Test 2 - L11/12 Diabetics Flashcards

1
Q

Rapid Insulin: Compare/contrast to endogenous Insulin
and Regular insulin

(do not need to know specifics just know RAPID)

A
  • Rapid insulin readily form monomers in solution V.S Regular Insulin although still classified as a Rapid therapy needs more time to break down into monomers from its hexameric state

-given preprandial/ prior to meal to mimic insulin stimulation via nutrient intake

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2
Q

What is the route of admin for DPP4 inhibitors
A) slow IV infusion
B) syringe
C) Butt chug
D) oral

A

D) oral

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3
Q

The 2 drugs which were used by celebrities for weight loss (not lizzo tho)

A

Semaglutide was the main one
tirzepatide also mentioned

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4
Q

A) which of the 3 DPP4 inhib drugs are eliminated through biliary excretion
B) why is this beneficial for diabetic patients

A

A) Linagliptin eliminated via biliary secretion,

B) Beneficial in diabetic patients since it’s not being eliminated in kidneys. So no dose adjustment is required

(remember that CKD is common in diabetic patients)

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5
Q

Regular Insulin (Intravenous Injection)

Compare/contrast to endogenous Insulin:
- Rate
- Mech

A
  • Regular Insulin is slower than endogenous Insulin but is still considered RAPID
  • Delay is caused by Regular insulin forming NON-COVALENT HEXAMERS in solution. (requires time to break into monomers; active form)

*Regular Insulin is only suitable for intravenous use and given preprandial/ prior to meal to mimic insulin stimulation via nutrient intake

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6
Q

1) What was a severe side of DPP4 inhibitors

2) what was a possible side effect of DPP4 and GLP1 drugs but has not yet shown in human data

A

1) Increased risk of pancreatitis (severe)

2) Pancreatic cancer seen in animals but not in humans so far

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7
Q

Intermediate Insulin:
- Name
- Composition
- cause of time delay

*other concerns about absorption

A
  • NPH Insulin :
  • is a suspension of human sequence insulin aggregated with protamine and zinc
  • protamine and Zinc are aggregates causing delayed activity

-Intermediate and Long acting insulin mimic 24hr basal insulin secretion

** NPH action is unpredictable bc of variable rate of absorption. You can also find drugs which come as a mix of regular and NPH insulin

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8
Q

1) what is the usual 1st line treatment in T2DM IF the patient does not suffer from any renal deficiencies.

2) what happens if the person suffers from renal impairment and cannot eliminate the drug from their body
****
(This is Black box I forgot to mention on the main card)

A

1) Metformin

2) Metabolic acidosis

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9
Q

Long Insulin (3)
- names
- Why does it take longer/ Administration
(2 act similar, 1 has its own mechanism)
- purpose

A

Insulin: Glargine, Detemir, Degludec

A) Glargine soluble at pH 4 but poorly soluble at pH7
making it take longer to solubilize staying in system longer.When injected SUBCUTANEOUSLY forms fine precipitant in interstitial fluid.

B) Both Detemir and Degludec are insulin administrations prolonged by binding to albumin in the blood. (normal insulin is never bound)

C) Intermediate and Long acting insulin mimic 24hr basal insulin secretion

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10
Q

Metformin

A) class
B) mechanism
C) use
D) Sides/metabolism

A

A) Biguanide drug

B) Inhibits Gluconeogenesis in Liver
-* Unlike insulin does not cause Hypoglycemia or Weight Gain (Sulfonylureas/Insulin = fat)

C) **most common 1st LINE THERAPY for T2DM

D) Bc Metformin is 100% excreted by Kidneys as active compound it should be used with caution in patients with decrease GFR/CKD why?

** BC improper elimination of Metformin can lead to increased metabolic acidoses

** Since Metformin acts locally on liver it affects hepatic metabolism of lactic acid = accumulation
(do not confuse this with drug being metabolize by liver. it is not)

** GI side effects of nausea, diarrhea

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11
Q

Aside from controlling/lowering blood glucose through stimulation of B cells and inhibiting gluconeogenesis what were the other 2 unique positive benefits (1 of is tech a side effect)

A

DRUG: GLP1-agonist
2) 1) benefit is that is cardio protective
2) Unique side is its effect on CNS for feeling of satiety

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12
Q

Glyburide, Glimepiride, Glipizide

A) class
B) use/requirements
C) MECH

A

A) Sulfonylurea drugs; But also Insulin Secretagogues

B) Used in early T2DM If Metformin alone cannot control blood Glucose and require functioning B cells
(useless in T1D)

C) Blocks K+ channelse making inside of cell more positive leading to Ca+ Channel depolarization. Ca+ leads to B- Cell depolarization and INSULIN secretion

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13
Q

These 2 drugs are both responsible for side effects of Nausea/ vomiting , Diarrhea and GI effects

A

Metformin and GLP-1 ( glp1 only nausea/vomit)

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14
Q

Sulfonylureas:
Glizipide: 1/2 life; admin when
+ general side effects (including the other sulfur drugs)

A

Glizipide -Shortest half life and administered pre-prandial

Sulfonyl Side Effects:
- weight gain -> increased appetite **
- Hypoglycemia
- Sulfer allergy
- increased CV mortality **

