genito-urinary Flashcards
Renal stones: epidemiology
- 10-15% lifetime risk.
- Males > females - 2:1 ratio.
- Common among 30-50 y/o.
Renal stones: aetiology?
rf?
Diet e.g. high protein, high salt diet,
- Congenital abnormalities.
- Metastable urine.
- Hypercalciuria/ high urate/ high oxalate.
- Dehydration!resulting in a concentrated urine - seen particularly in those
working in hot climate - Infection.
RF
- Family history
- Diet e.g. high protein, high salt diet, chocolate, tea, strawberries, rhubarb - all increase oxalate levels
- male
- caucasian
- obesity
- dehydration resulting in a concentrated urine - seen particularly in those
working in hot climate
- meds inc antacids, carbonic anahydrase inhibitors and NA+ and Ca2+ containing meds
Renal stones: pp?
most common sites in ureter?
Stones form from crystals in supersaturated urine.
- 80% are calcium based e.g. calcium oxalate.
1. crystal-like structures AKA urinary/kidney stone can formif small - can pass in urineBUT if it remains in kidneys - can grow BIGGER and = form kidney STONE
- → can lead to an OBSTRUCTIONwhich can increase pressure in tubule. ALSO there is inflammation due to ostructionthis pressure can cause irritation. this irritation and inflammation = RENAL COLIC!!!
- IF stone gets tucks at those sites of ureter constriction - RENAL COLIC can also occur - BC increase in pressure in ureter - THUS stretching of fibres = irritation and pain
- bc of the irritation and increase in pressure proximally = OEDEMA can occur and ureter will contract more vigorously trying to push stone OUT = OEDEMA HYPERPERISTALSIS
- Sites of ureter constriction (where it contracts the smooth muscle:
- Pelviureteric junction
- Pelvic brim
- Vesicoureteric junction (connection between ureter and urinary bladder)
Renal stones: symptoms?
- Loin pain -> groin pain.
- ACUTE flank pain which can radiate to back OR towards groin - ‘Renal colic’ - pain caused by a blockage in the urinary tract.Rapid onset - woken from sleep
• Pain that results from upper urinary tract obstruction
• Excruciating ureteric spasms - patient is writhing in pain
• Pain is from loin to groin and comes and goes in waves as the ureters
peristalise - UTI symptoms e.g. dysuria, urgency, frequency.
- Recurrent UTI’s.
- Haematuria.
Renal stones: management?
- Strong analgesic for renal colic e.g. IV DICLOFENAC
- Antiemetics to prevent vomiting
- IV fluids
Stones less than 5mm in lower ureter 90% pass spontaneously
Stones larger than 5mm with pain and not resolving
Medical expulsive therapy:
• ORAL NIFEDIPINE (A CCB)!!!!!!!!!! or alpha blocker e.g. ORAL TAMSULOSIN can
promote expulsion and reduce analgesia requirements
If still not passing then:
• Extracorporeal shockwave lithotripsy (ESWL) - ultrasound fragments
stone - breaks up stones using shock waves
Percutaneous nephrolithotomy (PCNL) - keyhole surgery to remove
stones that are large, multiple or complex
Renal stones: investigations?
-
Urine dipstick:
• Usually positive for blood - may show haematuria
• Also looks for red cells, protein and glucose- and 24hr urine - calcium, phosphate and oxalate, urate, cysteine and xanthine levels!! - can show us what types of kidney stone
-
Bloods:
• Serum urea, electrolyte, creatinine and calcium, crp
• FBC AND MG, CA, Phosphate levels -
KUBXR - Kidney Ureter Bladder X-ray:
• FIRST LINE INVESTIGATION
• 80 % sensitive
• See stone in line of renal tract
NCCT-KUB - Non-contrast Computerised Tomography: CT Scan
• GOLD STANDARD
• Very rapid
• 99% sensitive for stones - DIAGNOSTIC
Ultrasound
Shows kidney stones and renal pelvis dilatation well but ureteric stones
can be missed - can show acoustic shoadowing
• Sensitive for hydronephrosis (if obstruction is in ureter)
AKI: investigations?
What is the affect of AKI on creatinine and urine output?
Aim is to establish whether AKI is pre-renal, renal or post-renal
- Check potassium!
- Bloods: creatinine, U+E.
- Urine output.
- Auto-antibodies.
-
Urine dipstick:
• Can suggest infection (leucocytes + nitrites) and glomerular disease
(blood + protein) -
Blood count - FBC, U&E
- high CREATININE (diagnostic)
- may alos have raised urea and nitrogen
- anaemia and very high ESR suggests myeloma or vasculitis
as underlying cause
- Creatinine is raised.
- Urine output is reduced.
AKI: rf?
- Increasing age.
- CKD.
- HF.
