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PATHO FINAL
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WHAT ARE THE EXOCRINE FUNCTIONS OF THE PANCREAS?


SECRETES ENZYMES AND AN ALKALINE SUBSTANCE


WHAT DO THE ALPHA AND BETA CELLS SECRETED BY THE ISLETS OF LANGERHANS ASSOCIATED WITH


BETA - INSULIN
ALPHA - GLUCAGON


WHAT DOES INSULIN DO BESIDES GLUCOSE REGULATION?


REGULATES POTASSIUM LEVELS.  IF THERE IS TOO MUCH INSULIN, POTASSIUM WILL DROP.  IF TOO MUCH INSULIN IS GIVEN THE HEART CAN STOP


DESCRIBE TYPE I DIABETES


BODY DOES NOT MAKE INSULIN.  WHEN THEY ARE HOME THEY HAVE TO TAKE INSULIN INJECTIONS.

TYPE II IS INSULIN RESISTANCE-PERSON MAKES INSULIN, BUT THEIR BODY DOES NOT ABSORB INSULIN AND USE IT AS THEY SHOULD. THEY USUALLY TAKE ORAL MEDICATIONS, NOT INSULIN.

GESTATIONAL DIABETES: INSULIN GIVEN USUALLY BY PUMP. ORAL MEDS ARE TERATOGENIC. 

ALL FORMS REQUIRE WEIGHT LOSS, EXCERCISE, AND FOOD TO SUPPORT.

ONLY ABOUT 10% OF DIABETICS ARE TYPE I


WHY ARE MOST DIABETICS IN HOSPITAL SETTINGS GIVEN INSULIN INJECTIONS, EVEN TYPE II AND GESTATIONAL?


BECAUSE PTS ARE OFTEN NPO AND CAN'T TAKE OTHER MEDS.  ALSO, SOMETIMES THEY HAVE SPIKED AND NEED TO BE REGULATED.
STRESS AND DECREASED ACTIVITY IN HOSPITAL SETTING ALSO USUALLY RESULT IN INSULIN ADMINISTRATION. INFECTIONS AND ILLNESS ALSO INCREASE BLOOD SUGAR


DESCRIBE TYPE I DIABETES


COMES FROM IMMUNODESTRUCTION OF THE BETA CELLS.
CLINICAL MANIFESTATIONS: THIRSTY, POLYURIA, HUNGRY, LOSE WEIGHT, TIRED, LETHARGIC, AND VISUAL CHANGES
CHECK BLOOD GLUCOSE LEVELS


WHAT DO WE WANT OUR GLUCOSE LEVELS TO BE AT?


FASTING: 127
AIC: 7


WHAT ARE SOME TREATMENTS FOR DIABETES I?


CARB COUNTING, EXERCISE, INSULIN REPLACEMENT THERAPY


HOW CAN INSULIN BE GIVEN?


REGULAR INSULIN-CLEAR-GIVEN IN SLIDING SCALE INSULIN (MAY BE GIVEN TO TYPE II IN HOSPITAL) - FAST ACTING-WORKS WITHIN MINUTES

MPH-NOVALOG-CLOUDY-LONGER ACTING INSULINS

LANTIS - TAKES ABOUT 24 HOURS BEFORE IT TAKES EFFECT

APRIDA - FAST ACTING INSULIN


HOW OFTEN DOES BLOOD SUGER MONTIORING NEED TO BE PERFORMED ON A PERSON WITH INSULIN DRIP?


EVERY HOUR


DESCRIBE TYPE 2 DIABETES MELLITUS


*INSULIN RESISTANCE AND A REDUCATION IN ADEQUATE ..?
*OBESE
CLINICAL MANIFESTATIONS: MAY BE NONE. VISUAL CHANGES, NEPHROPATHY, CORONARY ARTERY DISEASE, PERIPHERAL VASCULAR DISEASE, RECURRENT INFECTIONS, NEUROPATHY (IE FEET AND HANDS ARE NUMB AND TINGLE AT SAME TIME)



WHAT ARE THE TYPE II DIABETES DIAGNOSTIC CRITERIA?


BLOOD GLUCOSE LEVEL IS CHECKED: USUALLY COMES FROM GLUCOSE TOLERANCE AND POSTCRANIAL?

NEED TO DETERMINE TYPE I OR TYPE II: USUALLY COMES FROM 3 HOUR GLUCOSE TOLERANCE AND CRANIAL?


DESCRIBE GESTATIONAL DIABETES?


GLUCOSE INTOLERANCE WITH THE ONSET OF PREGNANCY. OCCURS 4-14% OF PREGNANCIES. REQUIRES DIET MODIFICATIONS, EXERCISE, AND POSSIBLY INSULIN USUALLY IN PUMP FORM


WHAT ARE SOME COMPLICATIONS OF DIABETES (ACUTE)?


HYPOGLYCEMIA: COLD, CLAMMY, CONFUSED. PB AND MILK BEST TO GIVE. IF UNCONSCIOUS, GIVE D50 BECAUSE IT HAS A LOT OF GLUCOSE

DIABETES KETOACIDOSIS - DKA - DEHYDRATED AT CELLULAR LEVEL-USUALLY ALSO HAVE LOW POTASSIUM, GENERALLY PUT ON INSULIN DRIP. MAY HAVE ACETONE BREATH, KETONES PRESENT IN URINE 

HYPERGLYCEMIA HYPEROSMOLAR NONKETOTIC SYNDROM -HHNK - MAY BE THIRSTY, MAY BE IN COMA, NON KETOTIC EFFECT

THE SOMOGYI EFFECT: MAY FLUCTUATE RAPIDLY BETWEEN HYPER AND HYPOGLYCEMIA.   AND DAWN PHENOMENON




WHAT ARE SOME LESS ACUTE COMPLICATIONS OF DIABETES?


MICROVASCULAR COMPLICATIONS: IE RETINOPATHY, MAY ACTUALLY HAVE A STROKE IN THEIR EYES DUE TO LACK OF CIRCULATION. REGULAR EXAMS NEEDED.

MACROVASCULAR - BLOOD PRESSURE

NEUROPATHIES: NUMBNESS IN HANDS, FINGERS, TOES, FEET. MAY ALSO HAVE NEUROGENIC BLADDER IE THEY NAY NOT KNOW WHEN THEY NEED TO URINATE

INFECTION: ALL INFECTIONS MUST BE TREATED AS MAJOR INFECTIONS ESPECIALLY IF ON LOWER LEGS.


YOU HAVE INFLAMMATION OF THE LARGE INTESTINE, A CONDITION CALLED ULCERATIVE COLITIS.  WHAT IS THE MOST PROBABLE REASON THAT YOU WOULD DEVELOP IRON DEFICIENCY ANEMIA?


YOU ARE EXPERIENCING CHRONIC BLOOD LOSS IN YOUR STOOLS


YOU ARE PART OF THE HEALTH CARE TEAM AT A CLINIC FOR ADOLESCENTS WITH ANOREXIA NERVOSA. WHICH OF THE ASSESSMENTS THAT YOU PERFORM IS FOCUSED ON RECOGNIZING THE MOST COMMON CAUSE FOR MORTALITY IN THOSE WITH ANOREXIA NERVOSA?


CARDIOVASCULAR ASSESSMENT


WHICH DIETARY CHANGE WOULD BE RECOMMENDED FOR THE INDIVIDUAL WITH CELIAC DISEASE?


AVOID WHEAT, BARLEY, RYE, AND OATS


WHAT AFFECTS THE SENSATIONS OF HUNGER AND SATIETY AND THEREFORE PLAYS A MAJOR ROLE IN THE DEVELOPMENT OF OBESITY?


THE HYPOTHALAMUS


WHAT NUTRIENT DOES NOT CONTRIBUTE AS AN ENERGY SOURCE IN THE DIET?


VITAMINS


YOU ARE CARING FOR AN INDIVIDUAL WITH LIVER DISEASE, WHAT ARE YOU MOST CONCERNED ABOUT IN REGARDS TO THEIR NUTRITION?


PT MAY BE UNABLE TO ADEQUATELY STORE NUTRIENTS.
PT MAY BE UNABLE TO SYNTHESIZE NUTRIENTS
PT MAY BE UNABLE TO METABOLIZE MACRONUTRIENTS


YOUR PT HAS GALL BLADDER DISSEASE AND IS UNABLE TO STORE AND RELEASE ADEQUATE BILE TO THE SMALL INTESTINE. WHAT DIETARY MODIFICATIONS DO YOU SUGGEST?


DECREASE FAT INTAKE


YOU ARE WORKING IN THE NEWBORN NURSERY AND ARE AN ADVOCATE FOR BREASTFEEDING.  IT IS THE WINTER IN NORTHERN MINNESOTA AND YOU ARE CONCERNED WITH LOW SUNLIGHT EXPOSURE IN INFANTS WHO ARE BREASTFEEDING AS THEY MAY DEVELOP VITAMIN D DEFICIENCY. WHAT IS THE MAJOR MANIFESTATION OF BITAMIN D DEFICIENCY?


IMPAIRED MINERALIZATION IN GROWING BONES


YOU ARE PLANNING A NUTRITIONAL IN SERVICE TO YOUR CLINICS SERVICE AREA IN CALIFORNIA.  WHAT CONCEPT OF ALTERED NUTRITION SHOULD YOU FOCUS YOUR TALK IN ORDER TO ADDRESS THE LARGEST NUTRITIONAL PROBLEM IN YOUR AREA?


OVERNUTRITION


WHAT IS KNOWN ABOUT GLUCOSE TRANSPORT IN THE SMALL INTESTINE?


REQUIRES COTRANSPORT WITH SODIUM

OCCURS THROUGH ACTIVE TRANSPORT

MUST FIRST BE REDUCED AS IS RARELY CONSUMED IN THE TYPICAL DIET


HOW DO YOU THINK VITAMIN A AND C DEFICIENCIES AFFECT WOUND HEALING?


Wound healing would not occur without the support of vitamins A and C, which are essential for collagen formation


WHAT IS YOUR APPROXIMATE CALORIC REQUIREMENT PER DAY TO MAINTAIN YOUR BODY WEIGHT?


