Conditions Flashcards
(116 cards)
1
Q
UTI presentation
A
Dysuria, frequency, smelly urine
Very young; unwell, fail to thrive
Very old; incontinence, off their feet
2
Q
Renal inflammation terms
A
Urethra; urethritis
Bladder; cystitis
Ureter; ureteritis
Kidney; acute pylonephritis
Recurrent or prolonged kidney infection; chronic pyelonephritis
3
Q
Predisposing factors in UTI
A
Stasis of urine
- obstruction; congenital or acquired
- loss of ‘feeling’ of full bladder; spinal cord/brain injury
Pushing bacteria up urethra from below
- sexual activity in females
- catheterisation
Generalised predisposition to infection
- chemo, diabetes, immune system problems
4
Q
Describe obstruction in stasis of urine
A
Obstruction at level of urethra
- upper urethral and bladder dilatation
- bilateral hydroureter
- bilateral hydronephrosis*
- chronic renal failure
*hydronephrosis = water in kidney
Obstruction at level of renal pelvis; one side only
- unilateral hydroureter
- unilateral hydronephrosis
(so still have one functioning kidney)
5
Q
Consequences of obstruction
A
Proximal dilatation
Slowed urine flow; cannot flush out bacteria; infection
Slowed urine flow; sediments form; calculous formation; more obstruction
Cyclic TRIAD
6
Q
Obstruction in children
A
Numerous renal tract abnormalities
Always investigate at 1st presentation and send to paediatric surgeons
7
Q
Vesicoureteric Reflux
A
Decreased angulation of ureter at bladder
Opening at bladder is straight
inc pressure of urine in bladder causes reflux and leads to hydroureter
Common cause UTI in children
8
Q
Common causes obstruction in adults
A
Men;
- benign prostatic hyperplasia
Women;
- uterine prolapse
Both sexes;
- tumours and calculi
9
Q
Describe loss of “feeling” of full bladder (as a cause or urinary stasis)
A
Normally go to toilet and pass all urine
Decreased sensation; no sense when to micturate and do not know to empty it completely
Leave urine in bladder = high residual volume
Leads to stasis of urine and commonly UTIs
10
Q
Describe pushing bacteria up urethra from below
A
Sexual activity tends to move lower urethral flora up tract (in women back wall urethra just in front of vagina)
Catheterisation
- any instrumentation urinary tract tends to move lower urethral flora up tract
11
Q
UTI predisposition in females
A
- Short urethra
- Lack of prostatic bacteriostatic secretion
- closeness urethral orifice to rectum
- sexual activity
- pregnancy (pressure on ureters and bladder)
12
Q
Complications UTI
A
Acute
- Severe sepsis and septic shock
Chronic
- kidney damage; hypertension, chronic renal failure
- calculi - obstruction - hydronephrosis; hypertension and renal failure
13
Q
Normal Glomerulus
A
Afferent arteriole going in, efferent arteriole going out
“bag of capillaries”
14
Q
Glomerulonephritis (general)
A
Disease of glomerulus, large range of conditions
Can be inflammatory or non-inflammatory
Primary only affects glomerulus, secondary affects other parts of body i.e. SLE
Two types; proliferative and non-proliferative
Can cause nephritic syndrome and nephrotic syndrome
Usually non-proliferative causes nephrotic syndrome and proliferative causes nephritic syndrome
15
Q
4 common presentations of glomerulonephritis
A
- Haematuria
- Heavy proteinuria (nephrotic syndrome)
- Slowly increasing proteinuria
- Acute renal failure
16
Q
Main causes of haematuria
A
UTI
Urinary tract stone
Urinary tract tumour
*Glomerulonephritis less common but can cause haematuria
17
Q
US of kidneys
A
Urinary tract tone and tumour will show up so use as first investigation
18
Q
Immunoflourescence
A
Check for Ig deposition in mesangial area of glomeruli
19
Q
Complement system
A
System for punching holes in bacterial cell walls
20
Q
Describe membranous glomerulonephritis
A
Nephrotic syndrome, slowly progressive, mainly ages 30-50
Immune complex deposition activates complement (c3) which punches holes in BM
Leaky filter allows albumin into urine
Microscopic analysis = thickened BM
Immunofluorescence = diffuse IgG uptake
Steroids if begins to progress
21
Q
Diabetic nephropathy
A
- Glycated molecules
- matrix deposition in basal lamina underlying endothelium and mesangial matrix
- thickened but leaky BM and mesangial matrix compressed capillaries
