QUESTIONS

1. Where does Lasix act?
    
2. There are dopaminergic receptors in the kidney which, when stimulated, will increase renal blood flow, increase GFR, and increase sodium excretion.  Can dobutamine be used for these purposes instead of dopamine?
    
3. A dog with very bad degenerative joint disease is being given aspirin  2x daily.  Why might this patient be at greater risk for ARF than a dog not on aspirin?
    
4. When cisplatin is used to treat osteosarcoma & other tumors, it is frequently accompanied by saline diuresis.  Why diurese with saline?  Why not use something else?
    
5. Atrial Natriuretic Peptide has received attention lately in the treatment of ARF.  What is it supposed to do for the patient?
    
6. The kidney has two mechanisms for keeping GFR & renal blood flow relatively constant in the face of blood pressure changes.  Describe these two mechanisms (Hint:  one is the “myogenic mechanism” and the other is “tubuloglomerular feedback.”
    
7. What is the relationship between sympathetic nervous system stimulation and the secretion of renin?
    
8. Why is an alkalotic patient more susceptible to hypocalcemic tetany than an acidotic patient?
    
9. Calcium is absorbed throughout the nephron except for where?
    
10. What part of the nephron does PTH act on the increase Ca resorption?
     
11. Does PTH act on the GI tract to increase Ca absorption here?
    
    
    
    
     

ANSWERS

1. Lasix acts on the thick ascending loop of Henle.  It can induce increased tubular flow at this point thus is not helpful in flushing out debris upstream from here.  Don’t forget that it synergizes with Dopamine for diuresis.
   
   
   
   
    
2. No way.  Dobutamine causes vasoconstriction in the kidney which is just what you do not want.
   
   
   
   
    
3. Renal prostaglandins (esp. E & I)  have vasodilatory properties & are helpful in maintaining renal blood flow.  Removing these prostaglandins is not a big problem for normal kidneys but watch out if something happens on top of the aspirin admin.  FYI  ibuprofen is about equally as bad as naproxen & both are worse than aspirin.
   
   
   
   
    
4. Saline is the best fluid for providing sodium.   Lots of sodium means volume expansion/plenty of blood flow for the kidneys.  Also, all that sodium keeps the renin/angiotensin system quiescent (no afferent arteriole constriction).
   
   
   
   
    
5. Atrial Natriuretic Peptide causes diuresis.  It also causes vasorelaxation on the afferent arteriole (& may constrict the efferent arteriole) thus increasing GFR.  It also causes a natriuresis but I’m not really sure why that’s good since you want to retain Na+ to keep up blood volume, don’t you??
   
   
   
   
    
6. The Myogenic mechanism - when BP elevates, there is a reflex which causes arterioles to constrict .  This increases resistence so that the overall flow will stay constant.
   
   In Tubuloglomerular feedback, and increase in fluid flow through the tubule is perceived by the macula densa & a vasoconstrictor is emitted by the JGA to constrict the afferent arteriole.  (This vasoconstrictor is not a prostaglandin and is not angiotensin 2 - I don’t think any one knows its identity).
   
   
   
   
    
7. The indirect relationship:  the sympathetic nervous system causes vasoconstriction of the afferent arterioles.  The change in renal blood flow and tubular flow is sensed by renal baroreceptors & by the macula densa.  Renin gets secreted to assist vasocontriction.
   
   The direct relationship:  sympathetic neurons end in the vicinity of the JGA’s granular cells & directly stimulate them to secrete renin via beta two receptors.
   
   
   
   
    
8. Recall 45% Ca is ionized as Ca++ (active in nerve, muscle etc.), 40% Ca os reversibly bound to plasma proteins.  15% Ca is complexed in low molecular weight proteins.  As pH increases, more negatively charged areas are exposed on carrier proteins. This means more binding sites are available for Ca++.  This means less active Ca++ is available to do Ca++ dependent work.
   
   
   
   
    
9. Calcium is not reabsorbed from the descending loop of Henle.  Remember 98-99% of filtered calcium is recovered from the tubule & any protein bound Ca wasn’t filtered in the first place. 
   
   
   
   
    
10. PTH acts on the distal tubule.  Actually PTH inhibits calcium resorption in the prox. tubule but way way compensates in the distal tubule.  Tons of calcium is resorbed here.
    
    
    
    
     
11. Nope but active D3 sure does.