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DEMS > Unit I, week 1 > Flashcards

Unit I, week 1 Flashcards

1
Q

Smooth muscle contraction review

A

Actin = thin filament, myosin = thick filaments with cross bridges extending to contact thin filaments

Thin:thick filaments = 10:1 (skeletal muscle is 2:1)

Ca2+ entry into cell → Ca2+ + calmodulin → activate myosin light chain kinase → phosphorylates myosin → allows cross-bridge formation (cycling) to occur → smooth muscle contraction

Myosin light chain phosphatase breaks down this process and stops contraction

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2
Q

Types of motility in GI tract

A

Segmentation

Peristalsis

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3
Q

Segmentation

A

MIXING

Contraction is isolated, not coordinated with movement above and below, propel contents in both directions

When contracting area relaxes, contents flow back into original segment → mixing without net propulsion

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4
Q

Peristalsis

A

propulsive movement

Contractions of adjacent segments coordinated in proximal and distal manner → net propulsion of contents

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5
Q

Describe the general mechanism of peristalsis

A

Bolus of food distends intestinal wall → formation of contractile ring just proximal to bolus that pushes bolus distally

Longitudinal muscle contracts compacting bolus

At same time, intestine distal to bolus relaxes = Receptive Relaxation

Coordination requires nerves of myenteric plexus

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6
Q

In the stomach, peristalsis requires _______ coordinated by ________

A

BERs

vagal input

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7
Q

Smooth muscle in GI tract

A

Unitary (single unit) cell type:

  • Held together by adherens junctions
  • Communicate electrically via gap junctions
  • Pacemaker cells with spontaneous activity
  • Intrinsically produces BER and muscle tone without tension (myogenic properties)
  • Tension comes from NTs acting on muscle → role of ANS
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8
Q

Innervation of intestinal smooth muscle (3)

A

Sympathetic: epinephrine inhibits digestive function

Parasympathetic: rest-digest, sit-shit

ENS: bidirectional signalling between gut wall and ANS innervation

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9
Q

Basic electrical rhythm (BER)

A

cyclical changes in membrane polarization

Intrinsic property of smooth muscle cells in a given location (no external stimulus required) = MYOGENIC

Each depolarization does NOT cause contraction - contraction only occurs when depolarization exceeds specific membrane potential
–> Require NT input (ACh)

When membrane potential reached, muscle contracts at BER frequency

Force of contraction proportional to number of APs

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10
Q

BERs as you move along the GI tract

A

Different as you move along GI tract:

Stomach BER = 3 cycles per minute

Duodenum BER = 12 cycles per minute

Want things moving faster in the front so there isn’t backing up

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11
Q

Swallowing (deglutition)

A

swallowing initiated voluntarily but then sensory receptors in pharynx send impulses to swallowing center in brainstem → coordinate subsequent involuntary events

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12
Q

Phases of swallowing (3)

A

1) Voluntary
2) Pharyngeal
3) Esophageal

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13
Q

Voluntary swallowing phase

-what two steps of swallowing happen in this phase?

A

oral cavity bolus pushed by tongue to oropharynx

1) Tongue separates portion of food, moves it back into pharynx
2) Food pushes soft palate upward → constrictor muscle contracts, closing off nasopharynx → SWALLOWING NOW A REFLEX FROM HERE (involuntary)

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14
Q

Pharyngeal swallowing phase

-what two steps of swallowing happen in this phase?

A

directs food into esophagus, keeps it out of trachea

3) Respiration inhibited for 1-2 seconds centrally → larynx rises and glottis closes to prevent bolus from entering trachea
4) Upper esophageal sphincter (UES) relaxes

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15
Q

Esophageal swallowing phase

What step happens in this phase

A

5) Coordinated contraction (peristaltic wave) of middle and lower constrictor muscles propel bolus down esophagus

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16
Q

Esophageal peristalsis

A

Peristalsis propels bolus down esophagus in 5 seconds, and LES relaxes to allow bolus into stomach

LES prevents reflux of acid gastric contents into esophagus, but NOT a valve - just a thickening of muscle wall

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17
Q

What nerve controls esophageal peristalsis, what happens if it is damaged?

A

Controlled by vagus nerve (receives signals from swallowing center)

If vagus nerve severed, local myenteric complex can maintain swallowing

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18
Q

Function of stomach

A

storage, mixing, and slow controlled emptying

HCl disinfects food, denature, and digests proteins and produces IF

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19
Q

Receptive relaxation

A

vagally mediated inhibition of fundic body tone which permits volume expansion of stomach and storage of food without a concomitant rise in intragastric pressure

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20
Q

Gastric motility (3 steps)

A

1) After eating, contractions start in mid stomach, slow wave frequency → push bolus toward antrum
2) Contractions become stronger and faster in antrum, outrun bolus → contents forced backward = Retropulsion (breaks up food into smaller particles and mix with digestive juices (chyme))
3) Transient opening of pylorus allows small particles and chyme to leave stomach and enter duodenum

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21
Q

Gastric emptying

things that effect gastric emptying

A

controlled by pyloric sphincter, normally under high tone

1) Distension
2) Type of food
3) Gastrin
4) Detection of food in duodenum
5) Cholecystokinin

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22
Q

How does distention of the stomach effect rate of emptying?

A

Rate of emptying increased by distension: increased stretch → increased peristalsis through vagal/myenteric reflexes → decreased pyloric tone

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23
Q

How does type of food effect rate of emptying?

A

Carbs leave stomach in a few hours, protein rich food leaves more slowly, and fat leaves the slowest

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24
Q

How does gastrin effect rate of emptying?

A

Gastrin: hormone secreted in presence of food in stomach

Stimulates peristaltic contraction and decreases pyloric tone

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25
Q

How does detection of food in the duodenum effect rate of emptying?

A

Detection of food in duodenum → reflex inhibition of gastric peristalsis and increase in pyloric tone

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26
Q

How does cholecystokinin effect rate of emptying?

A

Cholecystokinin: secreted by enteric endocrine cells in response to arrival of fats in duodenum → inhibit gastric motility

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27
Q

Vomiting

4 steps involved

A

Centrally regulated by vomiting center in brain

Steps involved:

1) Salivation (HCO3-) and sensation of nausea
2) Reverse peristalsis from upper small intestine to stomach
3) Abdominal muscles contract and UES and LES relax
4) Gastric contents are ejected

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28
Q

Migrating motility complex

A

sweep down gastric antrum and along small intestines between meals (every 90 minutes)

Housekeeping role = remove bacteria and indigestible material

Peristaltic wave begins in stomach → ileocecal sphincter → repeat

Wave initiated by motilin hormone released from small intestine

Eating terminates MMC

DO NOT HAPPEN IN LARGE INTESTINE

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29
Q

Phases of migrating motility complex (MMC) (3)

A

Phase I: quiescence, occurs 40-60% of 90 min duration

Phase II: motility increases but contractions are irregular

  • Fails to propel luminal content
  • Lasts 20-30% of MMC duration

Phase III: 5-10 minutes of intense contractions
-From body off stomach to pylorus to duodenum to ileocecal valve - (pylorus fully opens)

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30
Q

Small intestine motility

A

Segmentation: chyme mixed with digestive enzymes and continually exposes surface to new contents for absorption

Peristalsis: propels chyme 1 cm/min

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31
Q

Gastroileal reflex

A

stomach activity stimulates movement of chyme through the ileocecal sphincter

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32
Q

Ileocecal sphincter

normal?
opened by?
closed by?

A

normally closed (to prevent reflux of bacteria from colon into ileum)

Opened by distention of end of ileum (local reflex)

Closed by distension of proximal colon (local reflex)

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33
Q

Gastrocolic reflex

A

food in stomach stimulates mass movement in colon

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34
Q

Distension in ileum → ?

A

Distension in ileum → relaxation of ileocecal sphincter → contents pass into cecum of large intestine

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35
Q

Types of motility in the colon

A

Haustration

Mass movement

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36
Q

Haustrations

A

muscles of colon wall contracted intermittently to divide colon into functional segments known as haustra

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37
Q

Mass Movement

A

giant migrating contraction 1-3X/day

does forward propulsion

Intense and prolonged peristaltic contraction that strips an area of large intestine clear of contents

Segmental activity temporarily ceases, loss of haustration

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38
Q

Defecation

A

1) Mass movements push feces into rectum which is usually empty
* *Gastrocolic reflex stimulates this

2) Feces enter rectum → distension of rectum → stimulate defecation reflex
* *Spinal mediated via pelvic nerves
- Reflex relaxation of internal anal sphincter and voluntary relaxation of external anal sphincter → defecation

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39
Q

Acid secretion

A

HCl

Kills bacteria (disinfects food at pH 1.0)

Begins protein digestion - denatures proteins and activates pepsinogen → pepsin

Acid producing parietal cells also secrete IF when secreting acid

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40
Q

Mucosal Defenses in Stomach

A

mucus layer and alkaline (HCO3-) layer at cell surface (surface mucus cells) protects stomach lining

Prostaglandins can increase mucus production

Tight junctions between cells prevent acid from infiltrating layers of wall

Rapid turnover maintains surface integrity

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41
Q

Phases of gastric acid secretion (4)

A

1) Basal interdigestive phase
2) Cephalic phase
3) Gastric phase
4) Intestinal phase

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42
Q

Basal (interdigestive) phase of gastric acid secretion

A

follows circadian rhythm

Rate of acid secretion lowest in morning before awakening, highest in evening

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43
Q

Cephalic phase of gastric acid secretion

A

initiated by smell, sight, taste, and swallowing of food

Mediated by vagus nerve

Accounts for 30% of total acid secretion

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44
Q

Gastric phase of gastric acid secretion

A

stimulated by entry of food into stomach

Food distends gastric mucosa → activate vagovagal reflex and local ENS reflex

Partially digested proteins stimulate antral gastrin G-cell→release gastrin

Responsible for 50-60% of total acid secretion

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45
Q

Intestinal phase of gastric acid secretion

A

presence of amino acid and partially digested peptides in proximal portion of small intestine stimulates acid secretion

Stimulate duodenal gastrin G-cells → secrete gastrin

Accounts for 5-10% of total acid secretion

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46
Q

Stimulation of vagus nerve results in what effects on the cephalic phase of acid secretion (4)

A

1) ACh release
2) Histamine release from ECL cells
3) Release of gastrin-releasing peptide from vagal enteric neurons
4) Inhibition of somatostatin release from delta cells in stomach

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47
Q

Parietal cells

A

secrete HCl and Intrinsic Factor into stomach

Stimulation of parietal cells causes them to significantly increase their secreting surface area → prodigious HCl output

→ Luminal pH of 2

Have lots of mitochondria: use lots of ATP to pump H+ against big gradient

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48
Q

Acid secretion stimulation

A

acid secretion stimulated by ACh, Gastrin hormone, and pancreas substance histamine → increase in Ca2+ and cAMP in cell → activation of distinct protein kinases that phosphorylate and increase activity of H+/K+ ATPase

