11 - Endocrine Case Study I

Question 1

Which lab values are associated with renal failure?

Answer 1

• Creatinine*** (primary)
• BUN
• Protein/RBCs in the urine

All of these things signal that the kidneys are not working

Question 2

If the patient is having shooting foot pain in the foot and has a history of renal failure, what types of things are you thinking?

Answer 2

• Gout
• Bone resorption of calcium

Gout would be more localized
Bone resorption of calcium would be more generalized throughout the foot

Question 3

What tests would you want to do in order to differentiate between these?

Answer 3

• PTH (parathyroid hormone, look for problems with calcium)
• Uric acid (for gout)
• Bone scan

Question 4

What is Procrit used for?

Answer 4

Procrit – synthetic errythropoetin (helps manufacture RBCs)

Question 5

What is Cellcept used for?

Answer 5

Cellcept – anti-rejection medication

This patient has had a kidney transplant

Question 6

What is Prednisone used for?

Answer 6

Steroid, used for rejection

Question 7

What can cause hyperglycemia in this patient?

Answer 7

• Prednisone can cause hyperglycemia

- This can be severe enough to induce a diabetic state

Question 8

What is renal osteodystrophy?

Answer 8

Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood. It’s common in people with kidney disease and affects most dialysis patients

Question 9

What is chronic renal failure?

Answer 9

• Slow, relentless loss of functional renal mass
• Primary-chronic glomerulonephritis, interstitial nephritis
• Secondary-diabetes, hypertension

Question 10

What is the clinical definition of chronic kidney failure?

Answer 10

Clinical definition - KNOW THIS

- GFR

Question 11

Describe the pathology of chronic kidney failure

Answer 11

• Kidneys will be reduced in size due to interstitial fibrosis and tubular loss
• Glomeruli will be solidified and may even become calcified
• Severe intimal thickening will be present in large and small renal arteries
• Multiple cysts can form
• Defect in glomerular filtration rate, specifically of nitrogenou waste
• The accumulation of nitrogenous waste leads to elevation in serum BUN and creatinine
• Defect in tubular handling of water, electrolytes, leading to hyperkalemia (can lead to cardiac arrest)

Question 12

What are the extra-renal manifestations of chronic renal failure?

Answer 12

• Nausea and vomiting, anorexia, colitis
• Anemia
• Impaired platelet aggregation
• Hypertension
• Cardiovascular disease
• Reduced lipoprotein lipase
• Chronic pulmonary edema
• Immune system blunting of the immune response
• Nervous system disturbances (sensory and motor neuropathy - demyelination)
• Parathyroid gland and bone problems

Question 13

Describe the anemia seen in chronic renal failure

Answer 13

Anemia-due to decreased production of erythropoietin, decreased red cell survival, poor nutrition, bleeding

Question 14

Describe the impaired pletelet aggregation seen in chronic renal failure

Answer 14

Disturbances of blood coagulation-impaired platelet aggregation, decreased release of platelet factor 3, thrombocytopenia

Question 15

Describe the hypertension seen in chronic renal failure

Answer 15

Hypertension-release of renin by diseased kidney (due to hypoperfusion of glomeruli), or increased intravascular fluid volume secondary to abnormal renal handling of salt and water

Question 16

Describe the cardiovascular disease seen in chronic renal failure

Answer 16

Cardiovascular disease-due to hypertension, calcium deposition, and hypertriglyceridemia

Question 17

Describe the reduced lipoprotein lipase seen in chronic renal failure

Answer 17

Reduced lipoprotein lipase (possibly due to insulin deficiency or resistance mediated by vitamin D deficiency and presence of nondialyzable inhibitor of LPL) results in decrease in levels of nonatherogenic containing lipoproteins and increase in proatherogenic LDL and VLDL

Question 18

Describe the nervous system disorders seen in chronic renal failure

Answer 18

Nervous system

• Disturbances in mentation, sensory and motor neuropathy
• Demyelination in peripheral nerves
• You will see a lot of neuropathic pain or lack of sensation due to demylination of peripheral nerves

Question 19

Describe the parathyroid glands and bone disorders

Answer 19

Parathyroid glands and bone

• PTH will be “turned on” due to hypocalcemia (from the renal retention of phosphate and decreased intestinal absorption of calcium)
• Lack of calcium absorption will lead to impaired conversion of vitamin D to its active form of 1,25-dihydroxycholecalciferol in the kidney, leading to further problems

Question 20

What is the effect of PTH being “turned on” due to low calcium?

Answer 20

A secondary hyperparathyroidism

Question 21

What are the effects of hyperparathyroidism?

