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Endocrine Exam 1 > 11 - Endocrine Case Study I > Flashcards

11 - Endocrine Case Study I Flashcards

1
Q

Which lab values are associated with renal failure?

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

All of these things signal that the kidneys are not working

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2
Q

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?

A
  • Gout
  • Bone resorption of calcium

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

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3
Q

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

A
  • PTH (parathyroid hormone, look for problems with calcium)
  • Uric acid (for gout)
  • Bone scan
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4
Q

What is Procrit used for?

A

Procrit – synthetic errythropoetin (helps manufacture RBCs)

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5
Q

What is Cellcept used for?

A

Cellcept – anti-rejection medication

This patient has had a kidney transplant

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6
Q

What is Prednisone used for?

A

Steroid, used for rejection

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7
Q

What can cause hyperglycemia in this patient?

A
  • Prednisone can cause hyperglycemia

- This can be severe enough to induce a diabetic state

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8
Q

What is renal osteodystrophy?

A

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

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9
Q

What is chronic renal failure?

A
  • Slow, relentless loss of functional renal mass
  • Primary-chronic glomerulonephritis, interstitial nephritis
  • Secondary-diabetes, hypertension
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10
Q

What is the clinical definition of chronic kidney failure?

A

Clinical definition - KNOW THIS

- GFR

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11
Q

Describe the pathology of chronic kidney failure

A
  • 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)
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12
Q

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

A
  • 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
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13
Q

Describe the anemia seen in chronic renal failure

A

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

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14
Q

Describe the impaired pletelet aggregation seen in chronic renal failure

A

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

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15
Q

Describe the hypertension seen in chronic renal failure

A

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

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16
Q

Describe the cardiovascular disease seen in chronic renal failure

A

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

17
Q

Describe the reduced lipoprotein lipase seen in chronic renal failure

A

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

18
Q

Describe the nervous system disorders seen in chronic renal failure

A

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
19
Q

Describe the parathyroid glands and bone disorders

A

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
20
Q

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

A

A secondary hyperparathyroidism

21
Q

What are the effects of hyperparathyroidism?

A
  • Subperiosteal bone reabsorption, primarily in the tips of distal phalanges and clavicles
  • Osteosclerosis
  • Irregular radiolucencies with expansion of bone (“brown cysts”)
22
Q

Describe the “brown cysts” of hyperparathyroidism

A
  • 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
23
Q

What is osteodystrophy?

A

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

24
Q

What is renal osteodystrophy?

A

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

25
Q

What are some types of renal osteodystrophy?

A
  • Osteomalacia of adults
  • Rickets of children
  • Osteopenia
  • Osteosclerosis
  • Osteitis fibrosa cystica ***
26
Q

What is osteitis fibrosa cystica?

A
  • 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)

27
Q

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

A

The laying down of bone

Build bone = osteoblasts

28
Q

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

A

75%

Bone inflammation with fibrous cysts

29
Q

What causes the bone changes seen in osteitis fibrosa cystica?

A

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

30
Q

How does decreased vitamin D lead to bone changes?

A

Decreased vitamin D leads to…

  • Decreased intestinal absorption of calcium
  • Hypocalcemia
  • Defective bone mineralization
31
Q

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

A
  • 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)
32
Q

How does metabolic acidosis contribute to bone changes?

A

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)
33
Q

Is chronic kidney disease always diagnosed?

A

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 ***

34
Q

What does chronic kidney disease lead to?

A
  • Bone pain
  • Muscle weakness
  • Deformities
  • Pathological fractures
35
Q

What lab findings will you see in chronic kidney disease?

A
  • Hyperphosphatemia
  • Hypocalcemia
  • Elevated alk phos
  • Increased PTH (particularly when assayed for C-terminal PTH, which is normally excreted only by the kidney)
36
Q

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

A
  • Decreased hemoglobin
  • Faulty production of erythropoietin
  • Low calcium
  • Low vitamin D
  • Low albumin
  • High PTH
  • High phosphate
  • High homocysteine
  • High inflammatory cytokines
37
Q

Why is albumin low?

A

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

38
Q

How do you treat endocrine abnormalities?

A
  • 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
39
Q

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

A
  • 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

Endocrine Exam 1 (18 decks)

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