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Phase 2a Sheffield Medicine > GU > Flashcards

GU Flashcards

1
Q

What is the function of calcitriol?

A
  1. Increased calcium and phosphate absorption from the gut

2. Suppression of PTH

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2
Q

What do people with CKD commonly present with?

A

hyperparathyroidism

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3
Q

How does CKD cause hyperparathyroidism?

A

Calcitriol deficiency, calcitriol supresses PTH therefore deficiency –> hyperparathyroidism

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4
Q

What is PTH secretion triggered by?

A

Low serum Ca

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5
Q

What are 3 ways that PTH increases serum calcium?

A
  1. Increased bone resorption
  2. Increased reabsorption of calcium at the kidneys
  3. Stimulates 1-hydroxylase –> 1,25 dihydroxyvitD –> increased calcium absorption from the intestine
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6
Q

What hormones are secreted from the posterior pit gland?

A
  1. ADH

2. Oxytocin

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7
Q

What is the function of ADH?

A

Acts on the CD, increases the insertion of aquaporin 2 channels –> H2O retention

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8
Q

What factors stimulate the release of renin?

A
  1. Sympathetic stimulation
  2. Decreased BP
  3. Decreased Na detected by the macula densa
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9
Q

What are the functions of ANP?

A
  1. Renal vasodilator
  2. Inhibits aldosterone
  3. Closes ENaC –> decreased Na reabsorption
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10
Q

Where does aldosterone act on?

A

CD

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11
Q

What is the action of aldosterone?

A
  1. Increases ENaC and H+/K+ pumps –> increased Na+ absorption and K+ secretion
  2. This causes H2O retention and increased BP
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12
Q

What anatomical structures make up the lower UT?

A

Bladder –> bladder neck, prostate gland –> urethra –> urethra and urethral sphincter

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13
Q

What are the functions of the bladder?

A
  1. Storage of urine
  2. Converts continuous process of excretion to an intermittent, controlled volitional processes
  3. Prevents leakage of stored urine
  4. Allows rapid, low pressure voiding
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14
Q

Describe the action of the detrusor muscle.

A

Storage - relaxes

Voiding - contracts

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15
Q

Describe the action of the urethral sphincter

A

Contracts during storage and relaxes during voiding.

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16
Q

What lines the bladder?

A

Pseudo stratified urothelium lines the bladder

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17
Q

Explain the physiology of micturition

A
  1. Bladder fills and stretch receptors are stimulated
  2. Afferent impulses stimulate Parasympathetic action of detrusor muscle –> contracts
  3. Urethral sphincters relax, mediated by the inhibiton of neurones
  4. PAG is stimulated.
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18
Q

Describe the fluid constituent in the body.

A

ICF – 28l

ECF – 14l

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19
Q

What is the ECF broken into?

A

Interstital –> 11l

Plasma –> 3l

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20
Q

What is the total body fluid?

A

42L

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21
Q

How much fluid is

Intravascular?
Extravascular?

A

Intravascular –> 3L

Extravascular –> 39l (ICF+interstitial)

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22
Q

What is the function of the prostate?

A

Secretes proteolytic enzymes into the semen which break down clotting factors in the ejaculate

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23
Q

What zone does prostate cancer usually affect?

A

peripheral zone.

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24
Q

What is a major worry for prostate cancer?

A

METASTASIS

To bone and lymph nodes.

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25
Q

What investigations would you do in suspected prostate cancer?

A
  1. Serum –> PSA
  2. Urine –> PCA3 and gene fusion products
  3. History of LUTS
  4. Trans-rectal LUTS
  5. Prostate biopsy
  6. DRE – Hard, irregular and craggy
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26
Q

What are some other causes of raised PSA?

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
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27
Q

What is the gleason score?

A

A score in prostate cancer, the higher the score the more aggressive it is.

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28
Q

What is the treatment for localised prostate cancer?

A
  1. Observation
  2. Radical prostatectomy
  3. Radiotherapy
  4. Adjuvant hormones
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29
Q

What is the treatment for metastatic prostate cancer?

A

Palliative treatment e.g. hormone therapy – androgen deprivation

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30
Q

What is an advantage for prostate cancer screening?

A

screening can lead to early diagnosis/early treatment and so cure or effective palliation

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31
Q

What are the disadvantages of prostate cancer screening?

A

Uncertain natural history, screening leads to overdiagnosis and over treatment

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32
Q

What is acute kidney injury?

A

Causes raised creatinine and reduced urine output

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33
Q

What are the risk factor of AKI?

A
  1. Increasing age
  2. CKD
  3. HF
  4. Diabetes mellitus
  5. Nephrotoxic drugs e.g. NSAIDs and ACEi
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34
Q

What are the prerenal causes of AKI?

A
  1. Hypertension
  2. Heart failure
  3. Nephrotoxic drugs
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35
Q

What are the renal causes of AKI?

A
  1. Nephrotoxic drugs
  2. Vasculitis
  3. AI
  4. Acute tubular necrosis
  5. Glomerulonephritis
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36
Q

What is a major complication of AKI?

A

Hyperkalemia which can lead to arrhythmias

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37
Q

How would you prevent Hyperkalemia in AKI?

A
  1. Give calcium gluconate to protect the myocardium

2. Give insulin and dextrose

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38
Q

How does insulin prevent kyperkalemia in AKI?

A

Drives K into cells and dextrose is given to rebalance the sugar.

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39
Q

What investigations should you perform in a patient with suspected AKI?

A
  1. Check K
  2. Bloods, creatinine, U +E
  3. Urine output
  4. Auto-antibodies
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40
Q

What is CKD?

