Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
87 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
glycogenolysis
|
conversion of glycogen into glucose in the liver & muscles
|
conversion of glycogen into glucose in the liver & muscles
|
|
|
glyconeogenesis
|
formation of glycogen from noncarbyhydrate sources - amino acids in the liver when there are excess amino acids and decreased carbohydrate intake
|
formation of glycogen from noncarbyhydrate sources - amino acids in the liver when there are excess amino acids and decreased carbohydrate intake
|
|
|
gluconeogenesis
|
formation of glucose from excess amino acids, fats or other noncarbohydrate sources
|
formation of glucose from excess amino acids, fats or other noncarbohydrate sources
|
|
|
glycogenesis
|
formation of glycogen from a carbohydrate source (glucose)
|
formation of glycogen from a carbohydrate source (glucose)
|
|
|
glycolysis
|
breakdown of glucose into 2 molecules of pyruvic acid and the formation of a small amount of ATB (energy source)
|
breakdown of glucose into 2 molecules of pyruvic acid and the formation of a small amount of ATB (energy source)
|
|
|
What is diabetes in relation to glucose?
|
excess glucose in blood or problem with glucose metabolism is indicative of what?
|
|
|
|
What is diabetes in relation to insulin?
|
Impaired insulin production or impaired insulin utilization are indicative of what?
|
|
|
|
Diabetes is a disease of what system? Why?
|
Endocrine; insulin is produced in the pancreas
|
|
|
|
Comorbitities
|
vascular problems; MI, stroke, blindness, amputations; kidney disease
|
|
|
|
normal fasting glucose
|
glucose level btwn 70 - 100
|
|
|
|
prediabetic fasting glucose
|
glucose level btwn 100 - 125
|
|
|
|
Diabetes is defined by what 3 measures? What are the lower limits?
|
Fasting blood glucose >/= 126; random plasma glucose >200; A1C >/= 6.5%
|
|
|
|
What is insulin?
|
a polypeptide hormone that regulates CHO (glucose) metabolism
|
|
|
|
What does insulin do?
|
1. promotes glucose uptake by target cells & provides for glucose storage as glycogen; 2. prevents fat & glycogen breakdown & inhibits gluconeogenesis (breakdown of proteins); 3. increases protein synthesis
|
|
|
|
How is insulin released?
|
1. continuous, pulsatile into blood stream & 2. increases w/ food consumption
|
|
|
|
Insulin is the only hormone known to have a direct effect on .....?
|
Hormone that has direct effect on lowering blood glucose levels
|
|
|
|
What does glucagon do
|
maintains blood glucose btwn meals & during periods of fasting.
|
|
|
|
Where are glucagon & insulin produced?
|
pancreatic islet beta cells produces what?
|
|
|
|
primary difference glucagon between insulin?
|
insulin lowers blood glucose level --- glucagon increases blood glucose level
|
|
|
|
what contributes to maintaining glucose level over time
|
glycogenolysis - contribution to glucose levels
|
|
|
|
What happens to glucose when insulin is absent or not working?
|
1. glucose can't enter cells; 2. excess glucose can not be stored in liver & muscle tissue; 3. glucose accumulates in blood = hyperglycemia
|
|
|
|
S&S to no glucose in the cells .... cell get no fuel so they starve & cant produce energy
|
Basis of S&S ....feeling of weakness & tiredness + weight loss as cell has no fuel;
|
|
|
|
S&S to no glucose in the cells .... brain sends message of hunger
|
Basis of S&S ....Polyphagia ... eat more yet lose weight + increased thirst;
|
|
|
|
S&S to no glucose in the cells .... excess glucose in blood leaves in urine
|
Basis of S&S .... polyuria ... b/c glucose particles are osmotic pull H2O
|
|
|
|
S&S to no glucose in the cells .... body breaks down other sources of fuels (fat & muscle)
|
Basis of S&S .... continued weight loss
|
|
|
|
S&S to no glucose in the cells .... breakdown of fat cells forms fatty acids which pass through liver to form ketones
|
Basis of S&S .... Ketonuria (ketones in urine) + Ketoacidosis (metaboic panel changes)
|
|
|
|
S&S to no glucose in the cells .... brain can't function w/out glucose
|
Basis of S&S .... CNS changes = dizziness, confusion, vision problems, changes in level of consciousness, coma
|
|
|
|
1 of 4 diagnostics for Diabetes
|
symptoms of diabetes ++ random plasma glucose >/= 200mg/dl .... have to take S&S into consideration not just rely on glucose level
|
|
|
|
2 of 4 diagnostics for Diabetes
|
****1 time fasting plasma glucose >/= 126mg/dl after fasting 8hrs .... best, doesn't need to be repeated
|
|
|
|
3 of 4 diagnostics for Diabetes
|
plasma glucose >/= 200mg/dl during oral glucose tolerance test (OGTT) .... measured at various intervals
|
|
|
|
4 of 4 diagnostics for Diabetes
|
****A1C >/= 6.5% .... measured at various intervals
|
|
|
|
What does H1C test?
