Renal Flashcards
Causes of AKI
Pre- renal (decreased vascular flow)
Renal (damage to glomerulus, intersitium or vessels)
Post-renal- blockage of urinary tract
Pre-renal causes of AKI
- hypovolaemia (dehyd, haemorrhage, D+V, burns, shock)
- reduced CO- HF, MI, sepsis
- Meds- ACEI, ARB, NSAIDs, loop diuretics, aminoglycosides
Renal Causes of AKI
- acute tubular necrosis
- *- vasculitis
- Glomerulonephritis
- *- infiltration- amyloidosis, myeloma, renal cancer
Post-renal causes of AKI
- Intrinsic- stones, clot, UT tumour
- Extrinsic- prostate, neurogenic bladder, blocked catheter
Presentation of AKI
- reduced UO
- colour change of urine (dark, brown)
Fluid overload
- Peripheral oedema
- pulm oedema- SOB, orthopnoea, PND, cough, crackles)
Uraemia
- confusion
- fatigue
- drowsiness, GCS
- N+V
- seizures
Diagnostic criteria fro AKI
1 of:
- raised Cr >=26 in 48hrs
- > =50% rise in Cr above baseline
- UO <0.5ml/kg/hr for at least 6 hours
definition of oliguria
<1ml/kg/hr infants
<0.5ml/kg/hr children
Adults:
<400-500ml daily in adults
17-21ml/hour
0.3-0.5ml/kg/hr
ix for ?AKI
- UO
- FBC, UE, CRP, Coag, LFT, CK
- *- urinalanysis
- *- immunology (autoantibs)
- renals USS
what urinanalysis results would suggest different causes of AKI
- negative- pre-renal
- blood and protein- glomerular
- white cell- infection/intersitital nephritis
what clasificaiton is used for AKI (stages)
- KIDGO
complications of AKI
- anaemia (EPO lacking)
- hyperkalaemia
- metabolic acidosis
- pulm oedema
- uraemia pericarditis
- total renal failure
Management of AKI
Pre-renal cause
- IV fluids
- Sepsis 6
- major haemorrhage protocol
Renal
- stop meds
- steroids
Post-renal
- catherterise
- surgery
General
- fluid balance (BP, skin turgor, JVP, fluid chart)
- monitor Na, K, Ca, Cr, glucose
- tx hyperkalaemia
- refer if no ID cause/moderate AKI
severe- haemodialysis
what is acute tubular necrosis
- ischaemic or nephrotoxic injury to tubular epithelial cells causing AKI
- results in detachment from BM
sx of acute tubular necrosis
- *- hypotension, fluid depletion
- exposure to nephrotoxic substances- contrast, aminoglycoside, abx, CT
- oligo/anuria
- *- poor oral intake, anorexia
- dizziness, malaise
ix ?acute tubular necrosis
- urinanalysis- muddy brown casts (epithelial cells)
* *****- urine Na conc, urine osmolality (ie conc)– high
management of acute tubular necrosis
- fluid balance
- remove toxic agents
definition of anuria
<100ml/day
what is the most common cause of CKD
diabetes
causes of CKD
diabetes
hypercholesterolaemia
HTN
glomerular disease
presentation of CKD
- asx in stages 1-4
- N+V, diarrhoea, anorexia, wt loss
- **- polyuria, nocturia, haematuria
- oedema, pleural effusions (SOB, cough, chest pain, orthopnoea)
- HTN
- *- bone pain, # (Ca, phosphate reab issues)
- *- prox muscle weakness (Ca, reabs issues)
- neuro- polyneuropathy, confusion
- uraemic pericarditis- chest pain worse on insp and lying), coughing
- skin pigmentation/darkening- pigments that are usually excreted are retained
ix ?CKD
- UE
- FBC- anaemia
- HbA1c, lipids
- PTH, Ca, Phosphate, vit D
- urinanalysis- proteinuria, haematuria
- urine albumin-Cr ratio– >3mg/mmol clinically relevant pronteinuria
- renal USS- obstruction, FH PCKD
Classification of CKD
1- eGFR >90 plus kidney damage (strctural/haematuria/proteinuria >3m) 2- eGFR 60-89 plus kidney damage 3a- eGFR 45-59 3b- eGFR 30-44 4- eGFR 15-29 5- eGFR <15
management of CKD
- monitor eGFR and alb-Cr ratio
- smoking, alcohol, wt/diet
- avoid NSAIDs and other nephrotoxics
- pneumococcal and flu jabs
- bisphos, vit D and Ca supplements
- PO iron, IV iron, recombinant EPO/erythropoietic stimulatign agent
- manage HTN
- statins
- antiplatelets
- renal replacement
indications for renal replacement therapy
Severe AKI
- unresponsive acidosis
- unreposnsive electrolyte abnormalities, esp hyperkalaemia
- oedema
- uraemia, seizure, GCS, encephalopathy
- pericarditis
LT
- CKD stage 5
types of renal replacement therapy
Intermittent haemodialysis-
- AV fistula
- *- 3-4 times p/w, 3-4 hours
- infection, thrombosis, aneurysm in fistula, stenosis, STEAL syndrome (distal limb ischaemia), **high output HF (increased venous retrun to heart)
Peritoneal dialysis
- pt can do in own time, independence
- bacterial peritonitis, peritoneal sclerosis, wt gain, **LT ascites
Continuous-
- on ward, more unwell pts
- no toxin build up
what would suggest O/E of a renal transplant
- mass palpable in iliac fossa (usually R)
- Rutherford Morrison (reverse hockey stick ie long curved scar, usually in RIF).
