Endocrine 3b+c Flashcards
Specialized glands and tissue of the endocrine system secrete____
hormones
Hormones_____
secreted into the blood, travel throughout the body
-only exert an effect on cells w/ receptors
CONTROL AND COORDINATE BODY FXNS
overlap w NS
Hormones characteristics
-specific rate/rhythm of secretion: diurnal, cyclic, dependence on circulating levels
-operate via feedback mechanisms
-only affect target cells w/ receptors
hormones are classified by
chemical structure-lipid soluble or water soluble, target organ, origin
possible hormone effects
-after plasma membrane permeability or membrane potential by opening/closing ion channels
-stimulate the synthesis of regulatory molecules (proteins)
-activate or deactivate enzyme systems
-induce secretory activity
-stimulate mitosis
endocrine organs
hypothalamus, pituitary gland, pineal gland, thyroid gland, parathyroid glands, thymus gland, pancreas, adrenal glands, ovaries, testes
lipid soluble hormones
-steroids
-hydrophobic signals
-circulate w. carrier protein
-receptor inside cell
1/2 life: hours to days
water-soluble hormones
-peptides, amines, glycoproteins
-hydrophilic
-circulate unbound
-receptors on cell membrane
1/2 life seconds to mins
examples of steroid hormones
cortisol, aldosterone, testosterone, estrogens
how steroid hormones work
- hormone diffuses
- gene activated
- protein synthesis
- new protein alters cell activity
examples of peptide hormones
insulin, glucagon, thyroid hormone, epinephrine, growth hormone, oxytocin
how peptide hormones work
- hormone binds to receptor
- cyclic AMP generated (2nd messenger)
- enzyme 1 –> 2-> 3activated
- Final product alters cell activity
hypothalamic-pituitary axis
anatomically and functionally connected
-hypothalamus secretes inhibiting/releasing hormones
-regulation secretion from pituitary
hypothalamus is link between ___and____
nervous and endocrine syestem
Pituitary hormones- anterior
-thyroid stimulating hormone (TSH)
-adrenocorticotropic hormone (ACTH)
-Prolactin (PRL)
-Growth hormone (GH)
-Follicle-stimulation hormone (FSH)
-Luteinizing hormone (LH)
TSH
stimulates secertion of throid hormone
ACTH
-stimulates adrenal cortex to secrete glucocorticoids
PRL
after birth stimulates mammary glands to synthesize milk
GH
stimulates mitosis and cellular differentiation
FSH
stimulates secretion of ovarian sex hormones, development of ovarian follicles and sperm production
LH
Stimulates:
-ovulation
-corpus luteum to secrete progesterone
-testes to secrete testosterone
Pituitary hormones posterior
Antidiuretic hormone( ADH), Oxytocin (OT)
ADH
Antidiuretic hormone
-acts of kidney, incr water retention
-also called vasopressin bc it can cause vasoconstriction
OT
-stimulates uterine contradiction during childbirth, flow of milk during lactation
-promotes feelings of sexual satisfaction and emotional bonding between partners
Thyroid gland
-located below larynx in the throat
-two lobes joined by central mass (isthmus)
-follicles filled with colloid, lined with cuboidal
Thyroid gland produces:
Thyroid hormone and calcitonin
TH production
-iodine transport stimulated by TSH: TH made in colloid of the follicle, secreted from epithelium
-TH can be free-floating in plasma or protein-bound (albumin, transthyretin)
-is amine hormone BUT lipid solublae
Regulating thyroid hormone levels
-negative feedback mechanism
-TH secretion stimulated by TSH, TRH secretion, cold (in infants)
-TH secretion inhibited by: dopamine, somatostatin, stress, blood levels of TH
Thyroid hormone effects
-determines basal metabolic rate (BMR)
-enhances effect of SNS( bc of incr adrenergic receptor production)
-promotes glucose catabolism, lipolysis
thyroid hormone effects in children______and in adults_____
children: critical for nervous, muscular, skeletal development
adults: normal functioning of nervous, muscular, CV, GI, reproductive syestems
Types of thyroid dysfunction
hyperthyroidism (thyrotoxicosis)
hypothyroidism (myxedema)
goiter
thyroid nodule
abnormal thyroid fxn test
Hyperthyroidism
overproduction/ secretion of TH
-enlargement of gland (adenomas, neoplasia)
-pituitary or hypothalamic dx
-overdose of thyroid meds
-excessive hormone release due to TSH receptor autoantibody–> graves dx (type 2 hypersensitivity)
Graves dx patho
-autoantibodies that stimulate TSH receptor in thyroid gland-persistent TSH “signal”-> excessive release of T3 and T4
–> Formation of autoantibodies by B cells
- thyroid-stimulating immunoglobulins (TSIs)
-Thyroid-stimulation antibodies (TSAbs)
Graves dx may develop into ___
hypothyroidism
-gland ablation (radiotherapy) or removal (sx)
-creation of more autoantibodies–> destroy gland
-creation of autoantibodies that block TSH receptor
Graves dx manifestations
Increased metabolism-increased appetite, weight loss, hyperthermia
-trachycardia and incr CO
-increased gluconeogenesis and lipolysis
-restlessness, agitation, anxiety
-exophthalmos- orbital connective tissue inflam/ weakening
-pretibial edema
Thyrotoxicosis
-thyrotoxic crisus, thyroid storm
-dramatic rise in TH, potentially lethal: undiagnosed graves dx
-hyperthermia
-trachycardia, heart failure
-delirium
-vomitting, diarrhea-> dehydraitons
Hyperthyroidism tx
-diminish production, secretion, or action of TH
antithyroid drugs
radioactive iodine therapy (destroy thryoid cells)
sx removal of adenoma or part of thyroid gland
excessive tx –> hypothyroidism
Hypothyroidism
underproduction/ secretion of TH
-Hypoplasia of thyroid gland (congenital)
-iodine deficiency
-pituitary or hypothalamic dx or injury
-tx for hyperthyroidism
-autoimmune destruction of thyroid follicles
–>hashimotos
Hashimoto patho
autoantibodies destroy follicle cells:
-Thyroglobulin (Tg Ab)
-Thyroidal peroxidase (TPO Ab)
-TSH receptor-blocking (THS-R block Ab)
low levels of T3 and T4
Hypothyroidism manifestations
decreased metabolism:
-hyperthermia, cold intolerance
-weight gain despite decr appetite
bradycardia and decr CO
increased cholesterol
muscle cramps, weakness, stiffness
decrease GI motility
myxedema (skin puffiness) and hair loss
lethargy, forgetfulness, depression
Hypothyroidism in children
cretinism- abnormal nervous syestem development- mental retardation
-slowed skeletal growth/maturation
-delayed puberty
+ all the other reg manifestations
Goiter
enlargement of thyroid gland
-typical lack of dietary intake of iodine
-reduced thyroid hormone secretion
-incr TSH secretion–> thyroid hyperplasia
(can also occur due to hyperthyroidism)- TSH-R stim Ab stimulates gland, leading to hyperplasia
Adrenal glands
-sits atop kidneys
Adrenal cortex produces-
corticosteroids:
-aldosterone (mineralocorticoids)
-cortisol (glucocorticoids)
-androgens (gonadocorticoids)
Adrenal medulla produces____
amines
-epinephrine, norepinephrine
Mineralocorticoids
regulates electrolytes(primarily Na+ and K+) in ECF
-Importance of Na+: affects ECF volume, blood volume, blood pressure, level of other ions
-importance of K+: sets RMP of cells
_____the most potent mineralocorticoids
Aldosterone
-Na+ reabsorption and water retention
-K+ excretion
Net result: increase blood volume and BP
Regulating aldersterone
stimulated by:
-decr blood volume and BP (RAAS)
-INCR K+ in blood
-ACTH release from PITUITARY GLAND
Inhibited by:
-ANP release from atria (incr blood volume and BP)
Hyperaldosteroniam pathogen
-neoplasm or hyperplasia of adrenal cortex
-excess renin secretion:
kideny dx/injury
heart failure
excessive laxative/ diuretic use
Hyperaldosteronism manifestations
-Na+ and water retention/ K+ and H+ excretion
-Hypertension- and organ damage that comes. w/ it
-tiredness, weakness, nocturia (low K+)
-metabolic alkalosis (H+ moves into cells to replace K+)
-renin levels decreased (primary) or increased (secondary)
Hyperaldosteronism tx
ALDOSTERONE RECEPTOR BLOCKERS
-removal of adenoma
Glucocorticoids
-keep blood sugar levels relatively constant
-maintain blood pressure by increasing the action of vasoconstrictors
cortisol the most significant bc:
-enhances breakdown of protein/fat to make glucose (gluconeogenesis + lipolysis)
-inhibits inflammation
-suppresses immune syestem
intended for surviving acute stress
Cortisol mechanism of action
bind to cytosolic receptor –> act as transcription factor
-promote breakdown of fat and protein
-promote synthesis of glucose (liver)
Cortisol- suppress immune activity
-reduce circulating lyphocytes, monocytes, eosinophils, basophils
-inhibit production of IL-2
-interfere with antigen processing
-decrease WBC migration into tissue
Regulating cortisol
-negative feedback mechanisim
-release stimulated by:
acth RELEASED FROM PITUITARY
emotional stress, bodily injury
-release inhibited by:
Fall in ACTH level
ACTH released:
-ACTH released in a diurnal pattern
peak between 6-8am
low between 12-2am
Hypercortisolism
-neoplasm of pituitary, adrenal cortex
overuse of corticosteroid medications
Cushing’s
redistribution of fat to face (“moonface”) and upper back (“buffalo hump”)
Hypercortisolism manifestation
-immune supression (inhibit transcription of pro-inflammatory genes)
-elevated blood glucose –> insulin resistance
-obesity / redistribution of fat
-muscle wasting (excessive breakdown of protein)
-loss of collagen (thin skin, poor wound healing)
-polydipsia and polyuria
-increased bone remodeling (weakening of bone tissue)
-hypertension (mechanism unclear)
Corticosteroids used for treating autoimmune conditions –>prolonged use leads to______
adrenal atrophy
Stopping corticosteroid tx:
-CRH/ ACTH signals suppressed
-Adrenal gland unresponsive –> adrenal insufficiency
-takes time to re-establish physiologic cycle of hormone release
Hypercortisolism tx
-sx/ radiation to treat tumor
-medication to block affects of cortisol
Hypercortisolism w/o tx leads to:
infections
complication from HTN
Hypocortisolism
-destruction/ dysfunction of adrenal cortex
~80% autoimmune
~TB infection
-deficient pituitary/ hypothalamic activity
Addison’s
-anti-adrenal antibodies
-decrease cortisol
-increase ACTH
Hypocortisolism patho autoantibodies
-adrenal cortex Ab (ACA)
-Steroid 21 hydroxylase Ab (21-oh Ab)
-other organs often targeted (thyroid, parathyroid, gonad, pancreas)
lymphocyte infiltration
destruction of cortex -> replacing cortical cells fibrous stroma
Hypocortisolism patho
-basal cortisol secretion is normal at first
-no increase in cortisol in response to stress, injury, trauma
-eventful destruction of tissue -> basal cortisol levels fall
-ACTH and CRH levels increase (because no negative feedback)
Hypocortisolism manifestation
-anorexia, weight loss
-GI issues; nausea, vomiting, diarrhea
-hyperpigmentation of skin (ACTH hypersecretion)
-hyponatremia
-prone to hypoglycemia (impaired gluconeogenesis); fasting can lead to coma quickly
-hypotension –> vascular collapse
Hypocortisolism tx
-glucocorticoid/ mineralocorticoid replacement therapy
-extra Na+
-additional cortisol for stressors: infection, sx, trauma
Pituitary gland
“master gland” of endocrine system
ADH stimulates thirst, causes water retention from ____
collecting duct of kidneys
increase in blood osmolarity
simulates release of ADH
Diabetes insipidus
insufficient ADH
-Polydipsia (abnormal thirst)
-Polyuria (dilute and large volume of urine)
-Nocturia (waking at night to pee)
dilute hypotonic urine- 10-20L/day
Diabetes insipidus : Central
disease of pituitary, hypothalamus
-head injury
-intracranial tumor collecting duct of kidneys
Diabetes insipidus: Nephrogenic
kidneys unable to respond
-inherited defect
-renal damage from drugs
DI pathogen: Central
initial edema/ shock from injury -> inhibit ADH release
-once healed -> ADH secretion resumes
DI Patho: Nephrogenic
-familial: defect in ADH receptor or aquaporin channel
-drug-induced: receptors sensitive to lithium and fluoride salts (reversible if exposure stops)
DI manifestation
-normal blood volume
-hypernatremia-> cell shrinking due to loss of osmotic balance
decreased responsiveness to stimuli
seizures
coma
Pancreas
exocrine and endocrine organ just behind stomach
-digestive enzymes, bicarbonate-> dudenum
-glucagon, insulin, somatostatin -> blood stream
pancreatic hormones
-glucagon
-insulin
glucagon
secreted by A or alpha (a) cells
-released between meals when blood glucose decreases
-liver stimulates glucogenesis, glycogenolysis
-adipose stimulates lipolysis, release of free fatty acids
insulin
secreted by B or beta cells
-secreted during and after meal when blood glucose and amino acid levels rise
-stimulates cells to absorb nutrients ->lowering blood glucose
-promotes synthesis of glycogen(liver, muscle), lipid (adipose) and protein
-suppresses use of already stored fats
hyperglycemic hormones raise blood glucose
glucagon
growth hormone
epinephrine/ norepinephrine
cortisol
Hypoglycemic hormones lower blood glucose
insulin
GIP (gastric inhibitory peptide), GLP-1 (glucagon-like peptide) (indirectly)
insulin is produced and secreted in response to_____
-increase blood glucose, amino acids, free fatty acids
-GI hormones (GIP, GLP)
proinsulin made of 3 peptides:
ABC
-C peptide cleaved
-A-B peptides =active insulin
-C peptide in blood an indirect measurement of insulin synthesis
Factors that inhibit insulin release:
decrease blood glucose
epi and ne
somatostatin
action of insulin
facilitates glucose transport into cells (not all)
incr glucose use and storage as glycogen
incr uptake of amino acids
incr uptake of free fatty acids and glycerol
stimulates production of lipids and proteins
incr uptake K+, mg2+, phosphate
GLUT receptors
GLUT1: brain cells
GLUT2; liver, kidney, intestinal, pancreatic cells
GLUT3: brain cells
all ^ insensitive to insulin
GLUT4: muscle and adipose cells highly sensitive to insulin
Diabetes insipidus
-hyposecretion of ADH or kidney insensitivity to ADH
-characterized by intense thirst and heavy urination
Diabetes mellitus
dysfxn of endocrine pancreas
-affects metabolism of fat, protein and carbohydrates
DM characterized by
hyperglycemia thqat results from:
secr in insulin secretion
decr in cell response to insulin
incr in hormones that oppose insulin
Diabetes dx
NORMAL: 90-100 mg/dL glucose and A1c , 6%
Diabetes: Hb1c >or =6.5 %
fasting blood glucose > or = 126 mg/dL
2 hr plasma glucose > or = 200 mg/dL
random plasma glucose . or = 200 mg/dL
HbA1c is
glycated hemoglobin:
-perm attachment of glucose to hemoglobin
-% Hb glycation proportionate to blood glucose level
Glycosylation
(glucose attatches to protein by enzyme)
-post-translation modification
-regulated by enzyme activity
-confers (+) biological properties to proteins
glycation
nonenzymatic attachment
a form of protein damage: impairs fxn and stability
Type 1 DM
little or no insulin secretion
loss of beta cells in the pancreas
-autoimmune:
body’s immune cells destroy beta cells
genetic predisposition + environmental trigger
-non-immune
secondary to other condition (pancreatitis)
idiopathic (no autoantibodies detected)
type 1 dm mechanism genetic factors:
unclear; may involve class ll human leukocyte antigen (HLAll)
type 1 dm environmental factors
-childhood infection ( enteroviruses, H.pylori)
-changes in gut microflora
-cow’s milk
-exposure to toxins
type 1 dm creation of autoantibodies
GAD65 (glutamic acid decarboxylase 65)
ZnT8 (zinc transporter)
IA2 (tyrosine phosphate-IA2)
–>Targetting pancreatic beta cells
by the time symptoms of t1dm occurs 90% of _____have been destroyed
beta cells
T1DM Symptoms
hyperglycemia
polydipsia- thirst
polyuria- peeing more
glucosuria- glucose in urine
polyphagia- hunger
weight loss
muscle wasting
acute complications with t1dm
diabetic ketoacidosis (DKA) with type 1 or 2
Diabetic ketoacidosis
type of metabolic acidosis
T1DM dx is usually occurs after first episode of DKA
-brought on by stress (trauma, infection, lack of insulin)
DKA presents with:
-lethargy
-labored breathing (kussmaul)
-fruity breath (acetone)
-hyperglycemia
-dehydration
-decr K+ (diuresis and vomiting)
Chem of DKA
-DECR IN insulin, incr in glucagon
-adipocytes release FFAs as energy source
-liver metabolizes FFAs to ketones->acetone, acetoacetic acid, beta-hydroxybutyric acid
Ketones ___blood pH
LOWER: BICARB BUFFERING SYSTEM QUICKLY overwhelmed
-hyperventilation and incr in H+ excretion in kidneys to compensate
-extra glucose pulls water/elertrolytes into kidney tubule-> polyuria dehydration
tx of t1dm
goal: to regulate blood glucose w/o episodes of hyper or hypoglycemia
-daily insulin
-self monitoring of blood glucose
-meal planning
-exercise
yearly screening for complications
Type 2 dm
chronic hyperglycemia
-insulin resistance (cells do not respond to insulin)
-improper beta cell fxn
causes by complex genetic, epigenetic, and environmental interactions
dm + obesity=
dm + obesity + htn=
diabesity
metabolic syndrome
T2DM effects
genetic -> obesity <- diet, inactivity
leads to adipokines, incr ffas, inflamm cytokine, decr activity of ghrelin
leads to insulin res and decr in beta cell mass n fxn
hpoinsulinemia, incr of glucagon
t2dm risk factors. causes
age, fam hx, genetic sus
inherited defects: B-cell fxn, insulin molecule, insulin receptors
obesity, htn, inactivity
metabolic syndrome: includes central obesity, dyslipidemia, htn, hyperglycemia
DM type 2 pathogenesis: insulin resistance
-resistance: diminished response of insulin-sensitive
contributors:
-abnormal insulin molecule
-high amount of insulin antagonists
-down-regulation of insulin receptor
-decr in activation of intracellular pathways
-alteration of GLUT proteins
-obesity
insulin resistance
down-regulation of insulin receptor, abnormal insulin molecules, alteration of GLUT proteins
decr activation of intracellular pathways, high amount of insulin antagonists= glucagon
Obesity
imbalance of energy intake and expenditure leads to expansion of adipose tissue (can be healthy or not)
inflammation or metabolic dysfxn
Healthy expansion of adipose tissue
incr in adipogenesis
decr cell volume
incr insulin sensitivty
decr inflammtion
Unhealthy expansion of adipose tissue
decr in adipogenesis
ince cell hypertrophy
decr insulin sensitivity
incr low grade inflammation
incr mo infiltration
CAN LEAD TO LIPOTOXIXITY- insulin res
____and_____affecting energy expenditure likely contribute to unhealthy expansion
genetic , endocrine
effect of obesity
-alterations in adipokines
-elevated serum free fatty acids and ectopic lipid deposits
release of inflamm cytokines from adipose tissue
-decr insulin-stimulated mitochondrial activity
-hyperinsulinemia and decr insulin receptor espression
adipokines-
hormones secreted by adipose cells:
adiponectin, leptin
Adiponectin
-compliments effects of insulin
-inversely correlated with body weight
-obesity decr adiponectin levels; contributes to insulin res
Leptin
-acts on recptor in hypothalamus
-decr food intake (signals satiety), incr energy expenditure
-scretion incr as adipocyte number and size incr
can lead to leptin resistance
leptin resistance
obese individuals have larger/more adipocytes
-incr serum levels of leptin
BUT are insensitive to its effects
promotes over-eating, excessive weight gain
-attributed to inherited defect in leptin receptor
Serum FFA and lipid deposits
-2 types of fat: visceral and subcutaneous
-Visceral (central) fat accumulation leads to adipocyte dysfxn
FFA metabolism is distributed-> dyslipidemia
inappropriate (ectopic) lipid deposition-detected by biomarkers in blood
release of inflamm cytokines from adipose tissue
chronic low grade inflamm
-released from intra-abdominal adipocytes or nearby mo:
TNF-a and IL-6
Acute phase reactants (fever, attract neutrophils)
two main effects on inflamm response in dm 2
1)induce insulin resistance: TNF-a phosphorylates insulin receptor, making it unresponsive to insulin
2)perpetuate associated conditions
-atherosclerosis
-fatty liver
-dyslipidemia
decreased mitochondrial activity
-insulin induces glucose uptake
-glucose used in cell respiration (in mitochondria)
cells(skeletal muscle, liver) become res to effects of insulin-> glucose not taken up effectively -> cell respiration and oxidative phosphorylation(makes ATP) become dysfxn -> leads to less ATP synthesis, more ROS production
effects of hyperinsulinemia
insulin receptors become desensitized due to the persistent presence of insulin
-insulin ‘signal” no longer processed by cells
-receptor expression downregulated
-hyperinsulinemia associated with increased risk for CAD, HTN
obesity has profound effects that induce_____
insulin resistance
Chronic DM complications
CV dx: micro and macrovascular
retinopathy
nephropathy
neuropathy
bladder dysfxn
Mucrovascular dx
dx of capillaries
-hyperglycemia alters cell metabolism
characteristic:
-EC hyperplasia
-thickening of extracellular matrix
-thrombosis
changes in capillary beds-> less tissue perfusion
