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Gu Flashcards

1
Q

What are the common causative bacteria of pyelonephritis?

A

E.coli (most common), klebsiella, proteus, enterococcus

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2
Q

What is the first line tx for pyelonephritis?

A

Ciprofloxacin/co-amixiclav

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3
Q

What additional medication other than antibiotics is needed for chronic pyelonephritis?

A

Blood pressure control

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4
Q

What is the first line antibiotic tx for epidiymo-orchitis?

A

doxycycline, cefixime, ciprofloxacin

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5
Q

What is the aetiology of epididymo-orchitis (for young vs older men)

A
  • <35 years: STI

>35 years: gram negative enteric organisms

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6
Q

What can prostatitis be a symptom of?

A

UTI

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7
Q

What is the first line investigation for prostatitis? and results?

A

DRE: gland feels nodular, boggy, tender and hot

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8
Q

What are the normal causative organisms for prostatitis?

A

gram negative organisms: E.coli, enterobacter, serratia. Sometimes STIs such as Neisseria gonnorhoea and and chlamydia trachomatis

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9
Q

What is the first line Abx tx for prostatitis?

A

Quinolones

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10
Q

What are the two subtypes of urethritis? And what is there differing presentation?

A

gonnococcal and non gonococcal. Gonococcal presents with discharge, non gonococcal doesnt

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11
Q

What is the treatment for gonococcal urethritis?

A

quinolones

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12
Q

What is the treatment for non gonococcal urethritis?

A

ceftriaxone

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13
Q

what is the difference between nephritic and nephrotic syndrome?

A
  • nephritic syndrome: haematuria, slight proteinuria, low urine volume, uraemia. Due to inflammation of the kidney
  • nephrotic syndrome: proteinuria, hypoalbuminemia, oedema, hyperlipidemia. Due to increased glomerular permeability
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14
Q

What are causes for nephritic syndrome?

A

Can occur due to antigen getting trapped in kidney

  • 1-3 weeks after a strep infection
  • viral infection
  • parasitic infection
  • IgA nephropathy (following upper rep infection)
  • ANCA associated nephritis
  • Good Pastures syndrome (anti basement membrane antibodies)
  • SLE
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15
Q

How does the liver compensate for the hypoalbuminaemia in nephrotic syndrome?

A

increased lipid synthesis

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16
Q

What are causes of nephrotic syndrome?

A
  • primary renal disease
  • minimal change disease
  • membranous nephropathy
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17
Q

How does glomerular disease affect the GFR?

A

Decreases it

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18
Q

What is minimal change disease?

A
  • cause of nephrotic disease

- loss of podocyte foot processes, vacuolation and appearance of the microvilli.

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19
Q

what is membranous nephropathy?

A

Thickening of the glomerular capillary wall. IgG deposited in subepithelial surface. Causes nephrotic syndrome

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20
Q

what do epididymal cysts present as (clinically and on dx)

A
  • lumps that can be painful once large. Well defined

- Dx via scrotal ultrasound. Transluminate shows clear and milky fluid

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21
Q

What is a hydrocele?

A

abnormal collection of fluid in tunica vaginalis (serous membrane covering the testes)

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22
Q

What are the three types of hydrocele?

A
  1. simple: accumulation of fluid. Scrotal enlargement with non tender, smooth swelling. If congenital, can disappear in the first years life. Can also occur due to trauma, oedema elsewhere, etc.
  2. Communicating: persistence of the processes vaginalis (failure to close). Also peritoneal fluid to freely communicate
  3. non communicating: imbalance of secretion and resorption of fluid
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23
Q

Dx of hydrocele?

A
  • ultrasound

- check beta HCG (teratoma) and alpha feroprotein

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24
Q

What are the possible complications of testicular torsion?

A

ischaemia, infarct and potential loss of testes due to ischaemia.

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25
Q

What is a variocele?

A

Abnormal dilation of testicular veins in the pampiform plexus.

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26
Q

how do varioceles present?

A

Scrotum feels like a ‘bag of worms’: hangs lower on one side

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27
Q

What side of the scrotum are varioceles more common on?

A

Left. Due to the angle of the left testicular vein entering left renal vein.

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28
Q

What are the possible complications of varioceles?

A

Infertility. the increased heat production can lead to reduced sperm quality

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29
Q

What are the three pathophysiology in erectile dysfunction?

A
  1. neurogenic (issue initiating due to nerve problems)
  2. arteriogenic ( failure to fill)
  3. venogenic (failure to store)
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30
Q

What is the normal physiology of an erection?

A

Nitrous oxide released neuronally. Leads to smooth muscle relaxation. Allows artery in flow and enlargement. Flows out when cAMP broken down by PDE-5 (venous channel opener). Involves pelvic plexus.

