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Step 1 (Let's Do This)! > GI > Flashcards

GI Flashcards

1
Q

MCC cause of ulcers, other than H. pylori?

A

NSAIDs

Inhibit Prostaglandin. Inhibit secretion of Mucin and Bicarb

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2
Q

What is the effect of insulin on glucose reabsorbtion in Small Intestine?

A

None! Insulin has no effect on secondary active transport. Only effects transport in adipose and resting muscles.
Glucose absorbed w/ Na into cell, and then transported out of cell into blood. However, Na reabsorbtion is energy dependent, so Glucose is cosnidered secondary ACTIVE transport.

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3
Q

What is the only substance in Small intestine absorbed independently from Na?

A

Fructose

Lipids

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4
Q

The two main causes of Metabolic Acidosis with normal anion gap are?

A

Diarrhea
Renal tubular acidosis

Both have high chloride

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5
Q

What is Invasive diarrhea?

A

Blood and WBCs in stool, and can give fever

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6
Q

Where is Gastrin produced?

Describe its regulation

A
  • G cells in antrum of stomach.
  • ↑by stomach distention, alkalinization, amino acids, peptides, vagal stimulation.
  • ↓by stomach pH
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7
Q

Which amino acids are potent stimulators for Gastrin release?

A

Phenylalanine and Tryptophan

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8
Q

What disease increase Gastrin release?

Chronic use of what drug also increase Gastrin?

A

Disease: Zollinger-Ellison
Rx: chronic use of PPI

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9
Q

What is the Fx of Gastrin?

A

↑gastric H+ secretion
↑growth of gastric mucosa
↑gastric motility

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10
Q

What effect does Ach have on GI?

A

Increases contractility and secretion

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11
Q

What is unique to hormone Gastrin?

A
  • only hormone to increase Gastric motility
  • only w/ negative feedback by stomach acid
  • only one w/ neural innervation (vagus via Ach and GRP)
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12
Q

Function of Cholecystokinin and location of source cells?

A

↑pancreatic stimulation by acting on neural muscarinic pathway
↑GB contraction
↓gastric emptying
↑sphincter of Oddi relaxation (allows pancreas secretion to move in duodenum

source: I-cells in duodenum, jejunum

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13
Q

What regulates CCK release?

A

↑by FA mainly, and amino acids

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14
Q

Where is Secretin made and what is its Fx?

A

S cells in duodenum
↑pancreatic and Liver HCO3- secretion
↑bile secretion
↓gastric acid secretion

HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function

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15
Q

What triggers Secretin release?

A

↑by acid, FAs in lumen of duodenum.

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16
Q

What is Somatostatin? What is it’s Fx?

A

Inhibitory hormone made by D cells of pancreas islets and GI mucosa. It has anti-growth hormone effects (inhibit digestion and absorption of material needed for growth)

Decreases ↓ the following:

  • secretion of gastric acid, pepsinogen, pancreatic and small intestine fluid
  • insulin and glucagon release
  • GB contraction
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17
Q

What regulates Somatostatin release?

A

↑by acid

↓vagal stimulation

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18
Q

What is funtion of Motilin and where is it released?

A

Regulates Migrating Motor Complexes, waves of electrical activity that sweep through the GI in a regular cycle during fasting. MMC trigger peristaltic waves, which facilitate transportation of indigestible substances such as bone, fiber, and foreign bodies from the stomach, through the small intestine, past the ileocecal sphincter, and into the colon. The MMC occurs every 90-120 minutes during the interdigestive phase (between meals), and is responsible for the rumbling experienced when hungry.

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19
Q

What is a Motilin agonist drug?

A

Erythromycin

Administration of a low dose of erythromycin will induce peristalsis

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20
Q

Does oral or IV glucose trigger higher insulin secretion? Explain

A

Oral glucose has >insulin release, due to GIP secretion from oral glucose (carbohydrates biggest stimulant of GIP)

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21
Q

What is Glucose-dependent insulinotropic peptide?

Where is it made?

A

Made from K cells (duodenum, jejunum)
GI hormone that ↓gastric H+ secretion (exocrine) and ↑insulin release (endocrine).

Also called Gastric Inhibitory Peptide (GIP)

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22
Q

What triggers GIP?

A

Oral glucose, carbohydrates.

Increase FAs, AAs

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23
Q

What is a VIPoma and what disease results?