- may have palpable AV fistula
- may have mutiple abdo scars due to dialysis insertion/exit sites (peritnoeal)
pathopysiology of renal arteyr stenosis
- atherosclerosis
- impaired renal BS
- juxtaglom apparatus detects
- renin released
- RAAS activated
- HTN
RAAS system
- low BP detected by juxtoglomerulus apparatus
- renin released
- angiotensinogen–> angiotensin I
- ACEI causes angio I–> II
- angio II causes aldosterone from adrenals plus vasoconstriction
- alosterone– reabs Na and water
where is angiotensinogen released from
liver
sx of renal artery stenosis
- **Flash pulm odema (recurrent)
- dyspnoea
- orthopnoea
- cough- frothy, blood
- wheezing
- weak, thirst, confusion, irritable (hypernatraemia)
- twitches, cramps, paralysis, arrhythmias (hypokalaemia)
- *- confusion, tremor (metabolic alkalosis)
- double vision, headaches
signs of renal artery stenosis
- sudden onset HTN
- tx resistant HTN
- worsening eGFR (ischaemia)- esp after starting ACEI
deranged U&Es - metabolic alkalosis
- HTN retinopathy on fundocscopy
ix ?renal artery stenosis
- UE, aldosterone to renin ratio
- renal USS
- duplex/doppler US
- CT/MRI angiography
tx renal artery stenosis
- diuretics
- angioplasty, stenting
- lifestyle
- manage diabetes
- antiplatelets, statins
presentation of glomerulonephritides
- asx
- nephritic or nephrotic syndromes
- chronic/end-stage- anaemia, bone disease
ix ?glomerulonephrtides
- bloods- inflam markers, protein levels, antibodies
- renal biopsy
What is Nephrotic Syndrome
- large proteinuria (>=3.5g/day)
AND - hypoalbuminaemia (<=30g/L)
- cause by non-proliferative glomerulonephritis
- also has hyperlipidaemia- liver compensates fro reduces albumin by also increasing lipid production
- loss of Ig proteins
- loss of antithrombotic proteins
sx nephrotic syndrome
- oedema- ascites, effusion
- immunosupression, recurrent infections
- clotting (urinary loss of antithrombotic proteins, increased prod of prothombotic factors)- renal vein thromb, PE, DVT
- frothy urine (proteinuria)
What is nephritis syndrome
- small proteinuria
- haematuria (micro or macro)
- reduced renal function– reduced UO– HTN
+- oedema - caused by proliferative glomerulonephritis
- red cell casts in urine (indicate glomerular damage)
Name some non-proliferative glomerulonephritis
- focal segmental glomerulosclerosis
- minimal change
- membranous glomerulonephritis
what type of renal syndrome do non-proliferative glomerulonephritides cause
- nephrotic
who does focal segmental glomerulosclerosis affect
adults
pathophysio of focal segmental glomerulosclerosis
- non proliferative
- segmental scarring of glomeruli and fusion of foot processes
- idiopathic
- HIV, lupus, reflux nephro
who does minimal changes disease tend to affect
2-6yo
causes of minimal change disease
- idiopathic
- paraneoplastic- Hodgkins
- drugs
sx of minimal change disease
- oedema / wt gain
- in a child
pathophysio of membranous glomerulonephritiis
- non-proliferative
- IgG deposition, thickening of glomerular cap wall
- glomerular PLA2R antigen targetting
- mostly caused by autoimmune disease
- can also be caused by infection, drugs, tumour
presentation of focal segmental glomerulosclerosis and membranous glomerulonephritis
- facial swelling
- oedema
- HTN
- renal failure (reduced UO)
who does membranous glomerulonephritis tend to affect
adults, slow
ix of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)
- urinanalysis- large proteinuria
- PLAR2 ab in urine (membranous)
- renal biopsy
management of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)
- prednisolone
cyclophosphamide/ciclosporin - salt/fluid restriction
- correct cause (infection, drug, autoimmune disease)
what would yuo see on renal biopsy of the different non-proloferative glomerulonephritides
focal segmental glomerulosclerosis
- segmental scarring of glomeruli
- fusion of foot processes
minimal changes
