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Labs Medicine > Diabetes, Glucose and Pancreatitis > Flashcards

Diabetes, Glucose and Pancreatitis Flashcards

1
Q

What pancreas cells have the exocrine function?

A

acinar cells secreting pancreatic enzymes into pancreatic ducts

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2
Q

What pancreas cells have the endocrine function?

A

islets of langerhan cells secreting hormones into blood vessels

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3
Q

What are the pancreatic enzymes?

A

alkaline fluid with bicarb and digestive enzymes:

amylolytic enzymes like amylase
lipase
phospholipase A2
cholesterol esterase
elastase
trypsin
chymotrypsin
carboxypeptidase
aminopeptidase
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4
Q

What are the three main endocrine hormones made by the pancreas?

A

insulin
glucagon
somatostatin

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5
Q

What cells produce insulin?

A

beta cells

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6
Q

What cells produce glucagon?

A

alpha cells

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7
Q

What cells produce somatostatin?

A

delta cells

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8
Q

Describe the changes from preproinsulin to insulin.

A

starts as preproinsulin, then the signal peptide is removed to make prosinulin, then the c-peptide is removed leaving just the A and B chain of insulin

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9
Q

What blood sugar is considered hypoglycemic in patients without diabetes? How about with diabetes?

A

Without diabetes: less than 40 mg/dL (although symptoms usually kick in at less than 55)

Less than 70 in diabetis

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10
Q

What is Whipple’s Triad (and why do we care about it)?

A

We care about it because if you meet the criteria for the triad, then you need to do a hypoglycemia workup for a non-diabetic patient

  1. recognize symptoms that could be caused by hypoglycemia
  2. Document that the plasma glucose concentrations are low when the symptoms are present
  3. show the symptoms can be relieved with administration of glucose
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11
Q

What is the differential diagnosis for hypoglycemia?

A

Diabetes mellitus
Drug-induced (most common cause–includes alcohol)
endogenous hyperinsulinism (insulinoma, sulfonylurea/glinide use, insulin autoimmune hypoglycemia)
accidental/maligious or surrepticious hypoglycemia (munchausen’s)
pseudohypoglycemia (wrong tube used)
Cortisol deficiency
malnourishment
critical illness

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12
Q

After Whipple’s triad is confirmed, what additional tests should be ordered?

A 
Insulin level
c-peptide
proinsulin
sulfonylura and glinide screen
beta-hydroxybutyrate

after treating the acute phase, patient should undergo a supervised fast until symptom recurrence or 72 hrs

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13
Q

If someone’s glucose is less than 55 mg/dl, what shuould their insulin be?

A

less than 3 mU/l

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14
Q

What is the only diagnosis that would cause a combination of elevated insulin level and low c-peptide level?

A

injection of insulin (because endogenous insulin would also cause c-peptide to be high)

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15
Q

What are the current diagnostic criteria for diabetes?

A
  1. fasting plasma glucose over 126 mg/cL
  2. HbA1c > 6.5%
  3. 2-hr value in an OGTT over 200 mg/dL
  4. Random plasma glucose concentration over 200 mg/dL WITH symptoms
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16
Q

If you run two tests for diabetes and the results are discordant, which test should be repeated?

A

the one that was diagnostic of diabetes

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17
Q

Which of the diagnostic criteria are now primarily recommended for the diagnosis of diabetes?

A

A1c over 6.5%

more convenient bc no fasting and there is correlation with retinopathy

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18
Q

At what A1c level does retinopathy increase?

A

over 5.5%

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19
Q

HbA1c is indicative of glucose control over 3 months. What other lab tests can be used as indicators of glucose control over a period of time?

A

Fructosamine (nonenzymatic glycation of glucose to the alpha terminus of proteins like albumin): 1-2 weeks

1,5-anhydroglucitol (renal absorption of this is inhibited by glucose, so measurements reflect blood glucose level over last 24 hrs - higher levels suggest higher blood glucose levels)

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20
Q

In what situations are HbA1c results not reliable?

A

hemoglobinopathies (if they don’t have any hemoglobin A, they obviously won’t have an A1c)

Hemolysis (shortened RBC lifespan will lower A1c)

Polycythemia or post-splenectomy (longer RBC lifespan will falsely elevate)

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21
Q

If the HbA1c is going to be unreliable in a given patient, what is the recommended alternative test?

A

fructosamine

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22
Q

What are the two entities that are of greatest concern in a diabetic with severe hyperglycemia and coma?

A

DKA and HHS

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23
Q

What lab tests should be ordered to differentiate between DKA and HHS?

A

serum glucose
serum electrolytes
UA with urine ketones
plasma osmolality
serum ketones (if urine ketones are present)
Arterial blood gas (if urine ketones or anion gap present)

24
Q

Which one (DKA or HHS) tends to occur at higher BS levels?

A

HHS is usually over 600 (and can exceed 1000)

DKA criteria are over 250 and will usually be less than 800

25
Q

Which one will have a lower pH

A

The names give it away - DKA

26
Q

Which one will have elevated urine and serum ketones?

A

DKA ( for the most part - HHS may have small amounts just due to dehydration)

27
Q

Which one will have elevated serum osmolality for sure?

A

Again, the name gives it away - HHS will have an osmolality above 320 mOsm/kg

DKA is variable

28
Q

Which one will have an elevated anion gap for sure?

A

DKA (HHS will be variable)

29
Q

Which type of diabetics are more likely to get DKA and which are more likely to get HHS?

A

Type 1 - DKA

Type 2 - HHS

30
Q

Which one comes on more insidiously?

