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  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
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