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ER Week 2 > Diabetes and Metabolic Syndrome Clinical Lecture > Flashcards

Diabetes and Metabolic Syndrome Clinical Lecture Flashcards

1
Q

What percentage of beta cell function needs to be lost before you get a diagnosis?

A

50-80%

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2
Q

What are some meds that can cause drug-induced hyperglycemia?

A 
glucocorticoids
OCPs
cyclosporine/tacrolimus/sirolimus
niacin
HIV protease inhibitors
thiazide diuretics
statins
gonadotropin releasing hormone aganoists
beta blockers, beta agaonists
megasterol
alcohol
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3
Q

How is gestational diabetes diagnosed?

A

oral glucose tolerance tests

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4
Q

Who do we screen for diabetes?

A

2012 ADA Guidelines

if BMI is equal or over 25 with at least 1 risk factor:
physical inactivity
first degree relative with it
high risk race
woman with a bid baby or hx of GDM
HTN
HDL less than 35 or triglycerides over 250
women with PCOS
AIC over 5.7%
history of CVD
other clinical conditions associated with insulin resistance (like acanthosis nigricans)

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5
Q

If you do’t have any of those criteria, what age do you start screening at?

A

45 yo and then every 3 years after tat

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6
Q

How do you make the diagnosis of diabetes?

A

fasting plasma glucose of 126 mg/dL on 2 separate occasions

random plasma glucose of 200 with symptoms

plasma glucose over 200 after an oral glucose load

AIc over 64.%

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7
Q

Prediabetes is defined as an A1c of what?

A

5.7 to 6.4%

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8
Q

A1c of 6% corresponds to what average daily blood sugar?

A

135

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9
Q

What should you check on exam for diabetes?

A 
height and weight
blood pressure
HEENT pupils and retinal exam
thyroid palpation
heart and lung
pulses
skin check
feet for sores and decreased sensation
reflexes
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10
Q

What are the microvascular complications of diabets?

A

reitnopathy (annual eye exam)
neuropathy (annual monofilament)
nephropathy (annual microalbumin screen)

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11
Q

What is an example of mascrovascular complication?

A

atherosclerosis - so CAD, stroke, claudication, etc.

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12
Q

What labs should you do on a diabetic?

A 
glucose (Fasting or random)
A1c every three months
Lipids
renal panel
microalbumin
TSH (common comorbid condition)
hepatic panel (comorbid with steatohepatitis)
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13
Q

Why do we do the A1c every three months?

A

three months is the lifespan of a RBC, so that’s how long it takes for the A1c to fully change

helps to appropriately assess for drug response

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14
Q

An incentivized approach includes what steps?

A
  1. measure A1c every 6 mo
  2. maintain A1c at individual target of less than 7% or 8% depending on patient
  3. measure LDL annually
  4. maintain LDL to elss than 100 or at level achieved by high dose statin
  5. BP less than 140/80
    6, annual proteinuria screen
  6. annual flu shots and pneumococcal vaccine UTD
  7. help them quit smoking
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15
Q

What did the Diabetes Control and Complicatons Trial prove?

A

conclusive evidence that intensive insulin therapy with tight blycemic ocntrol prevents or decreases the risk of chronic microvascular complications

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16
Q

Intensive therapy allows the use of insulin in a way that mimics the pancreas. What does this mean?

A

It means that you have a short release and a long release

the pancreas always has a basal release of insulin and a prandial release of insulin (so we mimic that with long acting and short acting insulin)

note that the pump does all of this on its own.

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17
Q

What’s the main biguanide and first line drug?

A

metformin (glucophage)

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18
Q

How much will metforming lower your A1c by?

A

only 1-2%

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19
Q

How many drugs does a person fail to reach a point where insulin is the only choice?

A

a combo of 3

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20
Q

What does metforming do?

A

decrease hepatic glucos eproduction

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21
Q

Does metformin cause hypoglycemia?

A

no!

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22
Q

What does metformin do to lipids?

A

lowers them

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23
Q

Why is metformin the first choice>

A

it decreases macrovascular complications

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24
Q

What are the main side effects for metformin?

A

diarrhea and abdominal bloating

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25
Q

What are the contraindications for metformin?

A 
renal impairment
cardiac/resp insufficiency, sepsis leading to hypoxia or reduced tissue perfusion
lactic acidosis
liver disease/alcohol abuse
radiographic contrast agents for testing
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26
Q

What vitamin should you give with metformin?

A

b12

27
Q

What are the three sulfonylureas?

A

glyburide
glipizide
glimepiride

28
Q

Why is glyburide not used much anymore?

A

super long half life

29
Q

How do the sulfonylureas work?

A

bind to sulfonylurea receptor on the beta cell to stimulate insulin release

30
Q

What are the side effects of the sulfonylureas?

A

hypoglycemia
weight gain
potential impairment of cardiac ischemic preconditioning

31
Q

What should you never use the sulfonylureas with?