Nodules of mesangial matrix = Kimmelsteil-Wilson lesions; gross excess mesagnial matrix forming nodules
Inevitable decline if
- Established diabetic neuropathy
- Continued poor diabetic control
22
Q
Crescentic glomerulonephritis
A
Pattern down microscope; many diseases cause it
23
Q
Granulomatosis with polyangitis
A
Form of vasculitis which affects vessels in kidneys, nose and lungs
Serum test shows presence anti-neutrophil cytoplasmic antibodies (ANCA)
*find this in serum but is not directed against glomerulus or deposited in kidney
fatal if left untreated; cyclophosphamide = 75% complete remission
24
Q
Nephrotic syndrome
A
Characterised by high protein in urine and often frothy
Also hypoalbuminaemia, oedema, hyperlipidaemia
25
Nephritic syndrome
Haematuria; macro/micro, red cell casts
May have small amounts protein
Hypertension (usually mild)
low urine vol <300ml/day
26
Post-infectious GN
Can occur after any infection, typically after strep pyogenes (typically 2weeks after)
Supportive treatment - usually resolves in 2-4weeks
27
Rapidly progressive GN
aka crescentic
All GN types can become RPGN however some types are only ever
Goodpasture's syndrome (immune mediated - high-dose immunosuppression)
Vasculitic disorders
28
IgA nephropathy
aka Berger's disease is most common type GN in adults
24-48hrs after URTI, may be relatively benign or lead to end-stage renal disease
Biopsy to confirm, steroids and cyclophosphamide (varied results)
29
Minimal Change GN
80% all nephrotic syndrome in children, 20% of adults
Supportive care, prednisolone can halt disease progress
30
Membranous GN
Slowly progressive
Mainly 35-50yo, caused by immune complex deposition
Microscopic analysis shows thickened glomerular BM and immunofluorescence shows IgG uptake
Steroids if begins to progress
31
Memranoproliferative GN
combined nephritic and nephrotic
Thickened BM AND mesangium
poor prognosis
32
```
BPE
BPH
BPO
BOO
LUTS
```
BPE - benign prostatic enlargement
BPH - benign prostatic hyperplasia
BPO - benign prostatic obstruction
BOO - bladder outflow obstruction
LUTS - lower urinary tract symptoms
33
Benign Prostatic Hyperplasia
Characterised by fibromuscular and glandular hyperplasia
Predominantly affects transition zone
Part of ageing process in male
progressive condition may result in BOO
34
Obstructive/voiding symptoms
Hesitancy
Poor stream
Terminal dribbling
Incomplete emptying
35
Irritative/storage symptoms
Frequency
Nocturia
Urgency +/- urge incontinence
36
Uncomplicated Benign Prostatic obstruction
Watchful waiting
Medical
- alpha blockers
- 5 alpha reductase inhibitors (finasteride/dutasteride)
- combination
Surgical Intervention
- TURP (prostate size <100cc)
- open retropubic or transvesical prostatectomy
- endoscopic ablative procedures
37
Alpha blockers
Main treatment LUTS due to BPO
Smooth muscle/bladder neck and prostate innervated by sympathetic adrenergic nerves (mostly alpha a1 subtype)
Side effects;
- hypotension, floppy iris syndrome (don't use if cataract surgery), retrograde ejaculation
38
5a reductase inhibitors
5a reductase converts testosterone to dihydrotestosterone which causes growth of prostate, so if we block production of this the prostate will shrink
Max effects takes ~6mnths to achieve
i.e. dutasteride and finasteride
Side effects
- breast growth
- sexual dysfunction
39
Complicated BOO
Progression LUTS, acute urinary retention, chronic urinary retention, urinary incontinence, UTI, bladder stone, renal failure
Surgery mostly; TURP
Alternative
- long term urethral or suprapubic catheter
- clean intermittent self-catheterisation
40
Upper UT obstruction
i.e. supravesical (above bladder)
PUJ
ureter
VUJ
Pain, frank haematuria, symptoms or complications
Signs; palpable mass, microscopic haematuria, signs of complications
Complications; infection, sepsis, renal failure
41
Lower UT obstruction
i.e. bladder outflow obstruction
```
bladder neck
prostate
urethra
urethral meatus
foreskin (e.g. phimosis)
```
acute retention, chronic retention, frank haematuria, recurrent UTI and sepsis, bladder stones, renal failure
42
Acute v chronic urinary tract obstruction
Acute
- renal function could be normal
- pain?
