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116 Cards in this Set
- Front
- Back
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Glucose is needed for
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Cellular function (fuel) for the brain and nervous system
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The nervous system and brain are the only things that can ____ glucose
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Mobilize glucose (move them) without carriers.
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Where can glucose not be stored
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CNS (brain) and The skin
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Blood glucose is controlled by
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Insulin, glucagon
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Insulin secreted by
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beta cells of the pancreas
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Glucagon is secreted by
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the alpha cells of the panceas
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Insulin and glucagon have most of their effects in
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the liver
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When there is an increase in gluoce levels what happens
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Insulin production is stimulated to make glucose move into the cells
|
|
|
When there is a decrease in glucose what happens
|
Glucagon is stimulated to promote Glycogenolysis (glycogen breakdown) and gluconeogenesis (amino acids and glycerol (fat) breakdown)
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Where is excess glucose stored
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IN the liver and muscle as glycogen
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What does insulin do
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Increase gluconeogenesis
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What affects blood glucose
|
Catecholamines, growth hormone,
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How do catecholamines affect blood glucose
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By epinephrine and norepinephrine
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What are the actions of catecholamines on in glucose control
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They affect glycogen stores and fatty acids increasing blood sugars and inhibiting insulin release.
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Why do catecholamines inhibit insulin release
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Because catecholamines are released in stressful situations so the body needs lots of energy… sugars…
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What affect does catecholamines have on b.s
|
they increase blood glucose by increasing glucose production for long periods of time and cause insulin resistance of the cells so the serum level of glucose stays increased.
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Which type of diabetes do catecholamines affect
|
Type 2, they have insul and glucose but because of the catecholamines, they have developed resistance of insulin to transport glucose into the cells.
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|
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What does growth hormone do
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Mobilizes glucose to increase blood sugars because gh stimulates new tissue synthesis (needs energy)
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When does gh affect blood sugars
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At night during sleep
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SO in the morning after gh has been working, a person is
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Hypoglycemia because the glucose has been used.
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|
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What doe glucocorticoid hormones do
|
Cortisol hormone causes glucose utilization to be decreased and cause gluconeogenesis (metabolism of fat and proteins)
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|
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What is Type I Diabetes Mellitus
|
Insulin Dependent because there is few or no functional beta cells in the islets of langerhans and so insulin production does not occur
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What MUST type 1 diabetes mellitus patients need
|
Exogenous insulin
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|
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When does type 1 occur mostly
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It develops during childhood
|
|
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What is a problem with type 1
|
Infection; usually upper respiratory
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|
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Symptoms of type 1 that usually occur before diagnosis
|
Polyuria, polydipsia, polyphagia but they LOSE weight, FRUITY breath because they excrete KETONES in their breath.
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|
|
Possible causes of type 1
|
Genetics, autoimmunity (T lymphs damage betas), environmental (seasonal)
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|
|
What is type 2 diabetes
|
Noninsulin dependent because the beta cells fail and cant keep up with the bodies demands for insulin. They either are not producing insulin or have become insulin resistance
|
|
|
The drug that has significantly altered the tissue to become sensitive to insulin again
|
Metformin
|
|
|
Type 2 diabetic issues are due to
|
80% obesity and 10% because they are over the age of 65 , and 60% of people with type 2 is genetic… simbling or parents have it too.
|
|
|
Why does being over 65 cause type 2
|
The pancreas ages and hormone production decreases including insulin hormone production decrease.
|
|
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With type 2 glucose metabolism is altered even though there is adequate because
|
There is not enough insulin receptors so the excessive glucose amounts cannot be transferred effectively into the cell and accumulation occurs – hyperglycemia.
|
|
|
What is gestational diabetes
|
Glucose intolerance developing in pregnancy predisposing mom to type 2 especially if they have a genetic predisposition
|
|
|
Complication of diabeties is what
|
Hyperglycemia, hypoglycemia, the somogyi effect,
|
|
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Which complication kills you
|
Hypoglycemia because it occurs so abruptly. Hyper is a slow uncomfortable progress
|
|
|
Hypoglycemia is caused by
|
Giving insulin, oral hypoglycemia agents, inadequate foot intake, alcohol, & exercise b/c more glucose is transported to the blood for energy… mostly when you give insulin and the patient doesn’t eat.
