Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endocrinology > T2DM Pharmacology > Flashcards

T2DM Pharmacology Flashcards

(56 cards)

Start Studying
1
Q

what are the insulin dependent mechanisms of treating T2DM

A

increasing insulin secretion (sulfonylureas, incretin mimetics, glinides, DPP-4 inhibitors)

decreasing insulin resistance abd reducing hepatic glucose output (glitazones)

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

what are the insulin independent mechanisms for treating T2DM

A

slowing glucose absorption from the GI tract (alpha-glucosidase inhibitors)

enhancing glucose excretion by the kidney (SGLT-1 inhibitors)

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

describe the relationship between cellular energy and insulin secretion in beta cells starting with blood glucose

A

increased blood glucose

glucose diffuses down conc gradient into B cell via GLUT2

phosphorylation of glucose by glucokinase

glycolysis of glucose - 6 - phosphate in mitochondrian making ATP

increased ATP/ADP ration

closure of ATP sensitive K+ channels

membrane depolarisation

opening of voltage activate Ca+ channels

release of intracellar Ca+

insulin secretion by exocytosis of storage granules

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

what are the components of KATP and their function

A

4 Kir6.2- form potassium channel

1 SUR1- regulates potassium channel activity

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

how does the ATP/ADP ratio determine the opening/ closing of KATP

A

ATP binds to Kir6.2- closes channel

ADP binds to SUR1 opening the channel

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

how do sulfonylureas (SU) act of KATP

A

displace ADP from SURI to close channel- cause depolarisation and the release of insulin

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

what do SU require

A

a functional mass of beta cells (to stimulate them to release insulin)

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

give exmaples of SU

A

gliclazine, glipizide

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

how do SU work

A

displace ADP from SUR1 subunit, closing KATP channel

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

what is the short ans long term effect of SU’s

A

decrease fasting and post prandial (after a meal) blood glucose

long term reduce the microvascular complications

undesirable weight gain

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

how long to peak release of insulin after SU

A

1-2 hours- some longer and shorter acting

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

what is the risk of the longer acting SU (glicazide, glipizide)

A

may cause hypos by excessive insulin secretion

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

who is most at risk of getting a hypo when using an SU

A

elderyl, reduced hepatic/ renal function, chronic kidney disease

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

when can SU be given

A

first line in those who cant tolerate metformin/ or with weight loss

second line in conjunction with metformin

third line in conjunction with metformin + thiazolidinediones/ other drugs

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

why do SUs cause weight gain

A

anabolic effect of insulin increased
appetite increased
urinary loss of glucose decreased

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

who should SUs not be given to

A

pregnant, breast feeding or elderly

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

are SUs dependent of glucose concentration

A

no work independently to it

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

how do glinides work

A

like SUs but action increased by glycaemia

bind to SUR1 to close the KATP channel and trigger insulin release

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

give examples of glinides

A

repaglininde

nateglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the onset of glinides

A

30-60 mins

promote insulin secretion in response to meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why are glinides sometimes better than SUs

A

less likely to cause hypos (than long acting SUs)

metabolised mainly by liver- safer than SUs in CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when can and cant glinides be used

A

can be used in conjunction with metformin and thiazolidinediones

cant be given in severe hepatic impairment, pregnancy and breast feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

is the insulin response greater to oral or IV glucose- why

Study These Flashcards
A

oral

the incretin effect (GLP-1 and GIP)

