MOD 10

Question 1

Endocrine system overview

Answer 1

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

Question 2

Nervous system

Answer 2

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

Question 3

Endocrine system response

Answer 3

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

Question 4

Tropic hormones

Answer 4

hormones that have other endocrine glands as their target

Question 5

non-tropic hormones

Answer 5

directly stimulate target cells

Question 6

Regulation abilities

Answer 6

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)

Question 7

Hormone transport for water-soluble hormones

Answer 7

-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

Question 8

Hormone transport for water-soluble hormones

Answer 8

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.

Question 9

Exocrine glands

Answer 9

use ducts to transport hormones/ enzymes
(salivary glands, sweat glands, gastrointestinal tract glands and exocrine pancreas)

Question 10

Endocrine glands

Answer 10

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

Question 11

Pancrease is exocrine or endocrine

Answer 11

It is both! exocrine because enzymes are excreted through ducts, and endocrine because hormones are excreted into blood stream

Question 12

Effects of aging on hormones

Answer 12

1. Decreased hormone secretion leads to increase risk for hormone deficiencies
   2.

Question 13

Glands to know

Answer 13

BRAIN: hypothalamus and pituitary
THROAT: thyroid and parathyroid
ABDOMEN: pancreas and adrenal

Question 14

Pituitary gland ADH

Answer 14

Antidiuretic hormone
Function: controls amount of urine produced in kidneys
Too much adh = fluid retention (SIADH)
Too little adh = profuse urine (D.I.)

Question 15

Pituitary gland TSH

Answer 15

thyroid-stimulating hormone
function: triggers the thyroid gland to grow and release thyroid hormones T4 & T3

Question 16

Pituitary Gland ACTH

Answer 16

adrenocorticotropic hormone
function: causes adrenal gland to release several hormones. the major one is cortisol (DEFICIENCY IS LIFE THREATENING)

Question 17

Pituitary gland GH

Answer 17

growth hormones
function: main hormone for body growth

Question 18

Reproductive hormones (pituitary gland)

Answer 18

oxytocin: stims uterine contractions
follicle stim hormone: ovulation and sperm production
luteinizing hormone: ovulation and testosterone product
prolactin: breast milk

Question 19

SIADH

Answer 19

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

Question 20

DI

Answer 20

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

Question 21

Hyperthyroidism and graves disease

Answer 21

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

Question 22

Thyroid storm

Answer 22

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

Question 23

hyperthyroidism

Answer 23

most common cause: autoimmune thyroiditis (hashimotos disease)
myxedema

Question 24

Hashimoto’s diseae (hyperthyroidism)

Answer 24

antithyroid antibodies destroy thyroid, can be inherited
Patho: decreased met, autoimmune disease, decreased T3 and T4, usually after thyroidectomy.

Question 25

hypothyroidism

Answer 25

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

Question 26

Hyperthyroidism

Answer 26

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

Question 27

hyperparathyroidism

Answer 27

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

Question 28

Parathyroid gland controls

Answer 28

calcium

Question 29

Hypoparathyroidism

Answer 29

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

Question 30

Adrenal glands medulla functions

Answer 30

Medulla (middle) exretes catecholamines (epinephrine and norepinephrine) that are responsible for fight or flight response

Question 31

Adrenal glands cortex functions

Answer 31

Cortex (covering) excretes cortisol, aldosterone, and androgens (sex hormones), these steroids help regulate the body's response to chronic stress

Question 32

Is medullary function essential for life?

Answer 32

No the sympathetic nervous system also secretes neurotransmitters epinephrine and norepinephrine, however adrenal cortical function is needed

Question 33

Adrenal cortex Cortisol

Answer 33

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

Question 34

Stress pipeline

Answer 34

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)

Question 35

Adrenal corticol Hypo secretion

Answer 35

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)

Question 36

adrenal cortical HYPER secretion

Answer 36

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)

Question 37

Pancrease is both

Answer 37

exocrine because of ducts and endocrine because it secretes hormones

Question 38

Pancrease and Glucagon

Answer 38

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

Question 39

Pancrease and Insulin

Answer 39

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

Question 40

high cortisol means you hold on to glucose why

Answer 40

because you need energy for fight or flight

Question 41

Stressful situations will release what

Answer 41

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)

Question 42

Loss of blood glucose control results from

Answer 42

-insufficient amount of insulin released -decreased sensitivity of insulin receptors

