Unit 3 Flashcards
Proton pump inhibitors
-prazole
Gastric ulcers
Histamine H2 receptor blockers
-idine
Gastric ulcers
Oral antidiabetics
-amide
Antidiabetic type 2
Bisphosphonates
-dronate
Osteoporosis
Hypothalamus
center of the endocrine system, negative feedback, controls pituitary
Adipose tissue
endocrine gland, secretes hormones for metabolism. Adinoectin and leptin. White vs Brown fat
Phychoimmunology
endocrine, NS, and immune system interact.
Sympathetic NS
is aroused during stress and causes the adrenal medulla to release catecholamines
Catecholamines
compounds that control stress response, fight or flight. Epinephrine, norepinephrine, dopamine
Cortisol
Glucocorticoid hormone from adrenal cortex, lipid and carb metabolism, stress response
Decrease: Wound healing, inflammation, bone formation
Increase: urine, GI secretions
Endorphins
Endogenous, modulate pain transmission
Growth Hormone (Somatotrophin)
Stimulates skeletal and visceral growth, increases after stress
Prolactin
Growth of breasts and milk, sexual satisfaction
Testosterone
regulate male sex characteristics
Neuroendocrine Theory of Aging
Cells are programed to die or lose function (menopause)
Aging Pituitary
Decrease in weight and blood supply
Aging Thyroid
Decrease in size, becomes fibrotic, decreases hormone secretion
Aging parathyroid
no changes
Aging Adrenal Glands
Increase fibrotic
Carpal Tunnel Syndrome
Common with acromegaly, diabetes, pregnancy, hypothyroidism
Posterior Pituitary
Only stores and releases hormones; Oxytocin and ADH
Oxytocin
Stimulates contractions, breast milk, and sleep rhythm
ADH
Vasopressin; reabsorbtion of water at kidneys and ACTH Release
Anterior Pituitary
Makes and stores hormones; Somatotropin, TSH, FSH, LH, Prolactin, ACTH, Lipotropin, MSH
Thyroid Stimulating Hormone
TSH; secretes Thyroxine (T3) and Triiodothyronine (T4)
Follicle Stimulating Hormone
Sex organs, develop follicle, estrogen secretion, and sperm maturation
Luteinizing Hormone
Ovulation, corpus luteum maintenance, progesterone and testosterone secretion
Adrenocorticotrophic Hormone
Adrenal cortex, release of corticosteroids
Lipotrophin
Break down fat and synthesize and corticosteroids
Melanocyte Stimulating Hormone
Produced melanin
Hyperpituitarism
Acromegaly, Carpal tunnel, over growth of body
Acromegaly
Excessive secretion of GH, affects face, hands, and head
Thyroid Gland
Produces Thyroxine (T3) and Triiodothyronine (T4) and calcitonin
Calcitonin
When calcium is high, calcitonin increases calcium excretion to lower blood levels
Parathyroid Hormone
When calcium is low, PTH increases calcium reabsorption and bone demineralization to lower blood levels; Stimulated by TSH
Hyperthyroidism
Increase in metabolic function; women more than men 4:1, Graves disease is common 85%, thyroid storm
Graves Disease
- Thyroid-stimulating immunoglobulins that react against thyroglobin; stimulates enlargement and excess secretion
-Increases SNS
-Hyperthyroidism, increased T4 production
Hyperthyroidism Clinical Manifestations
-Goiter: enlarged thyroid
-Increased: Nervousness, heat intolerance, tremors, heart palpitations
-Exophthalmos: protruding eyes
-Peri-Arthritis: tendon inflammation
-Myopathy: muscle weakness, dyspnea
Hyperthyroidism Diagnosing
Increased TSH, antithyroid hormones, TSI
Hyperthyroidism Therapy
Antithyroid medication, surgery, Radioiodine
Hyperthyroidism PT Implication
Exercise intolerance and capacity
Hypothyroidism
Generalized slowed metabolism; congenital or removal
Hypothyroidism Type I
Low functioning thyroid or impaired release; altered lipid metabolism
Hypothyroidism Type II
failure of the pituitary to release TSH