- no changes on light micro
- effacement of podocyte foot process on electrone
- no deposits or ig complements
Membranous
- Ig deposits on immunofluoresent staining
- thickened BM
Name proliferative glomerulonephritis
- IgA (berger’s)
- post- strep
- anti-glomerular BM
- rapidly progressive
what renal syndrome do proliferative glomerulonephritides tend to cause
nephritic
what is igA nephropathy
- igA deposits
- proliferative glomerulonephritis
- occurs post- URTI
sx of igA nephropathy
- frank haematuria
- after URTI
- can cause henoch-schonlein purpura in children- deposits in skin, GI tract
management f igA nephropathy
- ARB, ACEI (BP control)
- low cholesterol diet
- immunosupresison- steroids, cyclophosphamide, azathioprine for remission
most common proliferative glomerulonephritis
igA nephropathy/Berger’s
most common non-proliferative glomerulionephritis
adult- focal segmental glomerulosclerosis
children- minimal change
ix for any cause of ?nephritic syndrome/proliferative glomerulonephritis (frank haematuria)
- dipstick
- renal biopsy- to find cause
- serology for autoab
what is post-strep glomerulonephritis
- proliferative glomerulonephritis
- immune glomerular injury triggered by strep infection (2w following)
- generally self limiting
what is the specific antibody found in post- strep glomerulonephritis
anti-streptococcal antibody titres
management of post-strep glomerulonephritis
fluid balance
supportive
self limiting
what is anti-glomerular basement membrane disease
- autoimmune attack of basemement membrane antigens located in glomeruli and alveoli
sx anti-glomerular BM disease
- nephritic syndrome- haematuria, HTN, oedema
- haemoptysis, cough, SOB- Goodpasture’s syndrome!
what is a sepcific antibody found in anti-GBM disease
- anti-GBM antibodies
renal biopsy findings of the different nephritic, proliferative diseases
IgA- mesangial cells and matrix, crescents, igA deposits
Post-strep- exudative and proliferative, subepithelial humps
anti-GBM- igG deposits along basement membrane
What vasculitic diseases can affect the kidneys?
- necrotising small vessel vasculitis
- granulomatosis with polyangitis (wegner’s)
sx of necrotising small vessel vasculitis
rash
sinusitis
malaise, fever, wt loss
tx of necrotising small vessel vasculitis/ granulomatosis with polyangiitis
- steroids
- cyclophosphamide
- metho, azathioprine
sx of granulomatosis with polyangitis (wegner’s)
sinusitis
glomerulonephritis- proteinuria, haematuria
cough, haemoptysis
purpura, arthritis, scleritis/episcleitis
fever, malaise, weakness, wt loss
What is haemolytic uraemic syndrome
shiga toxin /verotoxin producing e.coli
- thrombin and fibrin deposition in renal, GI and CNS microvasculature
- haemolysis
- plts sequestered
sx of haemolytic uraemic syndrome
- after e.coli infection- gastroeneritis
- bloody diarrhoes, pain, vomiting
- haematuria
- oliguria
- jaundice
- anaemia sx
ix for haemolytic uraemic syndrome
- low plt, low Hb, elevated LDH, raised WCC
- red cell fragments on blood film
- rise in Ur and Cr
- LFTs to ddx HELLP
- CRP
- clotting- reduced values
- stool PCR, urine culture
- urinanalysis- haematuria, proteinuria
tx haemolytic uraemic syndrome
- fluid and electrloytes
- anti-HTNs
- dialysis
- plasma exchange
- liver, kidney transplants
what is lupus nephritis, sx
- lupus (fever, malaise, joint pain, malar rash)
- haematuria, proteinuria (forthy), HTN, oedema
tx lupus nephritis
- BP ctornol
- electrolyte and fluid
- steroids, cyclophosphamide
what is fanconi syndrome
- inadequate reabs in the Prox renal tubules
- caused by hypoxia, drugs, genetics, infiltration (myelome, wilsons)
sx of fanconi
- polyuria, polydipsia, dehydration
- rickets and osteomalacia (loss of phosphate)
- electrolyte disturbances– hypokalaemia
tx fanconi syndrome
- replace electrolytes and fluids
- kidney transplant
what inheritance pattern is PCKD
dominant OR recessive!
