Genitourinary Flashcards
1
Q
What are the names for kidney stones?
A
Nephrolithiasis, renal calculi, urolithiasis.
2
Q
What are the peak ages for kidney stones? Do they occur in children?
A
Peak age 20-40y.
Uncommon in children.
3
Q
What are kidney stones?
A
Very common problem where stones that form in the collecting duct of the kidney and are deposited anywhere (renal pelvis, ureters, urethra).
4
Q
What are the three common obstcrution sites for kidney stones?
A
PUJ - Pelvic-urethral junction.
VUJ - Vesico-urethral junction.
Pelvic brim - where ureters cross iliac vessel.
5
Q
What are seven risk factors for kidney stones?
A
Chronic dehydration, high salt diet, obesity.
Primary kidney disease, hyperparathyroidism.
UTIs, history of kidney stones.
6
Q
What are the types of kidney stones?
A
-Calcium stones are most common - calcium oxalate and calcium phosphate.
-Uric acid stones (not visible on XRAY).
-Struvite - produced by bacteria so associated with infection.
-Cystine.
7
Q
Describe the pathophysiology of kidney stones.
A
Excess solute in collecting duct which saturated urine which favours crystallisation.
-Stones then cause outflow obstruction, causing dilation and obstruction of renal pelvis.
8
Q
How do kidney stones present?
A
Colicky unilateral loin to groin pain that comes in waves.
-Restlessness due to pain, N+V.
-Haematuria, dysuria and oliguria.
9
Q
What are the first line and gold standard investigation for kidney stones?
A
1st line - XRAY.
GS - Non-contrast CT scan.
10
Q
What are the investigations for kidney stones in children and pregnant women?
A
USS - less radiation.
11
Q
What other investigations are used in the investigations for kidney stones?
A
Urinalysis - UTI.
Bloods.
12
Q
How are kidney stone symptoms managed?
A
Hydration and analgesia (NSAIDs).
13
Q
How are kidney stones managed?
A
If they’re small (<5mm) they can pass spontaneously.
If larger, elective surgery is done:
-ESWL (shockwave lithotripsy) - shock waves to break apart stones.
-PCNL (percutaneous nephrolithotomy).
14
Q
What are the lifestyle changes for kidney stones?
A
Healthier diet, exercise, less sodium and less protein.
15
Q
What are three complications of kidney stones?
A
Obstruction which can lead to AKI.
Infection leading to pyelonephritis.
Recurrence.
16
Q
What is obstructive uropathy?
A
The blockage of urinary flow which affects either one or both kidneys.
17
Q
What is obstructive nephropathy?
A
When the kidney function is affected by the obstruction.
18
Q
What are the most common causes of obstructive uropathy?
A
Stones and BPH.
19
Q
What is acute kidney injury?
A
Abrupt decline in kidney function characterised by increased serum creatinine and decreased urine output.
20
Q
What does acute kidney injury result in?
A
Electrolyte imbalances and azotaemia (build up of waste products).
21
Q
What are the three different classification criteria of acute kidney injury?
A
- Rise in serum creatinine >26 micromol/L within 48h.
- 1.5x baseline serum creatinine in 7 days.
- Urine output <0.5ml/kg/hr for >6h.
22
Q
What are the four normal functions of the kidney?
A
Water/hormone homeostasis.
Removal of waste/toxins.
RBC production by EPO.
Activates vitamin D.
23
Q
What are 8 risk factors for acute kidney injury?
A
CKD, hypertension, HF, diabetes, liver disease, old age, nephrotoxic drugs, cancer.
24
Q
Give some examples of nephrotoxic drugs.
A
DAMN - Diuretics, ACE-i/ARBs, metformin, NSAIDs.
-Antidepressants, Abx, contrast media.
25
What are the three categories of causes for AKI?
Pre-renal, intra-renal and post-renal.
26
What is the most common cause (classification) of acute kidney injury?
Pre-renal.
27
Explain the pathophysiology of pre-renal AKI.
Due to hypoperfusion due to:
-Dehydration, hypotension, HF, shock, liver disease and bleeding.
