- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
66 Cards in this Set
- Front
- Back
|
A 63-year-old female is evaluated for a humeral fracture sustained during a fall because of lightheadedness. For the past 2 months, she has become progressively fatigued and absent-minded. She has lost her appetite with weight loss, and is constipated. She has been urinating several times per night and complains of thirst; however, a test for diabetes was negative. Her blood pressure is 110/70 mm Hg, heart rate is 80 bpm, palpation of the thyroid is normal. Her mucus membranes are somewhat dry and sticky. An x-ray reveals a fracture of the mid-left humerus but there is also the suggestion of some lytic lesions of the proximal humerus. Serum creatinine is 2.1 mg/dL (normal 0.6-1.2 mg/dL), with normal electrolytes and glucose levels, but serum calcium is 13 mg/dL (normal 9.0-11.0 mg/dL), hemoglobin is 9.2 g/dL (normal 12.0-16.0 g/dL, female ). Parathyroid hormone is low (9 pg/mL). What is most likely causing her problems?
|
important info: loss of appetite, weight gain, urinating a lot, thirst, dry and sticky membranes (dehydrated); fracture (Ca problem); serum creatinine is elevated (kidney problem); hypercalcemia; anemia; LOW PTH
SO HIGH Ca, and LOW PTH Multiple myeloma |
|
High Ca and High PTH indicates?
|
problem with PT gland secreting too much PTH
gives PTH dependent hyerpcalcemia |
|
High Ca and Low PTH indicates
|
PTH normally raises Ca and Ca lowers PTH
so something else is increasing the Ca aka PTH independent hypercalcemia |
|
Low Ca and High PTH indicates?
|
appropriate response to low Ca (secondary hyperparathyroidism)
something else in the body is causing you to not have adequate response to PTH |
|
How can malignancy cause hypercalcemia? 2
|
stimulate osteoclasts
Secrete parathyroid hormone related protein (PTHrP) |
|
describe the summary of hypercalcemia due to malignancy
|
Tumor invades bone (such as multiple myeloma or bony metastases of some solid tumors).
They secrete cytokines and chemokines which increase the expression of RANK ligand on marrow stromal cells. RANK ligand binds to RANK on osteoclast precursors. This stimulates osteoclast formation and activity, causing bone resorption and hypercalcemia. |
|
summarize humoral hypercalcemia of malignancy
|
Systemic tumors (such as breast cancer) can secrete parathyroid hormone related peptide (PTHrP).
PTHrP is able to bind to and activate the PTH receptor on bone causing bone resorption PTHrP also increases distal renal tubular calcium reabsorption. Both contribute to hypercalcemia |
|
What will usually happen to PTH levels with hypercalcemia of malignancy?
|
it will be LOW
high calcium will feedback inhibit the PTH |
|
How can you lower serum free Ca levels in this patient? general mechanisms (3)
|
Dilute Ca in the Blood
increase Ca excretion by kidney Keep Ca in bone (prevent resorption) |
|
a patient is dehydrated with presumed prerenal azotemia. What would be the best treatment for hypercalemia? why?
|
IV normal saline
restores volume status and dilutes Ca in the blood, this facilitates urinary calcium excretion |
|
what does the body do to calcium when the body is dehydrated?
|
reabsorb more calcium
|
|
What diuretic will increase Ca excretion by the kidney?
|
Loop diuretic
(Furosemide) |
|
When might you use a loop diuretic to treat hypercalcemia? 2
|
if they develop edema after IV saline
in a pt with symptomatic hypercalcemia and heart failure (feurosemide) |
|
What happens to bone with primary hyperparathyroidism and hypercalcemia of malignancy?
|
adenoma -->PTH
Bone metastisis-->cytokines tumor-->PTHrP all increase bone resorption which then releases Ca and Phospate |
|
What hormone decreases osteoclast activity?
|
Calcitonin
|
|
MOA of calcitonin?
|
in bone: decrease Ca, P resorption (this is the major mech)
in kidney at pharmalogical doses: Increase Ca/P excretion |
|
Calcitonin use? and MOA?
