Digestion Flashcards

1
Q

Why is the mouth acidic?

A

Anaerobic environment => carb turned into lactic acid => pH < 5.5 => tooth decay/demineralization => cavities

Higher pH => enzymes non functional

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2
Q

2 major + 3 minor digestive enzymes found in saliva?

A

Major:
Alpha-amylase
Lingual lipase

Minor:
Superoxide dismutase
Glutathione transferase
Immunoglobulin A

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3
Q

Function of alpha amylase?

A

Initiates digestion of amylose/amylopectin chains => maltotriose, maltose, amylose, glucose, oligosaccharides

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4
Q

Function of lingual lipase?

A

Initiates hydrolysis of long chain TGs into diacylglycerol and free FAs (pH~4)

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5
Q

Function of superoxide dismutase?

A

Reduces highly reactive superoxide holecules

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6
Q

Function of Glutathione transferase?

A

Detoxification

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7
Q

Function of IgA?

A

Antibacterial

Main Ig in saliva => immunity

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8
Q

What is meth mouth?

A

Meth acts on alpha-adrenergic receptors => reduces saliva => counteract buffering of acids => BEAUTIFUL tooth decay

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9
Q

pH of stomach? Regulated how?

A

Enzymes are activated by pH~1-2

Regulated by ANS and hormones controlled by Vagus Nerve

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10
Q

Cell types in gastric mucosa of stomach + secretory product

A

Mucous surface cells+ Mucous (neck) or foveolar cells => producing mucous HCO3, H2O => protective barrier from corrosive gastric acid and digestive enzymes

Oxyntic (parietal) cells => H/Cl/IF/H2O

Peptic (chief) cells => pepsinogen, H2O

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11
Q

All secretory mucosa cells therefore produce?

A

Water

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12
Q

Secretions of parietal cells are stimulated by?

A

Located in fundus:

Histamine via H2 receptor

Gastrin => via CCK2/gastrin receptor => histamine

Vagus nerve => via ACh/M3

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13
Q

Chief (zygomenic/peptic) cells produce? Regulated by?

A

Pepsinogen = proenzyme of pepsin => cleaves peptide bonds at hydrophobic/aromatic AAs such as phe,trp,tyr

Stimulated by: vagus nerve, acidic conditions, hormones gastrin/secretin

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14
Q

Function and location of Enterochromaffin-like and G cells?

A

Enteroch.. ELC:
Found in gastric glands => stimulated by gastrin, pituitary adenyl cyclase-activating peptide => inhibited by somatostatin

G cells:
Found in pyloric antrum => secretes gastrin => increased by vagus nerve activity or large amounts of AAs in stomach

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15
Q

Function of PGE2?

A

Decreases parietal cell secretion of gastric acid

Increases mucus production

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16
Q

What is misoprostol? What is it used for?

A

= synthetically produced PGE1 => prevent gastric ulcers (short term care)

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17
Q

Where in the GI is gastrin produced?

A

Antrum of stomach until end of jejunum

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18
Q

Where in the GI is CCK and Secretin produced?

A

Beginning of Duodenum until end of Ileum

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19
Q

Where in the GI is GIP and Motilin produced?

A

Beginning of Duodenum until end of Jejunum

20
Q

5 major digestive hormones?

A

Cholecystokinin CCK

Enteroglucagon

Gastrin

GIP (gastric inhibitory peptide)

Motilin

Secretin

Somatostatin

VIP (vasoactive intestinal polypeptide)

21
Q

Function of Gastrin (this is a Q on the exam for sure)?

A

Inhibited by pH<4 and somatostatin
Stimulates HCl, IF, pepsinogen, rening, histamine

=> Increases smooth muscle contraction of stomach

22
Q

Which hormones promote smooth muscle relaxation aka decreased smooth muscle contraction?

A

GIP

VIP

23
Q

Which hormones inhibit stomach emptying and HCl?

A

CCK
Enteroglucagon
Somatostatin

24
Q

What is Achlorhydria and Hypochlorhydria?

A

=> production of HCl in stomach is absent/low => due to destruction/damage of parietal cells

=> increase in pH, bacterial growth, diarrhea
=> decrease of essential ion absorption

25
Q

What is GERD?

A

Gastroesophageal Reflux Disease

=> basically when the upper sphincter in the stomach is absent/damaged => acid exposure to lower esophagus => cancer

Treatment: H2 blockers => block histamine action on parietal cells or Proton pump inhibitors => same result => lower pH

26
Q

One of the liver functions is production of coagulation factors. What do they do?

