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Session 2 CM endo4
CM- Endo -4- Parathroids/Calcium lect 9-12
| Question | Answer |
|---|---|
| Where does the inferior parathyroid gland develop from embryologically | the third pharyngeal pouch |
| Where does the superior parathyroid gland develop from embryologically | develops from the fourth pharyngeal pouch along with the thyroid gland |
| How do the parathyoid glands normally look, how big are they, how much do they weigh | typically ovoid in shape, yellow-tan colored and measure 5mm x 3mm x 1mm and weight on average 35mg glands are soft in texture and highly vascular |
| Where do you typically find the superior parathyroid glands | they are typically found close to and often within the capsule of the superior pole of the thyroid gland -lie approx 1 cm above the junction of the inferior thyroid artery and recurrent laryngeal nerve at the level of the cricoid cartilage |
| Where do you typically find the inferior parathyroid glands | commonly located on the posterior lateral aspect of the lower thyroid gland pole. -lie below the junction of the inferior thyroid artery and anterior to the recurrent laryngeal nerve |
| What arteries supply the parathyroid glands | superior thyroid artery, inferior thyroid artery |
| what veins supply the parathyroid glands | superior thyroid vein, middle thyroid vein, inferior thyroid vein. |
| What nerve supplies the parathyroid gland | middle cervical ganglion, inferior cervical ganglion |
| What is the job of chief cells in the parathyroid and how do they appear microscopically | chief cells manufacture PTH -stain darker, smaller and are many in number |
| What is the job of Oxyphil cells of the Parathyroid and how do they appear microscopically | function is unknown, stain lighter, larger and are few in number |
| What is the main function of the parathyroid gland | maintain normal calcium homeostasis between 8.5- 10.2 mg/dl |
| What is the normal range of [Ca++] | 8.5 to 10.2 mg/dl |
| How does the parathyroid manage calcium levels | senses changes in ambient levels of extracellular calcium and respond by secreting PTH (parathyroid hormone) |
| What does PTH (parathyroid hormone) do | increases calcium resorption from the bone and kidney |
| What does a rise in serum calcium do to PTH secretion | a rise in serum calcium concentration acts as a negative feedback loop and reduces PTH secretion |
| Where can we get calcium from and how is it eliminated from the body | calcium can be absorbed from the diet or resorbed from the bone. Excess is excreted by kidney |
| HOw much calcium intake does a young adult require, and how much does a child need | young adult needs 12-15 mg/kg/day a child needs double to triple the adult requirements during growth spurts |
| Why do adults over 50 need more dietary calcium | they have a decrease in intestinal calcium absorption |
| How much of the calcium ingested is actually absorbed, where is it abosrbed | only 20-30% of calcium ingested is actually absorbed into ECF, Primarily absorbed in the small intestine |
| What compound helps in absorption of dietary calcium and phosphorus | 25-OH vit. D |
| Does the kidney excrete a lot of calcium | NO. Kidney is very efficient at resorption of excreted calcium only a small amount is excreted unless hypercalcemia is present |
| Where is the majority of the calcium in the body found | 98% stored in the skeleton as hydroxyapatite |
| Of plasma calcium what is the only biologically active form of calcium | ionized calcium is the biologically active form of Calcium |
| What can protein bound calcium aid in | can dissociate from carrier to defend against low serum levels of Calcium (hypocalcemia) |
| What plasma proteins bind calcium | albumin 80% Gobulin 20% |
| What will you see in total calcium vs ionized calcium in low protein states | in low protein states total calcium will be decreased but ionized calcium will not |