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49
Q

Effect of ACh on gastric acid secretion

A

from vagus nerve stimulation, binds muscarinic receptors on basolateral membrane → activate G-protein → increase [Ca2+] in cell

–> increase activity of H+/K+ ATPase in parietal cells

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50
Q

Effect of Gastrin on gastric acid secretion

A

bind gastrin receptors, also increases intracellular Ca2+

–> increase activity of H+/K+ ATPase in parietal cells

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51
Q

Effect of Histamine on gastric acid secretion

A

binds H2 receptors → activate G-protein → turn on AC → increase cAMP in cell

–> increase activity of H+/K+ ATPase in parietal cells

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52
Q

Direct pathway of acid secretion stimulation

A

ACh, gastrin, and histamine directly stimulate parietal cell, triggering secretion of H+ into lumen

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53
Q

Indirect pathway of acid secretion stimulation

A

ACh and gastrin stimulate histamine release from enterochromaffin-like cells (ECL) → histamine acts on parietal cell

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54
Q

H+/K+ ATPase and gastric acid secretion

A

H+ transported across apical membrane via H+/K+ ATPase

Primary active transport

Also drives Cl- and H2O movement into cell

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55
Q

Cl-/HCO3- anion exchanger and gastric acid secretion

A

HCO3- transported across basolateral membrane in exchange for Cl- via Cl-/HCO3- anion exchanger

Downhill movement of HCO3- drives Cl- into cell against gradient

When H+ transported out of cell → increase [HCO3-] in cell via CARBONIC ANHYDRASE activity

Secondary active transport

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56
Q

Cl- facilitated diffusion and gastric acid secretion

A

Cl- accumulation in cell due to Cl-/HCO3- exchanger, transported across apical membrane by Cl- facilitated diffusion = passive transport, CFTR channel

Cholera toxin → constitutively activate this channel

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57
Q

How does water travel in the stomach?

A

H2O follow HCl from blood into lumen via transcellular pathway

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58
Q

Alkaline tide

A

high pH of venous blood leaving stomach due to HCO3- transport

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59
Q

Protective barrier of gastric surface

A

Epithelial cells, mucous, and bicarbonate provide barrier to dissipation of massive pH gradient and harmful effect of acid

Mucous secreted by Goblet Cells and Mucous Neck Cells of the gland

  • Mucous forms an unstirred gel layer in which H2O is trapped
  • Serves as neutralization zone, so acid is neutralized
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60
Q

Carbohydrate absorption and digestion general rules

A

Only simple monomeric sugars can be absorbed!

Amylase is the major enzyme in saliva and pancreatic secretions

Other dietary sugars like sucrose and lactose can be digested at the surface of enterocyte

Plant starch amylopectin is largest single source of carbs in our diet

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61
Q

what types of nutrients are transported in the venules vs. lacteal vessel?

A

Venule → other nutrients (not fat) enter venule and portal vein

Central lymphatic lacteal vessel → products of fat digestion enter lacteal and blood stream at thoracic duct

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62
Q

Proteolytic enzymes from pancreas first secreted as what? why?

A

First secreted as inactive precursors (zymogens, proenzymes)

→ Prevent enzymes from digesting pancreatic membranes and each other before they are needed

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63
Q

In stomach: pepsinogen –> ?

In duodenum: trypsinogen –> ?

–> then goes on to do what?

A

In stomach: pepsinogen (proenzyme) → pepsin by stomach acid

In duodenum: trypsinogen → trypsin by brush border (microvillar) enzyme called enteropeptidase/enterokinase

*Trypsin → more active trypsin produced from trypsinogen and converts all other zymogens to active enzymes

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64
Q

Amylase

A

catalyzes hydrolysis of internal a-1,4 linkages, converts amylose and amylopectin → maltose, maltotriose, and a-limit dextrin

Free glucose is NEVER the product of amylase digestion

Cellulose = B-1,4 linked polymer → cannot be digested = “fiber”

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65
Q

Mucosal Sucrase-Isomaltase (SI)

A

last stage of small intestinal digestion of branch points of starch to glucose, breaks 1,6 linkages

Convert a-limit dextran → glucose

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66
Q

Mucosal Maltase-Glucoamylase (MGA)

A

inal step in small intestinal digestion of linear forms of starch to glucose

Convert maltotriose → glucose

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67
Q

Sucrase

A

converts sucrose → glucose and fructose

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68
Q

Trehalase

A

converts trehalose → glucose

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69
Q

Lactase enzyme deficiency

A

lactose intolerance due to deficiency of lactase enzyme that converts lactose to glucose and galactose

Absence of brush border enzyme lactase

Unabsorbed lactose draws water into intestinal lumen → osmotic diarrhea

Gut bacteria flora metabolize unabsorbed lactose → gases

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70
Q

Carbohydrate uptake

A

intestinal sugar transportes transport monosaccharides (glucose, galactose, and fructose) from intestinal lumen to blood

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71
Q

Na+-Dependent Glucose Transporter (SGLT1)

A

brush border/apical membrane of enterocytes, transports glucose and galactose with Na+ from lumen → cytosol

Requires sodium as a co-transporter

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72
Q

Genetic absence of SGLT1 → ?

A

glucose-galactose malabsorption → diarrhea upon sugar ingestion due to reduced small intestine Na+ fluid absorption and fluid secretion secondary to osmotic effect of non-absorbed monosaccharide

Potentially fatal

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73
Q

Na+-Independent Fructose Transporter (GLUT5)

A

apical transporter, transports fructose from lumen into cytosol

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74
Q

Na+-Independent Fructose Transporter (GLU2)

A

basolateral and transports all three monosaccharides from cytosol to blood

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75
Q

Protein digestion: begins in ______ where what happens?

ends where?

A

begins in stomach - Pepsin breaks down 15% of proteins to small peptides

ends in small intestine

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76
Q

Small intestine in digestion of proteins

A

pancreatic proteases like trypsin, chymotrypsin, carboxypeptidase and elastase break down proteins to oligopeptides di/tri peptides and amino acids

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77
Q

Endopeptidases vs. Exopeptidases

A

Endopeptidases: secreted, hydrolyze interior peptide bonds

Exopeptidases: secreted, hydrolyze one AA at a time from carboxy (C)-terminus of proteins and peptides

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78
Q

Endopeptidases include…(3 examples)

A

Trypsin
Chymotrypsin
Elastase

*all secreted as zymogens

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79
Q

Exopeptidases (2 examples)

A

Carboxypeptidases A and B (secreted as zymogen, Pro-Carboxypeptidase A and B)

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80
Q

Brush border proteases (3)

function?

A

peptidases break down oligopeptides into amino acids, dipeptides, and tripeptides

1) Aminopeptidase
2) Dipeptidyl aminopeptidase
3) Dipeptidase

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81
Q

Intracellular peptidases

A

peptidases in enterocyte can break down di/tri peptides into amino acids

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82
Q

Steps of small intestine protein digestion (5)

A

1) Activation of trypsinogen→ trypsin by brush border enterokinase
2) Activation of all other precursors by trypsin
3) Trypsin, chymotrypsin, elastase, carboxypeptidase A and B, all hydrolyze protein to amino acids and di-, tri-, and oligopeptides
4) Brush border proteases hydrolyze oligopeptides to amino acids
5) Pancreatic proteases digest themselves and each other

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83
Q

four mechanisms of protein uptake

A

1) Na+-dependent cotransport
2) Sodium independent transporters of amino acids
3) Specific carriers for small peptides (di/tri) linked to H+ uptake (cotransporter)
4) Pinocytosis of small peptides by enterocytes (infants)

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84
Q

Na+-dependent cotransport

A

di and tripeptides are absorbed intact

Cotransporters utilize the N+/K+ ATPase gradient are major route for different classes of amino acids, water follows

Broken down into AAs by cytoplasmic peptidases in the enterocyte

AAs exit basolateral membrane of enterocyte by facilitated diffusion and enter blood capillaries

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85
Q

Bile acids

A

Primary bile acids are produced in the liver from cholesterol
Secondary bile acids are formed by bacteria in the intestine and colon
Bile acids are complexed with glycine or taurine to make bile salts
Bile is recycled during a meal by uptake in distal ileum = enterohepatic circulation

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86
Q

Pancreatic lipase

A

Converts triglyceride (unabsorbable) into a 2-monoglyceride and two free fatty acids (absorbable)

Fat droplets emulsified by bile salts and lecithin to form 1 um particles → increase surface area for digestion by lipase and colipase

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87
Q

Pancreatic colipase

A

protein that anchors lipase to surface of droplets

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88
Q

Pancreatic Micelles

A

products of lipase digestion (2’-monoglycerides and fatty acids) are solubilized in bile-salt micelles

Cylindrical structure, hydrophilic groups pointing out, hydrophobic part inward

Required to transport products of fat digestion through “unstirred” water layer near surface of enterocytes

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89
Q

Steps of lipid movement across enterocyte into lacteal

7 steps

A

1) products of lipase digestion (2’ monoglycerides and fatty acids) solubilized in bile salt micelles
2) Bile salt micelles allow transport through “unstirred water”
3) When lipids strike cell surface → diffuse passively into enterocyte
4) → packaged into chylomicrons (triglycerides, phospholipids, cholesterol, apolipoproteins)
5) → incorporated into secretory vesicles in golgi
6) → vesicles migrate to basolateral membrane and released into interstitial space by exocytosis
7) → enter lacteals (too large for capillaries)

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90
Q

Fat soluble vitamin absorption

A

(A, D, E, K): absorbed same as fat and cholesterol

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91
Q

Steatorrhea

A

excessive loss of fat in stool as well as lipid soluble vitamins

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92
Q

Absorption of water-soluble vitamins

A

B vitamins, C vitamins, Niacin, Folic acid, Pantothenic acid, and Biotin

Absorbed by cotransport with Na+ or by passive diffusion

Absorption complete in upper small intestine except for B12

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93
Q

Absorption of B12 (cobalamin)

4 steps

A

B12 absorption in distal ileum in complex with IF

Dietary proteins contain B12 (cobalamin) - important for RBC production

1) B12 binds salivary R protein in stomach
2) Pancreatic proteases remove R protein in duodenum
3) IF from stomach then binds B12 in duodenum
4) IF/B12 complex binds specific B12-IF receptor in terminal ileum enterocyte membrane

Impairment of B12 absorption → pernicious anemia

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94
Q

Water absorption in jejunum

A

absorption of sugars and amino acids in cotransport with Na+ causes Cl- to follow, and H2O to follow for osmotic reasons = PARACELLULAR pathway

Osmotic gradient due to solute deposition in confined regions between cells → driving force for H2O absorption

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95
Q

Crypts vs. Villi with water reabsorption:

A

Crypts = net fluid secretion from cells

Villi: net fluid absorption, vill surface area > crypt surface area

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96
Q

Ileum and water absorption

A

most nutrients already absorbed → continues to absorb H2O

Cl- absorbed by TRANSCELLULAR pathway involving Cl-/HCO3- exchange in apical membrane and facilitated diffusion across basolateral membrane

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97
Q

Colon and water reabsorption

A

Na absorption via apical Na+ channels (epithelial sodium channel, ENaC)

Aldosterone promotes ENaC water reabsorption and K+ secretion

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98
Q

Potassium Absorption

A

passive process

Paracellular movement in jejunum (due to low [K+] in intercellular space from Na+/K+ ATPase) but transcellular in colon

In severe diarrhea, when fluid loss is substantial, can cause hypokalemia
-Give K+ with oral rehydration fluids

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99
Q

Calcium and Magnesium absorption

A

Ca2+ and Mg2+ compete for uptake by cells - ONE OR THE OTHER

Ca2+ enters enterocyte passively down its electrochemical gradient in proximal intestines

Uptake of Ca2+ in intracellular calcium stores maintains the gradient
Ca2+ ATPase pumps calcium out to the blood

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100
Q

Vitamin D absorption

And effect on Calcium absorption

A
  • synthesized in skin, or absorbed by intestine
  • 25-hydroxylated in liver
  • 25-OH VitD is 1-hydroxylated in kidney in presence of PTH
  • VitD binds to cytoplasmic receptor, activating transcription/translation

**VitD stimulates uptake if Ca2+ by increasing Ca2+ binding proteins and Ca2+ ATPase molecules

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101
Q

Iron absorption

A

regulated absorption in proximal intestines

Transported across apical membranes as either heme or Fe2+ (Receptor mediated)

Two possible fates:

1) Binds apoferritin → ferritin stays in cell and is lost when cell dies
2) Binds transferrin (carrier protein) → leaves cell and goes into blood

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102
Q

Osmotic diarrhea

A

caused by impaired digestion or defects in absorption

Causes: Lactase deficiency, ileal resection (bile salts not absorbed), Celiac disease (gluten sensitivity with gliadin-induced destruction of villi)

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103
Q

Secretory diarrhea

A

may be caused by vibrio cholerae

Increases cAMP levels in cells and activates CFTR chloride channel → water into lumen

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104
Q

What effect will Loperamide have on secretory diarrhea caused by cholera?

A

Loperamide will have NO impact on someone who has cholera induced diarrhea

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105
Q

Oral rehydration

A

antibiotics plus KHCO3 to prevent hypokalemia and metabolic acidosis, glucose or amino acids with NaCl to facilitate the absorption of electrolytes and water

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106
Q

Oropharynx function:

Teeth + lips → ?
Mastication, saliva → ?
Tongue → ?
Pharynx →

A

Teeth + lips → biting and grinding
Mastication, saliva → conversion of bite into small, soft, lubricated bolus
Tongue → push bolus into pharynx
Pharynx → move bolus from mouth to upper esophagus

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107
Q

Function of esophagus (3)

A

Transport: conduit for food and water from oropharynx to stomach

Barrier: protection of mediastinum and lungs from ingested food/water

1-way system → prevent reflux of gastric contents into pharynx or airway

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108
Q

Esophageal Motility disorders

typical presenting symptoms (2)

diagnosis (2)

A

Symptoms:
**dysphagia to BOTH solids/liquids
chest pain

DX:
Exclude structural lesion (upper endoscopy, barium esophagram)
Esophageal manometry

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109
Q

Structural Esophageal disorders

typical presenting symptoms (3)

A

luminal narrowing/obstruction

Symptoms: Dysphagia to solids → liquids much later, Weight loss, heartburn

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110
Q

Diseases of esophageal motility (3)

A

1) Achalasia: abnormal peristalsis, failure of LES relaxation
2) Spastic disorders of esophagus
3) Scleroderma (weak peristalsis)

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111
Q

Diseases of esophageal structure (4)

A

1) Esophageal strictures
2) Extrinsic compression
3) Eosinophilic Esophagitis (EoE)
4) Esophageal rings

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112
Q

Gastroesophageal reflux disease (GERD)

Pathophysiology

A

pathologic reflux of gastric juice (acid) into esophagus due to reduced LES tone

Acid in esophagus or airway → symptoms and/or esophageal damage

Esophagus lacks defenses (mucous secretion, alkalinity) against acid

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113
Q

Causes and risk factors of GERD

A

Inappropriate LES relaxation
**hiatal hernia

Risk factors: alcohol, tobacco, pregnancy, obesity, fat-rich diet

Rare: Zollinger-Ellison, Sjogren’s, Scleroderma

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114
Q

Symptoms of GERD (4)

A
  • *Heartburn: burning sensation, substernal or epigastric, rises in chest
  • May be positional (lying down)
  • Often postprandial (After meals)

**Regurgitation with acidic taste

Cough, throat clearing, hoarseness

Damage to enamel of teeth

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115
Q

Treatment of GERD (2)

A

antacids, anti-secretory medications (PPI)

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116
Q

Complications of GERD (2)

A

Barrett’s esophagus, ulceration with stricture

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117
Q

Diagnosis of GERD (4)

A

usually by symptoms

response to acid suppressive therapy (PPIs)

Endoscopy: usually for refractory symptoms
**Vast majority normal

-Ambulatory pH testing
Transnasal catheter or wireless capsule

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118
Q

Achalasia

A

cardinal motility disorder of esophagus

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119
Q

Causes of Achalasia (5)

A

damage to myenteric plexus ganglion cells (between inner circular and outer longitudinal muscle of the muscularis propria layer)

1) Idiopathic - affects both genders, all races, adults - VAST MAJORITY

2) Pseudoachalasia (secondary achalasia)
- Direct mechanical obstruction of LES
- Infiltrative submucosal invasion
- Paraneoplastic → ab to myenteric plexus
* *Chagas disease

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120
Q

Pathophysiology of Achalasia

A

1) Impaired relaxation of lower esophageal sphincter
- Due to selective loss of inhibitory neurons in myenteric plexus → unopposed excitatory (ACh) neurons → hypertensive, non relaxed esophageal sphincter

2) Absence of normal peristalsis in distal esophagus

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121
Q

Symptoms of achalasia (7)

A

**Dysphagia to solids AND liquids

Weight loss
Regurgitation
Chest pain
Difficulty belching
Heartburn
Hiccups
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122
Q

Diagnostic testing for achalasia

A

Esophageal manometry

Barium swallow study (“bird beak sign” due to buildup and distention of esophagus)

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123
Q

Treatment of achalasia

Medical therapy (3)
Endoscopic therapy (3)
Surgical therapy (1)
A

Medical therapy:

1) Nitrates (stimulate intracellular Ca2+ → SMC relaxation)
2) Ca2+ channel blockers
3) Sildenafil

Endoscopic therapy:

1) GE junction botulinum toxin injections → inhibit ACh release from nerve endings
2) Pneumatic balloon dilation → tear LES muscle fibers
3) POEM: Per-Oral Endoscopic myotomy

Surgical: Surgical Myotomy

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124
Q

Barrett’s Esophagus - what is the histological change?

A

metaplasia of lower esophageal mucosa from stratified squamous epithelium → nonciliated columnar epithelium with goblet cells

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125
Q

Barrett’s Esophagus

A

Consequence of GERD, response of lower esophageal stem cells to acidic stress

Significant risk of developing dysplasia to esophageal adenocarcinoma

Endoscopy with biopsies every 3-5 years to assess for dysplasia

Dysplasia → much greater risk for esophageal cancer development

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126
Q

Treatment of Barrett’s Esophagus (2)

A

Esophagectomy

Endoscopic treatment for HGD and early esophageal adenocarcinomas

  • Ablation of Barrett’s tissue
  • Endoscopic resection of lesions
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127
Q

Esophageal Adenocarcinoma

  • malignant proliferation of what?
  • Risk factors? (7)
  • Most common where?
A

malignant proliferation of glands in LOWER ⅓ of esophagus

Risk factors: old age, smoking, obesity, GERD, BARRETT’S ESOPHAGUS, radiation exposure
-More common in men

Rising incidence in US and Europe - most common type in West

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128
Q

Squamous cell esophageal cancer

  • malignant proliferation of what?
  • Risk factors? (8)
  • Most common where?
A

squamous cell epithelial malignancy in UPPER or MIDDLE third of esophagus

Risk factors = IRRITATION:

  • Old age, alcohol/tobacco use, hot tea, achalasia (rotting food in esophagus), esophageal web (traps rotting food), esophageal injury (e.g. lye ingestion)
  • More common in men and african americans

Declining incidence in US/Europe, more common worldwide

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129
Q

Symptoms of esophageal cancer

A

weight loss, hemoptysis, chest pain, anemia
Progressive dysphagia to solids → liquids

Does not cause sx until advanced

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130
Q

Esophageal strictures

cardinal symptoms

A

benign or malignant

Cardinal symptom = dysphagia to solids

-Painless, symptoms on regular/daily basis, progressive, weight loss

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131
Q

Causes of

Benign esophageal strictures

Malignant esophageal strictures

A

GERD, radiation, caustic ingestion, congenital

*Rule out cancer with biopsy during EGD

Malignant: squamous cell carcinoma, adenocarcinoma

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132
Q

Eosinophilic Esophagitis (EoE)

A

Chronic immune/antigen mediated esophageal disease

Diagnosis:

  • Symptoms of esophageal dysfunction and dysphagia
  • Vomiting, pain, dyspepsia, progressing to odynophagia and stenosis
  • Eosinophilic infiltrate in esophagus
  • Absence of other potential causes of esophageal eosinophilia
  • Can cause esophageal strictures → ringed appearance
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133
Q

Demographics of Eosinophilic Esophagitis (EoE)

A

Most common less than 40 years of age
White males classic
Commonly associated with other allergic diseases (asthma, atopic dermatitis, seasonal allergies, food allergies)

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134
Q

Treatment of Eosinophilic Esophagitis (3)

A

3 D’s

Drugs: steroids (topical&raquo_space;> systemic), swallowed topical steroids
Diet: elemental diet (allergen-free)
Dilation

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135
Q

Diagnosis of oropharyngeal disease

A

History, physical exam = MOST helpful

Barium swallow

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136
Q

Barium swallow

A

xray video of mouth and throat under direct observation while patient chews and swallows various consistencies of radio-opaque barium

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137
Q

Causes of esophagitis

A

inflammation and injury to esophageal mucosa

1) Chemical injury:
- Reflux of gastric contents** most common
- Acids, alkalis, alcohol, tobacco

2) Medications

3) Infection:
- Fungal (Candida) → white plaques
- Viral (HSV, CMV, adenovirus) → punched out ulcers, viral inclusions

4) Immune related:
- Eosinophilic esophagitis
- Dermatologic diseases (lichen planus)

5) Radiation, trauma
6) Graft-versus-host disease

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138
Q

Reflux esophagitis

2 clinical features

what happens if left untreated?

