PATHO FINAL FALL 2024 (GOLDSMITH ONLY)

what do the parathyroid glands do

maintain calcium levels

what does the adrenal glands do

metabolize nutrients, adapt to stress, maintain salt balance

what does the thyroid do

control bodys metabolic rate

does anabolism require ATP

yes

does catabolism require ATP

no it makes ATP

excess glucose is stored as

glycogen in the liver and skeletal muscles

can the brain store glycogen

no so blood glucose conc is highly regulated

when you are fasting what happens

the body burns fatty acids to spare glucose for the brain, AA can be converted to glucose by gluconeogenesis

excess amino acids

converted to glucose and fatty acids stored as TG in adipose

what is the main site of AA storage via structural proteins

muscles

absorptive state

glucose for major energy source, glycogen, TG, protein synthesis and storage, excess stored as TG fat

postabsorptive state

nutrients not being absorbed, TG, proteins and glycogen broken down to use glucose for energy for energy, conserves glucose for the brain, produce new glucose

things that increase blood glucose

absorption from GI tract

hepatic glucose production through glycogenolysis and gluconeogenesis

things that decrease blood glucose

transport glucose into cells for utilization for energy and for storage

urinary excretion of glucose

pancreas is organized into

islets of langerhans

beta cells produce

insulin

alpha cells produce

glucagon

somatostatin does what

inhibits alpha and beta from D cells

epsilon cells

increase ghrelin increasing hunger

gamma or f cells

pancreatic polypeptides appetite control secreted post prandial

insulin lowers

blood glucose, fatty acid, and amino acid levels and promotes their storage

insulin stimulates what

glycogenolysis and gluconeogenesis

where does insulin stimulate glycogenesis

skeletal muscle and liver cellss

increase in blood glucose concentration

increases insulin secretion bringing glucose down to normal level

what causes a decrease in glucose

inhibits insulin secretion shifts metabolism from absorptive to post absorptive state

what stimulates insulin secretion

elevated blood amino acids, GI hormones, PNS

type 1 diabetes

insulin deficiency

type 2 diabetes

reduced sensitivity of target cells to insulin

how does glucose enter the beta cells

facilitated diffusion via GLUT 2

parasympathetic stimulation secrets

islet beta cells

glucagon

promotes glycogenolysis

stimulates gluconeogenesis

promotes fat and protein breakdown

glucagon secretion increases when blood glucose concentration is

too low

excess glucagon can aggravate

hyperglycemia of DM

what are insulin antagonists

growth hormone, cortisol, epinephrine, glucagon

calcium homeostasis

involves immediate adjustments to control calcium in the blood

calcium balance

involves slow adjustments to maintain total amount of calcium

parathyroid hormone

secreted by parathyroid gland at back of thyroid

raises calcium in blood, signals bones, kidneys, intestines increasing plasma ca

lowers phosphate ions in the blood

rates of deposition and resorption causes

remodeling

what favors bone deposition

mechanical stress

too much bone resorption can do what to bones

weaken bones

when RANKL is secreted what happens

binds to RANK differentiate into osteoclasts and suppress absorption, increase osteoclast action, decreases bone mass

when osteoprotegerin is secreted what happens

RANKL bound not available to bind with RANK, blocks action decreases osteoclast action and osteoblast action outpases osteoclast action, increases bone mass

where does PTH release calcium

from labile pool in bone fluid for immediate need, stimulating transfer of ca across osteocytic osteoblastic bone membranes, quickly replaced from mineralized bone

PTH promotes slow transfer of

calcium and phosphate from stable pool of minerals in bones for chronic need, localized dissolution of ca in bones into the ECF

where is there a fast and slow exchange of Ca

between bone and plamsa

PTH signals kidneys to do what

conserve ca and eliminate phosphate, inverse relationship because they are in equilibrium within bone crystals conc must be constant

what does vitamin d do to intestinal calcium absorption

increase because PTH promotes intestinal absorption of ca and phosphate and activating vitamin D

what is the primary regulator of PTH

plasma conc of ca PTH increases in response to decrease of ca in blood

what does calcitonin do

lowers ca level in blood, protects against hypercalcemia

what is phosphate metabolism controlled by

same mechanisms that regulate calcium metabolism

decreases plasma ca

stimulates parathyroid glands, increases PTH, increases plasma conc also inhibits thyroid c cells

increases plasma ca

stimulates thyroid c cells increase calcitonin, decreases plasma ca, inhibits parathyroid glands

hyperparathyroidism

excessive secretion of PTH, can cause hypercalcemia and hypophosphatemia, reduce excitability of muscle and nervous tissue, thinning of bones and kidney stones

hypoparathyroidism

deficient secretion of PTH, leads to hypocalcemia and hyperphosphatemia increase neuromuscular excitability

Vit D deficiency

decreases intestinal absorption of calcium

rickets, osteomalacia

each adrenal gland has

steroid secreting portion and catecholamine secreting medulla

adrenal medulla is

inner core of adrenal gland, modified part of sympathetic system and postganglionic neuron, stores and secretes E and NE, released in the blood by sympathetic stimulation

when E and NE are released into the blood by sympathetic stimulation they are

neurohormones

epinephrine effects

fight or flight constricts most blood vessels raising total peripheral resistance, dilates blood vessels supply heart, skeletal muscle, bronchiole smooth muscle opening airways

epinephrine promotes

glycogenolysis (liver and skeletal muscles) and gluconeogenesis in liver (from lactate)

stimulates glucagon secretion

lipolysis

causes CNS arousal and alertness

stress response

pattern of reactions to a situation that threatens homeostasis, common responses to noxious stimuli

general adaptation syndrome

to noxious stimuli

hypothalamus activates

sympathetic and CRH- ACTH cortisol system activated increasing blood glucose

what maintains BP and blood volume

RAAS and vasopressin

lack of aldosterone leads to

hypovolemic shock- death

chronic activation of the stress response leads to

HTN, hyperglycemia, FA

cortisol breaks down

fat proteins and carbs

follicular secretory cells

makes thyroid hormones, enclose inner lumen filled with colloid which is the extracellular storage site for thyroid hormones

what is the main constituent of colloid

thyroglobulin

c cells

in interstitial space between follicular cells secrete calcitonin

how are thyroid hormones made

tyrosine and iodide occurs on thyroglobulin molecules in colloid by lipophilic diffusion (needs TGB and albumin binding molecule)

what form of thyroid hormone is more potent

T3

what does T4 lose when converted to T3

converted outside the thyroid loses iodines in liver or kidney

thyroid hormone effects on intermediary metabolism

small amounts promote glucose to glycogen conversion and protein synthesis, lg amounts promote glycogen to glucose conversion and stimulate protein degradation

thyroid hormones sympathomimetic function

increase target cells responsiveness to E and NE

thyroid hormones cardiovascular function

increase HR, and contraction, cause peripheral vasodilation

thyroid hormone growth and nervous system function

simulate GH secretion. IGF 1 production increased protein synthesis

what regulates thyroid hormone secretion

hypothalamus pituitary thyroid axis

TSH from anterior pituitary stimulates release of thyroid hormones and

maintains structural integrity, and increased hormone feeds back to decrease TSH secretion

TRH from hypothalamus turns on TSH secretion

increase TRH secretion exposure to cold in newborns

thyroid hormone increases

basal metabolic rate and catecholamine effect, heat production

hypothyroidism in adults

myxedema puffy appearance in face

hashimotos thyroiditis

hashimotos thyroiditis

follicular cell destruction by CD8 MHC and CD4 IFN gamma activates macrophages causes injury to thyrocyte

hypothyroidism from birth

produce cretinism, dwarfism, mental retardation

causes of hypothyroidism

deficiency of TRH, TSH, iodine, or thyroid hormone

symptoms of hypothyroidism

weight gain, fatigue, cold, slow weak pulse, slow reflexes

treatment of hypothyroidism

replacement therapy with exogenous hormone

hyperthyroidism symptoms

high BMR ,sweating, heat, weight loss with increased appetite, increased heart rate, strength of contraction, excessive degree of mental alertness

graves disease

autoimmune, antibodies TSI stimulate TSH, release T3 and T4, negative feedback to anterior pituitary no TSH, bulging eyes

thyroid storm

thyrotoxicosis, hyper symptoms, treat with cooling blankets, protect heart with beta blockers, antithyroid medications

goiter

enlarged thyroid gland TSI TSH overstimulation

hypothyroidism goiter

primary thyroid gland failure lack of iodine TSH stimulates cell growth to increase number and size

hyperthyroidism goiter

graves increase TSI or secondary to hypothalamus stimulates anterior pituitary TSI binds TSH causing continuous stimulation or TRH/TSH stimulation for secondary

what is the only hormone that decreases glucose

insulin from GLUT on skeletal and adipose

what signals proteins for insulin

TK leading to enzyme modification, fat protein synthesis and growth and gene expression

diabetes is also known as the

exaggerated postabsorptive state

type 1A diabetes

immune mediated, genetic predisposition, HLA markers

type 1B diabetes

idiopathic disease, genetic pattern, no autoimmunity, beta destruction

resistin is a hormone/ adipokine increased when

in obesity promoting resistance

adiponectin is a hormone decreased when

in obesity decreased insulin effects