MOD 10 Flashcards
Endocrine system overview
The use of chemical messengers (hormones) to control the flow of information between different tissues and organs of the body, interacts with the nervous system
Nervous system
Fast response but short-acting
function using neurotransmitter molecules transported by neurons over a short distance to muscles and glands that respond within milliseconds. but is short-lived
Endocrine system response
Slow response but long-acting
hormones released from glands directly into the bloodstream
tend to take much longer than the response to neurotransmitters but once initiated they tend to be much more prolonged than those induced by the nervous system
Tropic hormones
hormones that have other endocrine glands as their target
non-tropic hormones
directly stimulate target cells
Regulation abilities
negative feedback (most common)
-deficiency of factors stimulates release hormones to increase factor until it is in normal range then the stimulus is ended and hormone release stops
positive feedback (rare)
-hormone secreation stimulates additional hormone secretion (feedback loops)
Hormone transport for water-soluble hormones
-Hormones are not bound to protein = water soluble
-hormones decompose quickly and require frequent or continuous synthesis
-Examples of water-soluble hormones are insulin, pituitary hormones, and parathyroid hormones
Hormone transport for water-soluble hormones
lipid soluble hormones ARE bound to protein molecules
they have longer half-life and are produced in a more cyclic pattern
availability is dependent on having enough protein to bind to target tissues
steroid and thyroid hormones are lipid-soluble
take longer to effect the body but last longer.
Exocrine glands
use ducts to transport hormones/ enzymes
(salivary glands, sweat glands, gastrointestinal tract glands and exocrine pancreas)
Endocrine glands
ductless
excrete hormones into surrounding tissue or through the bloodstream
(thyroid gland, pituitary gland, adrenals, endocrine pancreas)
The duration of endocrine transmission is prolonged because kidneys have to filter blood
Pancrease is exocrine or endocrine
It is both! exocrine because enzymes are excreted through ducts, and endocrine because hormones are excreted into blood stream
Effects of aging on hormones
- Decreased hormone secretion leads to increase risk for hormone deficiencies
2.
Glands to know
BRAIN: hypothalamus and pituitary
THROAT: thyroid and parathyroid
ABDOMEN: pancreas and adrenal
Pituitary gland ADH
Antidiuretic hormone
Function: controls amount of urine produced in kidneys
Too much adh = fluid retention (SIADH)
Too little adh = profuse urine (D.I.)
Pituitary gland TSH
thyroid-stimulating hormone
function: triggers the thyroid gland to grow and release thyroid hormones T4 & T3
Pituitary Gland ACTH
adrenocorticotropic hormone
function: causes adrenal gland to release several hormones. the major one is cortisol (DEFICIENCY IS LIFE THREATENING)
Pituitary gland GH
growth hormones
function: main hormone for body growth
Reproductive hormones (pituitary gland)
oxytocin: stims uterine contractions
follicle stim hormone: ovulation and sperm production
luteinizing hormone: ovulation and testosterone product
prolactin: breast milk
SIADH
too much adh fluid retention
s/s fluid overload especially in lungs and brain
-high b/p, bounding pulse, low hct/hgb)
concentrated urine (high urine osmolarity)
high specific gravity
at risk for seizures and dyspnea
TX: hypertonic solution
DI
kidneys excrete h2O
s/s polyuria >200ml/hr , concentrated blood, dehydrated, High Na, low B/P, thirst, weak pulse, high hct/hgb
High serum osmolarity and hypernatremia (high na)
low specific gravity
at risk for hypovolemic shock
TX: Isotonic
Hyperthyroidism and graves disease
etiology: autoimmune abnormalities (IgG) called graves diseae
common cause: benign tumors, thyroiditis
incidence: less common, 20-40 yr olds, women
patho: excess excretion of t4 and t3
s/s: weight loss, tachycardia, heat intolerance, diarrhea, hypermetabolism, exophthalmos (Permanent eye bulging), insomniaT
Thyroid storm
aka thyroid crisis
life threatening
marked by elevation of body temp (105-106F) and tachycardia or heart palpitations, high b/p
s/s: chest pain, dyspnea, potential heart failure, and cardiac arrest
TX: Drugs to lower temp, heart rate, and b/p
usually occurs in the first 12 hours after a thyroidectomy
hyperthyroidism
most common cause: autoimmune thyroiditis (hashimotos disease)
myxedema
Hashimoto’s diseae (hyperthyroidism)
antithyroid antibodies destroy thyroid, can be inherited
Patho: decreased met, autoimmune disease, decreased T3 and T4, usually after thyroidectomy.
