G & E EXAM 2

acidemia

elevates ionized calcium

albumin

what is calcium bound to?

ionized (free)

which form of calcium is biologically active?

excreted in urine

what happens to the majority of calcium that is ingested

bone

where is calcium stored

calcitriol/1,25 dihydroxy vitamin D

what controls active CALCIUM absorption in the gut

duodenum

where is the majority of calcium absorbed in the small intestine

proximal convoluted tubule

major site of calcium reabsorption in the kidney

passive

method of calcium reabsorption in the PROXIMAL convoluted tubule

active

method of calcium reabsorption in the DISTAL convoluted tubule

distal convoluted tubule

where does PARATHYROID hormone act in kidney?

behind thyroid

location of parathyroid glands

increases osteoclast activity

function of PTH on bone

increases calcium reabsorption

function of PTH on kidney

increases vit D which increases calcium absorption

function of PTH on intestines

chief cells (of the parathyroid)

cells that secrete parathyroid hormone

parathyroid hormone

increases osteoclast and calcium, causes bone RESORPTION

 low calcium, high PO4, low OH vit D

factors that STIMULATE parathyroid hormone secretion

high calcium, low PO4, high OH vit D

factors that INHIBIT parathyroid hormone secretion

parathyroid, vitamin D (1,25 OH), FGF23

hormones that regulate calcium homeostasis

bones (osteoporosis), groans (bone/abdominal pain), stones (renal stones), anxiety, depression, cognitive dysfunction

symptoms of HYPERcalcemia

PTH-mediated hypercalcemia (primary hyperparathyroidism)

HYPERcalcemia with HIGH PTH

parathyroid adenoma

most common cause of hypercalcemia with HIGH PTH

parathyroid adenoma

benign functioning tumor of one parathyroid gland

increased Ca absorption, increased bone turnover (Ca release), and increased calcium reabsorption

how does high PTH lead to hypercalcemia

non-PTH mediated

hypercalcemia with low PTH

familial hypocalciuric hypercalcemia

inherited mutation of calcium sensing receptor (CaSR), leading to HYPERcalcemia

non-PTH mediated

HYPERcalcemia from other organs that control calcium (bone, kidney or gut)

malignancy, thyrotoxicosis, immobility

causes of bone resorption that lead to hypercalcemia

high Ca intake, CKD, high vitamin D intake

causes of increased gut absorption that lead to hypercalcemia

milk alkali syndrome

a condition arising from excessive intake of calcium and absorbable alkali, leading to HYPERCALCEMIA (non-PTH mediated)

increased 1-alpha-hydroxylase

activates vitamin D and increases calcium absorption

surgery (when indicated) or cinacalcet (surgery not indicated)

treatment of PTH mediated hypercalcemia

treat underlying cause

treatment of non-PTH mediated hypercalcemia

cinacalcet

agent used to treat HYPERcalcemia by increasing sensitivity of the calcium-sensing receptor (CaSR) in the parathyroid gland.

trousseau sign

a medical sign indicating HYPOcalcemia, characterized by hand spasm when blood flow is restricted to the arm (ex: BP cuff)

paresthesia, muscle spasm, cramps, trousseau and chvostek signs

symptoms of HYPOcalcemia

primary hypoparathyroidsim

Hypocalcemia with low PTH

calcitriol and calcium

treatment of Hypocalcemia with low PTH (primary hypoparathyroidism)

secondary hyperparathyroidism

Hypocalcemia with high PTH

decreased bone remodeling, renal Ca loss, vitamin D deficiency, malabsorption

causes of secondary HYPERparathyroidism

hormones, mechanical stress, medications

what affects bone remodeling

osteoblast

secrete OPG and inhibits RANKL when osteoclasts high

Osteoporosis

weakened bone structure with normal mineralization, making them more susceptible to fractures.

osteomalacia

normal bone structure with decreased mineralization leading to softer bones and greater risk of fractures.

older women (65+)

patient population with the highest risk of osteoporosis

parathyroid hyperplasia

generalized enlargement and overactivity of all four parathyroid glands due to cell overgrowth leading to HYPERparathyroidism

tertiary hyperparathyroidism

 develops after long-standing secondary hyperparathyroidism, most often with chronic kidney disease

raloxifene

estrogen like effect on bone, DECREASES resorption

denosumab

blocks RANKL, decreasing osteoclasts

hypothalamus

area of brain that releases Thyrotropin-releasing hormone (TRH)