Caloric requirements are determined based on the kcal/kg needed to maintain body weight. Caloric intake requirements depend on age, gender, activity level, current weight, pregnancy, and lactation. During times of growth, caloric requirements are higher. For example, caloric requirements are 115 kcal/kg at birth. This requirement decreases to 80 kcal/kg between ages 1 and 10 years and is about half of that (30 to 40 kcal/kg) in adulthood. Pregnancy demands add an additional 300 kcal/day. Lactation (breastfeeding) increases the requirement by 500 kcal/day.


WHAT DIETARY RECOMMENDATIONS WOULD YOU MAKE FOR THE INDIVIDUAL WHO IS NOT ABLE TO EFFECTIVELY PRODUCE OR UTILIZE BILE?


These individuals should consume a diet that has reduced fat and focuses on dietary fat sources that break down into shorter and medium (8 to 12 carbon) length fatty acid chains.


WHAT WILL HAPPEN TO NUTRIENT ABSORPTION IN CROHN DISEASE WHEN LARGE PORTIONS OF THE SMALL INTESTINE ARE INFLAMED?


 Virtually all nutrients are absorbed in the small intestine, with the exception of water and alcohol; loss of the absorptive surface of the small intestine will result in broad-range nutrient deficiencies.


Inflammation, particularly that which occurs with infection, stimulates the release of chemical mediators that promote insulin secretion. Insulin presence promotes the use of glucose for energy. How do you think this affects the adaptation to starvation?


 In the presence of insulin, body tissues continue to depend on glucose. Muscle mass quickly erodes. When 50% of protein stores are exhausted, recovery prognosis is poor.


WHY WOULD PANCREATIC DYSFUNCTION LEAD TO PROBLEMS WITH ABSORPTION?


Pancreatic enzymes are needed for the digestion and processing of all macronutrients, particularly fats. Without proper processing, these nutrients move quickly through the GI tract and are unable to be adequately absorbed.


YOU ARE PROVIDING NUTRITIONAL COUNSELING FOR A PERSON WITH CELIAC DISEASE. WHAT SPECIFIC FOODS WOULD YOU RECOMMEND AVOIDING? WHAT FOODS WOULD YOU SUGGEST AS SUBSTITUTIONS?


All wheat, rye, barley, and oats are excluded. This includes breads, cakes, cereals, pastas, beer, or any other foods made with these ingredients. Acceptable alternatives are milk and milk products, corn, rice, soy or potato-based grain products, eggs, peas, beans, nuts, seeds, tofu, fruits and vegetables, tea, and coffee.


HOW DO YOU MEASURE YOUR BMI?


 Do this by measuring your weight in pounds and converting this to kilograms (1 pound = 0.45 kg). Then, measure your height in inches and convert this to meters squared (multiply inches ×2.54 cm; divide this number by 100 cm/m; multiply this final number × itself to get meters squared). Then, the final step is to take your weight in kilograms and divide it by your height in meters squared.


GIVEN THAT VENTILATION-PERFUSION IS GRAVITY DEPENDENT, HOW DOES YOUR BODY POSITION AFFECT WHERE THE GREATEST VOLUME OF VENTILATION=PERFUSION OCCURS?


STANDING PROMOTES HIGHER RATIOS OF VENTILATION-PERFUSION IN THE LOWER BASES OF THE LUNGS; THE AREAS OF THE LUNG THAT ARE MOST DEPENDENT BECOME THE BEST VENTILATED AND PERFUSED.


HOW WOULD AN INEFFECTIVE RIGHT VENTRICLE AFFECT THE PULMONARY AND SYSTEMIC CIRCULATION?


AN INEFFECTIVE RIGHT VENTRICLE WOULD RESULT IN POOR MOVEMENT OF BLOOD INTO THE PULMONARY ARTERY AND PAST THE LUNGS.  THERE WOULD BE A BACK UP OF BLOOD SYSTEMICALLY RESULTING IN INCREASED HYDROSTATIC PRESSURE IN THE PERIPHERAL ORGANS AND TISSUES.


HOW WOULD MODERATE TO HEAVY AEROBIC EXERCISE AFFECT THE DEVELOPMENT OF COLLATERAL CIRCULATION OF THE HEART?


INCREASING DEMANDS WILL PROMOTE DEVELOPMENT OF COLLATERAL CIRCULATION.  THIS WILL INCREASE THE FUNCTIONAL RESERVES AVAILABLE TO THE HEART AND WILL PROMOTE MAXIMIZATION OF HEART PERFUSION.  THIS CAN BE BENEFICIAL IN TIMES WHERE PERFUSION IS SOMEHOW IMPAIRED.  BLOOD WILL STILL BE ABLE TO REACH A GREATER AMOUNT OF THE HEART THROUGH THESE COLLATERAL NETWORKS.


WHAT IS PERICARDITIS? WHAT WOULD BE THE PROBLEM WITH THIS CONDITION? WHAT CLINICAL MANIFESTATIONS DO YOU THINK WOULD BE PRESENT?


PERICARDITIS IS INFLAMMATION OF THE PERICARDIUM THAT CAN BE CAUSED BY INFECTION, MYOCARDIAL INFARCTION, MI, OR OTHER TRAUMA.  OFTEN THE CAUSE IS UNKNOWN.  THE MAJOR PROBLEM WITH THIS CONDITION IS RESTRICTION OF SMOOTH CARDIAC PUMPING DUE TO THE INFLAMED AND ROUGH PERICARDIAL MEMBRANES.  AS WITH OTHER INFLAMMATORY CONDITIONS, EXUDATE MAY DEVELOP.  CHEST PAIN IS A MAJOR CLINICAL MANIFESTATION.  PAIN WITH PERICARDITIS OFTEN WORSENS WITH INSPIRATION AND WITH LYING DOWN.  IF THE INFLAMMATION CREATES SUFFICIENT PRESSURE, CARDIAC COMPRESSION CAN RESULT (TAMPONADE) AND IMPAIR CARDIAC CONDUCTION AND CARDIAC OUTPUT.  CHRONIC INFLAMMAITON CAN RESULT IN CONSTRICTIVE PERICARDITIS, A CONDITION WHERE THE HEART IS ENCASED IN A RIGID SHELL.


WHAT WOULD HAPPEN IF THE AV NODE CONDUCTION WAS BLOCKED? WHAT WOULD HAPPEN IF THE BUNDLE BRANCH CONDUCTION WAS BLOCKED?


THE AV NODE PROVIDES THE ONLY CONNECTION BETWEEN THE TWO CONDUCTION SYSTEMS (ATRIA AND VENTRICLES); THE ATRIA AND VENTRICLES WOULD BEAT INDEPENDENTLY OF EACH OTHER IF THE TRANSMISSION OF IMPULSES THROUGH THE AV NODE WERE BLOCKED.  THE HEART RHYTHM WOULD BE INEFFICIENT; THE ATRIA WOULD NOT COMPLETELY EMPTY PRIOR TO THE VENTRICLES CONTRACTING.  THE BUNDLE BRANCH BLOCK WOULD PREVENT VENTRICULAR CONTRACTION.  IF UNILATERAL, ONE VENTRICLE WOULD BE AFFECTED.


WHAT HAPPENS TO PRELOAD WHEN VENOUS RETURN IS SLUGGISH? WHAT HAPPENS TO PRELOAD WHEN VENOUS RETURN IS EXCESSIVE AND CARDIAC MUSCLE FIBERS GET STRETCHED TOO FAR?


WHEN VENOUS RETURN IS SLUGGISH, LESS BLOOD ENTERS THE VENTRICLES AND THE PRELOAD IS REDUCED.  THIS LEADS TO DECREASED CARDIAC OUTPUT AS THE STROKE VOLUME IS LESS. THE HEART RATE WOULD HAVE TO INCREASE IN ORDER TO COMPENSATE.  WITH EXCESSIVE STRETCHING OF THE CARDIAC MUSCLE FIBERS ( OR WITH IMPAIRED CONTRACTILITY), PRELOAD IS EXCESSIVE AND THE HEART IS UNABLE TO OVERCOME THE PRESSURE IN THE VENTRICLES.


WHAT WOULD YOUR BODY NEED TO DO TO MAINTAIN OPTIMAL BLOOD PRESSURE IF YOU HAD INCREASED PERIPHERAL VASCULAR RESISTANCE (PVR) AS MAY OCCUR WITH ARTERIOSCLEROSIS ( A CONDITION OF STIFFENING OF THE ARTERIES)?


SINCE THE PRODUCT OF CARDIAC OUTPUT AND PVR COMPRISES BLOOD PRESSURE, AN INCREASE IN PVR WOULD REQUIR A DECREASE IN CARDIAC OUTPUT IN ORDER TO COMPENSATE AND MAINTAIN A STABLE BLOOD PRESSURE.  SINCE CARDIAC OUTPUT IS NEEDED TO CONTINUOUSLY PERFUS ORGANS, OFTEN CARDIAC OUTPUT WILL REMAIN STABLE AND HYPERTENSION IS THE RESULT.


DO YOU THINK THAT IT IS MORE PROBLEMATIC TO HAVE PERSISTENT ELEVATIONS IN SYSTOLIC OR DIASTOLIC BLOOD PRESSURE?


ALTHOUGH BOTH ARE PROBLEMATIC, PERSISTENT ELVATIONS IN DIASTOLIC PRESSURE INDICATE THAT THE INDIVIDUALS ARTERIES ARE NOT ALLOWED ADEQUATE REST BETWEEN CARDIAC CONTRACTIONS; THIS PRESENTS A GREAT DEAL OF STRESS ON THE ARTERIES WITHOUT AN ADEQUATE RECOVERY PERIOD.


THINK BACK TO THE LAST TIME YOU FELT DIZZY WHEN YOU STOOD UP TO FAST, WHY DO YOU THINK THIS OCCURRED? HOW DID THE BARORECEPTORS RESPOND?


ORTHOSTATIC HYPOTENSION CAN OCCUR FOR NUMEROUS REASONS INCLUDING DEHYDRATION OR LOW BLOOD VOLUME.  BARORECEPTORS RESPOND BY RECOGNIZING A DECREASED STRETCH IN THE VESSEL WALL.  THIS DECREASED STRETCH ON THE BARORECEPTORS SIGNALS A FALL IN BLOOD PRESSURE.  THE BARORECEPTORS THEN ALERT THE CARDIAC CONTROL CENTER TO TRIGGER THE SYMPATHETIC NERVOUS BRANCH TO VASOCONSTRICT THE VESSELS AND PROMOTE INCREASED PVR. HEART RATE IS ALSO INCREASED.