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31
Q

What type of medication is viagra?

A

PDE-5 inhibitor

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32
Q

What lobe is most affected in benign prostatic hyperplasia?

A

Median lobe

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33
Q

What scorring system is used for BPH?

A

I-PSS

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34
Q

What is the use of testosterone in BPH?

A
  • Testosterone required for the cellular changes that occur: increased hyperplasia and decreased apoptosis
  • testosterone is converted to its more potent form (DHT) by 5a-reductase
  • binds to receptors in the prostate: increased secretions and divisions
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35
Q

What receptor mediates smooth muscle contraction of the prostate in BPH?

A

a-1 adrenoceptor

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36
Q

What is the order of treatment in BPH?

A
  1. watchful waiting
  2. A1- adrenoceptor antagonist: doxasine
  3. 5a reductase inhibitor
  4. Surgery
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37
Q

What are the histology of the majority of bladder carcinomas?

A

transitional cell carcinoma

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38
Q

How does TCC of the bladder present?

A
  • painless haematuria (RED FLAG)
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39
Q

What is diagnostic for bladder carcinoma?

A

Flexible cytoscopy

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40
Q

What is the common spread of TCC of the bladder?

A

local –> pelvic structures –> lymphatic –> iliac and para-aortic nodes –> blood –> liver and lungs

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41
Q

What areas of the prostate are most affected in prostatic cancer?

A

Lateral nodes.

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42
Q

What type of cancer is prostatic (most often)

A

Adenocarcinoma

43
Q

What hormone drives prostatic cancer development?

A

Androgen

44
Q

What are the RF for testicular carcinoma?

A

undescended testis, HIV, FHx

45
Q

Where might testicular cancer metastasise to, and what can this present as?

A

To the lung. Dyspnoea

46
Q

What are the two types of testicular carcinoma and which is more common?

A

Seminoma and teratoma

47
Q

What hormone indicates testicular cancer?

A

increase of beta HCG

48
Q

Who is Wilhm’s cancer most prevalent in?

A

Children, as it is a nephroblastoma

49
Q

Where do transitional cell carcinomas of the kidney arise from?

A

Renal pelvis

50
Q

Where do renal cell carcinomas arise from?

A

Proximal renal tubular epithelium

51
Q

What is a unusual feature of renal cell carcinoma?

A

Can secrete PTH, ACTH, EPO, renin

52
Q

What is the gold standard dx for renal cell carcinoma?

A

IVU (intravenous pyelogram)

53
Q

What is the tx for renal cell carcinoma?

A

Partial or radical nephrectomy. Not radio/chemosensitive. Can use high dose IL-2

54
Q

What is the presentation of renal stones?

A

mainly asymptomatic. loin pain, LUTS, recurrent UTIs, haematuria, hypotension, decreased bowel sounds

55
Q

What is the differentiating feature of renal colic to peritonitis?

A
  • renal colic: can’t lie still
56
Q

What is the most common composition of renal stones, and the aetiology?

A
  • calcium oxalate
  • calcium: hypercalcaemia, increased PTH, increased calcium gut absorption, excess bone absorption
  • oxalate: high diet intake, low diet calcium, increased GI absorption due to disease
  • calcium oxalate ppt can form in the basement membrane of loops of henle
57
Q

What is gold standard dx for renal stones?

A

CT

58
Q

What cells control GFR?

A

mesiangial cells: smooth muscle cells

59
Q

What does the afferent arteriole detect and secrete?

A

Blood pressure and secretes renin

60
Q

What does macula densa detect?

A

sodium levels

61
Q

What is a nephron blood supply?

A

20% cardiac output. 1L/min

62
Q

What is the normal GFR?

A

~125l/min

63
Q

What is the presentation of AKI?

A

anuria (<100ml/24hrs)/oligouria. Large increase in serum creatinine levels (x1.5 base levels)

64
Q

What are the three catergories of AKI injury?

A
  1. pre renal
  2. renal
  3. post renal
65
Q

What are pre renal causes of AKI?

A

impaired perfusion of kidneys, GFR can’t be maintained. Volume depletion (D and V), hypotension, cardiac failure

66
Q

What are renal causes of AKI?

A

damage to kidney apparatus impairs function. Glomerular disease, tubular injury, nephritis (NSAIDs), vascular disease

67
Q

What are post renal causes of AKI?

A

obstruction of outflow

68
Q

What are possible complications of AKI?

A

volume overload, metabolic acidosis, electrolyte disturbance

69
Q

What are the 6 catergories of symptoms of CKD and why do they occur?