A

A long term condition where the kidneys function is compromised and may get progressively worse.

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41
Q

What are the signs of CKD?

A
  1. Proteinuria
  2. Haematuria
  3. Impaired eGFR <60ml/min
  4. Rise in serum Urea/creatinine
  5. Anaemia –> reduced EPO
  6. Bone disease
  7. Polyneuropathy
  8. CV disease
  9. Erectile dysfunction
  10. Raised PTH
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42
Q

What are the causes of CKD?

A
  1. Diabetes mellitus
  2. Hypertension
  3. Atherosclerotic renal vascular disease
  4. Congenital e.g. PKD
  5. UT obstruction
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43
Q

What is the appropriate management of CKD?

A
  1. Treat underlying cause
  2. Slow deteroriation of kidney function e.g. maintain Bp
  3. Reduce CV risk e.g. statins, smoking cessation
  4. Treat complications e.g. anaemia
  5. ESRF –> dialysis or transplant
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44
Q

What are the causes of raised UT pressure?

A
  1. Stone in lumen of UUT
  2. Tumour in the wall
  3. LUT outflow obstruction; BPH, Tumour and stone
  4. Bladder obstruction
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45
Q

What are the 4 causes of urinary tract colonisation?

A
  1. Diseases that require chemo or steroids e.g. diabetes and immunodeficiency
  2. Stones or tumour in the lumen of the UT
  3. Poor bladder emptying
  4. Catheterisation
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46
Q

What would be seen in electron microcsopy in a patient with minimal change disease?

A

Fused podocytes

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47
Q

What is the treatment for minimal change disease?

A

Steroids

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48
Q

What is an example of a loop diuretic and how does it work?

A

Furosemide –> acts on Na+/k2+/2Cl- transporter (NKCC2)

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49
Q

What are 3 potential side effects of Furosemide?

A

Hypokalemia, hypotension and dehydration

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50
Q

What is a potassium sparing diuretic and what does it act on?

A

Spironolactone –> works on RAAS rather than ion channels.

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51
Q

When would spironolactone be given?

A

In someone with poor K control.

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52
Q

What is incontinence?

A

Lack of voluntary control over urination or defecation.

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53
Q

What is the trend in incontinence?

A

More common in men as men have a bladder neck and a stronger urethral sphincter then women.

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54
Q

What information can you get from a bladder diary?

A
  1. Frequency
  2. Volume
  3. Functional capacity
  4. Incontinence
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55
Q

What are the 3 types of incontinence?

A
  1. Stress – associated with coughing and sneezing
  2. Urgency
  3. Mixed – stress + urgency
  4. Continuous – due to fistula
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56
Q

What is the cause of Stress incontinence in men and women?

A

In men - neurogenic or iatrogenic (prostatectomy)

In women - secondary to birth trauma

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57
Q

What is the treatment for female stress incontinence?

A
  1. Pelvic floor physio
  2. Duloxetine (concerns over SE’s)
  3. Surgery
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58
Q

What is the treatment for male stress incontinence?

A
  1. Artificial sphincter

2. Sling

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59
Q

What is an overactive bladder?

A

Urgency and frequency in the presence of local pathology that would account for these symptoms.

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60
Q

What is the treatment of an overactive bladder?

A
  • Behavioural E.g. limit caffeine
  • Pelvic floor physio
  • Muscarinic antagonists
  • Beta 3 agonists
  • Botox
  • Cystoplasty
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61
Q

What is the role of PMC/PAG in micturition

A

Coordination and completion of voiding.

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62
Q

Which group’s are at risk of hypervolemia?

A
  1. AKI patients
  2. CKD patients
  3. Heart failure patients
  4. Liver failure patients
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63
Q

Describe the presentation of Hypervolemia?

A
  • HR is normal, BP normal or high
  • JVP is high
  • Tissue turgor is normal
  • Urine output is normal
  • Weight is increased
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64
Q

What are the symptoms of hypervolemia?

A

shortness of breath and peripheral oedema

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65
Q

What is the effect on

creatine
Hb
haematocrit

in hypervolemia?

A

All reduced

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66
Q

How do you manage hypervolemia?

A
  1. Diuretics e.g. furosemide
  2. Fluid restriction
  3. Treat reversible causes
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67
Q

What are the reasons for a rising creatinine?

A
  1. Aggressive diuretics
  2. Extravascular hypervolemia but intravascular hypovolemia
  3. Progression of CKD
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68
Q

What are the signs of hypovolemia?

A
  • Tachycardia and Hypotension
  • Urine output reduced
  • Tissue turgor is reduced
  • Jugular venous pressure is low
  • Weight is also reduced
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69
Q

What are the symptoms of hypovolemia?

A

Thirst and dizziness

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70
Q

What is the effect on

Creatinine
Haematocrit
Hb

in hypovolemia?

A

All raised

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71
Q

Which groups are at risk of hypovolemia?

A
  1. Elderly
  2. Ileostomy patients
  3. Short bowel syndrome
  4. Bowel obstructions
  5. Those taking diuretics
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72
Q

Where may fluid accumulate in hypovolemia?

A
  • Pulmonary oedema
  • Pleural effusion
  • Ascites
  • Bowel obstruction
  • Intra-abdo collection
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73
Q

What is the management of hypovolemia?

A
  1. Oral fluid
  2. IV fluid if very ill
  3. Treat reversible causes
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74
Q

What are 3 examples of isotonic solutions?

A
  1. 5% Dextrose
  2. 0.9 NaCl
  3. Hartmann’s solution
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75
Q

Describe the movement of Crystalloid fluid

A

Intravascular to extravascular e.g. Gelofusine

Small molecules can pass through the CM.

