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ClinMed Endocrinology Exam 2 > ClinMed Endocrinology Exam 2 > Flashcards

ClinMed Endocrinology Exam 2 Flashcards

1
Q

Diabetes Mellitus

A

A chronic metabolic disease caused by either absolute or relative insulin deficiency and varying degrees of insulin resistance- long term complications are due to microvascular and macrovascular disease

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2
Q

What is the normal fasting glucose?

A

<100 mg/dl

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3
Q

What is the IFG range to be considered pre-diabetic?

A

100-125 mg/dl, 126 or more is considered DM

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4
Q

Diabetes diagnosing criteria is….

A

Random glucose over 200 mg/dl or more with symptoms is considered DM. Oral glucose tolerance test (OGTT): 2 hour value over 200 mg/dl is DM; 2 hour value 140-199 mg/dl is impaired glucose tolerance (IGT). Hemoglobin A1c > 6.5% is DM; 5.7-6.4 is prediabetes.

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5
Q

What are the treatment targets for diabetes?

A

Hemoglobin A1c should be 7%; target can be 6% in selected patients. BP should be <100mg/dl, but lower is better. Glucose target in ICU settings is 140-180 mg/dl.

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6
Q

What are the different types of diabetes?

A

Type 1 (genes, immune, environment), Type 2 (genes, insulin resistance), MODY- (at least 11 types, autosomal dominant-glucokinase, HNF alpha), LADA-latent autoimmune DM in adults, polyendocrine syndromes

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7
Q

What are the secondary causes of diabetes?

A

Catecholamines from a pheochromocytoma, Glucocorticoids-cushings in med or surg, GH in acromegaly (psych stress), glucagon in glucagonoma (rare), hypokalemia-decrease insulin secretion, islet destruction- hemochromatosis, pancreatitis, pentamidine, vacor (rat poison)

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8
Q

Characteristics of type 1 DM

A

Formerly called Juvenile onset DM, type 1 DM, insulin dependent DM. Islet cells in pancreas produce little or no insulin resulting in uncontrolled blood sugar and ketoacids. It is caused by islet cell destruction. It is often associated with specific inherited genes.

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9
Q

What kind of disease is DM type 1?

A

autoimmune disease with islet cell and insulin autoantibodies

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10
Q

What age do people typically get DM type 1?

A

can occur at any age, but most common in youth

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11
Q

How do you treat DM type 1?

A

can be treated with insulin, but not prevented (yet)

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12
Q

Physiologically, how does DM type 1 occur? How does it present?

A

Autoimmune destruction of beta cells for many years. It may present abruptly in DKA or more gradually as in LADA.

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13
Q

What are the genes and antibodies associated with DM type 1?

A

Genes- HLA DR 3/4, DQ8. Antibody markers: ICA- islet cell antibodies. Glutamic acid dehydrogenase- GAD IA2 insulin antibodies.

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14
Q

How is LADA different from other types of diabetes? How common is it?

A

Latent autoimmune diabetes in adults. May account for 2-12% of diabetes. Lower BMI than DM2, but overlap. Progresses to insulin dependence more rapidly than DM2. One definition: age > 30 years, at least 1 of 4 antibodies positive. Insulin not required for 6 months.

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15
Q

What are other names for DM type 2?

A

Formerly called adult onset DM

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16
Q

What is wrong in the body in DM type 2?

A

Islet cells can produce insulin, but the cells that normally respond (muscle, liver, fat) are resistant to its actions. Abdominal obesity in 90% of people. Insulin resistance often precedes the DM by many years. It is more common in adults BUT now more common than type 1 DM in youth. Preventable by attention to diet and exercise.

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17
Q

Is insulin resistance inherited?

A

Yes, it is a benefit in dealing with starvation, but a problem in dealing with overfeeding.

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18
Q

What are the main insulin sensitive tissues?

A

skeletal muscle, liver, fat

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19
Q

What does insulin resistance lead to?

A

Decreased glucose utilization (muscle), increased glucose production (liver), and increased free fatty acid release (fat). Weight gain and physical inactivity increase insulin resistance.

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20
Q

Type 2 diabetes is inherited insulin resistance aggravated by ….

A

obesity- metabolic syndrome present in >30% of the US population. Second “hit”- beta cells unable to keep producing elevated levels of insulin–> DM2. It is now more common in teenagers than DM1!

