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DEMS Unit 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Diabetes Definition

A
  • blood glucose that is inc. to the point that it would cause microvascular disease
  • fasting glucose > 126
  • 2 hr plasma glucose >200 during 75 g oral glucose tolerance test
  • sx of diabetes with random plasma glucose >200
  • A1C> 6.5%
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2
Q

A1C in Diabetes

A
  • > 6.5% on 2 occasions is diagnostic
  • represents avg blood sugar over last 3 months
  • must be in absence of other medical illness
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3
Q

Fasting Glucose in Diabetes

A

->126 mg/dl

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4
Q

2 Hr Plasma Glucose in Diabetes

A

->200 mg/dl during 75g OGTT

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5
Q

Random Plasma Glucose in Diabetes

A

->200mg/dl with sx of diabetes

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6
Q

Impaired Glucose Tolerance/Impaired Fasting Glucose

A
  • prediabetic
  • inc. risk for macrovascular disease (CAD, CVD)
  • 10% risk per year of progressing to T2DM
  • impaired fasting glucose: 100-125
  • impaired glucose tolerance: 140-199 during OGTT
  • A1C: 5.7-6.4%
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7
Q

Sx of Diabetes

A
  • polyuria
  • polydipsia (excessive thirst)
  • blurry vision
  • weight loss
  • sx present at ~90% loss of beta cell function in pancreas
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8
Q

Type 1 DM

A
  • due to autoimmune destruction of beta cells in pancreas
  • results in insulin deficiency
  • occurs in childhood
  • evidence of insulin deficiency: low C peptide
  • low genetic contribution
  • positive antibody blood tests
  • normal weight
  • predisposed to DKA
  • insulin sensitive
  • not related to vaccine exposure
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9
Q

Type 2 Diabetes

A
  • most common form of diabetes
  • insulin resistance
  • more common in adults
  • more common in hispanics, blacks, native americans, and pacific islanders
  • overweight
  • sedentary lifestyle
  • strong genetic component
  • DKA unlikely
  • no beta cell autoimmunity but beta cells are dysfuctional (dec. insulin secretion)
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10
Q

Gestational Diabetes

A
  • weight gain/pregnancy
  • resolves after delivery
  • inc. risk of T2DM in future
  • risks: big baby, delivery complications, child at risk for T2 also
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11
Q

Pancreatic Diabetes

A
  • insulin deficiency for beta cell destruction
  • diarrhea and steatorrhea
  • underweight
  • lack glucagon in addition to insulin
  • may occur in alcoholics
  • prone to hypoglycemia
  • inc. peripheral neuropathy
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12
Q

Stages of T1DM

A
  • genetic predisposition
  • overt immunologic abnormalities
  • progressive loss of insulin release
  • overt diabetes
  • no C-peptide
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13
Q

4 Autoantigens Characteristic of T1DM

A
  • insulin
  • glutamic acid decarboylase 65 (GAD65)
  • tyrosine phsophatase protein (IA2)
  • zinc transporter (ZnT8)
  • individuals with 2 or more autoantibodies will progress to T1D
  • also genetic risk factors such as HLA DR3/4
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14
Q

Possible Environmental Factors of T1DM

A
  • not vaccines
  • viruses
  • hygiene hypothesis
  • diet (formula)
  • obesity
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15
Q

C Peptide

A

-marker of endogenous insulin

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16
Q

Normal Plasma Glucose Values

A

-fasting

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17
Q

Diabetic Ketoacidosis

A
  • severe hyperglycemia
  • anion gap metabolic acidosis
  • inc. ketones
  • low insulin/glucagon ratio permits ketogenesis in the liver
  • counter regulatory
  • hormones are elevated
  • most common precipitating cause is infection
  • tx: volume replacement, insulin, potassium
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18
Q

Signs of Hypoglycemia

A
  • adrenergic: sweating, tremor, tachycardia
  • neuroglycopenic: confusion, convulsions, LOC
  • pts can be unaware due to dec. adrenergic warning signs
19
Q

Maturity Onset Diabetes of Young (MODY)

A
  • autosomal dominant

- linked to mutaitons in glucokinase gene and mitochondrial genes

20
Q

Macrovascular Disease Associated with DM

A
  • MI
  • stroke
  • peripheral vascular disease
  • lipid lowering significantly dec. mortality and CV events in pts with DM
  • legacy effect: early blood sugar control in DM leads to dec. CV events 10-20 yrs later
21
Q

Vascular Wall Response to Diabetes

A
  • abnormal endothelial cell function
  • abnormal vascular smooth muscle cell function
  • inflammation and dec. fibrinolysis
22
Q

Tx to Prevent Complications of DM

A
  • B blockers
  • antihypertensives
  • lipid lowering agents
  • ASA in high risk pts
23
Q

Microvascular Disease Mechanisms in DM

A
  • polyol pathway-> sorbitol, fructose
  • non-enzymatic glycosylation-> AGEs
  • elevation of protein kinase C
  • oxidative/carbonyl stress
24
Q

Microvascular Diseases Associated with DM

A
  • retinopathy- hypoxic stress-> neovascularization
  • nephropathy
  • neuropathy-> ulceration
25
Q