A

Clinical features: heartburn and regurgitation

If left untreated → severe ulcerations, strictures, Barrett’s esophagus, and adenocarcinoma may develop

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139
Q

Causes of reflux esophagitis

A 
transient LES relaxation
decreased LES tone
hiatal hernia
increased intraabdominal pressure
delayed gastric emptying
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140
Q

Sequence following GERD all the way to cancer

A

GERD-Barrett Esophagus (metaplasia)-Dysplasia-Esophageal Adenocarcinoma

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141
Q

Zenker’s diverticulum

A

outpouching of pharyngeal mucosa through an acquired defect in muscular wall (false diverticulum)

Uppermost esophagus, above esophageal sphincter

Regurgitation, halitosis, and aspiration

Associated with reduced UES compliance

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142
Q

Esophageal webs

A

protrusion of esophageal mucosa

Often in UPPER esophagus

Presents with dysphagia for poorly chewed food

Increased risk for esophageal squamous cell carcinoma

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143
Q

Esophageal Varices

A

Dilated submucosal veins in LOWER esophagus

Due to PORTAL HTN and shunting of blood from portal to system venous system

Left gastric vein backs up into esophageal vein

Presentation: PAINLESS hematemesis

Associated with cirrhosis - most common cause of death in cirrhosis

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144
Q

Mallory-Weiss Syndrome

A

Longitudinal laceration of mucosa at gastroesophageal junction

Caused by vomiting usually due to alcoholism of bulimia

Presents with PAINFUL hematemesis

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145
Q

Tracheoesophageal Fistula

most common variant
presentation

A

congenital defect resulting in a connection between the esophagus and trachea

Most common variant = proximal esophageal atresia with distal esophagus arising from trachea

Presents with vomiting, polyhydramnios (baby can’t swallow amniotic fluid), abdominal distension (breathing into stomach), and aspiration

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146
Q

Congenital esophageal stenosis

A

Anomaly demonstrates significant narrowing of mid-esophagus

→ Esophageal web/rings, muscular hypertrophy, inflammation

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147
Q

Cardia contains what cell type and secretes what?

A

Gastric pits contain mucous cells that secrete mucus and small amount of pepsinogen

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148
Q

Fundus contains what gland type? (cells in this gland?)

A

Contain gastric pits with OXYNTIC glands = mucous cells, parietal cells, chief cells, endocrine cells, and enterochromaffin cells

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149
Q

Antrum contains what gland type? (cells in this gland?)

A

Contains PYLORIC glands = mucous cells, endocrine cells, G cells (produce gastrin), and D cells (produce somatostatin)

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150
Q

Stomach function

A

1) Receptive relaxation
2) Digestion/mixing
3) Slow release of chyme into duodenum
4) Parietal cells secrete HCl to disinfect food, and IF for B12 absorption

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151
Q

Movement of liquids and solids in stomach

A

Liquids rapidly emptied from proximal stomach to duodenum

Solids initially stored in proximal stomach and then move to antrum

  • -> Vagally mediated segmented contractions originating in mid-body of greater curve mix food
  • -> When food particles 1 mm or less, it empties into pylorus

Inhibitory mechanisms in small intestine prevent it from being overwhelmed by rapid entry of nutrients from stomach
-CCK, secretin, GIP, pH receptors, osmoreceptors, etc. in duodenum reflexively inhibit gastric emptying

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152
Q

Mucosal protective factors that prevent self-destruction

A

Prostaglandin E2 and Prostacyclin → stimulate bicarb secretion, mucus, and mucosal blood flow

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153
Q

H. Pylori Gastritis:

Epidemiology

A

most common cause of gastritis, typically in ANTRUM

  • adult prevalence of H. pylori correlates with crowded living conditions and socioeconomic status during childhood
  • Transmission occurs person-to-person, especially among children - fecal-oral and environmental spread
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154
Q

H. pylori bacteria

A

gram-negative spiral

produces abundant urease which produces ammonia and raises local pH

→ escape acidic gastric juice and burrow through mucus layer to colonize surface epithelium of gastric mucosa

Elicits robust inflammatory response → active/chronic gastritis

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155
Q

Virulence factors of H. Pylori (6)

A

1) Flagella to maneuver through gastric mucous
2) Adhesion molecules bind to gastric foveolar cells
3) Acid resistance with urease
4) CagA protein: decreased cell adhesion-associated with both gastric and duodenal ulcers and cancer
5) VacA: exotoxin → pores in membrane
6) Minimization and evasion of immune response

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156
Q

H. Pylori mucosal biopsy reveals what?

A

Mucosal biopsies indicate presence of urease (CLO) - use pH sensitive test medium

Shows infiltration of gastric mucosa with neutrophils (active gastritis) or lymphocytes (chronic gastritis)

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157
Q

diagnosis of H. pyloris infection

A

1) Mucosal biopsy
2) Culture (least sensitive)
3) Blood antibody test
4) Urea breath test
5) Stool antigen test

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158
Q

Blood antibody test for H. Pylori

A

H. pylori produces circulating antibody that can be detected on ELISA - BUT can’t be used acutely to determine effect of abx

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159
Q

Urea breath test

A

urea radiolabeled ingested with liquid meal, if urease present, can be detected by analysis of expired breath

Virtually 100% PPV and 95% NPV

PPI can result in false negative test

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160
Q

Stool antigen test

A

similar performance characteristics of UBT, most commonly used test in outpatient setting to confirm eradication

161
Q

Spectrum of disease with an H. Pylori gastritis infection

A

Asymptomatic

Gastritis

Peptic ulcer disease - both duodenal and gastric ulcers

Neoplasia (gastric cancer, lymphoma)

162
Q

Treatment of H. pylori Infection

A

course for 7-14 days

Triple therapy: Proton pump inhibitor + Amoxicillin + Clarithromycin

Quadruple therapy = PPI + bismuth + tetracycline + metronidazole

Confirm eradication (stool antigen)

163
Q

Diseases associated with H. Pylori

A

Gastritis, gastritic and duodenal ulcers, gastric adenocarcinoma, gastric lymphoma

164
Q

Eosinophilic gastritis

A
  • infiltration of gastric wall with eosinophils
  • Allergic disease (e.g. cow’s milk) and parasitic infection

Symptoms: delayed gastric emptying, associated peripheral eosinophilia

TX: corticosteroids, surgery

165
Q

Granulomatous gastropathy

A

Associated with Crohn’s, sarcoidosis, and infection

166
Q

Autoimmune Gastritis

A

**CD4+ T cells against parietal cells

Anti-parietal cell and anti-Intrinsic Factor antibodies
+/- pernicious anemia

Most common in scandinavian / N. Euro descent

Can develop intestinal metaplasia → higher risk of gastric cancer

Histology: lymphocyte and plasma cell infiltrate in the body of stomach and glandular atrophy

167
Q

Gastropathy

A

gastroduodenal injury with little or no inflammation associated with lesion

168
Q

NSAID-Induced Injury:

cause
risk factors
treatment

A

Gastropathy

Cause: prostaglandin depletion

Increased risk: elderly, prior ulcer disease

Treatment: PPIs - healing usually occurs even if NSAID is continued

169
Q

Ulceration vs. erosion

A

Ulceration = > 5mm in diameter, depth breaches muscularis mucosa

  • Often gastric ulcers but can also be in duodenum
  • Increased risk for GI bleed

Erosion = not below mucosa

170
Q

Ethanol-Induced Injury

A

lesion similar to NSAID induced lesions, can occasionally cause serious bleeding, but rare

171
Q

Stress related mucosal injury

A

hemorrhages and erosions of stomach and duodenum in patients under “physiologic stress”

Morphologically resembles acute gastritis

Patients with CNS injury, prolonged mechanical ventilation, coagulopathy, and burns - NOT pts in coronary care units

172
Q

What kind of ulcers?

Trauma, shock, sepsis → ?

Burns → ?

Intracranial disease → ?

A

Trauma, shock, sepsis → stress ulcers

Burns → Curling’s ulcers
-Due to hypovolemia and decreased blood supply

Intracranial disease → Cushing ulcers
-Increased ICP → increased vagal stimulation → increase ACh → increased acid production by parietal cell

173
Q

Pathogenesis of stress related mucosal injury

A

most patients not acid hypersecreters but due to mucosal ischemia/vasoconstriction

174
Q

Peptic ulcer disease

A

acid mediated ulceration of distal stomach or proximal duodenum

175
Q

Pathogenesis of peptic ulcer disease

A

gastroduodenal mucosal defenses unable to protect epithelium from corrosive effects of acid and proteases (pepsin)

Primarily disease of failed mucosal integrity, NOT excess acid/pepsin secretion

176
Q

Predisposing factors for gastric ulcer vs. duodenal ulcer

A

gastric ulcer: H pylori infection, NSAID use

duodenal ulcer: H. pylori and ZE syndrome

177
Q

Symptoms of peptic ulcer disease

A

Asymptomatic, or burning epigastric pain relieved by food or antacids, may awaken patient from sleep

“Nocturnal pain relieved with antacids” = most specific sxs

178
Q

Complications of peptic ulcer disease (3)

A

Bleeding (15%)

Perforations/Penetration (5%) → acute development of peritonitis

Obstruction (2%) → nausea, vomiting, early satiety
Due to repeated ulceration and formation of scar tissue

179
Q

Treatment of peptic ulcer disease

A

PPI and H.pylori eradication are cornerstones of therapy

Severe acute bleeds → PPI drips used in ICU to tightly control pH

180
Q

Systemic presentation of gastric carcinoma (5)

A

1) Acanthosis nigricans
2) Leser-Trelat sign (seborrheic keratoses)
3) Spread to left supraclavicular node (Virchow’s node)

Distant mets:

4) Sister Mary Joseph nodule: periumbilical region (intestinal type)
5) Bilateral ovary mets = Krukenberg tumor (diffuse type)

181
Q

Gastric Adenocarcinoma types (2)

A

1) diffuse type

2) intestinal type

182
Q

Diffuse type

A

signet ring cells, diffusely infiltrate gastric wall

Can cause desmoplasia = thickening of stomach wall (linitis plastica)

183
Q

Intestinal type

A

large, irregular ulcer with heaped up margins

Most common in lesser curvature of antrum

Associated with H. pylori, autoimmune gastritis, nitrosamines (smoked food, Japan), blood type A

184
Q

Epidemiology of gastric adenocarcinoma

A

90% of all malignant gastric tumors

2nd most common malignancy in the world (but not USE)

185
Q

Prognosis of gastric adenocarcinoma

A

related to depth of invasion (worse if in muscular layer)

High mortality unless disease detected early

5-year survival = 30% (90% for early cancer)

186
Q

Symptoms of gastric adenocarcinoma

early vs. late

A

Early: dyspepsia, dysphagia, nausea
Late: weight loss, anorexia, early satiety, anemia