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76
Q

What is haematuria?

A

Blood in urine

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77
Q

What are the causes of haematuria?

A
  1. Kidney tumour, trauma, stones and cysts
  2. Ureteric stones or tumours
  3. Bladder infection, stones or tumours
  4. BPH or prostate cancer
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78
Q

A patient presents with haematuria, what tests should you order?

A
  1. Urinalysis
  2. Urine cytology
  3. Abdo US and Abdo CT
  4. Cystoscopy
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79
Q

What is renal colic?

A

A pain you get when urinary stones block part of your urinary tract (Kidneys, ureter, bladder and urethra)

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80
Q

What are the symptoms associated with renal colic?

A
  • Colicy pain
  • Nausea and vomiting
  • Pain during urination
  • Severe low abdo or groin pain
  • Urinating less frequently
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81
Q

What are the causes of renal colic?

A
  1. UT stones
  2. UTI
  3. Pyelonephritis
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82
Q

What investigations would you do for renal colic?

A
  • Bloods inc, calcium, phosphate, urate
  • Urinalysis
  • MCS MSU
  • NCCT-KUB – gold standard
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83
Q

What is the treatment for Renal colic?

A
  • Analgesia e.g. NSAIDs – diclofenac
  • Anti-emetics
  • Check for sepsis
  • Treat underlying cause.
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84
Q

What are the functions of the kidney?

A
  1. Filters and exretes waste products from the blood
  2. Regulates BP
  3. Retains albumin
  4. Reabsorption of Na, Cl, K, glucose, H2O, Amino acids
  5. Synthesis EPO
  6. Converts 1-hydroxyvitD to 1.25-dihydroxyvitD
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85
Q

What is the equation for GFR?

A

Um x urine flow rate / Pm

  • Um = concentration of marker in urine
  • Pm = concentration of substance in plasma
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86
Q

What is a typical GFR?

A

120ml/min

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87
Q

What is used to estimate GFR?

A

Creatine

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88
Q

What are 3 features of a good marker substance?

A
  1. Not metabolised
  2. Freely filtered
  3. Not reabsorbed/secreted
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89
Q

What is the affect of afferent arteriole vasoconstriction?

A

Decreased GFR

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90
Q

What is the affect of efferent arterial vasoconstriction?

A

Increased GFR

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91
Q

Where does the bulk of reabsorption happen in the kidneys?

A

PCT

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92
Q

What are 7 things absorbed at the PCT?

A
  1. Sodium
  2. Chlorine
  3. K
  4. Glucose
  5. Water
  6. Amino acids
  7. Bicarb
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93
Q

What is fanconi syndrome?

A

failure of the nephron to absorb essential ions. Sugar and AA are therefore present in the urine.

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94
Q

What is the signs of fanconi syndrome?

A
  1. Sugar in the urine
  2. Acidotic due to bicarb in the urine.
  3. Rickets/ osteomalacia
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95
Q

What are the causes of fanconi syndrome?

A
  1. Myeloma

2. Cystinosis

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96
Q

Why do we have a countercurrent multiplier system?

A

Generates hypertonic medullary interstitium for H2O Reabsorption

Na+ moves out of the ascending limb which increases medullary osmolality –? H2O follows

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97
Q

Describe tubuloglomerular feedback

A

Macula Densa cells of the DCT lie between the AA and EA. They detect NaCl and use this as an indicator of GFR.

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98
Q

What happens when the macula densa detect’s raised NaCl

A

AA Constriction

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99
Q

What happens when the macula densa detects lowered NaCl

A

Renin secretion

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100
Q

What two cell types exist in the CD?

A
  1. Principal

2. Intercalated

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101
Q

What does aldosterone do?

A

Aldosterone regulates sodium reabsorption

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102
Q

How can aldosterone cause hypokalemia?

A
  • Aldosterone secretion causes increases sodium reabsorption
  • Sodium reabsorption leads to K secretion therefore Hypokalemia
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103
Q

How do NSAIDs effect GFR?

A

NSAIDs inhibit prostaglandins –> so lead to AA vasoconstriction = Reduced GFR.

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104
Q

How do ACEi effect GFR?

A

ACEi cause EA Vasodilation = reduced GFR.

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105
Q

What factors govern renal K?

A
  1. Na+
  2. Aldosterone
    Sodium is responsible for volume control
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106
Q

What hormones increase Na reabsorption?

A
  1. Aldosterone

2. Angiotensin 2

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107
Q

What can decrease Na absorption?

A

ANP

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108
Q

What is the function of EPO?

A

Stimulates bone marrow to allow for RBC maturation.

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109
Q

What is benign prostatic hyperplasia?

A

Prostate enlargement

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110
Q

What is PSA?

A

a glycoprotein secreted by the prostate into the blood stream

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111
Q

What are the symptoms of Benign prostatic hyperplasia?

A
  1. Increased frequency of micturition
  2. Nocturia
  3. Hesitancy
  4. Post-void dribbling
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112
Q

What is the treatment of Benign prostatic hyperplasia?

A
  1. Mild symptoms – watchful waiting
  2. Alpha 1 antagonists e.g. tamulosin
  3. 5-alpha reductase inhibitors
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113
Q

How does Tamsulosin work?

A

By relaxing the smooth muscle in the bladder neck and prostate so increases urinary flow, improving obstructive symptoms.

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114
Q

How do 5-alpha reductase inhibitors work?

A

By blocking the conversion of testosterone to dihydrotestosterone (the androgen responsible for prostatic growth)

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115
Q

What investigations should be done in benign prostatic hyperplasia to rule out carcinoma?

