Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IDT Spring > Diabetes Lec 4-5 > Flashcards

Diabetes Lec 4-5 Flashcards

1
Q

SC insulin takes about __ hours before reaching a max, therefore it should be injected about ___ min before meals

A

2, 30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does zinc change the diffusion of SC insulin?
a. increases diffusion
b. decreases diffusion
c. inhibits diffusion
d. limits diffusion

A

b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

______ insulin is what is secreted in response to elevated blood glucose

A

mature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The structure of insulin is comprised of?

A

along helix B chain and 2 short helices of A chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the three short acting insulins called?
what are the advantages of this form of insulin?

A

lispro (humalog), insulin aspart (novolog), and glulisine
-more rapid onset than regular insulin
-reduces risk of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the structural significance of the short-acting insulins?

A

they prevent formation of oligomers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the long-acting insulin called?

A

glargine (lantus, toujeo)
detemir (levemir)
degludec (tresiba)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

why does glargine (lantus, toujeo) have a pl (isoelectric point) that is more basic than insulin and why is this important?

A

Because of 21-G on A chain and (mainly) 2 arginine at the C-terminus of the B chain. They increase basicity to precipitate at injection site. this makes it act for a longer period of time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

For detemir (levemir), __________ is bound to B chain K29 which allows it to bind to ______ and slowly dissociate

A

myristic acid, albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

for degludec (tresiba), it’s structure has a deletion of ________ and an addition of a __________ attached to B-Lys29 via a glutamic acid spacer. It self-associates into multi-_______ resulting in an ultra-long peak

A

B-Thr30, 16-carbon fatty diacid, hexamers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rank the order of insulin meds from longest acting to shortest acting

A

Glargine -> Detemir -> NPH -> Regular -> lispro/ aspart/glulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Once a glucagon emergency kit is reconstituted, how long can it be used for?

A

not long, it should be used immediately after reconstitution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the mechanism of action of sulfonylureas?
what gives them their hypoglycemic effect?

A

close K+ channels located on beta cells to promote insulin release from beta cells
modification of the structure to contain a urea group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List the drugs classified as sulfonylureas

A

-drugs ending in amide
-glipizide
-glyburide
-gliclazide
-glimepiride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the mechanism of action of meglitinides?

A

same as sulfonylureas: close K+ channels located on beta cells to promote insulin release from beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the drugs classified as meglitinides

A

nateglinide, repaglinide, and mitiglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which sulfonyureas/meglitinides are selective for SUR1-type channels?

A

tolbutamide, chlorpropamide, nateglinide, and mitiglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which sulfonyureas/meglitinides are non-selective for SUR1/SUR2-type channels?

A

glibenclamide, glimepiride, and repaglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the mechanism of action of biguanides?

A

indirectly activates AMPK and reduces cytosolic dihydroxyacetone phosphate while raising cytosolic NADH/NAD+ ratio
-decreases hepatic glucose production by inhibiting gluconeogenesis and intestinal absorption of glucose, and improves insulin sensitivity

20
Q

what drugs are classified as biguanides?
what is a potential adverse reaction of biguanides?

A

metformin and buformin (can cause toxic lactic acidosis), and phenformin (withdrawn due to toxic lactic acidosis)

21
Q

what drug is co-administered with metformin?

A

glyburide

22
Q

what can toxic lactic acidosis cause? (adverse rxn to biguanides)

A

death, hypothermia, hypotension, and resistant bradyarrhythmias

23
Q

why does phenformin have a greater risk of toxic lactic acidosis than metformin?

A

because it is more lipophilic and and may bind more strongly to mitochondria to inhibit oxygen consumption causing a shift to anaerobic glycolysis

24
Q

why is metformin formulated with hydrochloride?

A

because it has a nearly permanent positive charge

25
Q

what is the mechanism of action of thiazolidinediones (glitazones)?
they are approved as combo therapy with?

A

improve insulin sensitivity by agonizing PPARy and reduce insulin resistance in T2DM.
sulfonylureas, metformin, and insulin

26
Q

what are the names of the thiazolidinediones (glitazones)?
dosing? adverse reactions?

A

pioglitazone: 15-45mg qd
rosiglitazone: 4-8mg qd -> has adverse cardiovascular effects
Troglitazone: withdrawn due to drug induced hepatitis
Lobeglitazone
-all drugs have warnings of monitoring liver function

27
Q

thiazolidinediones should not be used in pts with ______ impairment because they may cause _____ retention leading to possible cardiac failure
a common side effect from these drugs is?