WHAT IS THE MECHANISM FOR DEVELOPMENT OF VENOUS THROMBI FORMATION IN AN INDIVIDUAL ON BED REST?


SKELETAL MUSCLE CONTRACTION PLAYS A MAJOR ROLE IN AIDING BLOOD RETURN TO THE HEART.  BED REST DECREASES EXTREMITY SKELETAL MUSCLE CONTRACTION AND BLOOD POOLS IN THE LOWER EXTREMITIES.  BLOOD STASIS ALLOWS COAGULATION AND FORMATION OF THROMBUS.


WHEN PREPARING AN INTRAVENOUS FLUID OR MEDICATION, ALL AIR MUST BE REMOVED FROMT HE TUBING OR SYRINGE.  DESCRIBE THE CONSEQUENCE OF BEING CARELESS IN AIR REMOVAL


SMALL AMOUNTS OF CIRCULATING AIR ARE OF LITTLE CONSEQUENCE.  INSERTION OF AIR GREATER THAN ABOUT 100 ML OR MORE CAN LEAD TO SUDDEN DEATH AS AIR BUBBLE COALESCE (AIR EMBOLI) AND PHYSICALLY OBSRUCT THE FLOW OF BLOOD IN THE MAIN PULMONARY ARTERY, RIGHT SIDE OF THE HEART, AND CAN CAUSE RIGHT VENTRICULAR FAILURE.  THEN LEFT VENTRICULAR FAILURE, NO PUMPING OF BLOOD FROM THE LEFT VENTRICLE, SEVERE HYPOTENSION, SHOCK AND DEATH


BASED ON THE PRESSURE DIFFERENTIAL BETWEEN THE RIGHT AND LEFT SIDES OF THE HEART, DO YOU THINK IT IS MORE COMMON TO HAVE A LEFT TO RIGHT OR RIGHT TO LEFT SHUNT? WHICH ONE WOULD MOST LIKELY RESULT IN CYANOSIS?


THE LEFT SIDE OF THE HEART HAS A GREATER PRESSURE SO A LEFT TO RIGHT IS MORE COMMON.  A RIGHT TO LEFT IS MOST LIKELY TO RESULT IN CYANOSIS AS DEOXYGENATED BLOOD IS DISTRIBUTED SYSTEMICALLY.


LOW DOSE DAILY ASPIRIN IS COMMONLY USED TO PREVENT MI.  ASPIRIN REDUCES PLATELET AGGREGATION.  HOW WOULD THIS MEDICATION HELP TO PREVENT MI?


ASPIRIN REDUCES THE ACCUMULATION OF PLATELETS AT THE SITE OF INJURY.  IF THE ATHEROSCLEROTIC PLAQUE BREAKS OFF, PLATELETS ARE LESS LIKELY TO ACCUMULATE AT THE SITE IN SUFFICIENT QUANTITIES TO OBSTRUCT THE LUMEN OF THE ARTERY.


HOW DO YOU THINK PHARMACOLOGIC INTERVENTIONS DIFFER BETWEEN SYSTOLIC AND DIASTOLIC LEFT VENTRICULAR FAILURE?


SYSTOLIC FAILURE IS TREATED WITH DRUGS THAT IMPROVE CARDIAC CONTRACTILITY OR REDUCE PERIPHERAL RESISTANCE.  DIASTOLIC FAILURE IS TREATED WITH DRUGS THAT INCREASE THE RELAXATION AND PROLONG THE DIASTOLIC PHASE OF THE CARDIAC CYCLE


HOW ARE COMPENSATORY MECHANISMS SIMILAR BETWEEN SHOCK AND HEART FAILURE? HOW ARE THESE DIFFERENT?


BOTH INVOLVE STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM, THE RENIN ANGIOTENSIN MECHANISM, AND VASOMOTOR TONE.  THE GOALS ARE DIFFERENT.  SHOCK COMPENSATION AIRMS TO INCREASE VASCULAR VOLUME, TONE, AND SHUNT BLOOD TO VITAL ORGANS; HEART FAILURE COMPENSATION AIMS TO REDUCE THE WORKLOAD ON THE HEART.  SINCE WORKLOAD ON THE HEART IS GREATLY INCREASED WITH HEART FAILURE, ANOTHER DIFFERENCE CAN BE THE HYPERTROPHY CHARACTERISTIC OF HEART FAILURE NOT NECESSARILY FOUND WITH SHOCK.


IN EVALUATING MODIFIABLE CARDIOVASCULAR RISK FACTORS FOR YOUOR PATIENT, WHICH IS NOT CONSIDERED MODIFIABLE?


FEMALE GENDER

POORLY CONTROLLED DIABETES, HYPERLIPIDEMIA, AND HYPERTENSION ARE ALL MODIFIABLE


YOUR PATIENT IS EXPERIENCING PERIPHERAL EDEMA, HEPATOMEGALY, ASCITES, AND SPLENOMEGALY. WHICH OF THE FOLLOWING CONDITIONS WOULD BE CONSISTENT WITH THE PTS FINDINGS?


RIGHT SIDED HEART FAILURE






















































































































































































IT IS A VERY HOT SUMMER DAY, YOUR NEIGHBOR STOPS AT YOUR HOUSE AFTER JOGGING 5 MILES.  SHE IS SWEATING AND TELLS YOU SHE FEELS DIZZY AND THIRSTY AND CANT MAKE IT HOME.  YOU CHECK HER BLOOD PRESSURE AND FIND IT TO BE LOW. WHAT COULD YOU DO RIGHT INYOUR HOME TO RAISE HER BLOOD PRESSURE?


HAVE HER DRINK A LARGE GLASS OF COOL WATER


YOUR NEIGHBOR AGAIN COMES TO YOUR DOOR. SHE HAS BEEN RUNNING IN THE SNOW AND IT IS VERY COLD OUTSIDE. SHE HAS A HEADACHE AND HER HEART IS POUNDING. YOU CHECK HER BP AND FIND IT TO BE HIGH. WHAT COULD YOU DO THIS TIME RIGHT IN YOUR HOME TO DECREASE HER BLOOD PRESSURE?


HAVE HER LAY DOWN ON YOUR COUCH


WHICH SITUATION OF ALTERED PERFUSION COULD BE TRIGGERED BY COPD?


VENTILATION PERFUSION MISMATCHING


WHICH MECHANISM INCREASES PERIPHERAL VASCULAR RESISTANCE AND CONTRIBUTES TO THE DEVELOPMENT OF HYPERTENSION?


AIMPAIRED SODIUM EXCRETION BY THE KIDNEYS


WHY IS IT NECESSARY FOR URINE TO BECOME CONCENTRATED BEFORE IT IS EXCRETED?


SEVERE HYPOTENSION AND HYPOVOLEMIA WOULD RESULT IF TUBULAR FILTRATE WERE EXCRETED IN THE FORM IT IS IN WHEN IT LEAVES BOWMANS CAPSULE.  OF THE 125 ML/MIN OF URINARY FILTRATE FORMED IN THE GLOMERULI, ONLY 1 ML IS ACTUALLY EXCRETED WITH THE OTHER 124 ML RETURNED BACK INTO THE BLOOD BY REABSORPTION


WHY WOULD THE INDICATION FOR URINE COLLECTION INFLUENCE THE METHOD SELECTION?


TESTS THAT DETERMIEN THE PRESENCE OF A PATHOGEN REQUIRE STERILE COLLECTION METHODS.  TESTS THAT IDENTIFY URINE CHARACTERISTICS DO NOT NEED STERILE COLLECTION


WHAT MECHANISMS OF INFECTION AND INFLAMMATION MAY CONTRIBUTE TO DAMAGE TO RENAL STRUCTURES?


INFLAMMATORY RESPONSES STIMULATE CHEMICAL MEDIATORS TO WIDEN THE JUNCTIONS BETWEEN ENDOTHELIAL CELLS IN THE RENAL CAPILLARIES IN ORDER TO PROMOTE MOVEMENT OF FLUID OUT OF THE VASCULAR SPACE.  VASODILATION OF ARTERIOLES IS ALSO INDUCED TO BRING MORE BLOOD FLOW TO THE SITE OF INJURY.  THESE MECHANISMS PROVIDE THE NECESSARY IMMUNE CELLS TO SITES OF DAMAGE FORDEFENSE AGAINST PATHOGENS.  EDEMA RESULTING FROM THESE MECHANISMS MAY DIMINISH THE FUNCTION OF THE TISSUE.  OBSTRUCTION OF VASCULAR AND TUBULAR FLOW MAY ALSO RESULT, INCREASING THE RISK OF DAMAGE DUE TO INCREASED PRESSURE IN THE KIDNEYS


REDUCED PERISTALSIS WOULD SLOW THE MOVEMENT OF STOOL THROUGH THE LARGE INTESTINE.  HOW MIGHT THIS AFFECT WATER CONCENTRATION IN THE STOOL?


WATER MOVEMENT OUT OF STOOL CONTINUES AS LONGAS THE STOOL REMAINS IN THE COLON, INCREASING THE RISK FOR CONSTIPATION


WHAT ARE SOME COMMON REASONS THAT INTESTINAL MOBILITY CAN BE REDUCED, LEADING TO SLOWED INTESTINAL SMOOTH MUSCLE CONTRACTION?


INTESTINAL MOTILITY CAN BE SLOWED BY REDUCED ACTIVITY, MEDICATIONS THAT ALTER MEUROMUSCULAR CONDUCTION, AGING, FREQUENT USE OF LAXATIVES, AND FACTORS CONTRIBUTING TO CONSTIPATION.


WHAT WOULD YOU EXPECT STOOL IN THE ASCENDING COLON TO HAVE MORE WATER CONTENT THAN STOOL IN THE DESCENDING COLON?


INCREASING WATER IS ABSORBED FROM FECAL MATTER AS IT IS PROPELLED THROUGH THE LENGTH OF THE LARGE INTESTINE.  FECAL MATTER FORM THE CECUM INTO THE ASCENDING COLON RETAINS MUCH OF ITS WATER CONTENT.  STOOL AT THE DISTAL END OF THE DESCENDING COLON HAS LOWER WATER CONTENT REFLECTING THAT OF NORMAL STOOL.


WHY DO BLOODY STOOLS SUGGEST THE POTENTIAL DIAGNOSIS OF CANCER?


