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50 Cards in this Set
- Front
- Back
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Type 1 Diabetes
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"Hard Core"
15% -juvenile onset (12-16) -insulin taken -pancreas is broken |
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Type 2 Diabetes
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"Adult Onset"
85% -generally older 40+ |
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Pancreas cells
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Alpha Cells
-Glucagon -Stores excess glucose in the liver Beta Cells -Insulin -assist glucose in getting into cells |
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what happens when blood sugar gets low?
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alpha cells release glucagon which changes glycogen back to glucose
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what happens when blood sugar rises?
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beta cells release insulin to help glucose back into cells
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Simple VS Complex Carbs
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Simple
-jelly -candy -soda Complex -pasta -bread -rice |
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Insulin
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patients take different types at different times, take list with the patient
we do NOT give prehospital take a little less then enough to cover all the glucose, (attempt to keep hyperglycemic) |
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Hyperglycemia S/S
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similar to flu (without the fever)
-flushed -N/V -Eventually Coma (takes a few days) |
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Flu Like symptom diabetic recommendations
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-continue to take insulin
-body is utilizing glycogen stores for energy & requires insulin -if not taking insulin? flu like symptoms (hyperglycemia) |
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Diabetes complications 4
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1) feet and toes lack circulation and require amputation
-due to hyperglycemia, proteins and ketones being used for energy 2) Blindness -eye capillaries get clogged with lipids 3) ASHD -atherosclerotic heart disease due to increased lipids in blood -higher incidence of stroke and heart attack 4) Nueropathy -loss of sensation in limb -foot care and infections, due to lack of circulation -comorbid factor |
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Oral Glucose
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takes a long time to work
IV access is preferred -make sure line is patent, otherwise necrosis occurs 15g |
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Glucagon
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commonly carried by spouses
given IM condition of liver determines efficacy |
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Steps for patient refusal
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call endocrinologist
1) accurate description of scene, vitals, and treatment 2) somebody to take care of patient 3) plan for complex carbs intake -D50 is a simple sugar, u need a long lasting solution -generally soup and sandwitch, chicken and rice soup or pasta/rice |
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insulin shock
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may present similarly to ETOH
able to answer questions, but look and behave in a staggering pattern |
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Diabetic Ketoacidosis
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Hyperglycemia caused
-fatty ketones and lipids used instead of glucose -fruity breath (bad wine & vomit) -kussmaul respirations (deep rapid, try to blow of excess acid |
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causes of fruity breath
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1) homeless alcoholics
2) starvation diet 3) diabetic ketoacidosis |
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insulin reaction
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"LOW"
-Type 1 too much insulin not enough food, immediately causes AMS -extremely diaphoretic and pale -normal BP/PR/RR |
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Hyperosmolar Hyperglycemic non Ketotic coma
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-type II diabetes
-insulin is being produced but not enough (CBG > 1000 in some cases) -pt may be insulin resistant -COMA -polyphasia, polyuria, polydipsia -high mortality rate |
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major endocrine glands
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-pituitary
-thyroid -parathyroid -adrenal cortex & medulla -pancreatic islets -ovaries and testes |
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hormone classifications
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catagories
-proteins -polypeptides -derivatives of amino acids -lipids Steroids (manufactued by endocrine cells from cholesterol) -cortisol -aldosterone -estrogen -progesterone -testosterone Non-steroid made from amino acids -insulin -parathyroid hormone |
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positive vs negative feedback
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positive (continue to go)
-child in birth canal causes more oxytocin to be released = more contractions negative (homeostasis) -eating causes rising glucose in blood stream, insulin released to lower glucose levels |
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specific disorders of the
pancreas thyroid adrenal |
pancreas
-diabetes mellitus (type I and II) -hyperosmolar hyperglycemic non-kinetic coma thyroid -hyperthyroidism -hypothyroidism -myxedema -thyroid storm -thyrotoxicosis adrenal -addison disease -cushing disease |
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endocrine vs exocrine
pancreas endo vs exo |
endocrine = hormones to bloodstream
exocrine = hormones secreted through a duct to the inner or outer surface of the body acini = exocrine glands, produce digestive substances islets of laangerhans = endocrine produce hormones |
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glucagon 2 major effects
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glycogenolysis = stimulates the liver to release glucose stores from glycogen and other storage sites
gluconeogensis = glucose formation through the breakdown of fats and fatty acids, thereby maintaining a normal blood glucose level |
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Growth Hormone
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insulin atagonist (decreases insulin effects on cell membranes)
-secreted by the anterior pituitary -triggered by many physiological stimuli including A. stress B. exercise C. sleep D. Hypoglycemia |
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normal glucose range
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60-120 mg/dl
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3 main components of food
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1) Carbs
-sugary, starchy foods -near instant energy -yield glucose 2) fats 3) proteins |
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primary functions of insulin
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1) increase glucose into cells
2) increase glucose metabolism by cells 3) increase liver glycogen levels 4) decrease blood glucose concentration toward normal levels |
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hormone release from LIVER? & absorption
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stimulated by food in the duodenum
gall bladder releases bile salts enzymes and salts -nuetralize acids -emulsify fats absorption carbs = simple sugars (glycogen) fats = fatty acids & glycerol (lipoproteins) proteins = amino acids (proteins) |
