Anti inflammatory: inhibits activity of phosphlipase A2, thus reducing LT, PG production

• decreased capillary permeability of WBC
• decrease immune system function

Metabollic effects

• raise blood glucose for immediate use
• glucogenesis from amino acids
• increased appetitie

• increase blood sugar
• suppress the immune system
• aid in fat, protein and carbohydrate metabolism

• hypothalamus is stimulated (stress, pain, sleep, trauma)
• hypothalamus releases corticotropin-releasing hormone (CRH)
• CRH acts on the anterior pituitary
• ACTH is released and acts on adrenal cortex
• adrenal cortex releases cortisol
• cortisol acts on target organ(s)

• it is critical to balance stress in the body
• without cortisol the body will not balance to homeostatsis during stressors
• cortisol helps protect from damaging effects of stress by suppressing inflammation/immunity

• regulate Ca+
• parathyroid hormone (PTH) acts on bone and renal tubules to cause increase calcium levels

• increase osteoclast activity
• increase release of calcium from bone matrix to ECF
• increase renal calcium reabsorption
• activates vitamin D

• acts as a potent vasoconstrictor in its own right
• acts as anti0diuretic hormone (anti-pee)

• decreased ADH: increase urine output
• Increased ADH: decreased urine output

• large excretion of dilute urine (4-12L/d)
• polyuria
• polydipsia (increased thirst)
• dehydration
• increased plasma osmolarity (stimulates osmoreceptors)
• UA has low SG
• hypernaturemia (>145)
• dry mucous membrames

• SG is decreased (1.000-1.005)
• water loss in plasma

• sodium increases (>145)
• water loss in plasma

• no water or PO fluids for 4-18 hours
• patient with DI continues to have high urine volume output
• kidneys cannot concentrate urine

• give synthetic ADH to determine if kidneys can concetrate urine
• this test will tell us isf they have neurogenic DI or nephrogenic DI

• independent secretion of ADH from a non-endocrine source
• oat cell (small cell carcinoma of the lung), cancer in duodenum/pancrease and lymphomas
• surgeries are notorious
• drugs (chemo, thlenol, thiazide diuretics)

• hyponatremia (110-115)
• increased risk of seizures
• mental status change
• decreased plasma osmolarity from volume expansion
• increased levels of ADH
• urine hyperosmolarity (concentrated)

• hypertonic NaCl for sodium replacement
• PO fluid restriction to 600-800 mL/d
• Lasix
• Lithium to interfere with aDH at the kidney level
• montior I&O, urine SG, CV changes, mental status

• increased GH in childhood
• overgrowth of long bones
• increased activity of the bones at the epiphyseal plates

enlargement of the visceral organs with connective tissue changes

• left ventricular failure is prominent
• nerves can become entrapped related to overgrowth of bone and skin: foot drop, muscular atrophy, weakness

• increase metabolic rate and decrease carbohydrate tolerance (loss of insulin sensitivity from increased growth hormone, connective tissue in pancreas becomes fibrotic)

autoimmune process

• increase levels of IgG, which bind to TSH receptors, mimicking TSH & increasing the production of T4

condition when thyroid grows larger than normal

• you will see exopthalmos (protrusion of eye) and associated lid lag

• increased metabolism/metabolic rate
• nervousness
• hadnd tremor
• goiter
• exophalmos
• hair is fine, thinning
• warm, moist baby-butt skin

• TSH decreased
• Free T4 should be increased

• TSH increased
• increased T4

failure of the gland to produce thyroxine

• Hasimoto's thyroiditis
• patient treated with RA12 for Graves disease
• iodine deficiency
• medications: sulfonamides, lithium carbonate
• post-surgical
• congenital

Failure of HPT axis

• hypothalamic lesion

• pituitary lesion

• increaed TSH
• decreased T4

• decreased TSH
• decresed T4

• slow mental activity
• depression
• fatigue
• weight gain
• dry coarse skin
• menorrhagia (heavy periods)
• myxedema

What is myxedema (fat face)

Cushing's disease

The patient is not able to respod to stressor because there are already high levels. Can be very damaging because we can't mobilize glucose like we normally would. Immune response will be down all the time. More likely to become sick.

Excess secretion of cortisol with or withoug pituitary involvement

• usually from elevated levels of ACTH from anterior pituitary; sometimes from adrenal neoplasm

Cushing's Disease

Role of exogenous glucocorticoid therapy?

• accumulation of adipose tissue
• protein wasting
• hyperpigmentation
• HTN
• mental status changes
• poor wound healing

salt retention from cortisol and increased blood volume because of dual mineralcorticoid effect.

(cortisol is a good-enough fit for the aldosterone receptors)

Addison's disease

Hypercortisolism develops from inadequate stimulation by ACTH or decreased production of cortisol by the adrenal cortex

Decreased cortisol and aldosterone

• when cortisol, aldosterone and adrogens and all decreased
• increased ACTH but inadequate synthesis and secretion of cortisol
• possible autoimmune

increased ACTh from anterior pituitary

decreased cortisol

• weakness
• fatigue
• mental confusion from hypoglycemia
• hypotension
• hypovolemia from decreased aldosterone
• salt cravings
• hyperpigmentation
• vitiligo

loss of sodium

increase in potassium

excess PTH (parathyroid hormone)

often related to renal failure → decreased Vit D activation → decreased GI absorption of calcium → decreased serum Ca++ → PTH stimulation

"stones, bones, abdominal groans, psychic overtones"

renal stones, bone pain, fracture, nausea, vomiting, constipation, PUD, pancreatitis, depression, fatigure, anxiety

Increased PTH with Decreased serum calcium. Chronic low serum Ca++ (from less absorption, renal failure, or external cause) stimulates PTH secretion from parathyroids

Decreased PTH with decreased serum Ca++ (the parathyroid cannot respond to the low Ca++)

Decreased PTH with increased serum Ca++ (if serum Ca++ is high for some reason, parathyroid does not respond. Would be corrected with correction of serum Ca++)

hypocalcemia

chvostek's sign

Trousseau's sign

parathesias

seizures

dysrhythmias

hyperosmotic hyperglycemic nonketonic coma

Glucose > 800 mg/dl

Type 2

severe dehydration from osmotic diuresis and electrolyte shifting

AGE End products

atherosclerosis is accelerated poor circulation and sugary blood make more susceptible to infections, gangrene and amputation

Diabetes Insipidus

Limit water intake

If still pee a lot then it's true DI

Decreased urine is not DI

Give synthetic ADH

Draw blood to test ADH level

see if kidney can produce concentrated urine

If positive response: primary problem is decreased production (neurogenic)

If negative (no response): problem is nephrogenic - renal tubules are not sensitive to ADH