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236 Cards in this Set
- Front
- Back
What are the two types of diabetes
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Type 1
Type 2 |
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What is diabetes?
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Diabetes is a disorder of carbohydrate metabolism.Diabetes is the most common edocrine disorder,.
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What does Insulin do in mormal body functioning?
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Insulin pulls glucose out of the blood stream and into the cells.
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What does Glucagon do in normal body functioning?
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Gulcagon inhibits the effects of insulin thus preserving glucose leves in the blood.
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What are the symptoms of diabetes?
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sustained hyperglycemia polyuria, poly dipsia, ketonuria and weight loss
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At what age does type 1 diabetes become evident?
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Juvenile onset of diabetes, usually begins @ age 11-13 with abrupt syptoms.
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What is the primary defect of type 1 diabetes?
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Destruction of pancreatic beta cells--thus a lack of insulin.
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If the body goes without insulin in type 1 diabetes where does the body get glucose for energy?
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Ketoacidosis
D/T lipids being used for energy leaving ketoacid as waste and lowers pH blood (more acidic) |
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Over time what problems can diabetes cause?
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HTN, heart disease, blindness, renal failure neruopathy, amputations, impotence and stroke.
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What is the most prevelant form of diabetes?
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Type 2
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What is almost always present in type 2 diabetes?
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OBESITY--with little risk of ketoacidosis
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What is the age onset of type 2 diabetes?
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Middle age
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Why does type 2 diabetes form?
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It's a result from Insurlin resistance and imparied insulin secretion
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What type of diabetes do pregnant women get?
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Gestational Diabetes
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What is gestational diabetes caused from?
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It's due to the placenta producing hormones that antagonize insulin
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The production of ? rises during gestationl diabetes?
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Cortisol rises to a lever 3X normal
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What are the shortterm complications usually seen with type 1 diabetes?
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HYPER or HYPO glycemia, ketoacidosis
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What can result from untreated HYPERgylcemia?
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Ketoacidosis and DEATH
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What are the most commen long term complications of diabetes?
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The disruption of blood flow from macro or microvascular damage.
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What are some MACROvascular complication damage?
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CARDIOVASCULAR (leading cause of death)Heart disease, HYPERtention, Atherosclerosis (develops early), HYPERglycemia, Altered Lipid metabolism
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What are some MICROvascular complication damage?
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Retinopathy, Nephropathy, Neuropathy, Gastroparesis, Amputations, Erectile dysfunction
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What can Nephropathy cause?
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Proteinuria, Decreased GFR, HTN
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What does Retinopthay cause?
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BLINDNESS (DM major cause of blindness)
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Is Gestational diabetes difficult to control? Why?
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Yes, since plecenta producing hormones antagonize insulin's action makeing mother HYPERglycemic so baby secretes insulin.
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What does Gestational Diabetes cause?
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FAT BABIES
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When does gestational diabetes usually subside?
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Usually within 6 weeks post-pardum
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How often should a pregnant Type 1 or 2 diabetic test insulin?
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6-7 times per day due to pregnancy
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How do you determaine if your patient is diabetic?
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Test plasma glucose-on TWO SEPERATE days, BOTH tests MUST be POSITIVE
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What type of tests are administered to determain plasma glucose?
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1. Fasting Plasma Glucose(FPG)
2. Casual Plasma Glucose 3. Oral Glucose Tolerance(OGT) |
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How would you administer a Fasting Plasma Glucose test?
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Administer 8-10 hours after last meal.
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What is the Normal levels for a FPG, Casual glucose test and OGT?
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FPG NORMAL= 100mg/dl POSITIVE=>126
Casual glucose= <200mg/dl OGT NORMAL= <200mg/dl @1hr. POSITIVE= <140mg/dl @2hr |
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How do you administer the ORAL glucose test?
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Give load of 75gm and measure glucose @ hr1 and hr2
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What is the Glucose test reading for a pre diabetic? (borderline diabetic)
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Fasting Glucose of 100-125mg/dl
Glucose tolerance test of 140-199mg/dl |
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What are some metabolic symptoms of PRE-DIABETES? (borderline diabetic)
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B/P > than 140/90, Fasting Bld. sugar >110, Triglycerides >150, HDL<40 in males and <50 in females
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What is the treatment for type 1 diabetes?
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Diet, Exersise, Insulin, Monitoring BS Hemoglobin A1c, and Urine glucose.
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Thwat are the treatments for Type 2 diabetes?
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Lifesytle Changes-then add 1agent then 2 agents then 3 agents then agent plus insulin then only insulin
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What should glucose be BEFORE meals? AFTER meals?
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BEFORE- 90-130
AFTER-100-140 should test 2hrs after meal |
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What does a Glycosylated Hemoglobin test reflect? (HA1c)
NORMAL LEVEL? |
The average glucose lever over 2-3 months
NORMAL is LESS than 7 |
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What system controls the release of insulin?
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Sympathetic Nervous System
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What is the stivulus for the SNS to release insulin?
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GLUCOSE
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Which receptor activation promotes insulin secreation?
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Beta 2adrenergic receptor activation
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Which receptor stimulation inhibits insulin secreation?
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Alpha Andrenergic Stimulation
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What indicates that the pancreas is still producing some insulin?
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C-peptide in the blood
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What part of the pancreas is in charge of insulin production?
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Beta cell of the islets of LANGERHANS
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What is the ANABOLIC ACTIONS due in the body?
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Anabolic actions CONSERVE ENERGY & Build energy stores, PROMOTE SYNTESIS of complex organic molecules
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What is the METABOLIC consequences of lack of insulin?
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CATABOLIC MODE-Where glycogen is convereted to glucose LEADING TO KETOACIDOSIS
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What do Catabolic reation due in the body?
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PROTEINS CONVERT to AMINO ACID
Fats into glycerol and fatty acids |
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What does Insulin DEFICIENCY PROMOTE?
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HYPERglycemia which INCREASES GYCOGENOLYSIS
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What can an increasing gluconeogenesis cause?
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Ketoacidosis occurs seconday to disruption of glucose and fat metabolism
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How does insulin get into the body when it is needed?
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while eatting insulin is secreted based on the food, if your not eating insulin isnt produced
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What can shut off insulin?
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Exercise
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What are the types of insulin medications used?
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SHORT duration= RAPID or SLOW acting, Intermediate duration, LONG deration
|
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What afe the types of RAPID ACTING insulin? How RAPID is the onset?
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HUMALOG-onset 15-30min lasts 3-6hr.
NOVOLOG(analog of human insulin)-onset10-20min lasts 3-5hr APIDRA(synthetic analog of human insulin)-onset 10-15min lasts 3-5hrs |
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What are the SLOWER actiing insulin? onset?
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HUMULIN R/ NOVOLIN R onset 30-60 minutes peaks 1-5 hrs. lasts up to 10hr.
|
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What is the most common use of SLOW acting insulin? How is it given?
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Most commonly used in NPO surgical cases
ONLY IV INSULIN FORM |
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What are the INTERMEDIATE duration insulins?
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HAGEDORN (NPH)-regular insulin with protamine to retard absorption
LANTUS |
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What does insulin look like?
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All clear EXCEPT NPH its cloudy
|
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What are the concentrations of insulin?
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100units/ml & 500units/ml
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What is the ONLY insulin safe for mixing with sort acting insulins?
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NPH
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What should you administer for an insulin overdose or hypogycemia?
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ORAL glucose tab
PARENTERAL gulcagon IV glucose |
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How is Insulin administered?
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SUBQ
INHALATION (exubera) IV (only REG insulin) |
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What insulin injection site has the most consistent absorption rate?
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ABDOMEN
|
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How is insulin stored?
|
Store unopened vial in fridge until open then store room temp for 1 month--prefilled syringers store needle up for up to 1 week
|
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What are some drug interactions that will cause HYPOglycemia?
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Sulonylureas, troglitazone, ETOH and Beta-adrenergic blockers
|
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What interacts with insulin to make pt. HYPERglycemic?
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Thiazide diuretics, glucocoticoids, and sypathomimetics--must increase insulin with these meds.
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What do BETA-andrenergic blocking agents due to the awareness of insuling reactions?
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Delays awareness of insulin-induced HYPOglycemia by masking symptoms associated with SNS
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What are the ORAL HYPOglycemic drugs for type 2 diabetes?
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Sulfonylureas such as TOLBUTMIDE
Meglitinides such as REPAGLINIDE or NATEGLINIDE |
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IMPORTANT things to know about TOLBUTMIDE
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Concomitant use of NSAIDs, Sulfa antibiotics,Ranitidine and Imetidine can ^ risk of HYPOglycemia
|
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Which patients should avoid the use of TOLBUTAMIDE?
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PREGNANT or BREAST FEEDING
|
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What can Beta Blockers due when used with TOLBUTAMIDE?
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can mask hypoglycemic s/s and suppres insulin release
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What interacts with Repaglinide?
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Gemfibrozil-inhibits etabolism of Prandin causing higer levels
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What levels should you watch when taking METFORMIN?
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Monitor for elevated SERUM CREATINE levels
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How does METFORMIN lower blood glucose levels?
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It decreases the production of glucose by the liver (NOT by promoting insulin secreation)
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Where is METFORMIN absorbed? Excreated?
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Absorbed in intestine
Excreted by kidneys |
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What is METFORMIN used for?
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Polycystic ovary syndrome
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What should patient avoid while taking METFORMIN? Why?
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ETOH, ^risk of lactic acidosis
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What do THIAZOLIDINEDIONES do?
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They increase target cell to respond to insulin
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Who are THIAZILIDINEDIONES used in?
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Insulin resistant patients
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What are two types of THIAZOLIDINEDIONES?
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Avandia and Actos
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What is the half life of Avandia?
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3-4 hours
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What are some side effects opf Aandia?
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fluid retention, lopid ^ plasma levels of avandia
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What is the most important remember about GLITIZONES such as Actos?
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DO NOT GIVE TO CARDIAC PATIENT WITH HEART FAILURE
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What are the alpha-glucosidease inhibitors?
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Acarbose
Miglitol Muraglitazar |
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What does ACARBOSE decrease absorbtion of?
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IRON in anemia & CARBS
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Waht is a CAUTION of ACARBOSE?
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HEPATIC DYSFUNCTION
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Who is MIGLITOL effective in?
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Hispanics & African Americans
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Is Miglitol associated with hepatic dysfunction?
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NO
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Which Alpha glucosidase inhibitor is EXPERIMENTAL?
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Muraglitazar
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How should you educate your patient about ALPHA-GLUCOSIDASE INHIBITORS?
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TThey may cause GI problems such as flatulence & diarrhea
DOES NOT CAUSE HYPOglycemia when used as MONOTHERAPY |
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What are some NEW INJECTABLE drugs for diabetes?
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SYMLIN & BYETTA
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What is BYETTA derived from?
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Lizard spit
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In adjunctive terapy what can BYETTA improve?
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Glycemic control in patients with type 2 diabetes
|
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What is Ketoacidosis?
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EMERGENCY--derangement of glucose and fat metabolism
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What are some characteristics of KETOACIDOSIS?
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hypERglycemia,Ketoacids,Hemoconcentration,Acidosis, COMA
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Treatment for Ketoacidosis?
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IV Insulin replacement, Bicarb, H2O & Saline (Iso or Hypotonic), K replacement (monitor ECG), Normalize BS levels
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What should you watch for when treating ketoacidosis?
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SWITCH TO HYPOglycemia
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What is Rheumatoid Arthritis? (RA)
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Auto immune inflammatory disorder-when body attacks joints-progressive-crippleing
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What is GOUT?
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Recurrent inflammatory disorder characterized by HYPERuricemia & episodes of severe pain. Typically in LG toe
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When is RA usually present?
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Usually in 30s or 40s-3x greater in Females, >60 equally effect in gender
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Treatment for GOUT?
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Relieve symptoms, Maintain joint function and ROM, Minimize systemic involvement, Delay progression of disease.
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What are the s/s of RA?
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Symetric joint stiffness & pain(worse in AM, Joints warm, tender, swollen, tired, weak, anorexia and wt loss, vasculitis.
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What are the classes of Antiarthritics?
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NSAIDs-nonsteroidal anti inflammatory drugs
DMARDs-disease-modifying antiheumatic drugs GLUCOCORTICOIDS-adrenal corticosteroids |
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What is the advantage of combining NSAIDs and DMAEDs?
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Fast acting and inexpensive
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What is the maintenance dose of NSAIDs and DMARDs?
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7.5-20mg/week
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What should be monitored when useing NSAIDs with DMARDs?
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LIVER & KIDNEY FUNCTION
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What is the most rapid acting DMARD?
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RHEUMATREX
1ST CHOICE OF DMARD |
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what drug used with Rheumatrex is used to produce remission of RA symptoms?
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Hydroxychloroquine (Antimalarial drug)
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What is the dosage and toxicity of Hydroxychloroquine?
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Dosage 200mg BID or 400mg QDay
Toxicity - risk of irreversible retinal damage. |
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What is Azulfidine used for?
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Retard joint deteriation // once used for IBS.
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What's the #1 reason for discontinuing Azulfidine?
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GI problems (divide dose to decrease affect)
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What are the adverse affects of Azulfidine?
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Hepatitis and Bone Marrow Supression - Rare.
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Remicade in combo with Rheumatrex for RA patients/crohns disease and ankylosing spondylitis not for use in what type of patient?
|
DO NOT USE in patients with HEART FAILURE can cause new onset heart failure.
^ risk of lymphoma. |
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Uses of Enbrel
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Moderate/severe MA
Ankylosing Spondylitis, Psoriasis, Psoriatic arthritis. |
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What are the adverse affects of Enbrel?
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Infection, Injection site reaction, Interracts with Live Vaccines.
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What is Arava?
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Powerful DMARD, LAST RESORT
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What are the side affects of Arava?
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Diarrhea, Reversible Alopecia, Resp Infection, Rash, Nausea, Inhibits NSAIDS ^Liver damage with Hepatotoxic drugs.
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What is Kineret?
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DMARD for SERIOUS ACTIVE RA.
Blocks receptors for Interleukins-1. |
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Is Kineret approved for SUBQ injections?
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YES
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What are the adverse affects of Kineret?
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Injection site reactions (1st month of treatmetn), Serious infection.
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What is Gout?
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Recurrent infammatory disorder.
Uric acid crystals collecting in a joint. |
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What is Hyperuricemia?
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Excessive uric acid production and impaired renal excretion.
|
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How does Gout progress?
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4 Stages
1) Asymptomatic hyperuricemia 2) Attacks of acute gouty arthritis.. 3) Symptoms subside 4) Tophaceous gout |
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What is the Therapy for Gout?
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Relieve Inflamation, reduce hyperuricemia
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What are the drugs for Gout?
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Colchicine, Indocin, Zyloprim, Benemid, Anturane.
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What is Colchicine?
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Anti-inflamatory agents that target Gout.
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What are the uses of Colchicine?
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Treat acute Gout, Reduce attacks, Abort impending attack.
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What are the adverse affects of Colchicine?
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N,V & D + ABD Pain = STOP DRUG
Caution: cardiac, renal, GI disease, elderly, pregnancy. |
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When administering Colchicine, what should you do?
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Make sure IV line is patent.
Mix 20ml NS & IV push slow 5-10 minutes |
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What is Zyloprim?
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Reduces uric acid levels and inhibits production.
|
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What are the uses of Zyloprim?
|
LONG TERM USE - Chronic tophaceous gout #1 Choice. HYPERuricemia due to CA Chemo
|
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What are the adverse affects of Zyloprim?
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Rash = discontinue, Hypersensitivity syndrome, Mild GI, Neuro.
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Zyloprim drug interractions?
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Inhibits hepatic drug enzymes, Anti-Coags and CA drugs (decrease warfarin dose), Rash with ampicilin.
|
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How should Zyloprim be administered? Why?
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With plenty of liquids to avoid renal damage.
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What is the action of Probenecid?
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Inhibits reabsorption of uric acid in renal tubules.
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How should Probenecid be administered?
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With 2-3L of H2O and food.
|
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What are the drug interractions with Probenecid?
|
ASA interferes with uricosuric action = reduce indocin and other sulfonamide dosages.
Mild GI effects. |
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What is Cacium?
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Element - critical to blood coagulation and Bone, Nerve, Muscle, and Heart function.
|
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How does the body regulate Calcium?
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Parathyroid Hormone, Vitamin D, and Calcitonin.
|
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Where is Ca stored in the body? How much?
|
98% of Ca stored in BONES
|
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WHere is Ca absorbed?
|
In the SMALL INTESTINE
|
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What are the Ca requirement for 9-18 & 51<
|
9-18y/o= 1000mg/day
51 or <= 1200mg/day |
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What decreases aborsorbtion of Ca in the body?
|
Glucocorticoids, Brans and Whole Grains
|
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What increases absorbtion of Ca?
|
Parathyroid Hormone
Vit D |
|
What is the NORMAL value for total serum Ca in body?
|
10mg/dL
50%bound to proteins 50%free |
|
Bone undergoes continuous remodeling, What are OLD bone deposits? NEW bone deposits?
|
OLD-osteoCLASTS
NEW-osteoBLASTS |
|
What are the 3 ways Ca adjusts in the body?
|
1.ABSORBTION from INTESTINE
2.Excretion by KIDNEY 3.RESORBTION/depostion by Parathyroid hormone, VitD, & Calcitonin |
|
What is Cacium?
|
Element - critical to blood coagulation and Bone, Nerve, Muscle, and Heart function.
|
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How does the body regulate Calcium?
|
Parathyroid Hormone, Vitamin D, and Calcitonin.
|
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Where is Ca stored in the body? How much?
|
98% of Ca stored in BONES
|
|
WHere is Ca absorbed?
|
In the SMALL INTESTINE
|
|
What are the Ca requirement for 9-18 & 51<
|
9-18y/o= 1000mg/day
51 or <= 1200mg/day |
|
What decreases aborsorbtion of Ca in the body?
|
Glucocorticoids, Brans and Whole Grains
|
|
What increases absorbtion of Ca?
|
Parathyroid Hormone
Vit D |
|
What is the NORMAL value for total serum Ca in body?
|
10mg/dL
50%bound to proteins 50%free |
|
Bone undergoes continuous remodeling, What are OLD bone deposits? NEW bone deposits?
|
OLD-osteoCLASTS
NEW-osteoBLASTS |
|
What are the 3 ways Ca adjusts in the body?
|
1.ABSORBTION from INTESTINE
2.Excretion by KIDNEY 3.RESORBTION/depostion by Parathyroid hormone, VitD, & Calcitonin |
|
WHat are the causes of HYPERcalcemia?
|
Cancer, HYPERparathyroidism, VitD intox, Sarcoidosis, Use of Thyazide Diuretics, Osteoperosis
|
|
What are the treatments for HYPERcalcemia?
|
Decrease intestional absorbtion, Mobilization from bones, Take Iso tonic saline Diuretics,Glucocorticoids, Calcitonin, Biophosphonates, Inorganic Phos, Gallium Nit.
|
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Signs and symptoms of HYPOcalcemia?
|
^ Neuromuscular excitability (Convultions,Tetany, Spasms of the Pharynx)
|
|
What are the treatments for HYPOcalcemia?
|
CaCL (in severe cases, asses for brady if taking dig.), Ca supplements, VitD
|
|
Other disorders involveing Ca?
|
Rickets, Osteomalacia, Paget's disease, Osteoperosis, HYOPO/HYPER parathyroidism
|
|
What is Osteoporosis?
|
Ca motabolism = low bone mass, ^bone fragility
|
|
Preventative measure for Osteoperosis?
|
WT. bearing exersizes
NO SMOKING NO DRINKING |
|
Treatment for osteoperosis in WOMEN?
|
Antiresorbtion threapy drugs, Drugs that promote bone formation
|
|
What are the the Antiresorbiton therapy drugs used?
|
Foxamax
Evista |
|
How do you administer FOSSAMAX?
|
Once daily or Once weekly
|
|
what is the common side effect of FOSSOMAX?
|
GI
|
|
What is the ONLY drug that INCREASES bone FORMATION in osteoperosis?
|
FORTEO
|
|
What is the side effects of EVISTA?
|
^ RISK of DVT and PULMONARY EMBOLIS
|
|
What is required for absorbtion of Vit D? Where is it absorbed?
|
Bile and Sun light
small intestine |
|
What are the daily dosages of vit D in ages 0-50
50-70 & 70+ |
Chilren (birth -50y/o) = 200IU/day
50-70 = 400IU/day 70 + 600IU/day |
|
What function does the thyroid hormones of the body have?
|
profound effects on Metabolis, Cardiac funcion, Growth and Development
|
|
What do the thyroid hormones stimulate?
|
the metabolic rate of most cells and ^ force &rate of cardiac contraction
|
|
What are the 2 active thyroid hormones in the body?
|
TRIODOTHYRONIN (T3)-more potent than T4
THYROXINE (T4)-converted to T3 in most tissues |
|
What are the Thyroid Function tests?
|
TSH-Most sensitive method 2 diagnose HYPOthyroidism
T4 Test-measures total thyroxine Confirms Diagnosis T3 Test-measures total Trilodothyronine-tests for HYPERthyrodism |
|
What is SEVERE dificiency of thyroid hormone called?
|
MYXEDEMA in adults
CRETINISM in children |
|
What are some clinical presentations of HYPOthyroidism in adults?