187
Q

Genetics in gastric adenocarcinoma (3)

A

1) Wnt signalling pathway activation (can occur with loss of APC as in FAP)

2) Loss of CDH1 (mutation or methylation)
- Common in diffuse type cancers

3) Amplification of Her2/neu
→ TX with trastuzumab (TKI)

188
Q

3 gastric polyp types

A

1) Hyperplastic polyps
2) Gastric adenomas
3) Fundic gland polyps

189
Q

Hyperplastic polyps

A

proliferation of gastric foveolar cells (mucus producing)

Arise from chronic inflammation

Found in gastric body autoimmune gastritis and H. pylori infection with chronic atrophic gastritis

*Rare malignant potential
> 1 cm → increased risk of dysplasia or adenocarcinoma

190
Q

Histology of hyperplastic polyps

A

Histology: inflammation and edema, cystically dilated foveolae

typically in antrum of stomach

191
Q

Gastric adenomas

A

arise from dysplastic epithelial cells, risk progression to adenocarcinoma

Premalignant - Should be removed endoscopically

Familial adenomatous polyposis (FAP) → multiple polyps and adenomas

192
Q

Histology of gastric adenomas

A

dark, atypical cells

193
Q

Fundic gland polyps

A

dilated oxyntic glands lined by flattened parietal and mucous cells (most common type of gastric polyp)

Unrelated to H. pylori infection
Typically due to PPI use

Benign - No malignant potential
Increased incidence with FAP

194
Q

Histology of fundic gland polyps

A

cystically dilated oxyntic gland

195
Q

Stromal Tumors

A

benign gastric tumors arising from supporting tissues

Leiomyomas and Lipomas → malignant leiomyosarcoma, liposarcoma

Usually asymptomatic, but larger ones can present with abdominal pain and GI bleeding

TX = surgical resection

196
Q

Gastrointestinal stromal tumors (GISTS)

A

subtype of stromal tumor

Express c-KIT (CD117) transmembrane receptor tyrosine kinase → TX with imatinib (receptor tyrosine kinase inhibitor) and surgical resection

Mesenchymal neoplasms derived from interstitial cells of Cajal (pacemaker cells)

197
Q

Neuroendocrine Tumors: Carcinoid tumors

A

arise from enterochromaffin or enterochromaffin-like cells in intestinal tract

Well-differentiated endocrine neoplasm

Can be associated with MEN1

Histology: Nests and trabeculae of monomorphic cells

Sporadic type → higher rate of malignant behavior
Atrophy associated → typically indolent

198
Q

Gastric Lymphoma

A

Strong association between H. pylori infection and primary gastric B-cell lymphoma

Low grade clonal proliferation of B-cells in H. pylori induced gastric MALT → lesion may progress to high-grade lymphoma → require surgical resection and chemo/radiation

199
Q

Hypertrophic Pyloric Stenosis

A

hyperplasia of pyloric muscularis propria → obstructs gastric outflow

Presents in 2-3rd week of life with regurgitation and persistent projectile, nonbilious vomiting (DEVELOPS AFTER YOU ARE BORN)

More common in boys

Presents as firm ovoid abdominal mass

TX: surgical splitting of muscularis propria (“myotomy”)

200
Q

Menetrier disease

A

very rare

Mucous cell hyperplasia

Gastric acid secretion low-normal

Signs/symptoms: abdominal pain, weight loss, N/V, hypoalbuminemia

201
Q

Zollinger-Ellison Syndrome

A

neuroendocrine tumor in pancreas or duodenum

Gastrin secreted leading to hyperplasia of parietal cells

Signs/symptoms: chronic diarrhea, abdominal pain, peptic ulcers

202
Q

4 Layers of GI tract

A
  1. mucosa
  2. submucods
  3. muscularis externa
  4. Serosa adventitia
203
Q

Mucosa

A

epithelial layer + lamina propria (underlying loose, vascularized CT) + muscularis mucosae (thin layer of smooth muscle underlying this)

204
Q

Cells in Epithelial layer

A

contains enteroendocrine cells (secrete into blood) and M cells (immune sampling cells)
Contain IgA receptor that are ingested and transported into lumen → first defense layer

205
Q

Basal lamina

A

underlying epithelial cells, specialized to allow molecules across epithelium of gut

206
Q

Lamina propria

A

contains capillaries and WBCs (including MALT)

Lymphocytes, plasma cells, and macrophages scattered throughout lamina propria

207
Q

Submucosa

A

connective tissue (more dense than mucosa), larger blood vessels, nerve plexes, glands, lymphatic nodules

208
Q

Nerve plexus within submucosa

A

Meissner’s nerve plexus

209
Q

2 divisions of muscularis externa

A

inner circular and outer longitudinal smooth muscle layers

210
Q

Function of muscularis externa

A

Peristalsis and churning of lumenal contents

211
Q

Nerve plexus within muscularis externa

A

Auerbach’s plexus between inner circular and outer longitudinal smooth muscle

212
Q

Layers of stomach

A
  1. inner circular
  2. outer longitudinal
  3. oblique smooth muscle (churning)
213
Q

Serosa/adventitia

A

outer covering of squamous epithelial cells separated from underlying muscular layer by thin CT layer

  • Adventitia = above diaphragm (esophagus), no outer squamous layer
  • Contains large blood vessels and nerves
214
Q

How do we avoid digesting ourselves?

A
  • Mucosae lining the tube creates a microenvironment at surface of the tube that is resistant to proteolytic digestion
  • Mucin = heavily glycosylated, heavily hydrated, resistant to proteolysis → prevent digestion and protective layer from bacteria
215
Q

Prevention of bacterial infection along the GI tract

A

Lymphoid tissue present as scattered individual cells and as lymphatic nodules

Peyer’s patch: group of lymphatic nodules

M-cells: specialized epithelial cells, function in antigen-uptake
- Phagocytose luminal contents and present antigens to underlying lymphocytes and macrophages

Plasma cells in nodules release IgA immunoglobulins that bind to receptors on epithelial cells and are transcytosed to lumenal surface → antibacterial agents
Prevents pathogenic colonization and adherence

216
Q

Neural control of GI tract (2)

A

1) Enteric neurons: lie outside CNS, produce local gut motility
2) Parasympathetic and sympathetic fibers: directed by CNS, enables coordinated input → coordinated peristalsis and effects on blood vessels (PS) and glands (S)

217
Q

Function of esophagus

A

convey ingested material from pharynx to stomach (no digestion)

218
Q

Location of pancreas

A

posterior to stomach, anterior to thoracic spine/ribs in retroperitoneum

219
Q

Blood supply of pancreas

A

superior pancreaticoduodenal and splenic arteries (branch off celiac axis) and inferior pancreaticoduodenal artery (branch off the SMA)

220
Q

Exocrine function of the pancreas

made up primarily of what two types of cells?

3 major functions

A

made up of epithelial cells with acinar glands (Acinar cells)

1) Secrete digestive enzymes as pro-enzymes/zymogens and amylase/lipase as active enzymes in response to cholecystokinin
2) Produce large amounts of bicarb and water in response to secretin→ maintain flow throughout ducts, keep zymogens inactive with low pH, protect pancreas and duodenum/ileum from low pH
3) Trypsin inhibitor in pancreas deactivates any trypsin prematurely activated

221
Q

Pathway of pancreatic excretions

A

enzymes secreted across apical cell membrane into tiny ductule at center of each acinus

→ ductules coalesce into larger exocrine duct system of pancreas

→ main (ventral) duct and ampulla of Vater

222
Q

Endocrine function of the pancreas

A

pancreatic islet cells produce insulin, somatostatin, VIP, glucagon, and others

223
Q

Acute pancreatitis

A

when pancreatic enzymes are inappropriately and prematurely activated resulting in autolysis of the gland → severe inflammation and necrosis of pancreatic tissue

224
Q

Labs used for diagnosis of acute pancreatitis

A

serum amylase and lipase elevated > 3x upper limit of normal

Lipase more specific for pancreatitis - rises within 1-2 hrs, remains high for 1 week

Amylase - rises and falls within 24-48 hrs - can be high due to other etiologies (mumps, Sjogrens, penetrating peptic ulcer, ectopic pregnancy, intestinal ischemia/trauma, etc.)

225
Q

Imaging used for diagnosis of acute pancreatitis (what are the benefits of each?)

A

contrast CT or ultrasound

US: best for gallbladder stones

CT: detects edema, calcifications, fluid collections (complications of acute pancreatitis)

226
Q

Pathophysiology of acute pancreatitis

A

caused by obstruction of pancreatic duct → stagnation of pancreas enzymes within duct lumen and activation of enzyme cascade

Lipase released from dying acinar cells → break down fats → fatty acids precipitate with calcium and form insoluble soaps

→ Coagulation necrosis of gland and hemorrhage into retroperitoneum

→ Intense infiltrates of neutrophils and apoptosis of epithelial cells

227
Q

Main causes of acute pancreatitis

A

1) Gallstone: most common cause of pancreatitis in US**
2) Ethanol
3) Other causes: tumors, surgical, congenital ductal abnormalities, Sphincter of Oddi dysfunction types 2 and 3, hyperlipidemia, blunt/penetrating trauma, drugs, hypercalcemia, infection, CF

228
Q

How does ethanol cause acute pancreatitis?

A

direct toxic effect on pancreatic acinar cells and ductal epithelium → premature release/activation of trypsinogen and stagnant flow of pancreas juice

229
Q

How do gallstones cause acute pancreatitis?

A

Stone lodges in distal common bile and/or ampulla → obstructing ventral duct and causing bile reflux into pancreas → zymogen activation

230
Q

Symptoms of acute pancreatitis

A

1) sudden onset severe pain in upper abdomen, radiating to back
2) Nausea/vomiting
3) Low grade fevers
* Self-limited

Elevated pancreatic enzymes in serum

231
Q

Treatment of acute pancreatitis (4)

A

1) admission, NPO, IV pain meds, IV fluids, time - supportive only usually

2) Consider ERCP for bile duct stone removal
- If persistent bile duct stone → requires extraction

3) Cholecystectomy to remove source of stones in some cases
4) Avoidance of alcohol is KEY

232
Q

Complications of acute pancreatitis (5)

A

1) Ileus (paralysis of gut)
2) Intra-abdominal hemorrhage (digestion through artery)
3) Pseudocyst formation
4) Severe pancreatitis → bowel/bile duct obstruction, shock, respiratory distress/failure/renal failure, death
5) Pancreatic necrosis → increases mortality significantly

233
Q

Chronic Pancreatitis

A

develops after repeated bouts of acute pancreatitis, permanent destruction of pancreatic parenchyma with replacement by fibrosis

234
Q

Main features of chronic pancreatitis (4)

A

1) Ductal strictures/stones → pain, exocrine failure
- NOT seen in acute pancreatitis **

2) Pancreatic pseudocysts → pain, nausea, vomiting
3) Acinar destruction → exocrine failure
4) Diabetes → endocrine failure (late)

235
Q

Diagnosis of chronic pancreatitis (7)

A

1) History and physical
2) Plan abd xray
3) CT
4) Endoscopic US
5) Rapid fat stool stain
6) 72 hour quantitative stool collection
7) Secretin stimulation test

236
Q

What does a CT of chronic pancreatitis show?