A
  • non-alpha, non-beta islet cell panreatic tumor.
  • Secretes excess VIP
  • causes WDHA syndrome: Water Diarrhea, Hypokalemia, Achlorhydria (no HCl acid made for stomach)
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24
Q

What is Fx and source of VIP?

A
  • From parasympathetic ganglia in sphincters, GB, SI.
  • ↑Intestinal H2O and electrolyte secretion
  • ↑relaxation of intestinal SM and sphincters
  • homologous to Secretin: ↑HCO3 pancreas release, decrease gastric H+ release
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25
Q

What stimulates VIP release?

A

↑by distention and vagal stimulation

↓by adrenergic input

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26
Q

What hormone is possibly implicated in ↑LES tone in Achalasia?

A

Nitric Oxide

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27
Q

What is Fx of Nitric Oxide?

A

Increases SM relaxation, including LES sphincter

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28
Q

What do Parietal cells release?

What are the stimuli for Parietal cells?

A

Parietal cells release HCl and Intrinsic factor.

They have 3 stimuli:

1) Neural: Ach (vagal)
2) Hormonal: Gastrin
3) Paracrine: Histamine

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29
Q

What secretes stomach acid?

What regulates this? What disease causes excess release?

A

Parietal cells (stomach). Gastrinoma is a tumor that causes continuous levels of acid release and ulcers.

↑by histamine, ACh, Gastrin
↓by Prostaglandin, Secretin, somatostatn, GIP.

“Don’t PaSS Gas”

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30
Q

What is the only part of stomach necessary for life?

What disease affects source cell?

A

Intrinsic Factor for Vit B12 absorption.

Autoimmune destruction of parietal cells, cause chronic gastritis andPernicious anemia

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31
Q

Where are Chief cells? What do they make, and what stimulates?

A

Chief cells in stomach. Make Pensinogen (active form Pepsin by H+) which digests Protein.

↑by vagal stiulation and stomach acid

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32
Q

Where is HCO3- made in GI?

Fx?

A

Mucosal cells in salivary glands, stomach, duodenum (Brunner’s glands), Liver, and Pancreas

Neutralizes acid. Trapped in mucosa and covers stomach epithelium.

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33
Q

What regulates HCO3- release in GI?

A

↑by panreatic and biliary secretion w/ Secretin (S-cells in duodenum, act on pancreas and Liver)

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34
Q

Effects of stomach distension?

A
  • ↑ACh and GRP (Vagal stimulation both)
  • Opens Pylorus
  • ↑Mucus lining stomach
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35
Q

What are Brunner’s glands?

What happens in hyertrophy?

A

Glands in duodenal submucosa. Secrete alkaline mucus.

Hypertrophy seen in Peptic ulcer disease.

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36
Q

What medication can inhibit Parietal cells? Be specific to PC stimuli

A

Atropine: blocks vagal stimulation by ACh on M3 receptor of PC. Does not effect G-cells. which use GRP.

H2 blockers: Stop Histamine (from ECL cells) action on PCs.

Misoprostal: Inhibit cAMP (Histamine, H2 receptor pathway)

PPIs stop all 3 stimuli (Ach, Gastrin, Histamine) by inhibiting ATPase (releases H+, stimulates by all 3).

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37
Q

What are pathways for Parietal cell production of stomach acid?

A

ACh acts on M3 receptor, Gastrin acts on CCKB receptor. Both activate Gq →IP3/Ca→activate ATPase (release H+).

Histamine ats on H2 receptor→cAMP→activate ATPase
(Gastrin acts on ECL cells→Histamine release)

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38
Q

What is Gastrin’s primary effect on Parietal cells?

A

Gastrin increases stomach acid primarily by acting on ECL cells, leading to histamine release Vs. acting directly on parietal cells

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39
Q

MOA of following on Parietal cell:
PG?
Misoprstol?
Somatostatin?

A

All 3 are Parietal cell inhibitors for Stomach acid release.

Activate Gi→inhibit cAMP→inhibit ATPase

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40
Q

What is pathway for Gastrin on Parietal cell?

A

Vagus stimulation→GRP acts on G-cells, release Gastrin →act on CCKB receptor→Gq stimulation→IP3/Ca2+→ATPase activation (H+ release)

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41
Q

Describe H+ source for Parietal cells and effect on outgoing venous blood

A

CO2 from arteria blood becomes H+ via Carbonic anhydrase pathway. HCO3- made as result leaving through venous blood (highest pH of any blood in body!)

