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Year 2 > Genitourinary: Part 1 > Flashcards

Genitourinary: Part 1 Flashcards

1
Q

Name 6 functions of the kidney

A
  1. Filter or secrete waste/excess substances
  2. Retain albumin and circulating cells
  3. Reabsorb glucose, amino acids and bicarbonates
  4. Control BP, fluid status and electrolytes
  5. Actiates 25-hydroxy vit D (hydroxylates hit to 1,25 dihydroxy vit D)
  6. Synthesises erythropoietin
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2
Q

Define GFR

A

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

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3
Q

What is th normal GFR in the body

A

120ml/min

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4
Q

What percentage of the cardiac output does each kidney receive

A

20%

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5
Q

What is the eGFR

A

Predicts creatinine generation (produced by muscle and only eliminated from the kidneys) - from age,gender and race

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6
Q

What factor is required for a normal GFR

A
  1. Everything is at a steady rate and extremes of muscle mass may be misleading (Body builders or amuptees)
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7
Q

Where do sugars, amino acids and bicarbonates get reabsorbed

A

PCT

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8
Q

Where is 70% of Na reabsorbed

A

Pct with water

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9
Q

What pathology can effect the PCT

A

Ischaemic injury resulting in acute tubular necrosis

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10
Q

What part of the kidney is most vulnerable to damage

A

PCT

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11
Q

What is Fanconi Syndrome

A

EFFECTS PCT

  1. Glycosuria
  2. Acidosis with failure of urine acidification
  3. Phosphate wasting resulting in rickets/osteomalacia
  4. Aminoaciduria
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12
Q

What causes fanconi syndrome

A

Cystinosis
Wilson’s
TENOFOVIR (used in HIV)

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13
Q

What is reabsorbed at the Loop of Henle

A

25% Na and water

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14
Q

What transporters are founding the loop of Henle

A

Na2KCl - more active here

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15
Q

Where do most diuretics work

A

Loop Of Henle as 25% of Na is filtered here

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16
Q

What is reabsorbed at the DCT

A

Na and water (5%)

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17
Q

What constitutes the juxtaglomerular apparatus

A

Macula Densa cells

Juxtaglomerular cells

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18
Q

Role of Macula dense cells

A

Sensitive to NaCl

Too much NaCl accumulate at macula dense, then afferent arterioles are CONSTRICTED to reduce GFR rate (less gradient)

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19
Q

When does the juxtaglomerular apparatus release RENIN

A

When it detects high solutes

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20
Q

What regulates re-absorption of solutes at the collecting duct

A

Aldosterone

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21
Q

How does aldosterone effect the collecting ducts

A

Increases transcription of enact channels which absorb Na+ in exchange for K+

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22
Q

What is secreted by the collecting duct into the urine

A

K+ and H+

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23
Q

How is water re-absorption handled i the collecting ducts

A

Water re-absorbed by aquaporin 2 channels

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24
Q

What is hyperaldosteronism

A

LOTS of Na reabsorption resulting in a negative lumen, K+ and H+ rush in causing hypokalaemic alkalosis

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25
Q

In what condition is hyperkalaeimc acidosis seen in

A

Addison’s

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26
Q

How is hyperkalaemic acidosis treated

A

Sodium bicarbonate

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27
Q

What causes hyperkalaemic alkalosis

A

Loop diuretics

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28
Q

Where is K+ absorbed

A

PCT and Loop of Henle

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29
Q

Where is K+ secreted

A

DCT

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30
Q

What governs secretion of K+

A

NA conc

Aldosterone

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31
Q

What compounds drive cellular K+ uptake

A

Insulin and Catecholamines

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32
Q

Way causes hypokalaemia

A

Loop Diuretics

Thiazide diuretics

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33
Q

What causes hyperkalaemia

A 
Spironolactone (aldosterone antagonist)
Amiloride (acts on eNAC channels)
ACEI
ARB
Trimethoprim (acts on enact channels but milder)
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34
Q

Are diuretics NEPHROTOXIC

A

No

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35
Q

How do diuretics cause nephrotoxic effect

A

They cause hypovolaemia

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36
Q

What two medications are extremely effective in advanced kidney disease

A

Thiazide and loop diuretics

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37
Q

What organ is responsible for maintaining plasma tonicity

A

Kidney

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38
Q

What detects water conc

A

Osmoreceptors in th hypothalamus

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39
Q

What is released in response to high conc in plasma

A

VASOPRESSIN

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40
Q

Role of vasopressin

A

Binds to V2 receptors and increases insertion of Aquaporin-2 in apical membrane

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41
Q

Where is vasopressin produced

A

Suprachiasmatic nucleus

42
Q

In which part of th kidney is erythropoietin produced

A

Renal cortex - acts as an oxygen sensor, blood flow and oxygen

43
Q

At what eGFR level is anaemia usually seen

A

<30

44
Q

When is erythropoietin production stimulated

A

In response to tissue hypoxia

45
Q

Why is there a drop in Ca during kidney failure

A

Kidney cannot hydroxylate and there is a drop in Ca (less re-absorption in the gut)