- Diabetes mellitus.
- Nephrotoxic drugs e.g. NSAIDs and ACEi.
AKI: aetiology?
pre-renal cause of AKI.
- Hypertension.
- Heart failure.
- Nephrotoxic drugs.
intrarenal:
- Nephrotoxic drugs.
- Vasculitis.
- Autoimmune.
- Acute tubular necrosis.
- Glomerulonephritis.
- Interstitial:- Acute intersitial nephritis - due to:
- Drugs, ischaemia, infections, connective tissue diseases, OR nephrotoxins,
Post-renal (10-25%): aka post-obstructive renal injury
- urinary tract obstruction at ureter, bladder or prostate
- Luminal: stones,
- Mural (wall):
- Malignancy e.g. ureteric, bladder or prostate, cervical cancers
- Benign prostate hyperplasia (BPH) (prostate enlargement)
AKI: management?
Treat underlying cause: if infection → ab, if renal stone → painkillers / stone removal, if obstructed catheter → flush it out
Stop nephrotoxic drugs:
Optimise fluid balance
UTI: define
the inflammatory response of the urothelium to bacterial invasion, usually
associated with bacteriuria (bacteria in urine) and pyuria (pus in urine)
• Defined as >105 organisms/ml or fresh mid-stream urine
UTI: which 5 pathogens account for nearly ALL ISOLATE from primary care ?
- KEEPS:
K = Klebsiella spp.
**E = E.coli - MOST COMMON** E = Enterococci P = Proteus spp. S = Staphylococcus spp. - coagulase negative
There is a much broader range of potential pathogens from hospitalised or
catheterised patients
UTI: rf>
- Post-menopausal BC
-
pH rises -> increased colonisation by colonic flora.
* 2. Reduced mucus secretion.*
-
pH rises -> increased colonisation by colonic flora.
- catheterization
- pregnancy - bc progesterone relaxes smooth muscle THUS causing stasis of urine - allowing bacteria to colonize esp up to KIDNEY
- FEMALE BC urethra is shorter so increased risk of developing UTI
- sexual intercourse
- condoms
- urinary tract MALFORMATION
- urinary stones
UTI: pp?
- contamination
- bacteria colonise bladder AND urethra
- inflammatory response
- NEUTROPHIL INFILTRATION
- bacteria multiply and evade immune system (virulence)
- ascension to the kidney
- colonization of the kidney
- bacteraemia - can get into circulation
UTI: investigations?
- Take a good history.
- Urinalysis - multistix SG.
- Microscopy; culture and sensitivity of mid-stream urine.
- In recurrent/complicated UTI renal imaging is important
which upper tract utis vs lutis?
- Upper tract:
• Pyelonephritis
- Lower tract: • Cystitis (bladder) • Prostatitis • Epididymo-orchitis • Urethritis
pyelonephritis: define and main symptoms?
Infection of the renal parenchyma and soft tissues of renal pelvis and upper ureter
pyelo = pelvis
nephro = kidney
so inflammation / infection of renal pelvis
main symptoms: - riad of: • **Loin/FLANK pain, fever and pyuria** - May have severe headache - Rigors UPPER UTI:
- same luti kinda symptoms but also
- vomiting
- flank pain (or back pain)
- fever
- rigors
- malaise
pyelonephritis: investigations?
- Tender loin on examination
- Urine dipstick:
• Detects nitrites - bacteria breakdown nitrates to release nitrites
• Detect leucocyte elastase
• Foul-smelling urine
• Dipstick positive for nitrites, leucocytes and protein - Midstream urine microscopy, culture and sensitivity - GOLD STANDARD for
diagnosis - Bloods:
• FBC - shows elevated white cell count
• CRP & ESR may be raised in acute infection - Urgent ultrasound:
- Detection of calculi, obstruction, abnormal urinary anatomy and
incomplete bladder emptying
- Detection of calculi, obstruction, abnormal urinary anatomy and
cystitis: define
and symptoms
infection/inflammation of bladder
- Dysuria
- Frequency
- Urgency
- Suprapubic pain
- Haematuria
- Offensive smelling/cloudy urine
- Abdominal/loin tenderness
prostatis: define and symptoms?
Infection and inflammation of the prostate gland
• Can be acute or chronic
- Acute prostatitis:
• Systemically unwell
• **Fever, rigors, malaise**
• **Pain on ejaculation**
• **Significant voiding LUTs e.g. poor intermittent stream, hesitancy,
incomplete emptying, post micturition dribbling, straining, dysuria
• Pelvic pain**
- Chronic prostatitis:
• *Acute symptoms (above) > 3 months*
• **Recurrent UTIs**
• **Pelvic pain**
- Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
- Uropathogens in urine.
urethritis: define and aetiology? and symptoms?
infection and inflammation of urethra
Urethral inflammation due to infectious of non-infectious causes
• PRIMARILY a SEXUALLY ACQUIRED DISEASE
STI’s e.g. gonorrhoea, chlamydia can cause them -
-
Gonococcal:
- Neisseria gonorrhoea
- Non-gonococcal:
- Chlamydia trachomatis - MOST COMMON CAUSE
Urethral pain/dysuria.- Urethral pain
- Penile discomfort
BPH: management?