| What can cause low protein states effecting total calcium readings | Cirrhosis or nephrosis |
| What is the formula to correct calcium in low protein states | (4 - measured albumin)x(0.8)+(measured calcium) |
| Where do we get Vit D3 | made via photogenesis in the skin and absorbed in dietary intake |
| Is Vit D3 biologically active | NO it must by hydroxylated by liver to form 25-OH Vit D (calcidiol) |
| What does 25-OH Vit D do | aids in absorption of calcium and phosphorus in the small intestines |
| What do the renal tubules do to Vit D3 | hydroxylate 25-OH Vit D to 1,25-OH Vit D (calcitriol) |
| HOw are Vit D metabolites eliminated from the body | Excreted primarily in bile |
| How does PTH keep serum calcium from falling below physiological concentrations | stimulates calcium movement from intestinal and renal tubular lumen and from bone fluid compartment into the blood |
| What does PTH do to phosphate level | keeps phosphate from rising above normal physiological level by increasing tubular excretion of phosphate |
| HOw does PTH act on bone | Directly activates osteoclasts stimulating bone resorption. |
| What effect does PTH have on kidney | directly causes increased resoprtion of calcium increases excretion of phosphorous increase conversion of 25-OH-D3 to 1,25-OH-D3 (calcitriol) |
| Does Direct effect does PTH have on GI | No direct effect on GI tract renal conversion of 25-OH-D3 to 1,25-OH-D3 by PTH indirectly provides the stimulus to increase calcium and phosphorus absorption in the intestines |
| What is secreted by the thyroid in response to hypercalcemia and which cell secrete it | Calcitonin secreted by Parafollicular cells (C-cells) |
| What does Calcitonin do | prevents increase in serum calcium and phosphorus (PTH antagonist) -Decreases renal absorption of calcium -decreases release of calcium and phosphorus from bone -No effect on intestinal absorption of calcium |
| What does Calcitonin do to Intestinal absorption of calcium | no effect on intestinal absorption of calcium |
| What effect does PTH have on Bone Kidney Intestine | Bone- ↑ Ca+ and ↑ Phosphorous Kidney- ↑ Ca+ but ↓Phos ↑1,25 OH D3(calcitriol) intestine- No direct effect |
| What effect does Vit D have on bone kidney intestine | Bone- NO effect Kidney- ↓ Ca+ Intestine- ↑Ca+, ↑Phos |
| What effect does Calcitonin have on bone kidney intestine | Bone-↓Ca+ resorption, ↓Phos resorption Kidney-↓Ca+ resorption, ↓Phos resorption Intestine- No direct effect |
| What effect does Thyroid T4 have on bone kidney intestine | Bone- ↑Ca+ Kidney- Intestine- ↓Ca+, ↓Phos |
| What effect does Glucocorticoid have on bone kidney intestine | bone- ↑Ca+ kidney-↓Ca+ intestine-↓Ca+ |
| What effect does Insulin and Furosemide have on bone kidney intestine | bone kidney- ↓Ca+ Intestine- |
| What effect does Thiazide have on bone kidney intestine | bone- Kidney- ↑Ca+ Intestine- |
| What effect does metabolic acidosis have on bone kidney intestine | Kidney- ↓Ca+. ↓Vit D Intestine- ↓Ca+, ↓Phos |
| What is the most common cause of hypercalcemia in hospitalized patients | Malignancy is the most common cause |
| How does metastases cause hypercalcemia | tumors metastasize to the bone and cause hyper calcemia |
| How do Solid Tumors such as lung-squamous cell, renal adenocarcinoma, breast cancer cause hypercalcemia | These tumors secret PTH related protein (PTHrP) which acts like PTH and causes ↑Ca/↓phos by stimulating osteoclastic resorption of bone. This suppress native PTH by ↑serum calcium |
| HOw does multiple myeloma cause hypercalcemia | abnormal plasma cells secrete osteoclastic activating factors leading to local bone destruction ↑Ca+ |
| How do Granulomatous diseases such as sarcoidosis, TB, histoplasmosis, and Coccidiomycosis cause hypercalcemia | Cuase ectopic secretion of 1,25-OH D3 leading to increase GI absorption of calcium and phosphorus |