28
Explain the pathophysiology of intra-renal AKI.
Due to disease within the kidney itself.
-Acute tubular necrosis (mc), interstitial nephritis, glomerulonephritis.
29
Explain the pathophysiology of post-renal AKI.
Due to obstruction:
-Stones and BPH.
30
How does AKI generally present?
Often asymptomatic until late.
-Oliguria, high creatinine, hyperuraemia (N+V, weakness), hyperkalaemia (arrhythmias, muscle weakness).
31
How does pre-renal AKI usually present?
Hypotension, signs of heart/liver failure.
-D+V, syncope, oedema.
32
How does intra-renal AKI present?
Infection signs and signs of cause (diabetes, glomerulonephritis, acute tubular necrosis).
33
How does post-renal AKI present?
With obstructive uropathy and LUTS.
34
What investigations are used to diagnose AKI?
-Bloods - U+E = eGFR, creatinine, K+, H+.
-Urinalysis - WBCs and nitrites (infection), protein and blood (nephritis), glucose (diabetes).
-USS - Obstruction.
35
How is AKI treated?
Correct the underlying cause:
-Pre-renal - Fluid rehydration.
-Post-renal - Relieve obstruction.
Stop nephrotoxic drugs.
36
How is severe AKI managed?
Dialysis.
37
What are five complications of AKI?
Hyperkalaemia, ESRF, metabolic acidosis, CKD, uraemia.
38
What is chronic kidney disease?
Decreased kidney function for more than 3 months which tends to be progressive and permanent. Characterised by eGFR.
39
What are the three definitions of CKD?
1. eGFR <60ml/min/1.73m2 for more than 3 months.
2. eGFR <90ml/min/1.73m2 with signs of renal damage.
3. Albuminuria >30mg/24h (ACR >3mg/mmol).
40
What are the five risk factors for CKD?
Old age, hypertension, diabetes, smoking, nephrotoxic drugs.
41
What are the most common causes of CKD?
Hypertension and diabetes.
42
What are three other causes of CKD?
Glomerulonephritis, PKD, obstruction.
43
What are the two classification criteria of CKD?
G score based on GFR.
A score based on ACR.
44
Describe the G score classification of CKD.
Based on eGFR:
G1 >90.
G2 - 60-89.
G3a - 45-59.
G3b - 30-44.
G4 - 15-29
G5 <15.
45
Describe the A score in the classification of CKD.
Based on ACR (albumin to creatinine ratio):
A1 - <3mg/mmol.
A2 - 3-30mg/mmol.
A3 - >30mg/mmol.
46
How does CKD usually present? When do symptoms start?
Usually asymptomatic often until ESRF.
Symptoms start due to uraemia.
47
Describe the presentation of CKD.
Fluid retention - oedema.
Oliguria, cramps, peripheral neuropathy, palpitations.
Uraemia effects - pruritus, pallor, nausea, appetite loss.
Anaemia and bone pain.
Hematuria.
48
Which investigations are used to diagnose CKD? Give the results.
Bloods - U+E = eGFR, creatinine, urea, phosphate and potassium. FBC = Anaemia.
Urinalysis - haematuria, proteinuria, glycosuria (if diabetic).
Renal USS.
49
What are the aims of CKD treatment?
-Slow the progression of disease.
-Reduce risk of CVD and complications.
-Treat complications.
50
How is CKD progression slowed?
Control diabetes and hypertension with:
-ACE-i/ARBs, CCBs.
-Metformin, sulphonylureas.
Treat the infection.
51
How is the CVD risk reduced in CKD?
Statins, aspirin, exercise and diet (less phosphate).
52
Why does anaemia occur in CKD? How is it treated?
Kidneys usually produce EPO which stimulates RBC production. CKD causes a drop in EPO so less RBCs.
-Treated with EPO and iron.
53
Why does renal bone disease occur in CKD? How is it treated?
High serum phosphate occurs due to low excretion by the kidney, vitamin D is low as it is activated by the kidney.