A

CT → dilated duct, atrophy, calcifications, pseudocysts

Mainstay of diagnosis

237
Q

What is the secretin stimulation test?

what is required for diagnosis of chronic pancreatitis?

A

tube in stomach and duodenum - duodenal bicarb response to secretin [HCO3-] less that 80 mEq/L after 2 hours = diagnostic of pancreatic exocrine failure

-Secretin should stimulate bicarb and water secretion from pancreas in normal patient

238
Q

Causes of chronic pancreatitis

A

typically chronic alcohol abuse +/- smoking

ALCOHOL = most common cause

Genetic conditions: CF, mutations in trypsinogen (PRSS), or trypsin inhibitor genes (SPINK), familial hypertriglyceridemia

239
Q

Pathophysiology of chronic pancreatitis

A

Replacement of healthy pancreatic tissue by hard, fibrous tissue, and possible atrophy of the gland

Pancreas juice becomes viscous and calcifications develop within duct

Fibrous tissue → strictures of duct

240
Q

Microscopic appearance of chronic pancreatitis

A

broad bands of scar tissue replace lost tubular tissue

Moderate numbers of lymphocytes/plasma cells present

Relative sparing of islet cells

241
Q

Symptoms of chronic pancreatitis (3)

A

1) Malabsorption
2) Pain (chronic, waxes/wanes, never disappears) - epigastric, radiates to back, worse after meals
3) Malnutrition

242
Q

What are the malabsorption problems seen commonly in patients with chronic pancreatitis? (4)

A

1) Dominant malabsorbed nutrient is lipid = steatorrhea

2 )B12 malabsorption (pancreatic enzymes cleage R-bond)

3) Can eventually get diabetes due to glucagon/insulin secretion
4) Vitamin K malabsorption → bleeding

243
Q

Steatorrhea in chronic pancreatitis

A

Dominant malabsorbed nutrient is lipid = steatorrhea (oily, foul smelling, and/or buoyant stools), flatulence, weight loss

Due to decreased lipase and colipase in duodenum and decreased duodenal pH

Malabsorption occurs in later stages since only 10-20% of acinar cells required for maintaining lipase reserve

244
Q

Complications of chronic pancreatitis (2)

A

1) Pseudocyst

2) **Ductal obstruction due to strictures or stones (NOT in acute pancreatitis)

245
Q

Pseudocyst

A

fluid collection of liquefied/auto-digested pancreatic parenchyma containing a mixture of pancreas juice and clumps of semi-solid, necrotic tissue surrounded by granulation tissue

Resolve as pancreatitis improves, but if they persist, may grow/push on adjacent structures and require drainage

246
Q

Treatment of chronic pancreatitis (5)

A

1) ETOH avoidance ** = Mainstay of treatment
2) Pancreas enzyme replacement for steatorrhea
3) ERCP and dilation, stent placement, or stone removal for duct obstruction
4) Celiac nerve block for pain
5) Surgical resection if refractory and severe

247
Q

What is ERCP?

A

endoscopic retrograde cholangiopancreatography= visusalization and palliative stent placement across bile duct stricture to relieve cholestasis symptoms

248
Q

When to use ERCP? (3)

A

Adenocarcinoma → Refer in patients to ERCP with stent if they have metastases, recurrent disease, or high surgical risk

Autoimmune pancreatitis → ERCP with placement of biliary stent effective in patients with jaundice or pruritus

Acute pancreatitis → consider ERCP for bile duct stone removal if it doesn’t pass on its own

249
Q

Pathophysiology of autoimmune pancreatitis

A

IgG-4 + Plasma cells and lymphocytes infiltrate pancreas and its vessels → localized or diffuse enlargement of pancreatic parenchyma and narrowing of pancreatic duct and/or bile duct

Glandular atrophy, ductal dilation

**calcifications and steatorrhea are NOT features of AIP (features of chronic pancreatitis)

250
Q

Symptoms of autoimmune pancreatitis?

A
  • chronic epigastric or diffuse abdominal pain +/- cholestasis (jaundice, dark urine, itching)
  • Typically males in ages 40-70

**Can masquerade as pancreatic cancer

251
Q

Diagnosis of autoimmune pancreatitis (3)

A

Elevated serum IgG-4

Elevated total IgG, ANA, and RF

CT, US, or MRI → focally or diffusely enlarged pancreas with decreased enhancement and loss of lobular contour

252
Q

Treatment of autoimmune pancreatitis (2)

A

6-week corticosteroid course (MUCH more treatable than cancer)

ERCP with placement of biliary stent effective in patients with jaundice or pruritus

253
Q

Neuroendocrine tumors of the pancreas

Histology

Presentation (3)

A

aka carcinoids

Histology: arise from enterochromaffin cells of lung, GI tract, or pancreatic islets

Presentation:

1) Most are clinically silent and detected on routine imaging
2) Larger ones cause pain
3) Symptoms of hormone excess (insulin, glucagon, gastrin, VIP, somatostatin)

254
Q

Diagnosis and treatment of neuroendocrine tumors of the pancreas

A

Diagnosis: imaging studies, FNA

Treatment: surgical resection or close observation in high surgical risk patients

255
Q

Adenocarcinoma of the pancreas epidemiology

A

4th leading cause of cancer mortality in men and women in US

5-year survival only 5%

256
Q

Adenocarcinoma of the pancreas histology

A

typically arise from ductal epithelial cells (acinar cells 5-10% of time)

Form primitive mucin-positive gland-like structures

Elicit strong fibrotic reaction (desmoplasia) → hard to penetrate with chemo

257
Q

Adenocarcinoma of the pancreas risk factors

A

family history, tobacco use, chronic pancreatitis, obesity, genetic syndromes (VHL, Peutz-Jeghers)

258
Q

Adenocarcinoma of the pancreas symptoms

A

usually present late, with locally advanced/metastatic disease

1) Weight loss, abdominal/back pain (late symptom)

2) **Symptoms of bile duct obstruction → jaundice, dark urine, pruritus
- Due to bile duct obstruction at head of pancreas

3) Hypercoagulable state (Trousseau’s syndrome)

259
Q

Adenocarcinoma of the pancreas diagnosis and treatment

A

Diagnosis: contrast abdominal CT, fine needle aspiration (FNA), biopsy
-Endoscopic ultrasound is test of choice to stage pancreatic cancer

Treatment: surgical resection

260
Q

4 names of proton pump inhibitors

A

Lansoprazole, Omeprazole, Esomeprazole, Lansoprazole

261
Q

How do PPIs get into cells and act?

A

prodrug → systemic circulation → diffuses into parietal cells → activated in canaliculi to sulfenamide → then “trapped”

262
Q

Mechanism of action of PPIs

A

Irreversibly inactivates H+-K+-ATPase

ONLY inactivates ACTIVE pumps
→ 2-5 days for steady state effect

Must take PPI before a meal so Cp max coincides with maximal pump secretion

Inactive pumps stored inside cell, put on membrane when active

Acid suppression for > 18 hours

263
Q

Uses of PPIs (5)

A

1) GERD (#1 agent)

2) Peptic ulcer disease
- Used in triple therapy in order to increase gastric pH and promote healing with H. pylori associated PUD

3) NSAID induced ulcers (prevention and treatment)
4) Prevention of stress gastritis (IV infusion)
5) Zollinger-Ellison Syndrome

264
Q

Side effects of PPIs

dosage reduction for who?
chronic use results in what?

A

Dosage reduction required for HEPATIC disease (not renal)

Remarkably safe drug, minimal side effects (headache, GI pain, nausea, diarrhea, constipation)

Acid rebound upon discontinuation (taper dose)
-Gastrin levels are increased due to decreased acidity, but proton pump is blocked so pH stays high → remove PPI → rebound acidity

Chronic use → increased fracture risk (decreased Ca2+ absorption), decreased Mg2+ absorption

265
Q

Misoprostol

mechanism of action
indication

A

Prostaglandin analog → acts on epithelial cells to decrease H+ secretion and increase mucus bicarbonate

Indicated for NSAID induced ulcers - not first line (PPIs are)

266
Q

Misoprostol

side effects (2)

A

diarrhea

uterine cramping, contraindicated in pregnancy

267
Q

Sucralfate

mechanism of action
side effects

A

Sulfated disaccharide Al+++ salt → binds necrotic tissue forming protective barrier
Activated by acidic pH → give on empty stomach

Not absorbed → few side effects (constipation)

268
Q

H2 antagonist drug names (3)

A

Cimetidine, Famotidine, Ranitidine

269
Q

H2 antagonists mechanism of action

A

competitive reversible block of H2 receptors on basolateral membrane

270
Q

H2 antagonists uses (3)

A

GERD
PUD (usually PPIs used instead)
Stress related gastritis (IV H2 antagonist)

271
Q

PPI vs. H2 antagonist (3)

A

Less efficacious than PPIs

More rapid onset of action than PPIs → better for acute gastritis

Better at blocking nocturnal H2 than meal stimulated (ACh-gastrin) acid secretion, but PPIs are still more effective

272
Q

Side effects of H2 antagonists (4)

A

Generally well tolerated

1) CNS dysfunction (mental status change) in elderly or renally impaired
2) Gynecomastia (chronic high dose cimetidine)
3) Tolerance possible with continued use

273
Q

DDIs and dosage reduction in who?

A

DDIs: Cimetidine inhibition of CYP450 metabolism**

Renal excretion - dosage reduction with renal dysfunction

274
Q

Antibiotic ulcer therapy

purpose?

