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WHAT CAN OCCUR IF HYPOGLYCEMIA IS NOT TREATED?
LOSS OF CONSCIOUSNESS, SEIZURES, COMA, AND DEATH.
HOW IS HYPOGLYCEMIA PREVENTED AND TREATED?
PREVENTION: CALCULATING AND ADMINISTERING INSULIN DOSAGES WITH REGARD TO NUTRITIONAL INTAKE AND PHYSICAL ACTIVITY

TREATMENT: ADMIN OF 15-20 G OF GLUCOSE. THE METHOD DEPENDS ON LEVEL OF CONSCIOUSNESS. IF PERSON IS ABLE TO SWALLOW, FRUIT JUICE, HONEY OR CANY MAY BE GIVEN. IT IS REPEATED IN A FEW MINUTES IF IT DIDN'T WORK.

GLUCAGON MUST BE ADMINISTERED PARENTERALLY, IM, OR SUB Q IF PERSON IS UNCONSCIOUS
WHAT IS DKA?
DIABETIC KETOACIDOSIS, A PROBLEM OF DEFICIENT INSULIN AND SEVERE HYPERGLYCEMIA LEADING TO A STATE OF METABOLIC ACIDOSIS AND SEVERE OSMOTIC DIURESIS. HAPPENS MOST OFTEN WITH TYPE I DIABETES AND USUALLY DEVELOPS OVER A FEW DAYS AND IS TRIGGERED BY INCREASED DEMAND FORINSULIN, AS WITH STRESS, INFECTION, OVERCONSUMPTION OF FOOD, PREGNANCY, OR NOT ENOUGH INSULIN ADMIN. ONSET OF DKA MAY BE THE EVENT THAT MAKES THE PERSON AWARE THAT THEY HAVE TYPE I DIABETES. BLOOD GLUCOSE CAN REACH AS HIGH AS 1000 MG/DL.
WHAT IS THE MECHANISM FOR DKA
LAKE OF INSULIN CAUSES MOBILIZATION OF FATTY ACIDS FOR ENERGY, LEADING TO INCREASED PRODUCTION OF KETONES. KIDNEYS CANT EXCRETE THE KETONES AND THE CELLS ARE UNABLE TO USE THESE BYPRODUCTS, ALLOWING THEM TO ACCUMULATE IN BLOOD. CAN PROMOTE OSMOTIC DIURESIS, ELECTROLYTE LOSS, AND DEHYDRATION
WHAT ARE S/S OF DKA?
SAME AS SEVERE HYPERGLYCEMIA, METABOLIC ACIDOSIS, AND DEHYDRATION. MANIFESTATIONS PRECEDING DKA ARE POLYURIA, POLYDIPSIA, POLYPHAGIA, NOCTURIA, WEIGHT LOSS AND FATIGUE. ABDOMINAL PAIN AND VOMITING ARE COMMON. WITH THE ONSET OF ACIDOSIS, BUFFER SYSTEMS ARE TAXED AND COMPENSATORY CHANGES OCCUR IN AN EFFORT TO IMPROVE THE ACIED BASE BALANCE IN THE BODY.
WHAT ARE KUSSMAUL RESPIRATIONS?
DEEP, RAPID RESPIRATIONS THAT RELEASE EXCESS ACIDS THROUGH THE LUNGS AND INTO THE ATMOSPHERE.  THE BREATH HAS A SWEET FRUITY ODOR CAUSED BY RELEASE OF ACETONE, A VOLATILE FORM OF KETONES.  THE DECREASED CIRCULATING BLOOD VOLUME PROMOTES TACHYCARDIA AND HYPOTENSION. ACIDOSIS TRIGGERS A DECREASED LEVEL OF CONSCIOUSNESS WHICH CAN PROGRESS TO COMA AND DEATH
WHAT DOES TREATMENT OF DKA FOCUS ON?
STABILIZING BLOOD GLUCOSE LEVELS, CORRECTING ACIDOSIS, REPLACING FLUIDS AND ELECTROLYTES, IMPROVING TISSUE PERFUSION. THEY ARE ACCOMPLISHED THROUGH IV ADMIN OF INSULIN, FLUID, AND ELECTROLYTE SOLUTIONS. ANY TRIGGERING CAUSES LIKE INFECTION MUST ALSO BE ADDRESSED. AFTER STABILIZATION, TREATMENT INVOLVES INITIATING OR RESUMING STRATEGIES TO MANAGE DIABETES EFFECTIVELY AND PREVENT FURTHER OCCURANCES OF DKA
WHAT IS HHNK?
HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME, PRIMARILY PROBLEM OF TYPE II IN OLDER ADULTS AND IS CHARACTERIZED BY: HYPERGLYCEMIA, OFTEN ABOVE 600 MG/DL, HIGH PLASMA OSMOLARITY, DEHYDRATION, LAKE OF OR MILD KETOSIS, CHANGES IN LEVEL OF CONSCIOUSNESS.
IN HHNK, WHAT DOES SEVERE HYPERGLYCEMIA RESULT FROM?
INCREASED INSULIN RESISTANCE AND EXCESSIVE CARB INTAKE.  HYPEROSMOLARITY FROM EXCESSIVE GLUCOSE AND INADEQUATE FLUID INTAKE RESULTS IN WATER SHIFTING FROM INTRA TO EXTRACELLULAR SPACES, LEADING TO CELLULAR DEHYDRATION AND CELL DEATH. THE PRESENCE OF GLUCOSE IN URINE IMPAIRS ABILITY OF KIDNEY TO CONCENTRATE URINE AND PROMOTES OSMOTIC DIURESIS. THIS EXACERBATES WATER LOSSES.
DESCRIBE ONSET OF HHNK
OFTEN GRADUAL AND RPESENTS OVER A PERIOD OF DAYS TO WEEKS. 
WHAT DO HYPERGLYCEMIA DN SOLUTE DIURESIS LEAD TO?
POLYURIA, POLYDIPSIA, POLYPHAGIA, WEIGHT LOSS, WEAKNESS, SIGNS OF DEHYDRATION LIKE LEG CRAMPS, POOR TISSUE TURGOR, COOL EXTREMITIES, AND TACHYCARDIA. INDIVIDUALS MAY ALSO PRESENT WITH RENAL IMPAIRMENT AND NEUROLOGIC CHANGES LIKE SEIZURES, HALLUCINATIONS, WEAKNESS, PARALYSIS, MUSCLE TREMORS, AND VISUAL CHANGES
APPROXIMATELY HHOW MANY INDIVIDUALS IN HHNK PRESENT IN STATE OF COMA?
ONE OUT OF FOUR. SOMETIMES PERSON IS NOT KNOWN TO HAVE DIABETES BEFORE HHNK.
WHAT CAN BE FOUND IN URINE DURING HHNK?
GLUCOSE IS PRESENT IN THE URINE AND KETONES ARE TYPICALLY ABSNET OR MINIMAL
HOW IS HHNK TREATED?
CAREFUL FLUID REPLACEMENT WITH A TONICITY MATCHED TO THE LEVEL OF HYPEROSMOLARITY, ALONG WITH POTASSIUM, MAGNESIUM, AND PHOSPHATE REPLACEMENT AND STABILIZATION OF BLOOD GLUCOSE LEVELS. ONCE PERSON IS STABILIZED ONGOING CARE IS NEEDED TO PREVENT FURTHER OCCURENCES THROUGH ONGOING MGMT OF TYPE II DIABETES.
DESCRIBE THE SOMOGYI EFFECT
IT IS THE PRESENCE OF REBOUND HYPERGLYCEMIA AS A REACTION TO INSULIN INDUCED HYPOGLYCEMIA.  INSULIN INDUCED HYPOGLYCEMIA TRIGGERS COMPENSATORY INCREASES IN CATECHOLAMINES, GLUCAGON, CORTISOL AND GROWTH HORMONE TO PROMOTE INSULIN RESISTANCE AND INCREASE CIRCULATING BLOOD GLUCOSE LEVELS.  OVERNIGHT HYPOGLYCEMIA IS MET WITH MORNING OR DAYTIME HYPERGLYCEMIA WHICH PROMPTS INCREASED EXOGENOUS ADMIN OF INSULIN WITH FURTHER AGGRAVATES SOLOGYI EFFECT AND POSES MAJOR CHALLENGE TO GLUCOSE CONTOL.
