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33 Cards in this Set
- Front
- Back
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Glucagon: what does it do, when is it secreted
What factors affect its secretion? |
Opposes the effects of insulin
Secretion in response to hypoglycemia Gluconeogenesis from the liver Other factors affecting its secretion Cortisol Exercise Infections Stress |
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Highest BG in the ______
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morning due to surge of counter-regulatory hormones, catecholamines
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Physiologic Insulin
How long is it secreted for? When does it peak? return to basal levels? |
Endogenous secretion over 24 hours
Insulin concentration peaks 30-45 minutes after meals Insulin levels return to basal levels within 2 – 3 hours Predictable absorption pattern in healthy individuals without diabetes |
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Carbohydrate Metabolism in Diabetes
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Muscle and fat cells lack sufficient glucose and react as if they were in the fasting state even when blood glucose levels are high
Results in metabolic abnormalities Hyperglycemia Glycosuria Loss of fluid from cells Breakdown of fat and proteins Continuous production of glucose by the liver |
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Explain:
Hyperglycemia Glycosuria Loss of fluid from cells Breakdown of fats and proteins Continuous production of glucose by the liver |
Hyperglycemia
Underutilization of glucose by fat and muscle cells Overproduction of glucose by liver Glycosuria Exceed kidney’s capacity to reabsorb glucose Excess spills over into urine Loss of fluid from cells Osmotic pull of glucose can draw water out of cells Osmotic diuresis from extreme hyperglycemia and glycosuria dehydration Breakdown of fats and proteins Adipose tissue and muscle cells metabolized to FFA and proteins as alternate fuel sources Continuous production of glucose by the liver Continuous hepatic glucose production leads to hyperglycemia during fasting state Lacking counter-regulatory effects of insulin |
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An immune-mediated destruction of β cells in the pancrea = DM ___
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Type 1 Diabetes Mellitus
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Types of antibodies and other factors involved in Type 1 DM immune response:
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Islet cell antibodies
Insulin antibodies Glutamic acid decarboxylase (GAD) antibodies - indicator that prolly have antibodies to B-cells as well Low C-peptide - cleaved portion of insulin, if it's low then not a lot of active insulin around - B-cells aren't cleaving it so there might be something wrong with them |
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Insulin resistance involving the muscle, liver, and adipocyte = DM ___
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2
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Amylin is indicated for Type I DM pts b'c....
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it's also secreted by B-cells...so if no B-cells need amylin and insulin
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effects of insulin on the liver
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Decrease glucose output
Increase glycogen synthesis Increase lipogenesis (triglycerides uptake) |
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effects of insulin in muscle
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Muscle
Increase glucose and amino acid uptake Increase glycogen synthesis |
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effects of insulin in adipose tissue
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Adipose tissue
Glucose converted to free fatty acids Stored as triglycerides |
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In the fed state, insulin...
amino acids are... |
Fed state
Insulin stimulates hepatic and muscle glycogen storage Also amino acid uptake by muscle |
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effects of stress on carb metab
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Stress
Glucagon and counter-regulatory hormones (epinephrine, cortisol, growth hormones) Increases hepatic glucose output |
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hyperglycemia leads to metabolic abrnomalities, explain the cause and effect of hyperglycemia in your own words.
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incr in osmolality -> loss of fluid from cells
need to get rid of serum glucose -> glucosuria need energy (organs starving) -> continuous hepatic prod of glucose ->b/d of fats and protein |
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what causes the following, specifically:
Hyperglycemia Glycosuria Loss of fluid from cells Breakdown of fats and proteins Continuous production of glucose by the liver |
Hyperglycemia
Underutilization of glucose by fat and muscle cells Overproduction of glucose by liver Glycosuria Exceed kidney’s capacity to reabsorb glucose Excess spills over into urine Loss of fluid from cells Osmotic pull of glucose can draw water out of cells Osmotic diuresis from extreme hyperglycemia and glycosuria dehydration Breakdown of fats and proteins Adipose tissue and muscle cells metabolized to FFA and proteins as alternate fuel sources Continuous production of glucose by the liver Continuous hepatic glucose production leads to hyperglycemia during fasting state Lacking counter-regulatory effects of insulin |
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Common signs of metabolic syndrome is skin disorder called _____ _____, include...
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acanthosis nigricans
Velvety brown or tan areas of thickened skin Neck Armpits Knees |
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Risk Factors for Metabolic Syndrome, give all 5.
