Endocrine Flashcards

1
Q

Major endocrine glands and hormones

A
  • Glands: hypothalamus, pituitary, thyroid, parathyroid, pancreas, & adrenals
  • Hormones: a chemical messenger with a target cell; insulin, oral contraceptives, steroids
  • Receptors/Effect: intracellular signals (ATP, ADP, cAMP pathways); direct stimulation (transport channels & aquaporin production)
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2
Q

Describe the functions of the hypothalamus & pituitary glands

A
  • regulates growth hormone both releasing & inhibiting; thyrotropin releasing hormone; & corticotropin releasing hormone
  • positive & negative feedback loops
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3
Q

Describe the feedback loops related to the hypothalamus

A
  • Hypothalamus -> thyrotropin releasing hormone (TRH) -> anterior pituitary -> TSH -> thyroid -> T4 & T3
  • Normal body temp. -> increased body temp. -> thermostat in hypothalamus activates cooling mechanism -> blood vessels in skin dilate & sweat -> body temp. decreases -> normal body temp. -> body temp. decreases -> thermostat in hypothalamus activates warming mechanisms -> blood vessels in skin constrict & shivering -> body temp. increases -> normal body temp.
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4
Q

Describe a positive feedback loop

A
  • the loop will continue with more and more until told to stop (ex: pregnancy won’t stop until birth, blood clot formation to stop bleeding)
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5
Q

Describe the functions of the thyroid gland

A
  • Free and total thyroid: T4/T3 (mostly makes T4)
  • Metabolism
  • Temperature management
  • Respiration
  • Growth & development
  • Negative feedback loop
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6
Q

Signs and symptoms of hypothyroidism

A
  • Fatigue*
  • Bradycardia
  • Muscle weakness*
  • Dry skin
  • Neck swelling (Goiter)
  • Constipation
  • Increased weight gain*
  • Cold imbalance*
  • Facial edema
  • Irregular menstrual period
  • Increased cholesterol
  • Hair loss
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7
Q

Supplementation for hypothyroidism

A
  • T4 Synthroid: Levothyroxine
  • T3 Cytomel: Liothyronine
  • T4/T3 combination: Armour Thyroid
  • T4 has a long half life (7-10 days)
  • onset of action takes 3-5 days and peaks ~6 wks
  • T3 has more side effects
  • T4 is metabolized first & because it’s potent you can see if the pt will have any ADRs quicker
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8
Q

Describe Hashimoto’s disease

A
  • most prevalent hypothyroid disease
  • inherited with unknown gene expression
  • women more than men
  • 40-60 yrs of age
  • immune cells target & destroy thyroid tissue
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9
Q

Describe Myxedema Coma

A
  • severe form of hypothyroidism
  • 20-60% mortality rate
  • no edema/no coma
  • deteriorating mentation
  • Tx: supportive care, IV levothyroxine, & reverse underlying cause if known
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10
Q

Signs and symptoms of hyperthyroidism

A
  • Artial fibrillation
  • Heart failure
  • Osteoporosis
  • Thromboembolism
  • Tremor
  • Tachycardia/Tachypnea
  • Altered mental status
  • Fatigue
  • Muscle weakness
  • Heat intolerance
  • Nervousness
  • Neck swelling (Goiter)
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11
Q

Treatment for hyperthyroidism

A
  • Propythiouracil (PTU): blocks new hormone synthesis, blocks T4 -> T3 conversion, preferred agent given dual mechanism, 3x daily, bone marrow suppression & hepatotoxicity
  • Methimazole: blocks only new hormone synthesis, minor hepatotoxicity, 1x daily
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12
Q

Describe Graves disease

A
  • hyperthyroid disease
  • autoimmune disorder
  • rapid/irregular HR
  • osteoporosis
  • muscle weakness
  • vision changes
  • weight loss
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13
Q

Describe thyrotoxicosis

A
  • 1% prevalence: most common cause of Graves disease, could also be gestational or drug induced
  • 1% will experience thyrotoxicosis crisis “Thyroid Storm”: extremely elevated T4 and T3; 20% mortality rate
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14
Q

Treatment for thyrotoxicosis “Thyroid Storm”

A
  • symptom management with beta blocks (slows HR)
  • Thionamides (some side effects): propythiouracial (PTU) & methimazole
  • Iodine (some side effects): blocks new hormone synthesis & release; tachyphylaxis ~2 wks
  • Radioactive Iodine (permanent)
  • Thyroidectomy (permanent)
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15
Q

Describe the effect iodine has on the body

A
  • gives an overload of the thyroid
  • if seen on a patient chart it means they are getting ready to go into a procedure
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16
Q

Describe radioactive iodine

A
  • radioisotopes
  • radioactive uptake deposited in thyroid (apoptosis)
  • destruction of cells & increased incidence of cancer
  • diet alone not sufficient
  • 131 iodine use for thyrotoxicosis (medical radioactive iodine): T1/2 of ~8 days; dry eyes/mouth, neck pain, taste changes
  • 129 iodine from nuclear fission: T1/2 ~15.7 million yrs
  • 127 iodine is not radioactive
17
Q

Describe the parathyroid

A
  • 4 glands: embedded, bilateral, and posterior
  • Parathyroid hormone: PTH, maintains calcium (direct impact on bone/99% calcium is stored), ionized
  • Negative feedback: PTH & iCalcium
18
Q