A
  1. IPSS prostate score questionnaire
  2. DRE
  3. PSA to rule out prostate cancer
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116
Q

What is the treatment for prostate carcinoma?

A
  • Radial prostatectomy or radiotherapy

- Remove the androgenic drive e.g. bilateral orchidectomy

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117
Q

What are the signs of prostate carcinoma?

A
  1. Increased frequency micturition
  2. Nocturia
  3. Hesitancy
  4. Post-void dribbling

SAME AS BENIGN PROSTATIC HYPERPLASIA.

118
Q

What tests for prostate carcinomas would you perform?

A
  1. Trans-rectal USS of prostate
  2. Serum PSA – will be elevated
  3. Trans-rectal prostate biopsy
119
Q

What is sepsis?

A

Potentially life threatening response to an infection.

120
Q

What is the treatment of sepsis?

A
  1. High flow oxygen
  2. Take blood cultures
  3. IV abx and fluids
  4. Check lactate
  5. Monitor hourly urine output
    Drainage to relieve pressure
121
Q

How would you diagnose urosepsis?

A

A symptomatic UTI combined with 1> of

  • Microbial resistance
  • Immunosuppression
  • Pressure
122
Q

Which 2 groups would you treat for bacteriuria?

A

Pregnant ladies and children

123
Q

What is septic shock?

A

Severe sepsis with persistent hypertension.

124
Q

What are the symptoms of Acute urinary retention?

A
  1. Painful
  2. Sudden onset
  3. > 500ml of urine in bladder
125
Q

What is a rare but serious cause of Urinary retention?

A

Spinal cord compression

126
Q

What are the causes of urinary retention?

A
  • UT stones
  • Tumours
  • Benign prostatic hyperplasia
127
Q

What investigations in Acute urinary retentions would you order?

A
  1. Clinical examination – palpable bladder
  2. MRI
  3. Bloods
  4. Neuro tests – pain in back, loss of anal reflex  all for spinal cord compression
128
Q

What is the treatment in acute urinary retention?

A
  1. Reassurance
  2. Catheterise
  3. Pain relief
129
Q

What do the cavernous nerves carry?

A
  • Parasympathetic – S2-S4

- Sympathetic T11-L2

130
Q

What waste products are removed from the blood in dialysis?

A
  1. Urea
  2. Creatine
  3. Potassium
  4. Phosphate
131
Q

How frequent are

Hospital haemodialysis
Home haemodialysis

A

Hospital haemodialysis –> 3-5 hours 3 times a week

Home haemodialysis –> 2-3 hours, 5 times a week

132
Q

Why do patients with home haemodialysis require less dietary restriction?

A

Due to more frequent haemodialysis.

133
Q

What are the complications of haemodialysis?

A
  1. Hypotension
  2. Cramps
  3. Nausea
  4. Chest pain
  5. Fever
  6. Blocked or infected dialysis catheter
134
Q

Who would be suitable for haemodialysis?

A
  1. People who live alone/frail/elderly
  2. People who fear operating machines
  3. People who are unsuitable for PD e.g. previous abdo surgery, abdo hernia
135
Q

How often is CAPD and APD done?

A

CAPD is done in 30-40 min exchanges, 3-5 times a day.

APD is done once overnight (8hrs)

136
Q

What is peritoneal dialysis?

A
  • Access point is when a peritoneal is placed into the peritoneal cavity through a SC tunnel
137
Q

What are complications of peritoneal dialysis?

A
  1. Infection e.g. peritonitis/catheter exit site infection
  2. Peri-catheter leak
  3. Abdo wall herniation
  4. Intestinal perforation
138
Q

Who is peritoneal dialysis good for?

A
  1. Young people/those in full time work
  2. People who want control/responsibility for their care
  3. People with severe HF
139
Q

What is the physiological process of an erection?

A
  1. Parasympathetic stimulation
  2. Arteriolar dissection
  3. Smooth muscle relaxation
  4. Testosterone
140
Q

What is the role of NO in erections?

A

NO is responsible for the smooth muscle relaxation in an erection
- Causes a fall in cytoplasmic calcium  smooth muscle relaxation

141
Q

What are the main causes of erectile dysfunction?

A
  1. Organic e.g. vasculogenic, neurogenic, hormonal and anatomical
  2. Psychogenic
142
Q

What are the characteristics of psychogenic erectile dysfunction?

A
  1. Sudden
  2. Situational
  3. Younger males affected
143
Q

What are 4 risk factors for Erectile dysfunction?

A
  1. Obesity
  2. Lack of exercise
  3. Smoking
  4. Diabetes mellitus
144
Q

What are the non pharmacological management of ED?

A
  1. Lose weight stop smoking

2. Education and counselling of patient and partner

145
Q

What is the first line pharmacological treatment of ED?

A

Phosphodiesterase inhibitors e.g. Viagra, Cialis –> vasodilation so increase arterial blood flow.

146
Q

What is the second line pharmacological treatment of ED?

A
  1. Intracavernous injections

2. Vacuum devices

147
Q

What is the third line pharmacological treatment of ED?

A
  1. Penile prosthesis implantation
148
Q

What is priapism?

A

Erection lasting over 4 hours, permanent ischaemic damage as a consequence.

149
Q

Describe the epidemiology of Kidney stones?

A

10-15% lifetime risk, Males > females 2:1 ratio, common among 30-50-year olds.

150
Q

What are the potential causes of stones in the UUT?

A
  1. Congenital abnormalities
  2. Metastable urine
  3. Hypercalcaemia/ high urate/ high oxalate
  4. Dehydration
  5. Infection
151
Q

What is the pathophysiology of stone formation?