|
RBCs/ hemaglobin circulates in the body live for about three months before they die.....when sugar sticks to these cells, it gives us an idea of how much sugar has been around for the preceding three months
|
|
|
|
Types of Diabetes
|
Type 1, Type 2, Gestational, Secondary; Genetic
|
|
|
|
Other names for Type 1 Diabetes
|
Juvenile onset or insulin dependent
|
|
|
|
Peak onset for Type 1 + more common in what race?
|
4-6 & 11-13 y/o; caucasions
|
|
|
|
cause/ origin of Type 1
|
1. destruction of pancreatic beta cells (80 - 90% reduction) so no insulin produced; 2. autoimmune; 3. genetic process; 4. virus (unsubstantiated)
|
|
|
|
What increases changes of getting Type 1?
|
close relative w/ Type 1
|
|
|
|
What is the most prevalent form of diabetes?
|
Type 2 ... 90% of cases in US
|
|
|
|
Age at risk for Type 2 Diabetes
|
adults >40 ... increasing # of children w/ diagnosis due 2 increased childhood obesity
|
|
|
|
Races at greatest risk for Type 2
|
Native Americans + African Americans
|
|
|
|
Reasons for hyperglycemia
|
1. secretion impairment & 2. insulin resistance ... greater problem
|
|
|
|
what disease processes accompany diabetes
|
Increased Cardiac Risk due to HTN, increased LDL, decreases HDL
|
|
|
|
differences btwn Type 1 & Type 2
|
1. races: Type 1 whites & Type 2 native americans + AA; 2. age of onset: Type 1 childhood & Type 2 adult; 3. insulin production: Type 1 no insulin produced & Type 2 insulin produced yet cells resistant
|
|
|
|
causes/ origin Type 2
|
1. insulin insufficiently or poorly utilized, 2. insulin resistance; inappropriate glucose production by liver, 3. ultimately insulin production decreases cause pancreas wears out - will ultimately need supplemental insulin
|
|
|
|
Why insulin insufficiently or poorly utilizied + insulin resistance?
|
decrease in # of receptors on cell membrane or decreased sensitivity of receptors (obesity contributes)
|
|
|
|
Describe onset of Type 2
|
gradual; often undiagnosed; marked hyperglycemia m/b 1st sign; hyperosmolar coma (fluid & electrolyte lose due to elevated glucose)
|
|
|
|
Classic symptoms of both Type 1 & Type 2
|
polydipsia + polyuria + polyphagia
|
|
|
|
Symptoms unique to Type 1
|
some fatigue & weight loss - body can't get glucose into cells so don't have energy & have to breakdown fats + protein for energy
|
|
|
|
therapy for Type 1
|
exogenous source of insulin
|
|
|
|
Symptoms unique to Type 2
|
Fatigue (more then type 1), vision changes, recurrent infections & prolonged wound healing = excess glucose & cardiac impairment
|
|
|
|
therapy for Type 2
|
lifestyle changes, oral antihyperglycemic drugs .... eventually most will require exogenous source of insulin
|
|
|
|
Other ways Diabetes presents
|
1. asymptomaticly (found incidentally); 2. ketoacidosis (children <6y/o / hyperglycemia >200); 3. metabolic acidosis (pH 7.5 or bicarb <15) ... will have Kussmals respiration (increased rate + depth)
|
|
|
|
10 things to look out for w/ Diabetes
|
1. always tired, 2. polyuria, 3. polyphasia, 4. polydipsia, 5. sudden weight loss, 6. wounds won't heal, 7. sexual problems (vascular problems) 8. blurry vision, 9. infections, 10. numb/ tingling in hands or feet
|
|
|
|
other names for Insulin Resistance Syndrome
|
Metabolic Syndrome, Syndrome X, Cardiovascular Dysmetabolic Syndrome
|
|
|
|
Metabolic Syndrome cluster of abnormalities
|
Increased risk of CV disease, elevated insulin & glucose levels, elevated triglyceride level, decreased HDL, increased LDL, HTN .... act synergistically to increase risk for CV problems
|
|
|
|
Metabolic Syndrome Risk Factors
|
Central obesity; 2. sedentary; 3. polysystic ovary syndrome; 4. urbanization = environmental factors; 5. Ethnicity = increase in AA; 6. family history; 7. gestational diabetes; 8. older adults ...... 9. overweight individuals w/ impaired glucose tolerance (prediabetes)
|
|
|
|
What is MODY
|
Mature Onset Diabetes of the Young = genetic defect of beta cell function, heredity mechanism that has some kind of mutation of autosomal dominant gene that disrupts insulin production as child reaches adulthood
|
|
|
|
Gestational Diabetes .... how detected, treated & duration
|
detected w/ GTT - treated w/ insulin during pregnancy (revert back post partum) - at greater risk for Type 2 in 5-10yrs
|
|
|
|
What is Secondary Diabetes
|
diabetes that develops as a result of another condition or medications
|
|
|
|
Conditions that result in Secondary Diabetes
|
1. Pancreatic disease or removal; 2. Cushing's Syndrome; 3. Hyperthyroidism; 4. TPN
|
|
|
|
Best determinant of long term diabetes control/ mgmt
|
Hemoglobin A1C < 7% ( norm is 4.5 - 5.7%)
|
|
|
|
Type 1 at greatest risk for what complication
|
rapid onset of hypoglycemia
|
|
|
|
Cause of hypoglycemia
|
Given the too much insulin .... 1. b/c they didn't eat; 2. b/c exercised more then usual; 3. dose too large
|
|
|
|
S&S of hypoglycemia
|
feel weak + hungry, tremors, *significant diaphoresis*, CNS changes - irritable, confused, blurred vision
|
|
|
|
4 Acute complications of Diabetes
|
1. Hypoglycemia (typ Type 1); 2. Hyperglycemia; 3. Diabetic Ketoacidosis (typ Type 1); 4. Nonketotic Hyperglycemia (typ Type 2)
|
|
|
|
Reasons for Hyperglycemia
|
1. don't have med dosed appropriately; 2. not following diet (too many simple carbs); 3. decreased level of exercise
|
|
|
|
What's going on with body that becomes Diabetic Ketoacidosis (DKA)?
