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Physiology > Endocrinilogy > Flashcards

Endocrinilogy Flashcards

1
Q

Glands of the endocrine system

A
  1. pituitary gland
  2. Hypothalamus
  3. Thyroid gland
  4. Parathyroid glands
  5. Adrenal glands
  6. Pancreas
  7. Gonads
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2
Q

low-density lipoproteins (LDLs)

A
  • carriers of cholesterol in plasma
  • stores cholesterol until needed, and moves it into the cell and undergoes steroid biogenesis
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3
Q

Pregnenolone

A

An intermediate of cholesterol during steroid biogenesis. Will be further modified into different steroid molecules and will become a steroid hormone.

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4
Q

Diurnal secretion

A

having a 24 hour period or cycle, daily

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5
Q

Sensitization

A

an increase in the affinity of a receptor to a hormone

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6
Q

Hypophysis

A
  • the pituitary gland at the ventral part of the brain
  • just below hypothalamus
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7
Q

Adenohypophysis vs Neurohypophysis

A
  • neuropophysis: posterior = neural tissue, downgrowth tissue from brain
  • adenoypophysis: anterior = non neural tissue, tissue from invagination of the roof of the mouth, called the hypophyseal pouch/ Rathke’s pouch
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8
Q

What produces the hormones that are secreted by the posterior pituitary?

A

hypothalamus

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9
Q

Infundibulum

A

pituitary stock that contains the axons of the neurons in the hypothalamus and blood vessels. End in the posterior pituitary to release hormones

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10
Q

Posterior pituitary hormones

A

Protein hormones translated from pre-prohormones
1. ADH/vasopressin: produced from supraoptic nuclei (SON) from the hypothalamus
2. Oxytocin: produced from the paraventricular nuclei of the hypothalamus

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11
Q

ADH/vasopressin

A
  • pro-prohormone is first translated to pro-pressophysin, then converted to ADH
  • causes vasoconstriction action during blood loss (hemorrhage)
  • has anti-diuretic actions to control fluid balance in body by reducing urination and increasing permeability of renal collecting ducts (adds aquaporin 2) and reducing the glomerular filtration rate
  • stimuli is high blood osmolarity or low blood volume
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12
Q

ADH deficiency

A
  • diabetes insipidus
  • hypothalamic/central diabetes insipidus: problem with ADH production
  • nephrogenic diabetes insipidus: problem of ADH action
  • polyuria: production of lare amounts of dilute urine
  • polydipsie: excessive thirst and fluid intake
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13
Q

Excess ADH syndrom

A
  • Syndrome of inappropriate ADH (SIADH)
  • feedback failure of ADH production
  • excess ADH production
  • increased water retention and decreased sodium reabsorption (decreased aldosterone secretion)
  • hypoantremia: low blood sodium levels
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14
Q

Oxytocin

A
  • released from posterior pituitary, produced from the paraventricular nuclei in the hypothalamus
  • stimulates milk let down, helps movement of sperm in female tract, and clamps ruptured blood vessels to prevent hemorrhage
  • positive feedback loop
  • problems with deficiency, but no problems with excess
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15
Q

Hypothalamo-hyposphyseal portal vessels

A
  • venous/portal vessels that run into the anterior pituitary
  • rise from median eminence-capillary bed
  • carry secretions from hypothalamus
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16
Q

Nuclei of the hypothalamus

A
  1. Parvocellular neurons: small cell bodies with short axons. Axons end in the median eminence which carry secretions into anterior pituitary
  2. Magnocellular neurons: among the largest cells in the brain. Synthesize oxytocin and ADH (made of PVN and SON nuclei)
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17
Q

Hormones of the Anterior Pituitary gland

A
  1. Gonadotropins: tropic hormones that stimulate growth and gonad activity (LH and FSH)
  2. Growth hormone: stimulates growth
  3. Thyroid-stimulating hormone: stimulates thyroid gland
  4. Prolactin: milk formation and acts on gonads
  5. Adrenocorticotropin (ACTH): acts on the adrenal gland
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18
Q

Hypothalamic-releasing hormones on anterior pituitary gland

A
  1. GnRH: stimulates release of LH or FSH
  2. GHRH: stimulates release of growth hormone
  3. TRH: stimulates release of TSH and prolactin
  4. PRFs: stimulates release of prolactin
  5. CRH: stimulates ACTH release
  6. SRIF: inhibits GH and TSH release
  7. PIF: inhibits TSH and prolactin (example: dopamine)
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19
Q

Growth Hormone (GH)

A
  • effects on muscle, liver, and adipose tissue
  • in muscles and liver, induces protein synthesis, anabolic action
  • in adipose tissue, induces lipolysis (breakdown of fats)
  • increase tissue growth of soft tissue and bone by somatodins
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20
Q

When is GH release the highest?

A

When it’s dark and during sleep

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21
Q

What is GH produced by?

A

somatotroph cells in the anterior pituitary gland

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22
Q

GH deficiency effects

A
  • dwarfism in juveniles
  • somatopause in adults (gradual decrease that occurs normally with age)
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23
Q

Types of dwarfism from GH deficiency

A
  1. Isolated growth hormone deficiency (Type 1): defect in GH production
  2. Laron-type: defect in GH action because of problems with receptors (IGF-1levels defects)
    - normal body proportions for age, and no intellectual disability
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24
Q

Acromegaly

A
  • GH excess in adults
  • no growth in height, but growth in the bones of the face, hands, feet, and cartilage
  • protruding jaw (prognathism)
  • hirsutism
  • gynecomastia (enlarged breast tissue in men)
  • increased release of glucose which leads to diabetes
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25
Q

Prolactin-releasing factors

A
  • TRH and oxytocin
  • gonadal steroid hormones: estrogen increases, progesterone inhibits
    mammary suckling
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26
Q

Excess prolactin

A
  • hyperprolactinemia
  • gonadal dysfunction
  • amenorrhea (lack of menustration)
  • reduced libido
  • treated with dopamine agonist to prevent PRL inhibition
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27
Q

Prolactin deficiency

A
  • hypoprolactinemia
  • gonadal dysfunction
  • impairment of lactation
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28
Q

Hyperglycemia, Hypopituitarism, Panhypopituitarism

A
  • Hyperglycemia: excess of all anterior pituitary hormones. Results in pituitary diabetes
  • Hypopituitarism: deficiency in one or more pituitary hormones
  • panhypopituitarism: deficiency in all pituitary hormones
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29
Q

Thyroid gland hormones

A
  1. T3
  2. T4
    They increase metabolic rate and heat production, enhance growth and CNS development and enhance sympathetic activity. They provide feedback inhibition at anterioir pituitary and hypothalamus levels (regulate TSH secretion by inhibiting TRH and TSH)
30
Q

TSH

A
  • peptide hormone produced by anterior pituitary cells called thyrotrophs
  • stimulates growth of the thyroid gland
  • trophic hormone: has effects on growth, nutrition, nd function of target tissue (thyroid gland)
  • belongs to group of pituitary hormone called glycoprotein hormones (contain sugar residues and have 2 subunits: alpha and beta. Beta subunit is the biologically active one)
31
Q

The basic unit of the thyroid gland?

A

Follicle (secretory parts), filled with protein-rich substance (colloid made of thyroglobulin) (colloid shrinks when gland is active)

32
Q

Thyroglobulin

A
  • precursor for thyroid hormone biosynthesis
  • glycoprotein
  • synthesized in the follicle cells of the rough endoplasmic reticulum
  • contains tyrosine residues as a template for thyroid hormones
  • NOT a thyroid hormone binding protein
33
Q

The thyroid hormone binding proteins

A
  1. TBG (most important): binds T3 and T4
  2. TBA: binds T3 and T4
  3. TBPA: binds T4 only
34
Q

What breaks down T3 to make it biologically inactive?

A

deiodinases

35
Q

Thyroid hormone excess

A
  • hyperthyroidism
  • increased basal metabolic rate
  • primary problem: thyroid gland (t3/T4)
  • secondary problem: pituitary gland (TSH)
  • tertiary problem: hypothalamus (TH)
  • Grave’s disease (most common): antibodies develop against TSH receptors (LATS antibodies). Large goiter in neck and overstimulation of thyroid gland, bulging of the eyes
36
Q

The 2 adrenal glands

A
  1. Adrenal cortex: produces the steroid hormones. Outer part of adrenal gland
  2. Adrenal Medulla
36
Q

Thyroid hormone deficiency

A
  • hypothyroidism
  • decreased metabolic rate
  • causes: deficiency in iodine (dietary), problems with thyroid gland (primary dysfunction)
  • Hashimo’s thyroiditis: antibodies develop against T3//T4 or thyroglobulin
  • Secondary/tertiary hypothyroidism: low levels of TSH and TRH. Atrophic thyroid glands (reduced in size, no goiter)
  • cretinism in utero
  • myxedema in adults
  • bradycardia
37
Q