Chronic
- renal function may be normal
- high pressure v low pressure
- partial or complete
43
UUT obstruction management
Resuscitation
- ABCDE
- IV, bloods, ABG, urine and blood culture, fluid balance
- IV fluids, broad ABs
- analgesia
- HDU care
Investigations
Emergency treatment of obstruction
- percutaneous nephrostomy insertion
- retrograde stent insertion
THEN treat underlying cause i.e. stone, ureteric tumour
44
LUT obstruction management
Retention; catheterise immediately
Resuscitation
- ABCDE
- IV, blood, ABG, urine and blood culture, fluid balance monitor
- analgesia
- HDU
Investigations; bladder scan, USS renal tract
Emergency treatment of obstruction
- urethral catheterisation
- suprapubic catheterisation
Treat underlying cause
45
Post obstructive diuresis
need fluid input/output chart to ensure they don't become hypotensive (kidney failure would become worse)
>200mls/hour
rare but can lead to life threatening Na and water depletion
46
Low pressure v high pressure chronic retention
Low pressure
- painless
- dry
- normal cr
- normal kidneys
High pressure
- painless
- incontinent
- raised cr
- bilateral hydronephrosis
47
Decompression haematuria
shearing of small vessels due to differing compliance of tissue layers
usually self-limiting
48
Differentials for blood in urine
1. UTI
2. Cancer
3. Stones
4. Glomerulonephritis with IgA being most likely
49
Renal replacement therapy
Means of sustaining life in patients sufferring from end-stage renal disease, usually at eGFR<10ml/min (but variable)
Types;
- renal transplant
- haemodialysis
- peritoneal dialysis
- conservative kidney management
50
Haemodialysis
Access
- Permanent; Arteriovenous fistula, AV prosthetic graft
- Temp; tunnelled venous catheter, temp venous catheter
Fluid balance usually restricted to 500-800ml/24hrs
Complications
- CV problems
- coagulation
- other; allergic, catastrophic dialysis accidents (rare)
51
Peritoneal Dialysis
Balanced dialysis solution instilled into peritoneal cavity via a tunnelled, cuffed catheter, using peritoneal mesothelium as a dialysis membrane
Fluid contains balanced conc of electrolytes, glucose is most common osmotic agent for ultrafiltration of fluid
Complications
- exit site infection, tunnel infection
- PD peritonitis
- ultrafiltration failure, tube malfunction
- encapsulating peritoneal sclerosis
- abdo wall herniae
52
Indications for dialysis
Advanced uraemia (GFR 5-10ml/min)
Severe acidosis (bicarb < 10mmol/l)
Treatment resistant hyperkalaemia
Treatment resistant fluid overload
53
Dialysis related drugs
Anaemia
- erythropoetin injections
- IV iron supplements
Renal bone disease
- activated vit D
- phosphate binders with meals
Heparin
Water soluble vitamins
54
Conservative kidney management
Supportive care
- priority for symptomatic management
- holistic multi-professional approach
- anticipatory care planning
55
Renal Transplant
Places in iliac fossa and anastomosed to iliac vessels, normal usually remain in situ (indications for nephrectomy include size and infection)
56
Immunosuppressive agents
```
Corticosteroids
Calcineurin inhibitors (cyclosporine)
Anti-proliferatives
mTOR inhibitors
Costimulatory signal blockers
Depleting agents
```
57
Immunosuppression protocols
Induction; basiliximab
Maintenance; tacrolimus + mycophenolate + steroids
Steroid free is possible
Others CNI-free using belatacept
58
Acute kidney rejection
T cell mediated
Banff I; Tubulointerstitial
Banff II; Arteritis/endothelialitis
Banff III; arterial fibrinoid necrosis
Antibody mediated;
Banff I; ATN-like
Banff II; capillaried and/or glomerular inflammation
Banff III; arterial inflammation
59
Transplant-related infection
Cytomegalovirus most important
~8% transplant recipients, despite prophylaxis
High mortality and morbidity if untreated
Recipient affected via;