presentation of autosomal dominant PCKD
asx unless cysts large/haemorrhagic
- loin pain
- haematuria
- stones
- HTN
- cyst infection- fever, pain, sepsis
- UTI, pyelonephritis
management of dominant PCKD
- annual monitoring USS< BP, UE
- drink water
- HTN control
- tx infections
- CT guided cyst aspiration
- tolvaptan- slows growth
- renal replacement therapy
sx of recessive PCKD
- affects fetus
- oligohydramnios
- underdeveloped lungs
infance
- abdominal mass
- resp failure
- portal HTN (cirrhosis)
- underdeveloped ear cartiliage, low set ears, flat nasal bridge
tx recessive PCKD
- tx renal failure, portal HTN
- renal replacement- most will dies in childhood if dont have this
what is alport syndrome
x linked
- defect in type IV collagen
- affects glomerular BM, cochlea, eyes
sx alport
- haematuria, proteinuria
- sensorineural deafness
- cataracts, corneal erosion later in life
management of alport syndrmoe
ACEI
renal replacement therpay
renal transplant
ix for inhertied renal disease (PCKD, alport)
UE, urinanalysis
USS
genetic testing
renal biopsy
cell type of renal cancer
95% RCC
sx renal cancer
2/3 are asx
- haematuria
- flank pain
- abdo mass
- HTN
- anorexia, wt loss
ix ?renal cancer
- HTN- aggressive (renin)
- FBC- polycythemia due to EPO
- ESR, UE
- ALP (bony mets)
- renal USS
- CT/MRI
what is the 2ww criteria for ?RCC
> =45 yo and
unexplained frank haematuria without UTI
OR
frank haematuria that perissts/recurs after successful tx of UTI
tx RCC
- surgical- nephrectomy
- CT/RT resistant
what is a wilms tumour
nephroblastoma
- children
- embryonal tumour of the kidney
sx wilm’s tumour
- abdo mass
- otherwise well child
- haematuria
- HTN
ix ?wilms tumour
- US/CT/MRI abdo
- assess function of contralateral kidney
tx wilms tumour
CT
excision, nephrectomy
RT
what is rhabdomyolysis
- breakdown of damage skeletal muscle
- causes myoglobin release
- kidney damage
causes of rhabdomyolysis
- trauma (crush, burns, ischaemia)
- heat (lightning, heat stroke)
- exertion (long lie, shivering, seizures)
- genetic disorders in metabolism
- hypothyroidism
- DKA
- electrolyte imbalances
- DUchenne
- infection
- inflammation
- drugs
what drugs may cause rhabdomyolysis
- statin (safety net muscle pain)
- cyclosporin
- erythro
- colchicine
- cocaine, ampehtamines, ecstasy, LSD
sx rhadomyolysis
- weakness
- soreness
- bruising
- dark urine
- fatigue, malaise, fever, N+V,
- confusion, agitation
ix ?rhabdomyolysis
- CK
- myoglobin- serum and urine
- K- may leak from injured tissue
- Cr
tx rhadomyoloysis
- IV fluids stat
- sodium bicarbonate meds- binds to myoglobin and alkalanises the urine
- diuretics
- tx and monitor for hyperkalaemia, hypocalacaemia
- dialysis
sx acute retention
- urgency, but cannot urinate
- lower abdo pain.discomfort
- normal renal function
sx chronic retention
- polyuria (8x p/d)
- hesitancy
- weakn/intermittent stream
- feeling need to urinate post-mic
- nocturia
- leakage
- urge incontinence
- cant tell when bladder is full
- mild discomfort lower abdo/pelvis
ix to differentiate acute and chronic retention
Residual volume
>1L in chronic
<1L in acute
Kidney function
deranged in chronic
normal in acute
what is high pressure urinary retention
- chronic retention with high intra-vesical pressure
- back up to kidneys- BL hydronephrosis
causes of retention
Obstruction
- stones
- strictures
- constipation
- mass in pelvis/GI
- blood clot
- foreigh bodies
- urethritis, cystitis, balanitis, prastatitis
Meds
- amphetamines
- Anticholinergics
- sypathomimetics
- muscle relaxants
- MSADs
- antipsychotics
- tricyclics
- opioids
Neuro- CNS damage, diabetes, MS, parkisons
Iatrogenic- spinal, joint surgery