CO2 + H2O–(CA)-↔ H2CO3↔ HCO3- + H+

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42
Q

Most basic blood in body location?

A

“alkaline tide”

highest pH blood is venous blood leaving stomach

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43
Q

What disease decreases?

How to Tx?

A

Diabetic Gastroparesis, due to neuropathy

Tx: Erythromyin increases GI motility
normal patient, drug would cause vomiting

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44
Q

Saliva source and consistency by source

A

Parotid gland: serous (THIN no mucin)

SM and SL gland: mixed, mucus and serous), THICK

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45
Q

What controls saliva secretion?

A

Parasympathetic AND Sympathetic
Para: ↑vol, thinner
Symp: ↓vol, thicker

No hormonal control. All neural control.

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46
Q

What are contents of saliva and purpose?

Tonicity and cause?

A
  • Salivary Amylase and Lipase (partial digestion, enough to taste)
  • HCO3-: neutralizes bacterial acids
  • Mucins lubricate foods
  • IgA

Chloride pump- NaCl reabsorbed into duct, but H2O is not→hypotonic saliva. Necessary for taste (food hypertonic in comparison, molecules flow to saliva).
This type of pump unique to saliva

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47
Q

Why can’t you taste Tofu?

A

Saliva lacks Proteases, protein digestion.

Tofu 100% pure protein

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48
Q

Rank fastest to slowest substances for stomach digestion

A

Normal saline > other liquids > CHO > Protein > Fats

Fats have most calories, need more time to absorb.

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49
Q

Stomach distension and duodenum distension effect on pyloric sphincter?

A

Stomach distension: Opens PS

Duodenum distension: Closes PS

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50
Q

What triggers Ileocecal valve opening and closure?

A

Opens: distension/stretch of ileum
Closes: cecum distension

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51
Q

What is RLS in bile salt formation?

Deficiency has what effect?

A

Cholesterol 7alpha- hydroxylase

Defiency: gallstones

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52
Q

What is Bile? Composition and Fx?

A

Dark green/yellowish fluid made by liver for lipid digestion in small intestine.

Composed of Bile acids, phospholipid, Cholesterol, Bilirubin, H2O, and ions.

Fx:

  • Digestion and absorption of lipids and fat-soluble vitamins.
  • Chol excretion (only means for body)
  • Antimicrobial activiy (via membrane disruption)
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53
Q

Bile salts vs Bile acids. Give pathway.

A

Bile salts make fat Micelle (fat surrounded by hyrdrophillic surface).
Bile acids are useless; hydrophobic

Chol→Bile acids–(conjugates w/ sugar Taurine or Glycine)–> Primary Bile salts –> Micelles

“MandMs, sugar coated fat candy”

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54
Q

Lack of Bile like what disease?

A

Pancreatitis

Celiac disease

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55
Q

What are Peyer’s Patches?

A

Unemcapsulated lymph tissue found in lamina propria and submucosa of ileum. Contain M-cells, which take up Ag. Produce secretory IgA

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56
Q

What is source of secretory IgA in Peyer’s patches?

A

Stimulated B-cells in germinal center of Peyer’s patches. They differentiate into plasma cells that reside in lamina propria. IgA part of secretary component of gut and line epithelium, targeting intraluminal Ags.

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57
Q

What bug invades Peyer’s patches? Describe disease Sx and bug MOA

A

Shigellosis-

  • Intestinal lumen infection by Shigella (mostly S. Sonnei)
  • Invades M cells (via endocytosis)→lyses endosome, multiplies, and spreads LATERALLY into other epithelial cells.
  • Sx: Ulcers, bloody stool w/ mucus
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58
Q

Direct vs Indirect Bilirubin

A

Direct: conjugated w/ gucuronic acid/ Water soluble.
Indirect: unconjugated. Water Insoluble

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59
Q

What is bilirubin pathway?

A

FA, pg 323

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60
Q

Describe Tonicity of Pancreas secretions and purpose.

Describe flow rate and content.

A

Isotonic fluid

Low flow: High Cl-
High flow: High HCO3-

Pancreas releases Bicarb rich fluid and digestive enzymes. Essential for life!

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61
Q

Describe Pancreas enzymes released on active form

A

Alpha-Amylase: Starch digestion
Lipase, Colipase,and Phospholipase A: Fat digestion
Proteases: Protein digestion

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62
Q

List types of Proteases released by Pancreas.

