Home > Flashcards > Print Preview
The flashcards below were created by user
on FreezingBlue Flashcards. What would you like to do?
5 functions of target cells
- 1. Alters plasma membrane permeablitity or membrane potential, or both, by opening or closing ion channels
- 2. Stimulates synthesis of proteins or regulatory molecules such as enzymes within the cell (growth hormone, testastarone)
- 3. Activates or deactivates enzymes
- 4. Induces secretary activity
- 5. Stimulate mitosis (aids in reproduction of the cell)
lipid soluble hormones. (like steroids). the hormone can go straight through plasma membrane into the cell.
Increase of receptors. Body adjusts to excessive amounts of hormones in the blood by producing more receptors on the target cell for that hormone.
Process that desensitizes the target cells due to prolonged exposure to high hormone concentration.
The target cells respond less vigorously to hormonal stimulation.
Prevents the target cells from overracting to persistently high hormone levels (like insulin resistence).
regulates metabolic activity through hormones
(reproduction, growth and developement, maintenence of electrolyte, water, and nutrient balance of the blood etc.)
secreated by the glads and travel through the blood to work on specific cells
specific cells that respond to specific hormones
- eat lots of sugar at frequent intervals
- insulin goes up--exessively
- stay up for extended period of time
- cells become numb to insulin (down-regulation)
- pancreas wears out after years (produce less insulin)
patient gets agressive symptoms
correct diabetes early on through
concentration of hormone in blood, determined by
- 1. rate of release
- 2. how quickly the hormone is inactivated (and removed from body).
the length of time it takes the blood level of a hormone to decrease by half (half as much hormone in the blood as origonally)
(hormone release) Humoral stimuli
hormone is secreted in direct response to changing blood levels of certain ions and nutrients
Ex. glucose up, insulin up (then glucose uptake--as in, it is stored in the muscles).
(hormone release) Neural stimuli
Nerve fibers stimulate hormone release
Ex. stimulation of the adrenal medulla to release epinephrine (adreniline) during stress
(hormone release) Hormonal stimuli
1 gland releasing a hormone that triggers another gland to release a hormone.
So endocrine glands release their hormones in response to hormones produced by other endocrine glands.
3 types of Hormone Release
- 1. Humoral Stimulus
- 2. Neural Stimulus
- 3. Hormonal Stimulus
Negative feedback system
stimulates hormone secretion--more hormone in blood. Target cells activated in large numbers. sends message back telling glands to cease producing that hormone.
Gland made of exocrine glands and indocrine glands. Behind liver. Secretes hormones. Some directly into the duodium.
Islets of Langerhans
In pancreas. Secrete insulin.
Within islet cells, beta cells
produce insulin. (lighter spot)
Within islet cells, within beta cells--alpha cells
Job is to move glucose out of the blood (where it has little value), into the cells.
- body breaks it into glucose in the stomach
- glucose moved to blood stream
- body recognizes glucose and pancreas secretes insulin
- insulin binds to glucose and moves into the cell
hormone secreted by alpha cells. Raises blood sugar levels (so we don't become hypoglycemic). i.e. when we're fasting, haven't eaten for a while, or are exercising.
It does this by breaking down glycogen
carbs that don't spike blood sugar levels. Insulin rises slower. Carbs that spike blood sugar lead to rapid and large amount of insulin which stay in the body longer than the sugar (which is where you crash)
If this is an on going cylce, it CAN be prediabetic.
Treatment of hypoglycemia
- Eat foods that don't raise the blood sugar levels rapidly
- Eat regularly (small meals)
Blood glucose levels
<110 is normal. >125 is diabetic.
Blood glucose levels chart
(get from powerpoint)
Negative Feedback System
Glucose up, pancreas secretes insulin, moves glucose to cells, blood levels of glucose equalize.
Glucose down, pancreas secretes clucagon, break up glycogen, sugar levels go up.
Autonomic Nervous System 2 Segments
Sympathetic Nervous System
Triggered by stress, exercise etc. Secretes empinephrum, stops insulin production.
Parasympathetic Nervous System
Triggered by sleep or rest. Starts insulin production.
