Urinary Flashcards

1
Q

Which diuretic might cause someone to present with a decrease in glucose tolerance, uricemia (uric acid in the blood) and hypokalaemia?

A

Thiazides

- effect the Na+/Cl- pump, sodium and glucose are absorbed together

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2
Q

Which diuretic can cause hypokalaemia , metabolic alkalosis and reversible ototoxicity?

A

Loop diuretics- potent naturiesis

- can also affect hair cells in the inner ear

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3
Q

What are loop diuretics used to treat?

A

Severe oedema, hyperkalaemia, hypercalcemia and acute renal failure (to increase urine flow)

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4
Q

Which drug reduces mortality by 30% in HF and LV dysfunction patients?

A

Spironolactone

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5
Q

Most common chief complaint associated with UTI in males?

A

Dysuria

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6
Q

Most likely UTI pathogen in a catheterised patient?

A

Staph. epidermidis

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7
Q

Describe the journey of a ureter

A

Arises from renal pelvis, descends on top of psoas major to reach the brim of the pelvis, crosses in front of the common iliac arteries, runs along the lateral walls of the pelvis, then curves antero-medially to enter the bladder

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8
Q

List the retroperitoneal viscera

A

SAD PUCKER

Suprarenal glans
Aorta/IVC
Duodenum (2nd and 3rd segments)

Pancreas
Ureters
Colon (ascending and descending)
Kidneys 
oEsophagus
Rectum
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9
Q

If you can see the hila of both kidneys and lumbar verterbrae, what level is the CT at?

A

L1-L2

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10
Q

How would a blockage of the Bowman’s capsule which causes an increase in pressure affect the net filtration pressure GFR?

A

It would decrease - there should be a movement from capillary - Bowman’s but it is harder to filter the blood out because the hydrostatic pressure in the Bowman’s is against the hydrostatic pressure in the capillary.

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11
Q

Describe normal oncotic pressure in Bowman’s capsule

A

Negligible- no proteins are filtered here

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12
Q

What would happen to GFR if glomerular oncotic pressure decreased?

A

It would increase
More oncotic pressure = more proteins = harder to filter
Less oncotic pressure = less proteins = easier to filter

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13
Q

Where has fluid leaked from if it has a very similar composition to plasma?

A

Bowman’s capsule

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14
Q

What constituent of the filtrate has a rate of urinary excretion > glomerular filtration in a healthy adult?

A

Glucose

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15
Q

Give the clearance equation

A

(Urine conc of substance x urine flow rate) / plasma conc

- units L/hr

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16
Q

What compensatory mechanism will occur in the nephron of a patient with orthostatic hypotension?

A

An increase in glomerular filtration rate of the same nephron.

  1. Immediately on standing BP falls
  2. Decrease in NaCl to macula densa
  3. Macula densa triggers 2 things - vasodilation of afferent arteriole to increase perfusion of kidney, and increased paracrine stimulation of JGA cells so more renin is released
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17
Q

Features of the ascending loop of Henle?

A

permeable to ions but impermeable to water
(thin ascending limb does minimal Na and Cl transport, thick ascending limb does more as it has NKCC and Na+K+ATPase)
ABSORB SOLUTE, WATER LOST

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18
Q

Features of the descending loop of Henle?

A

permeable to water and ions

H2O moves out and Na+ and Cl- move in so its more concentrated as you go down

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19
Q

What stimulates the granular cells of the JGA to release renin?

A

Drop in BP, decreased NaCl to macula densa, sympathetic stimulation

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20
Q

What does ADH do other than upregulate aquaporins?

A

Vasoconstriction - activates V1 receptor on VSM (vascular smooth muscle) - triggers thirst response from hypothalamus

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21
Q

What is diabetes insipidus?

A

Inability to reabsorb water from distal nephron due to failure of excretion or action of ADH

Central - damage to hypothalamus or pituitary , tx with nasal spray/ADH injections
Nephrogenic- insensitivity to ADH, tx with low salt low protein diet

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22
Q

What is dipsogenic diabetes insipidus (or primary polydipsia) ?

A

Damage to hypothalamus causing malfunction of the thirst mechanism

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23
Q

What is measured by urine specific gravity following water deprivation?

A

Renal concentrating ability

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24
Q

Which blood vessel relates to CCM?

A

vasa recta

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25
Q

What removes K+ from the body?

A

Calcium resonium (calcium gluconate stabilises myocardium and insulin redistributes)

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26
Q

What might cause hypokalaemia in a bulimic patient?

Give another cause of loss of serum potassium

A

Losing potassium from kidneys to correct acid balance
- she has a metabolic alkalosis from vomiting so not enough H+ in cells, so K+ leaves the blood to enter cells to try and compensate

Other cause is a thiazide diuretic

27
Q

How can trimethoprim affect potassium levels?

A

Competitive inhibitor for ENaC (similarly to amiloride) so causes hyperkalaemia

28
Q

What fluid replacement could you use for a surgical patient who is tachycardic with low bp?

A

Hartmann’s over 15 mins

29
Q

What fluid replacement could you give someone with severe diarrhoea?