A

=> clot formation/breakdown

Coagulation factors:
I = fibrinogen
II = prothrombin
V, VII, IX-XI

27
Q

Function of bile?

A

Fat emulsification

28
Q

How is hemoglobin degraded to bilirubin?

A

Spleen: heme+NADPH -> biliverdin + Fe3+
=> biliverdin + NADH -> conjugated bilirubin

Blood: transport by albumin

Liver: conjugated with glucoronic acid = make soluble => excreted in bile => small intestine

Intestine: bacteria => convert to urobilinogen/stercobilin => partly reabsorbed/excreted

29
Q

How is bilirubin measured/test?

A

Reported as conjugated: azo dye reacts directly with conjugated bilirubins => red/violet color

30
Q

Main points of detoxification process in liver? (Very likely on the exam)

A

Start with less polar molecule => phase I

Phase I: (increase polar nature, uses cytochrome p450)

1) oxidation => lipophilic => electrophile (some oxygen ring/double bond)
2) reduction => nucleophile (some special group attached)

Phase II: (permanently inactivate toxin/drug)

1) glutathione conjugation leading to R-SG (hydrophilic)
2) sulfation/acetylaction/glucuronidation

31
Q

Detoxification of alcohol?

A

Ethanol –alcohol dehydrogenase–> acetaldehyde (toxic) –acetaldehyde dehydrogenase–>acetic acid (vinegar)

First reaction is faster than second.

32
Q

Which organ is the only one capable of disposing cholesterol?

A

Liver => bile salts or distributed as LDL

33
Q

How do u get fat?

A

TGs are packed with cholesterol into VLDL => secreted into blood to deliver FAs to adipose cells

34
Q

What is the role of the gallbladder?

A

Stores/concentrates bile produced by liver => released into duodenum in response to CCK secretion

35
Q

What is bile?

A

Contains water, ions, lipids, proteins, bile acids and

Glycine- and taurine-conjugated bile acids => enables lipid degrading enzymes to act and promotes absorption of fats/fat soluble Vit

36
Q

What does CCK do?

A

Induces bile expression from gall bladder

Stimulates release of pancreatic digestive enymes: trypsin, chymotripsin, pancreatic lipase/amylase to aid fat/protein digestion

37
Q

Five F’s of cholesterol gallstone formation?

A

Cholesterol gallstones = type of cholelithiasis

Female
Forty
Fertile (had many pregnancies)
Fat
Fair

Think of that woman with the 19 kids and counting. Ridiculous

38
Q

2 functions/cell types of pancreas?

A

Exocrine function => release enzymes => proteases etc

Endocrine function => release hormones, under ANS control

=> alpha cell => sympathetic/adrenergic innervation => glucagon
=> beta cell => insulin, amylin
=> both: parasympathetic/ muscarinic innervation

39
Q

Other two cell endocrine pancreatic cell types and hormone associated with it?

A

Delta cells => somatostatin

Epsilon => ghrelin “hunger hormone”

40
Q

Small intestine portion, elongation factor, and absorbed molecule?

A

Elongated by x500 due to folds

Duodenum: Fe/Ca/Carb/Fat/Protein

Jejunum: Carb/Fat/Protein

Ileum: Fat/Protein/Bile salts/Vit B12

41
Q

Functions of ileum?

A

Provides continued digestion and absorption and immunoprotection

Absorption of Vit B12/IF/bile salts

42
Q

What is Pernicious Anemia?

A

Decrease in RBC count => decrease in absorbed B12 due to lack of IF

Cause: immune attack against IF/cells producing it

43
Q

Functions of large intestine by location?

A

Ascending: absorption of H2O/ions

Transverse: bacterial fermentation of nonabsorbed nutrients

Descending: storage of waste/indigestible stuff

44
Q

Importance of gut flora?

A
Bacteria 
digest/ferment carbs/proteins, 
aid absorption of lipids/Ca/Mg/Fe, 
augment levels of vit K/biotin=B7
Produces modified/secondary bile salts
Important for growth of intestinal lymph tissue 
Helps eliminate ingested carcinogens
45
Q

Problem with antibiotics and Clostridium difficile?

A

Barrier effect destroyed by antibiotics
=> C. Difficile releases toxins causing chronic diarrhea/bloating etc => pseudomembraneous colitis

Diagnosed via cell culture (cytotoxins)/EIA/PCR

Treatment: vancomycin, fecal transplant aka ingesting somebody else’s doodoo :o)