Renal and GU conditions Flashcards
Causes of acute kidney injury
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)
Acute kidney injury
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
What are the compensatory mechanisms for pre renal causes of AKI
- 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
Nephrolithiasis
-Investigations
RF
Pathophysiology
Symptoms
Investigations
Treatment
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
Chronic kidney disease
-Most common cause
RF
Pathophysiology
Symptoms
Investigations
Treatment
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
Complications of CKD
Anaemia - Due to decreased EPO
Osteodystrophy - Due to decreased vitamin D activation
Neuropathy + Encephalopathy - Due to accumulation of uremic toxins
Cardiovascular disease
Oedema - hypoalbuminemia
Differences between AKI and CKD
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
Benign Prostatic Hyperplasia
Last resort treatment
Which part of the prostate does it occur
RF
Pathophysiology
Symptoms
Investigations
Treatment
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
Name upper and lower UTIs
What are the main causative organisms?
RF of UTIs
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
Are females or males more susceptible to UTIs?
Females as they have a short urethra –> shorter distance for bacteria to travel to the bladder
Pyelonephritis
-Symptoms
- Investigations
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
What can chronic pyelonephritis lead to?
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.
What is sepsis 6?
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
Cystitis
-Treatment
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
Urethritis
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
Epididymo orchitis
-Symptoms
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
Nephrotic syndrome
Causes?
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
Nephritic syndrome
What conditions does it encompass and what are the typical presentations.
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.
IgA nephropathy (Berger’s disease)- treatment
RF
Pathophysiology
Symptoms
Investigations
Treatment
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
Post strep glomerulonephritis
- treatment
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
Goodpasture’s syndrome
-Investigations
RF
Pathophysiology
Symptoms
Investigations
Treatment
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)
