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78 Cards in this Set

  • Front
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Hormones

chemical messengers which are made by endocrine glands and are released into the blood stream.


can only affect target cells which express a specific receptor for that hormone

most common dysfunctions associated with hormonal regulation

1. production of too much or too little hormone


2. improper feedback


3. ectopic production of hormone

Neurons in the supraoptic and paraventricular nuclei of hypothalamus project axons which terminate in the posterior pituitary. These neurons make?

oxytocin and anti-diuretic hormone (ADH)

2 different type of cells based on staining characteristics

chromophobes(non-secretory)


chromophils(secretory)

chromophobe adenoma

the most overt symptoms of these begin tumors are due to the compression on the optic nerve and headaches due to increase in intracranial pressure.

bitemporal heminoplasia

defect in visual field on separate sides

where is ADH normally synthesized

in hypothalamic nuclei and axonally transported, stored and released from the posterior pituitary

ADH is released

in response to increased blood osmolarity in times of dehydration

ADH targets

the cells of the distal tubule and collecting duct of the kidney to promote water reabsorption from the filtrate or to produce a concentrated urine

Diabetes insipidus

insufficiency of ADH.


loosing fluid, and increasing sodium

neurogenic diabetes insipidus

occurs due to interruption of the synthesis, transport or release of ADH due to hypophysectomy, tumors, inflammation, vascular lesions

nephrogenic diabetes insipidus

occurs when renal tubes fail to respond to ADH

psychogenic diabetes insipidus

caused by extremely large intake of water producing decreased ADH levels

clinical manifestations of diabetes insipidus

polyuria


polydipsia


hypoosmolar urine;dilute urine


hyperosmolar plase; increased osmolarity in blood


hydronephrosis; enlarged kidneys

treatment for diabetes insipidus

oral hydration


desmioressin (vasopressin analog)

SIADH: syndrome of Inappropriate ADH secretion

excessive ADH secretion. hanging onto fluid and decreases sodium. dark urine


usually due to an ectopic problem



effects of excessive ADH

increased water reabsorption by the kidneys


hemodilution


hypervolemia; lots of fluid


hyponatremia; low sodium in blood

clinical manifestation of hyponatremia

140-130 impared taste; fatigue


130-120 muscle and GI cramping


115 confusion, lethargy, seizue

treatment for hyponatremia

correct underlying problem


hypertonic saline


fluid restriction

diseases of the anterior pituitary

GH-growth hormone


ACTH-adrenocorticotropic hormone


TSH-thyroid stimulating hormone

Child giantism

adenoma that produces excess amounts of GH


large tumor on pituitary gland

adult acromegaly

increased connective tissue and bone growth and deposition


increased insulin resistance leading to diabetes mellitus


Features: enlarged tongue jaw and forehead, hyperosteosis of vertebrae, enlarged sella turcica due to adenoma, enlarged hands and feet, increased sebaceous and sweat gland activity

child and adult dwarfism

in children short stature from birth give GH to kids for treatment, has potential for tumors.


in adults no symptoms occur with lack of only GH

Thyroid Gland

2 differnt endocrine cells: follicular cells and parafollicular cells

atrophy of thyroid gland

decrease in mass of gland due to lack of TSH. hypothyroidism

hypertrophy/hyperplasia of thyroid gland

increase in mass of gland due to excess TSH, or tumorous condition

goiter

enlarged thyroid gland due to a variety of causes

endemic goiter

lack of iodine in diet

neoplasms of thyroid

can cause hypertrophy/hyperplasia of gland

adenoma of pituitary gland

excess TSH which over stimulates thyroid gland

hyperthyroidism

thyroid gland dysfunction resulting in excessive TH production

primary hyperthyroidism

increased T3/T4 levels


decreased TSH levels in thyroid gland

secondary hyperthyroidism

increased T3/T4 levels


increased TSH production in anterior pituitary

Hypothyroidism

thyroid gland dysfunction resulting in decreased TH production

primary hypothyroidism

decreased T3/T4 levels


increased TSH levels in thyroid gland

secondary hypothyroidism

decrease T3/T4


decrease TSH levels in anterior pituitary

graves disease

hyperthyroidism


an autoimmune disease


antibodies that bind to and stimulate thyroid gland

what does a person with graves disease display

increased BMR, tachycardia, nervous, sweating, rapid weight loss, warm in the touch, loose stools. bulging eyes

exophthalmos

protrusion of eyeball from socket


increased extracellular infiltrate of extra ocular eye muscles


lids do not close properly leading to corneal erosions/ulcerations

thyroid "storm"

a rapid, sudden urge of TH symptoms of thyrotoxicosis worsen leading to death due to high output failure of the heart

given to block thyroid hormone synthesis

propylthiouracil

hypothyroidism

patients with low levels of TH are usually very lethargic, cool, low BMR, and with myxedema

myxedema

edematous condition of connective tissue surrounding the eyes, skin, limbs and in the tongue



autoimmune thyroiditits

immunoglobulins inhibit thyroid gland and provoke immune mediated destruction



what happens to the gland after autoimmune thyroiditis?

