Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > Pancreatic Hormones, Anti-diabetic agents and Hyperglycemic Drugs > Flashcards

Pancreatic Hormones, Anti-diabetic agents and Hyperglycemic Drugs Flashcards

1
Q

Pancreatic ‘juice’ comes from ______ cells –> is delivered to the

A

acinar cells –> duodenum via the ductal system

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

Beta cells secrete

A

insulin

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

Alpha cells secrete

A

glucagon

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

Omega cells secrete

A

somatostatin

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

High blood glucose levels stimulates

A

higher secretion rate

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

Low blood glucose levels stimulates

A

glucose transport into cells
inhibits glycogenolysis (breakdown of glycogen -> glucose)
inhibits gluconeogenesis

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

Type 1 DM is usually diagnosed in

A

early childhood to early adulthood

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

Type 1 DM is the

A

absolute deficiency of insulin (autoimmune disorder where your body destroys beta cells)

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

Treatment of Type 1 DM

A

insulin

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

Concerns for type 1 DM

A

DKA
infection
end-organ damage from untreated hyperglycemia

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

Type 2 DM risk factors

A

genetic factors
obesity
aging plays a role

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

Type 2 DM is

A

peripheral insulin resistance (decrease uptake of glucose in tissue)
insulin secretion does not maintain glucose homeostasis

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

Complications of DM

A

retinopathy
nephropathy
neuropathy
CV complications
gastroparesis, autonomic insufficiency

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

Insulin options

A

long acting
intermediate acting
rapid acting
short acting

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

Insulin is degraded in

A

the GI tract - so administered subcutaneously most commonly
IV administration for emergencies and DKA

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

Goals of giving insulin

A

to replicate normal physiologic insulin secretion
to replace basal insulin (overnight, fasting and between meals)
to provide bolus at meal time

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

Long acting insulin (basal insulin) includes

A

insulin glargine (Lantus)
insulin detemir (Levemir)

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

Insulin Glargine =
peak =
onset =
effective duration =
dosing =

A

long acting
no peak - flat prolonged effect
onset - 1-1.5 hours w/ max effect after 4 hours
effective duration - up to 24 hours
dosing - daily

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

Insulin Detemir =
onset =
peak =
effective duration =
dosing =

A

long acting
peak is 6-8 hours
effective duration up to 24 hours
dosing - twice daily

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

Intermediate acting insulin includes

A

NPH - neutral protamine Hagedorn

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

NPH - Neutral protamine Hagedorn =
administration =
onset =
peak =
duration of action =

A

intermediate acting insulin
subQ only (therefor not used for DKA)
onset 4-12 hours
peak 5.5 hours
duration of action 18-24 hours

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

Short acting insulin includes

A

regular (humulin, novolin)

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

Regular - Humulin, Novolin =
onset =
peak =
effective duration =
administration =

A

short acting insulin
onset - 30 min -5 hours
peak - 2-3 hours
effective duration - 8-12 hours
subQ and IV options

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Rapid acting insulin includes:

A

insulin lispro (Humalog)
insulin aspart (Novolog)
insulin glulisine (Apidra)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Insulin Lispro (Humalog) =
onset =
peak =
effective duration =

A

rapid acting insulin
onset - 10-15 min
peak - 30-90 min
effective duration - 3-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Insulin Aspart (Novolog)=
onset =
peak =
effective duration =

A

rapid acting insulin
onset = 15-20 min
peak > 1-2 hours
effective duration - 3-5 hours

27
Q

Insulin Glulisine (Apidra) =
onset =
peak =
effective duration =

A

rapid acting insulin
onset - 20-30 min
peak - 55 min
effective duration - 1-2.5 hours

28
Q

long acting insulin is mostly used for

A

replacing normal bodies insulin, what their metabolic need is

29
Q

rapid, short or intermediate acting insulin is used for

A

controlling sugars that we obtain when eating

30
Q

Typical dosing =

A

0.1 - 1.2 units/ kg/ day
Type 2 may require higher dosing due to resistance

31
Q

Adverse reactions to insulin

A

wt gain
somogyi effect
dawn phenomenon
hypoglycemia

32
Q

What is the somogyi effect?

A

If the blood sugar level drops too low in the early morning hours, hormones such as growth hormone, cortisol and catecholamines are released - these help reverse the low blood sugar level but may led to blood sugar levels that are higher than normal in the morning

33
Q

What is the Dawn Phenomenon?