Adrenal cortex hormones

A
  • steroid hormones
  • cortisol: the only adrenal hormone that provides feedback inhibition (at level of anterior pituitary and hypothalamus)
  • steroid intermediates: corticosteroids, androstenedione, and DHEA
  • DHEA and androstenedione are androgenic hormones
38
Q

Corticotrophin-releasing hormone (CRH)

A
  • produced by the hypotalamus
  • stimulates anterior pituitary to produce ACTH, which stimulates steroidogenesis in the adrenal cortex
  • CRH is potentiated in the presence of ADH to induce ACTH release
39
Q

ACTH

A
  • produced by corticotroph cells in the anterior pituitary gland
  • peptide hormone
  • trophic hormone as it stimulates adrenal blood flow, adrenal growth, and adrenal steroidogenesis
40
Q

POMC processing

A
  • ACTH and B-LPH are made from POMC
  • ACTH produce a-MSH (involved in pigmentation)
  • B-LPH produces B-MSH (also stimulates pigment)
  • B-LPH also gives rise to B-endorphins (opiate molecule)
  • ACTH and opiates are produced during stress
41
Q

Adrenal cortex zones

A
  1. Glomerular zone: outer zone. Produces Aldosterone. No metabolism
  2. Fascicular zone: middle zone, produces cortisol. Intermediate metabolism
  3. Reticular zone: inner zone, produces androgens. Sex characteristics
42
Q

Aldosterone

A
  • steroid hormone
  • upregulated proteins that move Na+ into the collecting duct cells (Na+ reabsorption)
  • result in increased Na+ channels in the luminal membrane and activate Na+/K+ ATPase
  • Stimulated by increased plasma K+ and Angiotensin II, to excrete K+ and retention of Na+
  • works to restore water and electrolyte balance
43
Q

Conn’s Syndrome

A
  • Excess aldosterone
  • increased Na+ retention and decreased K+ uptake into renal tubule
  • causes hypertension (volume excess)
  • causes alkalosis (increased urinary loss of K+)
44
Q

Cortisol

A
  • stimulates gluconeogenesis in the liver (anabolic)
  • increases blood glucose
  • glucocorticoid actions (glucose + cortex + steroid): regulation of glucose metabolism, synthesized in the adrenal cortex, steroid
  • prevents inflammation and autoimmunity during stress and provides energy source
  • stress stimulates hypothalamus to produce CRH, which acts on ant pituitary to release ACTH, and therefore adrenal cortex to release cortisol (then cortisol provides feedback inhibition)
  • levels of cortisol are highest first thing in the morning and during sleep, then fall throughout the day
45
Q

Adrenal insufficiencies

A
  • Primary: Addison’s disease. Defect in adrenal cortex. No feedback inhibition therefore high ACTH and increased skin pigmentation from POMC activity. Causes hypoglycemia (no gluconeogenesis), hypoantremia (low Na+ in blood), and hypovolemia )low blood volume), and hyperkalemia/hypotension (from high blood K+)
  • Secondary: defect at anterior pituitary. No ACTH i produced and will not stimulate adrenal cortex to produce cortisol. No increased POMC activity
46
Q

Cushing’s syndrom

A
  • prolonged exposure to cortisol
  • causes: pituitary tumor (high ACTH), adrenal tumor (high cortisol), ectopic tumor (produce ACTH and is not inhibited from feedback)
  • moon face
  • buffalo hump (fat deposit on back)
  • hirsutism
47
Q

DHEA

A
  • weak androgen that can be converted to testosterone or estrogen in other tissues
  • responsible for secondary sexual characteristics
  • produced by adrenal cortex
  • produced when pathways to cortisol and aldosterone are blocked
48
Q

Adrenogential Syndrome

A
  • pathway that makes aldosterone and cortisol are deficient, and all precursors end up making DHEA
  • results from excess androgens in adrenal cortex
  • in females, it causes masculinization of genitals
  • in males: pseudopuberty
49
Q

Hormones that regulate calcium

A
  1. Hypercalcemic hormones (increase calcium in blood): parathyroid hormone (PTH) and Vitamin D3
  2. Hypoglycemic hormone (decrease blood calcium): Calcitonin (CT)
50
Q