It is what is damaged when you are insulin resistent. When it is triggered, processes within the cell occur that open the protein channels for gulcose.
3 Actions of Insulin
- 1. Move glucose into the muscle where it promotes glycolysis (break down of glucose that produces ATP and provides short burst of energy)
- 2. Move glucose into the liver where it can be converted into glycogen (stored until needed).
- 3. Take glucose out of the blood and move it into the fat.
Insulin and weight gain
- more carbs
- more blood glucose
- more insulin
- more body fat.
- Influence energy metabolism
- Help the body reduce stress
regulates blood glucose (process is gluconeogenesis)
Breaks down fat and muscle to create glucose
Negative freedback system
- Hypothalamus --> (hormone)
- --> anterior pituitary --> (hormone)
- --> adrenal cortex --> cortisol (which inhibits the other parts of the system).
Excessive amounts of cortisol excreted (often caused by a tumor on the gland)
Resulting in a loss of muscle and bone protein.
Cushing's Syndrome Symptoms
- water and salt retention
- moon face
- distributed to nape of neck
- bruise easily
- poor wound healing
- buffalo hump
- stretch marks--they look pregnant
Hyposecretion (cortisol) OR Addison's Disease
(genetic--glands just don't work sufficiently)--opposite of Cushing's Syndrome
- Weight loss
- Decreased glucose and sodium
Raises glucose levels by doing two things
- 1. Lipolysis (fat--break-down of)
- 2. Glycogenolysis (break down of glycogen)
- secreted by the anterior pituitary gland
- both growth-promoting and metabolic actions
- increase size and number of cells (muscle and bone)
- encourages the use of fats for fuel, thus conserving glucose
Produce more growth hormone but your growth plates haven't fused yet so you grown tall but with normal body proportions
- Epiphyseal plates have closed
- Englarged bones in hands, feet, face
Pituitary dwartism (hyposecretion)
slowed long bone growth with normal body proportions
- Egyptian 1500 BC -- Pulyuria "frequent peeing" identified as a "sugar disease."
- Greece 14 AD -- Kidney disease
Diabetes historic diagnosis
- Lots of light colored pee
- Smelled like "sweet hay"
- Tasted like sugar
English physician who first documented the taste of pee.
Called the sweetness of diabetic pee "mellitus."
Early symptoms of diabetes
- Excessive urination
- Dry skin
- Boils and carbuncles (because they're secreting glucose in their sweat which attracts bacteria)
- Little perspiration
- Dry bowel movements
Early treatments of diabetes (we had no clue!)
- bear meat
- diluted wine
- herbs and grains
- avoidence of sex
- horse-back rides
- roast meat dripping in fat
- sweet pastries
- very few green vegetables
- diet-refrain from foods with sugar/starch
- eat meats, and green vegetables
Claude Bernard 19th century
Discovered that glycogen was stored in the liver, overproduction of glucose caused diabetes.
Paul Langerhans 19th century
Discovered "islet cells" in the pancreas (which secrete insulin and glucagon)
- 1. Eat--worsen disease and shorten life
- 2. Low calorie diet (starve)--lengthen life a little
Type 1 diabetes caused by...
Insulin Deficiency--your pancreas can't produce enough insulin
What causes a child to get diabetes?
Often it is an immune system problem that killed the beta cells
Milestones in diabetic studies
- Thomas Willis--sweet taste
- Dr. Dobson--boiled urine (sugar was left)
- Thomas Cawley--autopsies--shriveled pancreas
- Oscar Minkowski--took pancreas out of healthy dogs--> diabetic symptoms
- Sir Edward Albert Sharpeg--discovered insulin
- Fredrick Banting/Charles Best--tested with insulin injections
Short acting insulin
- (regular, lispro, aspart, glulisine)
- inject after eating
- works within 5-15 minutes. Peak 1-1.5 hrs. Lasts 3-4 hrs.
Long acting insulin
- (insulin glargine)
- slow release of insulin into the circulation
- 24 hrs.
- no peaks
- given once per day, before bedtime
- (insulin dtermir)
- 17 hrs.
- given twice daily
mixed insulin preparations
- Mix of fast and slow acting insulin.