THE BLOOD FLOW DEMANDS PLACED BY THE NEOPLASTIC CELLS DEPRIVE NEIGHBORING TISSUES OF ADEQUATE OXYGEN AND OTHER NUTRIENTS RESULTING IN TISSUE ISCHEMIA AND NECROSIS.  THE TUMOR CELLS CAN ALSO SECRETE ENZYMES THAT DEGRADE THE EXTRACELLULAR MATRIX AND ALLOW THE TUMOR TO MOVE INTO NEIGHBORING TISUES.  TUMOR GROWTH BEGINS TO ERODE THE GI WALL PROMOTING BLOOD ENTRY INTO THE GI TRACT TO BE INCORPORATED INTO STOOL


WHY ARE THE PEOPLE WITH HYPERPARATHYROIDISM AND HYPERCALCIURIA AT RISK FOR DEVELOPMENT OF RENAL CALCULI?


ELEVATED SERUM CALCIUM LEVELS ARE CHARACTERISTIC IN HYPERPARATHYROIDISM AND HYPERCALCIURIA.  IN PEOPLE AFFECTED BY THESE CONDITIONS, THE LARGE INTESTINE ABSORBS TOO MUCH CALCIUM.  EXCESS CALCIUM IN THE URINARY FILTRATE IS MORE LIKELY TO PRECIPITATE, PROMOTING THE DEVELOPMENT OF KIDNEY STONES.


WHY DO INDIVIDUALS SUFFERING FROM RENAL FAILURE BECOME ANEMIC?


THE HORMONE ERYTHROPOIETIN, ACTS ON THE BONE MARROW AND IS A STRONG INDUCER OF RED BLOOD CELL PRODUCTION.  DAMAGE AND REDUCED FUNCTION OF THE KIDNEYS RESULTS IN DECREASED PRODUCTION OF ERYTHROPOIETIN, THEREFORE, LESS STIMULUS TO PRODUCE RBC RESULTING IN ANEMIA.


WHY IS THE DIAGNOSIS OF NONRETENTIVE ENCOPRESIS LIMITED TO CHILDREN AT LEAST 4 YS OF AGE?


AS CHILDREN AGE, THEIR NEUROLOGIC SYSTEM CONTINUES TO DEVELOP, SO THAT THEY BECOME ABLE TO CONTROL ELIMINAITON OF BOTH URINE AND STOOL.  INTENTIONAL WITHOLDING OF STOOL ALSO REQUIRES WELL DEVELOPED NEURAL CONTROL IN ORDER TO INHIBIT THE RECTAL REFLEX AND URGE FOR STOOL ELIMINATION.  CHILDREN LESS THAN 4 YEARS OF AGE MAY NOT BE DEVELOPMENTALLY ABLE TO ACHIEVE THIS RESULT, EVEN IF IT IS DESIRED, AND THEREFORE ARE NOT CONSIDERED WHEN APPLYING THESE DIAGNOSTIC CRITERIA.


WHAT PROVIDES THE MOST OBJECTIVE MEASURMENT OF RENAL DYSFUNCTION?


GLOMERULAR FILTRATION RATE


A CHARACTERISTIC CHANGE IN STOOL THAT MAY INDICATE THE PRESENCE OF BLOOD INCLUDES WHICH ONE OF THE FOLLOWING?


MELENA


WHICH DIAGNOSTIC PROCEDURE ALLOWS ANALYSIS OF THE ENTIRE LARGE COLON?


COLONOSCOPY


WHICH FOOD SHOULD BE AVOIDED IN PEOPLE WITH RENAL CALCULI?


STRAWBERRIES


WHICH FOOD SHOULD BE AVOIDED IN PEOPLE WITH DIVERTICULAR DISEASE?


STRAWBERRIES


WHICH TYPE OF URINARY INCONTINENCE CAN BE ATTRIBUTED TO MUSCLE OVERACTIVITY


URGE INCONTINENCE


THE ENTERIC NERVOUS SYSTEM COMPONENT LOCATED BETWEEN THE CIRCULAR AND LONGITUDINAL MUSCLE LAYERS OF THE LARGE INTESTINE


MYENTERIC PLEXUS


THE AREA OF THE LARGE INTESTINE THAT ABSORBS THE MAJORITY OF WATER IS WHAT?


THE ILEUM


THE PROCESS BY WHICH FECAL CONTENTS ENTERS THE RECTUM IS KNOWN AS WHAT?


MASS MOVEMENT


WHAT IS THE AVERAGE VOLUME OF URINE ELIMINATED EACH DAY?


1500 ML


WHICH SPHINCTER IS MADE OF SKELETAL MUSCLE AND IS UNDER VOLUNTARY CONTROL?


EXTERNAL


WHAT DOES A URINE SPECIFIC GRAVITY OF 1:030 INDICATE?


CONCENTRATED URINE


WHICH OF THE FOLLOWING DIAGNOSTIC CRITERIA IS CONSISTENT WITH THE DIAGNOSIS OF ENCOPRESIS?


AGE OF 5 YEARS


WHAT DOES A GFR OF 95 ML/MIN INDICATE?


NORMAL RENAL FUNCTION


WHICH OF THE FOLLOWING INCREASES THE RISK FOR RENAL CALCULI?


DEHYDRATION


WHY DO AGE SPOTS FORM AS INDIVIDUALS AGE?


MELANOCYTES IN THE TRANSITIONAL LAYER OF SKIN, BETWEEN THE EPIDERMIS AND DERMIS, PRODUCE THE BROWN BLACK PIGMENT MELANIN.  PROLIFERATION OF MELANOCYTES WITH AGING PROMOTES THE FORMATION OF CONCENTRATED CLUSTERS THAT APPEAR ON THE SKIN SURFACE, ESPEIALLY AFTER PROLONGED EXPOSURE TO SUNGLIGHT.


HOW CAN THE ELDERLY PROTECT THEMSELVES FROM INFECTION?


PNEUMONIA AND INFLUENZA ARE AMONG THE TOP 10 CAUSES OF DEATH IN OLDER ADULTS. IMMUNIZATION AGAINST PNEUMONIA AND FLU CAN REDUCE BOTH MORBIDY AND MORTALITY AMONG THE ELDERLY


WHAT TYPES OF PHYSICAL ACTIVITIES ARE CONSIDERED WEIGHT BEARING? WHICH ARE NOT?


WEIGHT BEARING EXERCISES ARE ACTIVITIES THAT ARE USUALLY DONE WHILE STANDING.  THESE EXERCISES WORK AGAINST GRAVITY, STRENGHTENING BONES AND MUSCLES.   EXAMPLES OF WEIGHT BEARING EXERCISES INCLUDE WALKING, JOGGING, HIKING, MOWING THE LOWN, SKIING, SKATING, KARATE, BOWLING, TENNIS, SOCCER, BASEBALL, BASKETBALL, FOOTBALL, HOCKEY, DANCING STEP AEROBICS AND STAIRCLIMBING. WEIGHT TRAININ GWITH MACHINES AND FREE WEIGHTS ARE ALSO BONE BUILDING WEIGHT BEARING ACTIVITIES, AKA RESISTANCE EXERCISES. ACTIVITIES LIKE SWIMMING ARE NOT CONSIDERED WEIGHT BEARING SINCE WATER REDUCES THE EFFECTS OF GRAVITY


WHY WOULD METASTATIC DISEASE INCREASE CALCIUM LEVELS IN THE BLOOD?


CANCER OFTEN INCLUDES BONE AS A SITE FOR METASTASIS.  THE LYTIC EFFECTS OF THE CANCER CAUSES BONE RESORPTION AND DEMINERALIZATION.  INCREASING LEVELS OF CALCIUM ENTER THE BLOOD, INCREASING THE RISK FOR HYPERCALCEMIA.  HYPERCALCEMIA CAN LEAD TO ORGAN FAILURE, COMA, AND DEATH.


WHAT INFLUENCE DOES GEOGRAPHIC LOCATION HAVE ON VITAMIN D PRODUCTION?


SUN EXPOSURE IS PERHAPS THE MOST IMPORTANT SOURCE OF VITAMIN D BECAUSE EXPOSURE TO SUNLIGHT PROVIDES MOST HUMANS WITH THEIR VITAMIN D REQUIREMENT.  UV RAYS FROM THE SUN TRIGGER VITAMIN D SYNTHESIS IN SKIN.  SEASON, GEOGRAPHIC LATITUDE, TIME OF THE DAY, CLOUD COVER, SMOT AND SUNSCREEN AFFECT UV RAY EXPOSURE AND VITAMIN D SYNTHESIS


WHY ARE INDIVIDUALS ON ANTIPSYCHOTIC MEDICATIONS AT RISK FOR THE DEVELOPMENT OF PARKINSONIAN-LIKE SYMPTOMS?


THE MECHANISM OF ACTION OF ANTIPSYCHOTIC MEDICATIONS IS BLOCKADE OF D2 DOPAMINE RECEPTORS.  WHEN THE D2 RECEPTORS OF THE NIGROSTRIATAL PATHWAY (PART OF THE EXTRAPYRAMIDAL SYSTEM) ARE BLOCKED, IT PRODUCES MOVEMENT DISORDERS MUCH LIKE THOSE IN PARKINSON DISEASE, INCLUDING HYPERKINETIC MOVEMENT/TARDIVE DYSKINESIA.  ANTIPSYCHOTIC DRUGS CAN INDUCE EXTRAPYRAMIDAL SIDE EFFECTS OF DOPAMINE DEFICIENCY, INCLUDING MUSCLE STIFFNESS, MILD TREMORS, AND INCREASED SALIVATION


GENETIC INFLUENCES AS THE MAJOR DETERMINANTS OF AGING ARE THE FOCUS OF WHICH OF THE FOLLOWING THEORIES?


DEVELOPMENTAL THEORY


TYPICAL CHANGES IN TOTAL BODY WATER IN THE ELDERLY INCLUDE WHAT?


DECREASED TOTAL BODY WATER DUE TO DECREASE IN MUSCLE MASS


IMMUNE SENESCENCE IS CHARACTERIZED BY WHAT?


ENHANCED AUTOIMMUNE RESPONSE


AGE RELATED CHANGES AFFECTING NEUROLOGIC FUNCTION INCLUDE WHAT?


DECREASED NUMBER OF NEURONS


AN IMBALANCE IN BONE REMODELING CHARACTERISTIC OF OSTEOPOROSIS IS CAUSED BY WHAT?