A

insulin

they’ll go super hypoglycemic and besides - the person need to be able to make some insulin in order for these sulfonylureas to work. but we’ve already decided that he’s not making insulin because you decided to give him insulin!

don’t keep him on the sulfonylrueas just because of momentum

32
Q

What do the TZDs do?

A

increase the amount of glucose taken up by the muscle cells and keeps the liver from overproducing glucose

33
Q

What’s the tradeoff with those TCDs though?

A

THe good things: addresses primary defect, no hypoglycemia, lipid lower, and decrease macrovascular complications

BUT: side effects are bad: edema, precipitate CHF sometimes, increased fracture risk in women, increased MI in those who already have CV risk

34
Q

What do the GLP-1 agonist and DPP-IV inhibitors do?

A

activate the GLP-1 receptor to increase glucose depensend insulin secretion

decrease glucagon secretion

delay gastric emptyin

35
Q

What are the general side effects with these?

A

nausea, vomiting and pancreatitis (rare)

36
Q

What is the main GLP-1 receptor agonist?

A

Exenatide

also Liraglutide

37
Q

Why shouldn’t you give exenatide to patients who have had a history of thyroid cancer?

A

there has been dose and duration dependent thyroid C-cell tumors in animal studies

38
Q

Where do most of the drug-drug interactions with exenatide come from?

A

it slows gastric emptying, so it can alter the absorption of all oral medications (thyroid medications in particular)

39
Q

WHat enzyme needs to be inhibited to prevent the degradation o fGLP-1?

A

DPP-IV

40
Q

WHat are the sie effects of the DPP-IV inhibitors?

A

HA
GI upset
URTI
nasopharyngitis

41
Q

What’st he brand new diaabetes med that works in the kidney?

A

the sodium glucose cotransporter 2 inhibitor

Canagliflozin

42
Q

How does it work?

A

It blocks the rebsorption of glucose so they just pee it out

43
Q

Which requires higher insulin dosing - Typ1 or Typ2?

A

type 2

44
Q

What is the HA1c target according to the ADA?

A

less than 7%

45
Q

WHat is the fasting and pre-prandial glucose goal accoridng to the ADA?

A

less than 130

46
Q

WHat is the post-prandial glucose goal according to the ADA?

A

less than 180

47
Q

When shoul dyou consider a more stringent HbA1c target?

A

short disease duration
long life expenctancy (young)
no significant CVD

48
Q

When can cyou consider a less stringent HbA1? (7.5-8)

A 
hx of severe hypoglycemia
limited life expectancy (old)
advanced complications
extensive comorbid confitions
those whose target is difficult to obtain despite treatmen
49
Q

WIth oral therapy, you add additional meds, not substitue. What’s the exception?

A

IF you start insulin, you can start substracting oral therapies - especially if they don’t make sense

50
Q

What drug should all diabetics be on?

A

aspirin - helps prevent microvascular disease (not in kids obviously)

51
Q

What are some associated metabolic abnormalities seen in DM?

A 
steatohepatitis
elevated triglycerides (pancreatitis)
low HDL
hyperuricemia
acanthosis nigricans
52
Q

What are some other names for metabolic syndrome?

A

syndrome X
insulin resistance syndrome
dysmetabolic syndrome

53
Q

A patient will qualify for this diagnosis if he or she has at least three of what criteria?

A

waistline over 40 or 35 inches

BP of 130/85 or are taking BP medications to treat HTN

Tirglycerides above 150

fasting blood glucose of 100 or more

taking glucose lowering medications

high density lipoprotein level less than 40 for men or less than 50 in women

54
Q

What is the most common presenting symptom of metabolic syndrome

A

trick question - no symptoms

they’re usually picked up on incidental labs

55
Q

What is the first step in managing metabolic syndrome?

A

diet and exercise

reduce alcohol, stop smoking, etc

56
Q

If lifestyle changes don’t help, what drugs can you consider?

A

statins and ACE-i may be helpful

note that metformin has been found to help prevent the onset of diabetes in people with metabolic syndrome, but there are no guidelines yet

57
Q

A person with metabolic syndrome is ___ as likely to develop heart disease and ___ times as likely tod evelop diabetes as someone who doesn’t have metabolic syndrome

A

Your risk for heart disease, diabetes, and stroke increases with the number of metabolic risk factors you have. In general, a person who has metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes as someone who doesn’t have metabolic syndrome

58
Q

What percentage of people with normal body weight will have metaoblic syndrome?

A

5%

59
Q

WHat percent in those who are overweight?

A

22%

60
Q

What percent in those who are obese?

A

60%

61
Q

Adults who continue to gain fie or more pounds per year raise their risk of developing metabolic syndrome by what?

A

45%

62
Q

What percentage of the US population has metabolic syndrome?

A

32%

63
Q

What ethnic group has the highest rate of metabolic syndrome?

A

mexican americans - screen them starting in their 20s

64
Q

What percentage of people over 60 are affected?

A

40%

ER Week 2 (10 decks)

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