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MOD 3 > Diabetes Management > Flashcards

Diabetes Management Flashcards

1
Q

Genetics of Type 2 Diabetes

  • gene
  • level of risk for heterotyzgotes vs. homozygotes
  • frequency across ethnicities
A

SLC16A11 polymorphism: related to fat metabolism

Increased DM risk: heterozygotes (20%), homozygotes (40%)

Polymorphism Frequency: asian (10%), native americans and latin americans (50%) **low risk in white, everyone else is high risk**

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2
Q

Monitoring Diabetes Therapy

  • Short term
  • Long term
A
  • Short term: capillary glucose (finger forearm ear, continuous interstitial fluid)
  • Long term: hemoglobin A1C (glycated hemoglobin), fructosamine (glycacted albumin)
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3
Q

What is the rate of nonenzymatic protein glycation dependent on? (very obvious, don’t overthink it)

A

dependent on serum glucose concentration

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4
Q

normal insulin secretion: describe the graph over time.

A

regular phasic peaks (see figure)

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5
Q

What do you want to achieve with insulin injections

A

get a basal level + bolus components

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6
Q

How does “Reg Insulin” compare to “bolus”

A

more rounded peaks that span for more of the time. see figure

-regular is considered short-acting

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7
Q

Rapid-acting insulin (3)

Effects compared to Regular insulin in Type I DM

A
  • Lispro
  • Aspart
  • Glulisine
  • (inhaled insulin)

**Lispro vs Regular (type I DM): reduces hypoglycemia by about 15%

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8
Q

Long-Acting Insuline (2)

A
  • glargine
  • detemir
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9
Q

2 important facts about glargine

A
  • basal insulin, constant slow release
  • reduces nocturnal hypoglycemia
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10
Q

intermediate acting Insuline

A

NPH

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11
Q

Glargine vs. NPH (Type 1 DM)

A

reduces hypoglycemia by about 15%

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12
Q
  • Basal (2)
  • Bolus (3-4)
  • Insulin Pump (3)
A

-Basal: Glargine, detemir (long-acting)

-Bolus: glulisine, lispro, aspart, inhaled insulin (Afrezza)

-Insulin pump: glulisine, lispro, aspart

*“program” to calculate bolus dose based on carbs and blood sugar*

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13
Q

Which insulin drug should be avoided during pregnancy? Which is preferred?

A

Glargine insulin is class C drug and should be avoided during pregnancy

Detemir insulin is class B and is preferred during pregnancy.

(class B for BABY, i am in det to you for saving my baby)

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14
Q

Non-insulin therapy for what type of diabetes? List the 6 main drugs for treatment

A

Type II

1) K-channel
2) GLP-1
3) Metformin
4) SGLT2 inhibitors
5) Glucosidase inhibitors
6) Thiazolidinediones/Glitazones

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15
Q

possible MOAs of metformin (biguanides)

A
  1. decrease GNG (hepatic glucose production)
    - activates AMP kinase, inhibits mitochodnrial glycerophosphate dehydrogenase
  2. increases glycolysis
  3. increases peripheral glucose uptake
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16
Q

Most serious side effect of metofrmin

A

lactic acidosis (possible explanation is that metformin increases amount of NADH, and you need NAD with LDH to convert lactate –> pyruvate –> glucose)

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17
Q

Where is metformin cleared?

Contraindications

A

by the KIDNEY

reduced in rneal failure and in CHF

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18
Q

Metformin efficacy

A

1% reduction in hemoglobin A1C

-delays the onset of type 2 diabetes

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19
Q

SGLT2 inhibitors (3)

A

“flozin”

  • canagliflozin
  • dapagliflozin
  • empagliflozine)
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20
Q

Mechanism of SGLT2 inhibitors

A

Inhibits the subtype 2 sodium-glucose transporter in the renal proximal tubule

(if you inhibit this channel, you lose glucose in the urine which also will act as a diuretic and will lower BP)

blocks just about 300 calories from reabsorption

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21
Q

Other potential uses of SGLT2 (off-label): 7

A
  1. Type I DM (postprandial hyperglycemia)
  2. Obesity/metabolic syndrome/prediabetes
  3. Sleep apnea
  4. Osteoarthritis
  5. Cosmetic weight loss/performance enhancing drug
  6. CHF
  7. Hypertension
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22
Q

Side effects of SGLT2 inhibitors

A

increased vaginal candida infections, but not increased UTI at 12 weeks

(think of kidney leading to your vag)

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23
Q

Sulfonylureas + Glinides (K-Channel) MOA

A

ATP inhibits/closes the ATP-dependent K+ channel in the Beta-cell membrane, cell depolarizes, calcium rushes in, set up a phosphorylation cascade and secretes insulin

24
Q

List the 3 important Sulfonylureas and how long they last

A

12-24 hour

  • glymiperide
  • glyburide
  • glipizide
25
Q

List 2 important glinides and how long they last compared to sulfonylureas (both are secretagogues)

A

only 3 hours (sulfonylureas last 12-24)

  • repaglinide
  • nateglinide
26
Q

Secretagogues clearance (sulfonylureas and glinides)

A

Bother undergo hepatic metabolism (majority degraded in the liver)

-all are more effect in renal failure, since insulin is partially degraded in the kidney

27
Q

Side effects of secretagogues (2)