A

Stones form from crystals in supersaturated urine –> 80% are calcium based e.g. calcium oxalate

152
Q

What are the symptoms of stones?

A
  1. Loin pain  groin pain
  2. Renal colic – pain caused by a blockage in the urinary tract
  3. UTI symptoms e.g. dysuria, urgency and frequency
  4. Recurrent UTI’s
  5. Haematuria
153
Q

How can you prevent Stones?

A
  1. Staying well hydrated
  2. Low salt diet
  3. Healthy protein intake
  4. Reduced bmi
  5. Active lifestyle
  6. Deacidification of urine can prevent uric acid stones
154
Q

What is the treatment for stones?

A
  1. Conservative e.g. if stone is <5mm and in a safe location w/ no symptoms
  2. Medical e.g. nifedipine (CCB)
  3. Lithotripsy – fragment stones which will pass spontaneously
  4. Surgical – ureteroscopy – PCNL for larger stag horn ureteric tones
155
Q

Treatment for stag horn ureteric stones

A
  • Analgesia and anti-emetics
  • Observe for sepsis
  • PCNL
156
Q

Where do UT stones usually form?

157
Q

Where do UT stones usually get stuck?

A
  • Ureteropelvic junction
  • Pelvic brim
  • Vesoureteric junction
158
Q

Where does a transplanted kidney lie in the recipent?

A

Illiac fossa

159
Q

What is the selection criteria for a donor for kidney transplant?

A
  1. Blood relative
  2. ABO Blood group compatible
  3. HLA identical
  4. Excellent medical condition and normal renal function
160
Q

What 3 conditions can exclude a live kidney donation

A
  1. Renal parenchymal disease
  2. History of stones/frequent UTI/Hypertension/DM
  3. Recent malignancy
161
Q

What is the criteria for a cadaver donor?

A
  1. Irreversible brain damage
  2. Normal renal function
  3. No evidence of pre-existing renal disease or transmissible disease
  4. ABO Compatible and best HLA possible
162
Q

What kidney function tests can you perform?

A
  1. Serum creatine
  2. Creatinine clearance
  3. Urinalysis
  4. Urine culture
  5. GFR
163
Q

Give 5 contraindications for renal transplant

A
  1. ABO incompatibility
  2. Cytotoxic Ab’s against HLA antigens
  3. Recent malignancy
  4. Active infection
  5. AIDs
  6. Morbid obesity
  7. Age > 70
164
Q

How would you assess recipent and donor in transplants?

A
  1. HLA tissue typing (important to match DR antigens)
  2. Lymphocytotoxic cross matching – check there are no performed Ab against HLA antigens
  3. ABO blood group compatibility
165
Q

What 4 factors affect the longevity of a renal allograft?

A
  1. Age
  2. HLA matching
  3. Ischaemia time
  4. Number of acute rejection episodes
  5. Ethnicity
166
Q

What are the 2 major causes of Renal allograft failure?

A

chronic rejection and death with functioning graft

167
Q

What are 2 causes of death post kidney transplant

A

CV disease and infection

168
Q

What are 3 types of renal allograft rejection?

A
  1. Hyper-acute
  2. Acute
  3. Chronic
169
Q

Describe hyper-acute allograft rejection

A

preformed antibodies against HLA antigens of donor organs

Can be from blood transfusion, pregnancy, prior transplant and AI disease

170
Q

What would cause immediate graft loss?

A

Fibrinoid necrosis

171
Q

What is acute allograft rejection?

A

Activated T lymphocytes, occur within first 6 months –> often reversible w/ steroids

172
Q

What is chronic allograft rejection?

A

Slow and gradual decline in renal function, accompanied by proteinuria

173
Q

What is the Banff criteria?

A

diagnose allograft rejection

174
Q

What are the consequences of chronic immunosuppression?

A
  1. Malignancy
  2. Infection
  3. SE’s of other drugs
175
Q

What is transitional cell carcinoma?

A

AKA Urothelial carcinoma, effecting the

  1. Bladder
  2. Ureter
  3. Renal pelvis
176
Q

What is the epidemiology of TCC?

A

75% male and over 40

177
Q

What are the risk factors for TCC?

A
  • Smoking
  • Occupational exposure e.g. working in rubber factories
  • Increasing age
  • Male gender
  • Family history
178
Q

What are the symptoms for TCC?

A
  1. Painless haematuria
  2. Frequency
  3. Urgency
  4. Dysuria
  5. UT obstruction
179
Q

What investigations would you order in suspected TCC?

A
  1. Urine dipstick
  2. Blood tests
  3. Flexible cystoscopy = diagnostic
  4. Imaging of the URT
  5. TURBT –> trans urethral resection of bladder tumour
180
Q

What are the risks of flexible cytoscopy?

A
  1. UTI

2. Problems passing urine

181
Q

Why would you image the full URT in suspected TCC.

A

You would image the URT with suspected transitional cell carcinoma as you need to confirm there is no other TCC in the UT

  • CT, IVU, USS, and Xray
182
Q

What staging does TCC use?

A

TMN staging

183
Q

Why would you do a trans urethral resection of bladder tumour (TURBT)?

A

Histological and staining analysis.

184
Q

What is the treatment for non-muscle invasive bladder cancer?

A
  1. TURBT

2. Chemotherapy to reduce the risk of recurrence and progression to muscle invasion

185
Q

What is the treatment for muscle invasive bladder cancer?

A
  1. Radical cystectomy = gold standard
  2. +/- neo-adjuvant chemo
  3. Radical radiotherapy if not fit/unwilling to undergo cystectomy
186
Q

What is the treatment for T4 TCC (invasion beyond the bladder)

A
  1. Palliative chemo/radiotherapy

2. Chronic catheterisation for pain

187
Q

What helminth can cause Bladder cell carcinoma?

