Endocrine System and Diabetes Pathophysiology: Q&A, Exams of Pathophysiology

A concise overview of endocrine system pathophysiology, focusing on hormone actions, imbalances, and related diseases such as hyperthyroidism, hypothyroidism, addison's disease, cushing's syndrome, and diabetes mellitus. It includes key concepts, diagnostic approaches, and treatment options, presented in a question-and-answer format suitable for study and review. The material covers hormone secretion mechanisms, adrenal gland functions, and the pathophysiology of diabetes, including dka and hhs. It also addresses microvascular and macrovascular complications of diabetes, offering a structured approach to understanding these complex topics. Useful for medical and nursing students.

Typology: Exams

2025/2026

Available from 11/12/2025

DrShirleyAurora
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Pathophysiology Module 9
endocrine, paracrine, autocrine -
endocrine: hormones are released into circulation to act on a target organ๎˜โ˜‘๏ธ๎˜‚
paracrine: hormones act locally on cells close to where they are released
autocrine: hormones produce a biologic action on the cell that released them
transport carriers on which hormones? -
peptide and protein hormones: unattached โ˜‘๏ธ๎˜‚
steroid hormones: carrier protein
what are the different structural types of hormones? -
amines and amino acids โ˜‘๏ธ๎˜‚
peptides and proteins
steroids, made from cholesterol
function of hypothalamus -
link between NS and endocrine โ˜‘๏ธ๎˜‚
regulates homeostasis, body temp, hunger, behavior. emotion, pain
produces releasing hormones which stimulate pituitary to release stimulating hormones
What is the role of the pituitary gland? -
"master gland," โ˜‘๏ธ๎˜‚
stimulates target organs to secrete their hormones
anterior pituitary hormones -
GH, ACTH, TSH, FSH, LH, prolactinโ˜‘๏ธ๎˜‚
posterior pituitary hormones -
ADH and oxytocinโ˜‘๏ธ๎˜‚
ways hormones can be oversecreted -
1. target gland over-secretes due to pathologyโ˜‘๏ธ๎˜‚
2. pituitary or hypothalamus over-stimulates target gland
3. hormones produced from different site (tumor)
4. hyperactive genetic mutation of target hormone receptors
ways decreased hormone secretion happens -
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Pathophysiology Module 9

endocrine, paracrine, autocrine -  โ˜‘๏ธ endocrine: hormones are released into circulation to act on a target organ paracrine: hormones act locally on cells close to where they are released autocrine: hormones produce a biologic action on the cell that released them transport carriers on which hormones? - โ˜‘๏ธ peptide and protein hormones: unattached steroid hormones: carrier protein what are the different structural types of hormones? - โ˜‘๏ธ amines and amino acids peptides and proteins steroids, made from cholesterol function of hypothalamus - โ˜‘๏ธ link between NS and endocrine regulates homeostasis, body temp, hunger, behavior. emotion, pain produces releasing hormones which stimulate pituitary to release stimulating hormones What is the role of the pituitary gland? - โ˜‘๏ธ "master gland," stimulates target organs to secrete their hormones anterior pituitary hormones - โ˜‘๏ธ GH, ACTH, TSH, FSH, LH, prolactin posterior pituitary hormones - โ˜‘๏ธ ADH and oxytocin ways hormones can be oversecreted - โ˜‘๏ธ 1. target gland over-secretes due to pathology

  1. pituitary or hypothalamus over-stimulates target gland
  2. hormones produced from different site (tumor)
  3. hyperactive genetic mutation of target hormone receptors ways decreased hormone secretion happens -

โ˜‘๏ธ 1. congenital or acquired disorder of target gland

  1. pituitary doesn't secrete enough stimulating hormone
  2. hypothalamus doesn't secrete enough releasing hormone
  3. hormone is defective
  4. receptors of target organ don't respond lab values in primary vs. secondary hyperthyroidism - โ˜‘๏ธ primary: low TSH (thyroid is secreting a lot of hormone without being told by the pituitary) secondary: high TSH (pituitary is over-secreting it) both: high T3 and T Graves: anti-TSH antibodies T3 and T4 functions - โ˜‘๏ธ regulates metabolism, protein synthesis, mental development, sexual maturity, growth and development THRH --> TSH --> T3 & T primary hyperthyroidism is seen in - โ˜‘๏ธ Grave's disease toxic nodule hyperthyroidism clinical presentation - โ˜‘๏ธ weight loss, increased appetite, tachycardia, dyspnea, heat intolerance, tremor, nervousness Grave's: ophthalmopathy, exophthalmos, pretibial myxedema, diffuse goiter, thyroid bruit hyperthyroidism diagnosis - โ˜‘๏ธ lab values of T3, T4, TSH radioiodine uptake test, thyroid scans and ultrasound fine needle aspiration for benign vs. malignant hyperthyroidism treatment - โ˜‘๏ธ beta blockers: for tachycardia and anxiety methimazole, propylthiouracil: decreased thyroid hormone synthesis thyroid can be removed (but can lead to hypothyroidism)

aldosterone function - โ˜‘๏ธ triggers reabsorption of sodium and secretion of K in kidneys secretion caused by RAA or hyperkalemia aldosterone deficiency causes - โ˜‘๏ธ 1. lack of RAA stimulus from kidney disease or drugs

  1. ACE inhibitors
  2. adrenal cortex not secreting aldosterone (adrenal insufficiency) adrenal insufficiency causes - โ˜‘๏ธ 1. primary dysfunction of adrenal gland - Addison's disease
  3. decreased ACTH stim. from pituitary (secondary)
  4. decreased CRH from hypothalamus (tertiary) Addison's disease pathology - โ˜‘๏ธ insufficient cortisol and aldosterone secretion, with elevated ACTH levels Addison's disease clinical presentation - โ˜‘๏ธ low mineralocorticoids: hyponatremia, water loss, hyperkalemia loss of fluid: dehydration, orthostatic hypotension, decreased CO, fatigue, weak, salt craving low cortisol: lethargy, hypoglycemia, N+V, lack of appetite, weight loss high ACTH: high melanocyte-stimulation hormones: hyperpigmented skin Addison's disease diagnosis - โ˜‘๏ธ low cortisol and aldosterone aldosterone can't be measured so we'll see: hyponatremia, hyperkalemia high ACTH: inject to see if it increases cortisol, otherwise it's a primary issue with adrenals themselves Addison's disease treatment - โ˜‘๏ธ cortisol replaced for life (hydrocortisone) aldosterone replaced for life (Fludrocortisone) regular mealtimes, seek treatment for illness right away Cushing's disease - โ˜‘๏ธ overproduction of cortisol Cushing's syndrome causes -

โ˜‘๏ธ 1. latrogenic from long-term steroid treatment

  1. over-secretion by one or both adrenal glands
  2. overstim. of adrenal glands by ACTH secreting tumor in pituitary (Cushing's disease)
  3. overstim. of adrenal glands by an ectopic ACTH producing tumor Cushing syndrome clinical presentation - โ˜‘๏ธ buffalo hump, abdominal obesity, moon face, muscle weakness, easy bruising, thin skin, edema, striae, osteoporosis, acne, hirsutism, women are masc., immunosuppression, diabetes, cognitive changes Cushing's syndrome diagnosis - โ˜‘๏ธ 24 hr urine for elevated free cortisol saliva in cortisol in evening dexamethasone suppression test ACTH levels hypokalemia, hypertension ACTH low vs. high in Cushing's syndrome - โ˜‘๏ธ if low: adrenal glands are hyper-secreting on their own if high: something is oversecreting, such as a tumor Cushing's syndrome treatment - โ˜‘๏ธ Iatrogenic- taper off steroids surgical removal or radiation of tumor insulin and glucagon functions - โ˜‘๏ธ Insulin moves glucose into cells to reduce blood sugar levels. Glucagon causes a release of glucose into the blood when levels are low. which cells secrete insulin - โ˜‘๏ธ beta cells of pancreas Glycogenesis, glycolysis, gluconeogenesis, glycogenolysis - โ˜‘๏ธ Glycogenesis: insulin released, glucose taken up into the cells and stored as glycogen Glycolysis: glucose broken down for energy Gluconeogenesis: glucose formation Glycogenolysis: breakdown of glycogen to release glucose What is insulin resistance? -

oral antidiabetics - โ˜‘๏ธ WRITE DOWN insulin hypoglycemia - โ˜‘๏ธ <60 blood sugar, cognitive problems side effect of insulin therapy treat with 15-20 g glucose