Questions for midterm 3 Flashcards

1
Q

4 things present in the gastric secretion and where they come from

A

Mucus (goblet cells)
HCl (parietal cells - same as intrinsic factor)
Pepsin (chief cells)
Gastric lipase (chief cells)

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

3 ways the gastric epithelium protects itself from stomach acid

A

Mucus and bicarbonate layer
Tight junctions to prevent the penetration of HCl
Luminal membrane is impermeable to H+ ions

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

4 mucosal protective mechanisms

A

Mucus
Bicarbonate
Prostaglandins (mucosal blood flow)
Rapid turnover of mucosa

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

3 things H pylori secretes that can damage the epithelium

A

Urease (it neutralizes stomach acid and produces ammonia as a damaging byproduct)
Enzymes
Exotoxins

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

3 effects of H pylori on the epithelium

A

Mucosal damage
Inflammation
Mucosal cell death

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

3 ways H pylori is transmitted

A

Person to person
Exposure to gastric secretions
Water borne

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

6 ways to test for H pylori

A
Endoscopy and a biopsy
Culture
Breath test
Urease test
ELISA
Rapid test for H pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 ways to treat H pylori

A

Antibiotics

Proton pump inhibitors

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

What are 2 helpful actions of prostaglandins

A

Support platelets (helps the blood clotting function)
Protect the stomach (protects lining from effects of acid)
From COX 1

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

3 harmful effects of prostaglandins

A

Inflammation
Pain
Fever

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

Which COX pathway do you want to inhibit?

A

COX 2

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

3 functions of aspirin

A

Inhibits blood clotting
Prevents stroke
Prevents CV attack

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

Celecoxib

A

Selective COX 2 inhibitor

Good because it causes less bleeding and fewer ulcers

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

4 harmful effects of ASA and non-selective NSAIDS

A

Disrupt the mucosal barrier
Reduce bicarbonate production
Directly damage the gastric mucosal epithelium
Reduce the production of prostaglandins

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

Insulin

A

Released from pancreatic beta cells when there are high levels of glucose in the blood
Acts on the liver, adipose, and muscle to increase glucose uptake and storage, reduce gluconeogenesis, glycogenolysis, and glucose release

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

Glucagon

A

Release from pancreatic alpha cells when blood glucose levels are low
Acts on the liver to increase gluconeogenesis, glycogenolysis, and reduce glucose storage

17
Q

5 hormones from pancreatic islets and the cells they are released from

A
Insulin (beta)
Glucagon (alpha)
Somatostatin (delta)
Pancreatic polypeptide (PP cells)
Ghrelin (epsilon cells)
18
Q

Why do diabetic patients have increased appetite?

A

Her body is in starvation mode
No signals from ghrelin and no negative feedback from leptin
But not helping because she cannot use the glucose

19
Q

Incretins

A

Hormones from the gut that prepare the beta cell to secrete insulin

20
Q

Incretin effect in T2D

A

Lost

21
Q

GLP-1

A

From proglucagon, cleaved in intestinal L cells to GLP-1
Secreted from small intestine
Causes proliferation of beta cell and the release of insulin in response to glucose
Suppresses glucagon secretion
Inhibits gastric emptying/secretion/pancreatic secretion
Decreases food intake and body weight
Deficient in T2D

22
Q

GIP

A

Secreted from K cells in the first part of the small intestine
Enhances the release of insulin in response to infusions of glucose
No effect on satiety or body weight
Does not inhibit glucagon
Normal levels but decreased responsiveness in T2D

23
Q

GLP-2 function

A

Increases the size of the villi

24
Q

3 functions of GLP-1 in the beta cells

A

Increases insulin gene transcription
Leads to beta cell proliferation
Decreased beta cell apoptosis

25
Q

Why was GLP-1 approved to manage diabetes?

A

Glucose dependent insulin release (no risk for hypoglycemia)
Lowers blood glucose levels in normal people and those with T2D
Can help product enough insulin to overcome the resistance (to a point)

26
Q

Why is high glucose toxic for the beta cells?

A

Glucotoxicity

Lipotoxicity

27
Q

Is GLUT2 or GLUT4 insulin dependent?

A

GLUT4

Found in the muscle and adipose (need insulin to take glucose into cells)