Hypothyroidism Clinical Manifestations
Neuromuscular: decreased function and stiffness
Myxedema: non pitting edema of hands, feet, and scapula
Rheumatic symptoms
Hypothyroidism Diagnosing
Increased: TSH, cholesterol, phosphate, triglycerides
Decreased: T4
Parathyroid
Secrete PTH, on thyroid, 2
Hyperparathyroidism
Overactive parathyroid; disrupts calcium, phosphate and bone metabolism
Primary Hyperparathyroidism
Glands enlarge and interrupt PTH secretion
Secondary Hyperparathyroidism
-hypocalcemia
-glands become hyperplastic
Tertiary Hyperparathyroidism
Dialysis with long term secondary Hyperparathyroidism, glands become unresponsive
Hyperparathyroidism Clinical manifestations
Hypercalciuria, bone damage (osteoporosis), kidney damage, decreased NS function, muscle atrophy, GI disruptions
Hypoparathyroidism
Hypocalcemia; increased phosphate, NS irritability; decreased Ca+
Iatrogenic: Acquired, most common, gland damage or removal
Idiopathic: children, genetic or autoimmune
Hypoparathyroidism Clinical Manifestations
Neuromuscular irritability and calcification of organs
Adrenal Glands
Glands on kidneys, responses to stress
Adrenal Cortex
Secretes mineralocorticoids, glucocorticoids and androgrens
Mineralocorticoids
steroid hormones for fluid imbalances; aldosterone
Glucocorticoids
steroid hormones for metabolism of glucose, suppresses inflammation and immune functions; cortisol
Androgens
sex hormones, affect gonads
Adrenal Medulla
Secretes epinephrine and norepinephrine
Epinephrine
Fight or flight, increases response (adrenaline)
Norepinephrine
Same as epinephrine
Primary Adrenal Insufficiency
Addison Disease; insufficient cortisol release; removal/injury/radiation/cancer/infection
1) Decreased Cortisol Production
2) Aldosterone Deficiency
Primary Adrenal Insufficiency Pathogenesis: Decreased Cortisol production
less glucose production, Ca+, and stress resistance, weakness, increased ACTH
Primary Adrenal Insufficiency Pathogenesis: Aldosterone Deficiency
Fluid imbalances, increased NA excretion, dehydration, decreased heart activity
Primary Adrenal Insufficiency Treatment
Increase cortisol and fluids
Primary Adrenal Insufficiency PT Implications
Limited Stress (Addisonian crisis)
Secondary Adrenal Insufficiency
ACTH suppression = cortisol deficiency only
1) steroids
2) infection
3) pituitary removal
Adrenocortical Hyperfunction
Hypercorticolism, excess cortisol
Cushing Syndrome, Cushing disease, and Pseudo-Cushing syndrome
Cushing Syndrome
Hypercortisolism;
1) Hyperfunction of adrenal
2) Excess corticosteroids
3) excess ACTH
Cushing Disease
over secretion of ACTH from pituitary
Pseudo-Cushing Syndrome
emotional response causes symptoms
Adrenocortical Hyperfunction Clinical Manifestations
Hyperglycemia, high BP, muscles weakness, osteoporosis
Adrenocortical Hyperfunction Diagnosis
increased cortisol in urine and blood
Adverse Effects of Glucocorticoids
Mood, skin, GI, Bone, Fluid retention, infection, weakness
Conn Syndrome
Primary aldosteronism; adrenal glands hypersecrete aldosterone due to tumor; increases NA+ reabsorption
Adipokines
Proteins released by fat cells; autocrine hormones; decrease appetite
Visceral Fat
Bad, around abdomen releases cytokines that cause CVD and inflammation
bariatrics
study of obesity and weight management
Underweight BMI
<18.5
Normal BMI
18.5-24.9
Overweight BMI
25-29.9
Obese BMI
> 30
Obese Class I BMI
30-34.9
Obese Class II BMI
35-39.9
Obese Class III BMI
> 40
Type 1 DM
5-10%, abrupt, autoimmune
Type II Dm
90-95%, insulin resistance from B cell stress
Normal Glucose Lab values
A1C: 5.7%
Fasting: 99
GTT: 140
Prediabetes Glucose Lab Values
A1C: 5.7-6.4%
Fasting: 100-125
GTT: 140-199