A

Schistosomiasis

188
Q

What is the epidemiology of Renal cell carcinoma?

A

Incidence increases in those above 60 and male.

189
Q

What are the risk factors for renal cell carcinoma?

A

smoking, obesity and hypertension

190
Q

What disease can cause renal cell carcinoma?

A

Von Hippel lindau disease can cause renal cell carcinoma

  • AD, Loss of tumour suppressor gene VHL.
  • Lots of benign cysts grow –> some turn cancerous
191
Q

What are the signs of renal cell carcinoma?

A
  • Haematuria
  • Flank mass
  • Loin pain
192
Q

Do RCC present early or late?

A

RCC are rarely presenting with symptoms as they are often found early through incidental imaging

193
Q

What may RCC metastasise too?

A

lymph nodes
lungs
bones

194
Q

What is a variocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum

195
Q

Give two causes of varioceles?

A
  • RCC may cause L sided varicocele

- If the tumour obstructs where the gonadal vein drains into the renal vein.

196
Q

What investigations would you order in suspected RCC?

A
  • Ultrasound
  • Bloods  FBC + U+E, LFT, Ca profile
  • Abdo CT w/ contrast
  • Bone scan for boney metastasis
197
Q

What is the treatment for localised RCC?

A

Surgical partial nephrectomy

198
Q

What is the treatment for metastatic RCC?

A

Palliatve nephrectomy + radiotherapy

199
Q

What is the bozniak classification?

A

To help differentiate between benign cystic lesions and cancerous cystic lesions

200
Q

What is pyelonephritis?

A

Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis

201
Q

What is the cause of pyelonephritis?

A

UPEC. Typically, P pili –> infection usually in the bladder.

202
Q

What are the symptoms of pyelonephritis?

A
  1. Loin pain
  2. Fever
  3. Pyuria
    May also have a severe headache and be fluid deplete
203
Q

What investigations would you order in pyelonephritis?

A
  1. Urinalysis
  2. MCS MSU
  3. Bloods – raised WCC, ESR and CRP
204
Q

What is the treatment for pyelonephritis?

A

IV fluids and antibiotics e.g. gentamicin/co-amoxiclav

  • Drain obstructed kidney
  • Catheterise if necessary
  • Analgesics
205
Q

What is the likely cause of pyelonephritis in children?

A

Likely cause of pyelonephritis in children  reflux or structural/functional abnormalities.

206
Q

What are LUT symptoms?

A

Storage problems

  1. Straining
  2. Hesitancy
  3. Incomplete emptying
  4. Poor flow
207
Q

A 50yo man presents with LUT symptoms, what is the likely cause?

A

Benign prostatic hyperplasia.

208
Q

What investigation would you order in a patient with LUT symptoms?

A
  1. Urinary tests e.g. dipstick
  2. Urinary flow; maximum flow rate and residual volume are important
  3. Symptom assessment; International prostate scoring system
  4. Blood tests e.g. PSA, U+E
209
Q

What are the causes of nocturnal polyuria?

A
  1. Habiutal
  2. Congestive cardiac failure
  3. Sleep apnoea
210
Q

Describe the treatment for mild LUTs

A

reassurance, watch and wait

211
Q

Describe the treatment for moderate LUTs

A

Fluid management, avoid caffeine and bladder drill

212
Q

Describe the pharmacological management of LUTs

A
  • Alpha 1-blockers e.g. tamulosin

- 5 Alpha-reductase inhibitors

213
Q

How do Alpha 1 blockers and 5-alpha reductase inhibitors work in the treatment of LUTs?

A

Alpha 1-blockers cause vasodilation and so reduced resistance and bladder outflow

5- Alpha reductase inhibitors inhibit conversion of testosterone to dihydrotestosterone so reduce prostate size.

214
Q

What is a side affect of using Alpha 1-blockers in treatment of LUTs?

A

Tamsulosin

Hypotension + retrograde ejaculation

215
Q

What is the surgical treatment for benign prostate enlargement?

A

Transurethral resection of the prostate

216
Q

What are the consequences of untreated LUTs?

A

Consequences of untreated LUTS

  1. Bladder calculi (stones)
  2. UTI
  3. Urinary incontinence
  4. Reduced QOL
  5. Acute urinary retention
217
Q

What is Cystitis?

A

Inflammation of the bladder secondary to infection

218
Q

What are the symptoms of cystitis?

A
  1. Dysuria
  2. Frequency
  3. Urgency
219
Q

What are the risk factors for cystitis?

A
  1. Obstruction
  2. Previous damage to the bladder epithelium
  3. Bladder stones
  4. Poor bladder emptying
220
Q

What is the treatment for cystitis?

A
  • Over the counter painkillers

- Antibiotics if infection is confirmed

221
Q

What are the consequences of glomerulonephritis?

A
  1. Leaky glomeruli –> haematuria and proteinuria
  2. High BP
  3. Deteriorating kidney function
222
Q

What is the pathophysiology of glomerulonephritis?

A

Immunologically mediated – immunoglobulin deposits and inflammatory cells

223
Q

How can glomerulonephritis cause sepsis?

A

Becuase you lose Ig in the urine.

224
Q

What are the causes of acute nephritic syndrome

A
  1. ANCA
  2. Goodpastures
  3. SLE
  4. Post streptococcal infection – deposits immune complexes in the kidney
  5. IgA nephropathy
225
Q

What is the primary cause of acute nephrotic syndrome

A

Minimal change disease –> mainly in kids

226
Q

What investigations would you do in suspected glomerulonephritis/acute nephrtic syndrome?