A

renal, fluid
weight gain

28
Q

what are the names of the 2 aminocyclitols (a-glucosidase inhibitors) and their dosing
MOA?
common SEs?

A

acarbose: initial: 25mg tid at start of each meal maintenance: 50-100mg tid
miglitol: same dosing
inhibit a-glucosidase and pancreatic amylase to prevent glucose absorption
flatulence and diarrhea

29
Q

describe the “incretin effect”

A

higher lvl of insulin secretion when carb load is given orally than when given parentally which is caused mainly by GLP-1 and GIP

30
Q

what drugs are increatin based?

A

amylin agonists, GLP-1 agonists (the glutides +xenatide), DPP-4 inhibitors (gliptins)

31
Q

what is the MOA of pramlintide (aka Symlin)?
SEs?

A

it’s a synthetic analog of amylin: activates amylin receptors to extend gastric emptying to slow glucose absorption and potential appetite reduction
N/V, HA

32
Q

GLP-1 is derived from a larger peptide named ______

A

proglucagon

33
Q

what are the 2 forms of GLP-1 in bloodstream?

A

GLP-1 (7-37) and GLP-1 (7-36)

34
Q

Exenatide is a GLP-1 agonist that is a synthetic version of ______
it stops the liver from making too much ______
it reduces ______
it slows down ______ absorption
it slows _________ and stimulates ___________ secretion

A

exendin-4
glucose
appetite
glucose
GI emptying, glucose-dependent insulin

35
Q

Exenatide comes in two forms: Byetta and Bydureon, what is the dosing/administration of both?

A

Byetta: bid injection
Bydureon: qw injection

36
Q

Liraglutide is a GLP-1 agonist
Dosing?
what is an advantage of this med?
what is an associated risk?
what hormone can be monitored to determine this risk?

A

qd injection
causes weight loss
thyroid C-cell hyperplasia and C-cell tumors
calcitonin

37
Q

what is semaglutide’s dosing? (GLP-1 agonist)

A

qw injection

38
Q

what are common SEs of GLP-1 R agonists?

A

heartburn, N/V, diarrhea, and constipation

39
Q

All DPP-4 inhibitors name’s end in?

A

gliptin

40
Q

which DPP-4 inhibitors are class 1? (i played the SAX for Veronica)
which binding substrates do they inhibit?

A

saxagliptin and vigdagliptin
S2 and S1

41
Q

which DPP-4 inhibitors are class 2? (I put some Aloe on to Lin)
which binding substrates do they inhibit?

A

linagliptin and alogliptin
S2,S1,S2’, and S1’

42
Q

which DPP-4 inhibitors are class 3? (go SIT with the TENors)
which binding substrates do they inhibit?

A

sitagliptin (januvia) and tenegliptin
S2 extensive, S2, and S1

43
Q

MOA of SGLT2 inhibitors? why is this drug class more beneficial than the others?

A

block SGLT2 to increase renal glucose excretion to reduce plasma glucose levels and decrease weight
they don’t cause significant SEs

44
Q

what are the drug names of the SGLT2 inhibitors?

A

phlorizin, and all drugs ending in (gliflozin)

45
Q

which of the following is not a SE of SGLT2 inhibitors?
a. vaginal odor/discharge/itching
b. nausea/vomiting/diarrhea/constipation
c. UTI/polyuria
d. rhinorrhea/polydipsia/rash

A

b

46
Q

which drug classes are labeled as biologics?

A

amylin analogs, GLP-1 mimics, and DPP-4 inhibitors

47
Q

In summary:
what effect(s) do GLP-1 mimics have?
Sulfonylureas/meglitinides?
Biguanides?
Thiazolidinediones?
Symlin?
a-glucosidase inhibitors?
SGLT2 inhibitors?

A

stimulate insulin release and inhibit glucagon release
stimulate insulin release
improve insulin sensitivity and reduce hepatic glucose production
improve insulin sensitivity by targeting PPARy
lower blood glucose by activating amylin receptors
lower blood glucose by inhibiting a-glucosidase and pancreatic amylase
lower blood glucose by inhibiting reabsorption of glucose from kidney via inhibition of SGLT2 receptors

IDT Spring (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions