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DT4-Exam 1 > Pharm Diabetics- Melissa** > Flashcards

Pharm Diabetics- Melissa** Flashcards

1
Q

Describe briefly the 2 steps of insulin biosynthesis.

What is REQUIRED for insulin release by B cells?
What is released in granules containing insulin?

A

-Preproinsulin–> Proinsulin (RER)
-Proinsulin + Ca-dep endopeptidase make sec. granules
(golgi)

CALCIUM is required for release of insulin by B cells!!

Granules release: Insulin/C-peptide/Amylin

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2
Q

What are the three forms of insulin and how is it stored?

Which form is biologically active?

A

Insulin is chelated to ZINC + stored in secretory granules:

  • monomer (biologically active– short acting insulin)
  • dimer
  • hexameter (storage from– long acting insulin; larger complex, longer to diffuse)
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3
Q

What is the strongest stimulus of insulin release?

What are the 6 steps to insulin release + what is released along with insulin?

A

GLUCOSE = strongest stimulus for insulin release by B cells

Glucose uptake–> G6P–> ^ ATP/ADP ratio–>
CLOSE ATP-dep K+ channels–> OPEN VGCa++ channels–>
^ INTRACELLULAR Ca++–> release insulin, amylin, and C-peptide

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4
Q

Why is an oral glucose tolerance test superior to IV?

A

Oral glucose stimulates GASTRIN, SECRETIN, and other GI hormones that promote insulin release

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5
Q

How does glucagon influence insulin production?

A

Glucagon ^ insulin production as compensatory mechanism

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6
Q

What are 4 digestive hormones/ products that ^ insulin production?

What are four things that block insulin release

A
  • Gastrin and secretin (hormones )
  • AAs and FAs (products)

Blocked by: B2 ANTagonists, a2 agonist, diazoxide, somatostatin

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7
Q

What is different between human insulin and insulin analogs?
What are three rapidly acting insulin analogs?

**When is insulin used? When are the other drugs in this lecture used?

A

Analogs = insulin MONOMERS w rapid onset, short t1/2
Created by changing 1 or 2 amino acids

  • aspart
  • glulisine
  • lyspro

Insulin mainly for DM1, also for DM2 later in disease.
–>The other drugs are largely for DM2 NOT NOT DM1
(THANK YOU!❤️🙌)

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8
Q

Two therapeutic advantages to rapid insulin?
ROA?
compatible with NPH?

A
  • Give diabetics flexibility (less postprandial hyperglycemia)
  • MORE EFFECTIVE than insulin at lowering glucose
  • ROA: SQ, IV, pump (with a needle, NOT ORAL)
  • can be given with NPH
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9
Q

Which rapid acting insulin is fastest?

Which insulin is “short” acting?

A

Aspart; can take it 5 mins before eating

Short: regular human insulin

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10
Q

Which insulin is intermediate acting?

What is one potential problem with this form of insulin?

A

NPH insulin

  • Contains PROTAMINE, heparin antidote
  • Not good for fish allergy and must watch in patient with heparin OD
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11
Q

What are the two long acting insulins?

How are they given?

A

-Insulin Determir & Glargine=24hrs (degludec=42hrs)
(the “others”– the ones that aren’t made up of amino acid words like aspart)
-ROA: subQ

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12
Q

What are 4 factors influencing insulin action/ absorption?

A
  • blood flow (skin temp)
  • insulin prep (mixture short + long etc)
  • ^ physical activity = ^ absorption
  • site of injection
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13
Q

Rank injection sites in order of FASTEST to SLOWEST absorption:

A

abdomen–> arm–> thigh–> bum

** patients may get hypoglycemic from rotating to injection site with ^ absorbance

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14
Q

What are some circumstances that INCREASE insulin requirements?

A

Things that rev up the sympathetic nervous system like:

stress (physical or psychological) + HYPERTHYROID

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15
Q

What are some circumstances that DECREASE insulin requirements (3)?

A
  • N/V due to decreased caloric intake
  • HYPOthyroidism
  • liver or renal impairment
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16
Q

What is the primary ADR associated with insulin use?

+ special consideration when also using BBers

A
  • HYPOGLYCEMIA due to poor timing/ skipping meals or increased exercise
  • Remember that B-blockers will inhibit physiological response (sweats, tremors, dizziness, etc.)
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17
Q

Describe the symptoms of HYPERglycemia.

How can this occur when patient is on insulin regimen (3)?

A

Insulin prevents HYPERglycemia (loss of appetite, thirst, lethargy, fruity breath)

Can occur with the following:

  • too little insulin at last dose
  • ^ stress
  • overeating
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18
Q

What are the two ADRs that can occur at insulin injection sites?