What type of molecule is it released as?

A

Trypsin, Chymotrypsin, Elastase, Carboxypeptidase.

Secreted as zymogen, a proenzyme

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63
Q

What Pancreatic secretion released in inactive form?

How is it activated?

Premature activation when?

A

Trypsinogen

Converted to active form, Trypsin, by Enterokinase/Enteropeptidase enzymes only made in duodenal mucosa

Premature activation in Pancreatitis. Seen in Alcoholics,

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64
Q

Function of Trypsinogen

A

Once activated:

1) Protein digestion
2) Activate other proenzymes, and creation of more trypsinogen (positive feedback loop)

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65
Q

Describe Carbohydrate digestion in mouth

A

Salivary amylase: hydrolyzes alpha-1,4-linkages to yield disaccharides (maltose and alpha-limit dextrins)

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66
Q

Describe Intestinal Carb digestion.

A

Pancreatic amylase- Highest concentration in duodenal lumen, hydrolyzes starch to oligosacharide and disaccharides.

Oligosaccharide hydrolases: Brush border of intestine. Produce monosacharides from oligo- and di-

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67
Q

What is RLS for carbohydrate digestion?

A

Oligosaccharide hydrolases at brush border of intestine

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68
Q

What form can Carbohydrates be absorbed?

A

ONLY as monosaccharides (glucose, galactose, fructose) absorbed by enterocytes.

69
Q

How is Glucose, galactose, and Fructose absorbed?

A

Glucose and Galactose: SGLT1 (Na-dependent)

Fructose: Facilitated diffusion by GLUT-5

70
Q

How to test for GI mucosal damage?

A

D-xylose absorption test

distinguishes GI mucosal damage from other causes of malabsoption

71
Q

What is large colon significant for regarding electrolytes and pH state? during diarrhea?

A

Colon secretes K and HCO3-

In diarrhea: Metabolic Acidosis and Hypokalemia. Other morms of M.A. have Hyperkalemia.
Diarrhea also has normal anion gap (w HCO3 loss, ↑Cl-)

72
Q

What is absorbed in duodenum?

A

Fe2+ (“Fe goes INTWO the boweks)

Divalent Cations: Mg2+ and Ca2+

73
Q

What is absorbed in jejunum?

A

Folate and HCO3-

74
Q

What is absorbed in Terminal ileum?

A

Vit B12 (requires Intrinsic factor) and Bile acids

75
Q

Role of Sodium w/ small intestine reabsorbtion.

What uses secondary active transport in SI?

A

-Na necessary for all electrolytes and substances,
EXCEPT for FRUCTOSE

-Secondary active: Glucose and Proteins

76
Q

What are the salivary gland tumors?

A

Pleomorphic adenomaWarthin’s tumorMucoepidermoid carcinoma

77
Q

Describe Pleomorphic adenoma’s

A

-benign mixed tumorSx: painless, mobile mass made of cartilage & epithelium

78
Q

Describe Warthin’s tumor

A

-Benign-cyctic tumor w/ germinal centersaka: Papillary cystadenoma lymphomatosum

79
Q

What is a Mucoepidermoid carcinoma?

A

MalignantPainful mass, hasa mucinous & squamous portions involves facial nerves

80
Q

Failure of relaxation of LES (neurological cause) called?presentation on barium swallow?

A

Achalasia

Barium swallow: “bird’s beak”. Dilated esophagus w/ area of distal stenosis

81
Q

Cause of Achalasia?Effect on peristalsis and pressure changes

A

Loss of myenteric (Auerbach’s) plexus. Secondary disease due to Chagas. Unocordianted peristalsis and increased pressure to open LES

82
Q

What can you eat and not eat during Achalasia?

A

Dysphagia of solids & liquids

83
Q

What is associated w/ Achalasia?

A

Esophageal squamous cell carcinoma Scleroderma (CREST). Low pressure proximal to LES

84
Q

C/C: 46 yo male feels heartburn and feels like vomiting after lying down. Has trouble breathing, coughs at night, and feels like he may have asthma. What is it?

A

GERD

85
Q

GERD affect on LES?

A

Decrease LES tone

86
Q

Portal hypertension can have what affect on esophagus?

A

-Esophageal varices-PainLESS hematemesis of dialted submucosal veins in lower 1/3 of esophagus.

This is MCC of death in cirrhosis
Liver not Fx! Coag factors↓↓

87
Q

Non-infective causes of Esophagitis?

A

Chemical ingestionAcid Reflux (if not due to bug!)

88
Q

Bugs associated with eophagitis? Presentation w/ each

A

Candida = white pseudomembraneHSV-1= punched-out ulcersCMV= linear ulcers

89
Q

Who presents w/ Mallory-Weiss syndrome?

A

Drunks and bulimics(severe vomiting)

90
Q

What can Mallory-Weiss lead to?

A

Painful Hematemisis- throwing up blood! Mucosal lacerations

91
Q

Violent retching Transmural esophageal rupture. What is it?

Describe

A

BoerHaave Syndrome- Rupture of esophagus leading to air in the mediastinum & subcutaneous emphysema
aka: “Been Heaving Syndrome”

92
Q

Esophageal strictures are associated with what? 2 things…

A 
Lye ingestion- containing largely potassium carbonate or "potash"). In oven cleaners, drain openers
Acid reflux (GERD)
93
Q

triad of Plummer-Vinson syndrome

A
  • Dysphagia (due to esophgeal webs)
  • beefy-red tongue from atrophic Glossitis
  • Iron deficiency anemia
94
Q

Metaplasia where nonkeratinized stratified squamous cells replaced w/ intestinal cells (noncillaited columnar w/ goblet) in distal esophagus.

A

Barret’s esophagus

NCC cells w/ goblet cells

95
Q

What causes Barret’s esophagus?

A

GERD (acid reflux)

96
Q

Risk’s & association’s w/ Barret’s esophagus

A

Esophagitis
Esophageal Ulcers
increased risk of: esophageal ADENOCARCINOMA

97
Q

Types of cancer in esophagus. Sites affected, and demogprahics.

A

Squamous cell: upper 2/3, MC worldwide (outside US)Adenocarcinoma: lower 1/3, MC in USA

98
Q

Presentation of esophageal cancer?

A

Dysphagia- first solids, then liquidsWeight loss

99
Q

Risk factors for Esophageal cancer

A 
AABCDEFFGH
Achalasia
Alcohol- sqm
Barret's- adeno
Cigarettes-both
Diverticula (e.g. Zenkers)- sqm
Esophageal web- sqm
Familial Fat/obestity- adeno
GERD-adeno
Hot liquids- sqm
100
Q

Key Sx of Malabsorption diseases?

A

DiarrheaSteathorrheaWeight lossWeaknessVit & mineral deficiencies

101
Q

List malabsorbtion diseases?

A

Tropical sprueWhipple’s diseaseCeliac sprueDisaccharidase deficiencyAbetalipoproteinemiaPancreatic insufficiency”These Will Cause Devastating Absorption Problems”

102
Q

Differentiate Tropical Sprue & Celiac Sprue

A

Both similar. Tropical cause unknown, and can effect entire small GI

103
Q

Histo & IF of Whipple’s disease

A

PAS+ foamy macrophages in intestinal lamina propriaMesenteric nodes

104
Q

Sx of Whipple disease?

A

CardiacArthalgiaNeurologic “Foamy Whipped cream in a CAN”

105
Q

What is the MC disaccharidase deficiency? Type of diarrhea present?

A

Lactase!Osmotic diarrhea

106
Q

Lactase tolerance test is positive when…

A

Lactase administration–> Sx (bloating, osmotic diarrhea)& glucose rises only

107
Q

explain path of abetalipoproteinemia

A

↓apolipoprotein B made ->cannot make chylomicrons->↓ Cholesterol & VLDL secreted into blood->fat builds up in enterocytes

108
Q

When does abetalipoproteinemia present?

A

early in childhood, w/ neurological Sx

109
Q

What can cause pancreatic insufficiency?

A

CFobstructing cancerchronic pancreatitis

110
Q

What cant you absorb with pancreatic insufficiency?

A

cant absorb fat-soluble vitamins A, D, E, K –> neutral fat in stool

111
Q

HLA associations w/ celiac spru? Who gets it? What skin presentation associated?

A

HLA-DQ2 & HLA-DQ8Northern EuropeansDermatitis herpetiformis

112
Q

What Abs associated w/ celiac spru? Which one is used to test?

A

Abti-endomysial*Anti-tissue transglutaminase

113
Q

Cause of Cleft lip and cleft palate?