Question 43

Diabetes mellitus is different then

Answer 43

Diabetes insipidus

Question 44

Diabetes is a greek word that means what

Answer 44

large discharge of urine

Question 45

Both diabetes mellitus and diabetes insipidus produce what

Answer 45

polyurea, or large of amounts of urine. But that is the only thing they have in common

Question 46

Diabetes mellitus is a hormone imbalance of what

Answer 46

insulin from the pancreas that results in high blood glucose levels

Question 47

Diabetes insipidus is a hormone imbalance of

Answer 47

ADH from the pituitary gland that results in polyurea and loss of sodium through urine

Question 48

Diabetes mellitus clinical signs and tests

Answer 48

most common clinical sign: Hyperglycemia blood test for blood glucose: a finger stick/ blood draw other test: HbA1c test

Question 49

Diabetes pathophys overview

Answer 49

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

Question 50

normal blood sugar range

Answer 50

70-130 mg/ dL

Question 51

Diabetes Mellitus and HbA1c test

Answer 51

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) 2. The test does not require fasting or oral intake of glucose!! 3. Elevations above 6% (6) = early indicator of prediabetic state. The goal of therapy for diabetic patients is below 7%(7)!!

Question 52

Hypoglycemia

Answer 52

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

Question 53

Symptoms of hyperglycemia

Answer 53

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

Question 54

Signs of impending danger with hyperglycemia

Answer 54

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

Question 55

hypo vs hyper glycemia

Answer 55

give me some candy im cold and clammy = hypo skin hot and dry sugar high = hyper

Question 56

hyperglycemia

Answer 56

increased blood sugar > 130 before a meal

Question 57

Types of diabetes, Both are what

Answer 57

both result in high glucose, each is an insulin imbalance that results in 1 or 2

Question 58

DM 1 overview

Answer 58

Not enough insulin because there are insufficient beta cells to produce insulin

Question 59

DM 2 overview

Answer 59

too much insulin because the body does not recognize insulin so beta cells keep producing more and more

Question 60

Type 1 diabetes more details

Answer 60

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)

Question 61

S/s of T1D

Answer 61

-3' Ps Polyuria polydipsia polyphagia -weight loss -frequent infections (wound heal slow because of compromised immune system)

Question 62

Type 2 diabetes details

Answer 62

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.

Question 63

S/s of T2D

Answer 63

Weight gain, also the 3 P's, frequent infections, wounds slow to heal, associated with metabolic syndrome

Question 64

T2D risk factors

Answer 64

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

Question 65

Microvascular changes because of chronic complications from diabetes mellitus

Answer 65

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)

Question 66

Macrovascular changes because of chronic complications from diabetes mellitus

Answer 66

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

Question 67

s/s of peripheral neurological involvement include

Answer 67

decreased sensation, impaired sensation (numbness, tingling, intense pain) impaired GI motility, bladder dysfunction, and impotence.

Question 68

DKA and HHS

Answer 68

Diabetic ketoacidosis and hyperosmolar hyperglycemic state (HHS) are two fo the most serious acute complications of diabetes

Question 69

DKA

Answer 69

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

Question 70

HHS

Answer 70

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

Question 71

Hyperglycemia in the morning

Answer 71

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

Question 72

Somogyi phenomenon

Answer 72

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

Question 73

Dawn phenomenon

Answer 73

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

Question 74

Metabolic syndrome

Answer 74

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

Question 75

is metabolic syndrome a disease

Answer 75

it is not a disease instead it is a group fo risk factors It is reversible! can be resolved by lifestyle changes

Question 76

Metabolic disease risk factors

Answer 76

-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

Question 77

Adipocytes

Answer 77

fat cells can release hormoens that will either increase or decrease insulin sensitivity adipose tissue is considered another endocrine gland because it secretes estrogen

Question 78

Effects of aging on hormones

Answer 78

1. decreased hormone secretion→increase the risk of hormone deficiencies 2. 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 3. 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

Question 79

Hypothalamus gland

Answer 79

produces releasing and inhibiting hormones

Question 80

types of releasing hormones

Answer 80

thyrotropin-releasing gonadotropin-" corticotrophin-"

Question 81

Types of inhibiting hormones

Answer 81

somatostatin dopamine

Question 82

hypothalamus indirectly controls

Answer 82

because it regulates other glands it controls -body temp -blood osmolarity -blood hormone levels -inflammatory mediators -blood nutrients -emotions -pain -sleep cycle

Question 83

hypothalamic-pituitary axis

Answer 83

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

Question 84

IICP s/s

Answer 84

Increased b/p Decreased pulse Decreased resp (Opposite of shock)