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15
Q

Repaglanide

A) class (alt drug)
B) mechanism
C) use
D) side

A

A) Alternative to Sulfonylurea drugs
(which also enhance B-cell insulin release; secretagogue)

B) They inhibit K ATP channels in B cells for insulin release via depolarization through ca+ mech

C) They can be used as an alternative T2DM drug in patients who may have Sulfer allergy

D) Hypoglycemia

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16
Q

GLUTIDE/TIDE drugs (suffix)

A) class
B) mechanism
C) metabolism
D) sides

A

A) GLP1 Agonist (Liraglutide , Dulaglutide, Semaglutide (Ozempic), Exenatide
Tirzepatide (special one on separate card)

B) Has actions in 4 places:
1) CNS, -> reduced BW, producing satiety feeling (+ side effect)
2) muscle/fat, -> enhances insulin sensitivity
3) liver -> inhibits glujconeogeneis
4) Pancreatic B cell -> enhances Insulin synth, B cell Prolif, decreases B cell Apoptosis

C) Drugs given subcutaneously except for Rybelsus which is oral tablet
All drugs metabolized by DPP4

D) Nausea and vomit beginning of treatment

17
Q

Tirpezatide why it diff than other GLP1… lets get racist.. lets go to the beach

A

Tirpezatide is dif. from the other GLP1 Agonist bc it is a dual agonist working on GLP1 and GIP.
-“GIP released from K-cells in GI, same effect as GLP-1 on β-cells in pancreas
but additionally promotes fat storage and bone formation

18
Q

LIPTIN Drugs

A) class
B) mechanism/use
C) Admin and Metabolism **
D) Sides **

A

A) DPP4 inhibitors/ antagonist

B) Inhibit breakdown of GLP-1 so it stays in system longer but NOT AS EFFICIENT at reducing blood glucose as GLP-1 agonist is

C)*** Of DPP4 inhib. Linagliptin is only excreted primarily by biliary secretion and as a result doesn’t require dose adjustment for renal dysfunction or CKD

D) possible increase risk of pancreatitis however data was only seen in animal but not human data

19
Q

GLIFOZIN Drugs

A) Class
B) Mech
C) use/requirements to use
D) Sides ** (+1 & -1)/ pro/con

A

A) SGLT-2 inhibitors

B) Inhibit SGLT2 in proximal tub. reducing Gluc. reabsorption

C) Bc it acts on kidneys its efficacy is reduced in CKD patients. — Metabolism ->fecal elim

D) (pro) + side effect is reduced body weight as glucose is not being absorbed.
(con) increased risk of genital/ UTI bc bacteria munch on ur PP glucose

20
Q

SGLT-2 Side effects/warnings

what are the main 2 side effects and the drug which came with a black box warning

A

Side 1) increased risk of UTI and genital tract infections

(bc urinating glucose -> residual glucose on genitals -> bacteria eat)

Side 2) FOR insulin DEPENDENT T2DM
glucose remains normal while taking SGLT-2 inhibitors so insulin is withheld resulting in diabetic ketoacidosis

Black Box) Canaglifozin: increased risk of lower limb amputations due to infection

21
Q

How is circulating Insulin different in T2DM patients versus healthy individuals

A

T2DM have 10-20% total circulating insulin as proinsulin which still contains C peptide

22
Q

(1/4) T2DM Therapeutic approach: Education

A
  • Educate them about diet, exercise smoking
  • reducing body weight by 5-10% can reduce risk of T2DM by almost 60%
23
Q

(2/4) T2DM Therapeutic Approach: Medication

A

1) After changing lifestyle then Metformin can be introduced to lower blood glucose

2) Metformin + “others” - if greater reduction needed in blood glucose (Others = DPP4, GLP1 etc..)

3) If that doesn’t work: Metformin + “others” + Insulin

Adding insulin poses issue with weight gain cuz T2DM patients usually already fat

24
Q

(3/4) T2DM Therapeutic Approach: patients W/ atherosclerosis and CV disease

A

1) Use semaglutide; GLP1 Agonist

Promotes weight loss but also has protective heart functions

25
Q

(4/4) T2DM Therapeutic Approach: patients w/ MINOR Renal impairment or MINOR CKD

A

1) use SGLT2 inhib ; Glifozin drugs
(empagliflozin, canagliflozin, dapagliflozin)

2) SGLT2 inhibitors can reduce progression of CKD. If CKD is severe drugs don’t work for example a patient on DIALYSIS

3) You would use SGLT2 inhibitors in comb. with other drugs because it has lesser glycemic reducing effect
*NOT METFORMIN tho cuz it can make CKD worse/ requires healthy kidney function

26
Q

Pioglitazone

1) class
2) mech
3) use
4) side effects

A

1) class: Meglitinide drug

2) mech: increases expression of GLUT 1 & 4 in muscle, adipose and liver tissues

3) use: similar to metformin; effects on peripheral tissues to decrease blood glucose

4) side effects increase cardiac related health problems increase fluid retention - LIMITS USE OF DRUG
cardiac problem mentioned: angina pectoralis

27
Q

Insulin delivery:
- what is the most common route of administration
+ other routes
- cybersecurity issue

A

1) most common is injection via syringe
2) other routes:
Insulin pen (same shit)
Inhaling dry powder (Doing lines of that pow)

3) Remote insulin pump - people were hacking other peoples pumps LMAO