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Flashcards in Final- Ca and P Deck (23):

What is the role of PTH?

• Increases serum Ca by increasing renal tubular reabsorption
• Increasing resorption of bone-
• Promote activation of Vit. D to its active form. In kidney


What is the role of calcitonin?

Produced by C cells in the thyroid gland- decreases serum calcium
concentration by inhibiting PTH


What does Vit D do?

Activated vitamin D (calcitriol) increases calcium concentration by increasing absorption of Ca from the intestine and by enhancing PTH action on bone and kidney


What is the relationship between plasma ionic Ca and inorganic phosphate?

• Related reciprocally- and solubility is pH dependant.


What occurs w/ increasing pH ?

Promotes precipitation of ca phosphate salts into soft tissues
(vessels, lung, kidney
• increases in plasma Phosphorous decreases plasma calcium which increases PTH.


What percent of serum calcium is bound to albumin?

cent of serum calcium is bound to albumin?
• 50% bound to albumin. 40% ionized (active form) thus total
calcium is provided w/ a profile ! hypoalbuminemia can result in
decreased calcium so look at the albumin levels


what occurs w/ hypoalbuminemia?

Fraction of Ca bound to albumin decreased, thus absolute amount of albumin available is decreased and thus an apparent hypocalcaemia


What is the formula for corrected calcium?

Total calcium – albumin + 3.5. if corrected calcium calculation is
w/in reference interval you have hypocalcaemia b/c of


What occurs w/ acidosis and alkalosis and calcium?

Acidosis causes increased ionized calcium; alkalosis decreases ionized calcium
• hypocalcemia can result in tetany ,seizures, death if very hypocalcemic. If low calcium and acidic- pH shifts more total clacium in ionized form.
• Alkalsosis causes decrease ionized calcium. – shifts more ionized calcium to bound form- any time w/ alkalemia can have same total calcium as one w/ acidosis but w/ more clinical signs. b/c hypocalcemic can be more tragic.


What are common causes of hypocalcemia?

pancreatitis, eclampsia, ethylene glycol, renal dz, sepsis PEERS


What are uncommon causes of hypocalcemia?

Hypoparathyroidsm, nutritional secondary hyperparathyroidism
(inadequate intake of calcium, inadequate vitamin D and excess phosphorus); intestinal malabsorption (if not absorbing fats appropriately you are probably not absorbing vitamin d (DEAK). Also can see it K deficiency and increase in bleeding if the case as well; phosphate containing enzymes (fleet enemas), citrate toxicity (blood transfusion- anticoag used for blood transfusion- chelates calcium. If huge amount it can give a hypocalcemic effect.) hypomagnesemia (magnesium necessary for PTH production and secretion) , massive tissue degeneration (calcium can bind to necrotic tissue and cause hypocalcemia), hypercalcitonism (c cell thyroid tumor)


what are clinical signs of hypocalcemia?

Nervousness, anorexia, stilted gate, hyperventilation,
numbness, generalized tetany, seizures


You are presented w/ a 2 yar old dog that is vomiting and icteric. Slight decrease in PCV, inflammatory leukogram, slight decrease in calcium, cholesterol elevated above RI, total bilirubin increased, increase ALP and ALT. histopath shows pancreatitis; what is your most likely dx for the dec. in calcium.

This is a case of pancreatitis causing cholestasis (inflammation at the duodenum blocking the bile duct. Perform a PLI. If elevated- there is your answer. Dec. calcium b/c saponification of fat in the GI.


What are causes of hypercalcemia?

What are causes of hypercalcemia? remember HARDIONS
• Hypercalcemia of malignancy (tumor producing PTH rp- perirectal
apocrine gland carcinoma and dog s/w lymphoma(medialstinal lymphoma); granulomatous inflammatory dz (usually b/c increase
in vitamin D); Renal dz (can be primary or 2ndary- only 10% cases of small animal w/ primary renal dz. But renal dz 2ndary to hypercalcemia very common); idiopathic hypercalcemia of cats (diet, rx prednisone); vitamin D toxicosis (some rodentocites contain colicalciferal which causes hypercalcemia and the rat can get calcification of soft tissue); Grape and raisin toxicosis (renal fiaulre- not all dogs get it- idiosyncratic. Renal failure comes first and hypercalcemia is not what is causing reanl failure ); hypoadrenocorticsm –addisons dz- cortisol decreases calcium levels. Patients are deficient in mineralocorticoids resulting in hypercalcemia; usually these animals will have palpable mass in neck by the time you are seeing hypercalcemia.


What are clinical signs associated w/ hypercalcemia?

PU/PD- inhibit ADH receptors. Lethargy, weakness,
• Mineralization of soft tissue when calcium x phosphorous
product is greater 60 or 70- medical emergency- not quickly


What is the diagnostic approach to a case of hypercalcemia?

Look for cancer (lymphoma, hypercal. Of malignancy)- perform a
rectal exam. Often perirectal apocrine gland carcinomas are very malignant, renal dz, mass in cervical region, history of vit D ingestion, if still suspect neoplasia- perform PTH rp test.