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21
Q

What are the ADA guidelines for primary prevention of DM2?

A

Patients with IGT, IFG, or A1c 5.7-6.4% should be referred for weight loss and exercise programs. Higher risk patients (IGT+IFG and another risk factor such as A1c>6%, HTN, low HDL, high trig, or FH of DM) should be considered for metformin therapy.

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22
Q

What are some pharmacologic prevention therapies for DM2?

A

Metformin (risk reduction 26-31%), Glargine (RR 28%), Troglitazone (RR 55-75%), Rosiglitazone (RR 60%), Pioglitazone (RR 72%), GLP-1 (RR ?>80%). Surgery for obese people reduced risk by 79-87%.

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23
Q

Pathophysiology of DM 2?

A

Pancreas have impaired insulin secretion, and the liver has an increase in glucose production, the glucose travels to the peripheral tissues (like skeletal muscle) and there is insulin resistance in the tissues. This results in hyperglycemia.

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24
Q

What leads to beta cell dysfunction in type 2 DM?

A

elevated glucose levels and elevated free fatty acids- this is glucotoxicity and lipotoxicity

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25
Q

How much beta cell function is lost by the time impaired glucose tolerance occurs in type 2 DM?

A

80-90% loss of beta cell function; overt DM appears when there is any further loss in function. In IGT and early DM, this is reversible.

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26
Q

What happens in late DM type 2?

A

deposition of islet amyloid polypeptide; apoptosis of beta cells

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27
Q

What are some ways to monitor diabetes?

A

Serum glucose- fasting, random. Fingerstick glucose testing- use to adjust insulin regimen. Hemoglobin A1c- glycosylation of valine in the hemoglobin molecule. Urine ketone testing- sick type 1 pts.

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28
Q

Who can you refer a newly diagnosed diabetic to?

A

diabetes educator, nutritionist, exercise physiologist if necessary, when pharmacologic treatment is needed- continue diet and exercise

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29
Q

Tips for diabetic meal planning?

A

modest weight loss/caloric restriction, individualized meal plan, nutritionist referral, annual review

30
Q

Weight loss program for diabetes?

A

modest restriction in calories preferred, avoid rapis loss-regain cycle, very low calorie diets for markedly obese, behavior modification techniques

31
Q

Exercise program goal and tips for diabetics include:

A

To improve glucose control and reduce cardiovascular risk factors. Individualize program, aerobic exercise 50-70% of maximum O2 intake, 20-45 minutes at least 3 days per week, include warm up and cool down exercises, appropriate for patients’ age, health and lifestyle, patients on oral hypoglycemic agents or insulin must self-monitor glucose response.

32
Q

What could you do for increased hepatic glucose production in type 2 DM?

A

weight loss, exercise, biguanides, insulin, thiazolidinediones, possibly bile acid sequestrants

33
Q

What could you do for increased glucagon secretion in type 2 DM?

A

GLP-1 receptor agonists, DPP-IV inhibitors, amylin mimetics

34
Q

What could you do for increased appetite in type 2 DM?

A

GLP-1 receptor agonists, amylin mimetics

35
Q

What could you do for decreased insulin secretion in type 2 DM?

A

sulfonyureas, meglitinides, GLP-1 receptor agonists, DPP-IV inhibitors

36
Q

What could you do for impaired incretin effect in type 2 DM?

A

GLP-1 receptor agonists, DPP-IV inhibitors, possibly bile acid sequestrants

37
Q

What does incretin do?

A

A group of GI hormones that cause an increase in the amount of insulin released from the beta cells of the islets of Langerhans after eating, even before blood glucose levels become elevated.

38
Q

What could you do for decreased amylin secretion in type 2 DM?

A

amylin mimetics

39
Q

What could you do for carb absorption in type 2 DM?

A

Alpha-glucosidase inhibitors

40
Q

What could you do for increased rate of gastric emptying in type 2 DM?

A

GLP-1 receptor agonists, amylin mimetics

41
Q

What could you do for increased insulin resistance in type 2 DM?

A

weight loss, exercise, biguanides, thiazolidinediones, D2 dopamine-receptor agonists

42
Q

What is the MOA for sulfonylureas for increasing insulin secretion?

