extra Flashcards

1
Q

What is Levothyroxine (T4)?

A

Synthetic form of thyroid hormone; converted to T3 in the body.

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2
Q

What are the actions of Levothyroxine (T4)?

A

Increases metabolism, regulates growth, and energy production.

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3
Q

What are common side effects of Levothyroxine (T4)?

A

Hyperthyroid symptoms (tachycardia, insomnia, weight loss); cardiac events (arrhythmias at high doses).

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4
Q

What are Glucocorticoids?

A

Prednisone, Hydrocortisone: Mimic cortisol action.

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5
Q

What are the actions of Glucocorticoids?

A

Reduce inflammation, suppress the immune response, increase glucose production.

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6
Q

What are common side effects of Glucocorticoids?

A

Osteoporosis, weight gain, moon face, high BP, hyperglycemia, infection risk; long-term use: adrenal suppression.

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7
Q

What is Fludrocortisone?

A

Mimics aldosterone; regulates sodium and potassium balance.

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8
Q

What are the actions of Fludrocortisone?

A

Controls blood volume, pressure, and electrolyte balance.

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9
Q

What are common side effects of Fludrocortisone?

A

Hypertension, edema, hypokalemia, alkalosis.

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10
Q

What is Hormone Replacement Therapy (HRT)?

A

Estrogen & Progesterone: Treat menopausal symptoms (hot flashes, vaginal dryness).

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11
Q

What are the actions of Hormone Replacement Therapy (HRT)?

A

Protects bone density, alleviates symptoms.

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12
Q

What are common side effects of Hormone Replacement Therapy (HRT)?

A

Breast tenderness, nausea, headaches, VTE, breast cancer risk (long-term use).

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13
Q

What is the treatment for Hypothyroidism?

A

Levothyroxine (T4): Replaces thyroid hormone.

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14
Q

What is the impact of treating Hypothyroidism?

A

Corrects metabolic imbalance, alleviates symptoms like fatigue, weight gain, cold intolerance.

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15
Q

What is the treatment for Hyperthyroidism?

A

Methimazole, Propylthiouracil: Inhibit thyroid hormone production; radioactive iodine: Ablates thyroid tissue.

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16
Q

What is the impact of treating Hyperthyroidism?

A

Reduces thyroid hormone levels, normalizes metabolism.

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17
Q

What is the treatment for Adrenal Insufficiency (Addison’s Disease)?

A

Hydrocortisone (glucocorticoid) and Fludrocortisone (mineralocorticoid).

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18
Q

What is the impact of treating Adrenal Insufficiency?

A

Restores cortisol and aldosterone, reduces symptoms like fatigue, weight loss, hypotension.

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19
Q

What is the treatment for Cushing’s Syndrome?

A

Ketoconazole, Mitotane: Suppress cortisol production; surgical removal of tumors if necessary.

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20
Q

What is the impact of treating Cushing’s Syndrome?

A

Reduces excess cortisol, normalizes metabolism, and alleviates symptoms like weight gain, hyperglycemia, osteoporosis.

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21
Q

What is the treatment for Osteoporosis?

A

Bisphosphonates (e.g., alendronate), SERMs, calcitonin, Denosumab.

22
Q

What is the impact of treating Osteoporosis?

A

Prevents bone resorption, increases bone density, reduces fracture risk.

23
Q

What is the mechanism of Insulin?

A

Facilitates glucose uptake by cells.

24
Q

What are the actions of Insulin?

A

Lowers blood glucose and regulates fat/protein metabolism.

25
Q

What are common side effects of Insulin?

A

Hypoglycemia, weight gain, injection site reactions.

26
Q

What is Metformin (Biguanide)?

A

Reduces hepatic glucose production and increases insulin sensitivity.

27
Q

What are common side effects of Metformin?

A

Gastrointestinal issues (nausea, diarrhea), lactic acidosis (rare), B12 deficiency.

28
Q

What are Sulfonylureas?

A

Stimulate insulin secretion from pancreatic beta cells.

29
Q

What are common side effects of Sulfonylureas?

A

Hypoglycemia, weight gain, rash.

30
Q

What are DPP-4 Inhibitors?

A

Inhibit DPP-4 enzyme, enhancing incretin effect (increases insulin and reduces glucagon secretion).

31
Q

What are common side effects of DPP-4 Inhibitors?

A

Upper respiratory infections, headaches, gastrointestinal discomfort.

32
Q

What are GLP-1 Receptor Agonists?

