Renal (Ca, Mg, Po4)

Front 1

in what conditions is PTH secreted?

Back 1

low serum Ca, increased PO4, severe hypomagnesemia

Front 2

what are the hormones involved in regulation Ca, PO4, Mg levels in the body?

Back 2

PTH
Vit D
Calcitonin
phosphatonins

Front 3

PTH actions on kidney, bone, intestine?

Back 3

kidney: gets rid of PO4 in PT; increase Ca reabsorption and incrase active Vit D in DCT

bone: increase bone resorption

intestine: indirectly increease Ca and P absorption by increasing conversion to active vit D

Front 4

what does cinacalcet do?

Back 4

increases sensitivity of CSR to calcium (used to tx secondary hyperparathyroidism like in chronic kidney dz)

remember what CSR is?
in hypercalcemia, CSR activates to cause more excretion of Ca

Front 5

what is the vitamin D synthesis pathway?

Back 5

vit D3 from sun or diet --> 25 HCC (via 25-hydroxylase in liver) --> 1,25 DHCC (via 1 hydroxylase in kidney)

Front 6

what is 1-hydroxylase enzyme activity (and thus active vit D) increased by?

decreased by?

Back 6

inc by low P, low Ca, low calcitriol (=active vit D), inc PTH
dec by high levels of active vit D (neg feedback)

Front 7

what are the actions of vit D in the intestines, bone, PTH gland, kidneys?

Back 7

Intestine:- increase Ca, Mg and P reabsorption

Bone:- increase mineralization and enhance osteoclast activity (PTH required for Vitamin D effect on bone)

PTH gland:- Provides feedback to PTH gland - inhibit PTH secretion

Kidney:- Increased renal excretion of phosphate and decreased renal excretion of calcium maintains Ca-Pi balance

Front 8

what is useful in tx of hypercalcemia?

Back 8

calcitonin

Opposite effect on serum calcium as PTH
- Inhibits osteoclast-mediated bone resorption
-zIncreases renal excretion of calcium

Front 9

what is the normal level of calcium in serum?

-ionized ca?

Back 9

9-10.4 mg/dL

ionized= 4.8-5.2 mg/dL

Front 10

where is most of the calcium in the body?

Back 10

in the bone! (99%)

Front 11

what is the definition of hypocalcemia?

Back 11

total serum Ca < 9.0 mg/dl

ionized calcium <1.2 mmol/L (nl=1.2-1.3)

Front 12

what are causes of hypocalcemia?

Back 12

1) No PTH
-Hypo PTH, hypomagnesemia

2) Ineffective PTH (generally Vit D related)
-Vit D deficiency, malfunction
-Intestinal malabsorption Ca

3) PTH overwhelmed
Hyperphosphatemia (e.g. tumor lysis and rhabdomyolysis) -- PO4 will bind to Ca in the blood; so if you control PO4, you'll bring Ca back up

Front 13

what are teh clinical presentation of hypocalcemia?

Back 13

1) Neuromuscular (causes muscle contraction)
-Tetany, Trousseau’s and Chvostek’s signs
-Seizures, neuropsychiatric changes

2) Cardiovascular
-Prolonged QT interval, arrhythmias, hypotension, heart failure

3) Ectodermal (rare)
Coarse scaly skin, cataracts

Front 14

tx of hypocalcemia

Back 14

- correct underlying dz process
- IV calcium (Ca gluconate > Calcium chloride)
- oral calcium (calcium citrate, ca- acetate, ie tums)
- give vit D (to inc gut absorption of Ca)

Front 15

what is the definition of hypercalcemia?

Back 15

total serum Ca >10.4 mg/dl

ionized Ca >1.3 mmol/L

Calcium always has to be linked to protein when you discuss it??

Front 16

what are the causes of hypercalcemia?

Back 16

Bone (hyperPTH, tumor, acidemia, immobilization, vit A)

GI absorption (Vit D, sarcoid, milk-alkali syndrome)

Renal (ARF/immobilization, thiazide diuretics, familial hypercalcemia)

Front 17

how does hypercalcemia present?

Back 17

1) Cardiovascular
Vasoconstriction, Hypertension, short QT interval on EKG

2)Gastrointestinal
Ulcers, constipation, pancreatitis

3) Neuropsychiatric
Lethargy, obtundation, psychosis muscle weakness

4) Extraskeletal calcifications
Dermal, ocular, vascular (with infarction), visceral organs

Front 18

________ ___________ is the most common cause of hypercalcemia in all patients

Back 18

primary hyperparathyroidism

Front 19

T or F. Thiazide diuretics are useful for hypercalcemia therapy.

Back 19

F. Loop diuretics are useful, but not thiazide!!

thiazide diuretics would make hypercalcemia worse! the blockade of na/cl cotransporter causes an increase in the functioning of the na/ca antitransporter which is reabsorbing Ca's and leads to hypercalcemia.

Front 20

hypercalcemia related to _______ is the most common in hospitalized patients.

Back 20

malignancy

Front 21

what is the most important initial tx for hypercalcemia?

Back 21

aggressive volume replacement (But be careful in management of pts with CHF -- don't want them to have too much fluid)

Front 22

65 year old man with multiple myeloma presents with altered mental status and serum calcium of 10 mg/dL. Serum albumin is 1.2 mg/dL.
Is he hypercalcemic?

Back 22

remember Ca is always linked to protein, so you have to correct for hyperalbumic state.

Calcium is bound to albumin. Ionized calcium level may be elevated if albumin level is low.

Formula: Normal calcium range changes 0.8 mg/dL for each gram that albumin changes from 4.