A
  1. Weight gain (Because you have more insulin, and patients are still overeating)
  2. Hypoglycemia (in theory, the shorter acting agnets “glinides” should cause less hypoglycemia. there are no studies to demonstrate this benefit)
28
Q

GLP-1 analogs MOA

A

incretins: augment insulin release

recall GLP-1 and GIP are produced in the L-cell and K-cell respecitvely down in the gut. Released in response to feeding (rapid response)

29
Q

DPP-4 (dipeptidyl peptidase-4) inhibitors

A

DDP-4 is a protease that inactivates GLP-1 and GIP (cleaves N-terminal dipeptide)

Inhibitors indirectly increase insulin release by allowing GLP-1 and GIP (incretins) to stay activated

30
Q

Explain the incretin effect, and how this changes in Type 2 diabetes

A
  • Simple study shows that glucose given by mouth vs. infusion caused a greater insulin release
  • shows that something in gut is associated with agumentation of insulin release, and that is GLP-1
  • **the incretin effect is diminshed in Type 2 diabetes **
31
Q

Can GLP-1 agonists cause hypoglycemia?

A

NO, because they are stimulated when glucose is high, but when glucose comes down, the effect wears off. Nifty!

32
Q

GLP-1 activates what when Ca rushes into cell

A

increases cAMP production, enhancing phosphorylation (tied to G-receptor)

33
Q

half life of GLP-1 due to DDP-4

A

t1/2= 1-2 minutes

34
Q

List the 4 important DDP-4 inhibitors

A
  1. Sitagliptin
  2. Saxagliptin
  3. Linagliptin
  4. Alogliptin
35
Q

4 major GLP-1 agonists

A
  1. Exanatide
  2. Liraglutide
  3. Dulaglutide
  4. Albiglutide
36
Q

Exenatide MOA and pharmacokinetics

A

activates the GLP-1 receptor, 2 hour efficacy

37
Q

GLP-1 agonist

A

hypoglycemia (rare)

nausea and vomiting

pancreatitis

38
Q

which drug gets used the least due to less efficacy

A

glucosidase inhibitors

39
Q

MOA of glucosidase inhibitors and pharmacokinetics

A
  • delays digestion of complex carbs by inhibiting alpha-glucosidase at intestinal brush-border (delays sugar hydrolysis and glucose absorption)
  • reduces need for first phase inuslin release (decreases postprandial hyperglycemia)
  • acts in gut for about 2 hours
40
Q

2 glucosidase inhibitors and side effects

A

Miglitol and acarbose

gas-no hospitalizations of death

41
Q

MOA of thiazolidinediones/glitazones and pharmacokinetics

A

increase insulin sensitivity in peripheral tissue: binds PPAR-gamma nuclear transcription regulator

24 hour efficacy

42
Q

effect of PPAR-gamma stimulation

A

lipid synthesis and carbohydrate metabolism

43
Q

Thiazolidinediones side effects

A
  • weight gain
  • water retention - occasional CHF
  • distal extremity fractures in women
44
Q

Extra bonus benefit from thiazolidinediones in addition to 1% A1C reduction (pioglitazone only)

A

30% triglyceride reduction

45
Q

For each drug, decide whether + or -

INSULIN

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: +
  • weight gain: +
  • liver toxicity: -
  • lactic acid: -
  • gas: -
46
Q

for each drug, decide whether + or -

K- Channel secretogogues

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: +
  • weight gain: +
  • liver toxicity: -
  • lactic acid: -
  • gas: -
47
Q

For each drug, decide whether + or -

GLP-1 agonists

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: +
  • weight gain: - - -
  • liver toxicity: -
  • lactic acid: -
  • gas: -
48
Q

For each drug, decide whether + or -

DPP4 INHIBITOR

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: -
  • weight gain:-
  • liver toxicity: -
  • lactic acid: -
  • gas: -
49
Q

For each drug, decide if + or -

METFORMIN

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: -
  • weight gain: -
  • liver toxicity: -
  • lactic acid: +
  • gas: -
50
Q

for each drug, decide whether + or -

SGLT INHIBITORS

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: +
  • weight gain: - - -
  • liver toxicity: -
  • lactic acid: -
  • gas: -
51
Q

for each drug, decide whether + or -

alpha- GLUCOSIDASE INHIBITORS

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: -
  • weight gain: -
  • liver toxicity: -
  • lactic acid: -
  • gas: +
52
Q

for each drug, decide whether + or -

THIAZOLIDINEDIONES

  • hypoglycemia:
  • weight gain:
  • liver toxicity:
  • lactic acid:
  • gas:
A
  • hypoglycemia: -
  • weight gain: +
  • liver toxicity: +
  • lactic acid: -
  • gas: -
53
Q

combination therapy -efficacy

+exception

A

efficacy of different classes of agents is ADDITIVE

(exception: effects of GLP1 agonists and DPP4 inhibitors are not additive)

if a max dose of an agent is reached, then adding a second agent from that class will be ineffective

54
Q

For Type 2 DM patient not requiring insulin and with “good” insurance, what’s the stupid “Malchoff Algorithm”

A
  • metformin
  • liraglutide (GLP-1 agonist, or DPP4 inhibitor), canagliflozin (SGLT)
  • pioglitazone (thiazolidinediones), sulfonylureas
  • glucosidase inhibitor
55
Q

benefits of GLP-1 agonist exenatide

A
  • 0.8% decrease in A1C
  • 5 pound weight loss
56
Q
A

MOD 3 (19 decks)

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