endocrine Flashcards
Glands of the endocrine syndrome
Pituitary
Thyroid
Parathyroid
Adrenal glands
organs that also produce hormones
Pancreas
Gonads
Hypothalamus
hormones
Regulate water and electrolytes
Respond to adverse conditions such as infection, trauma, stress
Help with growth and development
Reproduction
Pregnancy maintenance
Digestion
Nutrient storage
Endocrine hormones can exert various effects on various organs
Ex. Estradiol
paracrine
produces action on other cells
autocrine
produces action on themselves
Hypothalamic horomone
Synthesis and release of Anterior Pituitary Hormones are regulated by releasing or inhibiting hormones from the hypothalamus
Hypothalamus hormones that regulate secretion of anterior pituitary hormones
GH-releasing hormone (GHRH)
Somatostatin
TRH
Corticotropin releasing hormone (CRH)
Gonadatropin releasing hormone (GH)
regulation of hormone levels
Hypothalamus activity is regulated by negative feedback mechanism
TSH–> T3T4
pituitary
pea shaped hormone locates at the base of the brain
Pituitary anterior lobe
Thyrotrophs-produce TSH
corticotrophs- produce corticotropin (ACTH)
Gonadotrophs - produce gonadotrophins (LH, FSH)
Somatrophs- produce GH
Lactotophs- produce prolactin
Putuitary posterior
stores and releases: antidiuretic hormone (ADH) and oxytocin
Both of these hormones are synthesized in the hypothalamus
Pituitary posterior
stores and releases: antidiuretic hormone (ADH) and oxytocin
Both of these hormones are synthesized in the hypothalamus
hypofunction of hormones
Congenital defect: gland/enzyme
Gland destroyed: blood flow, infection, inflammation, autoimmune response, neoplasm
Age, atrophy due to drug
Receptor defect
hyperfunction of hormones
Excessive hormone production
Excess stimulation
Hyperplasia
Hormone producing tumor
Drugs (steroids/cushings)
altered endocrine primary disorder
originate in the target gland producing the hormone
altered endocrine secondary diagnosis
gland is fine but the stimulating and releasing of a hormone is not
Ex thyroidectomy- eliminates TSH stimulation
altered endocrine tertiary disorders
results form hypothalamic dysfunction- both pituitary and target glands are under stimulated
hyperpituitarism
typical cause pituitary adenoma (benign tumor from anterior pituitary)
Less common cause: hyperplasia, carcinoma of the anterior pituitary, secretion of hormones by extra-pituitary tumors, hypothalamic lesions
Lactotrophic Tumors are most frequent
Small benign tumors composed of prolactin secreting cells causing hyperprolactinemia
In women: inhibit LH causing amenorrhea, galactorrhea, infertility
In men: ED and loss of libido
hypopituitarism
Decreased secretion of pituitary hormones causing hypofunction of the secondary organs- 70-90% of anterior pituitary must be destroyed to become evidence
Causes: congenital, acquired abnormalities that destroy anterior pituitary, deficiency of hypothalamic hormones, lesions
Gradual progressive loss- loss of GH, LH, FSH then eventual loss of TSH, ACTH*Maybe be manifested R/T hormone- GH loss decreased growth in children, decreased libio, ED, amenorrhea, then Hypothyroid
Growth hormone disorders
Growth hormone (somatotropin): essential for growth and aids in metabolic functions
Growth patterns are measured over time and is related to parent height as well
idiopathic short stature
short king because it be like that
psychosocial dwarfism
daddy why wont you love me
functional hypopituitarism, seen in some emotionally deprived children: poor growth, potbelly, poor eating and drinking habits
Classic growth hormone deficiency
Decreased lean mass, increased fat mass, hyperlipidemia, decreased bone mineral density, reduced exercise capacity and diminished sense of well-being
Associated with- increase central adiposity, insulin resistance, dyslipidemia (metabolic syndrome), elevated CRP
giantism
growth hormone excess before puberty
somatotroph adenoma
acromegaly
GH excess in adulthood
Precocious Puberty
Early activation of hypothalamic pituitary gonadal axis
Occurs before 6 in African American girls, 7 in Caucasian girls and 9 in boys of both races
Development of secondary sex characteristics and fertility
Tall stature in childhood and short stature in adulthood
Thyroid Gland
Body’s largest single organ specialized in hormone production
Thyroid hormone secretion regulated by the hypo-thalamic-pituitary-thyroid feedback
Thyroid hormone increases metabolism and protein synthesis
Thyroid Function Tests: T3, T4, TSH
hypothyroidism
General slowing down of the metabolic process
Most often caused by Hashimoto Thyroiditis-autoimmune disorder than can destroy the thyroid gland
Manifestations: gradual onset of generalized weakness, weight gain despite decrease appetite, cold intolerance, dry sterm-127kin, coarse, brittle hair, puffy face