A

used to eradicate H. pylori infection that damages epithelial cells and increases susceptibility to ulceration (associated with 85% of duodenal ulcers)

**Confirm eradication (stool antigen test)

275
Q

Triple therapy (ulcer therapy)

A

Clarithromycin-Amoxicillin/Metronidazole-PPI

276
Q

Quadruple therapy (ulcer therapy)

A

bismuth subsalicylate-Metronidazole-Tetracycline-PPI (or H2 Antagonist)

277
Q

Sequential therapy (ulcer therapy)

A

amoxicillin-PPI x 5 days, THEN clarithromycin-Tinidazole / Metronidazole-PPI x 5 days

278
Q

Ideal antacid has what properties? (5)

A

rapidly raise pH (to pH=4)

nonabsorbable

long acting,

no adverse effects

no drug-drug interactions

279
Q

Calcium carbonate (Tums)

A

Rapid, prolonged neutralization → rebound secretion

Safe, but NOT for chronic use (except when used as Ca2+ supplement)

Side effects: Constipation, hypercalcemia, renal calculi

280
Q

Aluminum hydroxide/Aluminum carbonate

A

Widely used

Binds phosphate in gut (used in CKD)

Side effect: constipation, CNS toxicity with chronic intake

281
Q

Magnesium hydroxide (milk of magnesia)

side effects

A

osmotic diarrhea

282
Q

Prokinetic agents (3)

A

Metoclopramide (Reglan)

Tegaserod, Cisapride

283
Q

Metoclopramide (Reglan)

Mechanism of action

A

dopamine antagonist → block presynaptic inhibition of ACh release → increase in coordinated contractions → enhance transit

Weak 5-HT antagonist at chemoreceptor trigger zone → relieve n/v

284
Q

Metoclopramide (Reglan)

side effects

A

somnolence, dystonic reactions, tardive dyskinesias (EPSEs)

285
Q

Tegaserod, Cisapride

Mechanism of action

A

5HT4 receptor agonists → direct stimulation of ACh release → increase coordinated contractions and transit in esophagus and stomach

286
Q

Tegaserod, Cisapride

use

A

reduces bloating of irritable bowel syndrome (IBS)

287
Q

Tegaserod, Cisapride

side effects

A

Cisapride → LIFE THREATENING ARRHYTHMIAS (increase QT)

Tegaserod → linked to strokes, MI, angina

288
Q

Epithelium in esophagus

A

non-cornified squamous epithelium

289
Q

Muscle within the esophagus

A

Upper portion → skeletal muscle, midway → mix skeletal/smooth, lower ⅓ → solely smooth muscle

290
Q

Mucus glands in esophagus

A

present in dermis → lubrication, assist in swallowing

291
Q

Esophageal gastric junction

A

contains small incomplete sphincter with maintained muscular contraction to prevent reflux of stomach contents

292
Q

Does the esophagus contain a mucous covering?

A

NO

293
Q

Cardia

A

small area with mucus secreting glands around entry of esophagus

294
Q

Fundus

A

main body of stomach, secretes acid, peptic digestive products, and mucus

295
Q

Pylorus

A

secretes mucous, contains endocrine cells that secrete gastrin hormone

296
Q

Surface mucous secreting cells

A
  • face cavity of stomach, arranged in folds along underlying lamina propria
  1. Contain large vesicles with mucins and bicarbonate → local discharge onto surface to provide viscous protective layer
    - Shelter epithelial cells against stomach acid and abrasion from churning chime
  2. Have short microvilli on surface with glycoprotein/glycolax covering
297
Q

Gastric pits

A

spaces between epithelial folds, continue deep into mucosa as one or more tubular gastric glands

298
Q

Gastric glands

A
  • contain differentiated epithelial cells crucial for function of stomach (digestion of food at acidic pH)
  • Stomach lumen extends to very body of gastric glands
299
Q

Stem cells of the stomach

A

Enable constant renewal of gastric epithelium (every 3-5 days)

  1. Deep in glands, turn over every 6-12 months
  2. Located in upper neck region, undifferentiated
    → downward to specialized cells on gastric glands
    → upward mucous-secreting cells
300
Q

Chief cells

A

protein secretors with apical granules and elaborate basal RER

  1. Secrete pepsinogen → converted to pepsin in presence of acid
  2. Pepsin: protease, optimal function at low pH
  3. Derived directly from stem cells
301
Q

Parietal cells (5)

A

unique acid producing cells

  1. H+/K+ ATPase pumps H+ ions into lumen of gastric glands against high concentration gradient
    pH of gastric juice = 1-1.5
  2. Extensive microvilli bordering canaliculi → enormous surface area for pumping H+ into lumen
  3. Lots of mitochondria
  4. Stimulated to produce acid by gastrin and histamine
  5. Secrete intrinsic factor
302
Q

Zollinger-Ellison Syndrome

A

excessive secretion of gastrin → overproduction of HCl by parietal cells → duodenal ulcers

303
Q

Enteroendocrine cells

A

APUD cells (amine precursor uptake decarboxylation), typically oriented toward vascular side to release into bloodstream

304
Q

4 types of enteroendocrine cells

A
  1. G-cells: secrete gastrin, located in pylorus
  2. A-cells: secrete glucagon
  3. EC-cells: secrete serotonin (serotonin also taken up and stored by platelets)
  4. D-Cells: secrete somatostatin, widely distributed in middle portion of stomach
305
Q

Rugae

A

Stomach

  • longitudinal folds in stomach wall
  • Disappear upon distension
306
Q

Plicae circularis

A

(small intestine)

  • permanent transverse-oriented folds covered with villi
  • Increase surface area of small intestine 8x
307
Q

Duodenum

A
  • low pH chyme from stomach enters duodenum upon relaxation of pyloric sphincter
  • Digestion continues in duodenum at higher pH and with enzymes released from pancreas and present at surface of intestinal mucosa
  • Absorption also occurs due to high surface area here
308
Q

Brunner’s glands:
Duodenum:
Jejunum:
Ileum:

A

Duodenum: Present
Jejunum: Absent
Ileum: Absent

309
Q

Goblet cells:
Duodenum:
Jejunum:
Ileum:

A

Duodenum: +
Jejunum: ++
Ileum: +++

310
Q

Lymphatic tissue:
Duodenum:
Jejunum:
Ileum:

A

Duodenum: +
Jejunum: ++
Ileum: ++++

311
Q

Plicae Circularis:
Duodenum:
Jejunum:
Ileum:

A

Duodenum: +
Jejunum: Best developed
Ileum: +

312
Q

Number of Villi:
Duodenum:
Jejunum:
Ileum:

A

Duodenum: Most numerous
Jejunum: decreased distally
Ileum: least abundant

313
Q

Parts of the intestine (5)

A
  1. Enterocytes
  2. Goblet mucous cells
  3. Enteroendocrine cells
  4. Intestinal glands
  5. Intestinal villi
314
Q

Enterocytes of the small intestine

A
  • epithelial cells, also contain microvilli on their surface,
  • increase surface area 30x
  • Glycolax and glycoproteins cover microvilli → digestive processes within glycolax due to digestive enzymes found in matrix
315
Q

Goblet mucous cells of small intestine

A

scattered between absorptive/digestive cells

  • Produce mucus for protection/lubrication
  • Least abundant in duodenum
316
Q

Enteroendocrine cells

A

also in SI, secrete different stuff than stomach ones

317
Q

Intestinal glands (3)

A
  1. Crypts of lieberkuhn
  2. Paneth cells
  3. Brunner’s glands
318
Q

Crypts of Lieberkuhn

A

simple tubular glands, penetrate from base of villi deeper into mucosa

  • Continuous with surface epithelium
  • Stem cells most abundant in lower third of crypts → give rise to other cells (mucous cells, enterocytes, Paneth cells)
319
Q

Paneth cells

A

contain large eosinophilic granules with lysozyme, phospholipase, and antibacterial peptides called defensins

320
Q

Brunner’s glands

A

only in duodenum, release contents into crypts

  • Secrete large amounts of mucins and bicarb to neutralize acid arriving in pyloric sphincter
321
Q

Intestinal villi

A

highly structured

  1. Loose lamina propria core containing small blood vessels, lymphocytes, and lymphatic spaces that joint at the lacteal
  2. Contains lacteals: larger lymphatic vessel in center of intestinal villa-> larger lymphatics and proceed to bloodstream via thoracic duct
322
Q

Function of lacteal (2)

A
  1. Passage for fluid entering lumen of intestine

2. Transport for lipoprotein droplets (chylomicrons) exocytosed by enterocytes on side facing lamina propria

323
Q

Enterocytes and fatty acids

A

take up fatty acids and monoglycerides form lumen of gut, and resynthesize them to di- and triglycerides → release them by exocytosis on opposite side
Nutrient taken up by capillaries via hepatic portal system of liver

324
Q

Digestion in the small intestine

A
  • Chyme neutralized → enzymes produced by pancreas and enterocytes digest proteins to AAs, complex carbs to single monomers (glucose, galactose), and lipids to fatty acids and monoglycerides
  • Muscularis externa: inner circular and outer longitudinal layers in intestine → movement of luminal contents by peristalsis
  • Segmented movement with alternate contraction and relaxation of segments → back and forth movements that agitates luminal contents
325
Q

Main pancreatic duct

A

Main pancreatic duct joins common bile duct near its entry to duodenum

  • Sphincter of Oddi (hepatopancreatic sphincter)
326
Q

Organization of pancreatic cells

A

Organized into cluster of pancreatic acinar cells arranged at end of common duct

327
Q

Basal side of acinar cells

A

full of RER, synthesis of proteins for secretion

328
Q

Apical side of acinar cells

A

secretory granules (zymogen granules) with packaged product that gets secreted into ducts

  • Most secreted enzymes initially inactive (zymogens)
  • Prevents autodigestion of proteins/lipids of pancreas en route via ducts to duodenum
329
Q

Inactivated enzymes secreted by pancreas (5)

A

trypsin, chymotrypsin, elastase, carboxypeptidase, triacylglycerol lipase

330
Q

Trypsinogen activated by ____

A

enterokinase

Not secreted by pancreas, membrane anchored enzyme in apical plasma membrane of duodenal digestive/absorptive cells (epithelial enterocytes)

331
Q

Trypsin

A

Activates other zymogens by proteolysis

332
Q

Amylase

A

degrades starch to glucose and maltose

Synthesized in active form in pancreas

333
Q

Ribonuclease

A

cleaves RNA

Synthesized in active form in pancreas

334
Q

Centroacinar cells

A

cells in acini, represent beginning of duct system
Secrete much of the volume of pancreatic juice (water, bicarb)
- Help Brunner’s glands neutralize acid
- Secretion under control of secretin and cholecystokinin

335
Q

Enterocytes of intestine

A

have complex glycolax at their surface

Some of final digestive processes occur in this layer just outside cell

336
Q

Digestion of starches

A

amylase (from pancreas) digestion → maltose and isomaltose → broken down by maltase and isomaltase (membrane-anchored enzymes in apical plasma membrane of enterocytes) → glucose

Glucose absorbed via nearby glucose transporters = most effective absorption instead of being consumed by bacteria

337
Q

Digestion of lactose

A

Lactase → on enterocyte surface, cleaves lactose → glucose + galactose

Absence of lactase → lactose intolerance because bacteria utilizes undigested lactose

338
Q

Three types of fluids secreted by salivary glands

A
  1. serous
  2. Mucous
  3. Mixed
339
Q

3 types of salivary glands

A
  1. submandibular
  2. sublingual
  3. parotid
340
Q

Type of fluid secreted by submandibular glands

A

mixed

341
Q

Type of fluid secreted by sublingual glands

A

mucous (lubricative and protective)

342
Q

Type of fluid secreted by parotid glands

A

serous (watery, contain enxymes- amylase, RNAse, DNAse)

