Number 1. (blank) patients have pancreatic beta cells that have lost the ability to produce insulin. This happens mainly in children. There is no insulin to assist glucose to enter most cells. Therefore blood glucose rises and is filtered in the kidney. If plasma glucose exceeds 400 mg/dl then kidney transporters are saturated (zero order kinetics) and glucose spills into the urine drawing water with it causing a diuresis. They exhibit polyuria (frequent urination) and polydipsia (constant thirsty). They are physically weak but their mind functions because brain cells take up glucose without insulin. High blood glucose causes neuropathies and blindness and also kidney damage. They do not feel pain sensation of injuries and infections begin. The immune system is compromised and wounds do not heal well. The child with (blank) fails to thrive without insulin hormone replacement therapy

Number 2. (blank) patients are usually older and obese but this metabolic disease is happening to obese children too. They make insulin in their pancreatic beta cells but secrete much of it in the precursor inactive form (proinsulin). Cellular receptors become resistance to insulin. Then cells do not take up glucose, plasma glucose rises and spills into the urine causing polyuria and polydipsia. Renal damage, neuropathies, injuries, wounds that do not heal and blindness occur. The sweat is sweet and fungal skin infections occur between body folds and these may eventually infect the blood. They are not dependent on insulin at first since their pancreas still makes plenty but their body is desensitized to it and needs higher concentrations of insulin to respond.

Number 3. (blank) is also called gestational diabetes. These patients have hyperglycemia which must be controlled to prevent the fetus from becoming a 10 to 14 lb baby due to elevated glucose causing fat deposition. The drugs to treat diabetes during pregnancy must not cross the placenta since hypoglycemia in the fetus would reduce brain development and a cause failure to thrive. Dietary controls and insulins are usually used since this protein hormone does not cross the placenta.

Number 4. (blank) (standard or tight) control of diabetes causes less risk of developing complications like nephropathies, blindness or neuropathies, cardiovascular disease, infections failing to heal resulting in amputations. If (blank) control is done well, longevity improves.

Number 5. To keep blood glucose below 140 mg/dl, close to the normal fasting range (80 to 110 mg/dl), the disadvantages are more needle sticks for drug administration and monitoring and regimentation about meals and medications. The cost of (blank) tight control treatment is higher and their is a greater risk of developing hypoglycemic emergencies which reduces brain function, and runs the risk of brain malfunctions, seizure, and death.

Number 6. There is a risk of organ damage if blood glucose is allowed to become twice the normal = 220 mg/dl for long periods of time. Kidneys fail, neuropathies begin and may progress to blindness. The immune system weakens, infections occur and wounds do not heal; basically health slowly declines.

Number 7. There is less risk of hypoglycemia causing sudden death. Life does not have to be quite so regimented . There are fewer needle sticks and cost of medications and monitoring is lower but cost of treatment fo complications adds up too unfortunately.

Number 8. In conscious patient they should eat sugar quickly before they lose mental acuity. In an unconscious patient, they should be infused with glucose or given an injection of glucagon (hormone from pancreas that raises blood sugar by breaking down glycogen stored in the liver).

Number 9. Hormone of the pancreatic beta cells and genetically engineered modications of it to make short intermediate and long acting insulins. MOA = Lowers blood sugar by causing insertion of glucose transporters into plasma membranes that take glucose out of blood and into cells. Insulin is required to treat Type I diabetics. It is eventually used in Type II diabetics after they no longer respond effectively to oral hypoglycemic agents. Mixtures of fast and slow insulins are used to keep insulin in the therapeutic window and plasma glucose in the normal range for longer periods of time with fewer injections. Usually insulin is injected subcutaneously, but it can also be delivered by intradermal pump (3 day supply) or by inhalation of insulin powder (exubera).

Number 10. 1st generation (6 hr duration) and 2nd generation (~24 hr action) sulfonylureas = oral hypoglyemic agents. MOA = they close ATP sensitive K channels to depolarize beta cells of the pancrease to open Ca channels and secrete more insulin. The sulfonylureas treat Type II diabetes. These drugs do not work in Type 1 diabetics who have no insulin to release. Sulfonylureas have the potential to cause hypoglycemia and allergic cross-reactions in those sensitive to sulfonamides.