A

Lypohypertrophy: ^ fat at injection site (insulin ^ FA synth)
Lipoatrophy: depression at injection site (immune rxn)

**patients must rotate injection sites

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19
Q

Describe two situations when patients might temporarily go on insulin regimen:

A
  • DM2 patients undergoing surgery or in ICU

- Gestational diabetes

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20
Q

Pramlintide: Drug class?
MOA (2)
ROA, with insulin?

A

Amylin Analogue

MOA:

  • Inhibit glucagon –> DECREASE hepatic GLUCOSE output
  • SLOW gastric emptying –> decrease appetite

ROA: SubQ, not in the same vial as insulin.

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21
Q

Pramlintide: ADRs (1) and CIs (2)?

A

ADR: HYPOGLYCEMIA
CI: noncompliant patients + gastroparesis (slows gastric empyting)

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22
Q

What are the two drug classes that INCREASE insulin release from pancreas?
List the drugs within these classes.

What type of DM should these NOT be used in?

A

Sulfonylureas:
Gen1: Tolbutamide, Chloropropamide (AMIDE)
Gen2: Glyburide, Glimepiride (IDE)

Metaglinides:
RepaGLINIDE + NateGLINIDE

*THESE (and any others that ^^ insulin) SHOULDN’T BE USED IN SEVERE DM2 PRONE TO KETOACIDOSIS

(usually DM2 doesn’t have this but it can in uncontrolled/ bad cases!!)

23
Q

Sulfonylureas:
What are the drugs in this class?
MOA–where do they bind ?
Extra pancreatic effects (2)?

A

Sulfonylureas:
Gen1: Tolbutamide, Chloropropamide
Gen2: Glyburide, Glimepiride

MOA: Act on PANCREAS
BIND +INHIBIT receptor near K+ channels–>^ INSULIN RELEASE

Extra pancreatic effects:

  • DECREASE hepatic gluconeogenesis
  • ^ # Glu transporters + peripheral insulin receptors
24
Q

Which sulfonylurea can be used to treat central DI?

Is this first or second line therapy?

A

Chloropropamide

  • ^^^s ADH
  • second line therapy for patients intolerant to desmopressin
25
Q

What are the 2 ADRs associated with Sulphonylureas only? (mainly 1st gen)

What ADR is assc with sulphonylureas AND metaglinides?

A
  • Water retention due to ^ ADH
  • cholestatic jaundice

Both sulfonyls and metaglinides ^^ insulin and therefore can cause hypoglycemia

26
Q

What are the differences between Gen1 and Gen2 Sulfonylureas?

Which have more ADRs and which are more potent?

A

Sulfonylureas:
Gen1: Tolbutamide, Chloropropamide
- LESS POTENT with MORE ADRS
- ^ binding displacement and DD interactions
- ^ ADH activity–> H2O retention–>wt gain

Gen2: Glyburide, Glimepiride
- MORE POTENT with LESS ADRs
(better choice unless treating DI)

27
Q

Drugs that induce hypoglycemia and DECREASE sulfonylurea +metaglinide clearance?

A

Azole antifungals (P450 INHIBITORS)

28
Q

Describe how ASN and NSAIDS interact with sulpholyulureas:

A

Interact with first generation drugs to displace protein binding–> ^ amount of drug

29
Q 
Metaglinides: List the two drugs in this class and their MOA.
Can they be adminstered in combo w other drugs?
A

Repaglinide + Nateglinide
MOA: similar to sulfonylureas (act at diff. site)
Can be given WITH metformin

30
Q

Which drug is in the Biguanide class?
What is its MOA (3)
Biggest Benefit?

A

Metformin (Is the “Big-UAN” ‘cause it’s most commonly used)

MOA: ALL EXTRAPANCREATIC EFFECTS

  • DECREASE hepatic glucose production
  • DECREASE GI glucose absorption
  • INCREASE peripheral insulin sensitivity (mm uptake, etc)

-Extrapancreatic so NO HYPOGLYCEMIA!!

31
Q

What are some advantages to treatment of DM2 with metformin (3)?

A
  • No hypoglycemia
  • Decreases hyperlipidimia + weight gain

(they give this in OBGYN for the sole purpose of weight loss?… not sure that its appropriate but they do.😱)

32
Q

List 3 ADRs assocated with metfromin.

When is it CI?

A
  • GI n/v/d
  • DECREASE B12 absorption
  • Lactic acidosis w/ ETOH

CI: Hx of keto/lactic ACIDOSIS, liver or renal disease, CHF
(will decrease renal perfusion –> ^ risk lactic acidosis)

33
Q

What other condition is metformin used to treat other than DM2? Describe the logic:

A

PCOS with insulin resistance:

Decrease insulin resistance–> ^ synth sex hormone binding globulin–> DECREASE circulating androgens

34
Q

Acarbose + Miglitol:
MOA and site of action?
When is it taken?