A
  1. anaemia –> decreased EPO production
  2. CNS (confusion, coma) –> advanced uraemia can cause decreased cerebral function, fits. Carpal tunnel syndrome due to amyloidosis
  3. CVS (HTN): BP not properly controlled
  4. Renal (nocturia, polyuria, haematuria)
  5. Bone (osteomalacia, bone pain, hyperparathyroidism): renal phosphate retention, impaired production o 1,25 dihydroxyvitamin D –> decreased calcium. Increased PTH, skeletal decalcification
  6. skin (Pruitus)
70
Q

What is the treatment for CKD?

A
  • renoprotective: control BP <120/80
  • ACE-I and ARB can reduce proteinuria.
  • dialysis and kidney replacement
71
Q

What is the aetiology of CKD?

A

polycystic kidney disease, HTN, DM, glomerular disease, urinary tract obstruction

72
Q

What is the pathophysiology of autosomal dominant polycystic kidney disease?

A

Polycystin mutation. Integral membrane protein that regulates tubular and vascular kidney development. Cysts develop, increase with age, renal enlargement and destruction

73
Q

What co-morbiditie is there with AD Polycystic renal disease?

A

SAH due to berry aneurysms

74
Q

what is the pathophysiology of autosomal recessive polycystic kidney disease?

A

Dilation and elongation of renal collecting ducts. Develops fibrosis and tubular atrophy and leads to end stage kidney disease.

75
Q

What often exists with AR polycystic kidney disease?

A

liver disease

76
Q

What scoring system is used for prostate cancer?

A

Gleason’s pattern scale. Looks at how much tissue looks normal and how much diseased

77
Q

Why might urine appear foamy?

A

Kidney disease

78
Q

What is GFR measured in?

A

ml/min/1.73m2

79
Q

how was diabetes lead to CKD?

A

glycation of glomerular endothelium, and efferent arteriole

80
Q

What arteriole in the kidney does HTN damage?

A

afferent

81
Q

What are the systemic effects of uraemia?

A

pruitus, yellow/grey complexion, nausea, reduced appetite, weakness

82
Q

What electrolyte imbalance commonly occurs due to CKD?

A

potassium

83
Q

What are the four intra renal catergories of AKI?

A

glomerular, tubular (necrosis in most cases), interstitial, vascular

84
Q

what is diagnostic for nephritic syndrome?

A

renal biopsy

85
Q

What are four physiological consequences of nephrotic syndrome?

A
  • loss of Abs due to proteinuria, reduce immunity
  • increased liveractivity due to hypoalbuminae leads to increased coagulation factors, increased cholesterol synthesis and increased albumin production
86
Q

What is the criteria of proteinuria for nephrotic syndrome?

A

> 3.5 g/24hrs

87
Q

what is the most common cause of nephrotic syndrome in children vs adults?

A
  • children: minimal change disease

- adults: membranous glomerulonephritis

88
Q

What cardiac compx do many polycystitic kidney patients have

A

ventricular hypertrophy

89
Q

What size of renal stones are left to pass spontaneously?

A

<5mm

90
Q

What is hydronephrosis?

A

Dilation of the renal pelvis

91
Q

What is the first line and gold standard dx for kidney cancer?

A
  • 1st line: USS

- gold standard: renal biopsy

92
Q

What is a common metastasis site of prostate cancer and the compx?

A

Bone, and sclerotic bone lesions

93
Q

What is the dx for prostate cancer?

A

USS and biopsy

94
Q

What is the classic triad for pylonephritis?

A

loin pain, fever, pyuria

95
Q

What is the acronym for remembering common caustive bacteria for cystitis?

A

KEEPS

96
Q

what factors are related to a low GFR?

A

High serum creatinine, older age, being Caucasian and high protein diet

97
Q

What is the treatment for hyperkalaemia?

A

calcium gluconate

98
Q

What drugs should immediately be stopped in AKI?

A

diuretics, ACEi, metformin and NSAIDs (DAMN)

99
Q

What is tamsulosin? What is it’s s/e?

A
  • used for BPH (alpha blocker)

- s/e: postural hypotension

100
Q

If someone is in AKI, what electrolyte should be carefully monitored?

A

Potassium. Unable to excrete it: can lead to hyperkalemia

101
Q

Where do thiazide diuretics work?

A

DCT

102
Q

What is the MoA of tamsulosin?

A

a1 adrenoceptor antagonist.

103
Q

How does postural hypotension occur as a s/e of tamsulosin?

A

via dilation of venous capacitance

104
Q

where are germinoma’s commonly found, and what can be presenting feature?

A
  • in the brain

- positive pregnancy test

GI P2a (12 decks)

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