Renal + Urology Flashcards

(80 cards)

1
Q

Define AKI?

A

Acute decline in GFR from baseline w/wo oliguria/anuria due to impaired perfusion, intrinsic renal disease, obstruction or nephrotoxin exposure.

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2
Q

What does an AKI cause?

A

Acid-base disturbances
Reduced clearance
Metabolic disturbances
Impaired volume regulation

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3
Q

List pre-renal causes of AKI?

A

Sepsis
HF
Hypovolaemia
Overdiuresis

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4
Q

List some intrinsic renal causes of AKIs?

A

Interstitial nephritis, glomerulonephritis, ATN (most common 3)

also, HUS, thrombosis, TTP

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5
Q

List post renal causes?

A

Mechanical outflow obstruction: tumour, lymphoma, prostate hyperplasia, strictures, renal calculi

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6
Q

What are the signs/symptoms of AKI?

A
Oliguria, anuria, dizziness,
Orthopnoea, nocturnal dyspnoea 
Hypotension, orthostatic hypotension 
Pulmonary oedema, peripheral oedema 
Vomiting, tachycardia 

Can be fever/flank pain/seizures/haematuria/arthralgias

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7
Q

How is AKI classified?

A

Creatinine >26.5mmol 48hrs
Increase creatinine >1.5x norm
Urine output <0.5ml/kg/min

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8
Q

Investigations for AKI

A

U+E - Met acidosis - inc urea, creatinine and k+
Urea:creatinine = 20:1 = pre renal cause
Catheter trial and urine output monitoring. If large UO initially -> obstruction
Urinalysis - WBCs, RBCs, Protein
Renal USS - ob/
Urine culture
FBC
Urine osmolarity - high if prerenal (concentrated)

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9
Q

How is pre renal AKI rx?

A

Volume expansion +/- RBC transfusion +/- vasopressin

Possible dialysis

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10
Q

How is obst AKI caused?

A

Catheterisation (all patients unless ruled out)

Stent/lithotripsy/TURP/percutaneous nephrostomy

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11
Q

What is BPH?

A

A benign increase in prostatic tissue resulting in lower urinary tract symptoms as a result of decreased lumen size and increased SM tone mediated by a adrenergic receptors.

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12
Q

What are the RFs for BPH?

A

Age >50, non asian, FHx, Male pattern baldness, metabolic syndrome, smoking

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13
Q

What are the signs and symptoms of BPH?

A

Storage - frequency, urgency, nocturia
Voiding - dribble, slow flow, straining, hesitancy
Fever + dysuria = complicated by UTI
Urinary retention = rare

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14
Q

What are the investigations for BPH?

A

PSA >4(age matched) suggests prostatitis / cancer
Urine flowmetry <20mls second = suggestive
Urinalysis - concomitant infection
Cystoscopy/uss - visualisation
DRE - enlarged prostate
Volume charting - differentiates from irritable bladder

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15
Q

What score is used to decide BPH therapy and quantify the burden of disease?

A

IPSS

International prostate symptom scoring

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16
Q

What are the Rx steps?

A
  1. A blocker - tamsulosin 0.4mg / alfulosin 10mg OD. Decrease SM tone
  2. Phosphodiesterase 5 inhibitor - tadalafil 20mg/sildenafil 25mg - inc LUT symptoms
  3. NSAIDS (increase flow and symptoms celecoxib 100mg OD
  4. 5a reductase inhibitors - Finasteride 5mg / Dutasteride 0.5mg
  5. SURGERY
    - TURP = most widely available and effective. More bloodloss though.
    - Alternatives - laser therapy/photoselective vapourisation/needle ablation

PROSTATE >80g = open prostectomy / open laser

Reassess Pt

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17
Q

Define CKD.

A

CKD is defined as a GFR <60mls/min for >3months duration

10% of adult population

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18
Q

What are the main RFs for CKD?

A

Age >50, DM, HTN, obesity, male, smoking, a/i causes, long term NSAID use

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19
Q

What are the S+S of CKD?

A

Oedema, dyspnoea/orthopnoea, Fatigue, N+V, pruritus, anorexia, arthralgia,
Haematuria (cola coloured), proteinuria (foamy coloured)
Seizures

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20
Q

What investigations confirm CKD?

A
GFR estimation <60mls/min
Creatinine - MEN >97mmol, WOMEN >105mmol 
Urinalysis - haematuria/proteinuria 
Renal USS - if hydro/intrinsic disease 
CT/MRI - stones lesions cysts 
Microalbuminuria - 30-300mg/day
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21
Q

What is acute epididymitis/orchitis?