A

Mimic GLP-1, enhancing insulin secretion and reducing glucagon release.

33
Q

What are common side effects of GLP-1 Receptor Agonists?

A

Nausea, vomiting, diarrhea, pancreatitis (rare).

34
Q

What are SGLT2 Inhibitors?

A

Inhibit SGLT2, preventing glucose reabsorption and promoting excretion in urine.

35
Q

What are common side effects of SGLT2 Inhibitors?

A

UTIs, genital infections, dehydration, hypotension, ketoacidosis (rare).

36
Q

What is the management for Type 1 Diabetes?

A

Insulin therapy: Basal-bolus regimens (long-acting insulin for basal coverage, rapid-acting insulin for meals).

37
Q

What is the goal for managing Type 1 Diabetes?

A

Tight glycemic control.

38
Q

What is the management for Type 2 Diabetes?

A

Metformin first-line; add-on therapy: Sulfonylureas, DPP-4 inhibitors, GLP-1 agonists, and SGLT2 inhibitors.

39
Q

What is the goal for managing Type 2 Diabetes?

A

Improve insulin sensitivity, control blood glucose, prevent long-term complications.

40
Q

What are the adverse effects of diabetic medications?

A

Insulin & Sulfonylureas: Hypoglycemia, weight gain; Metformin: Lactic acidosis (rare), GI issues; GLP-1 Agonists: Nausea, vomiting; SGLT2 Inhibitors: UTIs, ketoacidosis (rare).

41
Q

What drug interactions can affect diabetes management?

A

Corticosteroids, Beta-blockers, Thiazide diuretics: Can increase blood glucose levels; Alcohol: May increase hypoglycemia risk with insulin.

42
Q

What is the role of the hypothalamus in regulating pituitary hormone secretion?

A

The hypothalamus releases releasing hormones (e.g., TRH, CRH, GnRH, GHRH) and inhibiting hormones (e.g., somatostatin, dopamine) to control the secretion of pituitary hormones.

43
Q

What is an example of the hypothalamus’s role in hormone regulation?

A

TRH stimulates the release of TSH from the pituitary, which in turn regulates thyroid function.

44
Q

What are the mechanisms and causes of endocrine hypofunction and hyperfunction?

A

Hypofunction: Due to gland destruction, autoimmune conditions, or insufficient stimulation from the hypothalamus/pituitary (e.g., Addison’s disease, hypothyroidism); Hyperfunction: Caused by tumors, hyperplasia, or genetic mutations that increase hormone production (e.g., Cushing’s syndrome, Graves’ disease).

45
Q

What are the types of pituitary tumors and their effects on endocrine function?

A

Adenomas: Most common pituitary tumors, can be functioning (secreting hormones) or non-functioning (no hormone secretion); Prolactinomas: Overproduction of prolactin, leading to galactorrhea and hypogonadism; Corticotroph adenomas: Overproduction of ACTH, leading to Cushing’s syndrome.

46
Q

What are the clinical features, causes, and consequences of hypopituitarism?

A

Clinical Features: Fatigue, weight loss, cold intolerance, decreased libido, infertility, adrenal insufficiency, and growth retardation; Causes: Tumors, trauma, infections, autoimmune diseases, or genetic defects; Consequences: Impaired function of target glands (thyroid, adrenal, gonads), and growth failure in children.

47
Q

What are the manifestations of growth hormone deficiency and excess in children and adults?

A

Deficiency in Children: Short stature, delayed puberty, and growth retardation; Excess in Children: Gigantism (abnormal growth of long bones); Deficiency in Adults: Reduced muscle mass, increased fatigue, and low bone density; Excess in Adults: Acromegaly (enlargement of hands, feet, and facial features).

48
Q

What hormones are produced by the adrenal cortex?

A

Cortisol, aldosterone, and androgens.

49
Q

How is feedback regulation managed for adrenal hormones?

A

Cortisol is regulated by ACTH from the pituitary, which is controlled by the hypothalamus through CRH; Aldosterone secretion is influenced by angiotensin II, K+ levels, and ACTH.

50
Q

What are the stages of adrenal cortical insufficiency and their clinical significance?

A

Primary Adrenal Insufficiency (Addison’s disease): Deficiency in cortisol and aldosterone; caused by autoimmune destruction of adrenal glands; Secondary Adrenal Insufficiency: Due to pituitary failure (low ACTH levels); Acute Adrenal Crisis: Severe cortisol deficiency, characterized by hypotension.