| Why do thiazides sometimes cause hypercalcemia as a s/e | Increaes reabsroption of Ca+ at the distal tubule |
| How does lithium cause hypercalcemia | increases set point for PTH secretion you need higher levels of Ca+ to have negative feedback effects on PTH secretion |
| How does chronic Antacid use cause hypercalcemia | the aluminumin the antacid binds phosphate and decreases phosphorus which stimulates osteoclast resorption of bone |
| How does Vit D intoxication lead to hypercalcemia | increases GI absorption of Ca+ |
| how does Vit A intoxication lead to hypercalcemia | Increases osteoclastic activity |
| What is milk-alkali syndrome | occurs after ingestion of large amounts of calcium and alkai where metabolic alkalosis results in decreased renal excretion of Ca+ and later leads to hypercalcemia |
| How does hyperthyroidism cause hypercalcemia | Increased T4 stimulates osteoclastic activity and suppress Vit D |
| This is an autosomal dominant disease w/ Onset of Hypercalcemia in first two decades of life. Renal hypersensitivity to PTH renal absorp. of Ca+. PTH level normal Distinguish from Hyperparathyroidism by low 24-hour urinary Ca+ excretion. | Familial Hypocalciuric Hypercalcemia: Patients are asymptomatic: No PUD or kidney stones |
| abnormality in parathyroid glands that causes inappropriate PTH secretion. | Primary Hyperparathyroidism |
| What is the most common cause of hypercalcemia in outpatients | primary hyperparathyroidism |
| What is the primary cause of primary hyperparathyroid | 84% are due to a single parathyroid benign adenoma |
| Why do you still get PTH secretion from a parathyroid benign adenoma even when calcium levels are high | Tumor functions autonomously free from negative feedback so you will have ↑Ca+, ↑PTH, and ↓Phos |
| What is the minor cause of primary parathyroid | 15% are due to parathyroid gland hyperplasia Chief Cells enlarge and replace normal stromal fat. Usually hereditary and involve more than one gland |
| What does MEN stand for in regard to primary hyperparathyroid | Multiple Endocrine Neoplasia |
| What are the s/sx of MEN type I (werner's syndrome) | hyperparathyroidism (adenoma) peptic ulcer disease pancreatic islet tumors (insulinoma) pituitary adenomas |
| What are the s/sx of MEN type IIa (Sipple's syndrome) | Hyperparathyroidism Medullary Thyroid Cancer Pheochromocytoma |
| What gene is messed up in MEN I | menin Gene |
| What gene is messed up in MEN IIa | Ret proto-oncogene |
| What percent of primary hyperparathyroid is actually caused by malignant parathyroid carcinomas | 1% |
| what are really RARE causes of Primary Hyperparathyroid | Palpable neck mass of metastatic carcinomas of the lung, breast or kidney |
| What are the causes of secondary hyperparathyroid | Renal Failure Fanconi Syndrome Malabsorption |
| How does renal failure cause secondary Hyperparathyroid | Damaged kidney can't make enough Vit D (1,25OH-D3) Won't absorb calcium from GI tract Calcium will decrease PTH will increase Kidney also can't excrete phosphorus so ↑Phos |
| What would you labs likely show in kidney failure when testing for secondary hyperparathyroid | ↓1,25-OH D3, ↓Ca+, ↑Phos, ↑PTH |
| How does fanconi's syndrome cause secondary hyperparathyroid | Damage to proximal renal tubule ↓ Ca+ absorption and phosphorus in renal glomeruli; Leading to increased PTH |
| How does malabsorption lead to hyperparathyroid | causes severe Vit D deficiency, Reducing hepatic 25OH-D3, Impaired absorption of Ca+ and phosphorus in GI. Low Ca+ = High PTH |
| What would the labs look like in malabsorption when looking at hyperparathyroid | ↓25-OH D3, ↓1,25-OH D3, ↓Ca+, ↓Phos, ↑PTH |
| What is tertiary hyperparathyroid | autonomous parathyrod hyperfunction ↑PTH, This develops from long-term secondary hyperparathyroidism |
| When are you likely to see tertiary hyperparathyroid | seen after renal transplant and creates hypercalcemia |