|
Puffy expressionless face, Brittle/loss of hair, Lowered HR/Temp, Lethargy, Cold intolerence
|
|
WHat do the labvalues mean in HYPOthyroidism?
|
HIGH TSH = LOW T4 serum
|
|
What are the clinical presentation of HYPOthyroidism in children?
|
Mental retard, Derangement of growth, Large protrudeing tounge, Potbelly, Dwarfish appearance, Impaired NS, Bones, Teeth, and Muscles
|
|
What are the 2 major forms of HYPERthyroidism?
|
1. Graves'disease MOST COMMON
2.Plummer's disease-toxic nodular goiter |
|
What are the effects of HYPERthyroidism?
|
Thyrotoxicosis-EMERGENCY high levels of thyroid hormone Exophthalmoses-buldgeing eyes
Rapid HR w/dysrhythmias Nervousness, rapid speech, insomnia, muscle weakness, intolerence to heat, sweaty skin and wt loss |
|
Whom whould you refer your pt to if they have Toxic Nodular Goiter (Plummers disease)
|
SERGERY or RADIATION
|
|
What do you treat Tachycardia seconday to HYPERthyroidism?
|
PROPANOLOL
|
|
What are the lab values for HYPERthyroidism?
|
LOW TSH levels
|
|
What is the cause of HYPERthyroidism?
|
Thyroid-stimulating Immunoglobulins (TSI)
|
|
What is the treatment of HYPERthyroidism?
|
Surgical removal, Destruction of thyroid tissue with radioactive iodine-supress thyroid hormone release, Supress release with Anti-Thyroid drugs
|
|
What drug is used for all forms of HYPOthyroidism?
|
SYNTHROID
|
|
How does SYNTHROID work?
|
Its a Synthetic form of T4 that converts to T3
Protein bound 1/2 life = 7 days |
|
What are the adverse effects of SYNTHROID?
|
Tachy, Angina, Tremors
|
|
How does the drug PROPYLTHIOURACIL (PTU) work?
|
Inhibits thyroid hormone by preventing oxidation of iodine and inhibits iodinated tyrosine from coupling
|
|
What is the 1/2 life of PROPYLTHIOURACIL (PTU)?
|
75-120 min.
ONLY AVAILABLE ORALLY |
|
What are the theraputic uses of PTU?
|
Graves disease or in adjuct with radiation therapy
|
|
What are some adverse effects of PTU?
|
Agranulocytosis -CHECK WBC count
HYPOthyroidism Jaundice, fever/chills, sore throt, bleeding gums-STOP NOW |
|
How does Radioactive Iodine 131 work?
|
emits gamma and beta rays to cause distruction to thyroid tissue
|
|
What is the 1/2 life of Radioactive Iodine 131?
|
8 days
|
|
What is Radioactive Iodine 131 used for?
|
Grave's disease
|
|
What are the ADVANTAGES and DISADVANTAGES of using Radioactive Iodine 131?
|
ADVANTAGES:cheap less risk and discomfort, no sergery
DISADVANTAGES:delay in effect and incidence of delayed HYPOthyroidism |
|
What is NONRADIOACTIVE IODINE?
|
Strong iodine solution (lugol'g solution) that suppresses thyroid funciton in PREPERATION for THROIDECTOMY
|
|
What are some ADVERSE effects of NONRADIOACTIVE IODINE?
|
Brassy taste, buring in mouth/throat, Sore teeth & gums, Frontal HA,
|
|
What do the HYPOTHAMOUS & PITUITARY work?
|
They work together to regulate amost all BODILY processes
|
|
What Hormones do the hypothalamus and pituitary employ?
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15, 3 main agents for our foucus
1.GROWTH HORMONE (GH) 2.ANTIDIURETIC HORMONE (ADH) 3.PROLACTIN |
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What is the effects of GROWTH HORMONE?
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Promote growth, Protein Synthesee, & Carb. Motabolism
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What is the effects of an EXCESS and a DEFICIENT amount in children and adults?
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EXESS-children-gigantism adult-acromegaly
DEFICIENCY-children-short stature, adult-reduced muscle mass |
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what is the ONLY treatment for DEFICIENCY of GH?
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Replacement with human GH, some may respond to sermorelin which PROMOTES GH
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What is the treatment of Acromegaly?
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Surgery, radiation or SOMAVERT
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What should you check ANNUALLY in GH deficiency pt that are being treated with GH?