Diagnosis: elevated TSH, low T4 (primary)*Treatment: levothyroxine( synthroid)
myxedema
non-pitting edema- especially face
Myxedema coma: life-threatening , end stage hypothyroidism, coma, hypothermia, cardiovascular collapse, hypoventilation, hyponatremia, hypoglycemia and lactic acidosis
Treatment: aggressive supportive therapy i.e. cardiovascular, electrolytes, warming blanket
hyperthyroidism
High levels of thyroid hormone
Due to hyperactive thyroid gland- graves disease, goiter
Manifestations: nervousness, irritability, weight loss, tachycardia, palpitatins, SOB, excessive sweating, heat intolerance, exophthalmos
Treatment- radioactive iodine to eradicate thyroid gland, surgery, antithyroid drugs- PTU, methimazole, and drugs to control symptoms- Beta-Blockers
Thyroid storm
Life-threatening thyrotoxicosis- rare now because of good diagnosis tools
Caused when hyperthyroid is not adequately treated, precipitated by stress, infection, DKA, trauma or manipulation of the hyper active thyroid during thyroidectomy
Manifested: Very high fever, tachycardia, CHF, angina. Agitation, restlessness, and delirium- high mortality rate
Treatment- should be rapid- cooling w/o shiver response, fluids, glucose, steroids, PTU, methimazole, BB, NO ASA- increases levels of free thyroid hormones
Primary Cortical Insufficiency
Addison’s Disease- (rare) adrenal cortical hormones are deficient, ACTH levels are elevated because of lack of feedback
Autoimmune destruction of the adrenal cortex, before 1950’s TB was the major cause, metastatic CA, CMV, hemochromatosis
Manifestations: urinary loss of sodium, chloride and H2O, decrease loss of K+, decreased Cardiac output, hyperkalemia, orthostatic hypotension, dehydration, weakness and fatigue
Treatment- fludrocortisone, hydrocortisone
Primary Cortical Insufficiency
Addison’s Disease- (rare) adrenal cortical hormones are deficient, ACTH levels are elevated because of lack of feedback
Autoimmune destruction of the adrenal cortex, before 1950’s TB was the major cause, metastatic CA, CMV, hemochromatosis
Manifestations: urinary loss of sodium, chloride and H2O, decrease loss of K+, decreased Cardiac output, hyperkalemia, orthostatic hypotension, dehydration, weakness and fatigue
Treatment- fludrocortisone, hydrocortisone
Acute adrenal crisis
Life-threatening, can be caused by illness in someone with Addison’s disease
Manifestations- N/V, muscular weakness, hypotension, dehydration, and vascular collapse
Treatment- fluids both NS and D5W, glucocorticoid replacement therapy
Cushing Syndrome
Hypercortisolism from any cause
Manifesations- protruding abdomen, subclavicular fat pads, buffalo hump on back, moon face, weakness and thin extremities
Treatment- remove or correct the cause of hypercortisolism
Diabetes
The body primarily metabolizes glucose and fatty acids for energy
The brain does not produce or store glucose, but needs it exclusively for function
Tissues obtain glucose from the blood
Liver stores excess glucose as glycogen, and uses gluconeogenesis to convert amino acids, lactate and glycerol into glucose during fasting or when glucose intake does not keep up with demand
Blood glucose levels reflect the difference liver released glucose and the amount of glucose removed from blood by body tissues
Fats can be used for fuel during fasting or diabetes mellitus- the breakdown makes fatty acids that are converted to ketones in the liver (not converted to glucose)
Energy metabolism is controlled by several hormones: insulin, glucagon, epinephrine, GH and glucocorticoids
Insulin is the only hormone that controls blood glucose levels
Insulin facilitates the transport of glucose into body cells, decreases livers production and release of glucose into the bloodstream
Insulin decrease lipolysis and the use of the fats as fuel
Glucagon and epinephrine promote glycogenolysis
Glucagon and glucocorticoids increase gluconeogenesis
Type 1 Diabetes
Type I- beta-cell destruction, absolute insulin deficiency
Type 1A- immune mediated destruction of beta-cells (90%)
Occurs more commonly in children and adolescents
Genetic predisposition, environmental triggers, infection, and T-lymphocyte- mediated hypersensitivity
Type 1B-idiopathic
Strongly inherited
African americans and Asian
Risk for diabetes
Fasting glucose levels- plasma glucose levels after 8 hrs of fasting
< 100 mg/dl nml
100-125 mg/dl impaired fasting glucose (pre-diabetes)
>126 mg/dl provisional diabetes
Oral Glucose Tolerance Test- measures bodies ability to remove glucose from the body within 2 hrs after consuming 75g on glucose 300ml of water
<140mg/dl nml
140-199 mg/dl impaired (prediabetes)
> 200 provisional diabetes
HGA1C> 6.5 diabetes
Type 2 diabetes
Type II- insulin resistance, relative insulin deficiency
Relative insulin deficiency
90% of Diabetes casesOlder and overweight, recently obese children