A

failure of facial prominences to fuse.

Early pregnancy, 5 prominences fuse together to form face.

114
Q

Sx of Behcet syndrome? Understand each

Cause?

A

recurrent

  • aphthous ulcers- superficial ulcer of oral mucosa
  • genital ulcers
  • Uveitis

Immune complex vasculitis. Possibly after viral infection.

115
Q

What is cause of blisters of oral mucosa, when ruptures, are shallow, painful and red? On the lips as a cold soar.

What triggers this?

A

Oral Herpes- HSV-1

Primary infection in childhood. Virus dormant in ganglia of Trigeminal nerve

Cause: Stress or sunlight

116
Q

Cause of Oral Squamous cell carcinoma?

A

Tobacco and Alcohol

117
Q

Describe precursor for Squamous Cell Carcinoma (oral cavity)?
Give differential diagnosis

A

Leukoplakia- white plaque, squamous cell dysplasia. CANNOT be scrapped away.
Erythroplakia- vascularized leukoplakia and is highly suggestive of squamous cell dysplasia.

Dont confuse w/ Oral Candidiasis or Hairy Leukoplakia. Biopsy to rule of Cancer.

118
Q

Cause of Hairy Leukoplakia. Differentiate from precursor to oral squamous cell carcinoma.

A
  • White, rough (“hairy”) patch that arises on LATERAL tongue.
  • EBV induced, squamous cell hyperplasia. NOT- Premalignant.
  • Seen in immunocompromised (AIDS)
119
Q

What oral condition caused by Mumps virus?

Give Sx of infection throughout body.

A

Bilateral inflamed parotid glands

Orchitis, pancreatitis, & aseptic meningitis can present.

Orchitis can cause infertility if patient >10yo

120
Q

Which serum enzyme elevated w/ Mumps?

A

Serum amylase.

Can be caused by inflammation of parotid gland and/or pancreas, which both make the carb digestive enzyme

121
Q

Cause of unilateral salivary gland inflammation? Name of condition?

A

SIALADENITIS

Obstructing stone: Sialolithiasis
Can cause Staph aureus infection

122
Q

MC salviary gland tumor? Describe

A

Pleomorphic Adenoma

  • benign
  • biphasic. Stromal & Epithelial
  • high rate of recurrence. Irregular borders of tumor capsule→common incomplete resection in surgery
  • Mobile, & painless.
123
Q

Significance of pain for parotid tumor. Describe specific.

A

Facial nerve runs through parotid gland. Parotid tumor with facial pain sign of Malignant tumor.

  • Mucoepidermoid tumor
  • Pleomorphic adeoma that has become malignant (RARE!!)
124
Q

MC malignant tumor of salivary gland? Describe

A

Mucoepidermoud carcinoma

  • Mucinous & squamous cells.
  • parotid gland. Pain from facial nerve.
125
Q

Benign tumor w/ abundant lymphocytes and germinal centers?

A

Warthin tumor. @ parotid gland

strong embryo association of lymphoid tissue w/ parotid gland

126
Q

Sx of TE fistula

A
  • Vomiting
  • Polyhydramnios- excess amniotic fluid (can’t swallow!)
  • Abdominal distension- air from Trachea→distal esophagus
  • Aspiration
127
Q

What is Zenker’s Diverticulum?

Location & Sx?

A
  • Outpouching of pharyngeal mucosa through muscular wall. Not completely through, thus a false diverticulum.
  • UES @ junction of Esophagus & Pharynx
  • Sx: Dysphagia, obstruction, and halitosis
128
Q

Clinical features of Achalasia

A
  • dysphagia of solids and liquids
  • putrid breath
  • High LES pressure on monmetry
  • “Bird-beak” sign on barium swallow
  • ↑risk for esophageal SCC
129
Q

Risk factors for GERD

A
  • Alcohol & Smoking
  • Obesity
  • Fat-rich diet
  • Caffeine
  • Sliding Hiatal hernia
130
Q

Clinical presentation of GERD

A
  • Heatrburn (mimics chest pain)
  • Asthma (adult-onset) & cough
  • Damage to teeth enamel
  • Ulceration w/ stricture: loss or narrowing of lumer of lower esophagus
  • long-term: Barret’s esophagus
131
Q

MC cancer of esophagus in West? MCC?

A

Adenocarcinoma

Barret’s MCC

132
Q

Global, what is MC type of esophageal cancer?