46
Q

Actions of calcitriol

A

Increases Ca and phosphate absorption from the gut

Increases phosphate absorption
Suppresses PTH

47
Q

What disease is caused by calcitriol deficiency

A

Secondly hyperparathyroidism

48
Q

Consequences of secondary hyperparathyroidism

A
  1. Low Vit D results in low Ca and phosphate resulting in increased PTH which causes Ca and phosphate leeching out of the bones
  2. High PTH acts on osteoclasts increasing activity and reducing bone quality
49
Q

What consists of the upper urinary tract

A

Kidneys

Ureters

50
Q

What does the LUT consist of

A

Bladder
Bladder neck
Prostate gland
Urethra and urethral sphincter

51
Q

Function of LUT

A

Convert the continuous process of excretion to an intermittent, controlled volitional process - micturition

52
Q

Essential features of the LUT

A
  1. Low pressure and storage of urine to adequate capacity
  2. Prevent leakage of urine stored
  3. Allow rapid, low-pressure voiding at an appropriate time and place
53
Q

What MAP drives filtration in Bowman;s capsule

A

60-70 mmHg

54
Q

Physiology of Voiding

A
  1. Pontine micturition stimulates excitatory control to detrusor nucleus and inhibits ONUF’s nucleus
  2. Signal transmitted from root S3,4,5 via parasympathetic nervous system and results in contraction of detrusor muscles and relaxation of the urethraa
55
Q

How is urination stopped

A
  1. Pontine store .centre sends inhibitory signals to detrusor muscles and excitatory to onus’s
  2. Signal transmitted from T10, L1 and 2 via sympathetic nervous system = relaxation of th bladder and contraction of the urethral sphincter
56
Q

Describe the sacral micturition centre

A

initiates voiding when bladder is full automatically - inhibited VOLUNTARILY

57
Q

Consequence of cutting cord above S2,3,4

A

Only urinate when bladder is full, not voluntarily inhibited anymore

58
Q

Storage of th ebladder

A

500 ml

59
Q

What lines the bladder

A

Urothelium

60
Q

How many cells thick is urothelium

A

3-7 cells thick

61
Q

What stops reabsorption of urine

A

Umbrella cells

62
Q

Why do men have a greater voiding pressure

A

Longer urethra - more likely to develop retention

63
Q

Why do women have a lower voiding pressure

A

Shorter urethra - more likely to develop incontinence

64
Q

What do renal stones consist of

A

Crystal aggregates, stones from in collecting ducts and may be deposited anywhere from pelvis to urethra:

Consist of calcium oxalate and phosphate

65
Q

What are the there places renal stones tend to cause narrowing

A
  1. Pelvicureteric junction
  2. Pelvic brim
  3. Vesicoureteric junction
66
Q

Peak incidence of renal stones

A

20-40

67
Q

What gender are renal stones common in

A

Males

68
Q

Chances of recurrence after having a renal stone

A

50%

69
Q

Risk factors for renal stones

A
  1. Trauma/anatomical abnormalities
  2. Chemical composition of urine that favours stone crystallisation
  3. Dehydration - conc urine
  4. Infection
  5. Hypercalcaemia, hyperoxaluria, hypercalciuria and hyperuricaemia
    6/ Primary renal disease
  6. Drugs (diuretics, antacids, corticosteroids and aspirin + allopurional)
  7. Diet
  8. Gout
  9. Fam History
70
Q

What is supersaturation of urine

A

When urine solvent contains more solutes than it can hold in solution)

Heterogeneous nucleation occurs more rapidly than homogenous nucleation (where crystal must grow in a liquid medium with no surface on which a crystal can grow)

Requires less energy - cells adhere to renal papilla causing a seed crystal to grow

71
Q

What do most renal stones consist of

A

Calcium oxalate (60-65%)

Calcium phosphate (10%)

72
Q

Where are stones located

A

Collecting system or renal parenchyma

73
Q

Consequence of stones

A

Hydronephrosis - combination of obstruction and dilatation of renal pelvis that causes lasting damage to kidneys

74
Q

What causes hypercalciuria

A
  1. Hyperparathyroidism = hypercalacaemia
  2. Excessive intake of Ca
  3. Idiopathic hypercalciuria = increased absorption in gut
  4. Primary renal disease such as polycystic kidneys or medullary sponge kidney
75
Q

What causes hyperoxaluria (increased oxalate in urine)

A
  1. High dietary intake of oxalate rich food (spinach, rhubarb and chocolate)
  2. Low dietary ca resulting in decreased binding of oxalate so increased oxalate absorption and urinary excretion
76
Q