Metabolic abnormalities- insulin resistance, increased glucose production by liver, impaired insulin secretion by pancreatic beta- cells
Increased postprandial blood glucose levels
Genetic, behavioral, environmental factor leads to diabetes
Family history twofold-fourfold increased risk
Obesity, inactivity
Visceral obesity leads to increased postprandial glucose levels
Metabolic syndrome (syndrome X, insulin resistance): hyperglycemia, hypertriglyceridemia, low HDL, high LDL, elevated CRP
Diabetes detection
Type 1 rapid onset
Type 2 gradual usually detected through incidentsl blood tey
3 P’sPolyuria
Polyphagia
Polydipsia
Weight-loss (type I)
FBG<100
Casual or random blood glucose > 200mg/dl with 3P’s, and blurred vision
OGTT after 2hr >200mg/dl
HgA1c- >6.5
Diabetes management
Exercise (especially type 2)
Sulfonyurea’s (glipizide), meglitinides (repaglinide), biguinides (metformin), alpha-glucosidase inhibitors (acarbose), Incretin- based agents (exanatide), Insulin
Diabetic complications: Ketoacidosis
hyperglycemia, metabolic acidosis, acute life-threatening complication of uncontrolled DM
Usually affects Type 1, but can affect Type 2 (sepsis, severe trauma)
Lethargy, vomiting, abdominal pain, coma, fruity breath
Blood glucose levels > 250mg/dl
Low bicarbonate mild (15-18mmol/L, ph 7.25-7.3); moderate (10-<15 mmol/l, ph 7.00-7.24), severe (<10mmol/L, ph <7.0)
Leads to dehydration and electrolyte imbalance
Goal of treatment- hydration, treat metabolic and electrolyte imbalances- insulins by infusion
Hypoglycemia
Insulin reaction resulting from excess insulin, below normal blood glucose levels
Occurs most often in patients taking insulin, sulfonylurea
Over dose of insulin
Failure to eat
Exercise
Decreased need for insulin (decreased stress, meds)
Rapid onset-anxiety, tremors, tachycardia, cool clammy skin, incoherent, coma seizures- some people may have decreased reaction
Treatment- juice, candy, glucagon
Overdosage of insulin
Somogyi Effect: hypoglycemia in pre-dawn hours 2-4am
rapid decrease in blood glucose during nighttime hours
stimulates release of hormones: cortisol, glucagon and epinephrine, to increase blood glucose by lipolysis, gluconeogenesis, and glycogenolysis
Monitor glucose between 2-4 am, reduce insulin dose at bedtime
hyperglycemia
Dawn Phenomenon: Hyperglycemia on awakening
Headache, sweats, nightmares
increase bedtime dose of insulin
Ketoacidosis: with inadequate amounts of insulin sugar can not be metabolized and fat catabolism occurs Extreme thirst, polyuria, fruity breath, kussmaul breathing, rapid thready pulse, dry mucous membranes, poor skin turgor, blood sugar level> 250mg/dl
Chronic complications of diabetes: Diabetic Neuropathies
paresthesia, numbness, tingling, impaired pain, decreased ankle and knee reflexes, ED
Chronic Complications of diabetes: Diabetic Neuropathy
lesions that occur in the diabetic kidney, cause CKD- contributing factor- HTN, family history, smoking, HLD, poor glycemic control, increased urine albumin secretion >30mg/day
Chronic Complications of diabetes: Diabetic Retinopathy
most frequent cause of new blindness, characterized by abnormal vascular permeability, mircro-aneurysm, hemorrhage, scarring, retinal detachment- poor glucose control, HTN. HLD- should have regular dilated eye exams
Chronic Complications of Diabetes: Macrovascular complications
atherosclerosis, cerebral vascular disease, HTN, hyperglycemia, altered platelet formation, HLD- reduce risk factors
Chronic Complications of Diabetes: Diabetic Foot Ulcers
effect of neuropathy and PVD, should have full foot exam yearly
Chronic Complications of Diabetes: Infections
soft tissue, osteomyelitis, UTI, candida
Stress response
activation of sympathetic nervous system, hypothalamic pituitary adrenal axis, immune system working to protect body from intense demands
Alarm stage- activation of sympathetic nervous system
Resistance stage- body selects most effective defense
Exhaustion- physiologic resources are depleted, and signs of systemic damage appear
Adaptation
Individual has successfully created a balance between the stressor and the ability to deal with it
Affected by experience and previous learning, how fast it needs to occur, gender, age, health status, nutrition, sleep-wake cycles and psychosocial factors
Stress
Stress response is designed to be self-limiting and protective
Prolonged activation of stress response because of overwhelming or chronic stressor can be damaging to health
Acute stress reaction and acute hyperglycemia are concerning in people with critical injuries or illness
PTSD
Chronic activation of the stress response after experience that involved actual or threatened death or serious injury
S&S: states of intrusion (flashbacks),avoidance (emotional numbing), hyperarousal (intense activation of neuroendocrine system)