Serous epithelial cells also transport IgA class Ig that together with lysozyme and peroxidase provide antibacterial action

343
Q

Organization of salivary glands

A

Organized in acinar design:

Contraction of myoepithelial cells propel salivary secretions form acini

344
Q

Large intestine

A

cecum, appendix, transverse colon, descending colon, and rectum

  • Smooth, lacks plicae and villi
  • Contains numerous straight tubular glands/crypts
  • Epithelial layer: abundant mucous-producing cells and absorptive cells
345
Q

Function of large intestine

A

recovery of water and salt during concentration of fecal material

346
Q

Columns of morgagni

A

longitudinal structural folds of mucosa located near distal portion of rectum

347
Q

Lamina propria and submucosa of LI contain numerous _______

A

Lymphocytes

348
Q

___ of the wall of the colon is muscular

A

2/3

349
Q

Muscle in the colon

A
  • Large band of circular smooth muscle
  • Muscular specializations in longitudinal layer:
  1. Taeniae: bands in this layer - segmented contraction → sacculation of bowel which compresses and segments fecal material
  2. Anus: where circular layer is thickened to form internal anal sphincter
    • External anal sphincter is circular striated muscle
350
Q

Main distinguishing features of stomach: 3

A
  1. Thick mucosa, glands that branch deep into mucosa with acini at end of branches
  2. Acinar/Chief cells at end running down to muscularis mucosa
  3. pH = 1-2 → kill bacteria, and denature proteins
351
Q

Main distinguishing features of small intestine (2)

A
  1. Villi on surface specialized for absorption, lined by epithelium
  2. Small crypts at end of folded epithelium
352
Q

Main distinguishing features of colon (1)

A

thick mucosa with linear, highly regular crypts filled with mucous secreting cells

353
Q

General features of normal GI motility

A

Requires complicated coordination between CNS (SNS and PNS) and enteric nervous system with the gastric musculature

Gastric pacemaker cells: drive baseline motility of stomach (not well understood) - Interstitial cell of cajal

354
Q

GI motility in the proximal stomach (cardia, fundus, body)

A

area relaxes upon ingestion of food = Receptive relaxation

Main role of proximal stomach is storage with minimal pressure increase

355
Q

GI motility in distal stomach (antrum)

A

controls mechanical (grinding) and enzymatic digestion and processing → liquid chyme sent in small amounts to SI

Contraction of distal stomach → gastric emptying into duodenum

356
Q

Physiology of gastric emptying (4)

A
  1. Receptive relaxation (vagally mediated inhibition of body tone)
    - Swallowing induced vagal response
    - Gastric Accommodation: smooth muscle relaxation elicited by mechanical distention of stomach (gastric mechanoreceptors)
    - -Vasovagal response
  2. Liquid emptying by tonic pressure gradient
  3. Solid emptying by vagally-mediated contractions
  4. Residual solids emptied during non-fed state by MMC (migrating motor complex) every 90-120 minutes
357
Q

What can cause motility disorders? (4)

A
  1. chemical substances (inside and outside body) = NEUROPATHIC
  2. Diseased GI muscles: genetic defect (muscular dystrophy) or acquired (progressive systemic sclerosis) = MYOPATHIC
  3. Abnormalities of interstitial cells of Cajal - pacemaker cells
  4. CNS disorders (input for SNS and PNS)
358
Q

Function of colon

A

transport, store, and expel stool after absorbing majority of luminal fluid

359
Q

Two types of colonic motor activity

A
  1. Low amplitude tonic and phasic contractions for mixing luminal contents (Haustra)
  2. High amplitude propagated contractions (HAPCs) for propelling
360
Q

What increases colonic motility?

A

Colonic motility increases after meal (gastrocolonic response) and on awakening

361
Q

Causes of constipation (7)

A
  1. Drugs, mechanical
  2. Metabolic: DM, hypoK, hyperCa, hypoMg, hypothyroid
  3. Myopathy: amyloid, scleroderma
  4. Neurogenic: Parkinson’s spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s
  5. Other: pregnancy, immobility
  6. IBS-C
  7. Normal transit, slow transit, dyssynergic defecation
362
Q

Achalasia

A

esophageal motility disorder due to inflammatory destruction of neurons in myenteric plexus of esophagus

  • Predominant destruction of inhibitory neurons that affect relaxation of esophageal smooth muscle → failure of appropriate LES relaxation after swallowing → esophagogastric junction outflow obstruction
  • Spares cholinergic neurons that contribute to LES tone
  • Absence of peristalsis
363
Q

Symptoms of achalasia

A

dysphagia to solids and liquids, regurgitation of undigested food

364
Q

Diagnosis of achalasia

A

esophageal manometry → incomplete relaxation of LES, aperistalsis in smooth muscle esophagus

365
Q

Scleroderma

A

multi-system disorder, skin and GI involvement mostly

Small vessel vasculitis → vascular derangement and resultant smooth muscle atrophy and fibrosis of multiple organs

366
Q

Esophageal involvement in scleroderma (3)

A

Myopathic process

  1. Atrophy of smooth muscle → weak peristalsis → dysphagia
  2. Atrophy of smooth muscle → weak LES → GERD
  3. Unrepentant GERD → esophagitis → stricture
367
Q

Stomach involvement in scleroderma

A

delayed gastric emptying

368
Q

Diagnosis of esophageal involvement in scleroderma

A

esophageal manometry → weak/absent esophageal body peristalsis

Differentiate from achalasia due to weakened LES pressure

369
Q

Spastic disorders of esophagus

A

conditions of uncertain etiology, peristalsis preserved

370
Q

Symptoms of spastic disorders of esophagus

A

chest pain and dysphagia

371
Q

Pathophysiology of spastic disorders of esophagus

A

related to overactivity of excitatory nerves, and impairment of inhibitory innervation or overreactivity of smooth muscle response

EX) Jackhammer esophagus = lots of red on esophageal manometry, with high pressure and long contraction time

372
Q

Gastroparesis

A

“Stomach paralysis”, delayed gastric emptying in absence of mechanical obstruction

Impaired transit of food from stomach to duodenum

373
Q

Symptoms of gastroparesis

A

nausea, vomiting, bloating, early satiety, postprandial abdominal distension and pai

374
Q

Causes of gastroparesis (4)

A
  1. Idiopathic, post-infection
  2. Post-surgical (vagal nerve injury) or myenteric plexus injury
    COMMON with thoracic surgical procedures (lung transplant)
  3. Diabetic (autonomic neuropathy), medication related (opiates)
  4. Others: paraneoplastic, rheumatologic, neurologic, myopathic (scleroderma)
375
Q

Diagnosis of gastroparesis

A

scintigraphic gastric emptying (gastric emptying study)

376
Q

Management of gastroparesis (4)

A
  1. Lifestyle and dietary measures: small and infrequent meals, low-fat and low-residue diet, glucose control in diabetics
  2. Medications: prokinetic agents, antiemetics
  3. Gastric electric stimulation
  4. Surgery (removal of stomach) - last resort
377
Q

Chronic intestinal pseudo-obstruction (CIPO)

A

Signs and symptoms of mechanical obstruction of small bowel without a lesion obstructing flow of intestinal contents

  • Characterized by presence of dilation of bowel on imaging
  • Major manifestation of small intestinal dysmotility
378
Q

Complication of CIPO

A

small intestinal bacterial overgrowth: stasis → bacterial overgrowth → fermentation and malabsorption

379
Q

Causes of CIPO (4)

A
  1. Underlying neuropathic disorder involving enteric nervous system or extrinsic nervous system (Parkinson’s Shy-Drager syndrome, Diabetes)
  2. Infectious (Chagas)
  3. Myopathic disorder (involving smooth muscle)
    EX) Scleroderma, amyloidosis, eosinophilic gastroenteririts
  4. Or abnormality in interstitial cells of Cajal
380
Q

CIPO in children

A

mostly congenital, mostly primar conditions, absent MMC predicts need for IV nutrition, ⅓ of infants born die in 1st year of life

381
Q

Hirschsprung’s disease (2)

A

Congenital absence of myenteric neurons of distal colon (neuropathic motility disorder)

No reflex inhibition of the IAS following rectal distention (No Recto-anal inhibitory reflex)

382
Q

Dyssynergic defection

A

Disorder in coordination of pelvic floor musculature - paradoxical contraction of pelvic floor and external anal sphincter with attempts at defecation

383
Q

Diagnosis of dyssynergic defaction

A

anorectal manometry

384
Q

Treatment of dyssynergic defaction

A

Biofeedback therapy is effective

385
Q

Esophageal manometry

A

assessment of esophageal body peristalsis and upper and lower esophageal sphincter function

  • Transnasal, intraluminal manometry catheter containing pressure sensors → from nares into stomach, assess esophageal motility as patient swallows repeated small boluses of water
  • UES relaxation (red color) → esophageal peristalsis from top to bottom (proximal peristalsis of striated muscle and distal peristalsis of smooth muscle) → post-deglutitive LES relaxation
386
Q

Gastric emptying studies

A

Aka gastric scintigraphy

Low fat EggBeaters radiolabeled with 1 mCi Technetium 99, measure percentage remaining after certain amount of time

387
Q

Abnormal gastric emptying study

A

retention >60% at 2hr or >10% at 4hrs

388
Q

Wireless motility capsule (WMC)

A

used to assess for gastroparesis and motility disorders of small intestine and colon
- Measures pressure, temperature, and pH as it traverses GI tract

389
Q

Antroduodenal manometry

A
  1. Measure motility of SI with pressure sensors
  2. Measure pressure waves that result from phasic contractions of circular muscle layer
  3. Neuropathic process: discoordinated infrequent contractions
  4. Myopathic process: nothing happening even though nerves stimulating SI tract intact
390
Q

Sitz marker study

A

Colonic transit study

Swallow 24 capsules containing radiopaque markers on Day 1 → plain abdominal xray on Day 5

  • Less than 5 markers = normal
  • > 5 markers in recto-sigmoid suggests defecatory disorder
  • > 5 markers scattered throughout colon = slow transit
391
Q

Anorectal manometry

A
  1. Primary means of assessing defecation disorders
  2. Catheter with pressure sensors placed in anus and rectum
  3. Resting pressure, stimulated defecation, rectal sensation testing, and recto-anal inhibitory reflex testing are all tested
392
Q

Esophageal peristalsis is altered in (2)

A

achalasia, scleroderma

393
Q

LES relaxation is altered in

A

achalasia

394
Q

LES tonic contraction is altered in

A

scleroderma

395
Q

Gastric emptying is altered in (2)

A

gastroparesis, functional dyspepsia

396
Q

Small bowel peristalsis is altered in

A

CIPO

397
Q

Colonic transit is altered in

A

slow transit constipation (scleroderma)

398
Q

Sphincter dysfunction is altered in (2)

A

Hirschsprung’s, dyssynergic defecation

DEMS (10 decks)

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