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endo 1 > Dodge > Flashcards

Dodge Flashcards

1
Q

what groups have the highest incidence of diabetes

A

american indians and alaskan natives followed by hispanic

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2
Q

describe insulin

A
  • created in the BETA ISLET CELLS OF THE PANCREAS
  • Glucose levels > 70mg/dl cause INCREASE in SYNTHESIS and SECRETION OF INSULIN from the pancreas
  • Insulin Binds to cell receptors (TK) leading to a cascade of reactions –> translocation of GLUT4 to cell membrane

–> RESULT in INFLUX OF GLUCOSE, PROTEIN and GLYCOGEN synthesis, cell growth

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3
Q

Type I diabetes

A
  • caused by complete or near complete insulin deficiency (usually seen with >70% destruction of beta cells
  • Typically AUTOIMMUNE DESTRUCTION OF BETA CELLS, tend to be young
  • genetic, environmental and immunologic factors
  • Increased risk of celiac disease, thyroid disease
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4
Q

Type II diabetes

A
  • Results from INSULIN RESISTANCE, abnormal insulin secretion and abnormal fat metabolism
  • OBESITY, family history, sedentary lifestyle, HTN, dyslipidemia, etc is a risk factor
  • STRONGER GENETIC COMPONENT
  • Preceded by progressive insulin resistance

–> impaired fasting glucose, imapired glucose tolerance

–> metabolic syndrome (HTN, HLD, obesity)

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5
Q

Symptoms of diabetes

A
  • Frequent urination
  • always tired
  • always hungry
  • sexual problems
  • weight loss
  • wounds that won’t heal
  • vaginal infections
  • numb or tingling hands or feet
  • always thirsty
  • blurry vision

** THE ONSET OF SYMPTOMS can be SLOW and INSIDIOUS, esp in pts with type II DM**

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6
Q

When should you screen

A
  • screening individuals every 3 years starting at 45 years of age
  • Sceen earlier if patients is overweight with at least one additional risk factor (HTN, PCOS, SEDENTARY etc)
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7
Q

Prediabetes

A
  • increased risk of diabetes or intermediate hyperglycemia

-

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8
Q

Diabetes mellitus diagnosing

A

If someone has a hmoglobin A1c greater than 6.5% they have DIABETES

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9
Q

Type I diabetes mellitus

A

REQUIRE TX WITH INSULIN DUE TO INSULIN DEFICIENCY

  • Basal/bolus (most common)

–> once or twice daily long-acting insulin inject

–> short-acting insulin bolus for meals/snacks

  • Continuous infusion

–> aka insulin pump, continuous infusion of short-insulin

–> bolus of short-acting insulin with meals

  • Split/mixed

–> multipe daily injections of combination of long and short acting insulin (generaly worse glycemic control, more hypoglycemia)

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10
Q

Type II diabetes mellitus treatment

A
  • Do not routinely require insulin at diagnosis
  • many will eventually require insulin as the disease progresses
  • choice therapy depends on severity of hyperglycemia, patient comfort, patient willingness
  • typically will start with oral therapies and adjust as needed
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11
Q

describe the treatment options for varying levels of initial A1c

A
  • Meformin is the standard (7.5-9%)

>9 - two oral agens or insulin monotherapy

> 10-12% = strong recommendation for insulin therapy

> 10-12% with ketosis and or weight loss = insulin therapy required

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12
Q

describe diet and lifestyle changes

A
  • ADA recommends 150 minutes/weeks of moderate intensity cardio workouts

–> 3x/wk, no more than 2 days off in between

  • recommends resistance training at least twice per week
  • HYPO-CALORIC with LOW FAT or LOW CARBO intake

–> consistent carbohydrate intake, recommend 45-65% of total daily calories

**WEIGHT LOSS IS MORE IMPORTANT THAN CERTAIN COMBINATIONS OF NUTRIENTS**

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13
Q

METFORMIN

A
  • Decreases hepatic gluconeogensis and glucogenolysis with increase in peripheral insulin sensitivity and glucose uptake
  • SIDE EFFECTS = diarrhea, indigestion (resovle within weeks), LACTIC ACIDOSIS
  • CONTRAINdiCATIONS

–> renal or hepatic impairment (Cr > 1.5 mg/Dl in men or Cr > 1.4 inw omen) –> DO NOT USE

–> binge drinking, cirrhosis or use a radio contrast dye

–> predisposition for LACTIC ACIDOSIS (CHF or chornic hypoxemia)

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14
Q

describe Metformin dosing

A
  • Initial mono-therapy when single agent is used
  • Start dosing at 500mg once or twice daily with meals

- If patient continues to tolerate medication, double dose every 5-7 days until at goal of 1000mg twice daily (GOAL TX)

  • this should not be used in women who are PREGNANT or MAY BECOME PREGNANT
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15
Q

