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STEP1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Describe how glucose trigger insulin secretion from pancreatic beta cells.

A

GLUT2 transporter glucose into cell of pancreatic beta
glucose is broken down and increases the ATP
High ATP inhibits K+ channel.
Depolarization.
Voltage-gated Ca++ channel opens, and Ca++ comes in.
Ca++ causes the release of insulin vesicles

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2
Q

Which tissues in the body have insulin-dependent glucose transporters? What is the effect of insulin on these?

A

adipose tissue
skeletal muscle
**insulin also increases the amount of GLUT4 receptors on the surface

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3
Q

Describe the basic symptoms of diabetes?

A 
hyperglycemia
polyuria
polydipsia
polyphagia (can't get glucose you do have in your cells!)
weight loss (if Type I)
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4
Q

What is the dangerous thing to watch out for w/ Type I and Type II diabetes?

A

Type 1: diabetic ketoacidosis

Type II: HHS: hyperosmolar hyperglycemic state

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5
Q

Where are the beta cells and alpha cells located within the pancreas?

A

beta cells are inside. Think: insulin is inside.
alpha cells are on the periphery
delta cells are interspersed.

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6
Q

What is a strange thing that glucagon stimulates?

A

the release of insulin

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7
Q

T/F Insulin crosses the placenta.

A

False. it does not. glucose does

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8
Q

What are 2 weird functions of insulin?

A

Na+ retention in the kidneys

increased cellular uptake of K+ and amino acids (be are building things here, people!)

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9
Q

WHere is GLUT1 found?

A

brain, RBCs, cornea

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10
Q

Where is GLUT2 found?

A

pancreatic beta cells
kidney
liver
SI

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11
Q

Where is GLUT3 found?

A

brain

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12
Q

Where is GLUT5 found?

A

this is the fructose one
spermatocytes
GI tract

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13
Q

Which antibody is found in Type 1 diabetes?

A

islet cell antibody

for glutamic acid decarboxylase (GAD)

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14
Q

What is the genetic association w/ Type I diabetes?

A

HLA-DR3, HLA-DR4

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15
Q

What histo is seen in Type II diabetes?

A

islet amyloid polypeptide deposits

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16
Q

What are some different treatment options for neuropathic pain from diabetes?

A

gabapentin
pregabalin
duloxetine
amitriptyline

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17
Q

What are the 2 main categories of complications in diabetes?

A

non-enzymatic glycosylation

osmotic damage

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18
Q

what types of damage do you see with non-enzymatic glycosylation?

A

small vessel disease: retinopathy, glaucoma, neuropathy, nephropathy. leaky vessels. thickening of basement membrane
large vessel atherosclerosis contributor. Gangrene. MI.

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19
Q

What’s the deal with the retinopathy produced by diabetes?

A

nonprolif phase and then proliferative phase where you get the growth of a ton of blood vessels
leaky vessels. hemorrhage. blindness possible.
**may also see cotton wool spots (non-specific)

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20
Q

What types of damage do you see with osmotic damage in diabetes?

A

neuropathy (motor, sensory, autonomic)
cataracts
**think about sorbitol accumulation in tissue w/ aldolase reductase and without sorbitol dehyrogenase

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21
Q

Which tissues have aldolase reductase, but not sorbitol dehydrogenase? What is this MOA and damage?

A

Glucose–>Sorbitol via aldolase reductase
Sorbitol–>Fructose via sorbitol dehydrogenase

**schwann cells, lens, retina, kidney

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22
Q

Describe what is going on with DKA in T1DM emergencies.

A

insulin deficiency-determines severity
glucagon increases–>glucose increases & ketone bodies increase
**glucose leads to polyuria and dehydration
**ketone bodies are acids, leads to anion gap metabolic acidosis
get kussmaul respirations to try to compensate
no serum hyperosmolarity

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23
Q

Describe what is going on w/ HHS in T2DM emergencies.

A

no ketoacidosis
roughly normal insulin levels
this insulin inhibits lipolysis and ketone body formation
no kussmaul
extreme hyperglycemia>800
serum hyperosmolar>340!
Presenting symptoms: may be confusion, coma

24
Q

What is the treatment for diabetic ketoacidosis?

A

ICU
IV Fluids (To fix dehydration)
Insulin drip (for the purpose of inhibiting lipolysis and ketone formation)
Monitor anion gap acidosis
Give insulin or even insulin and glucose until gap is closed
fix potassium and magnesium

25
Q

What is the treatment for HHS?

A

IV fluids
insulin–for the purpose of decreasing serum glucose
potassium

26
Q

What are some common triggers of DKA in T1DM patients?

A 
undiagnosed diabetes-first presentation!
missed insulin doses
dehydration
alcohol or drug abuse
Severe medical illness (MI, CVA, trauma)
infection (pneumonia, gastroenteritis, UTI)
27
Q

What are the short-acting insulins used with meals?

A

aspart
glulisine
lispro

28
Q

What are the long-acting 24 hour insulins?

A

glargine

detemir

29
Q

Regular insulin is usu depleted at about ___ hours.

A

6 hours

30
Q

NPH is a type of insulin that lasts ___ hours.

A

12 hours, fully gone by 18 hours

31
Q

What are incretins?

A

made in GI
increase insulin secretion
messed up in T2DM

Ex: GLP-1

32
Q

What is the MOA of DPP-4 inhibitors?

A

inhibit DPP-4, which inhibits GLP-1 and other incretins

33
Q

What is the effect of incretin?

A

increase insulin
decrease glucagon
delays gastric emptying

34
Q

What are the DPP-4 inhibitors?

A

sitagliptin
saxagliptin
alogliptin
linagliptin

35
Q

What is the MOA of GLP-1 agonists?

A

act like an incretin

exenatide is made from a hormone found in Gila monster saliva

**increase satiety and may even cause weight loss!

36
Q

What are the SE of GLP-1 agonists?

A

nausea

increased risk for acute pancreatitis

37
Q

What are the GLP-1 agonists?

A

exenatide
liraglutide
albiglutide
dulaglutide

38
Q

What is the MOA of SGLT-2 inhibitors?

A

inhibit sodium glucose linked transporter in the kidney
blocks reabsorption of glucose

**can also cause weight loss

39
Q

What is the SE of SGLT-2 inhibitors?

A

need normal kidney
can increase risk of UTIs b/c of increased glucose down there
mycosis possible

40
Q

What are the SGLT-2 inhibitors?

A

dapagliflozin
empagliflozin
canagliflozin

41
Q

Which diabetes meds have hypoglycemia as an SE?

A

sulfonylureas

insulin

42
Q

Which drugs are not safe in patients with fluid balance problems, such as CHF?

A

TZDs

43
Q

Which drugs should not be used in patents with kidney dysfunction?

A

metformin
SGLT-2 inhibitors
sulfonylureas

44
Q

Which drugs may actually help w/ weight loss?

A

metformin
DPP-4 inhibitors
GLP-1 agonist
SGLT-2 inhibitors

45
Q

What is a useful diabetes med for patients with kidney dysfunction,b /c it is metabolized by the liver?

A

TZDs

46
Q

Which drugs decrease hepatic gluconeogenesis?

A

metformin

TZDs

47
Q

What is a possible non-insulin treatment for patients with organ failure?

A

DPP-4 inhibitors

48
Q

What are possible fatal effects of DKA?

A

cardiac arrhythmias b/c of altered K+ & Mg
-include Vtach and torsades de point(mg)
Mucormycosis–>brain abscess if sinus infection

49
Q

What are the biguanides and their MOA?

A

metformin
basically, decrease gluconeogenesis, increase glycolysis, increase peripheral glucose uptake and increase insulin sensitivity

**can be used if patients don’t have islet cell function

50
Q

What are the SE & contraindications of metformin?

A

GI upset

lactic acidosis–watch for patients w/ renal insufficiency

51
Q

What is the MOA of sulfonylureas? And the 2nd gen drugs?

A

inhibit K+ pump on pancreatic beta cells. Cause depolarization, ca++ influx and release of insulin

Glimepiride
Glipizide
Glyburide

52
Q

What are the SE of the 2nd gen sulfonylureas?

A

hypoglycemia

weight gain

53
Q

What are the 1st gen sulfonylureas and their potential side effects?

A

chlorpropamide
tolbutamide

disulfiram-like reaction
hypoglycemia risk

54
Q

What is the MOA of TZDs? What are they?

A

increase insulin sensitivity by binding to PPARgamma

regulates fatty acid storage and glucose metabolism

pioglitazone
rosiglitazone

55
Q

What are the SE of TZDs?

A

Weight gain
Edema->bad for CHF
hepatotoxicity

56
Q

What is the MOA of amylin analogs?

A

Pramlintide

decrease gastric emptying
decrease glucagon
**amylin usu released w/ insulin

57
Q

What is the MOA of the alpha glucosidase inhibitors?

A

Acarbose
Miglitol

intestinal brush border enzyme inhibitors
decreases carb absorption

GI disturbances!!

STEP1 (54 decks)

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