstructive uropathy
  • Renovascular disease
  • Drugs (long term NSAIDs)
  • Polycystic kidney disease
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15
Q

What investigations would you do for a patient with chronic kidney failure?

A
  • Bloods:
    • FBC, U&Es, LFTs, calcium, phosphate, PTH levels, glucose
  • Urinalysis & MCS:
    • To quantify proteinuria, exclude infection and look for casts
  • 24 hour urinary protein/creatinine clearance
    • To assess severity/ for nephrotic syndrome
  • CXR:
    • If suspecting pulmonary oedema
  • Renal USS:
    • If suspecting obstructive causes
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16
Q

Define nephrotic syndrome

A
  • Triad of:
    • Proteinuria (at least 3.5g/day)
    • Hypoalbuminaemia (<30g/l)
    • Oedema (due to decreased oncotic pressure and water retention)

Nephrotic syndrome is due to an increase in permeability (loss of selective permeability) of glomeruli to plasma proteins (itself due to thickening), causing massive proteinuria.

It is non-proliferative

Renal loss of thromboregulatory proteins or liporegulatory proteins may lead to hyperlipidaemia or venous thrombosis

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17
Q

List important primary and secondary causes of persistent proteinuria and the nephrotic syndrome

A

Primary causes:

  • Minimal change nephropathy
  • Membranous glomerulonephritis
  • Proliferative gloerulonephritis
  • Focal segmental glomerulosclerosis

Secondary causes:

  • Bacterial/viral infection
  • Drugs
  • Neoplasm
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18
Q

What is nephritic syndrome?

(not an objective)

A
  • Tetrad of:
    • Haematuria plus red cell casts
    • Oliguria
    • Proteinuria (can be less than 3.5g)
    • Hypertension

It is proliferative, with increased cell numbers as well as damage to the basement membrane

Common causes: IgA nephropathy & goodpasture’s disease

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19
Q

Define glomerulonephritis

List what it is due to

A
  • Glomerulonephritis is defined as inflammation of the glomerulus.
  • It is due to immunological damage to the glomerulus – either through:
    • autoantigens
    • antigens that get trapped in the nephron
    • immune complexes that have come from other regions
20
Q

Describe the pathological features of acute pyelonephritis

What complications can occur?

A

(infection of the kidney)

  • High fever
  • Loin pain with tenderness
  • Bacteriuria
  • Rigors, vomiting and oliguria are other common signs

Complications include sepsis, abscess and papillary necrosis.

21
Q

Describe the symptoms and signs of urinary tract infection

A

Lower UTI (cystitis) signs/symptoms:

  • Frequency & nocturia
  • Dysuria
  • Urgency
  • Haematuria
  • Smelly urine
  • Suprapubic pain/tenderness
  • Strangury:
    • painful, frequent urination of small volume, expelled only by straining despite a severe sense of urgency

Older patients may present with confusion and/or incontenence.

Younger patients may present with non-specific symptoms, such as fever and poor feeding, along with “failure to thrive”

22
Q

List factors that may predispose to UTI

A
  • Female sex (due to short urethra)
  • Pregnancy
  • menopause
  • Obstruction
  • Catheter
  • Diabetes
    • glycosuria, reduced host defences
23
Q

List the common pathogenic bacteria associated with urinary tract infection

A

E.Coli (75%)

Proteus (12%)

Klebsiella (4%)

S.Epidermidis (10%)

S.Faecalis (6%)

don’t forget TB.

24
Q

What investigations would you do for a patient with a suspected UTI?

A
  • Urine dipstick
  • Midstream urine MCS

If the patient is showing signs of sepsis, FBC, U&E, CRP, Blood cultures and Lactate should be taken.

25
Q

Describe the causes, symptoms and signs of acute and chronic ureteric obstruction

A

Causes include may be intraluminal, intramural or extramural.

  • Intraluminal: renal calculi, tumour, blood clots,
  • Intramural: stricture (TB, post-calculus, post-surgery), congential problems
  • Extramural: Pelviureteric compression due to: tumour, retroperitoneal fibrosis, diverticulitis, fibroids, BPH, AAA, pregnancy

Symptoms/Signs:

  • Varying loin pain
  • Anuria (if complete bilateral obstruction)/polyuria (if partial blockage causes renal impairment)
  • Loin tenderness, and palpable hydronephrotic kidney
26
Q

What are the causes of calculi in the kidney and ureter?

A
  • Renal calculi form in the collecting ducts and may be desposited anywhere from the renal pelvis to the urethra
  • Classic sites are the pelviureteric junction, pelvic brim and vesicoureteric junction
  • They are most commonly composed of calcium oxalate (75%), with the others being magnesium ammonium phosphate or urate based
27
Q

What are the clinical features of calculi in the kidney and ureter?

