15.8 - 15.10: Parathyroid gland, Endocrine pancreas, adrenal cortex / medulla Flashcards
What is the key cell within the parathyroid gland? What does this do?
- Chief cell
- Regulates free ionized calcium in the serum via PTH secretion
What percent of the Ca in the body is bound to proteins?
60%
What is the effect of PTH on the bones? How?
Increases osteoclast activity, by first activating osteoBLASTS, which then activate osteoclasts
What is the effect of PTH on the small bowel? How?
Increases small bowel reabsorption of Ca and Phosphate through vitamin D
What is the effect of PTH on the kidneys?
Increases renal calcium reabsorption, and decreases phosphate reabsorption
What are the cells that secrete bone? Resorb bone?
Secrete = Osteoblasts Resorb = Osteoclasts
How are osteoclasts activated?
Osteoblasts receive PTH signal, which then activate osteoclasts
Why is it important that PTH increases the excretion of phosphate?
Phosphate binds free Ca, so getting rid of it increases free Ca levels within the serum
What is primary hyperparathyroidism?
Excess PTH d/t a disorder of the parathyroid gland itself
What is the most common cause of primary hyperparathyroidism?
Parathyroid adenoma
True or false: a parathyroid adenoma is benign
True
Do parathyroid adenomas usually involve more than one gland?
No
What is the most common presentation of a parathyroid adenoma?
Asymptomatic hypercalcemia
What are the kidney problems that can arise from a parathyroid adenoma? (2)
- Nephrolithiasis (Ca oxalate stones)
- Nephrocalcinosis
What are the GI problems that can arise from a Parathyroid adenoma? (3)
- Constipation
- PUD
- acute pancreatitis
What is nephrocalcinosis?
Deposition of Ca into the tubules of the kidney, resulting in polyuria
What are some of the CNS disturbances that can be caused by hypercalcemia from a parathyroid adenoma?
Seizures
Depression
How can hypercalcemia cause acute pancreatitis?
Ca activates the enzymes in the pancreas
What is osteitis fibrosa cystica?
Resorption of Ca from the bone causes cyst formation in the bones
What happens to the following lab values with hyperparathyroidism:
- PTH
- Serum Ca
- Serums phosphate
- Urinary cAMP
- Serum alk phos
- PTH (increased)
- Serum Ca (increased)
- Serums phosphate (decrease)
- Urinary cAMP (increase)
- Serum alk phos (increase)
How does hyperparathyroidism cause increased urinary cAMP?
Gs coupled protein activation by PTH
What is the role of alk phos in bone normally? Why is it increased in hyperparathyroidism?
- Normally aids in the deposition of Ca onto bone by generating an alkaline environment
- Since PTH first activates osteoblasts, these cells secrete alk phos
What is the treatment for a hyperparathyroidism secondary to a parathyroid adenoma?
Surgical removal of the affected gland
What is secondary hyperparathyroidism?
Excess production of PTH d/t disease process extrinsic to the parathyroid gland
What is the most common cause of secondary hyperparathyroidism?
Chronic renal failure
How does chronic renal failure lead to hyperparathyroidism?
Decreased phosphate excretion leads to increased serum levels of phosphate, which binds Ca. Lower Ca levels then stimulate the parathyroid gland
What is the effect of a lack of phosphate excretion in chronic renal disease in terms of PTH secretion?
Higher phosphate leads to lower Ca, leading to increased PTH levels
What happens to the following lab values with secondary hyperparathyroidism:
- PTH
- serum ca
- serum phosphate
- alk phos
- Increased PTH
- Decreased serum Ca
- Increased serum phosphate
- Increased alk phos
What are the three major causes of hypoparathyroidism?
- Autoimmune damage
- Surgical excision
- DiGeorge syndrome
Which pharyngeal pouches fail to develop in DiGeorge syndrome? What is the genetic cause of this?
3rd and 4th
chr 22q del
What are the s/sx of hypoparathyroidism?
- Numbness and tingling
- Muscle spasms (tetany)
What happens to serum PTH and Ca levels with pseudohypoparathyroidism?
Both decreased
Where specifically does the numbness/tingling start with hypoparathyroidism?
Lips
What is the trousseau sign?
a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient’s hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm.
What is Chvostek sign?
a clinical sign of existing nerve hyperexcitability (tetany) seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped at the angle of the jaw (i.e. masseter muscle), the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia
What is pseudohypoparathyroidism?
When end-organs do not respond to PTH d/t a mutation in the Gs protein
What are the PTH and Ca levels with pseudohypoparathyroidism?
Hypocalcemia and increased PTH levels
What is the inheritance of pseudohypoparathyroidism? What are the physical deformities that can present with this?
AD
Short stature + short 4th and 5th digits
What are the cells that comprise the endocrine pancreas called?
Islets of Langerhans
What does a single islet of Langerhans contain?
multiple cells types, each producing one hormone type
What cells of the pancreas secrete insulin? Where are these cells in the islets?
- beta cells
- Center of islets
What cells of the pancreas secrete glucagon?
Alpha cells
Where in the islets of langerhans do the beta cells lie?
Center
What is the MOA of insulin?
Increases the movement of GLUT 4 receptors to the surface of cells
What type of hypersensitivity rxn occurs in type I DM?
Type IV
What are the HLA haplotypes associated with DM I?
DR3 and DR4
What is the classic histological finding of DM I?
Inflammation of the islets
What are the autoantibodies that can be seen with DM I?
against insulin
What causes the muscle wasting with untreated DM I?
Increased gluconeogenesis from amino acids
What are the risk factors for DKA?
Stress
Infection
How does stress cause DKA?
Epinephrine increases glucagon, exacerbating lipolysis
What are the three ketone bodies that are found in DKA?
- beta-hydroxybutyrate
- acetone
- acetoacetic acid
What, besides hyperkalemia, are the lab findings with DKA?
- Anion gap metabolic acidosis
- Hyperkalemia
What are the s/sx of DKA? What type of respirations?
- Kussmaul respiration
- Dehydration
- N/v
- mental status changes
Why the anion gap metabolic acidosis with DKA?
Increased ketonic acids
Why is there hyperkalemia with DKA? (2)
- Insulin causes K to go into cells, but there is none
- K is exchanged for H+ in the serum
True or false: despite having high potassium levels in the serum, DKA pts actually have lower K levels overall
True
What are the three measures to take to treat DKA?
- IVF
- Insulin
- Replace lytes
How can treating DKA lead to hypokalemia?
- Insulin will force K into cells
- Reversal of the acidosis
What is the classic DM II pt?
Obese middle aged adult
True or false: there is a strong genetic predisposition for DM II
True
How does DM II arise?
Decreased numbers of insulin receptors
Which has a stronger genetic inheritance, type 1 or 2 DM?
2
What are the histological findings of DM II?
Islets of Langerhans are filled with amyloid
What are the ssx of DM II, if any?
- Polyuria
- Polydipsia
- Hyperglycemia
What are the clinical values for random and fasting glucose levels to diagnose DM II?
- Random more than 200 mg/dL
- Fasting more than 126 mg/dL
What is the glucose tolerance test?
More than 200 mg/dL two hours after glucose load
What is the first line therapy for DM II?
Weight loss