| What are the s/sx of hypercalcemia | bones, stones, abdominal groans and psychic moans. |
| What musculoskeletal s/sx would you expect in hypercalcemia | muscle weakness (general malaise fatigue) Diminished deep tendon relfexes (hypotonia Pseodogout(calcium pyrophospahte crystals) Bone Pain due to osteitis fibrosa cystica |
| What is the classical skeltal finding in hyperparathyroidism | osteitis fibrosa cystica salt and peper looking loss of bone in distal phalanges and skull leads to bone cysts or brown tumors |
| What are brown tumors | brown tumors are more severe form of osteitis fibrosa cystica. Habe brown fibrotic tissue collections in cystic spaces of bone due to ↑PTH excessive bone absorption and pathologic bone fractures |
| Why do you get pruritis in hypercalcemia | calcification of skin |
| What is band keratopathy | calcification of the limbus of the eye |
| What GI s/sx will you have in hypercalcemia | Constipation Nausea and Vomiting Abdominal Pain (groans) -pancreatitis -peptic ulcer disease (PUD) anorexia |
| why do you get pancreatitis in hypercalcemia | from calcification of the pancreas |
| Why od you see Peptic Ulcer Disease PUD in hypercalcemia | high calcium stimulates gastrin release |
| What renal s/sx will you see in hypercalcemia | volume depletion due to polyuria(kidney is trying to get rid of excess Ca+ nephrocalcinosis Kidney Stones- calcium oxalate |
| What is Nephrocalcinosis | Calcification of renal tubules in hypercalcemia |
| What cardiovascular problems will you see with hypercalcemia | hypotension cardiac arrythmias -bradycardia -short Q-T interval -Heart Block |
| What neurologic s/sx will you see in hypercalcemia | psychosis personality changes confusion lethargy apathy obtundation coma |
| In hyperparathyroid what will you see in serum Ca+ Serum Phos PTH Other findings | Serum Ca+- ↑ Serum Phos- ↓ PTH- ↑ Other findins- Bone loss |
| In Primary Carcinoma what will you see in serum Ca+ Serum Phos PTH Other findings | Serum Ca+- ↑ Serum Phos- ↓ PTH- nl Other findins- PTHrp, lesion on C-xray bone lesions |
| In metastatic Carcinoma what will you see in serum Ca+ Serum Phos PTH Other findings | Serum Ca+- ↑ Serum Phos- nl PTH- ↓ Other findins- PTHrp, lesion on C-xray bone lesions |
| In Multiple Myeloma what will you see in serum Ca+ Serum Phos PTH Other findings | Serum Ca+- ↑ Serum Phos- nl PTH- ↓ Other findins- urine bence jones protein |
| In Sarcoidosis what will you see in serum Ca+ Serum Phos PTH | Serum Ca+- ↑ Serum Phos- ↑ PTH- ↓ Other findins- ↑1,25-OH D3 |
| In Vit D intoxication what will you see in serum Ca+ Serum Phos PTH | Serum Ca+- ↑ Serum Phos- ↑ PTH- ↓ Other findins- ↑1,25-OH D3 |
| In Milk Alakali Syndrome what will you see in serum Ca+ Serum Phos PTH | Serum Ca+- ↑ Serum Phos- nl PTH- ↓ Other findins- Hx PUD |
| In thryotoxicosis what will you see in serum Ca+ Serum Phos PTH | Serum Ca+- ↑ Serum Phos- nl PTH- ↓ Other findins- ↓TSH, ↑T4/T3 |
| What would you be looking for in FX for hypercalcemic patient | familial hypocalciuric hypercalcemia MEN syndromes |
| What would you be looking for in reviewing meds of hypercalcemic patient | thiazide diuretics Vit A or D lithium |
| What would you be looking for as a red flag for hypercalcemic patient in their past medical history | thryoid/adrenal disease history of kidney stones history or symptoms of cancer hypophophatemia in vegetarians and alcoholics |
| How do you calculate true calcium level | .8 x (4-measured albumin) + serum calcium |
| What labs values do you want to work up in hypercalcemia | Serum Ca+ Phosphorus level PTH TSH/free T4 Cortisol chest x-ray EKG 24 hour urine collection |
| What do you need to do if your patients calcium is 14mg/dl or greater | the need to be hospitalized, if in hypercalcemia crisis- dehydrated, encephalopathy, cardiac arrhythmias give them FLUID FLUID FLUID FLUID FLUID |