A

For years this was the mainstay of treatment for DM. These drugs bind to the sulfonylurea receptor of the beta cell; this is part of a potassium channel. The drug closes the channel leading to partial depolarization of the beta cell. The beta cell then triggers insulin release at a lower blood glucose level. These drugs differ in potency, half life and cost. They often result in weight gain.

43
Q

What are some first generation sulfonylurea hypoglycemic compounds and their dose ranges?

A

Tolbutamide (500-3000), Tolazamide (100-1000), Acetohexamide (250-1500), Chlorpropamide (100-500)

44
Q

What are some second generation sulfonylurea hypoglycemic compounds and their dose ranges?

A

Glyburide (1.25-20), Glyburide (micronized) (0.75-12), Glipizide (2.5-40), Glipizide (GITS) (5-20)

45
Q

What controversy is there between sulfonylureas and CAD?

A

They all bind to K ATP channels in beta cells to increase insulin secretion, but some also bind to these channels in heart muscle. It may interfere with protective adaptation to recurrent ischemia. Glyburide does this, but not glipizide, glomepiride, or glicazide.

46
Q

What drugs decrease insulin resistance? What is there MOA?

A

Metformin (glucophage)- works mainly on the liver to decrease glucose production. It also increases glucose uptake in the skeletal muscles. Thiazolidinediones (rosiglitazone-Avandia; pioglitazone-Actos)- work through PPAR gamma receptors

47
Q

What works best, monotherapy of metformin or glyburide, or combination therapy with both?

A

Combination therapy works best. Glyburide works better than metformin in the beginning, but as the weeks go on metformin works better.

48
Q

What should you be concerned about with Metformin?

A

There are risk factors for developing lactic acidosis.

49
Q

Who should you not give Metformin to because of the possibility of the development of lactic acidosis?

A

Metformin should not be prescribed to patients with renal dysfunction as indicated by Scr > or equal to 1.5 mg/dL in males, > or equal to 1.4 mg/dL in females. In patients > or equal to 80 years of age, creatinine clearance should be assessed prior to initiating therapy. Also, CHF requiring pharmacologic management, liver dysfunction, history of alcohol abuse/drinking, and acute or chronic metabolic acidosis.

50
Q

What is the MOA for PPAR activators?

A

They reduce insulin resistance. The pancreas produces insulin and it goes to the liver, muscles and adipose tissue. The liver has a decrease in hepatic glucose output. The intestines absorb glucose and blood glucose goes to the muscles and fat. The muscles and adipose tissue decrease in insulin resistance and increase glucose uptake.

51
Q

What is the MOA for thiazoladinediones?

A

They bind to PPAR gamma receptors. These receptors are most abundant in fat cells. They induce differentiation of preadipocytes into mature adipocytes. This increases the potential sites for fat storage and, the greater the INCREASE in peripheral fat, the better the DM response to TZDs.

52
Q

What is the cause of insulin resistance in tissues and how do thiazoladinediones help with this?

A

Evidence suggests that intramyocellular, intrahepatic, and possibly intraislet cell lipid may be the cause of insulin resistance in these tissues. TZDs result in the transfer of fat from these tissues and from intrabdominal fat to new peripheral fat deposits.

53
Q

What are some complications that go along with TZDs?

A

LFT elevations (rare), sodium retention (edema, CHF), decrease in bone density - increase in fracture risk, PPAR gamma stimulation in bone marrow precursors favors adipocyte formation over osteoblasts, CAD risk with rosiglitazone- rx now severely limited- excess CAD not seen with pioglitazone.

54
Q

What is the MOA of alpha glucosidase inhibitors? What is an example of one?

A

Alpha glucosidase inhibitors prevent the digestion of carbs. They prevent carbs from being converted into simple sugars (monosaccharides), becaue they must be converted before they are absorbed through the insestines. Precose is an example of a alpha glucosidase inhibitor.

55
Q

What are the directions for insulin therapy?

A

1.) Bedtime NPH with daytime oral agent- best is metformin to avoid weight gain. 2.) Twice daily NPH + regular insulin. 3.) Basal insulin plus premeal boluses- insulin pump OR glargine + rapid acting insulin- lispro, aspart, or glulisine. You can take regular insulin before each meal and NPH at night.