-Secondary hyperparathyroidism occurs due to more PTH secreted due to low calcium and high phosphate (increased osteoclast and more bone resorption).
-This leads to osteomalacia, osteosclerosis and osteoporosis.
-Treated with vitamin D and biphosphonates.
54
How is oedema and metabolic acidosis treated in CKD?
Oedema - loop diuretic and fluid restriction.
Metabolic acidosis - sodium bicarbonate.
55
How is ESRF managed in CKD?
RRT - dialysis and kidney transplant.
56
What are five complications of CKD?
Anaemia, osteodystrophy, neuropathy, encephalopathy and CVD.
57
What is a UTI?
An infection anywhere in the urinary tract.
58
What are the locations of UTIs?
Upper (kidney) - pyelonephritis.
Lower (bladder and onward) - cystitis, prostatitis, urethritis, epidydymo-orchitis.
59
How are UTIs caused?
Bacteria enter the urinary tract from the poo.
60
What are the organisms that cause UTIs?
KEEPS:
Klebsiella, E. coli (mc), enterococcus, pseudomonas/proteus, staph saprophyticus/aureus.
61
What is the most common organism that causes UTIs?
E. coli.
62
Why are females much more affected by UTIs?
As the urethra is much shorter and closer to the anus so it is easier for bacteria to colonise.
63
What is the general presentation of UTIs?
Dysuria, suprapubic pain/discomfort, higher frequency, urgency, incontinence, haematuria, foul smelling and cloudy urine.
64
How do UTIs usually present in the elderly?
Confusion.
65
What is the 1st line investigation for UTI? What does it show?
Urine dipstick - leukocytes, nitrites and haematuria.
66
What is the gold standard investigation for UTI? What does it show?
Midstream MC+S to confirm UTI and to identify the causative organism.
67
What is the usual management of UTIs?
Antibiotics:
-Trimethoprim and nitrofurantoin.
-If not appropriate, use amoxicillin or cefalexin.
68
What is pyelonephritis?
Inflammation of the kidney due to bacterial infection.
69
What causes pyelonephritis?
Usually E. coli (can be other KEEPS) that is most commonly acquired by ascending transurethral spread but also can be blood and lymphatics.
70
Who is pyelonephritis most common in?
Females under 35y/o.
71
What are five risk factors for pyelonephritis?
Urine stasis (stones), renal structural abnormalities, catheters, diabetes, female.
72
How does pyelonephritis present?
Triad - loin/back pain, fever, N+V.
-Systemic illness, appetite loss, haematuria, pyruia.
73
How is pyelonephritis diagnosed?
Usual UTI (urinalysis/midstream MC+S).
-USS/CT KUB to exclude kidney stones/abscesses.
74
How is pyelonephritis treated?
Analgesia and paracetamol for symptoms relief.
-Antibiotics: Co-amoxiclav, cefalexin, trimethoprim.
75
What is the sepsis 6?
6 things to do if sepsis is suspected:
-3 tests - blood lactate, cultures and urine output.
-3 treatments - oxygen, broad-spec IV Abx, IV fluids.
76
What is a complication of pyelonephritis?
Chronic pyelonephritis (recurrent episodes of pyelonephritis) which leads to CKD and ESRF.
77
What is cystitis?
Inflammation of the bladder.
78
Who does cystitis occur in?
Children, females, pregnancy, those with catheters.
79
What are three risk factors for cystitis?
Urine stasis, bladder lining damage, catheters.
80
How does cystitis present?
Usual UTI symptoms:
-Suprapubic tenderness/discomfort, increased frequency, urgency, haematuria, incontinence and dysuria.
81
How is cystitis diagnosed?
Urinalysis/midstream MC+S.
-STI testing, cystoscopy for bladder cancer.
-If male, DRE for prostate cancer/BPH.
82
How is cystitis treated?
Antibiotics:
-Trimethoprim and nitrofurantoin.
83
How is cystitis treated in pregnancy?
-Trimethoprim not used in 1st trimester as it inhibits folate synthesis.
-Nitrofurantoin not used in 3rd trimester.
-Use alternative antibiotics - amoxicillin and cefalexin.
84
What is prostatitis?
Inflammation of the prostate that can be acute or chronic.
85
What causes prostatitis?
Unclear cause.
86
How does chronic prostatitis present?
3 months of:
-Pelvic pain, LUTS, sexual dysfunction, pain when defecating, tender/enlarged prostate.
87
How does acute prostatitis present?
The same as chronic prostatitis but with fever, myalgia, nauseam fatigue and even sepsis.
88
What investigations are used to diagnose prostatitis?
Urinalysis, midstream MC+S, NAAT testing to rule out STIs.
-DRE.
89
How is acute and chronic prostatitis treated?
Acute - Antibiotics, analgesia, laxatives.
Chronic - Tamsulosin (relaxes muscle), analgesia, antibiotics, laxatives.
90
What are three complications of acute prostatitis?
Sepsis, prostate abscess, chronic prostatitis.
91
What is urethritis?
Urethral inflammation with or without infection.
92
What is the most common cause of urethritis?
Usually STI - chlamydia.
93
What are the causes of urethritis?
Infective - gonorrhoea and chlamydia (mc).
Non-infective - trauma, stricture, irritation, stones.
94
What are risk factors for urethritis?
Gay sex, anal sex, unprotected sex, lots of sexual partners.
95
How does urethritis present?
Dysuria, urethral discharge (blood/pus), urethral pain, penile discomfort).
96
How is urethritis diagnosed?
NAAT test to detect STI.
Urinalysis and midstream MC+S.
97
How is urethritis treated?
Depends on underlying cause:
-Gonorrhoea - IM ceftriaxone and azithromycin.
-Chlamydia - Azithromycin or doxycycline.
98
What is epididymo-orchitis?
Inflammation of the epididymis, extending to the testes.
99
What causes epididymo-orchitis?
Urethritis (STI, <35y) or cystitis (KEEPS, >35y).
100
How does epididymo-orchitis present?
Unilateral scrotal pain and swelling.
-Dragging, heavy sensation with tenderness.
101
How is pain in epididymo-orchitis relieved?
Relieved with elevating the testes.
102
What is the key differential diagnosis in epididymo-orchitis?
Testicular torsion.
103
How is epididymo-orchitis diagnosed?
NAAT testing for STI.
Urinalysis and midstream MC+S for UTIs.
USS to rule out torsion and tumours.
104
How is epididymo-orchitis treated?
UTI - Co-amoxiclav, ofloxacin, levofloxacin.
STI - IM ceftriaxone, doxycyline, ofloxacin.
105
What are five complications of epididymo-orchitis?
Chronic pain, chronic epididymitis, testicular atrophy, infertility, scrotal abscess.
106
What are four cancers that affect the genitourinary system?
Prostate, testicular, bladder and kidney.
107
What is the most common cancer in men?
Prostate cancer.
108
What is the most common type of prostate cancer?
Adenocarcinoma of the outer zone of peripheral prostate.
109
How aggressive is prostate cancer?
Varies - most are slow-growing but some are aggressive and spread to lymph nodes and bones.
110
How do prostate cancers grow?
Via androgens as they are androgen dependent.
111
What are four risk factors for prostate cancer?
Family history, higher age, Afro-Caribbean ethnicity and anabolic steroids.
112
How does prostate cancer present?
With LUTS but also systemic cancer symptoms.
-Bone pain, weight loss, night sweats, fever, fatigue.
-Also, haematuria, erectile dysfunction.
113
What are the investigations for prostate cancer?
DRE and PSA testing.
-Cancerous prostate is firm, hard, irregular and asymmetrical.
-PSA antigen is specific to prostate but unreliable with false positives.
114
What is the gold standard investigation for prostate cancer?
Transrectal USS and biopsy.
115
What is the grading system for prostate cancer?
Gleason score - higher is worse.
116
How is a local, non metastasised prostate cancer treated?
Prostatectomy and radiotherapy.
117
How is metastatic prostate cancer treated?
Chemotherapy, radiotherapy, bilateral orchidectomy and hormone therapy.
118
In prostate cancer, why is a bilateral orchidectomy and hormone therapy successful?
Less testosterone and less growth of cancer due to it being androgen dependent.
119
What is the most common cancer in men aged 20-45?
Testicular cancer.
120
What are the types of testicular cancer?
Germ cell and non-germ cell.
121
What is the most common testicular cancer?
Germ cell - >90%.
122
What are examples of non-germ cell testicular cancers?
Sertoli, Leydig, teratomas.
123
Where does testicular cancer normally metastasise to?
Lymphatics, lungs, liver and brain.
124
Describe the prognosis of testicular cancer.
90% cure rate.
98% 5-year survival.
125
Which condition is testicular cancer associated with?
Gynecomastia (2% have testicular tumours).
126
What are four risk factors for testicular cancer?
Cryptorchidism (undescended testes), infertility, family history, HIV.
127
How does testicular cancer present?
Painless lump in testicle (can be painful).
128
What investigations are done in testicular cancer?
Doppler USS - lump doesn't transilluminate.
-Tumour markers - AFP (teratoma), HCG (teratoma/seminoma), LDH.
129
What is the first line treatment for testicular cancer?
Radical orchidectomy with sperm storage with radiotherapy.
-If metastasised, treat it.
130
What are two complications of testicular cancer?
Infertility and hypogonadism.
131
What are the types of bladder cancer?
Transitional cell carcinoma, squamous cell carcinoma.
Rare causes - adenocarcinoma, sarcoma.
132
What is the most common type of bladder cancer?
TCC - 90%.
133
Where does bladder cancer usually metastasise to?
Lymph nodes, bones, lung, liver.
134
What are the risk factors of bladder cancer?
Occupational exposure to dyes/paints/rubber.
-Hairdresser, painter, mechanic.
-Others: Smoking, age, male, chemo/radio.
135
How does bladder cancer usually present?
Painless haematuria.
-Sometimes with symptoms of systemic spread (weight loss, fatigue, pain, fever).
136
What is the gold standard investigation for bladder cancer?
Flexible cystoscopy and biopsy.
137
How are prostate and bladder cancer staged?
Using TNM staging.
138
How is bladder cancer treated?
Surgery - TURBT (transurethral resection of bladder tumour).
-Chemotherapy and radiotherapy.
139
What is the last resort treatment for bladder cancer?
Cystectomy - removal of urinary bladder.
140
What is the most common type of kidney cancer?
Renal cell carcinoma.
141
Where does RCC affect? Who is it most common in?
The PCT epithelium. More common in men.
142
Where does kidney cancer metastasise to?
Bone, liver and lungs.
143
What are four risk factors for kidney cancer?
Smoking, hemodialysis, hereditary, Von Hippel Lindau syndrome (auto dom, loss of tumour suppressor gene).
144
How does kidney cancer present?
Often asymptomatic.
-Triad - Flank pain, haematuria and abdominal mass.
145
What are the investigations for kidney cancer?
1st line - USS.
GS - CT chest/abdo/pelvis.
Biopsy.
146
How is kidney cancer treated?
Nephrectomy, chemo and radio.
147
What is a Wilms tumour?
Renal mesenchymal stem cell tumour seen in children.
Very rare and known as nephroblastoma.
148
What is benign prostate hyperplasia?
Hyperplasia of the inner transitional zone of the prostate which partially blocks the urethra.
149
Is BPH rare?
No it is very common and affects older men.
150
What are risk factors for BPH and what is protective?
Increased age is a RF and castration is protective (less testosterone, smaller prostate).
151
How does BPH present?
LUTS:
-Storage (FUNI) - Frequency, urgency, nocturia, incontinence.
-Voiding (SHIPP) - Straining, hesitancy, incomplete emptying, post-piss dribbling, poor stream.
-Anuria if urethra blocked.
152
What are red flags in BPH?
Haematuria and dysuria.
153
What are LUTS?
Lower urinary tract symptoms.
-Storage (FUNI) - Frequency, urgency, nocturia, incontinence.
-Voiding (SHIPP) - Straining, hesitancy, incomplete emptying, post-piss dribbling, poor stream.
154
How is BPH diagnosed? What is the differential diagnosis.
DRE (prostate exam) - smooth and enlarged.
-DDx - prostate cancer (hard, firm, irregular, asymmetrical).
155
What is the management for BPH?
-Lifestyle, drugs and surgery.
156
What are the first and second line drugs for BPH?
1st - Alpha blocker (tamsulosin) - relaxes the bladder neck.
2nd - 5-alpha reductase inhibitors (finasteride) - decreased testosterone production which decreases prostate size.
157
What is the surgical treatment for BPH?
TURP (transurethral resection of prostate).
158
How are scrotal masses considered?
All considered cancer until proven otherwise.
159
What is testicular torsion?
The spermatic torsion twists on itself, resulting in the occlusion of the testicular artery causing ischaemia.
160
What happens if testicular torsion isn't treated?
Leads to infarction and necrosis.
161
What is the typical patient in testicular torsion?
Teenage boy.
162
What is a risk factor for testicular torsion?
Bell clapper deformity.
-Fixation of testicle to tunica vaginalis is absent so the testicle hangs more horizontally than vertically.
163
How does testicular torsion present? Which reflex is lost?
Severe unitesticular pain, abdominal pain and N+V.
-Cremasteric reflex is lost.
164
How is testicular torsion diagnosed?
1st line - surgical exploration.
USS to check blood flow.
165
How is testicular torsion treated?
Urgent surgery within 6h (95% successful) to correct testicle position or remove if necrosed.
-Analgesia.
166
What is a varicocele?
Distended papilliform plexus due to increased left renal vein and left testicular pressure.
-Described as a bag of worms.
167
How common are varicoceles?
Affects 15% of males.
168
How are all scrotal masses diagnosed?
USS scrotum.
169
What are epididymal cysts?
Fluid filled cyst usually above and behind testicles.
No treatment.
Transilluminates.
170
How common are epididymal cysts?
Common, affects 30% of males.
171
What is a hydrocele? What are the symptoms and how does it appear on USS?
Fluid collection in tunica vaginalis, transilluminates.
-Non-tender, soft and painless.
172
What is nephritis?
Inflammation of the kidneys.
173
What is glomerulonephritis?
Umbrella term for conditions that cause inflammation around the glomerulus and nephron.
174
What is nephritic syndrome? What is the criteria?
Group of symptoms, not a diagnosis.
-No set criteria but has four features:
1) Haematuria.
2) Oliguria.
3) Proteinuria.
4) Fluid retention.
175
What is nephrotic syndrome? What is the criteria?
Group of symptoms, not a diagnosis but indicates an underlying disease.
1) Hypoalbuminaemia (less than 25g/L).
2) Proteinuria (more than 3g/24h).
3) Hypercholesterolaemia.
4) Peripheral oedema.
176
Which two conditions present as nephrotic and nephritic?
-Diffuse proliferative glomerulonephritis.
-Membrano-proliferative glomerulonephritis.
177
What are the causes of nephritic syndrome?
Systemic - SLE, Goodpasture's, post-strep glomerulonephritis.
Renal - IgA nephropathy.
178
What are the gold standard investigations for glomerulonephritis?
Kidney biopsy and microscopy.
179
What other investigations are done in glomerulonephritis?
Urinalysis, bloods, USS kidney.
180
How is nephritic syndrome treated?
Treat underlying cause, control BP (ACE-i, ARBs) and corticosteroids to reduce inflammation.
181
What is IgA nephropathy?
Most common cause of primary glomerulonephritis where IgA is deposited into the kidney which results in inflammation and damage.
182
How does IgA nephropathy present?
Visible haematuria 1-2 days after tonsillitis viral infection.
183
How is IgA nephropathy diagnosed?
Immunofluorescence microscopy - IgA complex deposition.
184
How is IgA nephropathy managed?
Non-curative, 1st line is to control BP.
185
How often does IgA nephropathy progress to ESRF?
30% of the time.
186
What is post-strep glomerulonephritis? How does it present?
Nephritic syndrome which presents with visible haematuria 1-3 weeks after pharyngitis from group A/B haemolytic strep.
187
How is post-strep glomerulonephritis treated?
Self-limiting, usually full recovery.
188
Describe the pathophysiology of Goodpasture's disease in glomerulonephritis. How does it present?
Anti-GBM antibodies attack glomeruli and pulmonary basement membranes causing glomerulonephritis and pulmonary haemorrhage.
-Presents with AKI, SOB and haemoptysis.
189
When do patients usually get IgA nephropathy and post-strep glomerulonephritis?
-IgA nephropathy - 20s.
-Post-strep glomerulonephritis - under 30y.
190
Describe the pathophysiology of nephrotic syndrome.
Inflammation leads to damage to podocytes, allowing protein leakage. Increased liver activity to increase albumin so there is also an increase in cholesterol.
-Reduced oncotic pressure leading to oedema.
191
What are three primary causes of nephrotic syndrome?
-Minimal change disease (mc children).
-Focal segmental glomerulosclerosis (mc adults).
-Membranous nephropathy.
192
Describe minimal change disease. How common is it in adults?
25% of adult cases.
-Normal appearance on microscopy but abnormal function.
-Causes nephrotic syndrome.
193
What is focal segmental glomerulosclerosis? What is the appearance on biopsy?
Scarring of glomeruli caused by sickle cell, HIV.
LM - Plaque/scarring.
EM - GBM thickening.
194
What is membranous nephropathy? How common is it in adults?
Thickened glomerular basement membrane (GBM). Idiopathic. APA2 antibody present. 25% of adults.
195
What is found on needle biopsy for membranous nephropathy?
FM - IgG and C3 deposits on GBM.
EM - GBM thickening.
196
What are the secondary causes of nephrotic syndrome?
DDANI:
-Diabetes (mc), drugs, autoimmune, neoplasia, infection (hep/HIV).
197
How is nephrotic syndrome managed?
Treat underlying cause and complications.
-Steroids (prednisolone) for 12 weeks.
198
How are most glomerulopathies treated?
Immunosuppressants (steroids).
Controlling BP (ACE-i, ARBs).
199
What is polycystic kidney disease?
Genetic condition where the kidneys develop multiple fluid-filled cysts and the kidney function is impaired.
200
What causes PKD?
Familial inherited.
201
Describe the inheritance of PKD?
Auto dom (mc) - Mutated PKD1 (85%) or PKD2 (15%). More males presents at ages 20-30.
Auto rec - less common, disease in infancy with high mortality.
202
Describe the pathophysiology of PKD.
Cysts develop and grow over time in tubular portion of kidney.
Leads to compression of renal architecture and vasculature.
Progressive impairment - gets bigger and worse with time.
203
How does PKD present?
Bilateral flank/back or abdominal pain.
-Hypertension, headache and LUTS.
204
How is PKD diagnosed?
Kidney USS, renal biopsy and genetic testing.
205
How is PKD treated?
Non-curative.
-Tolvaptan can slow cyst development.
-Antihypertensives for htn an analgesics for pain.
-Dialysis and kidney transplant if ESRF.
206
What is a major complication of PKD?
Associated with berry aneurysms - can cause subarachnoid haemorrhages.
207
What is the most common bacterial STI in the UK?
Chlamydia, followed by gonorrhoea.
208
How much people have symptoms with chlamydia?
Men, 50% asymptomatic.
Women, 75% asymptomatic.
209
How are STIs diagnosed?
NAAT testing.
210
How do STIs present?
Men - testicular pain, discharge, LUTS.
Women - discharge, dysuria, pain, LUTS.
211
What is the difference between uncomplicated and complicated UTI?
Uncomplicated - Bladder and lower.
Complicated - Extending to kidneys.
212
What is the Gleason score?
Based on prostate histology and helps determine which treatment is most appropriate.