A
  • Renal colic:
    • Excruciating ‘loin to groin’ spasms, with nausea and vomiting, patient often cannot lie still
    • Occurs if stone is impacted in the ureter
  • Dull loin pain:
    • If the stone is in a major/minor calyx
  • UTI:
    • Secondary to the partial/complete obstruction

There are few clinical signs on examination

28
Q

Describe the presenting features of renal cell carcinoma (adenocarcinoma of the kidney)

A
  • Vascular tumours arising from the proximal tubular epithelium
  • Account for 90% of renal tumours
  • Main risk factor is haemodialysis

Presentation:

  • 50% are incidental findings
  • 10% present with classic triad of haematuria, loin pain & an abdominal mass plus vague B symptoms
  • Invasion of left renal vein to a varicocele (rare)
  • There may be signs of polycythaemia/hypertension (if renin/EPO secretion)
29
Q

Describe the cause and effects of bladder calculi

A

Causes:

  • Bladder outflow obstruction
    • BPH, bladder neck elevation, high residual volume, infection, neurogenic bladder, urethral stricture
  • Presence of a foreign body
  • Upper urinary tract stone passing down

Presentation:

  • Present with UTI symtpoms, as there is often bacteriuria (frequency, pain and haematuria)
  • sudden termination of voiding
  • pain relieved by lying down
  • retention
  • nocturia
  • hesitation.
30
Q

Describe the pathology and risk factors for transitional cell carcinoma of the bladder

A
  • Transitional cell epithelium lines the calyces, renal pelvis, ureter, bladder and urethra
  • Bladder tumours are 50x more common than tumours of the ureter/renal pelvis

Risk factors;

  • Smoking
  • Aromatic amines: rubber/plastic/dye industry workers
  • Chronic cystitis
  • Pelvic irradiation
31
Q

How does transitional cell carcinoma of the bladder present?

A
  • Painless haematuria +/- clots: most common presentation
  • Recurrent UTI
  • Voiding symptoms
  • Pain from invasion of local structures
32
Q

List the common causes of outlet obstruction of the bladder

A

Can be luminal, mural or extramural

  • Luminal:
    • Bladder tumour
  • Mural:
    • Urethral stricture (post-calculus/infection)
    • Congenital abnormalities
    • Neuropathic bladder
  • Extramural:
    • BPH/prostatic carcinoma
    • Phimosis/paraphimosis (tight foreskin)
33
Q

What is benign prostatic hyperplasia?

Signs and symptoms?

A

Benign nodular/diffuse proliferation of glandular layers of the prostate, leading to enlargement of the inner transitional zone

Symptoms:

  • Filling symptoms (due to bladder overactivity)
    • Frequency (nocturia)
    • Urgency (/strangury)
  • Voiding symptoms (due to bladder outlet obstruction)
    • Hesitancy
    • poor/intermittent stream
    • Post-void dribbling
    • Strangury
    • Retention with overflow incontinence/acute retention
34
Q

What is the pathology and natural history of adenocarcinoma of the prostate gland?

A

Prostate carcinoma:

  • Most are adenocarcinomas, arising in the peripheral prostate
  • Spread can be local (seminal vesicles/bladder/rectum), lymphatic or haematogenous, classically to bone
35
Q

Discuss the diagnosis of bladder infection

A

A urinary tract infection is defined as the presence of bacturia >100,000 organisms/ml.

Lower tract symptoms include frequency, urge, dysuria, haematuria and abdominal pain, without fever. White cells are an indicator of an immune process.

Generally the sample is monoclonal. Polyclonal samples may suggest contamination.

Presence of inflammatory cells helps differentiate between asymptomatic bacturia and UT

36
Q

What is a urethral stricture?

A

A urethral stricture is a scar of the urethral epithelium, which commonly extends into the underlying corpus spongiosum

The fibroblastic activity leads to a shortening of urethral length, and narrowing of luminal size

37
Q

What are the causes of a urethral stricture?

A
  • Blunt perineal trauma:
    • straddle injury, pelvic fracture
  • Iatrogenic:
    • traumatic catheter insertion/long term catheterisation
  • Gonococcol/non-gonococcal urethritis (uncommon)
  • Balanitis xerotica obliterans
    • Characterised by white atrophic plaques leading to phimosis
38
Q

How does a urethral stricture present?

A
  • Obstructive voiding symptoms that worsen gradually:
    • Initial frequency/dysuria
    • Hesitancy/straining
    • Urinary retention
    • Splayed stream (if meatal stricture present)
  • On examination there will be form areas consistent with periurethral scarring
  • The patient is often <50, and there will be no prostate abnormalities
39
Q

What is phimosis?

(pathology)

What are causes and how does it present? (children and adults)

A
  • Narrowing of the preputial orifice, most often idiopathic
  • Other causes are congential, chronic balantitis (irritation of head of penis) or traumatic forcible retraction of the foreskin
  • In children it may present as ballooning of the foreskin and poor stream during urination
  • In adults it presents as pain during intercourse and inability to retract the foreskin
40
Q

What is paraphimposis?

(pathology)

Causes?

Presentation?

A
  • Results from pulling a tight foreskin over the glans, obstructing venous return, leading to a swollen, painful glans
  • As the glans swells, it becomes increasingly difficult to replace the foreskin
  • It can occur aften an erection or following urethral catheterisation (thus important to replace foreskin)
41
Q

Describe the pathology, causes and presentation of an epididymal cyst

A
  • Common, due to cystic degeneration of epididymal structures
  • Associated with polycystic kidney disease and cystic fibrosis
  • They should be:
    • Cystic (transillumates)
    • Separate from the testes, almost always be at the upper pole
  • The contained fluid may be clear, or contain sperm and be milky
  • They can be painful or their bulk can be troublesome
42
Q

Describe the pathology, causes and presentation of a hydrocele

A
  • Most common cause of scrotal enlargement
    • Fluctuant swelling that transilluminates
  • It is an excessive collection of serous fluid in the processus vaginalis
  • Congential hydroceles
    • Assoiated with a hernia sac and patent processus vaginalis
  • Primary (idiopathic) hydrocele
    • aka ‘vaginal hydrocele’ separate from the peritoneal cavity
  • Secondary hydroceles
    • Fluid collects due to underlying inflammation in the epididymis/testes, or an underlying cancer
  • Most hydroceles are not troublesome
43
Q

Describe the pathology, causes and presentation of a variocele

A
  • A varicocele is when veins (pampiniform plexus) become enlarged inside your scrotum
  • Often first manifests in adolescence
  • It feels like a ‘bag of worms’ on palpation and they may only be palpable in the standing position
  • It is associated with reduced spermatogeneis and subfertility
  • The left testicular vein drains to the left renal vein at right angles, rather than the right testicular vein that that drains obliquely into the IVC
  • Valvular incompetency at the junction of the left renal vein is the pathological process leading to a varicocele
44
Q

What is testicular torsion?

How does it occur? (causes)

How does it present?

How is it diagnosed?

A

Testicular torsion occurs when the spermatic cord (from which the testicle is suspended) twists, cutting off the testicle’s blood supply. The testicle twists upon its pedicle, obstructing venous return

Causes:

  • Usually due to a congential abnormality e.g. maldescention/bell-clapper testes
  • Presents in 12-18 year olds with a history of mild trauma or partial torsion (pain)

Symptoms:

  • Sudden onset severe pain in the groin/lower abdomen (T10)
  • Often accompained by vomiting

Signs on examination:

  • Unilateral hot, swollen, tender testis, sometimes lying high and transveres within scrotum

Diagnosis:

  • Dopplet USS may help in showing a lack of blood supply to the testes
  • Surgical exploration may be neccessary for diagnosis
45
Q

What is epididymo-orchitis?

How does it occur?

How does it present?

How is it diagnosed?

A

Acute epididymo-orchitis is a clinical syndrome consisting of pain, swelling and inflammation of the epididymis +/- testes

Causes:

  • Acute infections usally arise due to an ascending infection via the vas deferens:
    • After gonoccal/non-gonococcal urethritis
    • After UTI due E.Coli
  • Can spread haematogenously e.g. in mumps or TB

Symptoms:

  • Painful swelling of the epididymis
  • Often with secondary hydrocele
  • History of discharge (STI) / dysuria (UTI)

Signs on examination:

  • Examination of the prostate may reveal co-exsitent prostatitis, with a positive Phren’s test

Diagnosis:

  • From symptoms
46
Q

How are tumours of the testis classified?

Describe the pathology

A

Seminoma or non-seminomatous germ cell tumours (NSGCTs)

Seminoma:

  • Arises from the cells of the eminiferous tubules, in 30-40 year olds
  • It has a solid appearance macroscopically

NSGCTs:

Include teratomas, yolk sac tumours and choriocarcinomas

47
Q

What are the three questions should be asked to differentiate between scrotal swellings

A
  1. Can I get above it?
    • YES: Tumour, Hydrocele, Spermatocele
    • NO: Hernia
  2. Is it one lump or two?
    • YES: Spermatocele, Hernia
    • NO: Tumour, Hydrocele (usually tight)
  3. Is it transilluminable?
    • YES Hydrocele
    • NO: Tumour, Hernia, Spermatocele

CP1 (13 decks)

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