Sulfonylureas

A
  • Stimulate insulin secretion by pancreas beta cells
  • Decrease the microvascular complications of diabetes
  • ASE: weight gain, hypoglycemia, increased CV events
  • Decrease efficacy with time, therefore will need increasing dose
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16
Q

Thiazolidinediones

A
  • act on receptor in muscle, fat and liver to sensitize them to insulin (PPAR gama gene)
  • Less effective than sulfonyurea, metformin
  • increased risk of fluid retention and CHF; contraindicated in NTHA class III or IV
  • reported increased risk of bladder cancer with > 1 year of use
17
Q

Glitinides

A

- similar to sulfonylureas, stimulate beta cells

18
Q

Alpha-glucosidase inhibitors (Acarbose)

A
  • prevent absorption of simple sugars by decreasing carbohydrate breakdown
  • less effective but less wieght gain
19
Q

DPP-4 inhibitors (sitagliptin)

A
  • DDP-4 degrades incretin (which stimulates insulin secretion)
  • increased incretin leads to increase insulin secretion
  • Few ASE: pancreatitis, angioedema, urticaria
20
Q

GLP-1 Receptor antagonist (exanatide)

A
  • Increase insulin and decrease glucagon, increase anxiety
  • no hypoglycemia, causes weight LOSS
  • ASE: increase hypoglycema with combination, pancreatitis
21
Q

Sodium-glucose co-transport 2 (SGL T2) inhibitors (canagliflozin)

A
  • newest class, block glucose reabsorption in the kidney
  • less hypoglycemia, causes weight loss
  • ASE: dehydration (glucosuria), fungal genital infections
  • Do not use in Chronic kidney disease
22
Q

Insulin therapy (type II) dosing

A
  • MOST EFFECTIVE medication to lower A1c
  • typically Start with long-acting insulin ONCE DAILY

–> 0.1-0.2 Units/kg initially –> 10 units minimum

–> monitor daily morning fasting glucose and titrate insulin until goal of 70-130mg/dl

- Initial goal of insulin therapy is to obtain fasting glucose levels less than 130 mg/dL in the morning

–> if A1c is still not in range after 3 months add MEALTIME SHORT-ACTING INSULIN (designed to mimic insulin production by the pancreas)

23
Q

What are the glycemia treatment goals

A
  • A1c =
  • Preprandial glucose (fasting) = 70-130 mg/dL
  • peak postprandial glucose =
24
Q

What types of annual screening: ***

A
  • Spot urine albumin-to-creatinine ratio (normal < 30 mg/g)

–> if > 30mg/g, recheck to confirm

  • foot exam with monofilament testing

–> assess loss of protective sensation

–> check for pulses, ulcers, nail pathology

  • Dilated eye exam by ophthalmologist

–> monitor for diabetic retinopathy

25
Q

Diabetic ketoacidosis

A
  • More often seen in type 1
  • often onset within 24 hrs; nausea, vomiting, abdomianl pain
  • elevated glucose = polyuria + N/V = dehydration
  • increased ketosis (fatty acid release) due to low insulin and high glucose
  • caused by increased insulin requirements (infection, pregnancy, ischemia, or non-compliance)
26
Q

Hypoglycemia

A
  • occurs with glucose < 70 mg/dl (increase epi and glucagon

  • diphoresis, pale, tremor, tachycardia; can progress to coma in some circumstances
  • can be accidental or intentional overdose of insulin
  • treat with glucose tabs, dextrose and or glucagon
27
Q

Hyperglycemia hyperosmolar state (HHS)

A
  • more commonly seen in elderly type 2 DM
  • infection, ischemia, non-compliance
  • onset over weeks; weight loss, decreased intake, polyuria
  • dehydration on exam (tachycardia, hypotension
  • no ketosis
28
Q

what are the emchanisms for neuropathy

A
  • increased intracellular glucose leads to formation of advanced glycosylation end produces (AGEs)
  • bind cell surface receptors, non enzymatic glycosylation
  • accelerate athersclerosis, promote glomerular dysfunction, reduce NO syntheiss, and endothelial damage
29
Q

opthalamologic compliactions

A
  • # 1 cause of blindness in US
  • PROLIFERATIVE RETINOPATHY

–> neovascular due to hypoxemia (new vessels rupture easier = hemorrhage)

–> hemorrhage leads to fibrosis and eventual retinal detachment

–> prevention is the best intervention, although photocoagulation can be used to preserve vision

  • Non-proliferative retinopathy

–> vascular microaneurysms, blot hemorrhages, cotton-wool spots

–> retinal ischemia via change in retinal blood flow, increased vascular permeability

  • can only havemacular edema when non proliferative retinopathy present
30
Q

neurologic complciations

A
  • distal symmetric polyneuropathy is common (stock and glove distribition)
  • numbness, tingling, sharpness, burning
  • loss of proprioception, ankle reflexes and sensation
  • Autonomic neuropathy (noradrenergic, cholinergic)

–> effect CV, GI, anhidrosis

endo 1 (17 decks)

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