Patho Test 4

• Growth hormone (GH)
• Thyrotrotropic hormone (TSH)
• Adrenocorticotropic Hormone (ACTH)
• Melanocyte stimulating hormone (MSH)

• Somatotropin
• Prolactin
• Luteotropic hormone
• Follicle stimulating hormone
• interstitial cell stimulating hormone

Antidiuretic Hormone (ADH)

Oxytocin

• Triiodithyronine (T3)
• Thyroxine (T4)
• Calcitonin

Parathormone (PTH)

• Endocrine function insulin
• Glucagon
• Digestive enzymes

• Glucocorticoids (cortisone, cortisol)
• mineral corticoids (aldosterone)
• sex hormones (androgens)

Catechaloamines (Epinephrine, norephinephrine)

• Comes from the Anterior Pituitary
• Acts directly on bones and other tissues to stimulate growth

• comes from the Anterior Pituitary
• stimulates the thyroid gland

• comes from the Anterior Pituitary
• stimulates the adrenal cortex

• comes from the Anterior Pituitary
• stimulates darking of the skin

facilitates reabsorption of H2O in the kidneys

Control body metabolism and influence physical and mental

growth, nervous system activity, protein, fat, carbohydrate metabolism, reproduction

lowers serum calcium levels, inhibits bone reabsorption

regulates calcium and phosphorus metabolism

enables glucose to freely enter cells, helps muscles and tissue oxidation of glucose, promotes stoarge of glycogen

increases gluconeogenesis in the liver

decreases protein synthesis, regulate serrum glucose by increasing rate of gluconeogenesis, suppress the inflammatory and immune responce, increase fat mobiliaztion, support adaptation during stressful situations

Facilitate reabsorption of NA+ and elimination of K+

responsible for development of secondary sex characteristics

initiates stress response

causes vasoconstriction

Responsible for secondary sex characteristics, mammary duct system growth of graafian follicle in women

• Decrease in the # of receptors
• imparied receptor function
• andtibodies against receptors (autoimmune)
• abnormal receptor number

• absence or impaired development of gland
• gland destroyed
• decline in function

• excessive stimulation
• hyperplasia
• hormone producing hormone

defect in target gland responsible for producing the hormone

• target gland normal
• deficient RH and SH from pituitary system

results from hypothalamic dysfunction

interruption of the physical connections between the hypothalamus and the pituitary gland can cause disease

A syndrome characterized by high levels of ADH in the absence of normal physiologic stimuli for its release

Ectopic secretion of ADH by tumor cell

pituitary surgery, post-op clients, positive pressure ventilation, medications, disease and injury to the CNS

water intoxication due to water retention that leads to hyponatremia, hypoosmolarity, urine inappropriately concentrated w/ respect to serum osmolarity

• concentration of the blood
• Normal 270-295

135-145

40-45%

10-20

• decreased serum osmolality
• decreased sodium level
• increased urine osmolality
• decreased hematocrit
• decreased BUN

• insufficiency of ADH, leading to polyuria and polydipsia
• hx of head injury, pituitary tmor, craniotomy

• Neurogenic (central)
• Nephrogenic

• insufficient ADH
• may follow head injury or surgery near the lesion area

• End organ failure
• insensitivity of the renal tubule to ADH
• drugs and disorders damage the renal tubule

• Partial or total inabilty to concentrate urine. Insufficient ADH secretion causes secretion of large volumes of dilute urine, leading to an increase in plasma osmolatity
• urine out put 3 to >12 L/day
• Specific Gravity 1.00-1.005
• Dehydration can develop rapidly

• measure of concentration of urine
• Normal 1.010 - 1.020

• Monitor fluids
• Replace Fluids
• Check neuro states
• Check vital signs
• check muccous membranes

