Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
20 Cards in this Set
- Front
- Back
|
WHAT ARE THE COUNTERREGULATORY HORMONES AND WHAT IS THEIR ROLE IN RELATION TO THE PANCREATIC HORMONES?
|
GROWTH HORMONE - SECRETES CORTISONE, INCREASES BS
CATECHOLAMINES - EPINEPHERINE AND NOREPINEPHERINE, INCREASE BS WHEN PERSON IS UNDER STRESS CORTISOL - FROM ADRENAL GLANDS |
|
|
WHAT IS THE ROLE OF INSULIN?
|
INSULIN CAUSES GLUCOSE TO MOVE INTO CELLS SO THEY CAN GET ENERGY.
|
|
|
KETONES ARE A BI-PRODUCT OF WHAT?
|
FAT BREAKDOWN
|
|
|
IF KETONES ARE FOUND IN THE BLOOD, WHAT IS THAT INDICATIVE OF?
|
THE BODY IS USING FAT STORES BECAUSE THERE IS NOT ENOUGH GLUCOSE TO USE FOR ENERGY.
|
|
|
DIABETES HAS INCREASED INCIDENCE IN WHAT POPULATIONS?
|
ELDERLY AND MINORITY.
SPECIFICALLY: 1. NATIVE AMERICANS 2. HISPANICS 3. AFRICAN AMERICANS 4. ASIANS |
|
|
DM - TYPE 1
|
INCIDENCE 5-10%
ONSET 11-13 YEARS OF AGE LEAN BODY TYPE RAPID ONSET AUTOIMMUNE (BODY DESTROYS OWN BETA CELLS) POSITIVE ANTIBODY IN ISLET CELLS SEVERE INSULIN DEFICIENCY |
|
|
DM - TYPE II
|
>90%
ONSET >40 YEARS OLD ASSOCIATED WITH OBESITY SLOW ONSET INSULIN RESISTANCE WITH NORMAL OR DECREASED INSULIN SECRETION |
|
|
OTHER CLASSIFICATIONS OF DM
|
GDM (CAN PREDISPOOSE FOR TYPE II LATER IN LIFE)
CUSHINGS SYNDROME DRUG-INDUCED |
|
|
CUSHINGS SYNDROME
|
PROLONGED EXPOSURE TO EXCESSIVE GLUCOCORTICOID HORMONES WHICH ARE NATURALLY EXCRETED BY THE ADRENAL GLAND. CAN ALSO OCCUR DUE TO PHARMACOLOGICAL USE OF STEROIDS USED IN INFLAMMATORY CONDITIONS.
S/S: MUSCULAR WEAKNESS, THIN SKIN, EASY BRUISING, WEIGHT GAIN IN FACE, DEPRESSION, S/S OF DM |
|
|
CLIINICAL MANIFESTATIONS OF TYPE I DM
|
POLYDIPSIA - EXCESSIVE THIRST
POLYURIA - EXCESSIVE URINATION POLYPHAGIA - EXCESSIVE HUNGER WEIGHT LOSS FATIGUE |
|
|
WHY DO PT. HAVE POLYURIA WHEN THEY HAVE DM
|
FLUIDS MOVE FROM CELLS TO BLOODSTREAM
INTRAVASCULAR COMPARTMENT BECOMES HYPERTONIC FLUID GOES TO KIDNEYS AND IS EXCRETED |
|
|
WHY DO PATIENTS GET EXCESSIVELY HUNGRY WHEN THEY HAVE DM
|
THE CELLS ARE STARVING BECAUSE GLUCOSE IS NOT GETTING TO THEM.
|
|
|
CLINICAL MANIFESTATIONS OF TYPE II DM
|
3 P'S PLUS ANY OF THESE:
RECURRENT INFECTIONS GENITAL PRURITUS VISUAL CHANGES PARESTHESIAS (NUMBNESS/TINGLING - ESP. IN LEGS FINGERS) |
|
|
HOW IS DM DIAGNOSED?
|
CAN BE MADE FROM ANY OF THE 3 CRITERIA:
FASTING PLASMA GLUCOSE: BS>126 MG/DL WITH NO CALORIC INTAKE FOR AT LEAST 8 HR. S/S PRESENT + RANDOM PLASMA GLUCOSE >200 MG/DL OGTT- PLASMA GLUCOSE>200MG/DL AT 2 HOURS AFTER A 75MG GLUCOSE LOAD |
|
|
HOW IS DM CONFIRMED AFTER DIAGNOSIS IS MADE?
|
TEST IS CONFIRMED ON A SUBSEQUENT DAY USING ANY OF THE 3 METHODS USED TO DIAGNOSE.
|
|
|
IMPAIRED GLUCOSE TOLERANCE RANGE
|
140-199
|
|
|
IMPAIRED FASTING GLUCOSE
|
100
|
|
|
NORMAL FASTING GLUCOSE RANGE
|
70-100
|
|
|
GLYCOSYATED HEMOGLOBIN. WHAT IS IT AND WHAT ARE THE GOALS?
|
TEST USED TO MONITOR BG
TAKE AVERAGE BG FOR 90-120 DAYS NORMAL IS 4-6% IDEAL GOAL IS 7% OR LESS |
|
|
WHY IS URINE KETONE MONITORED?
WHEN SHOULD TEST BE PERFORMED? |
KETONES ARE A BIPRODUCT OF FAT BREAKDOWN.
INDICATES IMPENDING DKA PERFORM TEST DURING ILLNESS, STRESS, BG>250, PREGNANT, S/S DKA |