- transmission from donor tissue
- reactivation of latent virus
60
Acute Kidney Injury
Increase in serum creatinine by >26.5micromol/l within 48hrs or to 1.5x baseline or Urine vol <0.5ml/kg/hr for 6hrs / <300mls in 12hrs
Dangers
- Acidosis
- Electrolyte imbalance
- Intoxication TOXINS
- Overload
- Uraemic complications
Prevention better than treatment, pre-empt development
RFTs, urine dipstick, FBC, USS, blood gases
61
Medicines to stop on sick days
ACEIs, ARBs, NSAIDs, diuretics, metformin
62
Hyperkalaemia
Stabilise (myocardium)
- calcium gluconate
Shift (K intracellularly)
- salbutamol
- insulin-dextrose
Remove
- diuresis
- dialysis
- anion exchange resins
63
Urothelial tumours
Malignant tumours of lining transitional epithelium (urothelium)
- any point from renal calyces to tip of urethra
Most common site = bladder (90%)
64
Bladder cancer
Most commonly transitional cell carcinoma
Where Schistosomiasis is endemic then SCC is common tumour type
Risk factors;
- TCC - smoking, aromatic amines, non-hereditary genetic abnormalities (e.g. p53 and Rb)
- SCC - chronic cystitis, pelvic radiotherapy
Symptoms
- painless haematuria, occasionally symptoms due to invasion/mets
- recurrent UTI
- storage bladder problems
Investigation;
- Urine culture
- cytourethroscopy
- UT imaging; US
- urine cytology
- BP, U&Es
65
Bladder cancer diagnosis, staging and treatment
Diagnosis
- cytoscopy and endoscopic resection (TURBT)
- EUA to assess bladder mass/thickening before and after TURBT
Staging
- cross sectional imaging (CT/MRI)
- bone scan if symptomatic
- CTU for upper tract TCC
Treatment
- endoscopic or radical
66
Grades of TCC
G1; well diff (commonly non-invasive)
G2; mod diff (often non-invasive)
G3; poorly diff (often invasive)
Carcinoma in situ (CIS) - non-muscle invasive but V aggressive (different treatment)
67
Low grade non-muscle invasive bladder cancer treatment
Endoscopic resection followed by single chemotherapy within 24hrs
Prolonged endoscopic follow up for mod grade tumours
Consider prolonged course of intravesical chemo for repeated recurrences
68
High grade non-muscle invasive bladder cancer treatment
V aggressive; 50-80% risk progression to muscle invasive stage
Endoscopic redection alone not sufficient
CIS considerintravesical BCG therapy
Patients refractory to BCG need radical surgery
69
Muscle invasive bladder cancer treatment
Neoadjuvant chemo for local and systemic control followed by either
- radicao radiotherapy and/or
- radical cystoprostatectomy or anterior pelvic exenteration with urethrectomy
- extended lymphadenectomy
Radical surgery combined with incontinent urinary diversion
70
Bladder cancer prognosis
Dependent on
- stage
- grade
- size
- multifocality
- presence of concurrent CIS
- recurrent at 3months
Non-invasive, low grade bladder TCC; 90% 5yr survival
Invasive, high-grade bladder TCC; 50% 5yr survival
71
Upper tract TCC
Main symptoms
- frank haematuria
- unilateral ureteric obstruction
- flank/loin pain
- symptoms of nodal or met disease
Investigation
- CT-IVU or IVU
- urine cytology
- ureteroscopy and biopsy
Most treated by nephro-ureterectomy, but if unable then endoscopic treatment
In all cases high risk of synchronous and metachronous bladder TCC
72
Renal Tumours
Benign; oncocytoma, angiomyolipoma
Malignant;
- renal adenocarcinoma; commonest adult renal malignancy, most arise from proximal tubules
73
Renal adenocarcinoma
Risk factors
- FH
- smoking
- anti-hypertensive meds
- obestiy
- end stage renal failure
- acquired renal cystic disease
Asymptomatic 50%, flank pain, mass, haematuria 10%, paraneoplastic syndrome 30%
CT scan abdo/chest, provides radiological diagnosis and complete TNM, bloods, US optional
Treatment
- surgical; laparoscopic radical nephrectomy
- curative if
74
TNM staging renal cancer