• Polyuria, nocturia, thirst, polydipsia
• increase plasma osmolality
• decrease urine spenific gravity
• decreased urine osmolality
• hypovolemia, tachycardia, decreased b/p

pituitary tumors < 10 mm

pituitary tumors >10 mm

occurs in adults who are exposed to continuously excessive levels of GH

• slow progression, increased amounts of GH can't stimulate further lone bone growth, the result is connective tissue and bony proliferation
• Diabetes mellitus may occur when the pancreas is unable to secrete enough insulin to offset the effects of GH

GH secreting pituitary adenoma

enlaged tongue, interstitial edema, large sebaceous and sweat glands, coarse hair, enlarged bones of face, hands, feet, soft tissue overgrowth, HTN, heart failure

occurs in childern and adolescents, excessive secretion of GH by adenomas. Epiphyses not fused, excessive skeletal growth occures

low GH in children can lead to

condition that results from increased levels of thyroid hormone. could be due to graves disease, adenomas, carcinomas, pituitary issue

Graves disease

• result of increased circulating thyroid hormones
• increased T3, T4, decreased TSH
• clubing fingers, Tremors, increaed diarrhea, Menstrual changes (amenorrhea), intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, increase systolic BP, breast enlargement, weight loss, muscle wasting, nervousness, increased appetite

• more common in women, Familial tendency, autoimmune disease
• Thyroid autoantibodies are found in more than 95% of clients

suppression of TSH and TRH, increased iodine uptake, increaed thyroid gland metabolism, lead to enlargment of the gland

• enlarged thyroid gland
• can be seen ini both hypo and hyperthyroidism

subcutaneous swelling legs and hands

Exophthalmos (Bulging eyes), Edema of the orbital contents, protrusion of the globe can occur which can lead to visual disturbances, irritation, pain

• excerbation of hyperthyoidism
• worsened thyrotoxic state that can be fatal if not treated
• death can occur w/i 48hrs
• most frequently occurs in undiagnosed, partially treated and stressed individuals

infections, cardiopulmonary disorders, emotional distress, poor preparation for thyroid surgery

most common throid disorder due to deficient productoin of thyroid hormone by the throid gland

• loss of functional throid tissue
• leads to decreased production of TH
• that leads to increased production od TSH
• that may lead to goiter

• due to problem w/ pituitary gland and insufficient TSH
• pituitary tumors
• Decreased TSH, decreased TH

nonbacterial inflammation preceded by a virus

• destruction of thyroid tissue
• ex-Hashimoto disease

hair loss, apathy, lethargy, dry skin (coarse & Scaly), muscle aches and weakness, constipation, intolerance to cold, receding hairline, facial & eyelid edema, Dull-blank expression, extreme fatigue, thick tongue, slow speech, anorexia, brittle nails and hair, menstrual disturbances

late: subnormal temp, bradycardia, weight gain, decresed LOC, thickened skin, cardiac complications

• alteration in the composition of the dermis and other tissues
• protein-mucopolysaccharide complex binds w/ water

• excerbation of Hypothroidism
• decreased LOC, hypothermia, hypoventilation, hypoglycemia,
• LIFE THREATENING

occurs in infants as a result of absent thyroid tissue and hereditary defects in thyroid hormone synthesis

due to untreated congenital hypothyroidism

• most common cause is exposure to ionizing radiation during childhood. Small thyroid nodule or metastatic tumor in lungs, brain, bone
• s/s due to pressure on surrounding tissue

• manifestation of hypercortisolism from any cause
• Cushing disease
• Benign or Malignant adrenal tumor
• Ectopic Cushing
• Iatrogenic Cushing

excessive anterior pituitary secretion of ACTH. Most individuals have a pituitary microadenoma which secretes ACTH

non-pituitary ACTH secreting tumor small cell carcinoma of the lung

longterm use of pharmacologic glucocorticoids

personality changes, moon face, increase susceptibility to infection, gynecomastia, fat deposits on back, osteoporosis, hyperglycemia, CNS irritability, NA and Fluid retension, Thin extremities, GI distress (Increase acid), amenorrhea, hirsutism, thin skin, purple striae, bruises and petechiae

excess facial hair

• adipose accumulation in trunk, face, cervical areas, sodium and water retention,
• "Moon face, truncal obesity, buffalo hump"