You are presented w/ a 6 year old dog that is vomiting and weak. Elevated NCC, increase in lymphocytes. (lymphocytosis- lymphoma, addisons, excitement, infection- things to think about) BUN increase, creatinine increase, calcium increased, phosphorous increased. Ionized Ca is elevated, albumin is normal, sodium decreased, potassium elevated, chloride decreased, decreased tC02, increased anion gap. USg 1.018, 6.0 pH urine.
• What is on your ddx?

Has a metabolic acidosis- increase in the anion gap tells you
he has unmeasured anions present. Look at soidum, high potassium think about addisons b/c of lack of mineralocortoids. Anything less than a 23 Na:K ratio think of addisons. ! probably addisons this case the Na:K
ratio is 17. If prerenal azotemia- dehydration in the dog
should have USG greater than 1.030- not the case here.
o You perform a endocrine ACTH stim test and serum cortisol
levels before are .04 and after are .09! case of hypoadrenocroticsm. After stimulation >10 should be the case. Not here.
Side note- medullary wash out- need sodium to concentrate urine. Need sodium and urea. If hyponatremic can cause inability concentrate urine. Always look at electrolytes


You are presented w/ an 8 year old dog with normal PCV, elevated NCC, and segs and lymphocytes elevated 2.5 times greater than RI. (erlihcia, lymphoma, excitement etc). BUN elevated, creatinine elevated, CA elevated (erlichia wont cause hypercalcemia- ruled out), elevated phosphorus, elevated TP, normal albumin, increased globulin. Look at the liver panel- normal cholesterol, increased bilirubin, increased ALP and ALT. chem panel- Na normal, K elevated, Cl normal, TC02 decreased, anion gap- increased. USG is 1.011, pH is 6.5, 2+ protein, 2+ bilirubin.

The dog is hyperbiliruminemic in dog that is not anemic w/ elevated ALP and Alt tin there is cholestasis and possibly mild hepatocellular damage. Animal is hyperkalemic due to metabolic acidosis or there is renal issue and cant get rid of potassium. Increase in anion gap- elevated anions that are not measured. Lactic acid or phosphate is possible. Don’t think of antifreeze b/c has hypercalcemia not a normal situation-would be hypocalcemic. Urine- isosthenuric w/ azotemia you think of renal damage. Can have mineralization of kidney tubules or hypercalcemia is interfering w/ ability to concentrate. You perform a needle aspirate and detected lymphoblasts on the liver ! ddx- lymphoma.


You are presented w/ a 6 month old female cat w/ acute onset of tachypnea, vomiting, weakness, stress leukogram. glucose is elevated, Bun elevated, creatinine elevated, Ca is highly elevated, Phosphorous elevated, K is elevated, USG is 1.022. (cat is not pre renal azotemia from dehydration- would have USG greater than 1.035.blood gas- Ph is acidic, Pc02 elevated, Po2 is decreased, Hc03 is normal.

There is a metabolic acidosis and respiratory acidosis.
• Calcium phosphorous product- 171.
• Case of cholecalciferol toxicosis.


What is the importance of phosphorous in the body?

Mineralization of bone, critical for high energy posphoryl units of metabolic intermediates, structural phosphoproteins and phospholipids, inorganic phosphate anions play a role in acid base metabolism.


What regulates phosphorous in the body?

PTH decreases phosphorous, decreasing renal tubular reabsorption, calcitonin decreases P by inhibiting PTH stimulated bone
resorption, increasing movement into tissues and decreasing renal tubular resorption of P.
Vit D increases by stimulating absorption from intestine and kidney and inhibiting PTH synthesis


What causes hypophosphatemia?

Most marked decrease seen in patients w/ metabolic acidosis due to
increased urinary loss (phosphates eliminated w/ excess acid)
• Patient w/ diabetic ketoacidosis may have life threatening hypophasotemia due to increased urinary loss both from acidosis and osmotic diuresis.
• Primary hyperparthyroidsim (renal loss), hypercalcemia of malignancy (PTH rp inhibits P reabsorption), vitamin D deficiency, respiratory alkalosis, decreased intestinal absorption of P, renal tubular defects (fanconi syndrome) chronic renal failure in horses
Similar causes of hypophosphatemia also cause hypercalcemia, such as primary hyperparathyroidism and hypercalcemia of malignancy. Hypercalcemia may result in mineralizatoin of kidney, w/ resulting decreased in GFR, subsequent normal or increased serum P concentration


What are causes of hyperphosphatemia?

Decreased GFR, either result of prereanl azotemia- decreased blood
flow to kidney, renal dz is most common cause of
• Ruptured bladder or ureter or urethra obstruction will also cause retention of phosphorus.
• Other causes- vit D intoxication, acute acidosis as a result of decreased use of phosphorus (chronic acidosis will cause decrease in P), excessive P intake, primary hypoparathyroidsm