WHEN DO INDIVIDUALS WITH MORNING HYPERGLYCEMIA NEED TO TEST THEIR BLOOD GLUCOSE LEVELS TO DETERMINE PRESENCE OF SOMOGYI EFFECT?
MIDDLE OF THE NIGHT.  IF THE INDIVIDUALS IS HYPOGLYCEMIC AT THAT TIME ADJUSTMENTS IN THE EVENING SNACK OR INSULIN MAY BE NEEDED.
DESCRIBE THE DAWN PHENOMENON
PERSONS BLOOD GLUCOSE LEVEL WHEN WAKING IS HIGHER THAN LEVEL BEFORE GOING TO BED. IT IS RELATED TO HORMONE RELEASE LIKE GROWTH HORMONE, CORTISOL, GLUCAGON, AND CATECHOLAMINES, USUALLY BETWEEN 4-9AM WHICH TRIGGERS INSULIN RESISTANCE AND RELEASE OF GLUCOSE FROM LIVER. MGMT REQUIRES LIMITING OR REGULATING EVENING SNACKS OR INCREASING ORAL GLYCEMIC AGENTS IN TYPE II OR INSULIN DOSES IN TYPE I
IN CHRONIC COMPLICATIONS OF DIABETES MELLITUS, WHAT HAPPENS IN TISSUES THAT REQUIRE INSULIN FOR TRANSPORT OF GLUCOSE?
HYPERGLYCEMIA CAUSES DEGENERATIVE CHANGES BY THICKENING THE BASEMENT MEMBRANE, PROMOTING COAGULATION, OBSTRUCTING PERFUSION, INDUCING HYPOXIA, AND PRODUCING TISSUE NECROSIS. 
IN CHRONIC COMPLICATIONS OF DIABETES, WHAT OCCURS IN TISSUES THAT DONT NEED INSULIN FOR GLUCOSE TRANSPORT?
EXCESS GLUCOSE CAUSES FLUID TO OSMOTICALLY SHIFT INTO THESE CELLS AND CAUSES THEM TO RUPTURE.
HOW ARE CHRONIC COMPLICATIONS OF DIABETES CLASSIFIED?
MICROVASCULAR-SMALL VESSELS
MACROVASCULAR-LARGE VESSELS
NEUROPATHIES
WHEN IS AN INDIVIDUAL LESS LIKELY TO DEVELOP CHRONIC COMPLICATIONS IN DIABETES?
IF BLOOD GLUCOSE IS KEPT BETWEEN 70-120 MG/DL
HOW ARE THE MICROVASCULAR COMPLICATIONS MOST LIKELY TO PRESENT?
IN THE RETINAS, AKA RETINOPATHY AND IN THE KIDNEYS, AKA NEPHROPATHY.  ONE MECHANISM FOR THIS IS PRESENCE OF EXCESS GLUCOSE WHICH BINDS TO COLLAGEN AND PROTEINS IN BLOOD VESSEL WALLS.  THIS IS CALLED GLYCOSYLATION.  THE RATE OF GLYCOSYLATION IS PROPORTIONATE TO THE LEVEL OF HYPERGLYCEMIA
WHAT DOES THE PERMANENT GLYCOSYLATION ALTERATION OF COLLAGEN AND PROTEINS IN THE BLOOD VESSEL WALLS LEAD TO?
HARDENING AND TICKENING OF CAPILLAARY BASEMENT MEMBRANE, RESULTING IN OBSTRUCTION OR RUPTURE OF CAPILLARIES.  ULTIMATELY THIS LEADS TO NECROSIS AND LOSS OF FUNCTION IN THOSE TISSUES.
WHAT CAN THE RETINAL ISCHEMIA RELATED TO OBSTRUCTION AND RUPTURE OF CAPILLARIES IN RETINOPATHY LEAD TO?
BLINDNESS. 
WHAT CAN THE DEVELOPMENT OF COMPLICATIONS ALSO BE RELATED TO?
AN ACCUMULATION OF SORBITOL, A SUGAR ALCOHOL DERIVED FROM METABOLISM OF EXCESSIVE GLUCOSE BY ALDOSE REDUCTASE, AN ENZYME, IN TISSUES THAT DON'T REQUIRE INSULIN. SORBITOL IS THOUGHT TO PROMOTE OSMOSIS OF FLUID INTO THE LENSE AND MAY ALSO BE DIRETLY TOXIC TO CELLS.