|
Acute, symptomatic/severe hypercalcemia
Works in 4-6 hrs Lowers serum calcium concentration by a maximum of 1 to 2 mg/dL Tachyphylaxis - efficacy is limited to the first 48 hours also Paget's Disease and Osteoporosis MOA: in bone: decrease Ca, P resorption (this is the major mech) in kidney at pharmalogical doses: Increase Ca/P excretion |
|
What will produce a more sustained lowering of serum Ca (than Calcitonin)?
|
Bisphosphonates
|
|
drugs ending in -dronate are what?
|
Bisphosphonates
|
|
Etidronate is what kind of drug?
|
Bisphosphonates
INHIBIT OSTEOCLASTS |
|
Zoledronic acid is what kind of drug?
|
Bisphosphonates
INHIBIT OSTEOCLASTS |
|
MOA for Bisphosphonates
|
adsorb to hydroxyapatite in bone (stick on)
concentrate at site of active remodeling INHIBIT OSTEOCLASTS |
|
clinical use of bisphosphonates?
|
Acute, symptomatic/severe hypercalcemia
chronic--osteolytic bone lesions of cancer Osteoporosis and Paget's disease |
|
side effect of Etidronate?
|
osteomalacia
crappy remodeling (because you actually apoptose the osteoclasts) |
|
Esophagitis is a side-effect of what hypercalcemic drug class? prevention?
|
Bisphosphonates (inhibit osteoclasts)
tell the pt to sit up for 60 minutes and take on empty stomach |
|
Osteonecrosis of the jaw is a side-effect of what hypercalcemic drug class?
|
Bisphosphonates
(inhibit osteoclasts) |
|
major side effect of Zoledronic Acid?
|
Renal tox
(Bisphosphonates- inhibit osteoclasts) |
|
How can PTH secretion be reduced? 2 (general)
|
Raise serum levels of free Ca
Sensitize the Ca sensing receptor to Ca |
|
what does Cinacalcet do?
|
sensitizes the Ca receptor on the prathyroid gland
decreases PTH release thus decreasing Ca levels PTH WILL BE SHUT OFF AT LOWER CALCIUM LEVELS |
|
Clinical use of Cinacalcet? MOA?
What is it primarily used for? |
Hypercalcemia associated with PARATHYROID CARCINOMA
Secondary hyperparathyroidism in chronic kidney disease MOA: sensitizes the Ca receptor on the prathyroid gland decreases PTH release thus decreasing Ca levels |
|
Why would you not use Cinacalcet to treat hypercalcemia of malignancy?
|
there isn't an increase in PTH levels
|
|
Side effects of Cinacalcet?
|
Hypocalcemia (Ca receptor sensitizer)
|
|
Vitamin D deficiency can lead to what 2 problems?
|
Kids: Rickets (nutritional problem, lack of sun/dietary def)
Adults: Osteomalacia |
|
What is the primary cause of hypocalcemia with a vitamin D deficiency?
|
decreased intestinal absorption of Ca
|
|
describe the effects of inadequate intestinal absorption of Ca and P
|
|
|
low plasma P will do what?
|
increase free Ca levels
because it doesn't bind it |
|
What will you use to treat Rickets?
|
Vitamin D preparation
|
|
what is Cholecalciferol?
|
pure Vitamin D3
--inactive form! needs to be activated by kidney |
|
what is Ergocalciferol
|
pure Vitamin D2
less potent but again, still inactivated |
|
what is Calcitriol?
|
1,25 dihydroxyvitamin D3
ACTIVATED good to go vitamin D |
|
what would be the effects of having no PTH?
|
No Vitamin D induced Ca absorption
No bone resorption No calcium reabsorption and excretion of phosphorus from the kidney |
|
What contributes to hypocalcemia from hypoparathyroidism?
|
reduced vitamin D3 intestinal Ca absorption
reduced bone resorption reduced renal distual tubular calcium reabsorbption reduced renal phophaturic effect |
|
What happens to Ca with hypoparathyroidism?
|
goes down
|
|
What happens to P with hypoparathyroidism?
|
possibly normal or hyperphosphatemia
|
|
What would you use to treat hypoparathyroidism?
|
Vitamin D and calcium supplements
|
|
how does chronic kidney disease lead to secondary hyperparathyroidism?
|
|
|
if you have secondary hyperparathyroidsim, what will happen to bone?
