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General Flashcards

1
Q

Functions of the kindey

A
  • Filter or secrete waste/excess substances
  • Retain albumin and circulating cells
  • Reabsorb glucose, amino acids and bicarbonates
  • Control BP, fluid status and electrolytes
  • Activates 25-hydroxy vitamin D (by hydroxylating it to form 1,25 dihydroxy
    vitamin D)
  • Synthesis erythropoietin
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2
Q

Define GFR

A

Glomerular filtration rate

Volume of fluid filtered from the glomeruli into Bowman’s space per unit time (mins)

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3
Q

Normal GFR

A

120ml/min (7.2L/h)

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4
Q

What % of the cardiac output does each kidney receive

A

20%

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5
Q

True or False:

eGFR can help predict creatinine generation

A

True
Creatinine is produced by muscles and eliminated (only) by the kidneys
Predicts Creatinine generation from age gender and race also

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6
Q

What is reabsorbed at proximal convoluted tubule?

A

Sugars
Amino acid
Bicarbonate
Main portion of Na+ (70%) and water follows

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7
Q

True or False:

PCTs are not vulnerable to ischaemic injury

A

False

ARE vulnerable to ischaemic injury, resulting in acute tubular necrosis

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8
Q

What part of nephron is most vulnerable to damage

A

Proximal Convoluted Tubule

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9
Q

Example of disease of PCT

A

Fanconi syndrome:

  • proximal tubular insult
  • caused by cytinosis, Wilsons and TENOFOVIR drug (used in HIV)
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10
Q

What can result from disease of the PCT

A

Glycosuria (glucose in urine)
Acidosis with failure of urine acidification
Phosphate wasting resulting in rickets/osteomalacia
Aminoaciduria (amino acid in urine)

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11
Q

What % of Na+ is reabsorbed by Loop of Henle

A

25%

and water follows

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12
Q

Example of a drug that can act on Loop of Henle

A

Loop diuretic

as alot of Na+ filtered here and water follows, if can block here can have a large effect

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13
Q

Example of loop diuretic

A

Furosemide

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14
Q

Which part of the LoH are sodium potassium chloride transporters more active?

A

Ascending loop

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15
Q

What % of sodium is reabsorbed in Distal Convulted Tubule

A

5%

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16
Q

What diuretics act on DCT

A

Thiazide diuretics e.g. Chlorothiazide

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17
Q

When would Juxtaglomerular apparatus release renin

A

Juxtaglomerular apparatus is a solute sensing organ.
If detects high solutes (e.g. Na+), it will think GFR is low so releases renin.
JXA effectively senses Blood Pressure

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18
Q

What part of nephron does salt handling

A

Collecting duct as by this point, most of salt has been reabsorbed

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19
Q

What ions are secreted by the collecting duct into urine

A

K+

H+

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20
Q

Name 2 hormones that act on collecting ducts

A

Aldosterone - increases the transcription of eNac channels which absorb Na+ in exchange for K+
Vasopressin - water is absorbed via aquaporin 2
channels

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21
Q

How does hyperaldosteronism lead to hypokalemic alkalosis

A

In hyperaldosteronism (high aldosterone) there is lots of Na+ reabsorption resulting in a negative lumen, consequently K+ and H+ rush in and this results in hypokalaemic alkalosis.

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22
Q

What can you give to correct hyperkalemic acidosis (like in Addisons)

A

Sodium Bicarbonate

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23
Q

Would you get alkalosis or acidosis with loop diuretics

A

Alkalosis

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24
Q

Which hormone acts on renal potassium control

A

Aldosterone

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25
Q

K+ is freely filtered and mostly reabsorbed in which parts of nephron

A

PCT

LoH

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26
Q

Effect of insulin or catecholamines on cellular K+ uptake

A

Increase uptake

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27
Q

Which K+ modifying renal medication cause hypokalemia

A

Loop diuretics

Thiazide diuretics

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28
Q

Which K+ modifying renal medication cause hyperkalemia

A
  • Spironolactone (aldosterone antagonist)
  • Amiloride (acts on eNac channels)
  • ACE inhibitors (Ramipril)
  • Angiotensin receptor blockers (ARB)
  • Trimethoprim (acts on eNac channels but milder)
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29
Q

Are diuretics nephrotoxic

A

Diuretics are NOT NEPHROTOXIC but hypovolaemia (which they can cause e.g. loop & thiazide diuretics) IS

Loop and thiazide diuretics together are extremely powerful and effective together resulting in profound diuresis

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30
Q

If plasma is too concentrated, what is released by hypothalamus/posterior pituitary to dilute it

A

ADH (vasopressin)