A
  1. Renal biopsy
  2. Urine dipstick ++++ protein
  3. Bloods – low serum albumin
  4. Look for AI
227
Q

What are the signs of acute nephrtiic syndrome?

A
  1. Inflammation of glomeruli
  2. Haematuria and Proteinuria
  3. Hypertension
  4. Fluid overload
  5. Oliguria
  6. Red cell clasts
228
Q

What signs are needed to make a diagnosis of nephrotic syndrome?

A
  1. Hypoalbuminaemia
  2. Oedema
  3. Heavy proteinuria
  4. Hypercholesterolaemia
229
Q

What can nephrotic syndrome be secondary to?

A
  1. Diabetes
  2. Amyloid
  3. Infection
  4. SLE
  5. Drugs
230
Q

What are the consequence of nephrotic syndrome?

A

Sepsis and venous thromboembolism.

231
Q

Treatment for nephrotic syndrome

A
  1. Treat complications e.g. diuretics for oedema, ACEi for proteinuria
  2. Treat the underlying cause
  3. Statins and anti-coagulation e.g. warfarin
  4. In children give steroids as minimal change disease is the most likely cause of disease
232
Q

What is the pathophysiology behind nephritic syndrome?

A

Immune complex deposition in glomerular capillary –>neutrophil recruitment –> inflammation and damage to the glomerular capillary membrane  RBC, WBC, Protein etc leaks into the Bowmans capsule and is excreted in the urine.

Simple –> podocytes or the BM aren’t working properly and so huge amounts of protein leaks into the BC and is excreted in the urine.

233
Q

What is the difference between nephrotic and nephritic disease?

A

Nephrotic disease - Damage to glomeruli allowing too much protein to pass through the urine. DOESNT INCLUDE BLOOD.

Nephritic disease - Proteinuria and haematuria, glomeruli injury.

234
Q

What is the treatment for renal artery stenosis?

A

ACE inhibitors e.g. ramipril

235
Q

A patient presents complaining that they are hardly passing any urine and in the small amount of urine they do pass there is blood in it. On further questioning they tell you they have recently finished a course of antibiotics (amoxicillin) for a chest infection they had 2 weeks ago. Their BP is high. What is the likely cause?

A

Nephrotic syndrome –> THEY PASS BLOOD!

236
Q

Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?

A

Nephrotic syndrome

237
Q

A 50 y/o M presents with haematuria. On examination he has HTN, increased serum Cr and urea, proteinuria and bilateral palpable costo-vertebral angle masses. You take a family history and find out that his dad died of a sub-arachnoid haemorrhage. What is the most likely diagnosis?

A
  • ADPKD.
  • Normally people present around 50 y/o.
  • Raised creatinine and urea indicate a kidney problem.
  • The kidneys can be HUGE in ADPKD hence the palpable masses.
  • Intracranial haemorrhages are an extra-renal manifestation of ADPKD.
238
Q

Why might someone with ADPKD have bilateral palpable costovertebral masses?

A

Cysts increase in size and cause renal enlargement. Often the kidney’s can be HUGE!

239
Q

A patient presents with haematuria. A MSU sample is taken and a blood film is done. The RBC’s look dysmorphic. Where in the urinary tract is the problem likely to be?

A

Dysmorphic signify glomerular origin, if RBC look normal its likely a LUT problem.

240
Q

Most common cause of renal cancer in kids

A

Wilms tumour

241
Q

What is the symptoms of type 1 prostatitis? (Acute bacterial prostatitis)

A
  1. Systemically unwell, fever
  2. Rigors
  3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow)
  4. Pelvic pain
242
Q

What are the symptoms of Type 2 prostatitis (chronic bacterial prostatitis)

A
  1. Recurrent UTI’s
  2. Pelvic pain
  3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow)
  4. Uropathogens in urine
243
Q

How long should a patient have symptoms of type 2 prostatitis for it to be chronic?

244
Q

What is the treatment of Type 1 prostatitis (acute bacterial prostatitis)

A

IV Abx e.g. gentamicin, co-amoxiclav for 2-4 weeks.

245
Q

What is the treatment of Type 2 Prostatitis (chronic bacterial prostatitis)

A

4-6 weeks quinolone e.g. ciprofloxacin

246
Q

What is the symptoms of Type 3 prostatitis (pelvic pain syndrome)

A

Pelvic pain.

247
Q

What investigations would you do in prostatitis?

A
  1. Urinalysis and MSU
  2. Semen cultures
  3. STI screen
  4. Bloods including MCS
248
Q

What is the NIDDK-classification for prostatitis?

A
  1. Type 1 – acute bacterial
  2. Type 2 – Chronic bacterial
  3. Type 3a – inflammatory chronic pelvic pain syndrome
  4. Type 3b – Non-inflammatory chronic pelvic pain syndrome
  5. Type 4 – asymptomatic inflammatory prostatitis
249
Q

What is the cause of urethritis?

A

STIs e.g. gonorrhoea and chlamydia

250
Q

What are the symptoms of urethritis?

A

Urethral pain and dysuria

251
Q

Describe the treatment of urethritis

A

Treat the underlying infection with Antibiotics + education

252
Q

What is epididymo-orchitis?

A

Inflammation of the epididymis and testicle

253
Q

What are the symptoms of epipidymo-orchitis?

A
  • Sudden onset tender swelling
  • Dysuria
  • Sweats/fever
254
Q

What is the aetiology of epipidymo-orchitis?

A
  • If under 35 = ST e.g. chlamydia

- If over 35 = UTI

255
Q

What investigations would you do in epipidymo-orchitis?