| what is the first step in tx of hypercalcemia | correct volume depletion FLUID FLUID FLUID normal saline 2-6 liters a day for 48 hours this volume expansion will enhance renal excretion of Ca+ |
| If you took the fluid therapy too far in hypercalcemic patient what can you order | Loop diuretics(furosemide;lasix) not thiazides to promote fluid excretion w/o calcium retention |
| What drugs would you probably stop in patient with hypercalcemia | stop thiazides, lithium or other Ca+ concentrating drugs |
| What will you need to order for patients suffering from hypercalcemia and renal failure | Dialysis will be required to remove calcium |
| If the cause of the hypercalcemia is hyperparathyroidism what will your patient need | patient will need surgery to correct the problem |
| you are preping a patient for parathyroidectomy what will you order to find the abnormal parathyroid gland that needs to be removed | you will order a sestamibi scan. it is absorbed by all thyroid and parathyroid tissue but gets stays in abnormal parathyroid tissue. |
| You have just finished a parathyroidectomy now what do you want to monitor your patient for | monitor for hypocalcemia |
| what do you first have to do in your hypercalcemic patient with hyperparathyroid before you can cut out the offending abnormal parathyroid gland | get patients calcium level decreased to a safe level as parathyroidectomy is not emergent (immediately needed) |
| If malignancy if found what should you do | refer to oncologist |
| What should you use in hypercalcemia with granulomatous disease | corticosteroids- hydrocrotisone which may increase digitalis toxicity, osteoporosis, elevated blood sugar |
| How does bisphosphonates aid in treating hypercalcemia | it binds hydroxyapatite crystals in bone matrix and prevent osteoclasts attaching to the bone to cause resorptiong of calcium and phosphorus |
| what is pamidronate | bisphophonate that prevents bone resorption least toxic s/e= transient increase in body temp mild GI distress mild hypophophatemia hypokalemia and hypomagnesemia |
| What hormone therapy may aid in tx hypercalcemia | calcitonin- inhibits bone resorption and increases excretion of calcium. Can provide analgesia for bone pain |
| What is plicamycin | osteoclast RNA synthesis inhibitor. Quick onset and lasts for several days but may cause thrombocytopenia, bleeding, is hepatotoxic and nephrotoxic |
| What are the s/e of using a bone resorption inhibitor like gallium nitrate | is nephrotoxic so caution in renal failure |
| What may be causes of hypocalcemia | hypoparathyroid-most common Extensive radiation- hungry bone syndrome after parathyroidectomy autoimmune hypoparathyroid Congenital Hypomagnesemia pseudohypoparathyroidism |
| What is the most common cause of hypoparathyroid leading to hypocalcemia | post surgical excision of all parathyroid glands during surgery in neck for thyroid, laryngeal or neck malignancies |
| Why would extensive radiation in the neck or face lead to hypocalcemia | it may cause destruction of all 4 parathyroid glands leading to hypoparathyroid and decreased PTH |
| What is hungry bone syndrome and why does it cause hypocalcemia | after parathyroidectomy- removal of the overactive parathyroid gland drops PTH levels alot. bones have been starved for ca+ by high PTH now start to hold onto ca+ to remineralize free Ca++ drops and you get hypocalcemia until PTH secretion resumes |
| How does autoimmune hypoparathyroidism cause hypocalcemia | polyglandular syndrome: HAM syndrome (hypoparathyroid-addison's-mucocutaneous candidiasis) is autoimmune destruction of parathyroid gland. Leads to hypocalcemia by age 7-10 |
| Which congenital defects are also associated with hypocalcemia | digeorge syndrome- congenital abscence of the glands Fetal alcohol syndrome teratogentic defects mutations of chromosome 3q |
| Why does hypomagnesemia cause hypocalcemia | low levels (<1.2mg/dl) of mangesium interfer with PTH activity may be caused by alcoholism, diarrhea, pancreatitis |