56
Q

What is a long acting, soluble, biosynthetic insulin example?

A

Insulin Glargine

57
Q

What is the difference between regular human insulin and insulin lispro?

A

Insulin lispro breaks up in the blood much quicker than regular human insulin. The peak time for lispro is 1 hour after subcutaneous injection, and the peak time in regular human insulin is 2-3 hours.

58
Q

Can you inhale insulin?

A

Yes, it was used like this around 2006-2007 but it is not used this way anymore. There were concerns on how it affects the lungs.

59
Q

How does Medtronic’s MiniMed Paradigm work when detecting glucose levels?

A

It measures glucose via a sensor under the skin, transmitting results to the insulin pump, which recommends insulin dosages.

60
Q

How do the new drugs, incretin mimetics, work for diabetes?

A

They are glucagon like peptide-1- increase insulin release from beta cells after oral glucose. They decrease glucagon secretion, slow gastric emptying, increase beta cell proliferation, decreases apoptosis, and decrease appetite-central action.

61
Q

What kind of drug is exantitide? What is it used for?

A

Exanatide- injectable synthetic peptide with GLP1 activity for diabetes- originally found in the saliva of the Gila monster- marketed as Byetta- useful in promoting weight loss. GLP-1’s are found more in people with normal glucose tolerance. They are in lower levels in people with diabetes.

62
Q

What are DPP-4 inhibitors? What are some examples and what are they used for?

A

DPP-4 INHIBITORS: Sitagliptin (Januvia), Vildagliptin (Galvus), Saxagliptin (Onglyza). They are oral blockers of dipepidyl peptidase 4 which is an enzyme that inactivates GLP1- minimal effect on weight

63
Q

Oral glucose and IV glucose work equally well, but IV insulin works much better than oral insulin. True or False?

A

TRUE

64
Q

What are some injectable incretins called?

A

Exenatide based: Byetta (SC BID), Bydureon (microspheres, SC q week) (Lyxumia- lixisenatide). GLP-1 Based: Victoza- liraglutide qd (Syncria- albiglutide)

65
Q

Bariatric Surgery vs Conventional Rx for diabetes, which has better results?

A

60 pts age 30-60, BMI >35, DM >5y
1:1:1 Gastric Bypass: Biliopancreatic Diversion: Medical Rx= 2 year F/U to DM remission (FG< 6.5) off meds, GB- 75%; BPD 95%; Med Rx 0%

66
Q

What are some examples of SGLT2 Inhibitors (new drug therapy for diabetes)?

A

Sodium-glucose Cotransporter 2- renal reabsorption of glucose- upregulated in DM Phlorizin- from apple tree bark- found to be glycosuric in 1886. Dapagliflozin, canagliflozin- selective SGLT2 inhibitor lowers glucose without insulin, weight loss via glucosuria (200-300 kcal/day). Canagliflozin (Invokana) approved in US April, 2013– $8.77/tablet. Dapagliflozin (Forxiga) approved in Europe.

67
Q

What is the function of glucokinase?

A

is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Glucokinase occurs in cells in the liver, pancreas, gut, and brain of humans and most other vertebrates. In each of these organs it plays an important role in the regulation of carbohydrate metabolism by acting as a glucose sensor, triggering shifts in metabolism or cell function in response to rising or falling levels of glucose, such as occur after a meal or when fasting. Mutations of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia.

68
Q

What is the threshold of insulin release set by glucokinase? What is MODY and Piragliatin?

A

GCK- catalyzes glucoseG6P in beta cells and thereby regulates glucose flux and sets the threshold for insulin release at about 5mM (90 mg/dl)
MODY 2- GCK mutations
Piragliatin- oral GCK activator- improves fasting and postprandial glucose

69
Q

What is a G-protein coupled receptor 40?

A

GLPC receptors affect insulin secretion– GLP1 and GIP receptors. Long chain free fatty acids increase glucose stimulated insulin release by binding to GPR 40 on beta cells. Oral agonists that bind to GPR 40 have been developed and are in human trials– TAK-875

70
Q

What are some future insulins?

A

Insulin + recombinant hyaluronidase -faster absorption. Smart Insulin- insulin released from polymer when glucose rises. Hepatic Targeted Insulin.

ClinMed Endocrinology Exam 2 (1 decks)

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