|
|
|
What is the sympogyi effect!!!!!!
|
Acute complication seen in type 1 diabetes mostly
|
|
|
What is seen in the symogyi effect
|
Hypoglycemia at night but in the morning they become hyperglycemic because of the counter regulation of hormones trying to balance the low levels.
|
|
|
The mechanism of symogyi effect
|
Hypoglycemia triggers glucagon response/stress response because blood sugars are low so gh, cortisol, glucagon or catecholamines secrete during the night which is when they are not suppose to be secreted (except gh) and causes a false state of rebound hyperglycemic to be seen in the morning, this is a problem because the dr gives insulin in the morning when they are NOT hyperglycemic causing them to be even more hypoglycemic then they were.
|
|
|
How is the symogyi effect caused
|
Because of the counter regulatory hormones GH, cortisol, catecholamines and glucagon
|
|
|
Symptoms of the symogyi effect is
|
1. Type 1 diabetics, 2. VIVID!! nightmares because of low sugars and 3. Have Headaches that wake them
|
|
|
SO when you see hyperglycemia in the morning you should
|
NOT assume insulin insufficiency because you will cause the symogyi effect and the patient will DIE!
|
|
|
Why does diabetic ketoacidosis occur
|
Because there is a lack of insulin causing fatty acids to be mobilized for energy
|
|
|
Who experiences diabetic ketoacidosis
|
Type 1 diabetics, mostly newly diagnosed b/c b.s. continue to rise with no way to counteract the high levels.
|
|
|
What is diabetic ketoacidosis
|
Hyperglycemia gone bad because glucose cannot be metabolized so fatty acids are metabolismed for energy
|
|
|
Symptoms of diabetic ketoacidosis
|
Polyuria, polydipsia, nausea, vomiting, fatigue, coma progressions
|
|
|
Why does coma progress with diabetic ketoacidosis
|
The hyperglycemia serves as an osmotic diuretic so the patient becomes dehydration because of excessive urination which causes hypokalemia because potassium is also secreted.
|
|
|
What is the most significant finding of diabetic ketoacidosis
|
Excessive ketoacids occurring with fatty acid leading to METABOLIC ACIDOSIS
|
|
|
What is hyperosmolar hyperglycemia nonketotic coma
|
HHNKC, Seen in type 2 diabetes! With a mortality rate of 40 to 70% It is NONKETOTIC! But still results in coma because of hyperglycemia and increased plasma osmolality
|
|
|
What is the seen in HHNKC
|
Plasma osmolality is elevated, plasma glucose greater than 600 mg/dL but no ketoacids.
|
|
|
Why does HHNKC have such a high mortality rate
|
Because ketoacidosis/metabolic acidosis is not seen like it is expected to be as a result of hyperglycemia so symptoms aren’t noticed, just though to be high sugar.
|
|
|
What are the signs of HHNKC
|
High osmolality pulls water out of the cells including neuro cells which decrease conscious levels. Siezures occur, hemiparesis, aphasia, muscle fasiculations, hyperthermia, and dehydration.
|
|
|
What are chronic complications of diabetes
|
Diabetic neuropathies, microvascular disease, macrovascular disease, & infections.
|
|
|
Diabetic neuropathy develops because
|
The nerve veseel is ischemic due to demyelinization of the Schwann cell.
|
|
|
What are the symptoms of diabetic neuropathy
|
Loss of feeling, touch, position sense, temperature and pain sensations and impotence of men. \
|
|
|
Microvascular disease includes
|
Retinopathy because fibrotic changes and new blood vessels develop in the retina and ischemia causing plasma leaks from the vessels.
|
|
|
Macrovascular disease include
|
Coronary artery disease, stroke, and peripheral vascular disease.
|
|
|
Infection in diabtes caused by
|
Increased glucose in body fluids provide energy of infection and decreases wbc to tissues, impairing phagocytosis and impairing sensations.
|
|
|
Glucose is needed for
|
Cellular function (fuel) for the brain and nervous system
|
|
|
The nervous system and brain are the only things that can ____ glucose
|
Mobilize glucose (move them) without carriers.