| What is pseudohypoparathryoidism | mutation in PTH receptor/resistance to PTH causes hypocalcemia |
| What are the clinical signs that a patient suffers from pseudohypoparathyroidism | short stature round faces mild mental retardation knuckle, knuckle, dimple dimple when they make a fist (short 4th and 5th metacarpal bones) nodules, sub q tissue calcifications obesity |
| what will you lab results be in a pseudohypoparathyroid patient | low Ca+, HIgh phos, High PTH |
| If patient is pseudohypoparathyroid what would you expect to see on a CT scan of the head and X-ray of the hand | CT scan of head: shows basal ganglion calcification X-ray of hand: loss of bone in distal phalanges/short metacarpals |
| if you suspect your patient may suffer from pseudohypoparathyroid what test can you run to help confirm you dx | have patient fast overnight measure labs at 8am then give the PTH at 9am 2 days in a row the see if there is a 10-20 fold increase in UcAMP if not they have pseudohypoparathyroid |
| What is the tx for pseudoparahypothryoid | since PTH is ineffective you need to give Ca+ and Vit D to correct hypocalcemia. |
| What do all the following have in common in regards to Ca+ Sepsis or Toxic shock syndrome Infiltrative disease: Hemochromatosis or Wilson’s disease Fat emboli Pancreatitis | they can all cause hypocalcemia |
| what effect can hypoalbuminemia have on Ca+ levels | it is a low protein state that can effect free levels of Ca+ don't forget you have to account for albumin levels when getting corrected Ca+ levels (measured Ca+) + ( 4.0-albumin) x 0.8 = corrected Ca+ |
| Why do loop diuretics (lasix) cause hypocalcemia | they increase renal excretion of calcium |
| HOw does alcohol cause hypocalcemia | suppresses PTH |
| HOw do aminoglycosides, cisplatin, and amphotericin B cuase hypocalcemia | cause low Mg+ decreases PTH efficacy |
| How do phenytoin and phenobarbital cause hypocalcemia | both break down Vit D which results in decreased Ca+ absorption in the gut |
| how does cimetidine cause hypocalcemia | lowers gastric PH as an H2 blockers this slows fat breakdown, fat is necessary to complex Ca+ for gut absorption |
| What do the following have in common in regards to Ca+ Fluoride High phosphate states high citrate states high bicarb states high lactate states | all cause chelation of Ca+ lowering free Ca+ levels causing HYPOCALCEMIA |
| What Malignancies are possible causes of hypocalcemia: | Osteoblastic Metastasis: Breast and Prostate cancers. Excess Calcitonin: Medullary Thyroid cancer |
| If you have a Vit D deficiency what will happen to Ca+ | you will have hypocalcemia |
| What are causes of Vit D deficiency | limited sun exposure rickets- can't convert 25OHD3 to 1,25OHD3 Osteomalacia |
| What is rickets | failure of normal bone mineralization at growth plate in children due to a lack of Vit D response |
| what are the s/sx of rickets | Infants are restless, sitting/crawling delayed, delayed fontanels closer Older infants: delayed walking due to pain, Bowed legs, knock-knees |
| What are the two types of rickets and their causes | rickets type I: defect in 1,25OHD3 hydroxylase in the kidney (can't change 25OHD3 to 1,25OHD3) Rickets type II: receptor deficiency to 1,25OHD3 |
| What will your labs look like in rickets | Low Ca+ Low Phos High PTH Low 25OHD3 |
| What is tx for Rickets type I and what is the tx for rickets type II | type I: calcitriol Type II: ergocalciferol |
| What is osteomalacia | failure of bone matrix to mineralize normally |
| What are the s/sx of osteomalacia | waddling gait- due to proximal muscle weakness and pain Deformities caused by fractures in ribs, vertebrae, and long bones Brisk deep tendon reflexes (from hypocalcemia) Muscle hypotonia (hypocalcemia) rarely tetany (hypocalcemia) |