What part of esophagus affected?

A

Squamous cell carcinoma (from irritation)

Upper or middle 1/3.

133
Q

Risk factors of squamous cell carcinoma of Esophagus?

A
  • MCC: EtOH & Tobacco
  • Hot liquids
  • Achalasia
  • Esophageal web- rotting food
  • Esohageal injury (i.e. lye ingestion)
134
Q

Sx of esophageal cancer

A
  • Progressive dysphagia (solids & liquids)
  • Weight loss
  • pain
  • Hematemesis (as cancer grows)
  • Hoarse voice (recurrent Laryngeal nerve)
  • cough (trachea)
135
Q

What are LNs for each 1/3 of Esophagus?

A

Upper: Cervical
Middle: mediastinal or tracheobronchial
Lower: celiac & gastric

136
Q

What is a congenital malformation of anterior abdominal wall leading to exposure of abdominal contents?

A

Gastroschisis

“schisis” = splitting

137
Q

What is an omphalocele? Cause?

A
  • Persistent herniation of bowel into umbilical cord. Contents covered by peritoneum & amnion of umbilical cord.
  • Results from failure of herniated intestines to return to body cavity during development
138
Q

Cause, Sx of pyloric stenosis

A 
-congenital hypertrophy of pyloric SM
Sx:
-projectile, non-bilious vomiting
-olive-like mass in abdomen (SM hypertrophy)
-visible peristalsis
-2 weeks after birth. Mostly males.
139
Q

What is Acute Gastritis?

A

acidic damage to stomach mucosa due to imbalance between stomach defenses and acidic environment. Causes erosion (loss epith layer), or ulcer (loss of mucosal layer)

Defenses: Mucin made by Fovelar cells, HCO3- secretion by surface epith, & blood supply (nutrients & carries away acid)

140
Q

Risk factors for Acute Gastritis?

A
  • Severe Burn (Curling Ulcer)
  • NSAIDS (inhibit PG)
  • EtOH
  • Chemotherapy
  • Increased intracranial pressure (↑vagal stimulation→↑Ach)
  • Shock, stress ulcers in ICU pts
141
Q

What are the types of Chronic Gastritis? Locations of each.

MCC>

A

1) Autoimmune destruction of parietal cells, Type A. Fubdus & body.
2) H pylori, Type B. Antrum. MCC

142
Q

Clinical Sx of Autoimmune chronic gastritis?

What Type of hypersensitivity is it?

A
  • Atrophy of mucosa w/ intestinal metaplasia
  • Achlorhydria w/ antral G-cell hyperplasia
  • Pernicious anemia (no IF)
  • Increased risk for gastric adenocarcinoma (intestinal type)

Type 4 HS. Abs develop later as S/E.

143
Q

MOA of H. pylori in Chronic Gastritis.Bug location?

A

Makes ureases and proteases that damage mucosal defenses w/ inflammation.

Bug superficial to stomach epithelial, does not invade.

144
Q

Sx and risk factors of H pylori chronic gastritis?

A
  • Epigastric abdominal pain
  • Increased risk of Peptic Ulcer Disease
  • Gastric adenocarcinoma (intestinal)
  • MALT lymphoma
145
Q

Peptic ulcer disease affects what site?

Causes?

A 
Proximal duodenum (90%) & Distal stomach
Gastric ulcer in stomach antrum.

Duodenal: H pylori (95%) & ZE syndrome
Gastric: H pylori (75%) & NSAIDS, bile reflux

146
Q

Biopsy and clinical Sx of Duodenal Peptic Ulcer disease?

A
  • Epigastric pain. Improves w/ meals→weight gain

- Biopsy: ulcer w/ hypertrophy of Brunner glands

147
Q

Rupture site risk for Gastric & Duodenal Peptic Ulcer Disease

A

Gastric: bleeding from Left gastric artery (Lesser curvature)
Duodenal: bleeding from Gastroduodenal artery or acute pancreatitis (another rupture risk). Both Posterior ulcers.

148
Q

Sx of Gastric Peptic Ulcer Disease

A
  • Epigastric pain that worsens w/ meals→weight loss

- Ulcer on lesser curvature of antrum

149
Q

Cancer risks/causes of Peptic Ulcer Disease types?

Differentiate benign and malignant look

A

Duodenal- generally benign

Gastric- ↑Gastric carcinoma
Benign: small ulcer (

150
Q

What causes intestinal metaplasia of stomach?