INCREASED BONE RESORPTION DUE TO INCREASED ACTIVITY OF OSTEOCLASTS


AGE RELATED CHANGES CONTRIBUTING TO IMPAIRED HEALING INCLUDE WHAT?


ATROPHIED CAPILLARY SUPPORT TO DERMIS


OSTEOPOROSIS IS THE RESULT OF AN IMBALANCE FAVORING INCREASED?


OSTECLASTIC ACTIVITY


WHAT IS PARKINSON DISEASE CHARACTERIZED BY?


LEWY BODIES


WHICH ONE OF THE FOLLOWING NEUROTRANSMITTERS IS DEFICIENT IN PARKINSON DISEASE?


DOPAMINE


MEMORY LOSS IN ALZHEIMER DISEASE RESULTS FROM IMPAIRED NEURAL CONDUCTION IN THE ??


HIPPOCAMPUS


  What are the major differences and similarities between the actions of the hypothalamus on the anterior versus the posterior pituitary gland? Why would this difference matter? What is an effective way to remember this difference?


  Major differences are that hormones travel on axons versus the portal vascular system and hormones are made directly in hypothalamus and released directly (unchanged) from the posterior pituitary whereas anterior pituitary can have many steps before getting to the target gland. The difference is important in the pathway, number of steps, target organs, and different hormones needed to induce a response. Effective ways to remember this will vary.  


  How do you usually respond to stress? Think about the last time you were in a haunted house or were really scared. How did your body respond? How does this correlate to the neuroendocrine response described in this section?


  Answers will vary. Should indicate catecholamines induce a neurologic response to receptive organs. For example, blood flow is shunted to vital organs such as the heart, brain, and lungs. As a result, heart rate increases, blood pressure increases, respiratory rate increases, and the person becomes much more alert. The skeletal muscles also become activated to allow a rapid escape. Blood is shunted away from the skin and stomach. So, the person will look pale or ashen and digestion is decreased.


  What effect do you think that drinking alcohol has on ADH levels?


  Alcohol decreases ADH levels causing the inability to retain fluids in the body. Diuresis and dehydration then occurs.  


  What would happen if you had a diet that did not include iodized salt?


  The follicles utilize iodide from dietary intake of iodized salt, combine this with tyrosine, an amino acid, and secrete this combination into the colloid portion of the follicle to form the thyroid hormones. Without iodized salt, you would be unable to produce the thyroid hormones.  


  Would loss of the adrenal cortex or the adrenal medulla be more problematic?


  Adrenal cortex. The adrenal medulla actions are also accomplished by the sympathetic nervous system, so the absence of the adrenal medulla is not life threatening.


  You are on a 1-week hiking trip and one of your friends forgets her glucocorticoid medication that she takes for severe asthma. Should she go back and get the medication or is she OK without it for that week?


  Yes. She absolutely needs to go back if she has been taking this medication for over 1 week. After a prolonged period of time, exogenous glucocorticoids result in adrenal atrophy and decreased cortisol production. This medication is tapered (gradually withdrawn) to allow stimulation of the adrenal cortex to increase endogenous production of cortisol. If she suddenly stops taking the medication she will possibly not have adequate cortisol and perhaps other adrenal hormones to survive.


  Map out how the negative feedback loop is impacted by an ACTH-dependent hypercortisolism versus a non–ACTH-dependent hypercortisolism


  The mechanism of excess cortisol can vary. If this is ACTH-dependent, hypercortisolism will not decrease ACTH production (the ectopic or excess production is independent of cortisol levels). If this is not ACTH-dependent, then ACTH levels should decrease in response to high cortisol levels but the cortisol will remain elevated.


  How would a deficiency of cortisol present in terms of clinical manifestations?


  Hypoglycemia, anorexia, nausea, vomiting, fatigue, weakness, weight loss, and poor stress response.


  Based on the sensations involved, what other nerves do you think are involved in the somatosensory system?


  The sensations of touch, temperature, pain, and body position are processed in the brain. These sensations promote responses, often in the form of reflexes, designed to provide a motor action to prevent/reduce injury. These responses involve the activation of motor neurons.  


  Have you ever banged your head and began rubbing it in response to pain? How might this action decrease the pain sensation?


  The rubbing action may decrease pain by stimulating the “closing of the gate,” inhibiting transmission of ascending pain impulses.


  Why is it necessary to control the amount of light entering the eye?


  The amount of light necessary for sight is regulated by pupil constriction to prevent damage and loss of acuity from too much light entering the eye and coming in contact with the retina. Dilation of the pupil in conditions of low light or darkness allows maximal light entry for sight, not otherwise possible.  


  Why does a vitamin A deficiency cause the development of night blindness?


  Inadequate levels of retinene are unavailable to combine with opsin to form rhodopsin, minimizing the ability of rods to transmit impulses resulting in decreased night vision.  


  What is the most likely explanation for the runny nose that occurs during crying?


  Channels involved in the secretion/release of tears promote movement of fluid from the lacrimal sac into the nasolacrimal ducts, which are excreted through the nose.


  What are the ways that we can voluntarily manipulate pressure changes in the ear?


  We are aware of the eustachian tube at work when we feel air pressure changing in our ears as we yawn, chew, or swallow.


  What are the risks to ear structures when the ears are irrigated?


  There is the chance of pain due to force of irrigation, temperature of irrigation solution, or mechanical injury to ear structures. Rupture of the tympanic membrane is also a risk.  


  What strategies can a person use to avoid barotrauma caused by air travel during an upper respiratory infection?


  Autoinflation measures (yawning, swallowing, and chewing gum), decongestants (intranasal or systemic), myringotomy for severe, recurrent problems may be helpful in the avoidance of barotrauma.  


  Why are anti-inflammatory medications preferred over narcotic analgesics in the treatment of fibromyalgia?


  nflammatory processes and release of inflammatory mediators may be responsible for the pain associated with fibromyalgia. Anti-inflammatory medications may be helpful in blocking the production of the byproducts of the cyclooxygenase pathway, decreasing pain. Narcotic analgesics may complicate the treatment of associated psychiatric disorders and could contribute to the development of addiction and/or tolerance due to the chronic nature of the condition.


  What is the most likely mechanism for the prevention of migraines with antiseizure medications?


  Antiseizure medications work by inhibiting neurotransmitter conduction, usually related to actions of the neurotransmitter GABA, potentially slowing impulses perceived as pain.  


  Why do people with macular degeneration have difficulty with night vision and color differentiation?


  Degeneration of the macular portion of the retina includes loss of photoreceptors, rods, and cones responsible for night vision and color differentiation.  


  What are the implications for older Americans who develop glaucoma? What lifestyle changes can they expect to experience?


  Progressive loss of vision reduces an individual’s ability to care for themselves. Activities of daily living may require assistance, increasing dependence. Loss of visual acuity may result in the inability to drive, promoting dependence. Inability to read or see the television may reduce quality of life.


  What other tissue types can be affected by decreased trophic signals of ovarian hormones? What other tissue types can be similarly affected?


  Any cell dependent on trophic signals will undergo atrophy if the frequency or intensity of the signal is decreased. These cells may include thyroid, uterine, ovarian, adrenal, and pituitary. Lack of demand can also stimulate the development of atrophy. Tissues at risk for atrophy due to decrease in demand include muscle, renal and bone.  


  How are defense mechanisms and the body protections affected in the person who is a mouth breather?


  The mouth may be used for ventilation when the nose is obstructed or in cases of an increased oxygen demand, such as vigorous exercise. The filtration properties and humidification are not as efficient; inspired air is more likely to contain foreign particles and excessive dryness than that inspired through the nose.


  How does your breathing change when you exercise? Why do you think this happens?


  Breathing rate and depth increase during exercise. In the process of exercise, cell metabolism increases dramatically. This produces excess acids that must be removed from the body to prevent acidosis. One mechanism for the removal of these acids is to discharge CO2 (an acidic gas) from the body through the lungs.


  What happens to your oxygen-attracting ability if you eat a diet low in iron?


  Iron is the magnet that has a high affinity for oxygen and pulls the oxygen onto the hemoglobin molecule. Theoretically, the body in iron-deficiency has a reduced oxygen affinity on the hemoglobin molecule. Since hemoglobin is the most efficient carrier of oxygen, lower oxygen on hemoglobin could mean lower oxygen to cells and tissues throughout the body.  


  What happens to oxygen and carbon dioxide transport if there is a lack of RBCs, as in severe hemorrhaging?


  RBCs are major carriers of both oxygen and carbon dioxide. Reduction in overall RBC concentration will result in a reduced carrying capacity of both gases. Although small concentrations of both gases are found dissolved in the plasma, effective transport to all tissues of the body is reduced without RBCs.


  Based on what you know about why and how SaO2, PaO2, and PaCO2 are measured, what factors do you think would affect these readings?


  Oxygen saturations are affected by iron-binding capacity, presence of oxygen, carrying capacity of hemoglobin; PaO2 is affected by a lack of or reduced concentration of oxygen intake including the presence and concentration of oxygen, altitude, and aging; PaCO2 is affected by conditions that cause CO2 retention or release of CO2 including fibrosis, air trapping, fluid accumulation in the alveoli, or excessive “blowing off” of CO2 as with the hyperventilatory state of anxiety.


  How long can you hold your breath? How do you feel while you are holding your breath? When you cannot hold your breath any longer and you start to breathe, how does your body respond?


  Breath-holding will result in signs of respiratory acidosis (CO2 retention); body initially will respond by increasing rate and depth of breathing to rid of the excess CO2 retained while holding breath.


  How does the body respond to low oxygen or increased carbon dioxide in the blood or tissues?


  The body responds by altering the pattern of breathing. In this case, the rate and depth of breathing would increase to attract more oxygen and release more carbon dioxide.


  How does the development of granulomas, fibrosis, and calcification in TB compare with other chronic inflammatory conditions, such as rheumatoid arthritis?