A

Infection of the epididymis with associated scrotal swelling, erythema, and LUT symptoms of <6weeks duration.
‘Orchitis’ added if concomitant swollen testicles.

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22
Q

What are the RFs for acute ep/orch?

A

<35 - think STI
>35 - think outflow problem

Sexual behaviour, BPH, immunosuppression, DM, amiodarone, urinary procedures (iatrogenic)

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23
Q

What are the signs and symptoms of acute ep/orch?

A

Swelling -> <6weeks duration, erythematous, diffusely enlarged rather than nodular
Unilateral pain - gradual onset
Swelling may oscillate during day-evening
Painful/frequent micturition
Purulent discharge
Pyrexia

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24
Q

What investigations confirm acute ep/orch?

A
Urine dip - +ve leucocytes 
Urine microscopy - >10 WBCs per unit at full power 
Urine culture
Purulent fluid culture
NAAT for gonorrhoea/chlamidya 
TB AFB testing if high suspicion
Duplex USS - enlarged epididymis.
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25
What are the Rxs for acute ep/orchitis?
Pain - ibuprofen/naproxen/paracetamol STD related - ceftriaxome IM 250mg + doxycycline BD 100mg Enteric - ofloxacin / levofloxacin 300/500mg OD Amiodarone - stop amiodarone TB - refer to specialist
26
What is testicular torsion?
Twisting of the testicle on the spermatic cord which leads to constriction of the vascular supply -> ensuing ischaemia and necrosis
27
What are the RFs for torsion?
Bellclapper deformity, age <25, neonate, trauma, exercise, cold weather
28
What are the S+S of torsion?
ACUTE onset severe pain, N+V, scrotal oedema and erythema, reactive hydrocele, high riding testicle ABSENT CREMASTERIC REFLEX sign No relief on elevation, abdo pain Fever = possible, dysuria = possible
29
What investigations confirm torsion?
EMERGENCY - "time is testicle" Colour flow doppler USS - absent supply Greyscale USS - see whirlpool sign Urinary WCC - N , FBC - N
30
What is there Rx for torsion in adults?
5-20mg morphine + 4mg ondansetron Urgent scrotal exploration and detorsion +/- clips which can prevent recurrence If loss of testicle then offer prosthesis
31
What is polycystic kidney disease?
Heterogenous group of diseases character by renal cysts and systemic and extrarenal manifestations.
32
What are the two mutations that cause PKD?
PKD1 85%, PKD2 15%
33
What is the pathophysiology of PKD?
Gradual growth of cysts until compression of ordinary renal vasculature and architecture Increases kidney size, interstitial fibrosis and atrophy. Results in progressive renal impairment until CKD
34
What are the signs a symptoms?
Cysts on imaging -> HHHH - HTN, haematuria, headaches, hepatomegaly. Abdo/flank pain Dysuria/fever/urgency/suprapubic pain if UTI concom Palpable cysts on kidneys Abdo hernias Chest pain - uncommon
35
What investigations are undertaken for PKD?
Renal USS - <30 - 2 cysts total, 30-59 - two bilaterally, >60 - 4 bilaterally If inconclusive - CT abdo Urinalysis - haematuria/proteinuria/albumin Genetic testing - PKD1/2 Lipids - low HDL, H LDL associated to poorer prognosis U+Es - N / H Other tests - CT for risk of CVA, KUB if suspect stones as alternate diagnosis, echo if comorbid valvular disease.
36
Define RAS
Narrowing of the lumen of the renal arteries. Angiographically significant if >50% decrease
37
What percentage is atherosclerotic vs fibrodysplasic?
90:10
38
What are the RFs for atherosclerotic RAS?
DM, HTN, smoking
39
RFs for fibrodysplasic RAS?
Smoking, medial fibroplasia/adventital
40
What are the S+S of RAS?
``` RF presence Onset HTN in >55yo /// Accelerated HTN Abdominal bruit Hx CAD, PVD, unexplained dec in renal function Refractory angina, hx hypokalaemia ```
41
What investigations confirm RAS?
Estimated GFR - N/H K+ - N/L Urinalysis - No protein/haematuria/WBCs/Sediment Renal angiography (CT/MRI) - Dec in lumen size >50% Aldosterone:renin ratio - < 20 = confirms RAS rather than CONNS (in which aldosterone is significantly higher)
42
What is the pathophysiology with regards to hypokalaemia in RAS?
When stenosis reaches >50%, compensatory mechanisms begin to fail. There is a decrease in endothelin secretion, and relative increases in renin and ang II due to underperfusion of the kidneys. Results in increased Na+ absorption and dec K+ -> hypokalaemia and an increase in BP
43
What is a UTI?
Infection of the urinary tract and subsequent inflammation of the epithelium.
