Clin Path - Ca, P, Mg, And Hormones

Front 1

Calcium fractions in serum/plasma

Back 1

-fCa2+ (free Calcium)
-Ca2+/Pr- (Protein Bound Calcium)
-Ca2+/A- (Calcium bound to Ions other than proteins)

Front 2

What regulates each calcium fraction in the blood?

Back 2

-fCa2+ = hormones
-Ca2+/Pr- = protein conc.
-Ca2+/A- = anion conc.

Front 3

What is filterable Ca2+?

Back 3

=fCa2+ + Ca2+/A-


-protein bound calcium should not pass through glomeruli

Front 4

Vitamin D Production
-describe process

Back 4

-hepatocytes or diet provide cholesterol which is converted by sunlight to cholecalciferol (Vit. D3)
-Cholecalciferol can also be provided by the consumption of plants
-Cholecalciferol moves to hepatocytes where hydroxylase converts it to 25-HCCC (calcidiol)
-25-HCC circulates in the blood and eventully passes through the glomerular filtration barrier
-25-HCC is converted to calcitriol by hydroxylase in renal tubular cells

Front 5

Which is more active calcidiol or calcitriol?

Back 5

-calcitriol by 25x

Front 6

Animal that cannot form calcitriol in its kidneys?

Back 6

-horse

-lacks 1a-hydroxylase

Front 7

PTH production in the parathyroid glands
-stimulated by

Back 7

-dec. [fCa2+]
-dec. [1,25-DHCC] (calcitriol)

Front 8

Activity of 1a-hydroxylase in the kidneys
-promoted by
-inhibited by

Back 8

Promoted by:
-dec. [fCa2+]
-inc. PTH

Inhibited by:
-inc [fCa2+]
-inc. [PO4]

Front 9

Calcium mobilization from bone
-promoted by

Back 9

-inc. PTH
-inc. [1,25-DHCC]

Front 10

Calcium absorption in intestine
-promoted by

Back 10

-inc. PTH
-inc. [1,25-DHCC]

Front 11

Urinary excretion of calcium
-enhanced by
-reduced by

Back 11

enhanced by:
-inc [fCa2+]

reduced by:
-dec. [fCa2+]
-inc. PTH
-inc 1,25-DHCC

Front 12

What processes increase [fCa2+]?

Back 12

-inc. mobilization of Ca2+ from bone
-inc. absorption of Ca2+ by intestine
-dec. excretion of Ca2+ by kidneys

Front 13

How is regulation of [fCa2+] different in horses?

Back 13

-no production of 1,25-DHCC in the kidneys
-absorption of dietary calcium from the intestine is not tightly regulated
-excess dietary Ca2+ is excreted by the kidneys

Front 14

What does a change in [tCa2+] represent?

Back 14

-change in one or more of the calcium fraction concentrations

Front 15

Samples that can be used for measuring fCa2+

Back 15

-serum
-heparinized blood
-heparinized plasma

-DO NOT USE EDTA or Citrate!!!

Front 16

Hypercalcemia
-causes

Back 16

-primary hyperparathyroidism
-Humoral hypercalcemia of malignancy (HHM)
-Hypervitaminosis D
-dec. Urinary excretion

Front 17

Primary hyperparathyroidism
-caused by

Back 17

-parathyroid adenoma or adenocarcinoma

Front 18

Primary hyperparathyroidism
-pathogenesis to hypercalcemia

Back 18

-inc. production of PTH
-inc. [PTH]
--inc. mobilization of Ca from bone
--inc. absorption of Ca from intestine
--dec. renal secretion of Ca
---increases [fCa2+]
----inc. [tCa2+]

Front 19

Humoral Hypercalcemia of Malignancy
-aka
-causes

Back 19

-aka: pseudohyperparathyroidism

causes:
-Neoplasms (canine lymphoma, apocrine gland carcinoma)
-PTH-rp

Front 20

HHM
-pathogenesis to hypercalcemia

Back 20

-Neoplastic cells
-inc. production and release of PTH-rp
--inc. [PTH-rp]
---inc. mobilization of Ca from bone
---inc. absorption of Ca from intestine
---dec. renal secretion of Ca
----inc. [fCa2+]
-----inc. [tCa2+]

Front 21

Hypervitaminosis D
-causes

Back 21

-rodenticides with cholecalciferol
-granulomatous inflammation

(relatively uncommon)

Front 22

Hypervitaminosis D
-pathogenesis to hypercalcemia

Back 22

-Excess Vit. D intake/production
--inc. [1,25-DHCC]
---inc. mobilization of Ca from bone
---inc. absorption of Ca from intestine
---dec. renal secretion of Ca
----inc. [fCa2+]
-----inc. [tCa2+]

Front 23

Decreased Urinary Excretion of Ca2+
-causes

Back 23

-Equine renal failure
-Canine renal failure
-Canine Addison's Disease

Front 24

Equine renal failure
-pathogenesis to hypercalcemia

Back 24

Renal disease destroys most equine nephrons
-dec. GFR
--dec. clearance of Ca & Ca/A-
---inc. [fCa2+] & [Ca2+/A-]
----increase [tCa2+]

dietary calcium excess is normally excreted by horse kidneys

Front 25

Canine Renal Failure
-pathogenesis to hypercalcemia

Back 25

Renal disease destroys most of the nephrons
-dec. GFR
--dec. clearance of A- (PO4, SO4, citrate)
---increased formation of Ca2+/A- complexes in plasma & complexes are not cleared
----inc. [Ca2+/A-]
-----inc. [tCa2+]

Front 26

Canine Addison's Disease (hypoadrenocorticism)
-pathogenesis to hypercalcemia

Back 26

Hypoadrenocorticism --> hypovolemia
-inc. activation of RAS
--inc. angiotensin
---inc. proximal tubular reabsorption of Na+ and Ca2+
----inc. [fCa2+]
-----inc. [tCa2+]

Front 27

Hypocalcemia
-causes

Back 27

-Hypoalbuminemia
-Primary hypoparathyroidism
-Hypovitaminosis D
-inc. urinary excretion
-Pregnancy, Parturient, Lactational

Front 28

Primary hypoparathyroidism
-causes

Back 28

Parathyroid gland destruction
-surgery
-others

(uncommon)

Front 29

Primary hypoparathyroidism
-pathogenesis to hypocalcemia

Back 29

-dec. production & release of PTH
-dec. [PTH]
---dec.mobilization of Ca from bone
---dec. absorption of Ca from intestine
---inc. renal secretion of Ca
----dec. [fCa2+]
-----dec. [tCa2+]

Front 30

Disorder seen with a decrease in Vitamin D, Phosphate, or Calcium

Back 30

-Rickets

Front 31

Hypovitaminosis D
-causes

Back 31

-chronic renal disease --> secondary renal hyperparathyroidism
-Pseudohypovitaminosis D (vitamin D dependent Rickets)
-dietary deficiency

Front 32

Chronic renal disease leading to hypovitaminosis D is most commonly seen in:

Back 32

-dogs
-cats
-cattle

Front 33

Pseudohypovitaminosis D
-Types

Back 33

-Type 1: defect in 1a-hydroxylase gene --> dec. Calcitriol formation

-Type 2: defect in the vitamin D receptor gene --> dec. cell response to calcitriol

Front 34

Describe how chronic renal disease causes secondary renal hyperparathyroidism

Back 34

Front 35

Effects noted with secondary renal hyperparathyroidism

Back 35

-inc. [PTH]
-dec. WRI [tCa2+]
-inc. WRI [Pi]
-possible azotemia

Front 36

Hypocalcemia due to Pregnancy, Parturition, or Lactation
-aka

Back 36

-milk fever
-puerperal tetany

Front 37

Pregnancy, Parturition, Lactation
-pathogenesis to hypocalcemia

Back 37

-Parturition --> lactation
--Rapid inc. in Ca loss in milk
---not mobilizing Ca from bones fast enough
----dec. [fCa2+]
-----dec. [tCa2+]

Front 38

Inc. urinary excretion of calcium
-causes

Back 38

-inc. urinary excretion of anions
-Furosemide (Lasix) treatment

Front 39

Increased urinary excretion of anions
-pathogenesis to hypocalcemia

Back 39

-Inc. anion loss in urine (AcAc, lactate, HCO3-)
--obligate loss of cations in urine (Ca, Na, K)
---hypocalcemia

Front 40

Furosemide Treatment
-pathogenesis to hypocalcemia

Back 40

-Inhibition of Cl- resorption in the ascending loop of henle
--reduced electrical gradient for Ca2+ resorption
---hypocalcemia

Front 41

Describe how inc. PO4 results in hypocalcemia

Back 41

-PO4/Ca2+ complexes form and are engulfed by macrophages --> dec. PO4 and Ca2+ conc.
-tissue becomes calcified after damage by primary disease

Front 42

[fCa2+]
-regulated by

Back 42

-body

Front 43

[fCa2+] sample collection
-preferred sample
-tubes used

Back 43

-serum (anaerobic)
-red top

Front 44

Why is handling of a sample for fCa2+ critical?

Back 44

-if aerobic, there is a binding of H+ and HCO3- leasind to a loss of CO2
-the decrease H+ bindingn to protein allows more Ca to bind to protein, causein a decrease in [fCa2+]

Front 45

Excpetions for when disorders of [tCa2+] are not typically disorders of [fCa2+]

Back 45

-dec. [tCa2+] due tp hypoalbuminemia ([fCa2+] not affected)
-binding of Ca2+ to anions ([fCa2+] not directly affected)

Front 46

Different forms of Pi depending on pH

Back 46

-H3PO4
-H2PO4-
-HPO42-
-PO43-

Front 47

Major factors that determine serum [Pi]

Back 47

-intestinal absorption
-renal excretion
-shifting between ICF and ECF
-animal age

Front 48

Pi
-sample to collect

Back 48

-non-hemolyzed serum or plasma

Front 49

Most common forms of Pi due to normal pH
-ratio

Back 49

-H2PO4- : HPO42-

-1:4 ration

Front 50

Hyperphosphatemia
-causes

Back 50

-dec. urinary PO4 excretion
-inc. PO4 absorption from intestine
-shift of PO4 from ICF to ECF
-Age
-others

Front 51

Dec. urinary excretion of PO4
-reasons

Back 51

-Prerenal, Renal, Postrenal disorder
-Primary hypoparathyroidism

Front 52

Prerenal, Renal, Postrenal disorder
-pathogenesis of hyperphosphatemia

Back 52

-dec. GFR
--dec. clearance of PO4
---inc. [PO4] --> inc. [Pi]

Front 53

Primary hypoparathyroidism
-pathogenesis of hyperphosphatemia

Back 53

-dec. production and release of PTH
--dec. [PTH]
---inc. tubular resorption of PO4
----inc. [PO4] --> inc. [Pi]

Front 54

Hemolysis/Delayed harvesting of Serum or Plasma
-pathogenesis of hyperphosphatemia

Back 54

-Prolonged in vitro storage of RBCs or in vitro hemolysis
--PO4 leaks out of RBCs
---inc. [PO4] --> [Pi]

Front 55

Shift of PO4 from ICF to ECF
-causes

Back 55

-Myopathies
-Acute tumor lysis syndrome

Front 56

Rhabdomyolysis
-types

Back 56

-exertional
-malignant hyperthermia

Front 57

Acute-tumor lysis syndrome
-define

Back 57

-rapid death of neoplastic cells
-lymphoma

Front 58

Inc PO4 absorption from the intestine
-causes

Back 58

-phosphate enema
-hypervitaminosis D

Front 59

Phosphate enema
-pathogenesis of hyperphosphatemia

Back 59

Phosphate enema (Na & PO4)
-inc. intestinal absorption of Na --> inc. [Na]
-increase intestinal absorption of PO4
--inc. [PO4] = inc. [Pi]
---inc. formation of Ca & PO4 colloid in plasma
----Ca & PO4 colloid enters macrophages
----- dec. [fCa2+]
------ dec. [tCa2+]

