Fatigue (Raff) Flashcards
A 48 year old woman comes to your office complaining of fatigue and tiredness. • Physical Examination: No obvious abnormalities. – BP - normal – Height/weight – BMI not increased – Menstrual History – menopause at 45 y.o. – Normal fasting blood glucose
List Top 3 Possible Diagnosis (endocrine obviously) in the order you would evaluate them
Adrenal insufficiency: order ACTH or co-syntropin test
Hypothyroidism
Hypercalcemia
You suspect your patient has Adrenal insufficiency. What labs would you order
ACTH stimulation test: baseline cortisol, and aldosterone levels
What imaging would you want to get if you suspect adrenal insufficiency?
If it looks like primary adrenal insuffiecinecy get a CT of the abdomen
if you suspect 2nd adrenal insufficiency get CT of the pituitiary
What is a very common cause of adrenal insuffiency?
Addisons
Explain secondary adrenal insuffiency
Pituitary is not putting enough ACTH out thus adrenal gland atrophies; ACTH will ALWAYS be elevated in primary adrenal insufficiency
What symptoms do you expect to see with hypercalcemia? What about hypocalcemia?
Hypercalcemia: weakness: bones/stone/groans
Hypocalcemia: tetany
What labs and test would you order for a pt you suspect has Hashimotos?
Get TSH levels
Primary hypthyroidism you would see elevated TSH
In secondary hypothyroidis you would see low or inappropriately not elevated TSH so levels may look normal
What tests would you order for a pt you suspect has Hypercalciuria?
Look at serum Ca+ levels: if elevated, order PTH levels
If Ca+ is elevated and PTH is elevated or inappropriately NOT low; likely primary hypercalcinemia–> a tumor is secreating PTH causing increase in Ca+ levels called primary hyperparathyroidism
What could cause Secondary Hypercalciuria?
A rPTH secreating tumor may do this
Where is Ca+ aborbed in the GI system?
GI Calcium Absorption
- 20-70% (highest in children) is Abosrbed and
- 90% in duodenum and jejunum
By what process is Ca+ absorbed in the GI tract?
- Energy-dependent, cell-mediated process regulated by 1,25(OH)2D
- Passive diffusional paracellular pathway
What promotes Ca+ absorption
what inhibits it?
Promotes: PTH which is released when there is low plasma Ca++
Inhibited by High plasma calcium thus no PTH is realsease
What affect does PTH have on the kideys?
The Intestine?
The bones?
Kidneys: Causes conversion of 25-hydroxyvitamine D–> 1,25-dihydroxyvitamin D
cause Ca abosrpiton in gut
Causes Ca++ bone Reabsorption
What are the mechanisms by which Ca+ is reaborbed?
- Energy-dependent, cell-mediated process regulated by 1,25(OH)2D
- Passive diffusional paracellular pathway
Calcium Receptor on Parathyroid Hormone Secreting Cells
see image
PTH controls calcium balance directly and indirectly through
1,25(OH)2D
Signs and symptoms of hypercalcemia
Bones, Stones, groans, moans and pyschiatric overtones
Fatigue and weakness, Constipation, Nausea and vomiting, Abdominal pain (ulcers)
Osteoporosis, Polyuria and polydipsia, Renal stones, Impaired memory, confusion, and depression, Drowsiness, Coma
Key diagnostic eval for pt with hypercalcemia
Patient history and review of old labs, Serum calcium, Albumin, Phosphorus
PTH: if LOW–> get PTHrP
Do a 24 hr urine calcium and creatinine, abdominal xray adn bone mineral density
DDx for Hypercalcemia:
_____• PTH is high or inappropriately not suppressed
_____• PTH is low
PTH dependent
PTH Independent
Causes of PTH independent hypercalcemia
Sarcoid granulomas, lytic lessions, Vit D intox, malignancy
PTH Dependent Causes of Hypercalcemia
- Primary hyperparathyroidism
- Familial hypocalciuric hypercalcemia
- Parathyroid Carcinoma
- Extremely rare
What group is it more common to see primary hyperparathyroidism in?
postmenopausal women
Stats on causes of primary hyerparathyroidism
85% adenomas
5-12% are 2 or more adenomas
8-15% hyperplasia
What do the following have in common?
- MEN 1
- MEN 2
- Familial Hyperparathyroidism
• Familial Hyperparathyroidism and jaw tumors
Primary Hyperparathyroidism Familial Syndromes
Primary Hyperparathyroidism Indications for Surgery
Symptomatic hypercalcemia
Calcium 1 mg/dl above upper limit of nl
Nephrolithiasis
Osteoporosis/Fragility fractures
Renal Insufficiency
Age less than 50 yrs.
Patient preference
Why can patients with primary hyperparathyroidism have hypercalciuria if PTH increases calcium reabsorption?
Tm is saturated thus Ca will spill over into the urine: it reaches its reabsorption limits
Why can pts with primary hyperparathyroidism have hypophosphatemia?
PTH inhibits Phosphate reabsorption in the proximal tubules resulting in hypophosphatemia
How is a Parathhyroidectomy perfromed?
• Small incision with Local anesthesia
Must have preoperative localization • Ultrasound
- 99m-technetium sestamibi • CTscan
- Intraoperative parathyroid hormone monitoring
- Need to see 50% decrease in PTH after removal of suspected adenoma
Medical Management of Hyperparathyroidism
- Optimize hydration
- Avoid calcium sparing diuretics
- Normal calcium intake
- Optimize vitamin D status
- Potential use of a calcimimetic
- Calcium sensing receptor agonist • Cinacalcet (Sensipar)
Mechanisms of Hypercalcemia of Malignancy
PTH related protein (PTHrP)
Osteolytic bone mets
Unregulated 1,25 dihrydoxy Vit D
Osteoclast activating factors
Ectopic PTH
What is PTH releated protein or PTHrP
- N-terminal homology with PTH
- Not measured by PTH assays
- Found in normal tissue
- May be important in fetal development
• Chromosome 12 ( PTH on 11 )