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31
Q

What is erythropoietin

A

Hormone that produces haemoglobin

Produced in response to tissue hypoxia

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32
Q

When can erythropoietin be given

A

In advanced kidney disease and anaemia to help increase O2 transport

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33
Q

In anaemia, what is expected GFR

A

GFR <30

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34
Q

True or false:

Renal cortex acts as an oxygen sensor

A

True

Blood flow and oxygen are matched

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35
Q

What reaction occurs in kidneys in production of vitamin D

A

25-hydroxy vitamin D is hydroxylated to form 1,25-dihydroxy vitamin D (calcitriol)

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36
Q

What is effect on Calcium levels in kidney failure

A

Kidney cannot hydroxylate 25-hydroxy vitamin D to calcitriol. Therefore Calcium cant be absorbed from gut and so would theoretically decrease

37
Q

Effects of calcitriol

A
  • Increases Ca2+ and phosphate absorption from the gut
  • Increases phosphate absorption to a lesser extent
  • Suppresses parathyroid hormone (PTH)
38
Q

What condition can result from calcitriol deficiency and why

A

Secondary Hyperparathyroidism

Low vitamin D results in low Ca2+ and phosphate resulting in increased PTH (which causes Ca2+ and phosphate leeching from bones as well as increased osteoclast activity and reduced bone)

39
Q

What comprises upper urinary tract

A

Kidneys

Ureters

40
Q

What comprises lower urinary tract

A

Bladder (reservoir)
Prostate gland (in men) (Uterus in women)
Urethra and urethral sphincter

41
Q

What is the function of (lower) urinary tract

A

Micturition
To convert the continuous process of excretion (urine production) to an
intermittent, controlled volitional process

42
Q

Essential features of lower urinary tract

A
  • Low pressure and insensible storage of urine of adequate capacity
  • Prevent leakage of the urine stored
  • Allow rapid, low-pressure voiding at an appropriate time and place
43
Q

What is the mean arterial pressure that drives filtration in the Bowman’s capsules

44
Q

Why is there a progressive reduction in pressure along the nephron

A

Due to reabsorption as you go along

Pressure in collecting duct system is 3-10mmHg

45
Q

Describe neuronal control of voiding

A

Pontine micturition centre stimulates excitatory control to detrusor nucleus and inhibits Onuf’s nucleus.
Signal is transmitted from spinal root S2-4 via the parasympathetic
nervous system and this results in contraction of detrusor muscles and
relaxation of the urethra.

46
Q

Which spinal roots stimulate urination (voiding)

A

S2-S4 (parasympathetic - cholinergic)

47
Q

Describe neuronal control of stopping urination (storage)

A

Pontine storage centre stimulates and sends inhibitory signals to
detrusor muscles and excitatory signals to Onuf’s nucleus
Signal is transmitted from spinal root T10 to L2 via the sympathetic nervous system and this results in the relaxation of the bladder and
contraction of the urethral sphincter

48
Q

What is the storage of the bladder

A

around 500ml

49
Q

Epithelium of bladder

A

Urothelium (transtitional)
Highly specialised stratified 3-7 cells thick
Umbrella structure that is completely impermeable so cannot reabsorb urine
Able to fold and unfold to increase volume

50
Q

Why are men more likely to develop problems with retention

A

Have a greater voiding pressure due to them having a longer urethra.
Thus more likely to develop retention.

51
Q

Why are women more likely to have problems with incontinence

A

Have a shorter urethra with lower resistance and thus higher flow rates

52
Q

What urology complications can occur if the spinal cord is cut above S2-4?

A

Will only be able to urinate when the bladder is full

Descending pathway will not be able to inhibit this

53
Q

Normal flow rates in men aged:
<40
40-60
>60

A

21ml/s (<40)
18ml/s (40-60)
13ml/s (>60)

54
Q

What can reduce flow rates

A

Obstruction within the lower urinary tract

Detrusor underactivity

55
Q

How much urine needs to be void for representative flow rate measurement

A

At least 125ml

56
Q

What is normal PVR (Post Void Residual)

57
Q

Examples of disease that can occur from elevated PVR (Post Void Residual)

A

Hydronephrosis

Elevated creatinine

58
Q

Example cause of high PVR (Post Void Residual)

A

Detrusor underactivity

59
Q

Complications of BPE

A 
Symptom progression (17-40%)
Infections (0.1-12%)
Stones (0.3-3.4%)
Haematuria 
Acute retention (1-2% per year)
Chronic retention
Interactive obstructive uropathy (<2.5%)
60
Q

What is main substance made by prostate

A

PSA

  • liquifies semen
  • glycoprotein produced by prostate cells
61
Q

What zone of the prostate is the urethra in

A

Transitional zone (adjacent to central zone and surrounded by peripheral zone)