BPH, prostate cancer, penile cotnriction bands, meatal stenosis, paraphimosis/phimosis
Gynae cancers, prolapse
name some antimuscarinic/anticholinergic drugs
- Antihistamines- promethazine, hydoxyzine, chlorpheniramine
- oxybutynin, solifenacin
- procyclidine (parkinsons)
- tiotropium/irpatropium
- atropine
anticholinergic drug mechanism
block the parasympathetic nervous system:
- block cholinergic or acetylecholin receptors
- antimuscarinics block muscarinic receptors
- antinicotinics block nicotinic receptors
effects of anticholinergic drugs on the body
- decreased smooth muscle motility in UT and increase tone of sphincters contorlling urination
- increase the heart rate,
- minimize vestibular issues
- help with motor sx in parkinsonss
- decrease gastric acid secretion
- relax muscles in airways
SE anticholinergics
Can’t pee, can’t see, can’t spit, can’t shit
- dry mouth, sore throat
- urinary retention
- mood changes, hallucinations, confusion
- above are sx of an overdose too
ix for retention
- genital and rectum
- urinanalysis
- post void residual volume, urodynamic testing
- cystoscopy
- USS, CT
tx retention
- 2 way catheter
- surgical dilatation
- analgesia
- acute- alpha-adrenoreceptor blocker (doxazosin, tamsulosin)
- chronic- intermittent catheterisation, indwelling
Men
- alpha adrenoceptor blocker (alfuzosin, doxazosin, tamulosin– selective alppa1)
- bethanechol chloride
- 5alpha reductase inhib- finasteride
- surgery
post obstructive diuresis
- UO >200ml/hr over 2 hours
- can cause electrloyte disurbance and hypotension
management of post obstructive diuresis
- monitor (bloods, wt, ABG, obs)
- USS renal
- CT KUB
- IV fluid relplacement, hartmans 50% of UO
- catheter- indwelling
- never TWOC
Hydronephrosis- what is it?
UT obstruction cause increased pressure in the kidneys
- kidney distension
- damage and loss of function
sx hydronephrosis
- flank/back pain- can be dull if chronic
- N+V
- fever
- infants- listelessness, FTT
ix ?hydronephrosis
- USS- distended
- urogram
- CT/MRI if ?cancer
- creatinine
- urinanalysis- ??infection
tx hydronephrosis
- watch and wait if mild
- preventative abx
- anatomical correction
- surgery to unobstruct
sx of renal vein thrombosis
- loin/flank pain
- oliguria
- haematuria
- N+V
- may also have PE
- asymmetrical lower leg oedema- back flow of venous blood
- frothy urine if due to nephrotic syndrmoe
signs of renal vein thromb
- lef variocele if L renal vein thrombosed
- dilated abdo veins
- peripheral oedema
- proteinuria
ix ?renal vein thrombosis
Cr, urinary protein doppler USS IV urogram CT/MRI ?cancer biopsy if ?nephrotic syndrome
management of renal vein thrombosis
- warfarin
- streptokinase to lyse if acute
- statin
- ACEI/ARBC or proteinuria
- tx underlying cause
- thrombectomy
- surgery- IVC filters, nephrectomy
Where to loop diuretics act in the kidneys, how do they work
- loop of henle- thick ascending
- inhibit NKCC2 transporter
- stop Na, K and Cl reabs
- reduced water reabs
SE loop diuretic
- hypokalaemia- stops K reabs
Where do thiazide- like diuretics act in the kidney, mechanism of action
DCT
NaCa cotransporter inhibition- less Cl ions and Na reabs from tubule into blood
Less water reabs
SE thiazide like diuretics
- gout flare
- hyperglycaemia
egs of thiazide like diuretics
indapamide
bendroflumethiazide
EGs of aldosertone antagonsists
spironolactone
eplerenone
location of action of aldosterone anatgonsists
DCT- inhibit aldosterone from binding
prevents water and Na reabs
SE of alosetrone anatgonsists
Hyperkalaemia
agranulocytosis
SE of ACEI
dry cough
hyperkalaemia
SE ARB
hyperkalaemia
eg of ACEI
ramipril
- pril
eg of ARB
