Posterior Pituitary - Patho

what controls the adrenal medulla?

direct innervation by the hypothalamus, produces fight or flight response - epinephrine, norepinephrine

pheochromocytoma

tumor of adrenal medulla (excess) by proliferation of chromaffin cells

etiology of adrenal medulla excess

hypothalamus innervation = persistent SNS activation, chromaffin cell tumors

sx of adrenal medulla excess

persistent SNS response = high HR/BP, anxiety, tremors, bounding palpitations, sweating

dx for adrenal medulla excess

scans, biopsy - benign or malignant tumors, 24 hour urine collection for catecholamines

tx for adrenal medulla excess

adrenergic blockers/beta blockers, surgery

ADH pathway

hypothalamus has osmoreceptors (osmolarity) and baroreceptors (blood volume). blood too concentrated or blood volume too low → hypothalamus stimulates posterior pituitary to release ADH → renal tubules to increase water conservation and decrease urine output. blood too dilute or blood volume too high → hypothalamus decreases stimulation of posterior pituitary to release less ADH → tells renal tubules to decrease water conservation and increase urine output

diabetes insipidus

low ADH → not enough water conservation → copious amounts of water excretion. urine is pale and water like.

etiology of diabetes insipidus

neurogenic = problem with gland, posterior pituitary fails to release ADH (brain lesion, infection, trauma, immune response), tx: ADH replacement therapy, correct underlying cause. nephrogenic = problem with kidney not responding to ADH due to renal tubule damage, ts: address renal dysfunction

sx of diabetes insipidus

polyuria up to 16L in a day, polydipsia, low specific gravity, thirsty, dehydrated

tx for diabetes insipidus

DDAVP, vasopressins (ADP)

SIADH

too much ADH → too much water conservation → blood gets dilute → hyponatremia (water intoxication)

etiology of SIADH

head trauma, increased intracranial pressure, meningitis, ectopic tumors, drugs

sx of SIADH

fluid volume excess, hyponatremia, decreased urine output, weight gain from water retention, high specific gravity, confusion, seizures

tx for SIADH

fluid restriction, address root cause

what does calcium regulation involve?

bones, C cells of thyroid gland, parathyroid gland, kidneys, GI system

abnormal calcium levels affect…

bones, muscle contractility, cardiac activity, blood coagulation

PTH

parathyroid hormone, gets released when blood calcium levels are low. Puts calcium in The Heme. stimulates calcium reabsorption in kidneys, stimulates kidneys to produce vitamin D, increases osteoclast activity to break down bones, increases absorption of calcium in the GI tract.

hyperparathyroidism

causes hypercalcemia.

hypercalcemia

most common cause is cancer, in glands, bones, or tumors that secrete PTH. sx: bones (bone pain), stones (kidney stones), groans (constipation), neurological (headache, confusion, coma)

hypoparathyroidism

causes hypocalcemia

hypocalcemia

caused by calcium or vitamin D deficiency, hypoparathyroidism, parathyroid gland dysfunction, GI absorption disorder. sx: CATS = Convulsions/Cramps, Arrhythmias, Tetany, Spasms/parethesia. think increased muscle excitability.

vitamin D

cholecalciferol. necessary to absorb calcium, get it by exposing skin to sunlight or absorption via GI tract (dairy, fortified foods). both forms must be converted by the kidneys into a form the body can use

osteomalacia/rickets

caused by vitamin D deficiency or hypocalcemia, causes inadequate bone mineralization. children = rickets, bowed legs, pigeon chest, from lack of vitamin D or calcium or malabsorption disorder. adults = due to not enough exposure to sunlight or kidney failure

chronic renal failures, calcium, and phosphate

chronic renal failure → can’t excrete phosphate → phosphate accumulation → phosphate binds to calcium in the blood → serum calcium levels lower → stimulates release of PTH → moves calcium from bones too blood = weakens bony matrix. Also, kidneys can’t convert vitamin D to its usable form to absorb calcium

osteoporosis

most common metabolic bone disease in the US, bone loss outpaces bone deposition = decrease in bone density = weakening of bony matrix = increase risk for fractures

osteopenia is…

a precursor of osteoporosis

osteoporosis risk factors

POSTMENOPAUSAL WOMEN, lifestyle: heavy drinking, smoking, sedentary lifestyle, medications, glucocorticosteroids

advanced osteoporosis can cause…

compression fractures of vertebrae = kyphosis

pathologic fracture

bone breaks with normal activity, due to loss of bone integrity

compression fracture

vertebral compression fractures cause back pain and loss of height

dx of osteoporosis

bone density scans, also monitors condition through treatment

paget’s disease

genetic disorder with environmental triggers, not related to calcium or vitamin D, not entirely sure of the etiology. Is excessive bone turnover causing soft, brittle bones. Overactive osteoclast activity and disorganized osteoblast activity → bones get enlarged in some places, brittle in others.

sx of paget’s disease

pain, deformities, compression fractures, kyphosis, large forehead and scapula. tx: biphosphonate

risk factors for pathologic fractures/fractures

decreased activity, visual impairment, dementia, impaired cognition, medications like steroids

sx of fractures

pain, swelling, loss of mobility in affected area, deformity. stress fractures = in athletes that haven’t conditioned properly. spiral fractures may be an indicator of abuse

osteo myelitis

infection of the bone/bone marrow, very hard to treat

osteonecrosis

interrupted blood flow to the bone causing bone death