hypothyroidism
BMR: decreased
Weight: gain
Temp: cold Intolerance decreased sweating
GI: constipation decreased appetite
CV: decreased CO2, bradycardia
General appearance: brittle hair/nails, impaired menstruation
behaviors: mental and physical sluggishness, joint paint
Hyperthyroidism
BMR: increased
Weight: loss
Temp: heat intolerance, increased sweating
GI: diarrhea, increased appetite
CV: increased CO2, tachycardia and palpitations
Resp: dyspnea
Appearance: lid lag, decreased blink, Exophthalmos (fish eye)
behavior: restless, irritable, anxious, wakeful, sore
hyperparathyroidism
High calcium means “muscles are TOO calm”
pathophys: elevated calcium in serum, reduces calcium stores in bone, causing bone demineralization, leading to pathologic fractures and risk of injury
common in older women
characterized: bone pain weakness
s/s: Same as hypercalcemia, lethargy, drowsiness, Nausea/ vomiting, decreased DTR, and is greater risk for fractures
Rx: medications to decrease resorption of Ca++ from bone surgical removal of glands
Parathyroid gland controls
calcium
Hypoparathyroidism
Muscles cannot calm down!
etiology: atrophy, trauma, surgical removal along with thyroid
pathophys: decreased PTH, leads to decreased Vit D activation, leads to decreased Ca++ reabsorption
S/S: same as hypocalcemia, tetany, paresthesia (tingling in hands), irritability, and arrhythmias
Rx: vitamin D and Ca++ replacement
Adrenal glands medulla functions
Medulla (middle) exretes catecholamines (epinephrine and norepinephrine) that are responsible for fight or flight response
Adrenal glands cortex functions
Cortex (covering) excretes cortisol, aldosterone, and androgens (sex hormones), these steroids help regulate the body’s response to chronic stress
Is medullary function essential for life?
No the sympathetic nervous system also secretes neurotransmitters epinephrine and norepinephrine,
however adrenal cortical function is needed
Adrenal cortex Cortisol
Cortisol = stress hormone
1. helps regulate stress response
2. diverts metabolism from building tissues to supplying energy for dealing with the stress
3. causes s/s of chronic stress
(high blood levels of cortisol, affects reproduction, fat distribution, and macrophage functioning of the immune system)
End result of chronic stress: infertility, med section obesity, decreased immune functioning, risk of disease
Stress pipeline
Stress→hypothalamus→anterior pituitary→ACTH →adrenal cortex→cortisol release
cortisol release → increase blood glucose, increased heart rate, and decrease nonessential energy using activities (hormone production, bone formation, gastric mobility, rbc and WBC production→anemia and depressed immune system)
Adrenal corticol Hypo secretion
addisons disease
RF: atrophy of adrenal glands, fungal infections
s/s: hypoglycemia, hyponatremia, hyperkalemia (high potassium), bronze-like skin pigmentation, weight loss, hypoglycemia
ADH deficiency → dehydration.
DX: FBS, plasma cortisol, serum sodium all decreased, and potassium is increased
Adisson’s = arrows down (except hyperkalemia)
adrenal cortical HYPER secretion
Cushings disease
RF: hyperplasia of the adrenal gland
S/s: hypernatremia, moon face, buffalo hump, hypokalemia, increase masculinity among females (same as side effects of prednisone a corticosteroid med)
DX: FBS, Plasma cortisol, and serum sodium are all increased, and potassium is decreased
Cushing is pushing levels up (except hypokalemia)
Pancrease is both
exocrine because of ducts and endocrine because it secretes hormones
Pancrease and Glucagon
via the alpha cells in response to low blood glucose
-stimulates immediate breakdown of glycogen to be used for energy
-catabolic hormone also stimulates the breakdown of fats and proteins
-raises blood glucose levels
Pancrease and Insulin
via the beta cells in response to high blood glucose levels
-reacts with insulin receptor sites and stimulates movement of glucose into the cell
-anabolic hormone: stimulates synthesis of glycogen, fats, and proteins
-lowers blood glucose levels
high cortisol means you hold on to glucose why
because you need energy for fight or flight
Stressful situations will release what
epinephrine (sympathetic response) and corticosteroids
-all will decrease insulin sensitivity and increase glucose release
-all will increase the need for insulin (due to more glucose in the blood)
-the release of cortisol from the adrenal glands contributes to high BS and insulin resistance (metabolic syndrome)
Loss of blood glucose control results from
-insufficient amount of insulin released
-decreased sensitivity of insulin receptors
Diabetes mellitus is different then
Diabetes insipidus
Diabetes is a greek word that means what
large discharge of urine
Both diabetes mellitus and diabetes insipidus produce what
polyurea, or large of amounts of urine. But that is the only thing they have in common
Diabetes mellitus is a hormone imbalance of what
insulin from the pancreas that results in high blood glucose levels
Diabetes insipidus is a hormone imbalance of
ADH from the pituitary gland that results in polyurea and loss of sodium through urine
Diabetes mellitus clinical signs and tests
most common clinical sign: Hyperglycemia
blood test for blood glucose: a finger stick/ blood draw
other test: HbA1c test
Diabetes pathophys overview
disorder of the pancreas that alters the metabolism of glucose fats and proteins treatment is aimed at tightly regulating blood glucose using diet exercise and drug management → delay the onset and associated complications
normal blood sugar range
70-130 mg/ dL
Diabetes Mellitus and HbA1c test
Usually called an A1c test
1. provides a 3-month average glucose level (RBCs are freely permeable to glucose → gives glucose exposure over the life of the RBC (about 120 days)
- The test does not require fasting or oral intake of glucose!!
