Renal

Question 1

Laboratory findings acute renal failure: acid-base, electrolytes

Answer 1

Hyponatremia
Hypochloremia
Hypocalcemia

Hyperkalemia, hyperphosphatemia, hypercalcemia, metabolic acidosis (more severe, oliguric/anuric)

Fractional clearance:
Increased sodium, phosphorus

Question 2

Laboratory findings acute renal failure: urinalysis

Answer 2

Low USG despite dehydration
Microscopic hematuria
Glucosuria, increased urine enzymes —more substantial tubular damage)
Proteinuria (protein:crea >2:1) — glomerular disease
Casts
Erythrocytes
Leukocytes
Decrease urine crystals

Question 3

Chronic renal failure: primary glomerular diseases

Answer 3

• glomerular nephritis
• nonspecific glomerulopathy
• glomerular hypoplasia
• amyloidosis

Question 4

Chronic renal failure: primary tubularinterstitial

Answer 4

• acute tubular necrosis - incomplete recovery from
• pyeloneohritis
• nephrolithiasis
• hydronephrosis
• renal dysplasia
• papillary necrosis

— > all collectively named chronic interstitial nephritis

Question 5

Chronic renal failure: clinical signs

Answer 5

• weight loss
• ventral edema (small, between forelimbs)
• PU/PD
• rough hair coat
• anorexia
• poor performance
• dental tartar
• melena
• oral ulcers

Question 6

Acute renal failure: clinical signs

Answer 6

• Depression
• anorexia

— both more than expected from primary disease

• failure to produce urine despite fluid therapy (6-12 h)

• uremic encephalopathy (with fulminant ARF)

Question 7

What lesion do NSAIDS cause in kidney

Answer 7

papillary necrosis in renal medulla

Question 8

Ultrasonographic change typical for NSAID toxicity

Answer 8

renal medullary rim sign

= hyperechoic band parallel to corticomedullary junction

Question 9

NSAID nephrotoxicity - pathophysiology

Answer 9

PGE2 produced in the kidney, important regulator for renal blood flow

COX1 + 2 produce PG from arachidonic acid

hypoperfusion – upregulation of COX2 to increase PGE2 and renal blood flow = increased nephrotoxicity during hypovolemia

Question 10

Treatment of acute-on-chronic renal failure

Answer 10

Treatment as with ARF first (siehe ARF)

correction of acute component: dependent on acute insult
- correction of hypovolemia
- Treatment of ascending UTI
- removal of obstructing stones/calculi

Question 11

Explain the counter current exchange in the nephron

Answer 11

Thick ascending loop (impermeable to H2O) transports solutes (Na, Cl and K) out of the lumen into the interstitial (renal medulla) and causes a gradient for water to move from the lumen of the thin descending loop (permeable to water) into the blood

Question 12

How do loop diuretics work?

Answer 12

Furosemide

blocks co-transporter for Na/Cl and K in the thick ascending loop of Henle and therefore increases diuresis of Na, K, Cl and water (by making the medulla less hyper osmotic and more solutes in the lumen)

Side info: LaSIX called because it lasts six hours

Question 13

Bladder innervation

Answer 13

principal supply - pelvic nerves (sensory and motor fibers) –> sacral plexus mostly S2 + 3

Motor nerves: parasympathetic, terminate on ganglion in bladder wall, post-ganglionic (short) detrusor innervation

Skeletal muscle fibres: pudendal nerves - external bladder sphincter

sympathetic innervation: hypogastric nerves, mostly L2 mostly blood vessels stimulation

Question 14

Micturition

Answer 14

= autonomic spinal cord reflex

bladder filling - many superimposed micturition contractions
initiated by stretch reflexes (especially by posterior urethra) –> sensory signals then parasympathetic signals back both through pelvic nerves

not full bladder- contractions subside

beginning of micturition - initial contraction -> activation of stretch receptors = stronger sensory impulse = stronger reflex contraction
= self regenerating process (cycle repeated until ceasing of reflex)

when reflex powerful enough –> pudendal nerves to external sphincter –> inhibition

brain: higher centers keep final control (brain stem - mostly pons and cortex)
partial inhibition until desired, tonic contraction of external bladder sphincter can suppress micturition reflex
when time/desired –> cortical facilitate sacral parts and inhibit external sphincter

actual process:
abdominal contraction - increase in bladder pressure - extra urine in posterior urethra - stimulation of stretch receptors - micturition reflex - inhibition of external urethral sphincter

Question 15

What are the most important substances getting secreted in the urine?

Answer 15

Potassium
H+

Question 16

What causes increase in hydrostatic pressure of bowman’s capsule and what can it result in?

Answer 16

Urinary tract obstruction
Ca or Uric acid precipitation - stones
= decreases GFR and can lead to hydronephrosis

Question 17

What is the formula for renal blood flow?

Answer 17

(Renal artery pressure-renal vein pressure)/total renal vascular resistance

Renal vascular resistance = mainly interlobular arteries and afferent/efferent arterioles

Question 18

Aldosterone
- origin, stimulation, mechanism

Answer 18

Origin: zoma glomerulosa cells of adrenal cortex

Stimulation: increased extracellular potassium, increased angiotensin II (usually with low sodium, low blood pressure, volume deficit)

Mechanism: stimulation of Na/K ATPase in cortical collecting tubule, increased Na permeability on luminal side

Question 19

Angiotensin II
- origin, mechanism, effect

Answer 19

Origin: Angiotensin I –> II mostly lung, but also locally in kidneys by ACE

Mechanism:
1.) Aldosterone secretion – Na reabsorption
2.) Efferent arteriole constriction – decreased peritubular hydrostatic pressure – increased net reabsorption, reduction of renal blood flow – increased GFR
3.) Stimulation of Na reabsorption (prox tubule, loop of Henle, distal tubule and collecting ducts) – stimulates Na/K ATPase (basolateral), stimulates Na/H+ exchange (luminal), stimulates Na/HCO3 cotransport (basolateral)

Question 20

ADH
- origin, mechanism, effect

Answer 20

Origin: supraoptic nuclei of hypothalamus, stored in neurohypophysis (posterior hypophysis)

Mechanisms: binding to V2 receptors (late distal tubule, collecting tubule, collecting ducts) - release of cAMP - PKA - protein phosphorylation – movement of AQP-2 to luminal side - exocytosis with membrane = water channels

Effect: increased water permeability

Question 22

Factors that influence internal potassium distribution

Answer 22

• Insulin: increases intracellular K uptake
• Aldosterone: increases intracellular K uptake and increased K excretion

Question 23

Antibiotics concentrated in the urine

Answer 23

Penicillin, ampicillin, gentamicin, cephalosporins, TMS

Question 24

Preventative measures for urolithiasis (equine)

Answer 24

• Acidifying urine: Ammonium chloride, ammonium sulfate
• diet change: grass rather than legumes
• supplementation with 50g NaCl = promotes diuresis