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skeletal muscle, cardiac muscle, cartilage, bone, fibroblasts, leukocytes, mammary glands, liver
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insulin
-increased glucose uptake and glycogen synthesis, increased uptake of certain AA's glucagon -little effect |
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liver
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insulin
-increased glycogen synthesis, increased use of glucose for energy (glycolysis) glucagon -rapid increase in the breakdown of glycogen to glucose (glycogenolysis) and release of glucose into the blood -increased formation of glucose (gluecogenenesis) from AA's and fats -increased metabolism of fatty acids resulting in increased ketoes in the blood |
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adipose cells
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insulin
-increased glucose uptake, glycogen synthesis, fat synthesis, fatty acid uptake, increased glycolysis glucagon -high concentrations cause breakdown of fats (lipolysis) |
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nervous system
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insulin
-little effect except to increase glucose uptake in the satiety center glucagon -no effect |
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glucose storage around the body
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60% in a meal is stored in the liver as glycogen
muscles = muscle glycogen, can only be used by the muscles for energy (not into circulation) brain = no insulin effect, not very many glycogen stores |
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fat metabolism
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1/3 of glucose through liver is converted to fatty acids, and stored in adipose tissue
if no insulin -fat broken down for energy -cholesterol and triglycerides rise -acetate and betabutyric acid released |
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protein metabolism
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insulin causes proteins, cabs and fats to be stored
some are converted to glucose after breakdown in the liver if no insulin muscles are broken down allowing AA's to flood the system and be used for energy -increased urea excretion & protein wasting |
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4 mechanisms for achieving adequate blood glucose regulation are as follows
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1) the liver functions as a blood glucose buffer system, removing glucose form the blood (storing as glycogen), and returns glucose to blood when the glucose concentration and insulin secretion decline
2) insulin and glucagon function as a feedback control system. When glucose falls, glucagon is secreted to return to normal etc 3) low serum glucose levels stimulate the sympathetic system to release eppie, which has a glucagon like effect and promotes liver glycogenolysis 4) GH and cortisol play a role in long term hypoglycemic episodes. increase the rate of glucose production, and decrease rate of glucose use |
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Effects of diabetes mellitus 3
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1) decreased use of glucose by the body cells, with a resultant increase in CBG
2) markedly increased mobilization of fats from fat storage areas, causing abnormal fat metabolism, which may result in the short term in ketoacidosis and in the long term with atherosclerosis 3) depletion of protein in body tissues and muscle wasting |
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glucose spill
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when the amount of glucose entering the kidneys rises above the kidney's ability to reabsorb, glucose spills into urine, bringing water with it
dehydration results |
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acidosis in diabetes
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shift from carb burning to fat metabolism forms ketone bodies
-kausmall to compensate kidneys become overwhelmed profound acidosis and dehydration |
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Diabetes complications 6
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1) Blindness
2) kidney disease, 10%, require dialysis or or kidney transplant 3) peripheral neuropathy, nerve damage and foot infection 4) autonomic neuropathy -sexual function -bladder and bowel control -blood pressure 5) Heart disease and stroke 6) peripheral vascular disease 2ndary to atherosclerosis resulting in need for amputation |
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Insulin administration
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must be given IM
1-2 doses long acting each day frequent rapid acting insulin after meals OR insulin infusion pump, continuous dose of insulin, must check CBG often |
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Oral Hypoglycemic agents
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-stimulate release of insulin from the pancreas
-only effective in type II diabetes Common Drugs -chloropropamide -tolazamide -tolbutamine -acetohexamide -glipizide -glyburide |
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pioglitazone
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increases a patient's sensitivity to insulin
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glyburide & metformin
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lower blood sugar by causing more of the body's insulin to be released
decreasing the production and absorption of blood sugar helping the body use its own insulin more effectively |
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Hypoglycemia
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blood glucose below 80 mg/dl
symptoms occur at 60 mg/dl can also occur in non diabetics if physical exerted, ETOH/Drug effects, pregnancy or lactation, decreased intake diabetics -too much insulin -decreased dietary intake (missed meal) -admin of certain antibiotics Less common factors -chronic ETOH (depletes glycogen scores) -adrenal gland dysfunction -liver disease -malnutrition -pancreatic tumor -cancer -hypothermia -sepsis -beta blockers propanolol -admin of salicyliates in ill infants or children |
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Hypoglycemia S/S
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related to the release of epinephrine as the body tries to compensate for a drop in blood sugar, extreme hunger common
S/S -nervousness, trembling -irritability -psychotic (combative behavior) -weakness and in coordination -confusion -appearance of intoxication -weak, rapid pulse -cold, clammy skin -drowsiness -seizure -coma (severe cases) |
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Diabetic Ketoacidosis
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DKA
not enough insulin, glucose accumulates in blood, body changes from glucose to fat use -fatty acids & glycerol generated -acidosis causes loss of potassium from cells -sodium outside of cells decreases (replaced by hydrogen) ultimately -cardiac dysrhythmias -altered nueromusclar activity & seizure |
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DKA S/S
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slow in onset (12-48 hrs)
-diuresis -warm, dry skin -dry mucus membranes -tachycardia, thready pulse -postural hypotension -weight loss -polyuria -polydipsia -acidosis -ABD pain -anorexia, N/V -fruity breath -Kussmaul respiration in an attempt to reduce carbon dioxide -ALOC check for head injury, stroke, or drug OD |
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Hyperosmolar Hyperglycemic Nonktetotic Coma
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common in older patients with type 2 diabetes
or undiagnosed diabetes enough insulin to prevent metabolism of fats, but not enough to prevent glucose use by peripheral tissues or to reduce fluconeogenesis by the liver Hyperosmolar state, diuretic state CBG > 1000 |