- Given before breakfast and dinner.
- (trims down the amount of injections from 4 to 2)
- Syringe (anywhere where there is loose skin). Rotate the area.
- Pen injector devices
- Insulin pump--scheduled and set to inject regularly.
(agressive treatment--pancreas transplant, or islet cell transplants)
Diabetes Mellitus: Type 1
- Type 1
- Autoimmune disease
- Pancreatic islet B cell destruction
- Body does not produce sufficient amounts of insulin
- 100000000 cases per year
- 90% immune-medicated 10% Idiopathic (i.e. we don't know what causes the destruction of the B cells).
- Peaks of incidence in children before school age, again at puberty (Juvenile onset).
Diabetes Mellitus: Type 2
- Ciculating endogenous insulin is inadequate to prevent hyperglycemia
- OR increased tissue insensitivity (insulin resistence)
- 2500000000 cases per year (1 million more cases per year)
- Obesity, sedentary lifestyle, diet
- Predominantly in adults (now more in adolescents).
- Located paritally behind the stomach, triangular gland
- Aides in digestion
- Secretes alpha cells and beta cells
- Extremely potent hyperglycemis (1 molecule of glucagon can release 100 million glucose)
- 1. breaks down glycogen to glucose
- 2. Synthesis of glucose from lactic acid
- (releases clucose into the blood)
- Main effest is to lower blood glucose
- 1. Enhances membrane transport into cells
- 2. Inhibits breakdown of glycogen to glucose
- 3. Inhibits conversion of amino acids or fats to glucose
- Stimulated by elevated blood glucose levels
Etiology of Type 1 Diabetes
- Pancreatic B Cell destruction
- Circulating insulin is virtually absent
- Elevated plasma glucagon and glucose levels in the blood
Causes of Type 1 Diabetes
- mom has it 3% risk per child
- dad has it 6% risk per child
- caucasian most at risk
- Idiopathic- (we don't know what caused it)
- common in Asian or African
- Viral infection-
- viral infection during childhood, early adulthood, or a mom's pregnancy. Antibodies against virus--attack beta cells. Destroy beta cells.
Diagnose Type 1
- Urinalysis (analyze urine)
- --Glucosuria (sugar in urine)
- --Ketonuria (ketones in urine--from breaking down far for energy)
- Blood Testing
- -- >126 mg/dL (after 12 hour fast)
- --Hmoglobin A1C ---Assess diabetic control (blood glucose levels) over the lifespan of the red blood cell (RBC) (120 days)... >6HbA1C
Type 2 Diabetes statistics
- 25.8 million in 2010
- Most patients are 40+ yrs old and obese
- > 90% of all diabetes patiens have Type 2
- Predominantly seen in adults, but becoming more prevalent in children and adolescents
Does the pancreas produc insulin in type 2?
Yes, enough to prevent ketoacidosis but not enough to prevent hyperglycemia
Does location (distribution) of fat correlate with insulin resistance?
Yes, visceral obesity (abdominal fat) correlate with insulin resistance more than subcontaneous fat.
What makes you more prone to insulin resistence?
Type 2: What is insulin resistance syndrom?
25% of monobese, nondiabetic population has insulin resistance.
Gestational Diabetes Causes
- 1. Insufficient insulin release (not enough for you and the fetus).
- 2. Insulin resistance
Gestational Diabetes Risks
- Development of DM II later in life
- Complication duing pregnancy
- Future gestational diabetes
- Child at increased risk of obesity and DM II
- Daughters at higher risk of gestational and DM II
- Higher risk of DM I
Diabetes Insipidus Causes:
- 1. Failure of release antidiuretic hormone (ADH)
- 2. Failure ro recognize ADH
ADH conserves water--the lack (or resistance) of ADH lead to polyuria (peeing) and polydipsia (thirst)
Microvascular Diseases (destruction of small vessels)
- -Retinopathy--destroy vessels in the eye (patient goes blind)
- -Neuropathy--nervious system
- -Reproductive disorders
Macrovascular Diseases (destruction of large vessels)
- -Cardiovascular disease (myocardial infaction)
- -Cerebrovascular disease (stroke)
How do we get micro/macrovascular diseases?