44
What are the most common causative organisms?
E. coli - most common G -ve - klebsiella, proteus G+ve - Enterococcus/staphylococcus (Less common that g-ve) If catheter - candida/staph A - biofilm formation
45
What are the RFs for UTIs?
BPH, stones, recent surgery, recent hospitalisation, age >50, Hx UTI, catheterisation Unprotected sex
46
What are the S+S of UTI?
Frequency, dysuria, urgency, nocturia, terminal dribbling, large prostate, suprapubic pain, discharge Fever Rectal pain/ perianal pain / tender bladder/prostate
47
What are the investigations that confirm a UTI?
``` Urine DIP - +ve for WCC/nitrites Urine microscopy - WC/bacteria Urine culture - culture of organism Culture discharge CT/KUB/USS - if suspect concomitant blockage ```
48
List Rx for UTI (3 step)
1. Levi/ciprofloxacin 500mg OD/BD 7-14 2. Trimethoprim 500mg BD 7-14 3. Amoxicillin / clavulanate 500mg BD 7-14
49
What is nephrotic syndrome?
Presence of proteinuria >3.5g/24hrs Hypoalbuminaemia Peripheral oedema
50
What is the main cause of nephrotic syndrome in adults?
Diabetic nephropathy, Focal Segmetal GlomeruloSclerosis FSGS
51
Name a common cause of nephrotic syndrome in children?
Hodgkin
52
What are the S+S of nephrotic syndrome?
Peripheral oedema AKI If progresses haematuria Muerkes lines xanthalesmata (from hyperlipid) Facial oedema
53
What investigations confirm nephrotic syndrome?
Proteinuria >3.5g day Low serum albumin Cellular casts in urine microscopy SUGGEST ALTERNATE DIAGNOSIS BIOPSY = definitive diagnosis - not performed with cysts/hydronephrosis, infection
54
DEFINE Nephrolithiasis
Presence of crystalline stones in the urinary system
55
What are they usually formed from?
Oxalate, calcium, sodium and urticaria acid | Low ph and urine volume contribute as well as decreased magnesium and citrate -> inhibit stone formation
56
What are the RFs for renal stone formation?
Male Dec water, High salt, High protein, obesity, warm climate
57
What are the investigations that confirm kid stones?
Non contrast CT - shows all stones aside from rare indinavir stones Urinalysis - N unless infection. May be small haematuria Preg test - rule out ectopic
58
What are the signs and symptoms?
Acute severe flank pain May radiate to groin N+V Haematuria, inc urinary free, testicular pain, UNCOM - Tachycardia, fever, groin pain, hypotension, costovertabral angle tenderness
59
How are stones treated?
Tamsulosin0.4/alfulosin10mg - a adrenergic blockers - dec sm tone If fails / dependent on size: cystoscopy + laser therapy/shock wave lithotripsy
60
Ongoing rx for recurrent stones?
hyper URIC/calcuria/citrauria/cysteinuria = alkalinisation of urine with potassium citrate Hyper OXalauria = calcium citrate (ox chelator) + 2l urine output Dec dietary protein, salt and oxalate Inc citrus fruits
61
Define amyloidosis
An amyloid tissue deposition disease that may have a primary cause or be secondary to other diseases. Usually presents with unexplained weight loss, fatigue, and oedema resistant to diuretic therapy. Immunofixation of the serum and urine confirms the presence of monoclonal light chains in primary systemic amyloidosis. Biopsy verification of amyloid deposits is essential. Treatment includes appropriate management of resulting clinical syndromes, such as nephrotic syndrome, neuropathy, cardiomyopathy, and conduction disorders. Definitive treatment of primary systemic amyloidosis (AL amyloidosis) includes myeloablative high-dose chemotherapy, with stem cell reconstitution in selected patients, or chemotherapy. Any histological tissue specimen that binds the cotton wool dye, Congo red, and demonstrates green birefringence when viewed under polarised light is, by definition, an amyloid deposit. The patient with this deposit has amyloidosis. Deposits of amyloid may be localised in tissue or part of a systemic process. Progressive deposition of amyloid is disruptive to tissue and organ function and manifests its clinical sequelae by the dysfunction of those organs in which it deposits.
62
Epidemiology of amyloidosis
In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year There are no ethnicity studies specifically for amyloidosis MM + MGUS = B>W>A
63
Aetiology of amyloidosis