WHAT MAY ALSO BE INVOLVED IN THE DEVELOPMENT OF DIABETES?
REACTIVE OXYGEN SPECIES, AKA FREE RADICALS WHICH ARE RELEASED AS A RESULT OF TISSUE INJURY FROM EXCESSIVE GLUCOSE EXPOSURE.
BASED ON THESE POTENTIAL MECHANISMS, THE DEVELOPMENT OF NEPHROPATHY IS A CONSEQUENCE OF WHAT?
1. PROTEIN BREAKDOWN CAUSED BY HIGH GLUCOSE LEVELS AND INADEQUATE INSULIN
2. EXCESSIVE OSMOTIC DIURESIS AND GLUCOSURIA THAT OCCURS WITH HYPERGLYCEMIA
3. INTRAGLOMERULAR HYPERTENSION WHICH IS WORSENED IN THE PRESENCE OF SYSTEMIC HYPERTENSION.
DESCRIBE THE PATHO OF NEPHROPATHY
CHANGES IN GLOMERULAR CAPILLARIES INCREASE INTRAGLOMERULAR PRESSURE CAUSING HYPERTENSION IN KIDNEY. CHRONIC RENAL HYPERTENSION CONTRIBUTES TO GLOMERULAR SCLEROSIS, HYPOXIA, AND ULTIMATELY CHRONIC RENAL FAILURE
WHAT IS THE LEADING CAUSE OF END STAGE RENAL DISEASE, ACOUNTING FOR ALMOST HALF OF NEW CASES OF RENAL FAILURE?
NEPHROPATHY IN INDIVIDUALS WITH DIABETES.  THE PRESENCE OF CONTINUOUS PROTEINURIA IS A KEY MANIFESTATION OF DIABETIC NEPHROPAHTY AND PROGRESSIVE RENAL DISEASE.
WHAT MAY BE INDICATED FOR THOSE WHO DEVELOP CHRONIC RENAL FAILURE SECONDARY TO DIABETIC NEPHROPATHY?
PROTEIN RESTRICTION, DIALYSIS, OR RENAL TRANSPLANT
WHAT IS ESSENTIAL IN THE AVIODANCE OF MICROVASCULAR COMPLICATIONS?
STRICT BLOOD GLUCOSE CONTROL, A1C LESS THAN 7%, HYPERTENSION TREATMENT AND AVOIDING SMOKING
WHAT DO MACROVASCULAR COMPLICATIONS INCLUDE?
CORONARY ARTERY DISEASE, CEREBROVASCULAR DISEASE IE STROKE AND PERIPHERAL VASCULAR DISEASE
WHAT ARE THE MAJOR MECHANISMS FOR DEVELOPMENT OF MACROVASCULAR COMPLICATIONS?
RELATED TO THE ROLE OF DIABETES IN DEVELOPMENT OF ATHEROSCLEROSIS. HYPERGLYCEMIA, HYPERLIPIDEMIA, AND HYPERTENSION CONTRIBUTE TO THE DEVELOPMENT OF ATHEROSCLEROTIC PLAQUES BY INJURING THE INTIMA. LIPIDS ARE DEPOSITED ON WALLS OF LARGE VESSELS. LDLS ARE FOUND IN HIGH CONCENTRATIONS IN PEOPLE WITH DIABETES ESPECIALLY TYPE II.  HLDS ARE LOW.  PLATELETS ADHERE TO DAMAGED ENDOTHELIAL CELLS IN INTIMAL. LG VESSELS BECOME SCLEROTIC AND OBSTRUCTED.
WHAT WILL THE ATHEROSCLEROSIS OF DIABETES EVENTUALLY LEAD TO?
HYPOXIA AND EVENTUALLY ANOXIA, WHICH LEAD TO NECROSIS OF PERIPHERAL TISSUES.
WHAT IS THE PRESENCE OF MACROVASCULAR COMPLICATIONS IN THOSE WITH DIABETES?
MORE THAN HALF WILL DIE OF HEART DISEASE OR STROKE.
2-4 X MORE LIKELY TO HAVE HEART DISEASE OR STROKE THAN THOSE W/O DIABETES.