- Elevations above 6% (6) = early indicator of prediabetic state. The goal of therapy for diabetic patients is below 7%(7)!!
Hypoglycemia
Decreased blood sugar
MOST DANGEROUS
-occurs in starvation or if treatment of hyperglycemia with insulin lowers blood glucose too far
-CNS changes → due to the brain using glucose as its only source of energy
-S/S usually manifests when the blood sugar level is at or below 70 mg/dL
-irritable, mental confusion, shaky/trembling, diaphoretic → ultimately leads to a coma when blood sugar reaches 40-50 mg/dL
Symptoms of hyperglycemia
polydipsia = increased thirst→d/t increased tonicity of blood
glycosuria = sugar in urine
polyuria = increased urination from osmotic diuresis caused by glucose molecules attracting water
polyphagia = increased hunger → cells sense they are starving
ketoacidosis = break down of fats for energy → process stops at ketone level due to no glucose → results in increased ketones in blood
Signs of impending danger with hyperglycemia
Fruity breath: due to increased ketones in blood
dehydration: due to increased loss of water and electrolytes (hot and dry)
Kussmaul respirations: rapid deep breathing to blood off cot and acid to compensate for acidosis
hypo vs hyper glycemia
give me some candy im cold and clammy = hypo
skin hot and dry sugar high = hyper
hyperglycemia
increased blood sugar > 130 before a meal
Types of diabetes, Both are what
both result in high glucose, each is an insulin imbalance that results in 1 or 2
DM 1 overview
Not enough insulin because there are insufficient beta cells to produce insulin
DM 2 overview
too much insulin because the body does not recognize insulin so beta cells keep producing more and more
Type 1 diabetes more details
aka T1D, IDDM (insulin-dependent diabetes mellitus) or juvenile diabetes
-Onset in childhood or teenage years
-autoimmune destruction of beta cells → insulin-dependent genetic predisposition plus an environmental trigger like an infection T1D autoantibodies can exist for years before the onset of hyperglycemia
-at higher risk for other autoimmune diseases ( graves disease, R arthritis, addisons diseases etc.)
-requires lifelong insulin injections (insulin-dependent)
S/s of T1D
-3’ Ps
Polyuria
polydipsia
polyphagia
-weight loss
-frequent infections (wound heal slow because of compromised immune system)
Type 2 diabetes details
aka T2D, NIDDM, or adult onset diabetes
-not producing enough insulin or receptos have decreased sensitivity
-not necessarily insulin dependent - may be corrected with life style changes
-treat with diet, and exercise, antidiabetic medication and ultimately insulin therapy if other treatments are not effective.
S/s of T2D
Weight gain, also the 3 P’s, frequent infections, wounds slow to heal, associated with metabolic syndrome
T2D risk factors
Family hx: first degree relative
obesity
black, Hispanic, native American
gestational diabetes
age: over 45 but now being seen in much younger patients
smoking alcohol use sedentary noncompliant with high b/p meds
drug induced: corticosteroids cyclosporine and antiretroviral drugs
Microvascular changes because of chronic complications from diabetes mellitus
changes in smaller blood vessels
-more common in type 1 diabetes
-altered carbohydrate metabolisms thickening of basement membrane, decreased normal capillary permeability
-vessels most commonly involved, RETINAL (blindness, glaucoma, cataracts) RENAL ( chronic renal failure), PERIPHERAL (Impaired healing, increased gangrene)
Macrovascular changes because of chronic complications from diabetes mellitus
changes in larger blood vessels
-more common in type 2 diabetes
-chronic hyperlipidemia,atheroma formation, glycosylated proteins alter vessel endothelium leading to increased platelet aggregation
-vessels most commonly involved: CORONARY (myocardial infarction), CEREBRAL (stroke)
-PERIPHERAL NEUROPATHY IS COMMON TO BOTH TYPES
s/s of peripheral neurological involvement include
decreased sensation, impaired sensation (numbness, tingling, intense pain) impaired GI motility, bladder dysfunction, and impotence.