  TB is a chronic inflammatory condition caused by a bacterial infection. Chronic inflammation represents a persistent or recurrent state of inflammation lasting several weeks or longer. This state occurs when the acute inflammatory and immune responses are unsuccessful. Chronic inflammation can be related to an unrelenting injury, persistent infectious process, or an autoimmune condition. Cellular activity is notably different between acute and chronic inflammation. Monocytes, macrophages, and lymphocytes are more prominent in chronic inflammation. Monocytes circulate in the blood to the site of injury and mature into macrophages in the tissues. As monocytes mature into macrophages, they produce proteinases and fibroblasts. Proteinases are enzymes that destroy elastin and other tissue components. These enzymes help to break down dead tissue but, unfortunately, these enzymes do not discriminate. Proteinase activity is responsible for ongoing tissue destruction at and surrounding the site of the persistent injury. Fibroblasts are also active in chronic inflammation. Fibroblasts are responsible for collagen development, which contributes to the extensive scarring characteristic of chronic inflammation. Scarring can lead to permanent loss of function and deformity of the tissue or organ. In some cases, chronic inflammation results in granuloma formation. Granulomas are nodular inflammatory lesions that encase harmful substances. Granuloma formation is also regulated by macrophages. Granulomas typically form when the injury is too difficult to control by the usual inflammatory and immune mechanisms, such as with foreign bodies or certain microorganisms. One classic example of a microorganism that results in granuloma formation is Mycobacterium tuberculosis, the bacteria responsible for tuberculosis. By forming granulomas, macrophages protect healthy, unaffected surrounding tissue from further damage. Inside the granuloma, macrophages are busy phagocytizing harmful substances. As a result, necrosis fills the inside of the granuloma. Gradually, the necrosis diffuses through the granuloma wall and a fibrotic capsule remains  


  Based on the basic pathophysiologic processes, construct a treatment plan for a person with asthma. What environmental modifications would you make? What would be the goals of pharmacologic therapy?


  The treatment plan will include environmental modifications and targeted pharmacotherapy. Environmental modification will need to include reduction or elimination of exposure to the trigger. Immunotherapy (administration of “allergy shots”) is sometimes indicated. Medications need to address inflammation and the bronchoconstriction that characterizes asthma. Inhaled bronchodilators are used for quick relief of bronchoconstriction and can be used prior to exercise if the asthma is exercise induced. Inhaled anti-inflammatory medications are indicated for long-term control of chronic inflammation. Sometimes oral anti-inflammatory medications such as prednisone are indicated. The treatment plan will depend upon the severity of the condition.


WHERE IS EXCESS GLUCOSE STORED?


IN THE LIVER


WHAT DOES GLUCOSE IN THE BLOOD TRIGGER?


INSULIN RELEASE


INSULIN IS WHICH TYPE OF HORMONE?


IT IS AN ANABOLIC HORMONE NEEDED FOR GLUCOSE UPTAKE IN THE LIVER, MUSCLE, AND FAT CELLS, ETC


WHAT BODY STRUCTURES DO NOT REQUIRE INSULIN TO UPTAKE GLUCOSE?


BRAIN, RED BLOOD CELLS, KIDNEY, AND THE LENS OF THE EYE


WHAT ARE ANABOLIC HORMONES RESPONSIBLE FOR?


BUILDING COMPLEX COMPOUNDS IN TEH BODY SUCH AS BUILDING PROTEINS FROM AMINO ACIDS.


INSULIN HAS WHICH SEVERAL KEY FUNCTIONS?


PROMOTES GLUCOSE USAGE, DECREASING BLOOD GLUCOSE LEVELS

PROMOTES PROTEIN SYNTHESIS

PROMOTES FORMATION AND STORAGE OF LIPIDS
FACILITATES TRANSPORT OF POTASSIUM, PHOSPHATE, AND MAGNESIUM INTO THE CELLS


WHAT IS THE DIFFERENCE BETWEEN THE ENDOCRINE PANCREAS AND THE EXOCRINE PANCREAS WHICH ARE INNERVATED BY THE AUTONOIC NERVOUS SYSTEM?


THE ENDOCRINE PANCREAS SECRETES HORMONES LIKE INSULIN AND GLUCAGON.

THE ACINI CELLS OF THE EXOCRINE PANCREAS SECRETE DIGESTIVE ENZYMES AND ALKALINE FLUIDS THROUGH THE PANCREATIC DUCT INTO THE DUODENUM.


THE ISLETS OF LANGERHANS CONTAIN WHICH THREE MAJOR TYPES OF HORMONE SECRETING CELLS?


ALPHA: SECRETE GLUCAGON WHICH MOBILIZES GLYCOGEN FROM THE LIVER AND SUPRESSES INSULIN SECRETION. IT IS VERY HELPFUL IN MAINTAINING BLOOD GLUCOSE LEVELS BETWEEN MEALS.

BETA: SECRETE INSULIN WHICH PROMOTES GLUCOSE UTILIZATION

DELTA: SECRETE SOMATOSTATIN AND GASTRIN, WHICH REGULATE ALPHA AND BETA CELL FUNCTION BY SUPPRESSING THE RELEASE OF INSULIN, GLUCAGON, AND PANCREATIC POLYPEPTIDES.


THE PANCREAS ALSO CONTAINS F CELLS.  WHAT DO THEY DO?


USUALLY FOUND IN PERIPHERY OF THE ISLETS, THEY SECRETE PANCREATIC POLYPEPTIDES WHICH SUPPRESS DIGESTIVE ENZYME RELEASE FROM THE EXOCRINE PANCREAS.


WHEN IS INSULIN SECREATION INCREASED?


WHEN THERE ARE ELEVATIONS IN BLOOD GLUCOSE, AMINO ACIDS, POTASSIUM, PHOSPHATE, AND MAGNESIUM, AND GLUCAGON AND GASTRIN.

IT IS DECREASED IN SITUATIONS LIKE LOW BLOOD GLUCOSE, HIGH LEVELS OF INSULIN THROUGH NEG FEEDBACK, AND STIMULATION OF ALPHA CELLS.


WHAT IS THE MAJOR CHARACTERISTIC OF DIABETES INSIPIDUS?


A CONDITION OF INADEQUATE ANTIDIURETIC HORMONE


WHAT DOES THE ABSENCE, DEFICIT, OR RESISTANCE TO INSULIN LEAD TO?


A STATE OF HYPERGLYCEMIA WHICH IS A SIGNIFICANTLY ELEVATED BLOOD GLUCOSE LEVEL COUPLED WITH INABILITY TO TRANSPORT GLUCOSE AND AMINO ACIDS INTO THOSE CELLS THAT REQUIRE INSULIN FOR TRANSPORT.


BRIEFLY DESCRIBE TYPE I DIABETES


ONSET IS IN PUBERTY OR CHILDHOOD, PEAK AT 10-14 YEARS.  IT IS CAUSED BY INSULIN DEFICIT AND IS TREATED WITH INSULIN REPLACEMENT BLANCED WITH EXERCISE AND DIET


DESCRIBE TYPE II DIABETES


ONSET IS IN ADULT YEARS, USUALLY PEAKS AT 45 YRS, PREVALENCE INCREASES IN THOSE UNDER 45 YEARS OLD.  IT IS CAUSED BY INSULIN RESISTANCE OR IMPAIRED ABILITY OF THE TISSUES TO USE INSULIN; INSUFFICIENT INSULIN IN RELATION TO THE NEEDS OF THE BODY.  IT IS TREATED WITH DIET, EXERCISE, ORAL GLYCEMIC AGENTS, AND POSSIBLY INSULIN


DESCRIBE GESTATIONAL DIABETES


ONSET IS PREGNANCY AND PEAKS AT FIFTH OR SIXTH MONTH OF GESTATION.  IT IS CAUSED BY INSULIN RESISTANCE DURING PREGNANCY AS A RESULT OF TOO MUCH HORMONE PRODUCTION IN THE BODY (FOR THE PLACENTA); INABILITY TO MAKE THE ADDITIONAL INSULIN THAT IS NEEDED DURING PREGNANCY.  IT IS TREATED WITH DIET, EXERCISE, SOMETIMES INSULIN, AND DELIVERY OF THE BABY.


DESCRIBE THE ETIOLOGYOF TYPE I DIABETES


MULTIFACTORIAL AND INCLUDES BOTH GENETIC AND ENVIRONMENTAL INFLUENCES. 
AUTOIMMUNE RESPONSE: MOST BETA CELL ANTIBODIES ARE DIRECTED AGAINST GLUTAMIC ACID DECARBOXYLASE, GAD, A CHEMICAL IN THE BETA CELLS.  INFECTIONS LIKE MUMPS, GROUP B COXSACKIE VIRUSES OR INTRAUTERINE RUBELLA EXPOSURE MIGHT LEAD TO THIS AUTOIMMUNE CAUSE.

CYTOTOXIC T LYMPHOCYTES MAY DESTROY BETA CELLS.  AUTOIMMUNE DESTRUCTION TRIGGERS A CHRONIC INFLAMMATORY RESPONSE WHICH FURTHER DESTROYS BETA CELLS.


DESCRIBE PRE DIABETES


A STATE THAT CAN LEAST FOR SEVERAL YEARS, IT IS THE EARLY STAGES OF THIS CELL MEDIATED IMMUNE DESTRUCTION, ANTIBODIES AGAINST BETA CELLS ARE CIRCULATING, BUT HYPERGLYCEMIA IS NOT YET PRESENT.


AT WHAT POINT DO CLINICAL MANIFESTATIONS OF TYPE I DIABETES OCCUR?


WHEN AUTOIMMUNE PROCESSES DESTROY 80-90 PERCENT OR MORE OF THE BETA CELLS OF THE PANCREAS.  EVENTUALLY THE EXOCRINE PANCREAS BECOMES FIBROTIC WITH ATROPHY OF ACINAR CELLS.


HOW DOES TYPE I DIABETES ALSO AFFECT ALPHA CELLS?


IT RESULTS IN INCREASED LEVELS OF GLUCAGON BECAUSE GLUCAGON SUPPRESSES INSULIN PRODUCTION.  THIS, COUPLED WITH BETA CELL DESTRUCTION LEADS TO A STATE OF HYPERGLYCEMIA DN HYPERKETONEMIA.  HYPERGLYCEMIA IS A RESULT OF ACCUMULATIONS IN CIRCULATING BLOOD GLUCOSE UNMATCHED BY INSULIN FOR USE IN THE CELL.


WHAT DOES THE REDUCTION OR ABSENCE OF INSULIN ALLOW?