Serum albumin 1.2, down 2.6 from 4.0. His normal Ca should be 10-(2.6x0.8)=8 mg/dL.

Thus, his serum calcium of 10 is equivalent to a calcium of 12 in a patient with normal albumin.

so YES, he is hypercalcemic

(If there’s not enough protein in serum to bind Ca, then it will become ionized…not all of this Ca will stay in the serum and thus, total levels will decrease (although level of ionized Ca relative to normal will be elevated))

Front 23

65 year old man with multiple myeloma presents with altered mental status and serum calcium of 10 mg/dL. Serum albumin is 1.2 mg/dL. On exam, he is volume depleted.
How do you make his calcium level decrease?

Back 23

Replete patient’s vascular volume with saline. This will slow proximal nephron absorption of sodium and calcium. Also, volume repletion decreases TAL absorption of calcium.

Once patient volume replete, give furosemide with sufficient saline, so patient does not become volume depleted. Furosemide further decreases TAL calcium absorption.

Front 24

what's the big diff in PO4 vs Ca homeostasis?

Back 24

most of hte PO4 that we take in is excreted by kidney (so this is very important for pts with kidney dz).

most Ca is excreted in stool (2/3), kidney (1/3)

Front 25

which regulation hormone inhibits phosphorus reabsorption? where does it act?

Back 25

PTH; acts on proximal tubule

Front 26

An intoxicated, malnourished 45 yo patient with known alcoholism is brought to the ER by the police. He is given glucose containing fluids, vitamins, and admitted to general medicine. The next morning he is found to have hyperphosphatemia, rhabdomyolysis, and acute renal failure. What happened?

Back 26

The patient was probably phosphate depleted due to poor dietary intake, and had relatively low insulin levels. When he was given glucose containing solutions, his insulin levels rose, phosphate moved into cells, dropping serum phosphate to dangerously low levels

Rhabdomyolysis developed due to hypophosphatemia

Rhabdomyolysis released intracellular phosphate, so subsequently, serum phosphate levels rose.

Front 27

where are most of the cations (Ca, Mg, PO4) in the body: tissue or serum?

Back 27

tissue (so serum levels are NOT reflective of total body stores)

Front 28

what's the main diff of Mg reabsorption from Ca and PO4?

Back 28

most of it is taken up in the thick ascending limb of Henle -- 60% (Ca and PO4 is taken mostly up in the PT == check this!!

Front 29

etiology and presentation of hypomagnesemia

Back 29

etiology
- malnutrition, alcoholism, GI malabsorption
- renal wasting after cisplatin, amphotericin B, cyclosporin

presentation:
- muscle weakness, tremors, fasciculations, arrhythmias
-neuropsychiatric changes
- hypocalcemia, hypokalemia

Front 30

tx of hypomagnesemia

Back 30

- replace by IV or IM supplements

Front 31

etiology and presentation of hypermagnesemia

Back 31

etiology
- iatrogenic (pre-eclampsia), esp if renal failure present (can't excrete Mg)
- Mg containing antacids in ESRD pts

presentation:
- low: thirst, nausea, vomiting,
- mid: hypotention!!
- high: coma, resp paralysis



manifestations

Front 32

tx of hypermagnesemia

Back 32

- IV calcium gluconate
- loop diuretics, hemodialysis

Front 33

A weak patient is found to have hypokalemia and hypocalcemia refractory to potassium and calcium supplements. What’s going on?

Back 33

Magnesium is a necessary substrate or cofactor for important enzymes such as ATPase, GTPase, phospholipase C, adenylate cyclase and guanylate cyclase, which are important for renal transport of calcium and potassium.

Persistent hypocalcemia and hypokalemia may result from hypomagnesemia.

Treatment consists of giving all three cations.

Front 34

what is phosphatonins

Back 34

hormone that makes body get rid of phosphorus (nl physiology is not clear)

Front 35

what does acidemia do to serum ionized Ca levels?

Back 35

increases ionized Ca (vice versa for alkalosis --> would dec ionized Ca)

Front 36

what are the renal manifestations of hypercalcemia?

Back 36

1)ARF
-Vasoconstriction and decreased renal plasma flow and GFR
2) Volume depletion
-Inhibition of Na reabsorption and inability to concentrate urine
3) K and Mg losses due to Na wasting

Front 37

tx of hypercalcemia

Back 37

1) optimize renal excretion of Ca (by correcting vol depletion, loop diuretics -- not thiazides!!)

2) inhibit bone resorption with calcitonin and biphosphonates

Front 38

what are some causes of hyperphosphatemia?

Back 38

- tumor lysis, rhabdomyolysis

chronic renal failure (leading to inability to excrete PO4)

hypo-PTH

cathartics

Front 39

what are 3 consequences of hyperphosphatemia?

Back 39

- hypocalcemia
- Ca-Pi deposits in blood vessels, soft tissues, visceral
- secondary hyperparathyroidism (eg. in chronic kidney dz)

Front 40

tx of hyperphosphatemia

Back 40

-correct underlying dz
-oral phosphate binding agents (calcium and non-calcium based binders)

Front 41

what are some causes of hypophosphatemia?

Back 41

cellular shifts:
- glucose infusion after starvation
- common in severe alcoholism

renal losses:
- elevated PTH
-renal tubular defect

malabsorption (malnutrition, alcoholism)

vitamin D deficiency (can't absorb Pi in the intestines anymore)

Front 42

tx of hypophosphatemia?

Back 42

oral
- milk, cheese, eggs
- Na and K phosphate suplements

IV (Na or K phosphate salts)
- only use in emergencies bc can cause severe and symptomatic hypocalcemia