1 OUT OF 3 DIABETIC PTS OLDER THAN 50 ARE ESTIMATED TO HAVE PERIPHERAL VASCULAR DISEASE AND INTERMITTENT CLAUDICATION, A CONDITION OF FATIGUE OR ACHING IN THE LEG MUSCLES EVEN WHEN WALKING SHORT DISTANCES.

RISK OF LEG AMPUTATIONS IS 15-40 X GREATER FOR PEOPLE WITH DIABETES.
WHAT IS ONE OF THE MOST IMPORTANT PREDICTORS FOR MORTALITY IN PTS WITH TYPE I DIABETES?
AMPUTATION. MORTALITY RATE AFTER AMPUTATION IS ABOUT 2-8 X HIGHER THAN THOSE W/O AMPUTATION. AT DIAGNOSIS ABOUT HALF OF THOSE WITH TYPE II DIABETES PRESENT WITH MACROVASCULAR OR MICROVASCULAR COMPLICATIONS.
WHAT IS NEUROPATHY?
NERVE DEGENERATION THAT RESULTS IN DELAYED NERVE CONDUCTION AND IMPAIRED SENSORY FUNCTION. THEY CAN OCCUR IN SOMATIC, PERIPHERAL, AND AUTONOMIC NERVE CELLS
WHAT ARE NEUROPATHIES A RESULT OF?
THICKENING, SCLEROSIS, OBSTRUCITON, AND ISCHEMIA OF THE VESSELS THAT SUPPLY NERVE FIBERS

DEMYELINIZATION CAUSED BY IMPAIRED METABOLISM.
WHAT IS THE DIFFERENCE BETWEEN SOMATIC AND AUTONOMIC NEUROPATHIES?
SOMATIC NERVE DEGENERATION AND DELAYED CONDUCTION LEAD TO DECREASED SENSATION, NUMBNESS, TINGLING, WEAKNESS, MUSCLE WASTING, AND PAIN.

AUTONOMIC NEUROPATHIES LEAD TO BLADDER INCONTINENCE, IMPOTENCE, DIARRHEA, ERECTILE DYSFUNCTION AND POSTURAL HYPOTENSION. PREVALENCE OF AUTONOMIC NEUROPATHY INCREASES WITH AGE, DURATION OF DIABETES, AND INCREASED HEMOGLOBIN A1C
WHY ARE INDIVIDUALS WITH DIABETES ALSO AT RISK FOR DEVELOPING INFECTION?
1. EXCESS GLUCOSE IN BLOOD PROVIDES GOOD ENVIRONMENT FOR SOME PATHOGENS, ALLOWING RAPID PROLIFERATION
2. TISSUE ISCHEMIA FROM MICROVASCULAR AND MACROVASCULAR DEGENERATION DAMAGES TISSUE INTEGRITY AND ALLOWS ACCESS TO PATHOGENS
3. RBC DESTRUCTION AND HIGH LEVELS OF GLYCOSYLATED HEMOGLOBIN PREVENT RELEASE OF OXYGEN TO TISSUES
4. WBC ARE IMPAIRED WITHOUT ADEQUATE GLUCOSE TRANSPORT AND ARE UNABLE TO ENGULF AND REMOVE PATHOGENS
5. NEUROPATHIES PREVENT THE INDIVIDUAL FROM BEING ABLE TO SENSE BREAKS IN THE SKIN INTEGRITY ALLOWING PATHOGENS EASY ACCESS
6. RETINOPATHY MAY PREVENT THE PERSON FROM BEING ABLE T INSPECT FOR MANIFESTATIONS OF INFECTIONA DN WILL DELAY TREATMENT
HOW CAN INFECTION IN PEOPLE WITH DIABETES BE CONTROLLED?
TIGHT GLYCEMIC CONTROL IS KEY. ALSO SMOKING CESATION, MGMT OF HYPERTENSION, WEIGHT LOSS, LOWERING OFR LIPIDS.
WHAT IS THE ALPHABET METHOD OF EDUCATING ON COMPLICATION PREVENTION?
A: ADVICE TO FOLLOW DIET, WEIGHT LOSS, EXERCISE, AND LIFESTYLE MODIFICATIONS
B: BLOOD PRESSURE REDUCTION
C: CHOLESTEROL REDUCTION
D: DIABETES HYPERGLYCEMIA CONTROL
E: EYE SCREENING
F: FOOT CARE
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