It starts with GLYCOSYLATION.
amino acids + sugar (which makes glycosylation) --> glycated protein (ADD CHART FROM POWERPOINT) (happens when you have high levels of glucose over a long period of time).
Advanced Glycosylation End Products (AGE's) (product of glycosylation) leads to:
- 1. Increased vessel permiability (LDL's will penetrate the vessel wall --> Plaque).
- 2. Increased procoagulant ability (blood clots) --> heart attack or stroke
- 3. Vasoconstiction (vessels constricting) ... aids in cardiovascular disease.
How does AGE's affect you when you are diabetic (Put it all together). 3 factors:
- LDL's get into vessel wall --> plaque...so there is a decreased size where blood can travel.
- Vessel constricts
- You get blood clots that start to move through that narrow wall...it gets caught.
Numbness comes from
vessels being constricted so that blood doesn't get to that area. So the nerves die.
The higher the A1c the higher the risk of...
Platelet AbnormalitiesThrombus and Embolus
- atherosclerosis (myocardial enfarction)
- cerebrovascular accident (stroke)
- cardiovascular disease
Diabetic Retinopathy: nonprolifterative and proliferative
- Nonproliferative --no new vessel growth (damaged-thinner)
- Proliferative --new vessel growth (damaged-thinner)
Because the vessels are damaged, and thinner, they break. The body heals the vessel, but scars.
Diabetic Retinopathy Prevenative Treatment
- address the hyperglycemia
- reduce hypertension
- reduce hyperlipidemia (cholestrol)
- GOAL: stop prevention
- PREVENTION: reduce A1c (we want you at 6)
Diabetic Retinopathy Symptoms
- blurred vision
- dark floating spots
- loss of focus in the center of vision
- difficulty differentiating between colors
The higher the A1c the more likely...
that you get Diabetic Retinopathy.
- Kidney disease
- Progressive disease--it gets worse
- Protein that we want to keep for the body is being spilled into the urine because the kidneys are damaged
Diabetic Nephropathy: Identification
- Blood work--
- surum creatinine
- blood urea nitrogen (these things should be filtered out through the kidneys, but are not)
- glomerular filration rate goes down
- more protein in the urine
- Hematuria--presence of blood in the urine
Diabetic Nephropathy: Symptoms
- May have no symptoms
- Retention of fluid--> Edema (swelling)--> lungs, legs
- Hematuria (blood in the urine)
Diabetic Nephropathy: Treatment
- vigorous control of hyperglycemia
- reduce hypertension (angiotensin-converting enzyme (ACE) inhibitors)
- restrict dietary proteins
- prevention (normalization of blood glucose levels)
angiotensin-converting enzyme (ACE) inhibitors
- AC = Hormone that makes you retain water
- --> water goes up--> blood pressure goes up
AC + enzyme --> will not retain water
Nerve damage. Peripheral neuropathy--when the vessels constrict--> decreased circulation--> nerves get less blood and become damaged--> reduced sensation of the lower extremities.
Diabetic Neuropathy: Symptoms
- bilateral extremity pain
- progresses into numbness and sensory loss
- starts at toes and progresses up the leg
- modified gait (walk)
- repeated trauma (can't feel, so things happen)
- lack of circulation
- poor healing (because of little blood)
Diabetic Neuropathy: Identification--check for decreased sense of...
- touch (location of light touch)
- heat (hot/cold)
- pain (dull/sharp)
- vibration (tuning fork)
- position (movement)
Diabetic Neuropathy: Treatment
- decrease glucose levels
- pain control (over the counter, or codeine, narcotics)
- anticonvulsant, antidepressant medications
- referrals (podiatry, physical therapy, orthopedics, wound care)
Diabetic Neuropathy: Prevention
- decrease glucose levels
- foot care
Genitourinary and Reproductive Complication -- Males
- erectile dysfunction (can't obtain or maintain erection for intercourse)
- retrograde ejaculation (prostrate doesn't clamp down the urithra, so that sperm mixes with the urine)
Genitourinary and Reproductive Complication -- Females
- decreased libido (desire to have intercourse)
- reduce vaginal lubrication