Upper GI Diseases Flashcards

1
Q

What are the 3 parts of the stomach?

A

Fundus
Corpus (Body)
Antrum

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2
Q

Mucous cells produce….

Parietal cells produce….

Chief cells produce….

A

Mucus

HCl and IF

Pepsinogen

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3
Q

What stimulates mucous cells?

What stimulates chief cells?

A

Mechanical- chew and Bolus in stomach

Acetylcholine and gastrin

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4
Q

What stimulates parietal cells?

A

Acetylcholine, gastrin, and histamine

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5
Q

What do G cells produce?

What do D cells produce?

What do ECL cells produce?

A

Gastrin
Somatostatin
Histamine

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6
Q

What stimulates D cells?
What stimulates ECL cells?
What stimulates G cells?

A

Acid
Acetylcholine and gastrin
Protein products and acetylcholine

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7
Q

What 2 neurotransmitters are GI motility excitatory?

A

Acetylcholine and serotonin

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8
Q

What peptides are inhibitory to the GI?

A

GIP, somatostatin, vasoactive intestinal peptide

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9
Q

What does pepsinogen become?

A

It is inactive form of pepsin. Turns to pepsin when mixed with HCl. Splits and digests proteins

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10
Q

What affect does Prilosec have?

A

It’s an anti-secretory, so decreases HCl from parietal cells. Less HCl means less IF and no binding to B12 so could lead to B12 deficiency.

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11
Q

Which cells do Ach stimulate?

A

Parietal, chief, ECL, G-cells

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12
Q

Which cells does gastrin stimulate?

A

Chief, parietal, and ECL

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13
Q

What happens to somatostatin levels when pH decreases?

A

This means more acidic GI which means digestion needs to quit. Somatostatin is inhibitory so
More acid means more somatostatin (D cells)

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14
Q

3 phases of secretions to meal response:

A

Cephalic: HCl and pepsinogen when taste, smell, and see food.
Gastric: food in stomach stretches vagus nerve
Intestinal: stop secretions once pH is less than 2

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15
Q

What is UIE?

What is MALT?

A

Upper GI Endoscopy

Mucosa Associated Lymphoid Tissue (increased risk with PUD)

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16
Q

What is Peptic Ulcer Disease?

A

PUD

Ulcers in gastric mucosa of Antrum or duodenum that penetrate sub mucosa (deep)

17
Q

What are C/C and #1 cause of PUD?

A

Epigastric pain that is sensitive but not specific to PUD.

80-90% ulcers from Helicobacter pylori bacteria (2/3 of world carries it)

18
Q

Where are H pylori and why are they dangerous?

A

Live under mucus layer in stomach
Break down urea to
Ammonia so decrease acidity of stomach and survive longer.
They produce proteins that damage mucus cells to attract lymphocytes and inflame the area.

19
Q

Why can excessive ASA and NSAIDS use cause PUD? Why smoking?

A

Inhibits COX2 which makes pro and anti inflammatory chemicals. Less anti and more pro.
Less bicarbonate secretion so more acidic, less anti acid function and lowers LES pressure.

20
Q

What is primary PUD Tx?

A

7-14 days of 2 antibiotics with bismuth and an PPI.

Hard to stick with b/c abdominal pain and N/V.

21
Q

What meds help decrease acidic environment to help PUD healing?

A

Anti acids (tums, Mylanta)
Histamine receptor blockers (cimetidine, ranitidine or Zantac)
Proton pump inhibitor (omeprazole, -azoles, nexium)
Stomach lining protector (pepto bismol)

22
Q

What 3 things should be managed nutritionally for PUD patients?

A

Electrolytes from diarrhea, Ca and Vit D status and bone Fx risk, B12 deficiency from PPI.

23
Q

What foods increase GI acid?

A

Black and red pepper
Caffeine
Coffee with or without caffeine
EtOH

24
Q

What is Melena?

What is atrophic gastritis?

A

Black, tarry stools from bleeding in stomach.

Less parietal cell function so possible B12 deficiency (HCl, IF)–can happen from LT Nexium use

25
Q

What esophageal problem causes GERD and heartburn?

A

Decreased esophagus integrity. This means LES lets esophagus pressure dip lower than stomach pressure. Regurgitate.

26
Q

What is GERD?

A

Backward flow of gastric contents into esophagus from transient abd pressure or relaxed LES.

27
Q

What can cause GERD?

A

High stomach pressure. High gastrin, estrogen or progesterone secretions. Smoking (weaker LES). Meds like morphine. Obesity.

28
Q

What foods lower LES pressure?

A

Spearmint, peppermint, chocolate, alcohol, caffeine, chocolate, high fat foods.

29
Q

What are GERD s/s?

A

Increased saliva, dysphagia, belching, neck/head/jaw pain, heartburn

30
Q

What is Barrett’s esophagus?

A

Metaplasia, epithelial cells of esophageal mucosa are changed. Squamous cells become columnar cells. Only seen with biopsy.

31
Q

2 MNT Goals for GERD?

A

Increase LES strength (no smoking, less high fat food, lose wt, limit EtOH/caffeine/mint)
Decrease vol and frequency of reflux (sm meals, lose wt, no fluids with meals, increase fiber-constipation=more abd pressure)

32
Q

2 more MNT goals for GERD?

A

Less irritation to inflamed esophagus (no citrus, tomato, spicy, fizzy beverages)
Increase esophageal clearing time (don’t lay after eating, stop eating 2-3 hr before bed, elevate bed head, loose clothes)

33
Q

What are med Tx for GERD?

A

Anti acids (diarrhea, constipation), H2 blockers (stop after 2 wks of use), PPI for short term, Prokinetics to speed gastric motility and emptying (reglan)

34
Q

What is the surgical Tx for GERD?

A

Nissen fundoplication

Fundus of stomach is wrapped around lower esophagus to strengthen and support LES, prevents reflux.
Done laparoscopically

35
Q

What is gastroparesis and S/S?

A

Delayed emptying of stomach. N/V, satiety too soon, bloating and reflux. Common in young adults and DM pts (neuropathy)

36
Q

What do fat and fiber do to gastric emptying?

A

Slow it down so want to eat

37
Q

Gastroparesis MNT tips:

A

No bedtime snack, tender meats with crockpot, liquid/purée diet, limit quantities of cheese at once, no EtOH or fizzy bev, no meal replacement bars, walk after meals