Pathophys Exam 4

glucose/ fats

help body meet energy requirements

muscle/ liver

produces glucose

amino acids/ lactate

can be turned into glucose

GI tract/ liver

where glucose enters bloodstream from

glucose

present in higher concentrations in ECF than w/i cells

variable depending on cells

permeability of glucose

GLUT transporters

mediates diffusion of glucose

GLUT-1

blood brain barrier; insulin independent

GLUT-2

liver; insulin independent

GLUT-3

neurons; insulin independent

GLUT-4

muscle/ adipose tissue; insulin dependent

β cellls of Islets of Langerhans

produce insulin

insulin

regulate protein/ fat metabolism

glucose enters pancreatic β cells…

triggers insulin release into bloodstream

process after ingesting a meal

blood sugar rises —> glucose enters β cells —> β cells detect glucose/ generate energy —> exocytosis of vesicles w/ insulin into bloodstream

fasting state

glycogenolysis in liver/ muscle; insulin levels decrease; increased glucagon levels

lipolysis

breakdown of fat from adipose tissue; prumary source of energy in fasting state

neural regulation

SNS/ PNS related to carbohydrate metabolism/ glucose utilization

brain, mouth, β cells, hepatic portal vein

where glucose senstiive receptors are

PNS

stimulates insulin release; influences secretion activity; influences β cells

stress hormones (from injury, pain, illness) interact to

ensure continuous supply of glucose

corticosteroids

increase glucose/glucagon production

psychological stress causes

increase in blood glucose

Diabetes (DM)

pancreas doesn’t make enough insulin/ body doesn’t utilize insulin properly

hyperglycemia

too much glucose in blood

Type 1 DM (T1DM)

destruction of β cells; T-lymphocytes infiltrate islets/ destroy β cells —> cytokines; antibodies may be present

age peaks for T1DM

2, 4, 6, 10-14

Type 2 DM (T2DM)

resistance to action of insulin; affects 90-95% of individuals w/ DM

risk factors for T2DM

aging (loss of muscle mass/ increased visceral fat); sedentary lifestyle; obesity (excessive abdominal fat

symptoms of T1DM

polydipsia, polyuri, polyphagia, weight loss

prediabetes

impaired glucose tolerance/ fasting glucose; glucose levels higher than normal; warning sign of possible insulin resistance

prediabetes effect on organs’ response to insulin

less responsive to insulin

prediabetes effects on pancreas

tries to produce more insulin but cannot keep up

metabolic syndrome

abdominal obesity, HTN, T2DM, hypercholesterolemia, hypertriglyceridemia

metabolic syndrome complications

CVD, stroke

pathogenesis of T2DM

relative lack of insulin; impaired glycogen synthesis; impaired production of insulin

acute hyperglycemia causes

alterations in nutrition, inactivity, inadequate use of antidiabeteic medication, combination of factors

dawn phenomenon

early rise in bloood glucose that occurs w/o eating

hormones released in early morning

GH, cortisol, glucagon, epinephrine

diabetic ketoacidosis (DKA)

increased lipolysis/ conversion to ketone bodies; based on continued insulin deficiency

pH range of DKA

6.8-7.3 (metabolic acidosis)

DKA effects

osmotic fluid loss/ hyperkalemia

glycolsylated hemoglobin levels (HbA1c)

determines average amount of blood glucose over a period of 2-3 months; best indicator of long-term glucose management

exocrine glands

release substances through a duct

exocrine gland examples

eyes, mouth, skin, stomach, breasts, liver, pancreas, intestines

endocrine glands

secrete hormones into bloodstream

endocrine gland examples

pituitary, thyroid, adrenal glands

endocrine system

regulates growth, maturation, metabolic functions, fluid balance, response to stress, reproduction

positive feedback

neural/ chemical/ endocrine response increases synthesis/secretion of a hormone

negative feedback

changing chemcial/ neural/ endocrine response to a stimulus decreases synthesis/ secretion of a hormone

thyroid hormone regulation

T3/T4 signal hypothalamus/ pituitary to slow TRH/TSH production

hypothalamus (thyroid) secretes

TRH

anterior pituitary (thyroid) secretes

TSH

thyroid gland secretes

T3/T4

endocrine dysfunction causes

hypersecretion, hyposecretion, non-responsiveness

etiology of endocrine dysfunction

congenital, infectious, autoimmune, neoplastic, idiopathic, iatrogenic

primary endocrine disorders

intrinsic defects w/i the gland itself

secondary endocrine disorders

result from abnormal hypothalamic-pituitary secretions of trophic signals

growth hormone/ somatotropin

promotes growth in bones/ tissues, lipid metabolism, carbohydrate metabolism

growth hormone target organs

liver (IGF-1), adipose tissue

growth hormone gland

anterior pituitary

GH/ IGF-1

GH is released from anterior pituitary —> GH travels to liver —> liver produces/releases IGF-1 —> sitmulates bone growth, promote cell division/repair, support muscle growth