What causes uric acid stones to form

A

Hyperuricaemia with or without gout
Dehydration
Patients with ileostomies are at risk from dehydration and bicarbonate loss from GI secretion - acidic urine

77
Q

Uric acid is soluble in what pH

A

alkaline than acidic

78
Q

What are infective renal stones made of

A

Magnesium ammonium phosphate and calcium

79
Q

What causes infective stones

A

UTI:

Proteus mirabilis

80
Q

how do proteus mirabilis cause UTIs

A

Hydrolyse urea to ammonium hydroxide

Increased ammonium ions and alkalinity favour stone formation

81
Q

What causes cystine stones

A

Cystinuria - autosomal recessive condition affecting cysteine (AA) in epithelial cells of renal tubules and GI treat

Excessive urinary excretion and formation of cysteine stones

82
Q

Clinical presentation of renal stones

A
  1. Asymptomatic
  2. RENAL COLICS
  3. LOIN PAIN
  4. Fluid and diuretics make pain worse as peristaltic flow increases (if UT is obstructed)
  5. Dysuria/strangury (burning)
  6. Recurrent UTIs
  7. haematuria
    8/ Reduced bowel sounds
    9/ BP low
  8. SOCRATES
83
Q

What is dysuria

A

Difficulty peeing

84
Q

Clinical presentations associated with renal colics

A
  1. Rapid onset
  2. Pain resulting from upper urinary tract obstruction
  3. Excruciating ureteric spasms
  4. Pain from loin to ground comes and goes in waves as ureters peristalsis
  5. Nausea and vomiting
  6. Worse with fluid loading
  7. radiates to going and ipsilateral testis/labia
  8. can’t lie still
85
Q

Differential diagnosis of renal stones

A
  1. Vascular accident (ruptured aortic abdominal aneurysm) if over 50 years - until proven otherwise
  2. Bowel pathology (diverticulitis or appendicitis)
  3. Ectopic pregnancies or ovarian cyst torsion (do uric pregnancy test)
  4. Testicular torsion (loin pain and nothing else!!)
86
Q

How is renal stones diagnosed

A
  1. Vit D conduction - hypercalcaemia, recurrent UTIs and lots of rhubarb and tea
  2. Urine dipstick (positive for blood)
  3. Mid-stream specimen of urine sent for culture and sensnitivit y
  4. FBC
    Kidney Ureter bladder x-ray
  5. Non-contrast computerised tomography
  6. Ultrasound
87
Q

FBC result for renal stones

A
  1. Urea, electrolyte, creatinine and claim raised
88
Q

First line intervention for renal stones

A

X-ray

89
Q

What does x-ray show in renal stones

A

Stone in line of renal tract

90
Q

What is the gold standard for renal stones

A

Non-contrast computerised tomography (99% sensitive for stones)

91
Q

Pros of NCCT

A
  1. No contrast so doesn’t cause renal damage
92
Q

Con of NCCT

A

No functional info

Gives radiation dose equivalent to 18 months background radiation

93
Q

Role of ultrasound in kidney stones

A
  1. Kidney stones and renal pelvis dilatation well but ureteric stones can be missed
94
Q

What is ultrasound sensitive for

A

Hydronephrosis

95
Q

Cons of ultrasound in kidney stones

A

Poor at visualising stones in ureter

96
Q

When is ultrasound good for looking for kidney stones

A

Pregnancy or younger recurrent stone-formers (nor radiation risk)

97
Q

Treatment for kidney stones

A
  1. Strong analgesic for colics - IV DICLOFENAC
  2. Antibiotics for infection (IV GENTAMICIN or CEFUROXIME)
  3. Antiemetics
  4. Observe for sepsis
  5. Stones less than 5mm can pass
98
Q

What medication is given for stones greater than 5mm with pain

A
  1. ORAL NIFEDIPINE or alpha blocker (TAMULOSIN) - promotes expulsion and reduces analgesia requirement
If this still does not work: EXTRACORPOREAL SHOCKWAVE LITHOTRIPSY 
Endoscopy with YAG 
Percutaneous nephrolithotomy (keyhole surgery to remove stones )
99
Q

How are recurrent kidney stones prevented

A
  1. Over hydration
  2. Normal low ca dietary intake
  3. Low salt diet
  4. Reduce BMI
  5. Reduce animal proteins
  6. Active lifestyle
  7. Uric acid stones: Caused by long term allopurinol use
    Only form in acid urine
    Deacidification of urine - ORAL SODIUM BICARBONATE to alkalinise urine
    Cysteine stones: OVERHYDRATION
    Urine alkalisation
    Cysteine binders
100
Q

Name a cysteine binder

A

CAPTOPRIL

101
Q

Id hyperclacaemia is present in recurrent kidney stones what can be given for treatment

A

ORAL BENDROFLUMETHIAZIDE to increase ca excretion

Year 2 (155 decks)

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