A
  • Chronic autoimmune gastritis
  • Chronic H. pylori gastritis, thus:
  • Peptic Ulcer Disease
151
Q

What is presentation of Intestinal Gastric Carcinoma?

A
  • irregular ulcer w/ heaped up margins

- Lesser curvature of antrum (like gastric ulcer)

152
Q

What type of cancer is stomach mostly?

Describe how aggressive it is?

A

Adenocarcinoma

Early aggressive local spread & mode/liver metastasis.

153
Q

Risk factors for stomach cancer, intestinal type? Compare to Diffuse type

A

Intestinal metaplasia (H pylori, autoimmune gastritis)

  • Nitrosamines (smoked food…Japan)
  • Blood type A

These are NOT associated w/ Diffuse type

154
Q

Presentation of Diffuse type stomach cancer?

A
  • Signet ring cells in stomach wall
  • desmoplasia results in thickening of stomach wall; leathery (linitis plasticia). Response to invasive tumor w/ fibrotic tissue.
155
Q

Stomach Cancer general Sx

diffuse and intestinal type

A
  • Late weight loss
  • Abdominal pain
  • Anemia
  • Early satiety
  • Acanthosis nigricans
  • Leser-Trelat sign
156
Q

Common sites of metastasis for Gastric Carcinoma?

A
  • Liver
  • Subcutaneous Periumbilical region: Sister Mary Joseph nodule (intestinal stomach cancer)
  • Krukenberg tumor: bilateral ovaries. Abundent signet ring cells.
  • Virchow node (left supraclavicular node)
157
Q

Infant is born with Down syndrome. On X-ray, distention of stomach, duodenum, & thightened spincter is seen. What disease is present?
What is another high-yield Sx?

A

Duodenal Atresia

other Sx: Bilious vomiting

158
Q

What is Meckel’s Diverticulum and cause?

A

-Outpouching of all three layers of bowel wall, a true Diverticulum.
-Failure of vitelline duct to involute.
Early in embryogenesis, it connected yolk sac to midgut provided nutrients. For Meckel’s, duct partially closed.

159
Q

Cause of Mecinium passing through umbilicus?

A

Failure of vitelline duct to involute at all w/ zero closure.
In Meckel’s Diverticulum, there is all no involution, but partial closing of duct.

160
Q

Presentation of Meckel’s Diverticulum?

A

“Rule of 2’s”

  • Mostly no Sx
  • 2% of population (MC congenital GI problem)
  • 2inch long in small bowel, w/n 2 feet of ileocecal valve.
  • Presents w/n first 2 years of life w/ Bleeding, Volvulus, intussusception, or obstruction (mimics appendicitis).
161
Q

Twisting of bowel along mesentary?? Result of this?

Which sites for old and young?

A

Volvulus. Disruption and obstruction of blood supply (BVs in mesentery)

Elderly: Sigmoid colon
Young adults: Cecum

162
Q

MCC of intussusception in kids?

What location?

A

Lymphoid hyperplasia due to Rotavirus

Terminal ileum intussusception into cecum.

163
Q

MCC of intussusception in adults?

A

Tumor

164
Q

Clinical Sx of Intussusception?

A

Sx: Currant Jelly Stool (poop w/ blood and mucus), due to infarction caused by telescoping of segments.

165
Q

Which part of GI most susceptible to ischemic injury?

A

Small bowel. Use a lot of ATP for digestion.

166
Q

Cause of Small bowel Transmural infarction?

A

Thrombosis/embolism of SMA
Thrombosis of Mesenteric vein

Embolism: A fib,
Thrombosis @ SMA: Vasculitis (i.e. polyarteritis nodosa)
Thrombosis @ Mes Vein: PCV, Lupus anticoagulant

167
Q

What is Mucosal infarction of Small bowel and cause?

A

Hypotension.

Mucosa furthest away from blood, & first to become ischemic w/ ↓blood supply.

168
Q

Sx of Lactose intolerance?

A

abdominal distension & diarrhea after drinking milk.

Undigested lactose is Osmotically active (diarrhea)

169
Q

Causes of Lactose intolerance?

A

Lack of Lactase enzyme (brush border enterocytes)

  • Rare AR
  • Acquired: late childhood
  • Temporary: small bowel infection. Lactase injury susceptible

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