Front 60

Hypervitaminosis D
-pathogenesis to hyperphosphatemia

Back 60

-inc. intestinal absorption of PO4
-inc. mobilization of PO4 from bone
--inc. [PO4] = inc. [Pi]

Front 61

Difference between hypervitaminosis D and inc. PTH on phosphate

Back 61

-inc. PTH will also inc. PO4 renal excretion

Front 62

Affect of GH on Pi levels

Back 62

-GH will cause an increase in tubular PO4 absorption

Front 63

Hypophosphatemia
-causes

Back 63

-dec. PO4 absorption from intestine
-inc. urinary PO4 excretion
-shift in PO4 from ECF to ICF
-Defective mobilization of PO4 from bone (vs loss in milk)
-Equine renal disease (failure)

Front 64

Dec. PO4 absorption from the intestine
-cause

Back 64

-prolonged anorexia

Front 65

Inc. Urinary PO4 excretion
-cause

Back 65

-inc. PTH or PTHrp activity

Front 66

Magnesium
-most is found where

Back 66

-bones
-tissues

Front 67

In what animal is the amount of Mg in RBC not greater than the amount of Mg in plasma

Back 67

-Cattle

Front 68

How is Mg regulated

Back 68

-hormones

Front 69

Mg2+ assay
-samples to collect

Back 69

-serum or heparinized plasma

Front 70

Hypermagnesemia
-causes

Back 70

-Renal failure and causes of decreased GFR
-pseudohypermagnesemia from in vitro hemolysis or delayed removal of RBCs from serum (not cattle)

Front 71

Hypomagnesemia
-causes

Back 71

-Hypoproteinemia (prolonged anorexia, grass tetany)
-Osmotic diuresis
-ketonuria

Front 72

Grass tetany
-due to

Back 72

-cattle eating lush, green grass

Front 73

iPTH
-define

Back 73

-immunoreactive parathyroid hormone

Front 74

PTH
-secretion is stimulated by

Back 74

-dec. fCa2+
-dec. vitamin D

Front 75

Effect of inc. PTH on calcium and phosphorus

Back 75

-inc. Ca mobilization and resorbtion
-dec. phosphorus retention (promotes phosphaturia)

Front 76

PTH analysis
-sample collection

Back 76

-add protease inhibitor or freeze because susceptible to proteolysis

Front 77

PTH and fCa2+ relationship

Back 77

-inc. [fCa2+] expect dec. [PTH]
-and vice versa

Front 78

Inc. Serum PTH
-causes

Back 78

-neoplasm of the parathyroid gland
-hyperplastic parathyroid glands

Front 79

Hyperplastic parathyroid glands due to

Back 79

-chronic renal disease

dec. [fCa2+]:
-secondary renal hyperparathyroidism
-secondary nutritional hyperparathyroidism
-Vit. D dependent rickets

Front 80

Dec. Serum PTH
-causes

Back 80

-damaged parathyroid glands
-inhibited parathyroid glands

Front 81

Parathyroid gland inhibition
-due to

Back 81

-hypervitaminosis D
-hypercalcemic disorders

Front 82

PTH-rp
-normal physiological processes

Back 82

-promotes Ca2+ balance in the fetus
-produced by many cells
-low blood concentrations in healthy adults

Front 83

Human PTH-rp assays
-can be used for

Back 83

-dogs
-cats

Front 84

Inc. serum [PTH-rp] due to:

Back 84

-humoral hypercalcemia of malignancy

Front 85

HHM causes in
-dogs
-cats
-horses

Back 85

-dogs: lymphoma, apocrine gland carcinoma
-cats: carcinoma of the lung, kidney, bronchi
-horse: carcinoma