A

Potassium cannot be given quickly

1L 0.9% sodium chloride with 40mM potassium over 8 hours

30
Q

What fluid replacement would you consider for an elderly patient who is NBM?

A

NBM- must replace glucose
Elderly- dont fluid overload too quickly
1L 0.18% sodium chloride and 4% dextrose over 12hours

31
Q

Treatment for AKI and electrolyte imbalance that cannot be corrected by medication?

A

Haemofiltration - better then dialysis in acutely unwell haemodynamically unstable patients

32
Q

Urinary symptoms/AKI associated with hypotension and/or trauma are usually due to…

A

ACUTE TUBULAR INJURY

- if you dont know just say this

33
Q

How do the convoluted tubules regulate body pH?

A

Reabsorption of HCO3- (90% in PT)

34
Q

Screening for early kidney disease is important in…

A

Diabetics

35
Q

How does PTH affect the kidneys handling of phosphate?

A

Decreases reabsorption in PCT

36
Q

Short term and long term calcium regulation?

A

Short term- PTH

Long term- calcitriol

37
Q

Early sign of glomerulosclerosis in diabetic?

A

Microalbuminuria

38
Q

Pathological finding on biopsy for patient with rapidly progressive GN?

A

Glomerular crescents- leakage of fibrinogen into bowman’s space

39
Q

Action of which nerves cause detrusor contraction?

A

Parasympathetics from spinal cord to urinary bladder

40
Q

Stimulation of which receptor would reduce incontinence in a patient with OAB?

A

B3 receptors- would relax the detrusor muscle

41
Q

What innervates the EUS?

A

Somatic motor neurones- conscious control

42
Q

What is normal bladder capacity?

A

400-500ml

43
Q

Where is the detrusor muscle derived from embryologically?

A

Hind gut

44
Q

Radiopaque lesion present in bladder area, which other lab finding will be likely?

A

Hypercalciuria- secondary to bladder calculi

45
Q

Renal impact of AAA at L2-3?

A

Ureter trapping- unilateral hydronephrosis

46
Q

Describe urea concentration throughout the nephron. How does ADH play a role?

A
  1. Normal level until reaches the loop of Henle where urea concentrations are very high - most urea enters the nephron here from the medulla.
  2. Some more reabsorption happens in the PCT.
  3. Urea stays high in the DT because it is impermeable to it.
  4. In the collecting duct loads of urea gets pumped back into the medulla (recycling).

ADH stimulates even more urea uptake by activating urea transporters and urea is an osmole so water follows.

47
Q

Why does the IUS need to be stronger in men?

A

Prevent retrograde ejaculation

48
Q

What receptor is found on the IUS?

A

alpha 1

49
Q

Where in the nephron do amino acids and glucose get reabsorbed ? (bulk of reabsorption happens here)

A

PCT

50
Q

Describe reabsorption at the PCT

A

Reabsorption is isosmotic
• PCT responsible for ‘bulk’ reabsorption of
many solutes
• Very metabolically active, high concentration
of mitochondria
• Provide energy for Na/K ATPase

51
Q

What is sodium reabsorbed with and why?

A

Takes place in association with Cl- and HCO3-

Needed to maintain neutrality of cells

52
Q

Which substance is more concentrated at the end of the PCT than the beginning?

A

Creatinine

53
Q

Is urea actively secreted from renal tubular cells?

A

No it moves passively

54
Q

How does ADH cause water movement via urea recycling?

A

ADH increases number of urea transporters, more urea moves into medulla, water follows as urea is an osmole

55
Q

An increase in the conc of plasma potassium causes an increase in….

A

aldosterone release - aldosterone upregulates ROMK channels to increase K+ excretion

56
Q

In the presence of ADH the Distal nephron is permeable to …

A

water and urea

57
Q

What makes ammonia an effective urinary buffer?

A

The walls of the renal tubules are impermeable to NH4

+ - it becomes “locked” in the tubule

58
Q

Renal correction of acute hyperkalaemia will result in…

A

Acidosis

59
Q

What 3 components make up the filtration barrier?

A

Endothelial cells, BM, podocytes

60
Q

Where do you find the glomerulI?

A

In the renal CORTEX

61
Q

What is the tubuloglomerular feedback mechanism in high tubular flow?

A

Macula densa cells of the DCT epithelium detect osmolality or the rate of movement of Na+ or Cl- movement into the cells. The higher the flow of filtrate the higher the Na+ concentration in cells.

A signal is sent via the juxtaglomerular cells, triggered by
an increase in NaCl concentration of distal tubular fluid.
ATP released, converted to adenosine, binds with A1
receptor on afferent arteriole.

Further vasoconstriction of the smooth muscle of the
adjacent afferent arterioles and therefore ↓ RPF which in
turn ↓GFR. Renin synthesis inhibited.

62
Q

What is the tubuloglomerular feedback mechanism in low bp?

A

Release of prostaglandins – attenuate constriction of afferent arteriole

Renin released by juxtaglomerular cells. 3 stimuli responsible for release:
• Sympathetic nerve stimulation
• ↓ stretch of afferent arteriole
• Signals generated by macula densa cells in response to ↓NaCl delivery

RAAS system

63
Q

Fluid leaving the is….

A

hypotonic