| What are possible causes of osteomalacia | Malabsorption Impaired renal synthesis of 1,25 OH-D3 Phosphate Deficiency Drug induced Toxin induced |
| What will you find on labs in ostemalacia | decreased urinary calcium lose serum calcium low 25OHD3 incrased alkaline phophatase(from osteoblast) low phosphorous elevated PTH (response to low Ca+) |
| What will you find on x-ray in patient with osteomalacia | decreased bone density pseudofractures |
| What is the most common cause of ostemalacia | malabsorption |
| what is malabsorption | reduced absorption of Ca+ and Vit D results in fecal loss of Vit D and Ca+ |
| What are some common causes of Malabsorption | Crohn's disease Celiac's disease Chronich Steatorrhea Surgical Resection Biliary fistula |
| How do Crohn's and Celiac disease cause malabsorption | cause a reduced surface area to absorb calcium and phosphorus in GI |
| What may cause chronic steatorrhea causing malabsorption | pancreatitis |
| Why would surgical resection cause malabsrotption | if you cut out small intestine you are cutting out the area where absorption of vit D and calcium occurs so you get malabsorption |
| What is the tx for malabsorption | give large dose of ergocalciferol but you may still need to give an IM or IV dose because absorption is so reduced |
| What may lead to impaired renal synthesis of 1,25OHD3 | chronic renal disease-impairs production hypoparathyroidism-no stimuli to hydroxylate congenital absence of hydroxylating enzymes- Rickets type 1 malignant tumors secreting substances that suppress synthesis of 1,25OHD3 |
| what are some causes of phosphate deficiency | low dietary intake of phosphate excessive ingestion of aluminum hydroxide heritable x-linked hypophosphatemia Fanconi's syndrome Tumors |
| What drugs induce osteomalacia | excessibe bisphophonate use fluoride anticonvulsive meds |
| What toxins cause osteomalacia | aluminum lead cadmium |
| What do you see in the following lab results with hypoparathyroidism Ca+ PO4 PTH 25OHD3 | Ca+-↓ PO4-↑ PTH-↓ 25OHD3-nl |
| What do you see in the following lab results with hypoposphatemia Ca+ PO4 PTH 25OHD3 | Ca+-nl PO4-↓ PTH-nl 25OHD3-nl |
| What do you see in the following lab results with Vit D deficiency Ca+ PO4 PTH 25OHD3 | Ca+-↓ PO4-↓ PTH-↑ 25OHD3-↓ |
| What do you see in the following lab results with Malabsorption Ca+ PO4 PTH 25OHD3 | Ca+-↓ PO4-↓ PTH-↑ 25OHD3-↓ |
| What do you see in the following lab results with chronic renal failure Ca+ PO4 PTH 25OHD3 | Ca+-↓ PO4-↑ PTH-↑ 25OHD3-↓1,25OH-D3 |
| what is trousseau's sign | s/sx of hypocalcemia- infalte a b/p cuff above systolic pressure for a few minutes and then you get flexion of the writs and metacarpophalangeal joints; hyperextension of the fingers, flexed thumb on palm. |
| What is chvostek's I sign | tapping facial nerve causes twitching of the ipsilateral facial muscles |
| What is chvostek's II sign | tapping at zygomtaic prominence causes twitching in facial muscles circumoral muscles and orbicularis oculi on ipsilateral side |
| what are the Cardio Vascular s/sx of hypocalcemia | hypotension congestive heart failure |
| What changes will you see on an EKG with hypocalcemia | prolonged Q-T interval Prolonged S-T interval normal T waves |
| would the following indicate hyper or hypo calcemia Hyperirritability Anxiety Mood Swings Hoarseness (due to laryngospasm) Seizures Muscle cramps: involving lower back, legs and feet Parethesias: involving fingertips, toes, perioral) | hypocalcemia |
| What is the tx for hypocalcemia | IV infusion of Ca+ to restore normal levels chronic management w/ calcium carbonate Vit D supplement |
| If you have a symptomatic patient with clinical signs of hypocalcemia what do you need to do | immediate resuscitation check vitals for signs of sepsis/trousseau's Check surgical history for parathyroidectomy, pancreatectomy |
| Review last few slides | review last few slides |
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