Retinopathy Treatment and Prevention Strategies

A
  • annual opthalmologic exams
  • tight glycemic control
  • photocoagulation
  • intravitrial medication
26
Q

DM Nephropathy Pathogenesis

A

-hyperfiltration-> intrarenal and peripheral hypertension-> basement membrane thickening-> mesangial proliferation-> glomerular obliteration

27
Q

Rapid Acting Insulin Analogs

A
  • novalog (aspart)
  • apidra (glulisine)
  • humalog (lispro)
  • onset: 5 ming
  • peak: 1.5 hr
  • duration: 3-5 hr
  • subq or pump
  • given just prior to meal
  • dissociates into monomers after injection
28
Q

Rapid Acting Insulin: Inhaled

A
  • afrezza
  • onset: 5 min
  • peak: 1 hr
  • duration: 2 hr
  • set dose
  • administered just prior to meal
29
Q

Short Acting Insulin: Regular

A
  • Humulin R; Novolin R
  • onset: 30-60 min
  • peak: 2 hr
  • duration: 6-8 hr
  • subq, IV, infusion
  • inject 30 min prior to meal
30
Q

Intermediate Acting Insulin: NPH

A
  • Humulin N, Novolin N
  • onset: 1-3 hr
  • peak: 6-8 hr
  • duration: 12-16 hr
  • subq only (2x/day for basal coverage)
  • cloudy solution
31
Q

Long Acting Insulin

A
  • glargine (lantus)
  • detemir (levemir)
  • onset: 1.5 hr
  • no peak
  • duration: 24 hr glargine, 12-20 hr detemir
  • subq only
  • cannot be mixed in same syringe w/ other insulin
32
Q

Premixed Insulin

A
  • 70/30
  • 50/50
  • used twice a day just before AM and PM meals
  • subq only
33
Q

When to use insulin in T2DM

A
  • if lifestyle modifications and non-insulin combos don’t achieve target A1C
  • contraindications to other meds
  • when in hospital
34
Q

Glucose and A1C Targets in DM

A
  • fasting BG: 70-130

- 2 hr post meal BG:

35
Q

Diabetes Lifestyle Changes

A
  • less calorie dense/refined carbs
  • higher fiber, lean protein
  • smaller portions
  • inc. physical activity
  • weight loss
36
Q

Sulfonylureas

A
  • glyburide, glipizide, glimerpriride
  • close ATP sensitive K channels in B cell
  • bypass glucose control
  • must have some pancreas for this to work
  • pros: cheap, available in combo with other meds
  • cons: weight gain, hypoglycemia, loses effectiveness
37
Q

Biguanide: Metformin

A
  • potentiates supportive effect of insulin on hepatic glucose production
  • does NOT stimulate insulin secretion or inc. circulating insulin
  • risk lactic acidosis
  • pros: no hypoglycemia, cheap, no weight gain, combs
  • cons: GI side effects, risk of lactic acidosis
38
Q

Thiazolidinediones

A
  • pioglitazone (actos)
  • rosiglitazone (avandia)
  • inc. insulin sensitivity- adiponectin stimulation
  • cons: worsening of CHF, expensive, risk of bladder cancer
39
Q

Incretins

A
  • GLP-1- very effective for lowering glucose in diabetes
  • lowers glucose via multiple mechanisms
  • secreted by cells in GI tract in response to food intake
  • augments insulin secretion only if blood glucose is elevated
  • native GLP-1 is rapidly cleaved and inactivated in circulation by DPP-4
40
Q

GLP-1 Agonists

A
  • exenatide (byetta)
  • liraglutide (victoza)
  • exenatide Qwk (bydureon)
  • albiglutide (tanzeum)
  • dulaglutide (trulicity)
  • pros: multiple MOAs, effects are glucose dependent, weight loss
  • cons: subq injection, side effects, expensive
  • don’t combine with DPP-4
41
Q

DPP-4 Inhibitors

A

-sitagliptin (januvia)
-saxagliptin (onglyza)
-linagliptin (tradjenta)
-alogliptin (nesina)
-DPP-4 cleaves GLP-1
-pros: multiple MOAs, oral, once daily, weight neutral, combos
-cons: less potent, expensive, side effects
don’t combine with GLP1

42
Q

SGLT-2 Inhibitor

A
  • canagliflozin (invokana)
  • dapagliflozin (farxiga)
  • emplagliflozin (jardiance)
  • block glucose reuptake in the kidney-> pee out glucose
  • pros: novel MOA, weight loss, pill, combo
  • cons: inc. risk UTI, inc. risk low K, expensive
43
Q

Amylin

A
  • second peptide hormone secreted by B cells
  • actions: suppresses postprandial glucagon, slows gastric emptying, dec. food intake
  • T1DM: absolute deficiency
  • T2DM: initially elevated, then decline
44
Q

Amylin Analog

A
  • pros: multiple MOAs to reduce postprandial glycemia, induces weight loss
  • cons: subq up to 7x/day, side effects, expensive

DEMS Unit 2 (4 decks)

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