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)
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
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.
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)
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
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
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
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
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
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)
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
12
Q
Describe Graves disease
A
- hyperthyroid disease
- autoimmune disorder
- rapid/irregular HR
- osteoporosis
- muscle weakness
- vision changes
- weight loss
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
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)
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
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