What 3 areas does the parathyroid hormone act on

A
  • Kidneys
  • GI tract
  • Bones
19
Q

Describe the functions of the parathyroid

A
  • drop in serum ionized calcium levels promotes PTH release
  • rise in Vit D suppresses PTH
  • Renal effects: increased calcium reabsorption, phosphate excretion, & Vit D production
  • Bone effects: stimulates bone resorption & increases bone formation (indirectly & with normal levels)
  • Calcitonin (drives calcium into bone): produced via thyroid & opposes PTH, stimulates bone formation (lowering serum calcium)
20
Q

Describe abnormalities related to hypoparathyroidism

A
  • poor PTH secretion: reduced bone resorption/hypocalcemia
  • can supplement with calcium and Vit D
21
Q

Describe abnormalities related to hyperparathyroidism

A
  • excessive PTH secretion due to tumors and/or hypercalcemia
  • resection
22
Q

Describe Adrenocorticosteroids (ACTH)

A
  • Adrenal gland makes steroids in small doses
  • Cholesterol backbone
  • Glucocorticoids: cortisol/glucose metabolism; inflammation; immune system
  • Mineralcorticoids: aldosterone & fluid/electrolyte balance
23
Q

Describe glucocorticoids

A
  • Receptor binding: extra & intra cellular; DNA expression & protein synthesis
  • Increase in glucose: Liver - increased storage; Muscle/Adipose tissue - increased breakdown & decreased storage
  • Immune system suppression: decreased cytokine production & inflammatory markers, increased immature white blood cells
  • Local or systemic administration: joint injections, topical creams, & IV/Oral administration
24
Q

Adverse effects of Glucocorticoids

A
  • Adrencortical suppression
  • Connective tissue breakdown (muscles/tendons)
  • Peptic ulcers
  • Hypertension
  • Glucose control
  • Cushing syndrome (long term use)
25
Q

Adverse effects of Cushing syndrome

A
  • > 6mo on steroids
  • Moon face
  • Buffalo hump on back
  • Effects every system
  • Increased risk of bone fracture
  • Skin thinning
  • Adipose breakdown
  • Generalized: weight gain, slow healing of cuts, increased risk of infections, fatigue, & glucose intolerance
26
Q

Describe the pancreas

A
  • endocrine & exocrine gland (produces & excretes): digestive enzymes & insulin & glucagon
    -Cell types: α Glucagon; β Insulin; Δ Somatostatin (help tell the body you’re hungry); F Pancreatic polypeptide
  • Post-prandial: large rise in serum glucose, tissue mostly resistant to glucose (insulin facilitates transport intracellularly), hepatic tissue permeable (glycogen synthesis & phosphorylation
27
Q

Describe glycogenolysis

A
  • breakdown of glycogen
  • increases serum glucose levels
  • glucose broken down (glycolysis = pyruvate & ATP; Citric acid cycle = ATP)
28
Q

Describe gluconeogenesis via glucagon

A
  • Creation of glucose from non-sugars: amino acids, lactate, glycerol, & pyruvate
  • Lactate from anaerobic glycolysis due to exercise
  • Glycerol from adipose tissue: free fatty acids & glycerol
  • Amino acids: citric acid cycle
  • Balance with glycogen while supplies last
  • occurs after 12-14 hrs of starvation: gluconeogenesis is favored over glycogenolysis
  • slow not efficient process
29
Q

Describe glycolysis

A
  • glycogen stored in the liver is broken down into glucose via glycogenolysis
  • glucose in broken down = glycolysis
  • prioritization of use = glucose>glycogen>gluconeogenesis
30
Q

Medications used for pancreas issues/diabetes

A
  • Dextrose
  • Glucagon which can be administered via IM (intramuscular) shot
31
Q

What is the prevalence of diabetes and prediabetes

A
  • 1 in 10 people have diabetes and 1 in 5 of those people don’t know they have it
  • 1 in 3 people have pre diabetes and more than 8 in 10 of those people don’t know they have it
32
Q

Complications of diabetes

A
  • blindness
  • kidney failure
  • heart disease
  • stroke
  • neuopathy
33
Q

Treatment options for diabetes

A
  • Diet & exercise
  • Aspirin (bleeding risk)
  • ACE/ARB/Diuretics: “gold standard” (hypotension and act on the kidneys)
  • B-blocker: bradycardia
  • Insulin: hypoglycemia
34
Q

What are the 3 types of insulin

A
  • Short acting: mealtime insulin; 3x daily; Lispro (last 2-5hrs), Aspart (last 3-5hrs), & Glulisine (last1-2.5hrs)
  • Intermediate acting: Isophane; last up to 18-28hrs
  • Long acting: 1x daily; Detemir (last 6-24hrs) & Glargine (last 18-24hrs)
35
Q

Signs and symptoms of hypoglycemia

A
  • sweating
  • hunger
  • headache
  • blurred vision
  • extreme tiredness & paleness
  • dizziness
  • trembling
  • mood change
  • night sweats
  • tiredness at night
  • irritability upon waking
  • morning headache
36
Q

Symptoms of hyperglycemia (high blood sugar and very high blood sugar)

A
  • High: extreme thirst, frequent urination, headache, hunger, abdominal pain, blurry vision, warm/flushed skin, irritability
  • Very high/Diabetic Ketoacidosis: rapid/shallow breathing, vomiting, fruity breath
37
Q

How to monitor for low blood sugar (hypoglycemia)

A
  • Level 1 = 54-70 mg/dL; Level 2 = <54 mg/dL
  • Additional carbohydrate intake if <90 mg/dL; reduce re-exercise mealtime insulin
  • Check glucose at the end of each session
  • Rule of 15: 15g of carbs, check glucose in 15 minutes, repeat if <70 mg/dL