Thyrotropin-releasing hormone (TRH)

stimulates TSH release from pituitary

anterior pituitary

releases thyroid stimulating hormone (TSH)

thyroid stimulating hormone (TSH)

stimulates thyroid to release T3 and T4

T3 (triiodothyronine)

active thyroid hormone

TPO (thyroid peroxidase)

essential enzyme for thyroid hormone synthesis that catalyzes the iodination of thyroglobulin

iodine uptake, thyroglobulin production, iodination (TPO), coupling (TPO)

steps of thyroid hormone biosynthesis

thyroid binding globulin (TBG)

how is thyroid hormone transported in blood

intracellular (nucleus) (not a steroid though)

where is the thyroid hormone receptor

increases metabolic rate, fuel production, breathing rate, HR and contractility

function of THYROID hormone

Primary hypothyroidism

↓ T3/T4, ↑ TSH due to THYROID problem

secondary hypothyroidism

↓ T3/T4, ↓ TSH due to PITUITARY problem

fatigue, cold intolerance, weight gain, dry skin, bradycardia

clinical presentation of HYPOthyroidism

hashimotos (autoimmune thyroiditis)

most common cause of primary HYPOthyroidism (↓ T3/T4, ↑ TSH)

iodine deficiency

leading cause of goiter and HYPOthyroidism due to inadequate thyroid hormone production

T4 (levothyroxine)

treatment of hypothyroidism

difficult weight gain (children), overactive metabolism, increased adrenergic drive

clinical presentation of HYPERthyroidism

Primary hyperthyroidism

↑ T3/T4, ↓ TSH, due to THYROID problem

Secondary hyperthyroidism

↑ T3/T4, ↑ TSH, due to PITUITARY problem

graves disease

Most common cause of PRIMARY hyperthyroidism (↑ T3/T4, ↓ TSH), T3/T4 inhibits TSH secretion

autonomous nodules

thyroid nodules that produce T3/T4 independent of TSH (↑ T3/T4, ↓ TSH)

subacute thyroiditis

A painful inflammation of the thyroid gland often following a viral infection, characterized by transient primary hyperthyroidism (↑ T3/T4, ↓ TSH)

TSH secreting pituitary tumor

non-cancerous tumor in the pituitary gland, makes too much TSH → causes secondary hyperthyroidism (↑ T3/T4, ↑ TSH)

high thyroid hormone production

what is indicated by increased uptake on radioiodine scan

graves,toxic multinodular goiter, toxic adenoma

presents with increased radioiodine uptake

thyroiditis, iodine excess, exogenous thyroid hormone

presents with low radioiodine uptake

beta blocker, thioamides, radioiodine ablation, surgery

treatment of HYPERthyroidism

methimazole

an anti-thyroid medication used to treat hyperthyroidism by inhibiting thyroid hormone synthesis.

decreased TSH, T3, and T4 despite healthy thyroid

what happens to thyroid function during severe illness

multinodular goiter

indication of iodine degiciency

proptosis, dermopathy, diffuse thyroid nodularity, thyroid bruit

indication of graves disease

estrogen

increases TBG which INCREASES T3/T4 during pregnancy

hCG

mimics TSH and can cause decreased TSH in first trimester of pregnancy

hypothalamic nuclei

neuron cell bodies in the hypothalamus that REGULATE PITUITARY hormone secretion

median eminence

Region of the hypothalamus that links the nervous system to the endocrine system by releasing hormones into the blood

infundibulum

structure connecting the hypothalamus to pituitary gland, allowing for the transport of hormones between these regions

anterior lobe/ adenohypophysis/ pars distalis

PRODUCES and releases its own hormones, Controlled by releasing/inhibiting hormones from the hypothalamus

posterior lobe/neurohypophysis/pars nervosa

STORES and releases hormones made in the hypothalamus

sella turcica

bony structure that houses the pituitary gland, located at the base of the skull.

optic chiasm

X-shaped structure where optic nerves cross, located at the base of the brain

oxytocin and ADH (vasopressin)

hormones STORED (made by hypothalamus) and secreted by POSTERIOR lobe of pituitary

FSH (follicle stim),LH (luteinizing), TSH (thyroid stim), ACTH (adrenocorticotropic), GH (growth), PRL (prolactin)

hormones PRODUCED and secreted by ANTERIOR lobe of pituitary

GnRH, TRH, CRH, GHRH, dopamine

hormones released from HYPOTHALAMUS that regulate anterior pituitary hormones

GnRH (gonadotropin-releasing hormone)

stimulates FSH/LH release from anterior pituitary

CRH (corticotropin-releasing hormone)

stimulates ACTH release from anterior pituitary

GHRH (growth hormone-releasing hormone)

stimulates growth hormone release from anterior pituitary

dopamine

INHIBITS prolactin release from anterior pituitary

end organ hormones suppress hypothalamic and pituitary hormone secretion

negative feedback of hypothalamic-anterior pituitary hormones

non-functional

pituitary tumor that has no hormone secretion

non functional

most common type of pituitary tumor