A

a normal rise in blood sugar as a person’s body prepares to wake up
in the early morning hours, hormones () cause the liver to release large amounts of sugar into the bloodstream - for most people the body produces insulin to control the rise in blood sugar - if the body doesn’t produce enough insulin blood sugar levels can rise, causing high blood sugar in the morning before eating

34
Q

GLP-1 Agonists/ incretin Mimetics include

A

Exentidine
Liraglutide
Dulaglutide
All injectables - no oral form

35
Q

GLP-1 Agonists/ Incretin Mimetics MOA

A

promotes insulin secretion
enhances satiety
decreases postprandial glucagon secretion
promotes beta cell proliferation

36
Q

Oral Agents that primarily stimulate insulin secretion include

A

Sulfonylureas
Meglitinides

37
Q

Oral agents that increase insulin sensitivity include

A

Biguanides (metformin)
Thiazolidinediones (“glitasones”)

38
Q

Other oral agents

A

alpha-glucosidase inhibitors
dipeptidyl peptidase-4 inhibitors
sodium-glucose co-transporter 2 inhibitors

39
Q

Sulfonylureas MOA

A

stimulates release of insulin from the pancreatic beta cells
reduces production of hepatic glucose
increases sensitivity of insulin in the periphery

40
Q

Adverse reactions of Sulfonylureas

A

wt gain
hyperinsulinemia
hypoglycemia

41
Q

contraindications of Sulfonylureas

A

sulfa allergy
pregnancy

42
Q

Sulfonylureas: Use caution in

A

hepatic insufficiency
renal insufficiency
geriatric patients

43
Q

Sulfonylureas include

A

first generation: tolbutamide, Chlorpropamide
second generation: glyburide, glipizide, glimepiride

44
Q

Meglitinides “Glinides” include

A

repaglinide
nateglinide

45
Q

Meglitinides “Glinides” MOA

A

release insulin from the beta cells of the pancreas
rapid onset and short duration - chief difference from sulfonylureas

46
Q

Adverse reactions of Meglitinides “Glinides”

A

hypoglycemia
use caution with renal and hepatic insufficiency (Repaglinide)

47
Q

Biguanides: Metformin MOA

A

Decreases hepatic gluconeogenesis
Increases insulin sensitivity (enhances peripheral utilization)

48
Q

Metformin adverse reactions

A

abdominal discomfort

49
Q

Metformin contraindications

A

hepatic and renal impairment
DKA
AMI
CHF
IV contrast
Alcoholism
used with caution in the elderly

50
Q

Thiazolidinediones (glitazones or TZDs)

A

Rosiglitazone
Pioglitazone

51
Q

Thiazolidinediones (glitazones or TZDs) MOA

A

Increases insulin sensitivity - by activation of ppar-gamma receptors (regulates transcription of a number of insulin responsive genes)
enhances peripheral uptake of glucose
reduces hepatic glucose production

52
Q

Thiazolidinediones (glitazones or TZDs) contraindications

A

heart failure

53
Q

Thiazolidinediones (glitazones or TZDs) adverse reactions

A

wt gain
osteopenia
HA
Anemia
use with caution in patients with hepatic impairment

54
Q

Alpha-Glucosidase Inhibitors include

A

acarbose
miglitol

55
Q

Oral medications are only used for ______ DM

A

type 2

56
Q

Alpha-Glucosidase Inhibitors MOA

A

inhibitor of alpha-glucosidase in intestinal brush border
delay digestion of carbohydrates -> lower postprandial glucose levels

57
Q

Alpha-Glucosidase Inhibitors adverse reactions

A

GI intolerance

58
Q

Alpha-Glucosidase Inhibitors contraindications

A

IBD
colon CA or other conditions which predispose to obstruction or perforation

59
Q

Dipeptidyl peptidase-4 inhibitors include

A

Sitagliptin (Januvia)
Saxagliptin (Onglyza)

60
Q

Dipeptidyl peptidase-4 inhibitors MOA

A

inhibits the enzyme DPP-4 –> DPP-4 inactivates GLP-1 –> increase release of insulin and decrease release of glucagon

61
Q

Sodium- glucose co-transporter 2 inhibitors include

A

Canagliflozin
Dapagliflozin
Empagliflozin (Jardiance)

62
Q

Sodium- glucose co-transporter 2 inhibitors MOA

A

the SGLT2 reabsorbs filtered glucose in the tubular lumen of the kidney; therefore, by inhibiting this cotransporter, there will be decreased reabsorption of glucose
increased urinary excretion of glucose -> decreased serum glucose

63
Q

Sodium- glucose co-transporter 2 inhibitors adverse reactions

A

can cause vaginal candidiasis
UTI

Endocrinology (5 decks)

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