|
bone destruction
(due to CKD) |
|
secondary hyperparathyroidsim does what to phosphorus?
|
Exacerbates it
cant get rid of it from kidney resorption of bone |
|
What would you do for a patient with hypocalcemia and hyperphosphatemia from chronic kidney disease?
|
give calcitriol (active form of Vitamin D, kidney can't convert inactive form) and phosphate binders
|
|
What can happen to Ca levels if a patient with chronic kidney disease has high enough PTH levels?
|
normal serum Ca or hypercalcemia
|
|
What will happen to Ca absorption if you give calcitriol to a patient with chronic kidney disease and hypercalcemia?
|
increase
(via increasing Ca absorption) |
|
What is the difference between 1,25(OH)2D3 and Paricalcitol ?
|
1,25(OH)2D3 has a half life of hours ---> Increase serum Ca, decrease PTH secretion
1,25(OH)2D3 analogues have a half life of minutes-->Just decrease PTH secretion |
|
What is Paricalcitol?
|
1,25(OH)2D3 analogue
(decreases PTH without raising Ca) |
|
When might paricalcitol be useful?
|
When calcitriol causes unacceptably high serum Ca levels in patients with secondary hyperparathyroidism from chronic kidney disease
remember-->1,25(OH)2D3 analogues have a half life of minutes-->Just decrease PTH secretion |
|
What other drug can lower serum PTH levels in chronic kidney disease?
|
Cinacalcet
(Ca sensing receptor sensitizers) |
|
what do bisphosphonates do? used for?
|
Selectively inhibit bone resorption
Parenteral agents used for hypercalcemia used for osteoporosis |
|
how must you take bisphosphonates?
|
they have Very low oral bioavailability
must take on empty stomach, and sit up for 60 minutes after take to prevent reflux |
|
why can calcitonin be used for osteoporosis?
|
Inhibits bone resorption and Ca and P excretion by kidney
|
|
What is teriparatide? used?
|
Recombinant PTH
to treat osteoporosis--exogenous intermittent stimulation only hits osteoblast (the osteoblast does not then activate the osteoclast) so short half life leads to bone deposition |
|
Long term concern about increasing risk of osteosarcoma is associated with what drug?
|
Teriparatide (PTH analouge for osteoporosis)
|
|
What is Paget's Disease?
|
Disorder of increased skeletal remodeling
Uncontrolled osteoclastic bone resorption with secondary increases in bone formation New bone is poorly organized |
|
Tx for Paget's disease?
|
Calcitonin
Bisphosphonates --both decrease osteoclast activity and help reduce Ca resorption, prevent bad remodeling |
|
pt has tingling in fingertips, toes, and lips, muscle aches affecting their legs feet abdomen and face. Labs: low Ca, Low PTH, high Phosphorus, serum creatine normal. Treat with what?
A) cinacalcet B) Alendronate C) Vitamin D + Ca D) Teriparatide E) Calcitonin |
this is primary hypoparathyroidism
C) Vitamin D + Ca |
|
pt has excessive urination, abd pain, nausea, vom, loss appetitie, tires easily and some weakness. Recent kidney stone. Labs- high calcium, high PTH, low phosphours, high urinary calcium, high serum creatinine. What would you use to treat?
A) Alendronate B) Vit D + Ca C) Teriparatide D) Calcitriol |
person has PTH dependent hypercalcemia (primary hyperparathyroidism)
(serum creatinine is acutely high due to dehydration) tx is saline, bisphophonate, calcinet (Ca sensitizer) Answer: A) Alendronate |
|
pt has nausea, vomits, tires easily, weakness. Low Ca, high PTH, high phos, high serum creatinine. What would you use?
A) alendronate B) Teriparatide C) Calcitriol D) Calcitonin E) Paricalcitol |
secondary hyperparathyroidism, this dude has kidney problems (leading to high phos and creatine) most likely CKD
C) Calcitriol |
|
Patient complains of back pain and has BMD. Labs: Low Ca, high PTH, low Phosphate, normal serum creatinine.
Alendronate Teriparatide Calcitriol Calcitonin Paricalcitol Cinacalcet |
secondary hyperparathyroidism (vitamin D Deficiency in this case)
Calcitriol |