24
Q

describe the incretin effect

Study These Flashcards
A

ingestion of food stimulates release of GLP-1 and GIP from enteroendocrine cells in the small intestine
these enter the portal blood stream which goes to the pancreas
GLP-1 and GIP enhance (increment) insulin release from beta cells and delay gastric emptying (enhanced glucose uptake and utilisation)
GLP-1 decreases glucagon release from alpha cells
decreased glucose production

all together decrease the blood glucose

25
what are the gliptins, give examples
DPP-4 inhibitors: sitagliptin and others all ending in gliptins
26
what happens to the incretin effect in T2DM
is reduced
27
what terminates the actions of GLP-1 and GIP
the enzyme DPP-4
28
how do gliptins work
competitively inhibit DPP-4, prolonging the actions of endogenous GLP-1 and GIP, increasing plasma insulin
29
how can gliptins be administered
is orally active usually used in combo with SU, or metformin can be given as monotherapy
30
what are the effect and adverse affects of sitagliptin
no hypoglycaemia, weight neutral | nausea main adverse affect
31
what are incretin analogues | give examples
peptides that mimic the action of GLP-1 but are longer lasting as can resist breakdown by DPP-4 extenatide, liraglutide
32
how do incretin analogues work
bind as agonists to GPCR GLP-1 receptors that increase intracellular cAMP concentration in B cells to stimulate insulin secretion also; suppress glucagon secretion slow gastric emptying decrease appetite
33
are incretin analogue weight neutral
no cause modest weight loss, reduce hepatic fat accumulation
34
what are the adverse affects of incretin analogues
may cause nausea and pancreatitis (rare)
35
how are incretin analogues given
subcutaneously
36
what must happen to carbs before it is absorbed into the small intestine and how is this done
must be digested into monosaccharides | alpha-glucosidase (a brush border enzyme) breaks starch and disaccharides into absorbable glucose
37
how do alpha-glucosidase inhibitors work
when taken with a meal, delay absorption of glucose thus reduce post prandial increase in blood glucose
38
when are alpha-glucosidase inhibitors used
in T2DM inadequately controlled by life style measures or other drugs (not commonly used)
39
what are the adverse affects of alpha-glucosidase inhibitors
flatulence, loose stools, diarrhoea, abdominal pain, bloating (all due to undigested carb)
40
what are the pros and cons of alpha-glucosidase inhibitors
pose no risk to hypos | only moderately control glycaemia
41
what is the only theraputic biguanides
metformin
42
when is metformin used
is first line for T2DM irrespective of obesity, with normal hepatic and renal function
43
when is metformin contraindicated
in severe hepatic or renal impairment
44
what are the actions of metformin
reduce hepatic gluconeogenesis- stimulate AMP activates protein kinase increases glucose uptake and utilisation by skeletal muscle (increases insulin signalling) reduces carbohydrate absorption increases fatty acid oxidation
45
what are the desirable clinical effects of metformin
reduces microvascular complications of diabetes doesnt cause hypos given orally causes weight loss can be combines (insulin, thiazolidine, SUs)
46
what are the adverse clinical effects of metformin
lactic acidosis (rare)- avoid in patients with severe hepatic or renal disease/ excessive alcohol consumption
47
how do thiazolidineones (TZDs) work
enhance the action of insulin at target sites - do not affect insulin secretion - reduce insulin resistance activates PPARgamma - RXR complex which is a transcription factor that promotes the expression of genes encoding proteins involved in insulin signalling and lipid metabolism
48
why do TZDs have delayed onset
as work on transcription factors
49
what are the desirable affects of TZDs
promote fatty acid uptake and storage of adipocytes- rather than in skeletal muscle and liver reduce hepatic glucose output enhance peripheral glucose uptake dont cause hypos
50
what are the adverse affects of TZDs
weight gain fluid retention (Na+ absorption in the kidney) increased incidence of bone fractures
51
when should TZDs not be used
in heart failure- as increase circulating volume
52
give an example of TZD (a.k.a glitazones) used and what it can be used in combo with
pioglitazone | metformin, SUs
53
are SGLT2 inhibitors dependent on insulin
no
54
how do SGLT 2 inhibitors work
selsctively block the re absorption of glucose by SGLT 2 in the proximal tubule of the kidney nephron deliberately causes glucosuria cause a decrease in blood glucose with little risk of hypos
55
what are the secondary affects of SGLT 2
osmotic diuresus (water loss) and weight loss
56
give 3 examples of SGLT 2 inhibitors
dapagliflozin canaglifozin empagliflozin

Endocrinology (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions