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Phase 2a > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

What are the names for kidney stones?

A

Nephrolithiasis, renal calculi, urolithiasis.

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2
Q

What are the peak ages for kidney stones? Do they occur in children?

A

Peak age 20-40y.
Uncommon in children.

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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).

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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.

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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.

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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.

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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.

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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.

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9
Q

What are the first line and gold standard investigation for kidney stones?

A

1st line - XRAY.
GS - Non-contrast CT scan.

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10
Q

What are the investigations for kidney stones in children and pregnant women?

A

USS - less radiation.

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11
Q

What other investigations are used in the investigations for kidney stones?

A

Urinalysis - UTI.
Bloods.

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12
Q

How are kidney stone symptoms managed?

A

Hydration and analgesia (NSAIDs).

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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).

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14
Q

What are the lifestyle changes for kidney stones?

A

Healthier diet, exercise, less sodium and less protein.

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15
Q

What are three complications of kidney stones?

A

Obstruction which can lead to AKI.
Infection leading to pyelonephritis.
Recurrence.

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16
Q

What is obstructive uropathy?

A

The blockage of urinary flow which affects either one or both kidneys.

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17
Q

What is obstructive nephropathy?

A

When the kidney function is affected by the obstruction.

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18
Q

What are the most common causes of obstructive uropathy?

A

Stones and BPH.

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19
Q

What is acute kidney injury?

A

Abrupt decline in kidney function characterised by increased serum creatinine and decreased urine output.

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20
Q

What does acute kidney injury result in?

A

Electrolyte imbalances and azotaemia (build up of waste products).

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21
Q

What are the three different classification criteria of acute kidney injury?

A
  1. Rise in serum creatinine >26 micromol/L within 48h.
  2. 1.5x baseline serum creatinine in 7 days.
  3. Urine output <0.5ml/kg/hr for >6h.
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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.

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23
Q

What are 8 risk factors for acute kidney injury?

A

CKD, hypertension, HF, diabetes, liver disease, old age, nephrotoxic drugs, cancer.

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24
Q

Give some examples of nephrotoxic drugs.

A

DAMN - Diuretics, ACE-i/ARBs, metformin, NSAIDs.
-Antidepressants, Abx, contrast media.

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25
Q

What are the three categories of causes for AKI?

A

Pre-renal, intra-renal and post-renal.

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26
Q

What is the most common cause (classification) of acute kidney injury?

A

Pre-renal.

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27
Q

Explain the pathophysiology of pre-renal AKI.

A

Due to hypoperfusion due to:
-Dehydration, hypotension, HF, shock, liver disease and bleeding.

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28
Q

Explain the pathophysiology of intra-renal AKI.

A

Due to disease within the kidney itself.
-Acute tubular necrosis (mc), interstitial nephritis, glomerulonephritis.

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29
Q

Explain the pathophysiology of post-renal AKI.

A

Due to obstruction:
-Stones and BPH.

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30
Q

How does AKI generally present?

A

Often asymptomatic until late.
-Oliguria, high creatinine, hyperuraemia (N+V, weakness), hyperkalaemia (arrhythmias, muscle weakness).

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31
Q

How does pre-renal AKI usually present?

A

Hypotension, signs of heart/liver failure.
-D+V, syncope, oedema.

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32
Q

How does intra-renal AKI present?

A

Infection signs and signs of cause (diabetes, glomerulonephritis, acute tubular necrosis).

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33
Q

How does post-renal AKI present?

A

With obstructive uropathy and LUTS.

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34
Q

What investigations are used to diagnose AKI?

A

-Bloods - U+E = eGFR, creatinine, K+, H+.
-Urinalysis - WBCs and nitrites (infection), protein and blood (nephritis), glucose (diabetes).
-USS - Obstruction.

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35
Q

How is AKI treated?

A

Correct the underlying cause:
-Pre-renal - Fluid rehydration.
-Post-renal - Relieve obstruction.
Stop nephrotoxic drugs.

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36
Q

How is severe AKI managed?

A

Dialysis.

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37
Q

What are five complications of AKI?

A

Hyperkalaemia, ESRF, metabolic acidosis, CKD, uraemia.

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38
Q

What is chronic kidney disease?

A

Decreased kidney function for more than 3 months which tends to be progressive and permanent. Characterised by eGFR.

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39
Q

What are the three definitions of CKD?

A
  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).
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40
Q

What are the five risk factors for CKD?

A

Old age, hypertension, diabetes, smoking, nephrotoxic drugs.

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41
Q

What are the most common causes of CKD?

A

Hypertension and diabetes.

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42
Q

What are three other causes of CKD?

A

Glomerulonephritis, PKD, obstruction.

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43
Q

What are the two classification criteria of CKD?

A

G score based on GFR.
A score based on ACR.

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44
Q

Describe the G score classification of CKD.

A

Based on eGFR:

G1 >90.
G2 - 60-89.
G3a - 45-59.
G3b - 30-44.
G4 - 15-29
G5 <15.

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45
Q

Describe the A score in the classification of CKD.

A

Based on ACR (albumin to creatinine ratio):

A1 - <3mg/mmol.
A2 - 3-30mg/mmol.
A3 - >30mg/mmol.

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46
Q

How does CKD usually present? When do symptoms start?

A

Usually asymptomatic often until ESRF.
Symptoms start due to uraemia.

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47
Q

Describe the presentation of CKD.

A

Fluid retention - oedema.
Oliguria, cramps, peripheral neuropathy, palpitations.
Uraemia effects - pruritus, pallor, nausea, appetite loss.
Anaemia and bone pain.
Hematuria.

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48
Q

Which investigations are used to diagnose CKD? Give the results.

A

Bloods - U+E = eGFR, creatinine, urea, phosphate and potassium. FBC = Anaemia.
Urinalysis - haematuria, proteinuria, glycosuria (if diabetic).
Renal USS.

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49
Q

What are the aims of CKD treatment?

A

-Slow the progression of disease.
-Reduce risk of CVD and complications.
-Treat complications.

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50
Q

How is CKD progression slowed?

A

Control diabetes and hypertension with:
-ACE-i/ARBs, CCBs.
-Metformin, sulphonylureas.
Treat the infection.

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51
Q

How is the CVD risk reduced in CKD?

A

Statins, aspirin, exercise and diet (less phosphate).

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52
Q

Why does anaemia occur in CKD? How is it treated?

A

Kidneys usually produce EPO which stimulates RBC production. CKD causes a drop in EPO so less RBCs.
-Treated with EPO and iron.

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53
Q

Why does renal bone disease occur in CKD? How is it treated?

A

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.

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54
Q

How is oedema and metabolic acidosis treated in CKD?

A

Oedema - loop diuretic and fluid restriction.
Metabolic acidosis - sodium bicarbonate.

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55
Q

How is ESRF managed in CKD?

A

RRT - dialysis and kidney transplant.

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56
Q

What are five complications of CKD?

A

Anaemia, osteodystrophy, neuropathy, encephalopathy and CVD.

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57
Q

What is a UTI?

A

An infection anywhere in the urinary tract.

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58
Q

What are the locations of UTIs?

A

Upper (kidney) - pyelonephritis.
Lower (bladder and onward) - cystitis, prostatitis, urethritis, epidydymo-orchitis.

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59
Q

How are UTIs caused?

A

Bacteria enter the urinary tract from the poo.

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60
Q

What are the organisms that cause UTIs?

A

KEEPS:

Klebsiella, E. coli (mc), enterococcus, pseudomonas/proteus, staph saprophyticus/aureus.

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61
Q

What is the most common organism that causes UTIs?

A

E. coli.

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62
Q

Why are females much more affected by UTIs?

A

As the urethra is much shorter and closer to the anus so it is easier for bacteria to colonise.

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63
Q

What is the general presentation of UTIs?

A

Dysuria, suprapubic pain/discomfort, higher frequency, urgency, incontinence, haematuria, foul smelling and cloudy urine.

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64
Q

How do UTIs usually present in the elderly?

A

Confusion.

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65
Q

What is the 1st line investigation for UTI? What does it show?

A

Urine dipstick - leukocytes, nitrites and haematuria.

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66
Q

What is the gold standard investigation for UTI? What does it show?

A

Midstream MC+S to confirm UTI and to identify the causative organism.

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67
Q

What is the usual management of UTIs?

A

Antibiotics:

-Trimethoprim and nitrofurantoin.
-If not appropriate, use amoxicillin or cefalexin.

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68
Q

What is pyelonephritis?

A

Inflammation of the kidney due to bacterial infection.

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69
Q

What causes pyelonephritis?

A

Usually E. coli (can be other KEEPS) that is most commonly acquired by ascending transurethral spread but also can be blood and lymphatics.

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70
Q

Who is pyelonephritis most common in?

A

Females under 35y/o.

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71
Q

What are five risk factors for pyelonephritis?

A

Urine stasis (stones), renal structural abnormalities, catheters, diabetes, female.

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72
Q

How does pyelonephritis present?

A

Triad - loin/back pain, fever, N+V.
-Systemic illness, appetite loss, haematuria, pyruia.

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73
Q

How is pyelonephritis diagnosed?

A

Usual UTI (urinalysis/midstream MC+S).
-USS/CT KUB to exclude kidney stones/abscesses.

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74
Q

How is pyelonephritis treated?

A

Analgesia and paracetamol for symptoms relief.
-Antibiotics: Co-amoxiclav, cefalexin, trimethoprim.

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75
Q

What is the sepsis 6?

A

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.

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76
Q

What is a complication of pyelonephritis?

A

Chronic pyelonephritis (recurrent episodes of pyelonephritis) which leads to CKD and ESRF.

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77
Q

What is cystitis?

A

Inflammation of the bladder.

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78
Q

Who does cystitis occur in?

A

Children, females, pregnancy, those with catheters.

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79
Q

What are three risk factors for cystitis?

A

Urine stasis, bladder lining damage, catheters.

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80
Q

How does cystitis present?

A

Usual UTI symptoms:

-Suprapubic tenderness/discomfort, increased frequency, urgency, haematuria, incontinence and dysuria.

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81
Q

How is cystitis diagnosed?

A

Urinalysis/midstream MC+S.
-STI testing, cystoscopy for bladder cancer.
-If male, DRE for prostate cancer/BPH.

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82
Q

How is cystitis treated?

A

Antibiotics:
-Trimethoprim and nitrofurantoin.

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83
Q

How is cystitis treated in pregnancy?

A

-Trimethoprim not used in 1st trimester as it inhibits folate synthesis.
-Nitrofurantoin not used in 3rd trimester.
-Use alternative antibiotics - amoxicillin and cefalexin.

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84
Q

What is prostatitis?

A

Inflammation of the prostate that can be acute or chronic.

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85
Q

What causes prostatitis?

A

Unclear cause.

86
Q

How does chronic prostatitis present?

A

3 months of:
-Pelvic pain, LUTS, sexual dysfunction, pain when defecating, tender/enlarged prostate.

87
Q

How does acute prostatitis present?

A

The same as chronic prostatitis but with fever, myalgia, nauseam fatigue and even sepsis.

88
Q

What investigations are used to diagnose prostatitis?

A

Urinalysis, midstream MC+S, NAAT testing to rule out STIs.
-DRE.

89
Q

How is acute and chronic prostatitis treated?

A

Acute - Antibiotics, analgesia, laxatives.
Chronic - Tamsulosin (relaxes muscle), analgesia, antibiotics, laxatives.

90
Q

What are three complications of acute prostatitis?

A

Sepsis, prostate abscess, chronic prostatitis.

91
Q

What is urethritis?

A

Urethral inflammation with or without infection.

92
Q

What is the most common cause of urethritis?

A

Usually STI - chlamydia.

93
Q

What are the causes of urethritis?

A

Infective - gonorrhoea and chlamydia (mc).
Non-infective - trauma, stricture, irritation, stones.

94
Q

What are risk factors for urethritis?

A

Gay sex, anal sex, unprotected sex, lots of sexual partners.

95
Q

How does urethritis present?

A

Dysuria, urethral discharge (blood/pus), urethral pain, penile discomfort).

96
Q

How is urethritis diagnosed?

A

NAAT test to detect STI.
Urinalysis and midstream MC+S.

97
Q

How is urethritis treated?

A

Depends on underlying cause:

-Gonorrhoea - IM ceftriaxone and azithromycin.
-Chlamydia - Azithromycin or doxycycline.

98
Q

What is epididymo-orchitis?

A

Inflammation of the epididymis, extending to the testes.

99
Q

What causes epididymo-orchitis?

A

Urethritis (STI, <35y) or cystitis (KEEPS, >35y).

100
Q

How does epididymo-orchitis present?

A

Unilateral scrotal pain and swelling.
-Dragging, heavy sensation with tenderness.

101
Q

How is pain in epididymo-orchitis relieved?

A

Relieved with elevating the testes.

102
Q

What is the key differential diagnosis in epididymo-orchitis?

A

Testicular torsion.

103
Q

How is epididymo-orchitis diagnosed?

A

NAAT testing for STI.
Urinalysis and midstream MC+S for UTIs.
USS to rule out torsion and tumours.

104
Q

How is epididymo-orchitis treated?

A

UTI - Co-amoxiclav, ofloxacin, levofloxacin.
STI - IM ceftriaxone, doxycyline, ofloxacin.

105
Q

What are five complications of epididymo-orchitis?

A

Chronic pain, chronic epididymitis, testicular atrophy, infertility, scrotal abscess.

106
Q

What are four cancers that affect the genitourinary system?

A

Prostate, testicular, bladder and kidney.

107
Q

What is the most common cancer in men?

A

Prostate cancer.

108
Q

What is the most common type of prostate cancer?

A

Adenocarcinoma of the outer zone of peripheral prostate.

109
Q

How aggressive is prostate cancer?

A

Varies - most are slow-growing but some are aggressive and spread to lymph nodes and bones.

110
Q

How do prostate cancers grow?

A

Via androgens as they are androgen dependent.

111
Q

What are four risk factors for prostate cancer?

A

Family history, higher age, Afro-Caribbean ethnicity and anabolic steroids.

112
Q

How does prostate cancer present?

A

With LUTS but also systemic cancer symptoms.
-Bone pain, weight loss, night sweats, fever, fatigue.
-Also, haematuria, erectile dysfunction.

113
Q

What are the investigations for prostate cancer?

A

DRE and PSA testing.
-Cancerous prostate is firm, hard, irregular and asymmetrical.
-PSA antigen is specific to prostate but unreliable with false positives.

114
Q

What is the gold standard investigation for prostate cancer?

A

Transrectal USS and biopsy.

115
Q

What is the grading system for prostate cancer?

A

Gleason score - higher is worse.

116
Q

How is a local, non metastasised prostate cancer treated?

A

Prostatectomy and radiotherapy.

117
Q

How is metastatic prostate cancer treated?

A

Chemotherapy, radiotherapy, bilateral orchidectomy and hormone therapy.

118
Q

In prostate cancer, why is a bilateral orchidectomy and hormone therapy successful?

A

Less testosterone and less growth of cancer due to it being androgen dependent.

119
Q

What is the most common cancer in men aged 20-45?

A

Testicular cancer.

120
Q

What are the types of testicular cancer?

A

Germ cell and non-germ cell.

121
Q

What is the most common testicular cancer?

A

Germ cell - >90%.

122
Q

What are examples of non-germ cell testicular cancers?

A

Sertoli, Leydig, teratomas.

123
Q

Where does testicular cancer normally metastasise to?

A

Lymphatics, lungs, liver and brain.

124
Q

Describe the prognosis of testicular cancer.

A

90% cure rate.
98% 5-year survival.

125
Q

Which condition is testicular cancer associated with?

A

Gynecomastia (2% have testicular tumours).

126
Q

What are four risk factors for testicular cancer?

A

Cryptorchidism (undescended testes), infertility, family history, HIV.

127
Q

How does testicular cancer present?

A

Painless lump in testicle (can be painful).

128
Q

What investigations are done in testicular cancer?

A

Doppler USS - lump doesn’t transilluminate.
-Tumour markers - AFP (teratoma), HCG (teratoma/seminoma), LDH.

129
Q

What is the first line treatment for testicular cancer?

A

Radical orchidectomy with sperm storage with radiotherapy.
-If metastasised, treat it.

130
Q

What are two complications of testicular cancer?

A

Infertility and hypogonadism.

131
Q

What are the types of bladder cancer?

A

Transitional cell carcinoma, squamous cell carcinoma.
Rare causes - adenocarcinoma, sarcoma.

132
Q

What is the most common type of bladder cancer?

A

TCC - 90%.

133
Q

Where does bladder cancer usually metastasise to?

A

Lymph nodes, bones, lung, liver.

134
Q

What are the risk factors of bladder cancer?

A

Occupational exposure to dyes/paints/rubber.
-Hairdresser, painter, mechanic.

-Others: Smoking, age, male, chemo/radio.

135
Q

How does bladder cancer usually present?

A

Painless haematuria.
-Sometimes with symptoms of systemic spread (weight loss, fatigue, pain, fever).

136
Q

What is the gold standard investigation for bladder cancer?

A

Flexible cystoscopy and biopsy.

137
Q

How are prostate and bladder cancer staged?

A

Using TNM staging.

138
Q

How is bladder cancer treated?

A

Surgery - TURBT (transurethral resection of bladder tumour).
-Chemotherapy and radiotherapy.

139
Q

What is the last resort treatment for bladder cancer?

A

Cystectomy - removal of urinary bladder.

140
Q

What is the most common type of kidney cancer?

A

Renal cell carcinoma.

141
Q

Where does RCC affect? Who is it most common in?

A

The PCT epithelium. More common in men.

142
Q

Where does kidney cancer metastasise to?

A

Bone, liver and lungs.

143
Q

What are four risk factors for kidney cancer?

A

Smoking, hemodialysis, hereditary, Von Hippel Lindau syndrome (auto dom, loss of tumour suppressor gene).

144
Q

How does kidney cancer present?

A

Often asymptomatic.
-Triad - Flank pain, haematuria and abdominal mass.

145
Q

What are the investigations for kidney cancer?

A

1st line - USS.
GS - CT chest/abdo/pelvis.
Biopsy.

146
Q

How is kidney cancer treated?

A

Nephrectomy, chemo and radio.

147
Q

What is a Wilms tumour?

A

Renal mesenchymal stem cell tumour seen in children.
Very rare and known as nephroblastoma.

148
Q

What is benign prostate hyperplasia?

A

Hyperplasia of the inner transitional zone of the prostate which partially blocks the urethra.

149
Q

Is BPH rare?

A

No it is very common and affects older men.

150
Q

What are risk factors for BPH and what is protective?

A

Increased age is a RF and castration is protective (less testosterone, smaller prostate).

151
Q

How does BPH present?

A

LUTS:

-Storage (FUNI) - Frequency, urgency, nocturia, incontinence.
-Voiding (SHIPP) - Straining, hesitancy, incomplete emptying, post-piss dribbling, poor stream.

-Anuria if urethra blocked.

152
Q

What are red flags in BPH?

A

Haematuria and dysuria.

153
Q

What are LUTS?

A

Lower urinary tract symptoms.

-Storage (FUNI) - Frequency, urgency, nocturia, incontinence.
-Voiding (SHIPP) - Straining, hesitancy, incomplete emptying, post-piss dribbling, poor stream.

154
Q

How is BPH diagnosed? What is the differential diagnosis.

A

DRE (prostate exam) - smooth and enlarged.
-DDx - prostate cancer (hard, firm, irregular, asymmetrical).

155
Q

What is the management for BPH?

A

-Lifestyle, drugs and surgery.

156
Q

What are the first and second line drugs for BPH?

A

1st - Alpha blocker (tamsulosin) - relaxes the bladder neck.
2nd - 5-alpha reductase inhibitors (finasteride) - decreased testosterone production which decreases prostate size.

157
Q

What is the surgical treatment for BPH?

A

TURP (transurethral resection of prostate).

158
Q

How are scrotal masses considered?

A

All considered cancer until proven otherwise.

159
Q

What is testicular torsion?

A

The spermatic torsion twists on itself, resulting in the occlusion of the testicular artery causing ischaemia.

160
Q

What happens if testicular torsion isn’t treated?

A

Leads to infarction and necrosis.

161
Q

What is the typical patient in testicular torsion?

A

Teenage boy.

162
Q

What is a risk factor for testicular torsion?

A

Bell clapper deformity.
-Fixation of testicle to tunica vaginalis is absent so the testicle hangs more horizontally than vertically.

163
Q

How does testicular torsion present? Which reflex is lost?

A

Severe unitesticular pain, abdominal pain and N+V.
-Cremasteric reflex is lost.

164
Q

How is testicular torsion diagnosed?

A

1st line - surgical exploration.
USS to check blood flow.

165
Q

How is testicular torsion treated?

A

Urgent surgery within 6h (95% successful) to correct testicle position or remove if necrosed.
-Analgesia.

166
Q

What is a varicocele?

A

Distended papilliform plexus due to increased left renal vein and left testicular pressure.
-Described as a bag of worms.

167
Q

How common are varicoceles?

A

Affects 15% of males.

168
Q

How are all scrotal masses diagnosed?

A

USS scrotum.

169
Q

What are epididymal cysts?

A

Fluid filled cyst usually above and behind testicles.
No treatment.
Transilluminates.

170
Q

How common are epididymal cysts?

A

Common, affects 30% of males.

171
Q

What is a hydrocele? What are the symptoms and how does it appear on USS?

A

Fluid collection in tunica vaginalis, transilluminates.
-Non-tender, soft and painless.

172
Q

What is nephritis?

A

Inflammation of the kidneys.

173
Q

What is glomerulonephritis?

A

Umbrella term for conditions that cause inflammation around the glomerulus and nephron.

174
Q

What is nephritic syndrome? What is the criteria?

A

Group of symptoms, not a diagnosis.
-No set criteria but has four features:
1) Haematuria.
2) Oliguria.
3) Proteinuria.
4) Fluid retention.

175
Q

What is nephrotic syndrome? What is the criteria?

A

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
Q

Which two conditions present as nephrotic and nephritic?

A

-Diffuse proliferative glomerulonephritis.
-Membrano-proliferative glomerulonephritis.

177
Q

What are the causes of nephritic syndrome?

A

Systemic - SLE, Goodpasture’s, post-strep glomerulonephritis.
Renal - IgA nephropathy.

178
Q

What are the gold standard investigations for glomerulonephritis?

A

Kidney biopsy and microscopy.

179
Q

What other investigations are done in glomerulonephritis?

A

Urinalysis, bloods, USS kidney.

180
Q

How is nephritic syndrome treated?

A

Treat underlying cause, control BP (ACE-i, ARBs) and corticosteroids to reduce inflammation.

181
Q

What is IgA nephropathy?

A

Most common cause of primary glomerulonephritis where IgA is deposited into the kidney which results in inflammation and damage.

182
Q

How does IgA nephropathy present?

A

Visible haematuria 1-2 days after tonsillitis viral infection.

183
Q

How is IgA nephropathy diagnosed?

A

Immunofluorescence microscopy - IgA complex deposition.

184
Q

How is IgA nephropathy managed?

A

Non-curative, 1st line is to control BP.

185
Q

How often does IgA nephropathy progress to ESRF?

A

30% of the time.

186
Q

What is post-strep glomerulonephritis? How does it present?

A

Nephritic syndrome which presents with visible haematuria 1-3 weeks after pharyngitis from group A/B haemolytic strep.

187
Q

How is post-strep glomerulonephritis treated?

A

Self-limiting, usually full recovery.

188
Q

Describe the pathophysiology of Goodpasture’s disease in glomerulonephritis. How does it present?

A

Anti-GBM antibodies attack glomeruli and pulmonary basement membranes causing glomerulonephritis and pulmonary haemorrhage.
-Presents with AKI, SOB and haemoptysis.

189
Q

When do patients usually get IgA nephropathy and post-strep glomerulonephritis?

A

-IgA nephropathy - 20s.
-Post-strep glomerulonephritis - under 30y.

190
Q

Describe the pathophysiology of nephrotic syndrome.

A

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
Q

What are three primary causes of nephrotic syndrome?

A

-Minimal change disease (mc children).
-Focal segmental glomerulosclerosis (mc adults).
-Membranous nephropathy.

192
Q

Describe minimal change disease. How common is it in adults?

A

25% of adult cases.
-Normal appearance on microscopy but abnormal function.
-Causes nephrotic syndrome.

193
Q

What is focal segmental glomerulosclerosis? What is the appearance on biopsy?

A

Scarring of glomeruli caused by sickle cell, HIV.
LM - Plaque/scarring.
EM - GBM thickening.

194
Q

What is membranous nephropathy? How common is it in adults?

A

Thickened glomerular basement membrane (GBM). Idiopathic. APA2 antibody present. 25% of adults.

195
Q

What is found on needle biopsy for membranous nephropathy?

A

FM - IgG and C3 deposits on GBM.
EM - GBM thickening.

196
Q

What are the secondary causes of nephrotic syndrome?

A

DDANI:

-Diabetes (mc), drugs, autoimmune, neoplasia, infection (hep/HIV).

197
Q

How is nephrotic syndrome managed?

A

Treat underlying cause and complications.
-Steroids (prednisolone) for 12 weeks.

198
Q

How are most glomerulopathies treated?

A

Immunosuppressants (steroids).
Controlling BP (ACE-i, ARBs).

199
Q

What is polycystic kidney disease?

A

Genetic condition where the kidneys develop multiple fluid-filled cysts and the kidney function is impaired.

200
Q

What causes PKD?

A

Familial inherited.

201
Q

Describe the inheritance of PKD?

A

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
Q

Describe the pathophysiology of PKD.

A

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
Q

How does PKD present?

A

Bilateral flank/back or abdominal pain.
-Hypertension, headache and LUTS.

204
Q

How is PKD diagnosed?

A

Kidney USS, renal biopsy and genetic testing.

205
Q

How is PKD treated?

A

Non-curative.
-Tolvaptan can slow cyst development.
-Antihypertensives for htn an analgesics for pain.
-Dialysis and kidney transplant if ESRF.

206
Q

What is a major complication of PKD?

A

Associated with berry aneurysms - can cause subarachnoid haemorrhages.

207
Q

What is the most common bacterial STI in the UK?

A

Chlamydia, followed by gonorrhoea.

208
Q

How much people have symptoms with chlamydia?

A

Men, 50% asymptomatic.
Women, 75% asymptomatic.

209
Q

How are STIs diagnosed?

A

NAAT testing.

210
Q

How do STIs present?

A

Men - testicular pain, discharge, LUTS.
Women - discharge, dysuria, pain, LUTS.

211
Q

What is the difference between uncomplicated and complicated UTI?

A

Uncomplicated - Bladder and lower.
Complicated - Extending to kidneys.

212
Q

What is the Gleason score?

A

Based on prostate histology and helps determine which treatment is most appropriate.

Phase 2a (14 decks)

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