UNREGULATED MOBILIZATION OF FATS FOR ENERGY.  AS A RESULT, FAT OXIDATION PRODUCES HYPERKETONEMIA WHICH IS EXCESS CIRCULATING KETONE BODIES, COMPOSED OF ACETOACETIC ACID, ACETONE, AND B-HYDROXYBUTYRIC ACID, LEADING TO A STATE OF METABOLIC KETOACIDOSIS


WHAT CAN HYPERGLYCEMIA, EVEN WHEN NOT ASSOCIATED WITH KETOACIDOSIS, LEAD TO?


OSMOTIC DIURESIS WHICH IS A CONDITION WHERE EXCESS GLUCOSE PROMOTES THE ATTRACTION OF WATER INTO THE KIDNEYS THEREBY ELIMINATING GLUCOSE, ELECTROLYTES, AND WATER THROUGH URINE WHICH CAN LEAD TO SEVERE DEHYDRATION.  HYPERGLYCEMIA ALSO UNDERMINES WBC FUNCTION, PROMOTES INFECTION,AND IMPAIRS WOUND HEALING.


WHAT ARE THE THREE CLINICAL MANIFESTATIONS MOST COMMONLY ASSOCIATED WITH TYPE 1 DIABETES?


POLYDIPSIA-EXCESSIVE THIRST
POLYURIA-EXCESSIVE URINATION
POLYPHAGIA-EXCESSIVE HUNGER


WHAT ARE THE LAB LEVELS USED TO DIAGNOSE TYPE I DIABETES?


FASTING GLUCOSE OVER 126 MG/DL
RANDOME BLOOD GLUCOSE OVER 200 MG/DL

URINE IS CHECKED FOR KETONES AND CAN ALSO PROVIDE INFO ON PRESENCE OF HYPERKETONEMIA.  URINE KETONE LEVELS ARE PROPORTIONAL TO BLOOD KETONE LEVELS.

ISLET CELL AUTOANTIBODIES CAN BE DETECTED IN EARLY STAGES AS WELL AS AUTOANTIBODIES AGAINST GAD.

GLUCOSE TOLERANCE TEST: PERSON IS GIVEN 50-100 G OF GLUCOSE IN WATER AND BLOOD GLUCOSE IS TAKEN AT 1,2,3 HOURS: GREATER THAN 190 MG/DL AFTER 1 HOUR AND GREATER THAN 165 MG/DL AFTER 2 HRS IS ANOTHER DIAGNOSTIC CRITERIA

GLYCOSYLATED HEMOGLOBIN: HBA1C: 8% OR GREATER

URINALYSIS: GLUCOSE >15 MG/DL, KETONE PRESENT


WHAT IS THE GOAL OF TREATMENT FOR DIABETES TYPE I?


STABILIZE BLOOD GLUCOSE LEVELS WITHIN EXPECTED RANGE OF 70-120 MG/DL. 



WHAT SHOULD DIET INCLUDE FOR TYPE I DIABETES?


COMPLEX CARBS, PROTEIN, UNSATURATED FAT SOURCES WHILE LIMITING SIMPLE SUGARS, CHOLESTEROL, AND SATURATED FATS.  TYPICALLY THE CARB TO INSULIN RATIO NEEDED IS 10-15 G OF CARB TO 1 UNIT OF RAPID ACTING INSULIN.


HOW DOES EXERCISE HELP DIABETES?


EXERCISE DECREASES BLOOD GLUCOSE LEVELS THROUGH INCREASED GLUCOSE USAGE BY MUSCLE TISSUE.  INCREASES IN EXERCISE MUST BE MATCHED WITH REDUCTIONS IN INSULIN OR INCREASES IN FOOD UPTAKE.


WHY IS INSULIN NOT GIVEN ORALLY?


BECAUSE IT IS DESTROYED IN THE GI TRACT SO IT MUST BE GIVEN SUBQ OR BY INSULIN INFUSION PUMP.


WHAT CAN HAPPEN IF INSULIN IS INJECTED WITHOUT ADEQUATE DIETARY INTAKE?


HYPOGLYCEMIA, OR LOW BLOOD GLUCOSE LEVELS.


DESCRIBE THE VARIOUS TYPES OF INSULIN


RAPID ACTING (LISPRO): ONSET 15 MIN, PEAK 1 HR, DURATION: 2-4 HRS, ADMINISTER RIGHT BEFORE MEAL.

SHORT ACTING (REGULAR, HUMULIN): ONSET: 30 MIN, PEAK: 2-3 HRS, DURATION: 3-6 HRS: ADMINISTER THROUGHOUT THE DAY

INTERMEDIATE ACTING (NPH): ONSET: 2-4 HRS, PEAKS: 4-12 HRS, DURATION: 12-18 HRS, ADMINISTER THROUGHOUT THE DAY

LONG ACTING (ULTRALENTE): ONSET: 6-10 HRS, PEAKS: 8-12 HRS, DURATION: 18-26 HRS, ADMINISTER AT NIGHTTIME

OTHER (GLARGINE): ONSET: 2-4 HRS, PEAKS: PEAKLESS, DURATION: UP TO 24 HRS, ADMINISTER AT NIGHTTIME


DESCRIBE TYPE II DIABETES


A PROBLEM OF INSULIN RESISTANCE WHERE THERE IS REDUCED TISSUE SENSITIVITY TO INSULIN AND A REDUCTION IN ADEQUATE INSULIN SECRETION. 90% OF CASES ARE TYPE II. 


WHAT IS MODY?


MATURITY ONSET DIABETES OF THE YOUNG WHICH IS A RARE FORM OF TYPE II DIABETES THAT HAS A STRONG GENETIC COMPONENT (AUTOSOMAL DOMINANT INHERITANCE) AND IS FOUND TO AFFECT INDIVIDUALS YOUNGER THAN 25. 


WHAT IS SYNDROME X?


THE METABOLIC SYNDROME IS A CONDITION THAT INCLUDES INSULIN RESISTANCE AND A CONSTELLATION OF OTHER METABOLIC PROBLEMS INCLUDING OBESITY, HIGH TRIGLYCERIDES, LOW HDL, HYPERTENSION, AND CORONARY HEART DISEASE.  PEOPLE WITH TYPE II DIABETES MUST ALSO BE EVALUATED FOR THIS TO DETERMINE FULL RANGE OF METABOLIC ALTERATIONS.


DESCRIBE THE PATHO OF TYPE II DIABETES.


EXACT CAUSE UNKNOWN. MOST SIGNIFICANT RISK IS OBESITY. 90% OF THOSE WITH TYPE II ARE OBESE.  ALL OVERWEIGHT PEOPLE HAVE INSULIN RESISTANCE BUT ONLY THOSE WHO ARE UNABLE TO COMPENSATE BY INCREASING BETA CELL PRODUCTION OF INSULIN GO ON TO DEVELOP TYPE II.


WHAT ARE SOME RISK FACTORS FOR TYPE II DIABETES BESIDES OBESITY?


OVER 30 YRS OLD, FAMILY HX OF TYPE II, NATIVE AMERICAN, HISPANIC, OR BLACK.


HOW IS TYPE II DIFFERENT FROM TYPE I DIABETES?


THERE IS NO AUTOIMMUNE DESTRUCTION OF THE PANCREAS. INSTEAD, INSULIN RESISTANCE, OR A DECREASED SENSITIVITY TO INSULIN IN METABOLIC TISSUES, LIKE THE LIVER, SKELETAL MUSCLE, AND FAT TISSUE RESULTS IN INSUFFICIENT INSULIN USAGE.


HOW DOES OBESITY PROMOTE PERIPHERAL INSULIN RESISTANCE?


BY RELEASING FREE FATTY ACIDS AND CYTOKINES FROM ADIPOSE CELLS.  THESE CHEMCIALS INTERFERE WITH INSULIN SIGNALS, DISRUPT INSULIN RECEPTORS ON THE TARGET CELL PLASMA MEMBRANES, AND PROHIBIT INSULIN FROM FACILITATING THE ENTRY OF GLUCOSE INTO LIVER, MUSCLE, AND ADIPOSE TISSUES.


IN TYPE TWO DIABETES, SUBADEQUATE LEVELS OF INSULIN AND PERIPHERAL RESISTANCE TO INSULIN UPTAKE LEADS TO WHAT??


1. BETA CELLS DONT ADEQUATELY RESPOND TO CIRCULATING BLOOD GLUCOSE LEVELS.

2. THE RELEASE OF GLYCOGEN FROM THE LIVER COUPLED WITH THE SUPPRESSION OF INSULIN BY GLUCAGON PROMOTES EXCESSIVE CIRCULATING GLUCOSE.

3. THE INSULIN RECEPTORS IN THE LIVER, SKELETAL MUSCLE, AND ADIPOSE TISSUE ARE UNRESPONSIVE, THEREBY MAKING THE TISSUES UNABLE, OR RESISTANT, TO USING THE INSULIN.


IN TYPE II DIABETES GLUCAGON SECRETION IS SIGNIFICANTLY INCREASED.  WHAT THEN OCCURS?


GLUCAGON MOBILIZES GLYCOGEN FROM THE LIVER AND SUPPRESSES INSULIN SECRETION. ALTHOUGH THERE IS NO REDUCTION IN BETA CELLS, HIGH SERUM LIPID LEVELS, AS MAY OCCUR WITH OBESITY, ALLOWS FAT TO DEPOSIT IN THE PANCREAS, WHICH MAY LEAD TO SCLEROSIS AND FURTHER IMPAIR PANCREATIC FUNCITON. THIS RESULTS IN IMPAIRED METABOLISM OF CARBS, FATS, AND PROTEINS.


WHAT ARE SOME CLINICAL MANIFESTATIONS OF TYPE II DIABETES?


SOMETIMES IT IS THE TRIAD OF SYMPTOMS FROM TYPE I DIABETES.  PRIMARILY THE MANIFESTATIONS ARE RELATED TO LONG TERM COMPLICATIONS LIKE VISUAL CHANGES, CHANGES IN KIDNEY FUNCTION, CORONARY ARTERY DISEASE, PERIPHERAL VASCULAR DISEASE, RECURRENT INFECTIONS, OR NEUROPATHY. PRESENCE OF OBESITY AND HYPERLIPIDEMIA SHOULD HEIGHTEN SUSPICION THAT IT IS PRESENT.


WHAT ARE SOME OF THE DIAGNOSTIC CRITERIA FOR TYPE II DIABETES?


