Brainscape's Knowledge GenomeTM

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


See full index

Anatomy & Physiology 208 > Digestion II Study Guide > Flashcards

Digestion II Study Guide Flashcards

1
Q

term for a bolus of food after it is undergoing digestion in the stomach

A

chyme

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

how tunics are modified in stomach

A
  • Muscularis - added internal, oblique layer to allow increased mixing and churning – more intense mechanical breakdown
  • Mucosa - contains simple columnar epithelium made entirely of mucous cells – produces a cloudy, protective double layer of alkaline mucus
  • Dotted with millions of deep gastric pits
  • Gastric pits lead into the gastric glands responsible for producing gastric juice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

secretory cells in gastric glands

A

Mucus neck cells, parietal cells, chief cells, Eneteroendocrine cells

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

mucus neck cells

A

produce thin, soluble mucus

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

Parietal cells

A

produce HCL (pH 1.5-3.5, required to activate pepsin (breakdown proteins in stomach?)) and secrete intrinsic factor (required to absorb B12)

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

Chief cells

A

secrete pepsinogen (inactive pepsin) and lipases

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

Eneteroendocrine cells

A

secrete chemical messengers into lamina propria as well as gastrin

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

Mucosal barrier

A

produced to protect the stomach
- A thick coating of bicarbonate-rich mucus
- Tight junctions between epithelial cells
- Quick replacement of damaged mucosal cells by stem cells

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

Gastritis

A

Inflammation of the stomach in response to breaches of the mucosal barrier

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

peptic/gastric ulcers

A
  • Erosions of the stomach-wall – cause gnawing, epigastric pain
  • Pain typically appears 1-3 hours after eating and resolves with eating again, ulcers are linked to peritonitis and h. Pylori; a type of acid resistant bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

different functions completed in the stomach

A

Propulsion
Mechanical breakdown
Digestion
Absorption
Secretion of intrinsic factor

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

propulsion

A

peristalsis

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

Mechanical breakdown

A

churning

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

Absorption

A

only lipid soluble substances – alcohol and aspirin

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

Digestion

A

breakdown of proteins by HCl and pepsin (rennin in infants)

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

Secretion of intrinsic factor

A

essential for B12 absorption and maturation of RBCs

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

Gastrin

A

hormonal mechanism of regulation of gastric secretion
- Stimulates secretion of hcl by the stomach
- Stimulates secretion of gastrin antagonists by the SI

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

branch of the ANS that increases gastric secretions

A

parasympathetic

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

3 phases of gastric secretions

A

cephalic/reflex phase, gastric phase, intestinal phase

19
Q

cephalic/reflex phase

A

triggered by smell, taste, and sight; act via the vagus nerve

20
Q

Gastric phase

A

triggered by stretch receptors and/or chemical stimuli – partially digested protein, caffeine, rising pH
- Activates G cells (enteroendocrine cells) to secrete gastrin
- Gastrin initiates release of HCl
- Low pH (between meals) or firing of the SNS will inhibit gastrin

21
Q

Intestinal phase

A

Partially digested food enters the SI and triggers the release of intestinal gastrin
- Distension of the SI and or the presence of acidic, fatty, or hypertonic chyme will inhibit gastric secretions – protects the SI from excess acidity and being overwhelmed * enterogastric reflex and enterogastrones

22
Q

Enterogastric reflex

A

short reflexes by the enteric nervous system and long reflexes by the sympathetic and vagus nerves inhibit acid secretion

23
Q

Enterogastrones

A

duodenal enteroendocrine cells release secretin or cholecystokinin (CCK) to inhibit gastric secretions

24
Q

digestive function of liver

A

Production of bile
About 900ml per day
(additional functions: processed bloodborne nutrients, stores fat-soluble vitamins, and performs detoxification)

25
Q

bile

A

fat emulsifier

26
Q

Livers functional unit

A

liver lobules (hexagonal) composed of plates of hepatocytes
- Central vein: located in the longitudinal axis

27
Q

Hepatocyte

A

specialized liver cells that filter and process nutrient-rich blood
- Have increased numbers of rER, sER, golgi complexes, peroxisomes, and mitochondria

28
Q

Portal triad

A

located in each corner of the lobule
Hepatic artery
Hepatic portal vein
Bile duct

29
Q

Hepatic artery

A

supplies oxygen to the liver

30
Q

hepatic portal vein

A

brings nutrient rich blood from the intestines

31
Q

Bile duct

A

receives bile from the bile canaliculi

32
Q

function of hepatic macrophages

A

Exist in the liver sinusoids to remove debris and old RBCs

33
Q

portion of the SI that reabsorbs bile salts for recycling

A

ileum during enterohepatic circulation

34
Q

Bile salts

A

cholesterol derivatives that function in fat emulsification/absorption

35
Q

Bilirubin

A

yellow pigment formed from heme during breakdown of RBCs
- Metabolized by bacteria in the SI to stercobilin which gives feces a brown color

36
Q

pathway for bile moving out of the liver

A
  • Leaves liver via r and l hepatic ducts
  • R and l hepatic ducts fuse into common hepatic duct
  • Common hepatic ducts joins with cystic duct from gallbladder and forms the common bile duct
37
Q

Hepatitis

A

inflammation of the liver
- Typically, viral infection, but can be caused by alcohol, drug toxicity, or wild mushrooms
- Six viruses: a-f; 2 transmitted through food, remainder via blood

38
Q

Cirrhosis

A

progressive, chronic inflammation from hepatitis or alcoholism
- Liver activity is depressed
- Liver becomes fatty and fibrous
- Portal hypertension: flow of blood through the liver is obstructed

39
Q

gall bladder

A

Store and concentrate bile
- Muscular contractions release bile via the cystic duct – flows into the common bile duct

40
Q

gallstone

A
  • Caused by excess cholesterol or too few biles salts (cholesterol crystallized into stones)
  • Can obstruct the flow of bile from the gallbladder (painful when the gallbladder contracts against sharp crystals)
41
Q

Obstructive jaundice

A

blockage causes bile salts and pigments to build up in blood – results in yellowed skin

42
Q

Exocrine function of pancreas

A

production of pancreatic juice

43
Q

endocrine function of pancreas

A

secretion of insulin and glucagon via the pancreatic islet cells

44
Q

pancreatic juice

A

contains enzymes needed to break down all categories of foodstuffs (multiple ducts secrete into the duodenum via the main pancreatic duct)
- Contains electrolytes (primarily HCO3-)
- Watery, alkaline solution (pH 8) used to neutralize acidic chyme from stomach

45
Q

4 macromolecules digested by the digestive tract and the enzyme responsible for its digestion

A

Proteases – for proteins; secreted in inactive form to prevent self digestion
Amylase – for carbohydrates
Lipase – for lipids
Nucleases – for nucleic acids

Anatomy & Physiology 208 (35 decks)

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