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85 Cards in this Set
- Front
- Back
What 3 hormones does the pancreas secrete?
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insulin
glucagon somatostatin |
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What are the two types of tissue in the pancreas?
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1. Acini cells
2. Islets of Langerhans |
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What do acini cells do?
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Secrete digestive juices into the duodenum
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What do the Islets of Langerhans do?
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Secrete insulin and glucagon into the blood
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What are the 4 types of islet cells in the pancreas?
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1. Alpha cells secrete glucagon
2. Beta cells (Largest # of islet cells) secrete insulin 3. Delta cells secrete somatostatin 4. PP cells that secrete pancreatic polypeptide - unknown function |
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Normal glucose physiology incorporates the balance of ...
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food sources of glucose and the utilization of glucose (maintenance of normal blood sugar levels)
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Normal glucose range
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90 - 140 mg/dL
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Glucogenesis is
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the storage of glucose as glycogen in liver and muscle
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Lipogenesis is
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the storage of TG as fat (adipose tissue)
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Gluconeogenesis is
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the formation of glucose from non-carbohydrate sources such as lactate, pyruvate, amino acids, and glycerol
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In the endoplasmic reticulum, preproinsulin is cleaved into _____
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proinsulin
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Proinsulin is cleaved in the gogi apparatus to ____
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insulin which is then stored in the golgi apparatus
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Insulin circulates ____ in the blood
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unbound
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1/2 life of insulin is
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6 minutes
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insulin is cleared from the plasma within
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10 - 15 minutes
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The enzyme that is responsible for the breakdown of insulin is
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insulinase
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The insulin receptor on the cell contains two ___ subunits and two ____ subunits
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Alpha (outside cell) and
Beta ( inside cell) |
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When insulin binds the alpha subunit, a conformational change occurs in the beta subunit causing
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phosphorylation of tyrosine kinase, leading to several enzyme reactions
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Insulin binding to the cell causes
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increased uptake of glucose into the cell
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When glucose is transported into a muscle cell and not used, it is stored as
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glycogen
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The enzyme that is responsible for the breakdown of insulin is
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insulinase
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The insulin receptor on the cell contains two ___ subunits and two ____ subunits
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Alpha (outside cell) and
Beta ( inside cell) |
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When insulin binds the alpha subunit, a conformational change occurs in the beta subunit causing
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phosphorylation of tyrosine kinase, leading to several enzyme reactions
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Insulin binding to the cell causes
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increased uptake of glucose into the cell
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When glucose is transported into a muscle cell and not used, it is stored as
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glycogen
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When glucose is taken into the liver it is stored as
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glycogen
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Insulin promotes the formation of fatty acids from carbohydrates, which are stored in
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adipose tissue
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Excess fatty acid production leads to the formation of
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triglycerides (TG)
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True or False: The brain and neural tissue can store glucose
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FALSE
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When insulin is deficient, ___ are broken down
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triglycerides (via lipolysis)
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When glucose is taken into the liver it is stored as
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glycogen
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Insulin promotes the formation of fatty acids from carbohydrates, which are stored in
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adipose tissue
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Excess fatty acid production leads to the formation of
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triglycerides (TG)
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True or False: The brain and neural tissue can store glucose
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FALSE
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When insulin is deficient, ___ are broken down
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triglycerides (via lipolysis)
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Fatty acids are converted by the liver to
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phospholipids and cholesterol
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The breakdown of fatty acids produces
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acetoacetic acid
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Acetoacetic acid is broke down in to the ketone bodies
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acetone and bbeta hydroxy butyric acid
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Insulin makes the cell more permeable to
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amino acid transport
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Insulin favors the formation of ____ and _____.
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new proteins ; muscle growth
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Insulin increases activity of the
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Na-K-ATPase pump, driving potassium into the cell
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Increased plasma glucose causes
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Insulin release
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Insulin release is biphasic. The first phase occurs in ____.
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3-5 minutes
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Insulin release is biphasic. The second phase occurs in ___ and lasts ___.
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15 minutes; 2hours
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Factors other than increased plasma glucose that cause insulin secretion are:
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Increased levels of the following
1. amino acid presence 2. Gastrin 3. secretin 4. CCK 5. Gastric Inhibitory Peptide 6. Growth Hormone 7. Cortisol 8. Estrogen 9. Progesterone 10. Glucagon |
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Epinephrine causes increased plasma glucose by what mechanism?