|
|
|
Where can glucose not be stored
|
CNS (brain) and The skin
|
|
|
Blood glucose is controlled by
|
Insulin, glucagon
|
|
|
Insulin secreted by
|
beta cells of the pancreas
|
|
|
Glucagon is secreted by
|
the alpha cells of the panceas
|
|
|
Insulin and glucagon have most of their effects in
|
the liver
|
|
|
When there is an increase in gluoce levels what happens
|
Insulin production is stimulated to make glucose move into the cells
|
|
|
When there is a decrease in glucose what happens
|
Glucagon is stimulated to promote Glycogenolysis (glycogen breakdown) and gluconeogenesis (amino acids and glycerol (fat) breakdown)
|
|
|
Where is excess glucose stored
|
IN the liver and muscle as glycogen
|
|
|
What does insulin do
|
Increase gluconeogenesis
|
|
|
What affects blood glucose
|
Catecholamines, growth hormone,
|
|
|
How do catecholamines affect blood glucose
|
By epinephrine and norepinephrine
|
|
|
What are the actions of catecholamines on in glucose control
|
They affect glycogen stores and fatty acids increasing blood sugars and inhibiting insulin release.
|
|
|
Why do catecholamines inhibit insulin release
|
Because catecholamines are released in stressful situations so the body needs lots of energy… sugars…
|
|
|
What affect does catecholamines have on b.s
|
they increase blood glucose by increasing glucose production for long periods of time and cause insulin resistance of the cells so the serum level of glucose stays increased.
|
|
|
Which type of diabetes do catecholamines affect
|
Type 2, they have insul and glucose but because of the catecholamines, they have developed resistance of insulin to transport glucose into the cells.
|
|
|
What does growth hormone do
|
Mobilizes glucose to increase blood sugars because gh stimulates new tissue synthesis (needs energy)
|
|
|
When does gh affect blood sugars
|
At night during sleep
|
|
|
SO in the morning after gh has been working, a person is
|
Hypoglycemia because the glucose has been used.
|
|
|
What doe glucocorticoid hormones do
|
Cortisol hormone causes glucose utilization to be decreased and cause gluconeogenesis (metabolism of fat and proteins)
|
|
|
What is Type I Diabetes Mellitus
|
Insulin Dependent because there is few or no functional beta cells in the islets of langerhans and so insulin production does not occur
|
|
|
What MUST type 1 diabetes mellitus patients need
|
Exogenous insulin
|
|
|
When does type 1 occur mostly
|
It develops during childhood
|
|
|
What is a problem with type 1
|
Infection; usually upper respiratory
|
|
|
Symptoms of type 1 that usually occur before diagnosis
|
Polyuria, polydipsia, polyphagia but they LOSE weight, FRUITY breath because they excrete KETONES in their breath.
|
|
|
Possible causes of type 1
|
Genetics, autoimmunity (T lymphs damage betas), environmental (seasonal)
|
|
|
What is type 2 diabetes
|
Noninsulin dependent because the beta cells fail and cant keep up with the bodies demands for insulin. They either are not producing insulin or have become insulin resistance
|
|
|
The drug that has significantly altered the tissue to become sensitive to insulin again
|
Metformin
|
|
|
Type 2 diabetic issues are due to
|
80% obesity and 10% because they are over the age of 65 , and 60% of people with type 2 is genetic… simbling or parents have it too.
|
|
|
Why does being over 65 cause type 2
|
The pancreas ages and hormone production decreases including insulin hormone production decrease.
|
|
|
With type 2 glucose metabolism is altered even though there is adequate because
|
There is not enough insulin receptors so the excessive glucose amounts cannot be transferred effectively into the cell and accumulation occurs – hyperglycemia.
|
|
|
What is gestational diabetes
|
Glucose intolerance developing in pregnancy predisposing mom to type 2 especially if they have a genetic predisposition
|
|
|
Complication of diabeties is what
|
Hyperglycemia, hypoglycemia, the somogyi effect,
|
|
|
Which complication kills you
|
Hypoglycemia because it occurs so abruptly. Hyper is a slow uncomfortable progress
|
|
|
Hypoglycemia is caused by
|
Giving insulin, oral hypoglycemia agents, inadequate foot intake, alcohol, & exercise b/c more glucose is transported to the blood for energy… mostly when you give insulin and the patient doesn’t eat.