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EPIPHYSEAL STATUS
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What are some adverse effects of GH?
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HYPERglycemia, Antibodies to GH, Carpal Tunnel, Fatality in Prader-Willi syndrome pts., Interacts w/ Glucocorticoids
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What blood levels should be checked periodically in pts receiving GH?
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TSH LEVELS
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How is GH administered?
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.06mg SUBQ 3x per wk til goal height is metor until closure of epiphyseal plate--comes in powder form DONT SHAKE
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What is another name for GH--the drug name?
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SOMATROPIN
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What si PROLACTIN?
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Hormone produced by ANTERIOR PITUITARY that stimulates milk production after birth.
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What can hypersecreation of PROLACTIN in males and females cause?
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MALES-libido & potency reduced, Galactorrhea
FEMALES-amenorrhea, glactorrhea, infertility |
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What drug should be administed to suppress prolactin release?
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DOSTINEX
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What is THYROTROPIN (TSH)?
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Hormone that stimulates the thyroid gland function
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What are the effects of THYROTROPIN?
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Increase thyroidal uptake of iodine, ^synthesis of Thyroid Hormone, ^release of thyroid hormone &thyroidal growth
*USED TO DIAGNOSE THYROID CA* |
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What is CORTICOTROPIN (adrenocorticotropic hormone ACTH)?
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Acts on adrenal cortex to stimulate producion & release of adrenocortical hormones
*USED TO DIAGNOSE ADRENOCORTICAL DYSFUNCTIONp |
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What does the ANTIDIURETIC HORMONE (ADH) do in the body?
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It promotes renal conservation/ reabsorbtion of H2O
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What are the therapeutic uses of an ADH?
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Diabetes, Cardiac arrest, Postop abd distention, Hemophilla A, Von Willebrands disease
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How is ADH administered?
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PO, Intra-nasal, IV, SUBQ
*NOT IM* |
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What is the role of OXYTOCIN?
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Promote Uterine contractions and stimulate milk ejection
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What are THE TWO MOST FAMILIAR FROMS OF adrenocortical dysfunction?
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COUSHING'S SYNDROME--EXCESS adrenal hormon
ADDISONS DISEASE-adrenal hormone DEFICIENCY |
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What are the 3 classes of steroid hormones?
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1.Glucocorticoids
2.Mineralocorticoids 3.Androgens |
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What do MINERALOCORTICOIDS do?
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Influence renal processing of NA,K & Hydrogen
*ALDOSTERONE MOST IMPORTANT* |
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What are the physiologic effects of MINERALOCORTICOIDS?
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aldosterone acts on collecting ducts to promote NA reabsorbtion in exchange for secretion of K and H
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What is the causes of CUSHINGS SYNDROME?
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HYPERsecretion of ACTH, Glucocorticoids and administering glucocorticoids in Lg doses
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How does CUSHINGS SYDROME present?
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Obesity, HYPERglycemia, Glycosuria, HTN, Fluid and Elec. disturbences
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What are some treatments for CUSHINGS DISEASE?
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Surgicaly removal of adrenal gland, Replacement therapy, Irradation of pituitary gland
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What is clinical presentation of ADDISONS DISEASE?
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Wakness, Emanciation, HYPOglycemia, ^ pigmentation of skin and mucus membrane
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What are the clinical representations of ACUTE ADRENAL INSUFFICIENCY?
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HYPOtention, Dehydration, Weakness, Lethargy, GI symptoms
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What can cause ACUTE ADRENAL INSUFFICIENCY?
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Adrenal failure, Pituitary failure, Inadequate doeses of Corticosteroids, Adrenal crisis
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What is the treatment of ACUTE ADRENAL INSUFFICIENCY?
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RAPID relacement of fluid, salt, and glucocorticoids, Glucose
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what is the treatment of ADDISONS DISEASE?
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Replacement therapy with adrenocorticoids
HYDROCORTISONE DRUG OF CHOICE |
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What are some therapeutic uses of HYDROCORTISONE?
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Adrenal insufficiency, Allergic reactions, Inflammation and Treatment of CA
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What are some adverse effects of HYDROCORTISONE?
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In HIGH doses-Adrenal suppression, Cushing's syndrome
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What is the ONLY mineralocorticoid available?
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FLORINEF
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What are the Therapeutic uses for FLORINEF?
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Addisons disease, Primary HYPOaldoteronism, Congenital adreanl hyperplasia
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