T1; tumour <7cm within renal capsule
T2; tumour >7cm within renal capsule
T3; local extension outside capsule
- a into adrenal or peri-renal fat
- b into renal vein or IVC below diaphragm
- c into IVC above diaphragm
T4; invades beyond Gerota's fascia
75
Renal adenocarcinoma spread
Direct, venous invasion, Haematogenous, lymphatic
76
Renal adenocarcinoma prognosis 5yr
```
T1 95%
T2 90%
T3 60%
T4 20%
N1 or N2 20%
M1 median survival 12-18 months
```
77
Indications for renal imaging
```
Renal colic and renal stone disease
Haematuria
Suspected renal mass
UTIs
Hypertension
```
78
Renal imaging techniques
```
Plain film
Contrast studies - IVU, pyelography, cystography
US +/- contrast
CT and CTU
MR and MRU
Isotope scans
PET-CT
```
79
CT in renal imaging
Currently modality of choice for renal stones, staging renal tumours, investigation of haematuria
Disadvantages
- radiation dose
- cost
- contrast resolution less than MR
- contrast reaction and nephrotoxicity
80
Isotope scanning
DMSA
- look for renal scanning
MAG3
- assess renal function and drainage
Bone scan
- met disease eg. prostate cancer
81
Urolithiasis
Formation of stones in bladder or UT
Renal pain, ureteric colic (radiating to groin), dysuria, haematuria, testicular or vulval pain, urinary infection, loin tenderness, pyrexia
Bloods; FBC, U&E, creatinine, calcium, albumin, urate, parathormone, urine analysis and culture, 24hr urine collections
KUB Ultrasound, IVU, CT KUB
First line now commonly ESWL (breaks up stones) but not for stones >2cm
82
Stone types and incidence
```
Calcium oxalate - 45%
Calcium oxalate + phosphate - 25%
Triple phosphate - 20%
Calcium phosphate - 3%
Uric acid - 5%
Cystine - 3%
```
83
Indications for surgical treatment of stones
```
Obstruction
Recurrent gross haematuria
Recurrent pain and infection
Progressive loss of kidney function
Patient occupation
```
84
Bladder stones
Suprapubic/groin/penile pain
Dysuria, frequency, haematuria
Urinary infection
Sudden interruption urinary stream
Most treated endoscopically, larger stones can be treated by open excision
85
CKD Classification
Stage 1 = Normal or High GFR >90
Stage 2 = mild reduction GFR 60-89
Stage 3 = moderately impaired GFR 30-59
Stage 4 = severely impaired GFR 12-29
Stage 5 = Advanced or Dialysis <15
86
Wegener's Granulomatosis
Granulomatous inflammation in resp tract
Focal necrotising GN with crescents
Slightly more common in males
Affects whole body
- URT, LRT, heart (pericarditis)
87
Vasculitis
Diagnosis
- Blood in urine
- raised urea/creatinine
- raised alk phos, CRP, low albumin
- anaemia, thrombocytosis, leukocytosis
- hyperglobulinaemia, positive ANCA
Renal biopsy
88
ANCA in disease diagnosis
90% C-ANCA Wegener's granulomatosis
Usually P-ANCA microscopic polyarteritis
ANCA can be false positive; importance of renal biopsy
89
Infective endocarditis
Result of bacterial (or fungal) infection on cardiac valves
Typical infections
- Staph aureus
- Viridans strep
- enterococci
Leads to GN and small vessel vasculitis
Renal involvement
- abnormal urea/creatinine
- haematuria, red cell casts
- reduced complement levels
90
Multiple Myeloma
Monoclonal ploriferation plasma cells producing an excess of Igs and light chains
Clinical Features
- markedly elevated ESR
- anaemia
- weight loss
- fractures
- infections
- back pain/cord compression
Diagnosed by
- bone marrow aspirate
- BJP
- skeletal survey
91
Prostate cancer
Diagnostic triad of PSA, DRE and TRUS guided prostate biopsy
Weak stream, hesitancy, sensation incomplete emptying, frequency, urgency, urge incontinence, UTI
92
Normal PSA range
0-4ug/mL, age-related
<50yrs 2.5 upper limit
50-60yrs 3.5
60-70yrs 4.5
>70 6.5
If repeat PSA needed, check in at least 3weeks
93
Gleason grading
For prostate biopsies
Addition of most common and second-most common cell types together