How many does one need to have to be considered perdiabetic? |
Abdominal obesity
Men > 40 in Women > 35 in Triglyceride ≥ 150 mg/dL HDL Men < 40 mg/dL Women < 50 mg/dL High blood pressure ≥130/85 mmHg Fasting glucose ≥ 110 mg/dL 3/5 |
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Clinical Presentation Type 1
present with.. develop... |
Present with polydipsia, polyphagia, polyuria, and unexplained weight loss
Develop diabetic ketoacidosis if no insulin or under severe stress with excess of counter-regulatory hormones |
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Clinical Presentation Type 2
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Often present without symptoms until complications arise
Lethargy, polyuria, nocturia, polydipsia, weight gain can be seen at diagnosis |
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diff betw type 1 and 2 DM
% of Patients Age of onset Onset Presentation at diagnosis Obesity Treatment |
% of Patients: 5% - 10% / 90% - 95%
Age of onset: < 30 yr / > 40 yr Onset Abrupt / Gradual Presentation at diagnosis Acute symptoms Marked elevated blood glucose / May not be diagnosed until complications appear Obesity: Uncommon / Very common Treatment Insulin / Lifestyle modification, oral agents +/- insulin |
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Signs and Symptoms of Hyperglycemia
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Polyuria
Polydipsia Unexplained weight loss despite eating regular meals Blurred vision Slow healing cuts or sores Susceptible to infection |
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Signs and Symptoms of Hyp-O-glycemia
2 stages... +nocturnal sxs |
First stage
Adrenergic system – catecholamine release = -Anxiety -Shakiness -Sweating -Hunger tremors -Tachycardia Second stage Neuroglycopenic – CNS response to lack of glucose supply -Confusion -Irritability -Headache -Impaired mental function -Impaired vision -Motor in-coordination -Convulsion -Coma Nocturnal hypoglycemia Usually because of excess insulin therapy Symptoms usually do not awaken the patient |
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Hemaglobin A1c (HbA1c)
reflects glycemic control over... it measures the level of... |
2-3 months
glycation of HbA within red blood cells |
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A1c = ? plasma gluc
6% 7% 8% 12 think of this in relation to the AACE - American Association of Clinical Endocrinologists' guidelines and the acute/critical care guidelines for inpatient diabetics |
6% = 126
7% = 154 8% = 183 12% = 300 thus if we want BG 140-180, we're looking for a 1ac = 6.5-8% ish |
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DM2 diagnosis criteria
FBG RG HbA1c Normal Pre Diabetic |
FBG RG HbA1c
Normal <100 <140 <5.7 Pre <=125 <=199 <=6.4 Diabetic >=126 >=200 >=6.5% Diabetic |
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Glycemic Goals
ADA AACE |
American Diabetes Association (ADA)
A1c goal < 7% Pre-prandial plasma glucose 70 – 130 mg/dL Peak post-prandial plasma glucose < 180mg/dL American Association of Clinical Endocrinologists (AACE) A1c goal < 6.5% Pre-prandial plasma glucose < 110 mg/dL 2-hr post-prandial plasma glucose < 140 mg/dL |
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Long-term DM Complications
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Microvascular
Retinopathy Nephropathy Macrovascular Coronary artery disease Cerebral vascular disease Peripheral vascular disease Neuropathic Peripheral Autonomic |
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Background retinopathy (non-proliferative)
What causes it? can it be reversed? |
Arteries in retina leak forming small, dot-like hemorrhages
Possibly reversible with improved glycemic control |
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Advanced retinopathy (proliferative)
What causes it, how does it progress? can it be reversed? |
Poor circulation in retina causes ischemic areas
New, fragile collateral vessels develop New vessels hemorrhage easily Not reversible with improved glycemic control |
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Most common cause of death among patients with diabetes (75-80%)
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Cereberal & Coronary Disease - stroke, MI
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Autonomic Neuropathy
define it, and give 2 common resulting sxs. |
Dysfunction of nerves that control internal organs
GI = gastroparesis Inhibits gastric emptying time Bloating, difficulty swallowing, early satiety, reflux, anorexia, nausea, weight loss May vomit undigested food eaten hours to days earlier Improved glycemic control, metoclopramide, erythromycin can be helpful GU = sexual dysfunction PDE-5 inhibitors Often require max dose |
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The ABCs of DM Goals
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A1C <7%
BP <130/80 Cholest LDL <100, HDL >40/50, Total <200, TGs <150 mg/dL |