GHRH

growth release hormone

GHIH/ somatostatin

growth inhibiting hormone

growth hormone

small amounts released during sleep; greatest during adolescence/ decreased in elderely

growth hormone deficiency (GHD)

decreased GH secretion, defective GH action, impaired IGF-1 production

acquired GHD

brain tumors, TBI, cranial radiation therapy

GHD clinical manifestations

normal infant birth length/weight, hypoglycemia, seizures/ cerebral damage, underdeveloped male sex organs, below third percentile of growth, delayed dental eruption, thin hair/ poor nail growth

growth hormone excess

uncontrolled production of GH benign somatotrophic adenoma

pituitary giganticism

adenoma presenting in childhood

pituitary giganticism clinical manifestations

marked accelerated growth; untreated could growth to at least 8 feet

complications from pituitary giganticism

early cardiovascular death due to cardiomegaly/ HF

acromegaly

excess growth hormone during adulthood (40s-50s)

acromegaly clinical manifestations

progressively advancing shoe/ ring size, enlargement of frontal sinus —> prominent brow/ mandibular growth, hypertrophy of soft tissue, cardiomegaly/goiter, deepening of voice (thickening of vocal cords), sleep apnea (enlargement of tongue)

T3/ triiodothyronine

regulates body temperature, energy level, HR

T4/ thyroxine

growth/ development, metabolism

congenital hypothyroidism

cretinism (defects in mental/ physical development)

acquired hypothyroidism

Hashimoto thyroiditis/ autoimmune thyroididtis, radiation, surgical removal of thyroid, iodine deficiency

secondary hypothyroidism

defects in TSH production r/t head trauma

Hashimoto’s thyroiditis (HT)

autoimmune disorder of thyroid gland; hyperthyroidism —> hypothyroidism

pathophysiology of HT

immune system produces autoantibodies against thyroid proteins —> antibodies damage thyroid cells —> gradual destruction of thyroid tissue —> reduced production of T3/T4

hypothyroidism clinical manifestations

weakness, lethargy, cold intolerance, decreased BMR, bradycardia, moderate weight gain, hyperlipidemia, increased incidence of athersclerorosis, goiter, cool/dry skin, consipation, menstural irregularities

hypothyroidism myxedema

generalized non-pitting edema, edematous looking skin (glycosaminoglycans in interstial spaces), dry skin/hair

hypothyroid induced myxedema clinical manifestations

altered mental status, hypothermia, respiratory depression, hypercapnia, hypotension, coma

iodine hypothyroidism

required for T3/T4, low levels —> increased TSH release —> goiter

hyperthyroidism

Grave’s disease (increased synthesis/secretion of T3/T4), ingestion of excessive thyroid hormone

hyperthyroidism clinical manifestations

increased BMR, insomnia, restlessness, tremors, irritability, palpitations, increased HR, heat intolerance, diaphoresis, inability to concentrate, weight loss, amenhorrhea, thyrotoxicosis

exophthalmos

protrusion of eyeball due to tissue expansion behind eye

periorbital edema

swelling around eyes from fluid accumulation/ inflammation

diplopia

EOM muscle inflammation/ weakness

gritty/ irritated eyes

poor eyelid closure/ dryness

photophobia

eye surface inflammation

pretibial myxedema

localized, non-pittng edema/ indruated plaques on anterior lower legs

thyrotoxic crisis/ thyroid storm

TH levels rise dramatically; death can occur w/i 48 hours w/o treatment

thyrotoxic crisis causes

spontaneous, undiagnosed w/ Grave’s disease, physiologic stress

thyrotoxic crisis clinical manifestations

tachycardia, agitation/confusion, N/V/ abdominal pain/ diarrhea, high fever

only insulin dependent insulin transporter

GLUT-4

how DKA causes hyperkalemia

lack of insulin causes potassium to stay outside of cell

adrenocorticotropic hormone (ACTH)

triggers released by pituitary gland to stimulate release of cortisol from adrenal glands; responsible for release of androgens; stimulates of epinephrine/ neuroepinephrine

cortisol

regulates body’s stress response + fats/carbohydrates metabolism