|
SEVERE hyperglycemia - glucose >250 ... possibly as high as 1000+; Metabolic Acidosis - pH <7.3; Bicarb >15; Excess free fatty acids - Liver producing more ketones then can be lost through kidneys
|
|
|
|
S & S of DKA
|
fruity breath, tachycardia, decreased BP, increased RR .... if severe lose consiousness
|
|
|
|
Treatment for DKA
|
Insulin
|
|
|
|
onset of DKA is ...
|
slow & gradual
|
|
|
|
What is going on with body that causes Nonketotic Hyperglycemia
|
insulin present (glucose >600) but not effective ... effective enough to not produce excess ketones but not effective enough to move glucose into cells ==== blood is hyperosmolar (> 310) pulling H20 out of cells into vascular space to return blood to isotonic state
|
|
|
|
Why more CNS changes w/ nonketotic hyperglycemia?
|
movement out of cells ... including brain cells & fluctuation of H2O out of brain cells increases CNS changes
|
|
|
|
S&S of Nonketotic Hyperglycemia
|
1. altered reflexes; 2. hyperthermia; 3. aphagia (inability to swallow); 4. visual hallucinations; 5. seizures; 6. hemiporesis (weakness on 1 side of body)
|
|
|
|
What is Nonketotic Hyperglycemia often confused with?
|
Stroke
|
|
|
|
Treatment for Nonketotic Hyperglycemia
|
rehydrate + lower glucose level with insulin - give enough insulin to overcome resistance of cells
|
|
|
|
What are chronic complications of Diabetes?
|
1. Blood vessel disease - Angiopathy - affecting large & small vessels; 2. Neuropathy; 3. PVD; 4. impaired immune response; 5. increased infections; 6. Potassium imbalances
|
|
|
|
Macrovascular complication of Diabetes
|
atheroslerotic plaque - in part due to insulin resistance
|
|
|
|
Microvascular complication of Diabetes
|
Thickening of vessel membranes in capillaries & arterioles (limits blood flow) .... a. retinopathy = blindness; b. nephropathy = renal failure; c. dermopathy = skin problems/ increased incidence of skin breakdown
|
|
|
|
What is neuropathy & how does it manifest?
|
nerve damage - problem w/ nerve conduction .... numbness, tingling, pain in peripheral extremities, lack of sensation
|
|
|
|
Complications of Neuropathy & PVD
|
1. increased risk for amputation, 2. increased risk of wounds (bad infections & ulcers) + problems healing, 3. loss protective sensations - don't know have injury before it's really bad
|
|
|
|
What's going on that increases # of infections?
|
1. defect in mobilization of inflammatory cells (inflammatory system doesn't work optimally); 2. impaired phagocytosis; 3. persistent glycosuria may predispose to UTI; 4. excess glucose suppresses natural defense mechanisms like action of WBC; 5. bacteria LOVE sugar
|
|
|
|
Why does the body make more glucose when have an infection?
|
1. ned more energy to fight off infection & 2. stress response increases glucocorticoid hormone which stimulates gluconeogenesis
|
|
|
|
How is level of K+ affected by diabetes?
|
1. Insulin drives K+ into cells so when no insulin build up in blood = hyperkalemia; 2. Polyuria = excrete K+ leading to hypokalemia; 3. Low K+ can lead to elevated blood sugar since K+ required for converting glucose to glycogen that can be stored in liver; 4. loss of K+ affects cell membrane so disrupts Na+-K+ pump
|
|
|
|
How can best control complications?
|
VERY tight glucose control .... A1C < 7% + FBG <130
|
|
|
|
Goal of Diabetes Treatments?
|
Normalize glucose level
|
|
|
|
What are important lifestyle changes needed for controlling diabetes?
|
Diet - low in simple sugars & fat, adequate protein & complex carbs; Weight loss for obese w/ Type 2; Exercise - consistent & regular
|
|
|
|
When would a pancreas transplant be appropriate?
|
only for Type 1 diabetics
|
|