insulin resistance and increased gluconeogenesis

catabolism effects of cortisone on peripheral tissues, collagen loss leads to thin skin, easy bruising, capillaries more visible

high levels of ACTH, stimulates increased MSH

NA+ retention

suppression of immune system

cortisol effect

increased androgen levels

increased gastric acid secretions

destruction of bone proteins and aalteration in Ca+ metabolism

Addison disease

• autoimmune destruction of the adrenal glands is the most common cause
• 90% of tissue destroyed before symptoms
• characterized by elevated serum ACTH levels with inadequate corticosteroid synthesis and output
• add hormones

bronze skin pigmentation of skin, change in distrubution of body hair, GI disturbances, weakness, hypoglycemia, postural hypotension, weight loss

• profound fatigue
• dehydration
• vascular collapse
• renal shut down
• decreased serum NA
• increased K

• urinary loss of NA(Hyponatremia, loss of ECF), Cl, H2O
• decreased excretion of K+ (hyperkalemaia)

• Hypoglycemia
• Lethargy
• Weakness
• GI Symptoms
• Weight loss

low ACTH levels cause inadequate adrenal stimulation, adrenal atrophy, and corticosteroidogenesis

due to Exogenous steroids use (cannt be abruptly stoped due to "shutting off" of adrenal gland

• LIFE THREATENING
• precipitated by illness, stress, abrupt discontinuing of steroids

can cause N/V, muscular weakness, hypotension, dehydration, vascular collapse

care focused on dehydration

• S=salt (replace)
• S=sugar (replace)
• S=Steroids (replace)
• S= support
• S= search for cause

adrenal tumors, cushing syndroms, defects in steroid synthesis

• hypersection of estrogen (excess)
• development of female charcteristics

• hypersecretion of androgens (excess)
• development of male charcteristics

• A catecholamine producing tumor derived from the chromaffin cells of the adrenal medulla that contain sympathetic nevre cells
• most common 40-60 yrs, men and women affected equaly

hypertension, headaches, diaphoresis, tachycardia, palpitations, hypermetabolism, glucose intolerance, warmth, heat intolerance

cathecholamines

increased PTH levels results in increase serum Ca levels

greater than normal secreations of PTH by one or more of the parathyroid glands, cause unknown, maybe due to adenoma, carcinoma, inheritance

caused by increased PTH secondary to a chronic disease state. the most common cause is renal failure. Vitamin D metabolism is impaired in renal failure results hypocalcemia. The chronic renal failure induced hypocalcemia serves as a stimulus for increased PTH secretions

• abnormally lof PTH levels
• most common cause by damage to parathyroid glands during surgery ,
• a lack of PTH causes a depressed serum calcium level and an increased serum phosphate level due to increased renal reabsoprtion of phosphate

• muscle spasm (Chvostek's)
• hyperflexion (Trousseau's)
• Dry Skin
• Hair loss
• done deformities

• 1. more than one fasting plasma glucose level >or = 126 mg/dl
• 2. plasma glucose value in the 2 hr sample of OGTT > 200 mg/dl
• 3. Casual plasma glucose level > or = 200mg/dl with symptoms
• 4. HgbA1C= normal <7%

shows overal status of a person BS for the past few months

• Type 1
• Type 1.5
• type 2
• Gestational

• environmental-genetic factors result in Bcell destruction
• autoantibbodies detected of pancreas and B cells
• 95%
• peakage 11-13 years

• cause unknown
• no evidence of autoimmunity

Polyuria, polydipsia, polyphagia, weight loss, fatigue, increase frequency of infection, rapid onset, insulin dependent, familial tendency, peak incidence from 10-15 years

lack of insulin

to elevated glucose levels pull water from cells which results in intracellular dehydration

the effects of hyperglycemia as an osmotic diuretic renal threshold for glucose excreded

depletion of cellular stores of CHO, fats, proteins, resulting in cellular starvation

fluid loss w/ osmotic diuresis, loss of body tissue

metabolic changes

• 1. Peripheral insulin resistance
• 2. Deranged secrections of insulin by pancreatic cells
• 3. increased glucose production by the liver

obesity, diabesity, visceral fat

• 1. hyperglycemia
• 2. hypertension
• 3. hyperlipidemia
• High triglycerides (>150
• 4. Abdominal obsesity