leads to hypoxia and ischemia in tissues receiving blood from diseased capillaries
Intracellular effects of hyperglycemia
oxidative stress
incr in activation of polyol pathways
-metabolic pathways, leads to accumulation of sorbitol
-exhausts NADPH (req for neutralizing ROS)
incr activation of protein kinase C
-IC signaling protein inappropriately activated (cell proliferation)
incr glycation =AGE
-glucose irreversibly bound to things
incr activation of hexosamine pathways
-excess glucose directed to hexosamine pathway
-results in glycation (dysfxn) of signaling proteins
-contributes to oxidative stress
macrovascular dx
majority of diabetics succumb to coronary artery dx, atherosclerosis, aneurysm, stroke, peripheral artery dx
macrovascular dx mediated by____-
advanced glycation end-products (AGE)
aDVANCED GLYCATION END-PRODUCTS (AGE):
Attach to the receptor for AGE (RAGE)
promotes: oxidative stress
inflammation
endothelial cell dysfxn
VSM dysfxn
hyperlipidemia
Retinopathy
leading cause of blindness worldwide
already present in dm by time of diagnosis
-retina most metabolically-active structure in the body
vulnerable to changes in metabolism caused by hyperglycemia
-occurs in 2 stages: nonproliferation and proliferative
Nonproliferative retinopathy
microaneurysms )loss of supportive cells)
-incr capillary permeability:
heard exudates (fat)
edema
-ischemia and infarction
soft exudates
-hemorrhages
proliferative
neovasculation, ischemia causes release of VEGF
nephropathy
DM most common cause of end-stage renal dx/ kidney failure
-occurs more often in T1
-higher prevalence of T2 make up 50% of ESRD pts
-progressive changes in glomerular fxn that take many yrs to develop
-kidneys eventually fail
nephropathy, characteristic changes to ___
glomerulus
-enlarges
-basement membrane thickens
-mesangial cell sproliferate
-loss of podocytes : incr permeability
proteins lost in urine: proteinuria
-resistance to bloo dflow(changes to arterioles)
decr GFR
___made worse by renal dysfxn
controlling____ a key part of slowing progression of nephropathy
HTN
Neuropathy 3 types
-distal symmetric
-autonomic
-transient asymmetric (specific nerves/plexuses)
Neuropathy characteristics
demyleniation
nerve degeneration
slowed conduction
in neuropathy :
sensory deficit precedes motor deficit
begins distally, moves proximally
-attributes to metabolic and vascular dysfxn from hyperglycemia:
polyol pathways in neurons
microvascular dx-> ischemia
autoantibodies (sometimes)
neurotrophic factors defects (cannot repair damage)
Vascular dysfxn and neuropathy both contribute to ______
gangrene (body tissue death)
diabetic bladder dysfxn
mojority of DM pts experience bladder dysfxn
not life-threatening but severely impacted quality of life
dm bladder dysfxn casued by
hyperglycemia/glucosuria
-impaired metabolism
-oxidative stress
significant incr in urine voule (full of glucose)
-leads to tissue remodeling
-hypertrophy of smooth muscle (bc bladder working harder)
-decr in contractility
t2dm tx
primary tx-changing habits to reduce body weight
-diet, decr caloric intake
-exercise :decr postprandial blood glucose and triglyceride and cholesterol levels
-incr HDL (good cholesterol) levels
reduction in body weight can ____
sometimes reverse insulin resistance
if lifestyle changes do not decr hyperglycemia and HBA1c levels _____
pharm tx
Biguanides
metformin; 1st line drug for dm
decr hepatic glucose production
decr glucose absorption in gut
incr insulin sensitivity (liver, muscles, adipose)
Glitazones
activate transcription factor-> glucose homeostasis
-anti-inflamm, incr insulin sens, decr FFS and LDLS
Sulfonylureas
depolarizes pancreatic B-cells
stimulate insulin release
a-glucosidase inhibitors
prevent digestion of carbohydrates in intestines
naturally occurring in some foods (green teas, maitake mushrooms), not effective on its ownp
peptide mimetics
glucagon-like peptide (GLP) agonist (Ozempic)
gastric inhibitiry peptide (GIP) analog
incr insulin secretion
decr appetite
slow gastric emptying
Glycosurics
SGLT2 inhibitors
-inhibits glucose uptake in kidney tubule
decr glucose reabsorption and incr glucose exretion