DKA and HHS
Diabetic ketoacidosis and hyperosmolar hyperglycemic state (HHS) are two fo the most serious acute complications of diabetes
DKA
RF: Type 1 or type 2 diabetics, undiagnosed dm, cannot be producing any insulin whatsoever
Predisposing factors: illness, sepsis, stress, trauma, meds
presenting symptoms: polyuria, polydipsia, tissue dehydration, N/V, SZ’s coma, acidosis: kussmaul breathing, fruity acetone breath
Lab findings: extreme hyperglycemia, Ketones (blood, urine, breath)
Tx: rehydration iv fluids, iv insulin (hypo or iso), replace electrolytes as needed
HHS
high risk: type 2 diabetics, very old, very young, renal compromise
predisposing factors: sepsis/MI/ pancreatitis, low perfusion→glycogen from liver→ hi blood sugar→ thick blood→ dehydration
presenting symptoms: polyuria, polydipsia, tissue dehydration, N/V, SZs, coma NO ACIDOSIS
Laboratory findings: extreme hyperglycemia, no ketones
tx: rehydration and IV fluids, isotonic and hypotonic fluids, iv insulin, replace electrolytes as needed
Hyperglycemia in the morning
SOMOGYI phenomenon or Dawn phenomenon
important to determine which condition is causing the hyperglycemia, Both are caused by cortisol excretion during the night, both have normal blood sugar levels at night and high blood sugar in morning
Somogyi phenomenon
Caused by nighttime hypoglycemia which leads to a rebound hyperglycemia in the morning.
Blood sugar drops in nighttime→stress response→cortisol→stims gluconeogeneisis→blood sugar back up over correcting in the morning then levels out
boomerang curve
Dawn phenomenon
Blood glucose level gradually rises through night in response to cortisol release→stims the liver to excrete glycogen throughout the night so there is no hypoglycemic episode instead glucose rises steadily throughout the night
rises gradually like the sun at DAWN
Metabolic syndrome
one out of every 6 people (1 out of 3 adults) are effected
Runs in families, American, hispanics, asains, and NA. also known as syndrome X and insulin resistance syndrome.
To be DX you have to have at least 3 of the risk factors
is metabolic syndrome a disease
it is not a disease instead it is a group fo risk factors
It is reversible! can be resolved by lifestyle changes
Metabolic disease risk factors
-large waist size (abdominal fat deposits) 40 more inches for men and 35 for women
-cholesterol: high triglycerides: 150 mg/dL or higher
-cholesterol-Low “good cholesterol (HDL)
-High B/P
-blood sugar
this combination of RF double the risk of blood vessel and heart disease they also increase risk of diabetes by five times
Adipocytes
fat cells
can release hormoens that will either increase or decrease insulin sensitivity
adipose tissue is considered another endocrine gland because it secretes estrogen
Effects of aging on hormones
- decreased hormone secretion→increase the risk of hormone deficiencies
- decreased clearance of hormones: as renal function declines with aging some hormone levels can increase because they are not eliminated from the body in the urine or in the bile as they should be
- decreased receptor binding → The ability of receptors to bind hormones decreases with aging which can create erratic hormone levels resulting in s/s such as “hot flashes” during menopause
Hypothalamus gland
produces releasing and inhibiting hormones
types of releasing hormones
thyrotropin-releasing
gonadotropin-“
corticotrophin-“
Types of inhibiting hormones
somatostatin
dopamine
hypothalamus indirectly controls
because it regulates other glands it controls
-body temp
-blood osmolarity
-blood hormone levels
-inflammatory mediators
-blood nutrients
-emotions
-pain
-sleep cycle
hypothalamic-pituitary axis
hypothalamus to pituitary→ pituitary releases hormones →to peripheral glands
connects the posterior pituitary to the hypothalamus and allows the hormones required to initiate the fight or flight to release rapidly rather than go through general circulation
IICP s/s
Increased b/p
Decreased pulse
Decreased resp
(Opposite of shock)