losartan
candesartan
- sartan
CCBs mechanism of action
block Ca channels on BV and heart
relaxes smooth muscle
eg of CCBs
amlodipine
verapamil
SE CCBs
- peripheral oedema
- flushing
- constipation
Sx of pyelonephritis
- fever, N+V, aching, fatigue, confusion
- abdo/flank pain
- dysuria
- cloudy urine, haematuria, pyuria
- urgency/frequency
- fishy odour
organisms that commonly cause pyelonephritis
Gram -ve
- e.coli
- proteus
- klebsiella
- enterbacter
ix ?pyelonpehritis
- urinanalysis
- if catheter- check
- bloods, culture
- -> can make dx if loin/flank pain and confirmed UTI
diagnostic uncertainty:
- CTKUB ?stone
- kidney USS if recurrent, voiding custourethrography
- DMSA- radionucleotide
tx pyelonephritis in non pregnant women, men, indwelling catheters
1st line
- cefalexin 500mg BD 7 days
- coamox 500/125mg TDS 7 days
- trimethoprim 200mg BD 14 days
- cipro 500mg BD 7 days
tx pyelonephritis in pregnant women
cefalexin 500mg BD 7 days
what are kidney stones often made up of
- Ca oxalate
- Ca phosphate
- uric acid- dont show on XR
- struvite (mg, ammon, phos)
- cysteine
- Xanthine- dont show on XR
sx kidney stone
- flank pain
- becomes severe
- renal colic- spasmodic
- loin to groin
- haematuria
ix kidney stone
CT KUB
urinanalysis- blood
tx stone
- <5mm- can pass (CCBs, alpha adrenergic eg tamsulosin)
- hydration
- analgesia
- potassium citrate reduce formation
- lithotripsy
- surgery and stent
sx stress incontinence
- physical stress
- coughing, sneezing, laughing, bending. lifting, jumping, running, having sex
- muscles that support urethra are weak
sx of urgency incontinence/OAB
- sudden urge to urinate due to bladder contracting
sx overflow incontinence
- dribbling after micturition
- due to obstruction
medications that can cause incontinence
- diuretics
- antihypertensives
- sleeping tablets
- sedatives
- muscle relaxants
food,drink that can cause incontinence
- caffeine
- fizzy drinks
- chocolate,
- chillis, spice
- citrus, vit c
- alcohol
conditions/diseases that can cause incontinence
- neuro
- stones, UTI
- obstruction (tumour, constipation, prostate
- cauda equina
- retention (nocturnal)
- prolapse
ix incontinence
- bladder diary
- physical exam- pelvic floor, PR
- diptick
- USS bladder (overflow, retention)
- cystoscopy
- urodynamics
tx stress incontinence
- pelvic floor exercises
- topical oestrogen
- pessary/urethral insert
- bulking agents injected
- surgery- sling
- catheter
- absorbent pads
tx overactive bladder
- bladder training
- anticholinergics- oxybutynin, solifenacin
- mirabegron- beta-3-adrenergic agonist
- topical oestrogen
- imipramine- tricyclic
- botox
catheter - absorbent pads
tx cystitis
- trimethoprim 200mg BD 3 days OR
- nitro 100mg BD for 3 days
If recurrent - trimethoprim 200mg within 2 hours of sex
- 6m course of trimethoprim or nitro 100mg at night
what is interstitial cystitis, sx
chronic, mech unknwn
- urgency, frequency, nocturia
- suprapubic/pelvic pain
- may rdiate to groin, sacrum, vagina
- pain worse when bladder full
- dysuria
- pain better post void
- sx worse during menstruation
- dyspareunia
- often coincides with functional issues, SLE, asthma, TMJ
ix ?intersitial cystitis
rule out other causes:
- urinanalysis
- cervical swab (STI)
- urodynamics
- men- urethral swabs, prostatic secretion cultures– chronic prostatits
- cystoscopy with biopsy for diagnosis
tx intersitial cystitis
- reduce caffeine, alcohol, acidic foods and drink
- stress
- analgesia
- amytriptyline,. cimetidine
- pentosan - polysulfate sodium
- oxybutynin
- gabapentin
- ciclosporin
- intravescical lidocaine, botulinum toxin
- surgical ablaiton, augmentation cystoplasty