|
|
|
What is the sympogyi effect!!!!!!
|
Acute complication seen in type 1 diabetes mostly
|
|
|
What is seen in the symogyi effect
|
Hypoglycemia at night but in the morning they become hyperglycemic because of the counter regulation of hormones trying to balance the low levels.
|
|
|
The mechanism of symogyi effect
|
Hypoglycemia triggers glucagon response/stress response because blood sugars are low so gh, cortisol, glucagon or catecholamines secrete during the night which is when they are not suppose to be secreted (except gh) and causes a false state of rebound hyperglycemic to be seen in the morning, this is a problem because the dr gives insulin in the morning when they are NOT hyperglycemic causing them to be even more hypoglycemic then they were.
|
|
|
How is the symogyi effect caused
|
Because of the counter regulatory hormones GH, cortisol, catecholamines and glucagon
|
|
|
Symptoms of the symogyi effect is
|
1. Type 1 diabetics, 2. VIVID!! nightmares because of low sugars and 3. Have Headaches that wake them
|
|
|
SO when you see hyperglycemia in the morning you should
|
NOT assume insulin insufficiency because you will cause the symogyi effect and the patient will DIE!
|
|
|
Why does diabetic ketoacidosis occur
|
Because there is a lack of insulin causing fatty acids to be mobilized for energy
|
|
|
Who experiences diabetic ketoacidosis
|
Type 1 diabetics, mostly newly diagnosed b/c b.s. continue to rise with no way to counteract the high levels.
|
|
|
What is diabetic ketoacidosis
|
Hyperglycemia gone bad because glucose cannot be metabolized so fatty acids are metabolismed for energy
|
|
|
Symptoms of diabetic ketoacidosis
|
Polyuria, polydipsia, nausea, vomiting, fatigue, coma progressions
|
|
|
Why does coma progress with diabetic ketoacidosis
|
The hyperglycemia serves as an osmotic diuretic so the patient becomes dehydration because of excessive urination which causes hypokalemia because potassium is also secreted.
|
|
|
What is the most significant finding of diabetic ketoacidosis
|
Excessive ketoacids occurring with fatty acid leading to METABOLIC ACIDOSIS
|
|
|
What is hyperosmolar hyperglycemia nonketotic coma
|
HHNKC, Seen in type 2 diabetes! With a mortality rate of 40 to 70% It is NONKETOTIC! But still results in coma because of hyperglycemia and increased plasma osmolality
|
|
|
What is the seen in HHNKC
|
Plasma osmolality is elevated, plasma glucose greater than 600 mg/dL but no ketoacids.
|
|
|
Why does HHNKC have such a high mortality rate
|
Because ketoacidosis/metabolic acidosis is not seen like it is expected to be as a result of hyperglycemia so symptoms aren’t noticed, just though to be high sugar.
|
|
|
What are the signs of HHNKC
|
High osmolality pulls water out of the cells including neuro cells which decrease conscious levels. Siezures occur, hemiparesis, aphasia, muscle fasiculations, hyperthermia, and dehydration.
|
|
|
What are chronic complications of diabetes
|
Diabetic neuropathies, microvascular disease, macrovascular disease, & infections.
|
|
|
Diabetic neuropathy develops because
|
The nerve veseel is ischemic due to demyelinization of the Schwann cell.
|
|
|
What are the symptoms of diabetic neuropathy
|
Loss of feeling, touch, position sense, temperature and pain sensations and impotence of men. \
|
|
|
Microvascular disease includes
|
Retinopathy because fibrotic changes and new blood vessels develop in the retina and ischemia causing plasma leaks from the vessels.
|
|
|
Macrovascular disease include
|
Coronary artery disease, stroke, and peripheral vascular disease.
|
|
|
Infection in diabtes caused by
|
Increased glucose in body fluids provide energy of infection and decreases wbc to tissues, impairing phagocytosis and impairing sensations.
|