62
Q

Which zone of prostate is most often enlarged by prostate tumour

A

Peripheral zone

63
Q

Prostate cancer epidemiology

A 
Fam Hx in 5-10%
Mean diagnosis age is 72
Common in industrialised West
Most commonly diagnosed cancer in men
Lifetime risk ~15%
64
Q

What type of cancer is prostate cancer

A

Adenocarcinoma

65
Q

Where does prostate cancer spread

A

Spreads locally thorugh prostate capsule

Metastasises to lymph nodes and bone (sclerotic) and occasionally to lung, liver and brain

66
Q

Biomarkers for prostate cancer

A

Tissue biopsy
Serum (blood) Prostate-Specific Antigen or Prostate-Specific Membrane Antigen (more leakage of PSA, not more produced)
Urine - PCA3 or Gene fusion products (TMPRSS2-ERG)

67
Q

when would you see high PSA

A

Benign prostate enlargement
UTI
Prostatitis
(70% of men with high PSA do NOT have prostate cancer, 6% of men with prostate cancer will have a normal PSA)
higher PSA means higher risk of prostate cancer
>20ng/ml likely metastatic cancer (most common place is bone)
<2.5 not likely cancer

68
Q

Diagnosis of prostate cancer

A 
LUTS
PSA
Transrectal ultrasound scan
Prostate biopsy
Prostate cancer grading
69
Q

Grading of prostate cancer

A 
Gleason grading (from biopsy)
Partin's nomograms - combine clinical T stage, PSA and biopsy Gleason score
70
Q

Staging of prostate cancer

A

T stage:
T1-no palpable tumour on DRE
T2-palpable tumour, confined to prostate
T3-palpable tumour extending beyond prostate
N stage = MRI scan, CT scan, (laparoscopy)
M stage = Bone scan

71
Q

Treatment of Localised Prostate cancer

A

Curative - surgery; radiotherapy (external beam, brachytherapy); adjuvant hormones
If not then just observation (active monitoring/survellience

72
Q

Treatment of Locally advanced prostate cancer

A

Local control:

Surgery; radiotherapy + neoadjuvant hormone therapy

73
Q

Treatment of Metastatic prostate cancer

A

Palliative - Hormone therapy

74
Q

How could you confirm localised prostate cancer if high PSA is detected

A

Transrectal ultrasound

Biopsy of prostate gland

75
Q

Surgery for localised prostate cancer (also do radiotherapy)

A

Radical prostatectomy

Open, robotic (most robotic)

76
Q

What is focal therapy (prostate cancer)

A

High intensity ultrasound (HIFU), photodynamic therapy (TOOKAD)

77
Q

Pros of radical treatment of localised prostate cancer

A

Curative treatment
High mortality in prostate cancer
Reduced patient anxiety
Benefits of surgery shown by longitudinal studies

78
Q

Cons of radical treatment of localised prostate cancer

A

Disease of the elderly
Competing causes of death
30% of men with prostate cancer die OF prostate cancer
Adverse effects of treatment

79
Q

Treatment of metastatic prostate cancer

A 
Surgical castration
-reduced pain due to bony metastases
-prolonged survival
-median survival 2.5 years
Androgen deprivation therapy (GNrH analogues; LH antagonists)
80
Q

Prognosis of advanced prostate cancer

A

80% androgen-sensitive
Castration leads to remission of advanced disease (apoptosis of cancer cells)
Median response is 2 years

81
Q

What can be given if prostate cancer is castration-resistant

A

2nd line HRT: Abiraterone and Enzalutamide
Cytotoxic chemo
Bisphosphonates (Zoledronic acid)
Palliation

82
Q

Most common site of metastasis of prostate cancer

83
Q

Are majority or minority of prostate cancer cases T1c

A

Majority (detected on PSA testing)

84
Q

Reasons for screening for prostate cancer

A

Commonest cancer in men – lifetime risk c. 9%
Responsible for 10,000 deaths per annum in UK.
4th most common cause of cancer death.
3% of men will die of prostate cancer.

85
Q

Reasons against screening for prostate cancer

A

Uncertain natural history
Overtreatment
Morbidity of treatment

86
Q

Benefits of PSA testing

A

Early diagnosis of localised disease (cure)

Early treatment of advanced disease (effective palliation)

87
Q

Risks of PSA testing

A

Over-diagnosis of insignificant disease

Harm caused by investigation/ treatment

88
Q

Prevention of prostate cancer

A

Dietary

5 alpha-reductase inhibitors

Medicine Phase 2a GU (18 decks)

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