become fibriotic, infiltrated with lymphocytes, enlarged, eventually destroyed

cretinism

lacking TH during fetal development and immediately following birth. child is slow to reach major milestones, lethargic, sleepy, slow pulse, cold, stunted skeletal growth (dwarf) and mentally retarted. can be treated with supplemental TH

insulin

hormone naturally produced by the pancreatic beta cells in the islets of langerhan


functions to increase glucose transport into cells and lower blood glucose levels

diabetes mellitus

systemic condition that arises due to a lack of insulin



3 cardinal signs of diabetes mellitus

polyuria


polyphagia


polydipsia

type 1 diabetes mellitus

insulin dependent


juvenile onset


B-cells in pancreas destroyed


no insulin made


risk factor: HLA-DR3/ HLA-DR4


10% of cases

type 2 diabetes mellitus

non-insulin dependent


adult onset


B-cells make insulin


insulin receptors decreased or desensitized


risk factor: obesity


90% of cases

test used to measure blood sugar levels

fasting blood glucose: >126


random blood glucose: >200


glycated hemoglobin: elevated levels of hemoglobin A1C

diabetic ketoacidosis

insulin defieciency


metabolic enzymes don't work as efficiently, so energy failure then shock


direct relationship between volume and pressure. as volume increases, pressure increases

adrenergic response to insulin excess

anxiety


sweating


tremor


tachycardia


weakness

brain deprived of glucose in insulin excess

disorientation


convulsions


unconsciousness


insulin shock

hormones that increase blood sugar

growth hormone


epinephrine


cortisol


glucagon



hormone that decrease blood sugar

insulin

chronic complications of diabetes mellitus

arise from the hyperglycemic state over many years.


neuropathies, vascular disease, infections

Neuropathies complication of DM

sensory>motor


axonal degeneration


pain and other problems related to peripheral neuropathy

vascular disease complication of DM

microvascular: retinal arteries, renal arteries


macrovascular: atherosclerosis, coronary artery disease/ stroke, peripheral vascular disease, gangrenous necrosis/ amputation



infection complication of DM

increased risk due to:


impaired sensorium


sugar rich body fluids


impaired immune response due to abnormal blood supply/chemotaxis/phagocytosis

zona glomerulosa

secretes mineralocorticoids


aldosterone-promots sodium retention and potassium excretion

zona fasciculata

secrets glucorticoids


largest layer


cortisol:


increases blood glucose by stimulating gluconeogenesis and inhibiting glucose uptake


increases blood amino acid levels by promoting protein degradation


increases blood fatty acid levels by stimulating lipolysis

zona reticularis

secretes gonadocorticoids


androgens: stimulate masculinizing effects

cushing's disease

overactivity of adrenal cortex


increased ACTH production and release from anterior pituitary or elsewhere which stimulates the adrenal cortex and raising production and release of cortisol.


tumor

cushings syndrome

refers specifically to the clinical condition caused by hypercortisolism which can arise from a variety of causes-cushing disease being one of them

hypercortisolism effect on proteins

muscle wasting in extremities


poor wound healing


skin breakdown:less collagen synthesis, purple striae


protein matrix of bone breakdown

hypercortisolism effects on carbohydrate metabolism

increase gluconeogenesis


insulin resistance

hypercortisolism effects on adipose tissue

moon face


truncal obesity


buffalo hump

primary hyperaldosteronism (Conns disease)

hypertension and hypokalemia



hypertension

high levels of aldosterone on blood levels with some contribution from excessive sodium absorption and expansion of the extracellular fluid. kidney tubules demonstrate a sodium escape phenomenon in which they possess an intrinsic ability to release excess sodium into urine

hypokalemia

hypokalemic alkalosis: sodium increases and potassium decreases


tetany and muscle weakness


EKG abnormalities and other cardiac changes


less H+ ions in ecf, and more in ICF

hypersecretion of androgens from the zone reticularis

adrenogenital syndrome: development of masculine features in a female body

addisons disease

primary adrenal insufficiency


due to: infectious organism, autoimmune disorder, HLAB8/HLADR3

clinical manifestations of addisons disease

hypocortisolism and hypoaldosteronism

hypoaldosteronism

blood sodium levels fall, drop in blood volume and pressure


increased blood potassium levels

hypocortisolism

loss of permissive effects of catecholamine stimulation to blood vessels creating possible hypotensive crisis


decreased glucocorticoid effect producing hypoglycemia


muscle weakness


weight loss GI upset


bronzing of the skin(hyper pigmentation of ACTH levels are high and stimulates melanocytes)

pheochromocytoma

tumor of the adrenal medulla which synthesizes excessive catecholamines (adrenalin)


hypertension


diaphoresis


tachycardia and palpitations


elevation in basal metabolic rate