Number 11. ATP sensitive K channel closers are used to treat type II diabetes mellitus. Act like sulfonylureas by closing ATP sensitive K channels but only when incretin type digestive hormones are present. They are not chemically sulfonylureas. These drugs are taken before meals to depolarize beta cells to release more insulin and they work for about 2 hours postprandially when the incretin hormones are in the blood stream. They can cause hypoglycemia if plasma levels remain high too long.

Number 12. (blank) is a euglycemic agent that increases sensitivity of receptors to insulin. It stimulates glucose utilization in cells and decrease hepatic output of glucose into the blood by reducing glycogen break down and reducing glucagon release. It reduces glucose absorption from GI tract too. (blank) does not cause hypoglycemia. It prevents blood glucose from increasing but it can not cause blood glucose to fall below normal. It is used to treat Type II diabetes - not type I. Metformin can decrease LDLs, decrease TGs and increase HDLs a little so it is useful in patients with hyperglycemia and hyperlipidemia. It should not be used to alter lipids unless the patient also has type II diabetes.

Number 13. (blank) are insulin sensitizers. They sensitize muscle and liver to the actions of insulin by causing gene expression of insulin responsive genes by increasing peroxisome proliferator activator receptor gamma (PPARgamma) activity. These drugs need insulin to be active; they are used in type II diabetics to resensitize them to their own insulin. They cause weight gain which is problematic in type II diabetics. There are warnings posted that these drugs may be causing congestive heart failure. Special alerts recommend watching for rapid weight gain indicative of edema (fluid retention) and pitting edema and loss of cardiac function.

Number 14. (blank) are alpha glucosidase inhibitors. They inhibit alpha glucosidase in the brush border of the intestine. This inhibits carbohydrate digestion in the GI tract and prevent plasma glucose from rising rapidly after a carbohydrate (polysaccharide) meal. They prevent blood glucose from rising but do not lower blood glucose so they pose no threat of hypoglycemia. They are used to treat Type II (non-insulin dependent) diabetics. The undigested sugars can feed colonic bacteria and cause GI disturbances (flatulence and diarrhea). These drugs if combined with hypoglycemic agents can prevent hypoglycemic rescue with sugars. Glucose tablets or sports drinks containing glucose should be used instead. These drugs do not prevent blood glucose from rising if the patient drinks sports drinks or eats glucose containing foods.

Number 15. (blank)mimics incretin hormones. It is a peptide that must be administered by subcutaneous injection. It is an analog of the GI hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide(GIP) which increase insulin secretion, increase pancreatic Beta cell growth/replication to reverse diabetes. It slows gastric emptying and prolongs the feeling of fullness and may thereby decrease food intake resulting in weight loss. When added to sulfonylureas and/or metformin, it results in additional lowering of hemoglobin A1c by approximately 0.5% to 1%. It is used as an adjunct in the management of type 2 diabetes mellitus (noninsulin dependent, NIDDM). Because it slows gastric emptying time, it should not be given to patients who have a sluggish GI tract because it can cause stoppage of GI motility.

raises endogenous incretin levels by inhibiting their breakdown. This is a convenient oral once-a-day drug (100 mg per day). 
MOA = (blank) inhibits dipeptidyl peptidase IV (DPP-IV) enzyme resulting in prolonged active incretin levels. Incretin hormones [eg, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)] regulate glucose homeostasis by increasing insulin synthesis and release from pancreatic beta cells and decreasing glucagon secretion from pancreatic alpha cells which decreases hepatic glucose production from glycogen. incretin hormones are released by the intestine throughout the day in response to a meal; incretin hormones are rapidly inactivated by the DPP-IV enzyme which this drug inhibits thus keeping incretin hormones active longer. These cause a feeling of fullness and reduced appetite. They can cause weight loss and restore beta cells in the pancreas.

Number 17. (blank) is an amylinomimetic antidiabetic agent. Synthetic analog of human amylin cosecreted with insulin by pancreatic beta cells; reduces postprandial glucose increases via the following mechanisms: 1) prolongation of gastric emptying time, 2) reduction of postprandial glucagon secretion, and 3) reduction of caloric intake through centrally-mediated appetite suppression. This drug should not be given to diabetics with neuropathies slowing peristalsis or their GI tract may stop moving or become obstructed.