Primary amyloidosis (also known as immunoglobulin light chain amyloidosis, or AL): All are associated with clonal plasma cell dyscrasia, although in most instances this is of insufficient degree to qualify as multiple myeloma. Non-familial secondary amyloidosis (AA): Inflammatory polyarthropathies account for 60% of cases. Conditions include rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, and ankylosing spondylitis. Chronic infections, such as bronchiectasis, subcutaneous injection of illicit drugs, decubitus ulcers, chronic UTIs, and osteomyelitis can result in secondary amyloidosis Inflammatory bowel disease, specifically Crohn's disease, can result in secondary amyloidosis Castleman's disease is a lymphoproliferative disorder where the plasma cell variant can cause secondary amyloidosis. Also inherited forms
64
RFs for amyloidosis
``` STRONG MGUS Inflammatory polyarthropathy Chronic infections IBD Familial periodic syndromes ``` WEAK Castleman's disease
65
Sx of amyloidosis
COMMON RFs JVP Lower extremity oedema UNCOMMON Periorbital purpura Macroglossia OTHER COMMON Fatigue WL Dyspneoa ``` OTHER UNCOMMON Parasthesia Claudication Nausea Cramps Alternating bowel habit Orthostatic hypotension Submandibular salivary gland enlargement Hepatomegaly Should pad sign Weakness Sensory neuropathy Tinels Sx Phalens manoeuvre ```
66
Rx of amyloidosis
1) Stem cell transplantation = myoablative chemo -> SC reconstitution OR if not SCT candidate = Chemotherapy -> = Bortezomib
67
Prognosis / complications amyloidosis
The prognosis for patients with primary (i.e., immunoglobulin light chain) amyloidosis following treatment is dependent on the impact of the therapy in suppressing light chain synthesis. In patients who achieve a complete response to therapy, the 7-year survival approaches 80%. For patients who achieve a 50% reduction in therapy at 7 years, survival is 57%. Outcome is also determined by the severity of cardiac involvement. ``` COMPLICATIONS Rx related Chronic RF Progressive cardiomyopathy Conduction abnormalities Painful peripheral neuropathy Obstruction (macroglossia) Factor X deficiency Splenic rupture ```
68
Ix for amyloidosis
Detection of monoclonal protein in: Serum/urine Immunoglobulin free light chain assay - abnormal kappa to lambda ratio BM biopsy - clonal plasma cells Immunohistological studies of amyloid deposits - These can be attempted to distinguish the various forms of systemic amyloidosis. Beta-2-microglobulin - Predictive of survival in patients with amyloidosis.
69
Rx of CKD
STAGES 1-2 NO URAEMIA ACE or ARB + Statin + HTN Rx STAGES 3-4 NO URAEMIA SAME BUT Education re Renal replacement therapy IF NEEDED: Erythropoeitin stimulating agents - epoetin alfa / darbepoetin alfa Iron Vit D (ergocalciferol) Na Bicarbonate Stage 5 OR WITH URAEMIA DIALYSIS Continuous cycling peritoneal dialysis is done with a machine at night on a daily basis. Continuous ambulatory peritoneal dialysis is done on a daily basis. Patients manually exchange the peritoneal fluid. Haemodialysis is prescribed 3 times a week for approximately 4 hours each session. Transplant For patients with stage 5 CKD on dialysis, calcium, phosphorus, and intact PTH levels should be managed with phosphate binding agents, calcimimetics, active vitamin D analogues, or a combination of these based on serial laboratory assessments.
70
Prognosis CKD
Chronic kidney disease (CKD) is progressive and will eventually lead to end-stage renal disease (ESRD) and the need for renal replacement therapy (i.e., dialysis, transplant). CKD is a strong cardiovascular risk factor, and the majority of patients with CKD will die prior to reaching ESRD. As kidney function declines, complications such as anaemia and hyperparathyroidism develop that may contribute to worsening cardiovascular disease and renal osteodystrophy, respectively. There is no cure for CKD.
71
Complications of CKD
``` Anaemia Renal osteodystrophy CV disease Protein malnutrition Metabolic acidosis Hyperkalaemia Pulmonary oedema ```
72
Define hydronephrosis / obstructive uropathy
Obstructive uropathy is blockage of urinary flow, which can affect one or both kidneys depending on the level of obstruction. If only one kidney is affected, urinary output may be unchanged and serum creatinine can be normal. When kidney function is affected, this is termed obstructive nephropathy. Hydronephrosis refers to dilation of the renal pelvis and can be present with or without obstruction. A variety of conditions may cause obstructive uropathy. _______________ Blockage of urinary flow, which can occur at any level in the urinary tract. May affect one or both kidneys, depending on the level of obstruction. A number of underlying conditions can result in obstructive uropathy, most commonly urolithiasis and benign prostatic hyperplasia. Initial treatment is directed at relieving pressure on the kidneys to prevent obstructive nephropathy and irreversible renal damage. Prompt relief of obstruction usually leads to preservation of kidney function. This may involve a urethral catheter, ureteric stent, or nephrostomy tube, depending on the level and cause of obstruction. Subsequent treatment is targeted towards the underlying cause. Infection within an obstructed system must be treated promptly.