Answer 21

• Subperiosteal bone reabsorption, primarily in the tips of distal phalanges and clavicles
• Osteosclerosis
• Irregular radiolucencies with expansion of bone (“brown cysts”)

Question 22

Describe the “brown cysts” of hyperparathyroidism

Answer 22

• We want osteoclasts to go into overdrive, but there is a certain level of balance so osteoblasts have to as well
• You end up absorbing the calcium out of long bones, but when we try to put that calcium back, we can’t keep up with the osteoblasts, so we get the brown cysts or tumors forming

Question 23

What is osteodystrophy?

Answer 23

Osteodystrophy is a general term for a dystrophic growth of the bone.

Question 24

What is renal osteodystrophy?

Answer 24

A form of osteodystrophy

Bone changes due to kidney disease is known as renal osteodystrophy (uremic bone disease)

This is seen in patients with chronic renal failure

Question 25

What are some types of renal osteodystrophy?

Answer 25

- Osteomalacia of adults - Rickets of children - Osteopenia - Osteosclerosis - Osteitis fibrosa cystica ***

Question 26

What is osteitis fibrosa cystica? ***

Answer 26

- Proliferation of both osteoclasts and osteoblasts - The increase in osteoblastic (build) activity leads to an elevation of alkaline phosphatase - Bony trabeculae will appear frayed and fibrous tissues has formed in marrow spaces This whole process is called osteitis fibrosa cystica (which is a form of renal osteodystrophy)

Question 27

What causes the alkaline phosphatase levels to rise in osteitis fibrosa cystica? ***

Answer 27

The laying down of bone Build bone = osteoblasts

Question 28

What percent of chronic kidney disease patients show signs of osteitis fibrosa cystica?

Answer 28

75% Bone inflammation with fibrous cysts

Question 29

What causes the bone changes seen in osteitis fibrosa cystica? ***

Answer 29

1 - Abnormal metabolism of vitamin D 2 - Overproduction of PTH 3 - Chronic metabolic acidosis

Question 30

How does decreased vitamin D lead to bone changes? ***

Answer 30

Decreased vitamin D leads to... - Decreased intestinal absorption of calcium - Hypocalcemia - Defective bone mineralization

Question 31

How does the overproduction of PTH (parathyroid hormone) occur? ***

Answer 31

- Renal retention of phosphate causes hyperphosphatemia and even further hypocalcemia - The result is increased synthesis and secretion of PTH (which takes calcium from bone for the circulation)

Question 32

How does metabolic acidosis contribute to bone changes? *************

Answer 32

KNOW THIS - Metabolic acidosis inhibits the conversion of vitamin D into its active form - Metabolic acidosis also increases the solubility of bone mineral (bone degrades) - This further contributes to osteopenia (reduced bone mass of lesser severity than osteoporosis)

Question 33

Is chronic kidney disease always diagnosed?

Answer 33

Chronic kidney disease is greatly diagnosed - Phosphate levels begin to rise when GFR is around 60 mL/min, which is regarded as only a moderate decline in function by most physicians - You ALSO need to show that there is some renal failure for a CRF diagnosis KNOW the clinical diagnosis standards ***

Question 34

What does chronic kidney disease lead to?

Answer 34

- Bone pain - Muscle weakness - Deformities - Pathological fractures

Question 35

What lab findings will you see in chronic kidney disease?

Answer 35

- Hyperphosphatemia - Hypocalcemia - Elevated alk phos - Increased PTH (particularly when assayed for C-terminal PTH, which is normally excreted only by the kidney)

Question 36

As the glomerular filtration rate (GFR) decreases, what further changes will you see?

Answer 36

- Decreased hemoglobin - Faulty production of erythropoietin - Low calcium - Low vitamin D - Low albumin - High PTH - High phosphate - High homocysteine - High inflammatory cytokines

Question 37

Why is albumin low?

Answer 37

The patient is urinating the albumin out - the filtering holes in the kidneys are large, so the protein can easily escape

Question 38

How do you treat endocrine abnormalities?

Answer 38

- Treatment of hyperphosphatemia by reducing dietary intake of phosphate and decrease absorption of phosphate with intestinal phosphate binders (aluminum hydroxide) - Dialysis for severely high phosphate levels - Dietary supplementation of vitamin D

Question 39

What orthopedic treatment is needed for this case study? (numerous broken bones in the toes)

Answer 39

- Non-weight bearing (NWB) until bones are in reparative phase and abnormal lab values begin to correct with appropriate drug therapy - Not a whole lot we can do at this point - wheel chair for 2 months