Effect of parathyroid hormones

A
  • secreted by chief cells
  • increase plasma calcium
  • decrease plasma phosphate
  • target sire in kidney, bone, and GIT
51
Q

Hyperparathyroidism

A
  • high PTH and Ca and Vitamin D3, low PO4
  • soft tissue calcification (kidney stones)
  • weak bones (bone resorption)
  • GIT dysfunction
  • primarily caused by problems with parathyroid gland (high PTH)
  • secondary caused by low calcium that stimulate PTH, under rickets (juveniles) and osteolmalacia (adults) from impaired uptake from GIT and renal reabsorption failure
52
Q

Hypoparathyroidism causes

A
  • primary: low PTH from parathyroid
  • increase in neuromuscular activity since the threshold for excitation is lowered
  • tetany
  • asphyxia and death (tetanic spasms in bronchial tubes in the resp system, leading to problems breathing)
53
Q

Trousseau’s sign

A
  • hypoparathyroidism
  • involuntary contraction of the carpal muscles, due to hypocalcemia and tetany
54
Q

Chvostek’s sign

A
  • hypocalcemia
  • sign is tapping nerve along the cheek
  • tetany and snarl
55
Q

Pseudohypoparathyroidism

A
  • hypoparathroidism
  • tissue insensitivity to PTH action
56
Q

Calcitonin

A
  • peptide hormone
  • opposes PTH
  • produced by parafollicular cells (C-cells) in the thyroid gland connective tissue
  • lowers plasma calcium and phosphate
  • GIT is a major site of calcitonin action
  • used to treat postmenopausal osteoporosis (in the absence of estrogen, PTH action is not antagonized, so calcitonin is needed)
  • treatment for Padget’s disease
57
Q

Vitamin D3

A
  • steroid hormone that regulates plasma calcium and phosphate levels
  • main synthesis is in the skin from cholesterol in the liver then in kidney, then final conversion in the skin
  • raises both Ca2+ and PO3 reabsorption
  • main calcium absorption effects are in the GIT
58
Q

Rickets

A
  • deficiency in vitamin D3
  • found in juveniles
  • low calcium, poor bone formation, high bone resorption
59
Q

Pancreas

A
  • exocrine + endocrine gland (regulates blood sugar)
  • endocrine is found in the Islets of Langerhans
60
Q

Pancreas Islet cells

A
  1. Alpha cells: secrete glucagon
  2. Beta (most abundant): secrete insulin
  3. Delta: somatostatin (hypothalamic releasing factor that inhibits growth hormone and TSH. Made in hypothalamus and pancreas)
61
Q

Paracrine interactions in pancreatic islets

A
  • delta cells inhibit alpha and beta cells
  • beta cells inhibit alpha cells
  • alpha cells stimulate beta and delta cells
62
Q

Sympatheitc and parasympathetic effects on pancreas

A
  • sympathetic: high glucagon, low insulin
  • parasympathetic: high insulin, high glucagon
63
Q

insulin vs glucagon

A
  • insulin: for feasting. Anabolic. Lowers blood glucose
  • glucagon: for fasting. Catabolic. Breakdown of stored energy
64
Q

Structure of insulin

A
  • begins as single amino acid chain called proinsulin
  • connecting peptide or C-peptide is removed to convert proinsulin to insulin
  • insulin is composed of 2 chains: A and B chain
65
Q

What is the primary stimulus for insulin secretion?

A

High plasma glucose

66
Q

Main stimulus for glucagon secretion?

A

Low plasma glucose

67
Q

Diabetes mellitus

A
  • Insulin deficiency and glucagon excess syndrome
  • causes osmotic diuresis (elevated blood glucose causes some glucose to remain in renal tubules and increase osmotic force for water movement into the lumen)
  • cellular dehydration
  • hyperglycemia
  • high ketones from high liver processing of fatty acids, which causes acidosis and fruity breath
68
Q

Type 1 vs Type 2 diabetes mellitus

A
  1. Type 1: in juvenile, insulin-dependent. Autoimmune disease that attacks beta cells, causing loss of insulin secretion
  2. Type 2: in adults, insulin-independent: associated with insulin resistance from body from receptor degradation and obesiy
69
Q

Insulin Excess

A
  • causes: insulin-secreting tumor, insulin overdose, reactive hypoglycemia (hypersensitive beta cells)
  • symptoms: hypoglycemia, sympathetic activation, insulin shock
  • treatment: glucose for diabetics. Low carbohydrates for reactive hypoglycemia

Physiology (6 decks)

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