Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endocrinology > Endo-Pancreas > Flashcards

Endo-Pancreas Flashcards

1
Q

What is the primary function of insulin?

A

Insulin lowers blood glucose levels by promoting glucose uptake and storage.

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

What does glucagon do?

A

Glucagon increases blood glucose levels by promoting glycogenolysis and gluconeogenesis.

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

What are the two types of glucose uptake?

A
  • Insulin-dependent
  • Insulin-independent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is amylin’s role in glycemic regulation?

A

Amylin slows gastric emptying and promotes satiety.

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

What is glycogenolysis?

A

The process of breakdown of glycogen to glucose.

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

Which hormone is considered the primary stress hormone?

A

Cortisol

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

How does cortisol affect insulin response?

A

Cortisol inhibits the response to insulin and increases blood glucose.

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

What is the role of growth hormone in glucose metabolism?

A

Growth hormone increases glucose uptake by muscle and decreases blood glucose.

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

What is C-peptide and why is it important?

A

C-peptide is a marker of insulin production and is measured to assess β cell function.

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

What is the half-life of insulin?

A

The half-life of insulin is approximately 6 minutes.

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

What stimulates insulin secretion?

A
  • Increased blood glucose
  • Increased blood fatty acids
  • Increased blood amino acids
  • Gastric inhibitory peptide (GIP)
  • Vagal stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fill in the blank: The insulin receptor is composed of two subunits: ______ and ______.

A

[α] and [β]

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

What is the primary mechanism by which insulin decreases blood glucose concentration?

A
  • Increases glucose uptake
  • Promotes glycogenesis
  • Decreases gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the GLUT transporters and their roles?

A
  • GLUT-1: RBCs, brain, cornea
  • GLUT-2: beta cells, liver, small intestines, kidney
  • GLUT-3: brain, placenta
  • GLUT-4: skeletal muscle, adipose tissue
  • GLUT-5: spermatocytes, GI tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or False: Glucagon is the mirror image hormone of insulin.

A

True

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

What is the structure of glucagon?

A

Glucagon is a peptide hormone composed of 29 amino acids.

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

What triggers the release of glucagon?

A
  • Decreased blood glucose
  • Fasting state
  • Increased ingestion of protein
  • Physical exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the second messenger for glucagon?

A

cAMP

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

What is the function of somatostatin?

A

Somatostatin suppresses both insulin and glucagon secretion.

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

How does somatostatin inhibit insulin secretion?

A

It blocks voltage-gated calcium channels, reducing Ca++ influx.

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

What role does somatostatin play in paracrine interactions within the islets?

A

Insulin inhibits glucagon release, while glucagon stimulates insulin release.

22
Q

What is gluconeogenesis?

A

The synthesis of glucose from non-carbohydrate sources.

23
Q

What is glycogenesis?

A

The formation of glycogen from glucose.

24
Q

What is glycolysis?

A

The breakdown of glucose into pyruvate.

25
What is lipolysis?
The breakdown of triglycerides into fatty acids and glycerol.
26
What is ketogenesis?
The production of ketone bodies from fatty acids.
27
What is the role of glucagon in urea production?
Glucagon increases urea production by incorporating amino groups from amino acids.
28
Compare and contrast the pathogenesis of Type I & Type II DM induced hyperglycemia
Type I DM: high blood sugar due to impaired exocrine function of the pancreas glucagon action unopposed-tissues continue to produce glucose Type II DM: high blood sugar due to insulin desensitization The Pancreas produces insulin put tissues remain unresponsive
29
what does hemoglobin A1c measure?
Fraction of charged separated hemoglobin-hemoglobin bound to negatively charged glucose molecules
30
T or F: once glucose is bound to hemoglobin, RBCs remain glycated for the rest of their life span
true
31
what conditions can cause false positives of an oral glucose tolerance test for T1DM
malnutrition emotional stress: activation of HPA axis exogenous steroids: increase insulin resistance
32
why does T1DM cause polyuria?
glycosuria leads to osmotic diuresis and hypovolemia
33
Describe how T1DM causes polydipsia
polydipsia: increased sensation of thirst hyperglycemia pulls water into intravascular spaces leading to a hyperosmolar state which the hypothalamus perceives as dehydration even though tht pt. is drinking more water
34
dizziness and weakness is assoc. with what for T1DM
decreased plasma volume and hypokalemia to a smaller extent
35
T or F: glucose sensitive monitors measure capillary glucose levels?
False they measure interstitial glucose only
36
T or F: the goal of T1DM management is to normalize post-prandial blood glucose levels.
False the goal is to decrease Hgb A1c back down the normal range w/o significant hypoglycemia
37
T of F: fluctuations of blood glucose are more extreme for T1DM compared to T2DM.
True
38
hypoglycemia triggers the release of what NT?
epinephrine
39
Define Diabulemia.
intentionally skipping insulin injections to lose weight
40
A pt. w/ suspected T1DM should also be screened for these additional diseases?
Thyroid disease-TSH celiac disease
41
what is the biggest contributor of insulin resistance for T2DM?
OBESITY
42
T or F: lifestyle changes to reduce A1c is the most effective treatment for T2DM
True
43
T or F: microvascular complications are assoc. w/ insulin resistance.
False hyperglycemia contributes to microvascular complications while insulin resistance contributes to macrovascular complications
44
How long after a Dx of T2DM should the pt. be screened for albuminuria
5 yrs.
45
describe the pathogenesis of microvascular complications assoc. w/ DM.
glycosylation of blood vessels leads to increased vessel wall thickening and endothelial damage; this promotes intravascular coagulation leading to subsequent ischemia, microaneurysms, & neovascularization (more suspectable to hemorrhages)
46
what are common neuropathies assoc. w/ DM
gastroparesis, erectile dysfunction, cystopahties (eg: urinary incontinence, failure to void)
47
unlike T2DM, MODY is not assoc. w/ metabolic syndrome and occurs in adolsecent. what is the pahtogenesis
autosomal dominant; single gene defect in glucose-induced insulin release
48
what is LADA
AKA Diabetes 1.5 latent autoimmune diabetes that occurs later in adulthood
49
What are GLP-1 receptor agonists used for
treatment of obesity as a chronic disease
50
what is pre-diabetes defined as?
Hgb A1c 5.7-6.6% fasting BG: 100-125 GTT: 140-199
51
what is the pathogenesis of gestational diabetes
during pregnancy, pancreatic beta cells proliferate to hyperplastic proportions resulting in much higher fasting and increased insulin levels

Endocrinology (11 decks)

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