Endocrine System

Question 1

Negative feedback

Answer 1

product suppresses its own pathway (T3/T4 suppresses TRH/TSH)

Question 2

Positive feedback

Answer 2

product amplifies its own pathway (oxytocin in labor)

Question 3

autocrine signaling

Answer 3

cell sends signal to self

Question 4

paracrine signaling

Answer 4

cell sends signal to neighboring cell

Question 5

endocrine signaling

Answer 5

bloodstream is used for signal to reach distant target

Question 6

direct effects of hormones

Answer 6

hormone triggers effect - specific stimulation (insulin binds to insulin receptor, glucose uptake increases)

Question 7

permissive effects of hormones

Answer 7

increases responsiveness to another hormone; primes response (estrogen increased progesterone receptor expression in endometrium)

Question 8

downregulation of hormone receptors

Answer 8

when a hormone is persistently high, the cell makes fewer receptors so the same dose has less effect over time (beta 2 agonist overuse in asthma: frequent albuterol use -> B2 receptor down regulates on airway smooth muscle -> each puff bronchodilates less)

Question 9

upregulation of hormone receptors

Answer 9

when a hormone is consistently low, the cell makes more receptors to “listen harder” - sensitivity increases (hypothyroid: body’s tissues are under-stimulated; reduced negative feedback makes pituitary drive TSH up to push thyroid harder)

Question 10

Hypothalamic pituitary axis

Answer 10

system that links nervous and endocrine systems to regulate stress response, metabolism, and other functions through series of hormonal signals

Question 11

anterior pituitary

Answer 11

AKA adenohypophysis
hypothalamus sends releasing/inhibiting hormones thru a portal blood system (TSH, ACTH, GH, LH/FSH, prolactin)

Question 12

posterior pituitary

Answer 12

AKA neurohypophysis
hypothalamic neurons make ADH & oxytocin and send them down axons in the hypothalamo-hypophyseal tract (connection btwn hypothalamus & pituitary gland) and release them from the posterior pituitary when action potentials fire
-axons -> posterior pituitary (releases ADH, oxytocin made in hypothalamus)

Question 13

adrenal gland structure

Answer 13

cortex: outer layer
medulla: inner core

Question 14

adrenal cortex structure & function

Answer 14

steroid factory
-zona glomerulosa (aldosterone - salt)
-zona fasciculata (cortisol & glucose - sugar)
-zona reticularis (sex hormones)

Question 15

adrenal medulla function

Answer 15

alarm center; nerve signal from sympathetic system flips medulla on & epinephrine surges, heart/lungs/energy kick into high gear to respond NOW

Question 16

pathology of SIADH

Answer 16

-inappropriate antidiuretic hormone secretion
-disease of posterior pituitary
-cause: excess ADH (makes collecting ducts water-permeable -> free-water retention, diluted plasma & concentrated urine)
-headache, N, cramps, confusion, lethargy, hyponatremia
-water in blood, salt in urine

Question 17

pathology of diabetes insipidus

Answer 17

-insufficient amounts of ADH
-disease of posterior pituitary
-can’t hold water: polyuria, polydipsia, dehydration, high osmolality & hypernatremia, dilute urine, SG low
-kidneys fail to concentrate urine; lose free water, extreme thirst

Question 18

Acromegaly

Answer 18

-GH hypersecretion (adenoma: noncancerous tumor in adrenal glands)
-adults develop coarse facial features, enlarged hands/feet & tongue, hyperhidrosis - excessive sweating
-causes insulin resistance
-gigantism occurs w excess GH before epiphyseal closure (in kids)

Question 19

cushing syndrome

Answer 19

-disorder of adrenal cortex
-pituitary adenoma causing hypersecretion of ACTH -> adrenal cortisol excess
-central obesity, thin arms/legs (muscle loss)
-thin/frail skin, easy bruising, slow wound healing
-insulin resistance/diabetes, HTN, osteoporosis, mood/sleep changes

Question 20

hyperthyroidism

Answer 20

cause: Graves, toxic nodules/goiter, thyroiditis, excess exogenous hormone
labs: high T3/T4, suppressed TSH, radioactive iodine uptake test high in Graves/toxic nodules
clinical: tachy, heat intolerance, goiter, fast metabolism!

Question 21

hypothyroidism

Answer 21

cause: hashimoto autoimmune thyroiditis, iodine deficiency, postpartum thyroiditis
labs: low T3/T4, high TSH
clinical: brady, cold intolerance, dry skin/brittle hair, slow metabolism!

Question 22

characteristics of hashimoto’s disease

Answer 22

autoimmune, progressive destruction of thyroid; thyroid autoantibodies; may include transient hyperthyroid phase followed by hypothyroid

Question 23

compare/contrast hyper vs. hypothyroidism

Answer 23

hyper: anxiety, heat intolerance, sweating, palpitations, weight loss, tremor, fast metabolism
hypo: fatigue, cold intolerance, weight gain, dry skin, constipation, brady, myxedema w chronic disease, slow metabolism

Question 24

hypocortisolism

Answer 24

-primary: addison’s, autoimmune adrenalitis, symptoms after ~90% cortical destruction; fatigue, hyperpigmentation, anorexia/GI upset, salt craving, hyperkalemia
-secondary: prolonged exogenous steroid administration; exogenous glucocorticoids suppress ACTH -> adrenal atrophy; potential recovery w taper/cessation

Question 25

type 1 diabetes mellitus

Answer 25

autoimmune B-cell destruction -> absolute insulin deficiency glucagon: unopposed (a-cells keep firing) -> high lipolysis -> ketogenesis insulin sensitivity: usually intact sensitivity; problem is no insulin C-peptide: low/undetectable at/after diagnosis

Question 26

type 2 DM

Answer 26

insulin resistance (muscle/adipose/liver) & B-cell dysfunction (progressive secretory failure) liver: inappropriate hepatic glucose output (gluconeogenesis despite hyperglycemia) adipose/muscle: ectopic fat, lipotoxicity, inflammation -> impaired insulin signaling C-peptide: normal/high early (compensatory), then falls w B cell burnout

Question 27

acute complications of DM

Answer 27

hypoglycemia in DM usually caused by treatment triggers: late meals, extra exercise, alcohol, renal/hepatic impairment diabetic ketoacidosis: gap acidosis+ketones, glucose not necessarily extreme hyperosmolar hyperglycemic state: extreme hyperglycemia+hyperosmolarity, no significant ketosis

Question 28

chronic complications of DM

Answer 28

microvascular: retinopathy, nephropathy, neuropathy macrovascular: HTN, CAD, PVD, stroke, infections/poor wound healing

Question 29

physiologic differences btwn type 1 & 2 DM

Answer 29

type 1: onset - days to weeks; any age (often childhood/young adult) body type - lean/normal first presentation - polyuria, polydipsia, weight loss, fatigue; DKA is common at or before diagnosis type 2: onset - insidious (months to years), often found on screening body type - overweight/obese, acanthosis nigricans (hyperpigmentation in parts of skin) first presentation: polyuria/polydipsia, blurred vision, fatigue

Question 30

How do symptoms of hyperglycemia differ in type 1 vs 2

Answer 30

type 1: develops quickly, weight loss, ketosis/DKA common (absolute insulin lack -> lipolysis -> ketones -> metabolic acidosis) type 2: symptoms develop slowly over time, no ketosis BOTH: frequent urination, excessive thirst, fatigue, blurred vision, nocturia

Question 31

How do symptoms of hypoglycemia differ in type 1 vs 2?

Answer 31

type 1: occurs bc exogenous insulin, mismatched insulin/carbs, exercise, illness type 2: less common (unless on insulin) BOTH: low plasma glucose -> autonomic warning -> neuroglycopenia if untreated; tremor, palpitations, anxiety, sweating, hunger, tingling, confusion, slowed thinking, blurred vision, seizures, coma

Question 32

DKA and HHNK with diabetes

Answer 32

DKA: diabetic ketoacidosis; more common in T1D (total insulin deficiency) & involves high blood sugar w fat breakdown for energy, produces acidic ketones HHNK: hyperosmolar hyperglycemic nonketotic syndrome; more common in T2D - high blood sugar & severe dehydration w/o DKA, enough insulin to prevent ketosis

Question 33

Thyrotropin-releasing hormone (TRH) -> source, stimuli, targets, actions

Answer 33

source: hypothalamus stimuli: cold, stress, circadian input, low T3/T4, low metabolic rate targets: anterior pituitary thyrotrophs actions: stimulates TSH secretion

Question 34

Thyroid-stimulating hormone (TSH) -> source, stimuli, target, actions

Answer 34

source: anterior pituitary stimuli: TRH, low circulating T3/T4 targets: thyroid follicular cells actions: increases iodine uptake & thyroid hormone release; promotes thyroid growth

Question 35

What do high amounts of T3/T4 do to TRH/TSH?

Answer 35

suppress - negative feedback

Question 36

oxytocin -> source, stimuli, targets, actions

Answer 36

source: hypothalamus, released from posterior pituitary stimuli: nipple suckling, cervical stretch, psychological stimuli (infant crying) targets: breast myoepithelial cells, uterine myometrium actions: milk ejection, uterine contractions; positive feedback in labor

Question 37

Calcitonin -> source, stimuli, target, actions

Answer 37

source: thyroid parafollicular cells stimuli: high serum calcium target: bone (osteoclasts), kidney (minor) actions: reduced bone resorption to lower serum Ca2+; antagonizes PTH

Question 38

parathyroid hormone (PTH) -> source, stimuli, targets, actions

Answer 38

source: parathyroid chief cells stimuli: low Ca2+, high phosphate, low calcitriol targets: bone (osteoclast activation), kidney (increase Ca2+ reabsorption, decreases phosphate reabsorption), GI tract (vitamin D) actions: increases serum Ca2+, decreases serum phosphate, activates vitamin D production (calcitriol) -> resorted Ca2+ suppresses PTH

Question 39

glucagon -> source, stimuli, target, actions

Answer 39

source: pancreatic a cells stimuli: low glucose, amino acids, SNS (B receptors), stress target: liver, adipose tissue actions: increases glycogenolysis, gluconeogenesis, lipolysis, ketogenesis -> inhibited by insulin, somatostatin, high glucose

Question 40

insulin -> source, stimuli, targets, actions

Answer 40

source: pancreatic B cells stimuli: high glucose, incretins, amino acids, vagal acetylcholine targets: muscle, adipose, liver actions: increases glucose uptake, glycogen/lipid/protein synthesis, reduces hepatic glucose output, promotes potassium uptake into cells -> inhibited by SNS a2 receptors, somatostatin

Question 41

amylin -> source, stimuli, targets, actions

Answer 41

source: pancreatic B cells (cosecreted w insulin) stimuli: meal ingestion (co-released w insulin) targets: GI tract, pancreatic a-cells, CNS satiety centers actions: delays gastric emptying, reduces glucagon release after meals, increases satiety

Question 42

glucocorticoids (cortisol) -> source, stimuli, targets, actions

Answer 42

source: adrenal cortex stimuli: ACTH (driven by Corticotropin RH, stress, circadian rhythm) target: liver, muscle, adipose, immune cells, vasculature action: increases gluconeogenesis, antagonizes insulin, promotes protein/fat catabolism, anti-inflammatory, maintains vascular tone

Question 43

mineralocorticol (aldosterone) -> source, stimuli, targets, actions

Answer 43

source: adrenal cortex stimuli: RAAS (angiotensin II), high K+, ACTH targets: kidney distal nephron, colon, sweat glands actions: increases Na+/H2O reabsorption, K+/H+ secretion; raises extracellular volume and blood pressure