A

MOA:

  • Competitive inhibition of amylase + a-glucosidase
  • small intestine–> DECREASE starch absorption
  • taken immediately before meal
35
Q

List some ADRs (2) assocated with Acarbose and Miglitol.

With which drug are they worse?

A
  • GI pain, diarrhea, flatulance (worse with acarabose)

- hepatotocicity– must monitor liver fxn

36
Q

ThiaZOlinediones:
List the two drugs in this class.
What is the MOA (2)?

A

PioglitaZOne, RosiglitaZOne
(pio/rosi-GLITAZONE)

MOA:

  • Nuclear PPAR-Y Agonist–> ^ insulin response gene transcription–> ^ glucose uptake in skeletal mm
  • DECREASE hepatic glucose production
37
Q

Pioglitazone, Rosiglitazone:
Advantage to use?
ADRs (2 + black box)?

A

Advantage: no hypoglycemia

ADRs: hepatotoxic, edema/ weight gain, BLACK BOX FOR CHF EXACERBATION (esp. with Rosi)

38
Q

GLP-1 Agonists:
What are the two drugs in this class?
What is their MOA?
ADRs (3)? Which is the black box?

A

ExenaTIDE + LaragluTIDE

MOA:

  • ^^ GLP-1(=incretin hormone) secretion from intestinal cells w/ a meal–> ^^ insulin release
  • ^ glucose dependent insulin release

ADRs:

  • hypoglycemia
  • pancreatitis
  • *BLACK BOX: THYROID CANCER
39
Q

AloGLIPTIN, SaxaGLIPTIN, SitaGLIPTIN:
What is the drug class and their MOA?
ADRs?

A

MOA: DDP4 INHIBITORS

  • inhibit DDP4 which degrades GLP-1
  • ^ endogenous GLP-1

ADRs:
-Hypoglycemia
(lower than sulphonylureas and meglatides)
- Pancreatic, Renal and hepatotoxicity

40
Q 
CanaGLIFLOZIN + DapaGLIFLOZIN: 
Drug class and MOA?
A

Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors
MOA:
Inhibit SGLT2–> DECREASE proximal tubule reabsorption of glucose–> INCREASE renal excretion of glucose Requires good renal funciton

*If drug has “flo”=act on kidney, bc kidneys make the pee ‘flo’ .
Canagli’flo’zin + Dapagli’flo’zin

41
Q

Canagliflozin:

List the ADRs (3) and CI (1):

A

ADRs:

  • ^ UTI, especially in females
  • Hyperkalemia
  • HypoTN due to osmotic diuresis

**CI in patients with renal impairment!!

42
Q

Drugs classes that induce hypoglycemia (4)

A
  • Sulphonylureas + megalinides
  • Insulins
  • DDP4 Inhibitors
  • GLP-1 Agonists

(anything that ^^ insulin, and anything that DOES NOT ^^ insulin does NOT cause hypoglycemia, therefore benefit of all other drugs is less hypoglycemia.)

43
Q

Drugs classes that require Hepatic monitoring (3)

A
  • Acarbose
  • Thiazolinediones (have –glitazone in name)
  • DPP-4 inhibotors (have –gliptin in name)
44
Q

Drug classes that cause weight gain and water retention (2)

A
  • Thiazolinediones (-glitazone ‘s) + Chlorpropamide
45
Q

Diazoxide:

MOA/ Theapeutic use?

A

MOA: maintains ATP sensitive K+ channels OPEN–> DECREASE insulin release–> ^ Blood sugar

–patients with insulin secreting tumors

46
Q

Glucagon (Drug):

ROA, Therapeutic use:

A

ROA/Tx: IV, IM, SQ for hypoglycemia (admin prior to giving glucose IV)

47
Q

Drugs that stimulate insulin release:

A

Sulphonylureas and meglitinides

48
Q

Drugs that decrease hepatic glucose (4)

A

Biguanides
(metformin)

possibly pramlintide, sulphonylureas + metaglinides, thiazolinediones

49
Q

Drugs that dercrease carb absorption:

A

a-glucosidase inhibitors

acarbose, miglitol

50
Q

Drugs that are peripheral cell insulin sensitizers

A

Thiazolinediones
(Pioglitazone, Rosiglitazone)

Mary: I also think Metformin, Sulphonylureas/Metaglinides

51
Q

What is the #1 drug used to treat DM2?

A

METFORMIN

52
Q

Drugs that are black box for thyroid cancer?

What else can they cause?

A 
GLP analogs (exenatide, laraglutide) 
Also cause pancreatitis
53
Q

Two groups of drugs that can cause pancreatitis?

A

GLPs/DPP4i

54
Q

Drug contraindicated in CHF, liver, renal disease?

A

Metformin –> odd because it’s most commonly used in DM2 and these patients usually have several diseases!!

DT4-Exam 1 (17 decks)

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