```
ISUP GRADE GROUPING
Grade 1; 3 + 3 = 6
Grade 2; 3 + 4 = 7
Grade 3; 4 + 3 = 7
Grade 4; 8
Grade 5; 9 and 10
```
94
Low risk, localised prostate cancer
Treatments
- Surgery
- active surveillance
- EBRT
- brachytheraoy
- focal ablative therapy
Good prognosis
95
Intermediate risk, localised prostate cancer
Surgery, EBRT, brachytherapy +/- HT
Active surveillance
HT 2-3yrs
96
High risk, localised prostate cancer
EBRT and HT
Surgery and adjuvant EBRT and HT
HT 2-3yrs
97
testicular cancer
PC; usually painless lump, may be tender, inflamed, swelling, symtpoms/signs from nodal/distant mets
One of the commonest cancers in young men, peak incidence 3rd decade
Unknown aetiology but testicular germ cell neoplasia in-situ is a precursor
98
Tumour markers in testicular cancer
AFP - alpha fetoprotein (teratoma)
BHGG - human chorionic gonadotropin (seminoma)
LDH - lactate dehydrogenase (non-specific)
99
Lump in testis
Cancer until proven otherwise
Differentials; infection, epididymal cyst, missed testicular torsion
MSSU, testicular US and CXR, tumour markers
Radical orchidectomy essential, occasionally need biopsy normal contralat if high risk for tumour
Further treatment dependent on type, stage and grade
100
testicular cancer pathology
Seminoma; mainly 30-40yos
Non-seminomatous; mainly 20-30yos
101
Staging v Grading
Grading assesses aggressiveness i.e. high grade = poorly differentiated
Staging assesses spread
102
Testicular cancer prognosis
Good if treated
Stage 1 5yr = 99%
Stage 2/3 5yr = 96%
Stage 4 5yr = 73%
103
Transplant organ screening
Haematology
- cross match, FBC, clotting
Tissue typing
Us&Es, LFTs, amylase, phosphate
Virology
- HIV, HTLV, HepB, HepC, CMV, tocoplasmosis, syphillis
- EBV (paeds specifically)
- vCJD (tissues only)
104
UTI types
Kidney; acute/chronic pyelonephritis
Bladder; cystitis
Urethra; urethritis
Prostate; prostatitis
Epididymis/testis; epididymo-orchitis
105
UTI predisposition
```
Immunosuppression
Steroids
Malnutrition
Diabetes
Female
Sex and poor voiding habits
Congen abnorms
Stasis of urine
foreign bodies i.e. catheters
Oestrogen deficiency
Fistula between bladder and bowel
```
106
UTI Pathogenesis
Usually bowel organisms
- E coli, proteus, klebsiella, enterococcus
Transfer
- transurethral route
- bloodstream
- lymphatics
107
UTI Clinical features
Children; diarrhoea, crying, fever, nausea, vomiting, not eating
Adults; flank pain, dysuria, cloudy offensive urine, urgency, chills, strangury, confusion (v old people)
108
Clinical features of acute pyelonephritis
```
Pyrexia
Poor localisation
Loin tenderness
Signs of dehydration
Turbid urine
```
109
UTI investigations
MSSU
Urinalysis
- blood, leukocytes, protein, nitrites
Microbiology
- microscopy, gram staining
- bacteruria >10 to 5 CFU/ml
- culture and sensitivity
110
UTI treatment
Fluids
ABs; amoxicillin, cephalosporin, trimethoprim
SEVERE; IV ABs
111
Reflux nephropathy
```
UTIs in children
Damage caused by reflux and infection
Micturating cystogram (radionuclide 99Tc techniques)
Assess progression US scan and biochem
Surgery
```
112
Bacteriuria
>10 to power 5
Depends on clinical symptoms
Can be asymptomatic
113
Chronic pyelonephritis
```
Radiological diagnosis
scarring and clubbing
Hypertension/CRF
?reflux
15% progress to renal failure
```
114
Advice for recurrent UTI in young women
Fluid intake 2L/day
void every 2-3hrs during the day
Void before bed and before&after sex
115
Hyperkalaemia treatment
If severe enough to cause ECG changes then must first protect heart; calcium gluconate
Then serum concentration must be diluted; IV fluids, insulin
Overall body potassium can be considered; calcium resonium
Treatment underlying abnormality essential; i.e. AKI
116
Most common and rare type of stones in adults
Calcium oxalate
Rare = cystine stones