A
  1. Void urine
  2. Urethral swab
  3. MSU
    Rule out testicular torsion
256
Q

What is the treatment for epipidymo-orchitis?

A
  1. If STI aetiology suspected – refer to GUM and maybe give doxycycline
  2. If UTI aetiology suspected give quinolone (ciprofloxacin)
257
Q

What are UTIs?

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria.

258
Q

What are 3 causative organisms of UTIs?

A
  1. Uropathogenic strains of e.coli  UPEC
  2. CNS e.g. s. saprophyticus
  3. Proteus mirabilis
  4. Enterococci
  5. Klebsiella pneumonia
259
Q

What is the epidemiology of UTIs?

A

more common in women with short urethras and it’s proximity to the anus

260
Q

What is the pathology of UTIs?

A

Organisms colonise the urethral meatus and ascend via the transurethral route

261
Q

How can bacteria enter the UT?

A
  • Sex

- Catherization

262
Q

What are 3 bacterial virulence factors that aid their ability to cause UTIs?

A
  1. Fimbriae/pilli that adhere to urothelium
  2. Acid polysaccharide coat that resists phagocytosis
  3. Toxins
  4. Enzyme production e.g. urease
263
Q

Why does the vagina have lots of lactobacilli?

A

Maintain low pH for defence.

264
Q

What does Type 1 pili bind to and what does it cause?

A

Uroplakin and LUTI

265
Q

What does Type P Pili bind to and what does it cause?

A

Binds to gylcoproteins on urothelium to cause UUTI’s

266
Q

Why are post menopausal women more likely to get UTIs?

A
  1. pH rises –> increased colonisation by colonic flora

2. Reduced mucus secretion

267
Q

What is the host defence mechanisms against UTI’s?

A
  1. Antegrade flushing of urine
  2. Tamm-horsfall protein
  3. GAG layer
  4. Low urine pH
  5. Commensal flora
  6. Urinary IgA
268
Q

What is pyuria?

A

presence of leukocytes in the urine

269
Q

Give 3 examples of LUTIs

A
  1. Cystitis
  2. Prostatitis
  3. Epididymitis
  4. Urethritis
270
Q

Example of an UUTI

A

Pyeloneprhitis

271
Q

Investigations for a UTI

A
  1. Take a good history
  2. Urinalysis – multistix SG.
  3. Microscopy – culture and sensitivity of mid-stream urine.
  4. In recurrent/complicated UTI renal imaging is important
272
Q

What is the difference between complicated and uncomplicated UTI’s?

A
  • Someone with an abnormal UT
  • A man
  • A pregnant lady
  • Children
  • The immunocompromised
  • If it is recurrent
273
Q

First line treatment for uncomplicated UTIs

A
  1. Trimethoprim or nitrofurantoin for 3 days.

2. Increased fluid intake and regular voiding

274
Q

How does trimethoprim work?

A

Affects folic acid metabolism

275
Q

First line treatment for complicated UTIs

A
  1. Same for an uncomplicated UTI but MCS MSU is necessary

2. Patient would take a longer Abx course tailored to sensitivity

276
Q

What are the causes of recurrent UTIs?

A
  1. Re-infection
  2. Bacterial persistence
  3. Unresolved infection
277
Q

What is the definition of a recurrent UTI?

A

2 episodes in 6 months of >3 in 12 months.

278
Q

What is the management of recurrent UTIs?

A
  1. Increased fluid intake
  2. Regular voiding
  3. Void pre and post intercourse
  4. Abx prophylaxis
  5. Vaginal oestrogen replacement
279
Q

What is the pathophysiology of congenital polycystic disease.

A

Genetic mutation –> predisposition to cyst development –> cell proliferation and loss of planar polarity –>fluid secretion and cyst expansion

280
Q

What is the pathophysiology of acquired polycystic disease?

A

Cysts develop over time –> renal injury/ischaemia causes abnormal cell proliferation

281
Q

What are the 4 congenital causes of renal cysts?

A
  1. ADPKD
  2. ARPKD
  3. VHL
  4. OFD1 (Oral-facial-digital syndrome 1)
282
Q

What is autosomal dominant polycystic kidney disease?

A

An autosomal dominant condition characterised by progressive cyst development – cysts increase in size –> renal enlargement and loss of function causes kidney failure

283
Q

When does ADPK present?

A

Around 50 years old as there is more cysts.

284
Q

What is the cause of ADPK?

A

Mutation in PKD1 (more severe) and PKD2 is associated.

285
Q

What are the signs of ADPK?

A
  1. Hypertension
  2. Haematuria
  3. Polyuria
  4. Abdo/loin pain
  5. Palpable bilateral costo-vertebral masses
286
Q

How do you diagnose ADPK?

A
  1. Symptoms
  2. Family history
  3. High BP
  4. Urinalysis
  5. USS
287
Q

What is a prognostic marker for ADPKD?

A

TKV - total kidney volume

288
Q

What does a mutation in HNF1 beta cause?

A

AD tubulointerstitial kidney disease

289
Q

What is the difference in epidemiology of ARPK and ADPK?

A

ADPKD presents in middle age whereas ARPKD starts in infancy

290
Q

What are the features of acquired renal cystic kidney disease?

A
  1. No genetic mutation
  2. No family history
  3. Normal kidney size
  4. Risk factor for renal cell carcinoma
291
Q

Where is the access point in haemodialysis?

A

AV fistula

292
Q

Why might some patients have a PTFE graft instead of an AV fistula?

A

Pt may have atherosclerotic veins or previous fistulas.

Phase 2a Sheffield Medicine (10 decks)

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