- Mild symptoms: watchful waiting.
- Alpha-1-antagonists e.g. tamulosin.
Tamulosin is an alpha-1-antagonist. It works by relaxing the smooth muscle in the bladder neck and prostate and so increases urinary flow. This improves obstructive symptoms. - 5-alpha-reductase inhibitors. - 5-alpha-reductase inhibitor e.g. ORAL FINASTERIDE:
- will shrink prostate gland
- by inhibiting th conversion of testosterone → dihydrotestosterone
- Side effects; impotence, decreased libido
5-alpha-reductase inhibitors block the conversion of testosterone to dihydrotestosterone (the androgen responsible for prostatic growth).
BPH: symptoms?
- Increased frequency of micturition.
- Nocturia.
- Hesitancy.
- Post-void dribbling.
Poor stream/flow • Urgency • Haematuria - **hv to strain when urinating (to overcome obstruction)** - **dysuria**
BPH: pp?
baso NORMALLY after age 30. men produce 1% less testosterone AND 5-alpha reductase INCREASES W AGE (so increase in dihydrotestosterone levels)
normal prostate cells respond by —> living longer and multiplying
THUS entire prostate gland enlarges and hyperplastic nodules form
As the prostate gets bigger, it may squeeze or partly block the urethra
(narrows the urethra) This often causes problems with urinating
→ nodules compress prostatic urethra ans difficult for urine to pass → urine builds up in bladder causing it to dilate → smooth muscle walls contract harder → bladder hypertrophy where walls thicken and become easily irritated
(stagnation of urine in bladder promotes bacterial growth → UTIs
BPH: investigations?
-
Digital rectal exam - feel prostate and would feel enlarged but SMOOTH
- hard nodule = could be prostatic cancer
-
Serum prostate specific antigen (PSA):
• May be raised in large BPH (bc they’re produced by healthyprostatic luminal cells bc they’re more cells around making PSA)
CKD: define and aetiology?
CKD is longstanding, usually progressive, impairment in renal function (haematuria, proteinuria or anatomical abnormality) for more than 3 months
Defined as a GFR < 60mL/min/1.73 m2 for more than 3 months with/without evidence of kidney damage (haematuria, proteinuria or anatomical abnormality)
each cause basically leads to → an irreversible loss of nephron
- Diabetes mellitus.DIABETIC NEPHROPATHY - high blood glucose/hyperglycaemia = → increase in reactive oxygen species → increase in unecessary growth factors leading to oxidative stress - which lead to -? GBM thickening, sclerosis, - all these changes
- Hypertension. - leads to thickening of blood vessel AND narrowing of lumen THUS LESS blood flow to kidneys - this means decrease in FILTRATION thus DECREASE IN gfr
- reduced blood flow to nephron means cells detect this and renin is produced and RAAS is activated→ RAAS beign activated means → increase in HR and further HTN!!!
- this eventually will lead to glomerular sclerosis (aka thickening and hardening of muscles in bowman’s capsule in glomerulus itself) → leads to ischaemic injury → leads to NEPHRON LOSS
- Atherosclerotic renal vascular disease.
- Congenital e.g. PKD.
- Urinary tract obstruction.
ckd: pp?
CKD = loss of nephrons BC OF AKI, dm etc → glomerular hyperfiltration (bc blood gets diverted to nephrons that acc work) so in early stages glomerular hyperfiltration is tolerated and u get increase in GFR)
→ after a while → SCLEROSIS in nephron bc theres sm pressure
→ eventually glomerular sclerosis will lead to LOSS OF NEPHRON
in LATE stage: GFR decrease, urine output decreases and you begin to retain waste resulting in uraemia
CKD: symptos?
anaemia
retain more Na and H20 = increase in BP and peripheral oedema
hyperkalaemia → muscle weakness, ECG changes and fibrillations
- Mineral balance and osteodystrophy
- loss of nephrons → LESS calcitriol (kidneys can’t produce as much calcitriol as befre) → THUS decrease in Ca2+ reabsorption → HYPOCALCAEMIA → SECONDARY HYPER PARATHYROIDISM → renal OSTEODYSTROPHY
- also HYPERPHOSPHATAEMIA bc body can’t excrete phosphate out
- Proteinuria.
- Haematuria.
- Impaired eGFR <60ml/min.
- Rise in serum urea/creatinine.