A

HHS

31
Q

Why don’t you get ketogenesis in HHS?

A

people with Type 2 diabetes will still have some insulin usually, which blocks lipolysis and you don’t get the formation of ketone bodies

32
Q

What is the difference between serum osmolality and serum osmolarity and does it matter?

A

Osmolality is the # of moles of solute in a kg of H2O

Osmolarity is the number of moles in a liter of H2O

Osmolality is preferred since the mass of H2O is constant while the volume of H2O can change with temp, but the terms are used interchangeably because the changes of volume with temp are negligible for water

33
Q

What is the formula for calculating serum osmolality?

A

2Na+ + (glu/18) + BUN/2.8

34
Q

How does on calculate an osmolar gap?

A

osmolar gap = measured osmolality - calculated osmolality

note: a normal gap is less than 10 mOsm/kg

35
Q

Would you expect an osmolar gap in patients with HHS? why?

A

You would NOT expect an osmolar gap with HHS because glucose is in the equation for the calculated osmolality

36
Q

What are the causes of an increased osmolar gap?

A

Nonelectrolyte solutes like ethanol, ethylene glycol, methanol, mannitol, acetone and isopropyl alcohol

37
Q

What is the formula for calculating the anion gap?

A

Na+ - (Cl- + HCO3-)

Normal is 3-14 mmol/L

38
Q

What are some causes of an increased anion gap?

A

MUDPILES

methanol
uremia
DKA
paraldehyde/propylene glycole
isoniazid
lactic acidosis
ethylene glycol
salicylates
39
Q

What is the recommended screening approach for gestational diabetes?

A

Depends on who you ask:

ADA and WHO recommend a 1-step approach with at 75 g 2 hr oral GTT which requires a single elevated value for diagnosis

ACOG recommends a 2-step with an initial screening glucose challenge and then a 3-hr oral GTT in those who screen positive (this is the one that’s most commonly used in the US)

40
Q

What are the advantages and disadvantages of the 1-step screening approach?

A

only 1 visit necessary
more sensitive bc only requires one abnormal value

cons: implementation increases the diagnosis of GDM 2-3 fold because of that increased sensitivity

41
Q

What are the advantages and disadvantages of the 2-step approach?

A

pros: more specific because requires a follow-up test
cons: more expensive, more time-consuming

42
Q

How is the 1 hr GTT performed?

A

give a 50 gram glucose load (non-fasting)

then measure the glucose (normal is 60-130 mg/dL)

43
Q

How is a 3 hr GTT performed?

A

Measure fasting glucose
Give 100 g glucose load
measure plasma glucose at 1 hr, 2 hr and 3 hr

it’s positive if 2 or more glucose values are elevated

44
Q

What are the normal glucose value ranges (60 to ??) for the time points in the 3 hr GTT?

A

fatsing: 94
1 hr: 179
2 hr: 154
3 hr: 139

45
Q

How many patients fail the glucose screen and how many of them end up with a diagnosis of gestational diabetes?

A

Depending on the cutoff used, about 14-23% of women will fail the GTT, but only 8-11% who fail will be diagnosed with gestational diabetes

46
Q

What lab tests are recommended in a patient with acute RUQ/epigastric pain?

A

CBC, elecrolytes, BUN, Creatinine, glucose, ALT/AST, alk phos, bilirubin, lipase (NOT amylase)

47
Q

True or false: there is no correlation between the severity of pancreatitis and the degree of lipase elevation

A

true

48
Q

Besides elevated lipase and amylase, what other lab abnormalities can be seen in patients with acute pancreatitis/

A 
leukocytosis
hyperglycemia
hemoconcentration with Hct over 44% (harbinger of more severe disease)
Azotemia
Hyperbilirubinemia in 10%
transient elevations of AP, ALT, AST
Hypocalcemia
Hypoxemia
49
Q

What is macroamylase and how can it screw up the amylase test?

A

it’s a high molecular weight form of amylase in the patient’s serum due to binding of an immunoglobulin to amylase in the circulation

it’s too big to be excreted in urine, so you get an elevated amylase (seen in 1.5% of general adult population)

50
Q

What are some other causes of an elevated lipase?

A 
renal failure
acute cholecystitis
bowel obstruction/infarct
duodenal ulceration
pancreatis stone/tumor
post-ERCP
DKA
HIV
Macrolipasemia
celiac disease
drugs
idiopathic
51
Q

What are the most common causes of acute pancreatitis

A 
alcohol
stones
drug-induced
hypertriglyceridemia
ERCP
52
Q

What are some of the differences between acute and chronic pancreatitis?

A

Acute: usually not progressive, almost always painful, amylase an dlipase almost always elevated, diffusely involves pancreas with primarily neutrophilic response

chronic: progressive with permanent damage, can be asymptomatic or just pancreatic insufficiency without pain, amylse and lipase tend to be normal (burnt out), patchy focal disease with primarily mononuclear infiltrate and fibrosis

53
Q

How is chronic pancreatitis diagnosed?

A

Early or mild disease challenging to diagnose because amylase and lipase ar enot diagnostic

triad of pancreatic calcifications, steattorhea and diabetes mellitus is suggestive

may have high bili and alk phos

54
Q

How can you test for steatorrhea?

A

72 hr quantitative fecal fat is the gold standard

55
Q

How can you assess for exocrine dysfunction?

A

most use fecal elastase (low with insufficiency)

56
Q

What imaging modality is becoming the diagnostic test of chocie for chronic pancreatitis?

A

MRCP - can visualize calcifications and ductal obstruction

no contrast is needed and it’s non-invasive

Labs Medicine (27 decks)

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