RANDOM PLASMA ABOVE 200 MG/DL.
FASTING BLOOD GLUCOSE ABOVE 126 MG/DL.
FASTING PLASMA GLUCOSE BETWEEN 110 AND 125 MG/DL INDICATES IMPAIRED FASTING GLUCOSE.

PRESENCE OF RETINOPATHY, NEUROPATHY, AND NEPHROPATHY FOR SOM.

****PRESENCE OF ANTIBODIES AGAINST THE ISLET CELLS OR GAD WOULD INDICATE THAT THIS PERSON HAS TYPE I DIABETES, NOT TYPE II


HOW IS TYPE II DIABETES TREATED?


WEIGHT CONTROL THROUGH DIET AND EXERCISE.
CAN INCLUDE ORAL GLYCEMIC AGENTS OR INSULIN.
GOAL OF TREATMENT IS TO MAINTAIN OPTIMAL BLOOD GLUCOSE LEVELS.

PHYSICAL ACTIVITY IS HELPFUL BECAUSE IT INCREASES THE UPTAKE OF GLUCOSE BY THE MUSCLES WITHOUT INCREASING INSULIN NEEDS.  IT ALSO IMPROVES INSULIN SENSITIVITY AND LOWERS LONG TERM COMPLICATIONS OF DIABETES.

GLYCEMIC AGENTS ACT TO INCREASE INSULIN RELEASE BY THE BETA CELLS, INCREASE GLUCOSE PRODUCTION BY THE LIVER, OR INCREASE INSULIN UPTAKE.


DESCRIBE THE VARIOUS ORAL GLYCEMIC AGENTS


ALPHA-GLUCOSIDASE INHIBITORS (ACARBOSE, MIGLITOL): SITE OF ACTION: INTESTINES, SLOWS CARB DIGESTION.

BIGUANIDES (METFORMIN): SITE OF ACTION: LIVER, PREVENTS EXCESSIVE GLUCOSE RELEASE FROM THE LIVER, MAKES PERIPHERAL TISSUES MORE SENSITIVE TO INSULIN

MEGLITINIDES (REPAGLINIDE): SITE OF ACTION: PANCREAS, STIMULATES MORE SECRETION OF INSULIN FROM THE PANCREAS; SHORT ACTING

SULFONYLUREAS (TOLBUTAMIDE, GLIPIZIDE, GLYBURIDE, GLIMEPIRIDE): SITE OF ACTION: PANCREAS, STIMULATES MORE SECRETION OF INSULIN FROM THE PANCREAS

THIAZOLIDINEDIONES (ROSIGLITAZONE, PIOGLITAZONE): SITE OF ACTION: MUSCLE CELLS, INCREASES SENSITIVITY OF TISSUES (FAT, MUSCLE, LIVER) TO INSULIN.


DESCRIBE THE PATHO AND POTENTIAL COMPLICATIONS OF POLYURIA, NOCTURIA, AND GLUCOSURIA IN TYPE I DIABETES


HYPERGLYCEMIA OSMOTICALLY DRAWS FLUIDS INTO THE INTRAVASCULAR SPACE; GLUCOSE ALSO ACTS AS A DIURETIC; THIS LEADS TO LARGE VOLUMES OF URINE BEING FILTERED BY THE KIDNEYS AND EXCRETED; ALSO THE RENAL THRESHOLD FOR GLUCOSE IS EXCEEDED; THE KIDNEYS ALL THIS EXCESS GLUCOSE TO SPILL OUT INTO THE URINE. POTENTIAL COMPLICAITON IS DEHYDRATION


DESCRIBE THE PATHO AND POTENTIAL COMPLICATIONS OF POLYDIPSIA AND DRY MOUTH IN TYPE I DIABETES


HYPERGLYCEMIA OSMOTICALLY DRAWS FLUIDS FROM THE CELLS INTO THE INTRAVASCULAR SPACE, LEADING TO CELLULAR DEHYDRATION AND THE STIMULATION OF THIRST BY THE HYPOTHALAMUS. POTENTIAL COMPLICATION IS DEHYDRATION


DESCRIBE THE PATHO AND POTENTIAL COMPLICATIONS OF POLYPHAGIA, WEIGHT LOSS, AND FATIGUE IN TYPE I DIABETES


INSULIN DEFICIT DISALLOWS USE OF GLUCOSE FOR ENERGY; STORAGE OF FATS, PROTEINS, AND CARBS BEGIN TO DEPLETE, CELLS ARE IN A STATE OF STARVATION BECAUSE OF LACK OF NUTRIENTS, THEREBY INDUCING HUNGER.
POTENTIAL COMPLICATIONS ARE STARVATION, COMA, AND DEATH


DESCRIBE THE PATHO AND POTENTIAL COMPLICATIONS OF BLURRED VISION IN TYPE I DIABETES


LENS AND RETINA ARE EXPOSED TO HYPEROSMOLAR FLUIDS. CAN LEAD TO VISION IMPAIRMENT AND BLINDNESS.


DEFINE GESTATIONAL DIABETES


ANY DEGREE OF GLUCOSE  INTOLERANCE THAT OCCURS DURING PREGNANCY. IT IS USUALLY TEMPORARY. OCCURS BECAUSE OF INSULIN RESISTANCE THAT OCCURS DURING PREGNANCY AND BECAUSE OF AN INABILITY OF THE PANCREAS TO MAKE THE ADDITIONAL INSULIN NEEDED DURING PREGNANCY TO SUPPORT THE PLACENTA


WHAT ARE RISK FACTORS FOR GESTATIONAL DIABETES?


FAMILY HX OF DIABETES, FIVE + PREGNANCIES, AND A PREVIOUS LGA BABY.  IT OCCURS IN 4-14% OFF PREGNANCIES AND IS USUALLY DIAGNOSED IN THE FIFTH OR SIXTH MONTH.


WHAT ARE SOME TREATMENTS FOR GESTATIONAL DIABETES?


DIET MODIFICATION, EXERCISE, AND POSSIBLE INSULIN. TIGHT CONTROL OF BLOOD GLUCOSE IS NEEDED TO PREVENT OVERSTIMULATION OF THE FETAL PANCREAS DURING PREGNANCY.  ORAL GLYCEMIC AGENTS ARENT RECOMMENDED BECAUSE OF THEIR POTENTIALLY TERATOGENIC EFFECTS.


WHAT CAN UNTREATED GESTATIONAL DIABETES, OR POORLY CONTROLLED TYPE I OR TYPE II DIABETES IN PREGNANCY LEAD TO?


*FETAL MACROSOMIA
*HYPOGLYCEMIA FROM PANCREATIC HYPERPLASIA AND EXCESS INSULIN SECRETION IN THE NEWBORN
*HYPOCALCEMIA
*HYPERBILIRUBIEMIA
*A 5-10% INCIDENCE OF MAJOR DEVELOPMENTAL ANOMALIES LIKE SPINA BIFIDA OR HEART DEFECTS.

COMPLICAITONS FOR MOTHER INCLUDE A GREATER RISK FOR CHRONIC HYPERTENSION AND CESAREAN DELIVERY AND DEVELOPING TYPE II DIABETES AFTER DELIVERY


DESCRIBE ACUTE COMPLICATIONS OF DIABETES MELLITUS


RELATED EITHER TO HYPOGLYCEMIA OR STATE OF EXCESSIVE HYPERGLYCEMIA. RAPID ONSET AND OFTEN HAVE SIGNIFICANT MANIFESTATIONS OF ALTERED NEURAL FUNCTION.
ESPECIALLY IN THOSE WITH TYPE I, REGULATION OF GLYCEMIC CONTROL CAN BE CHALLENGING. SOMOGYI EFFECT AND DAWN PHENOMENON ILLUSTRATE ACUTE COMPLICATIONS.


DESCRIBE HYPOGLYCEMIA


VERY LOW BLOOD GLUCOSE, CLINICAL MANIFESTATIONS MAY BE WEAKNESS, PALLOR, COOL CLAMMY SKIN.
MANIFESTATIONS USUALLY PRESENT WHEN SERUM GLUCOSE IS LESS THAN 50 MG/DL WHICH MAY OCCUR IN SITUATIONS LIKE: HYPERINSULINEMIA (HIGH CIRCULATING INSULIN LEVEL) AS CAN HAPPEN WITH ADMIN OF EXOGENOUS INSULIN, INADEQUATE FOOD INTAKE OR VOMITING WHERE PRESENCE OF GLUCOSE IN BODY IS REDUCED, FREQUENT SIMPLE CARB INTAKE, STRENUOUS EXERCISE OR INFECTION WHERE USE OF GLUCOSE IS EXCESSIVE.


WHEN IS HYPOGLYCEMIA MOST OFTEN FOUND?


INDIVIDUALS WITH TYPE I DIABETES WHO ARE UNDERGOING INSULIN REPLACEMENT THERAPY.  ESPECIALLY INSULIN PUMP BECAUSE IT CONTINUOUSLY PUMPS INSULIN INTO BODY REGARDLESS OF MEAL SKIPPING OR EXERCISE HAS OCCURED.


WHAT IS HYPOGLYCEMIA PARTICULARLY PROBLEMATIIC FOR?


BRAIN, WHICH HAS AN ENERGY DEMAND TWICE THAT OF OTHER CELLS IN THE BODY. NEURONS ARE IN CONSTANT STATE OF METABOLIC ACTIVITY. CONCENTRATION NEEDS HIGH CONCENTRATIONS OF GLUCOSE.

LAKE OF GLUCOSE HAS BEEN FOUND TO IMPEDE THE SYNTHESIS OF ACETYLCHOLINE, A MAJOR BRAIN NEUROTRANSMITTER.


WHAT ARE THE MORE NOTABLE CLINICAL MANIFESTATIONS OF HYPOGLYCEMIA?


MOST NOTABLY RELATED TO NEURONAL DEPRIVATION OF GLUCOSE.

POTENTIAL S/S ARE POOR CONCENTRATION, EXTREME HUNGER, CLAMMY/COOL SKIN, BLURRED VISION, DIZZINESS, AND CONFUSION, DIFFICULTY WITH SPEECH, LACK OF COORDINAITON, STAGGERING GAIT, AND HEADACHE.  HYPOGLYCEMIC STATE ACTIVATES THE SYMPATHETIC NERVOUS SYSTEM WHICH CAUSES AN INCREASE IN THE PULSE ALONG WITH PALPITATIONS, SWEATING, ANXIETY, AND TREMORS. 


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