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Stimulation of the Beta-2 receptor in liver and adipose tissue when the SNS is stimulated
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Glucagon is secreted by
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alpha cells of the pancreas
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Glucagon induces
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1. the breakdown of glycogen into glucose
2. frees fatty acids and inhibits TG storage 3. increases blood flow through the kidney 4. inotropy (+) |
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Glucagon inhibits
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gastric acid secretion
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Glycogen release is inhibited by
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rise in plasma glucose
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Somatostatin inhibits
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glucagon and insulin secretion
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Diabetes Mellitus is defined by
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1. Fasting plasma glucose > 125mg/dl
2. Random plasma glucose > 200mg/dl |
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Causes of increased incidence of DM are
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1. Obesity
2. sedentary lifestyle 3. rise in elderly population |
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Type I DM is aka
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Insulin dependent or juvenile onset
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Type I DM is caused by
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lack of insulin secretion
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Type I DM is thought to be
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Autoimmune or viral related
Possibly familial Other immune disorders often present |
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Type I DM onset is often ____ and occurs around the age of ___.
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rapid or abrupt; 14
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Symptoms of Type I DM include
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1. Fatigue
2. Weight loss 3. polyuria 4. polydipsia 5. intravascular dehydration 6. ketoacidosis |
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Ketoacidosis represents
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SEVERE insulin deficiency
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Pancreatic transplants are showing promise for which type of DM patients?
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Type I
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Type II DM is aka
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Non-Insulin dependent DM
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Type II DM is caused by
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insulin resistance (decreased responsiveness of cell to insulin)
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Causes of Type II DM
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1. Age (often after 30)
2. Obesity (especially childhood) *Onset is usually gradual |
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Type II initially presents as
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Hyperinsulinemia
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Hyperinsulinemia results from
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chronic hyperglycemia
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Hyperinsulinemia causes the pancreas to
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burn out and lose the ability to produce insulin
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Type II DM is associated with
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Metabolic Syndrome
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Metabolic Syndrome includes
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1.Obesity (belly fat)
2. Hyperglycemia (FBS > 110) 3. Increased TG, LDL 4. Decreased HDL 5. hypertension |
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Other causes of insulin resistance
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1. Polycystic ovarian disease
2. gluccocorticoids (Cushings) 3. Steroid administration 4. Growth Hormone excess (Acromegaly) |
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In insulin deficiency, the body's utilization of fat for energy causes
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increased TG and lipid levels
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Increased TG and circulating lipids secondary to insulin deficiency causes
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angiogenic and atherosclerotic changes
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Insulin deficiency can lead to depletion of protein stores resulting in
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muscle wasting and muscle fatigue
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Polyphagia results from
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muscle wasting caused by insulin deficiency
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Polyphagia is
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increased appetite
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Hgb A1C is
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glycosylated hemoglobin which results from chronic protein metabolism secondary to insulin deficiency
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Glucosuria is
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glucose in the urine
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The concentration at which glucose will spill over into the urine is
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180-200mg/dl
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Glucosuria can lead to polyuria because
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when glucose spills into the urine, it takes water with it (hyperosmolar)
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Long term complications of DM include
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1. Thrombotic lesions
2. Heart disease 3. HTN 4. Blindness (25x more) - retinopathy 5. Neuropathy (50% of all DM pts) 6. Vagal denervation 7. Orthostatic hypotension 8. Painless myocardial ischemia 9. ESRD 10. Stroke 11. CAD 12. Athersclerosis |
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Vagal denervation secondary to diabetic neuropathy manifests as
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Tachycardia
dysrythmias loss of HR variability seen with deep breathing |
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Orthostatic hypotension secondary to autonomic neuropathy results from
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dysfunctional sympathetic nervous system that loses vasoconstrictive ability
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What type of induction is often preffered for DM patients?
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RSI
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Why RSI for DM patients?
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Autonomic neuropathy can cause delayed gastric emptying (increased risk of aspiration)
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What helps determine aspiration risk in DM patients?
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1. How long DM has existed
2. IDDM vs NIDDM 3. Autonomic neuropathy symptoms (i.e. orthostatic hypotension, vagal denervation) |
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For RSI in the DM patient with ESRD, what would you use for muscle relaxant?
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Depending on K+ level, may need to use roc instead of succs. perform thorough airway assessment
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