endocrine Flashcards

(54 cards)

1
Q

Glands of the endocrine syndrome

A

Pituitary
Thyroid
Parathyroid
Adrenal glands

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2
Q

organs that also produce hormones

A

Pancreas
Gonads
Hypothalamus

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3
Q

hormones

A

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

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4
Q

paracrine

A

produces action on other cells

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5
Q

autocrine

A

produces action on themselves

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6
Q

Hypothalamic horomone

A

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)

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7
Q

regulation of hormone levels

A

Hypothalamus activity is regulated by negative feedback mechanism
TSH–> T3T4

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8
Q

pituitary

A

pea shaped hormone locates at the base of the brain

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9
Q

Pituitary anterior lobe

A

Thyrotrophs-produce TSH
corticotrophs- produce corticotropin (ACTH)
Gonadotrophs - produce gonadotrophins (LH, FSH)
Somatrophs- produce GH
Lactotophs- produce prolactin

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10
Q

Putuitary posterior

A

stores and releases: antidiuretic hormone (ADH) and oxytocin
Both of these hormones are synthesized in the hypothalamus

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10
Q

Pituitary posterior

A

stores and releases: antidiuretic hormone (ADH) and oxytocin
Both of these hormones are synthesized in the hypothalamus

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11
Q

hypofunction of hormones

A

Congenital defect: gland/enzyme
Gland destroyed: blood flow, infection, inflammation, autoimmune response, neoplasm
Age, atrophy due to drug
Receptor defect

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12
Q

hyperfunction of hormones

A

Excessive hormone production
Excess stimulation
Hyperplasia
Hormone producing tumor
Drugs (steroids/cushings)

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13
Q

altered endocrine primary disorder

A

originate in the target gland producing the hormone

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14
Q

altered endocrine secondary diagnosis

A

gland is fine but the stimulating and releasing of a hormone is not
Ex thyroidectomy- eliminates TSH stimulation

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15
Q

altered endocrine tertiary disorders

A

results form hypothalamic dysfunction- both pituitary and target glands are under stimulated

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16
Q

hyperpituitarism

A

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

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17
Q

hypopituitarism

A

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

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18
Q

Growth hormone disorders

A

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

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19
Q

idiopathic short stature

A

short king because it be like that

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20
Q

psychosocial dwarfism

A

daddy why wont you love me
functional hypopituitarism, seen in some emotionally deprived children: poor growth, potbelly, poor eating and drinking habits

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21
Q

Classic growth hormone deficiency

A

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

22
Q

giantism

A

growth hormone excess before puberty
somatotroph adenoma

23
Q

acromegaly

A

GH excess in adulthood

24
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
25
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
26
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)
27
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
28
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
29
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
30
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
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
Diabetes management
Exercise (especially type 2) Sulfonyurea’s (glipizide), meglitinides (repaglinide), biguinides (metformin), alpha-glucosidase inhibitors (acarbose), Incretin- based agents (exanatide), Insulin
39
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
40
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
41
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
42
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
43
Chronic complications of diabetes: Diabetic Neuropathies
paresthesia, numbness, tingling, impaired pain, decreased ankle and knee reflexes, ED
44
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
45
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
46
Chronic Complications of Diabetes: Macrovascular complications
atherosclerosis, cerebral vascular disease, HTN, hyperglycemia, altered platelet formation, HLD- reduce risk factors
47
Chronic Complications of Diabetes: Diabetic Foot Ulcers
effect of neuropathy and PVD, should have full foot exam yearly
48
Chronic Complications of Diabetes: Infections
soft tissue, osteomyelitis, UTI, candida
49
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
50
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
51
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
52
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)