73
Epidemiology of hydronephrosis / obstructive uropathy
Unilateral obstructive uropathy is most commonly due to ureteral stones. Stones are more common in hot and dry climates and obesity appears to increase the incidence. The highest incidence is seen in adults aged 30 to 50. Prevalence of ureteric stones is estimated to be 10% to 15% Benign prostatic hyperplasia (BPH) is a common cause of acute and chronic bilateral obstruction. No men under 30 years have pathological evidence of hyperplasia of the prostate but nearly 100% of men in their 80s show evidence of the disease. Women with bilateral obstruction will most commonly be diagnosed with an anatomical problem such as a cystocele or a physiological problem such as neurogenic bladder. Cancer involving the pelvic organs or retroperitoneal space may cause unilateral or bilateral obstruction.
74
Aetiology of hydronephrosis / obstructive uropathy
Common causes include renal stones, benign prostatic hyperplasia, prostate cancer, and bladder tumours. Other less common causes include ureteropelvic junction obstruction, cystocele, herniation of the bladder into the inguinal canal, iatrogenic injury during gynaecological surgery, and pelvic malignancy.
75
RFs for hydronephrosis / obstructive uropathy
``` STRONG BPH Constipation Medication - anticholinergic agents, narcotic analgesia, alpha receptor agonists Stones SC injury MS Malignancy Posterior urethral valves Mental stenosis ``` ``` WEAK Pregnancy Haematuria Bladder hernia Cystocele Iatrogenic Urethral instumentation Retroperitoneal fibrosis ```
76
Sx of hydronephrosis / obstructive uropathy
``` COMMON Flank pain Fever LUTS Distended abdo Palpable bladder Inability to urinate Enlarged / nodular prostate Costovertebral angle tenderness ``` UNCOMMON Neurological disease OTHER COMMON Haematuria Increasing age Meatal narrowing ``` OTHER UNCOMMON Pelvic/abdominal malignancy Previous urethral instrumentation UTI as child Pelvic mass WL / LNs Recurrent UTIs Urinary incontinence ```
77
Ix for hydronephrosis / obstructive uropathy
``` 1st: Urine dipstick Renal US RFTs FBC CT pyelogram (non-contrast CT) ``` ``` CONSIDER PSA CT abdo pelvis CEA/CA125 Voiding cysturthrogram Bladder US MRI ```
78
Rx of hydronephrosis / obstructive uropathy
Anaglesia + rehydration Nephrostomy or ureteric stent ABx if septic IF STONES Alpha blockers - tamsulosin / alfuzosin IF BPH ALSO: 5a reductase inhibitors: Finasteride 5mg
79
Prognosis/complications of hydronephrosis / obstructive uropathy
Obstructive uropathy can result in permanent renal damage, but the majority of patients recover completely if the obstruction is relieved promptly. Although benign prostatic hyperplasia (BPH) is a common cause of obstructive uropathy, most patients with BPH do not go on to develop obstruction. COMPLICATIONS ``` Urethral trauma Ureteric stent displacement / occlusion Post-obstructive diuresis Severe sepsis/shock Renal failure - Unless obstruction is relieved, back pressure on the kidney can result in tubulo-interstitial fibrosis, tubular atrophy, and interstitial inflammation resulting in renal failure. ```
80
Define Glomerulonephritis
Glomerulonephritis (GN) denotes glomerular injury and applies to a group of diseases that are generally, but not always, characterised by inflammatory changes in the glomerular capillaries and the glomerular basement membrane (GBM). The injury can involve a part or all of the glomeruli or the glomerular tuft. The inflammatory changes are mostly immune mediated. Diseases include membranous GN, minimal change disease, focal and segmental glomerulosclerosis, immunoglobulin A nephropathy, forms of rapidly progressive GN (vasculitis and anti-GBM disease), and systemic lupus erythematosus nephritis as the more common forms; and glomerular damage in other systemic diseases such as diabetes, amyloidosis, myeloma, and a variety of infections.