70-110

• women <50
• men<40

<200

• women <35
• men <40

genital pruritus, visual changes, parethesias, fatigue

Fasting glucose >100 and <126 mg/dl

2 hour postload glucose level greater than or equal to 140 but less that 200 mg/dl

glucose intolerance first recognized during pregnacy, most likely in the third trimester. Following pregnancy glucose may normalize remaini impaired or progress to Diabetes Mellitus.

• lowered plasma glucose 45-60 mg/dl
• occcurs more frequently in individuals treated w/ insulin

tachycardia, diaphoresis, pallor, tremors, dizziness, headahcem visual changes

• Adrengic-pallor, sweating, tachycardia, sweating, palpitations, hunger, restlesness, anxiety, tremors, clammy skin
• Neurogenic- Fatigue, irritabilty, headache, visual changes, dizziness, convulsions

• most commonly occurs in Type 1 diabetics
• develops when ther is an absolute or relative deficiency of insulini and an increase in insulin counterregulatory hormones. Hepatic glucose production increases. peripheral glucose usage decreases, fat mobiliaztion increase and ketogenesis is simulated

catecholamines, cortisol, glucagon, growth hormone

are realses during a stress responce

type 1, illness, infection, trama, surgery, mi, stress evernt

• Hyperglycemia (BG 300-750)
• Ketosis (Ketones come from fat metabolism)
• Metabolc Acidosis (ketones acid) ,low bicarb <15, low pH <7.3

polyuria, polydipsia, N/V, Fatigue, hypotension, tachycardia, stupor leads to coma, abdominal pain, fruity breath, kussmauls respirations

• Hyperventilation
• rapid , deep

fluid loss from osmotic diuresis due to hyperglycemia

K+ normal or elevated (Met Acid= high K+), shift of H20 and K+ from EC due to hyperosmolarity of ECF due to hyperglycemia, NA normal or decreased

• more commonly seen w/ type 2 diabetes, levels of free fatty acid are in HHNKS are consistently lower than in DKA and is charcterized by a lack of ketosis
• insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly

• Glucose levels>600-2000 mg/dl
• Hyperosmolarity >350 mOsm/l

• 1.Major stress event
• 2. increased cortisol, glucagon, catecholamines
• 3. hyperglycemia
• 4. inadequate insulin secretion
• 5. Hyperglycemia
• 6. Osmotic Diuresis, Electrolye imblance
• 7.Extreme dehydration and intracellular dehydration
• 8. Nonketotic COMA, Death

• dehyration
• neurological signs-changes in LOC, seizures, visual loss, may mimic strock
• excessive thirst
• electrolye loss
• Potassium phosohorus sodium relacement needed, also rapid fluid replacement

• thickened vessel walls
• caused by ischemia, segmental demyelinization

• affects nerves that control sensations and muscle in the body
• loss feeling, touch, sensation
• burning pain

affects involuntary nerves controlling many body systems i.e bladder, GI sytem

retinal ischemia resulting from blood vessel changes and red blood cell aggregation

the glomeruli are injured by protein denaturation by high glucose levels and adverse effects of intraglomerular hypertension. Glomerular enlargement and glomerular basement membrane thickening result in diffuse intercapittary glomerulonecrosis. Proeinuria is a consistent sign of renal damage

• arise from development of atherosclerosis
• damage to endothelial later of arteries

coronary artery disease, Cerebrovascular diease, Peripheral vascular disease(see discolorarion, necrosis)

• common problem
• due to sensory impairment and motor weakess

• impaired vision
• impaired touch
• pathogens multiply
• decreased blood supply
• WBC function impairment