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Block 5 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What is the GALT (gastrointestinal-associated lymphoid tissue)? (where is it found and its purpose)

A
  1. GALT is a general term used to refer to all of the organized lymphoid tissues found in the small intestine. It is found in the mucosa and submucosa of small intestine lining.
  2. Function is to protect the body from foreign antigens and pathogens, while allowing tolerance to commensal bacteria and dietary antigens
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2
Q

What is the difference between MALT and GALT?

A

GALT is a subdivision of MALT and specifically located to the GI tract (small intestine)

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3
Q
  1. Location of lymphoid follicles?
  2. What is the purpose of lymphoid follicles found within the GALT and in between villi of small intestine?
A
  1. These lymphoid follicles are in mucosa and protrude into the lumen of the gut.
  2. It is the site where adaptive immune response is activated (T cells and B cells)
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4
Q
  1. What are Peyer’s patches?
A
  1. Clusters of lymphoid follicles found in the lining of small intestine
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5
Q
  1. What are M cells (microfold cells)
  2. What aspects of these cells allow it do its job (basolateral and apical surface)
A
  1. Microfold (M) cells are located in Peyer’s patches (PPs) of the small intestine. M cells actively transport luminal antigens to the underlying lymphoid follicles to initiate an immune response
  2. Basolateral surface forms fold around follicle (easy transport to APCs / lymphocytes) —> Apical surface lacks thick glycocalyx layer (easy uptake of antigens)
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6
Q
  1. Describe the Tolerogenic environment found in mucosal immunity.
  2. What happens when this tolerogenic environment is interrupted?
A
  1. This is general immune tolerance to the many antigens presented in gut. When non-harmful antigen is presented to M cell and lymphoid follicles then regulatory T-cells secrete TGF-beta and IL-10. These two signal molecules suppress T cell responses so there is no immune reaction to these non-harmful antigens.
  2. loss of tolerance is what causes food allergies, celiac disease, IBD, etc
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7
Q
  1. What is the secretory, Dimeric IgA immunity?
  2. where is found?
  3. Its purpose?
  4. Why does it not cause inflammation
A
  1. This is a type of primary antibody defense –> IgA antibody on surface of intestinal lining NEUTRALIZES pathogens instead of causing inflammatory response. Meant to prevent bacteria from crossing the intestinal lining.
    - -> Neutralization occurs bc IgA lacks Fc receptor which prevents complement activation
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8
Q

What causes secretion of IgA in small intestine? (4 steps)

A
  1. IgA can be produced by naïve B cells in GALT in response to stimulation by commensal microbes, microbial pathogens, or after vaccination.
  2. Regulatory T cells release TGF-beta and IL-10 which cause differentiation of plasma B cells to class switch and make IgA.
  3. Plasma B cells secrete dimeric IgA in lamina propria and dimeric IgA bind to poly-Ig receptor on basolateral surface of mucosal epithelial cells
  4. When on the apical side - poly-Ig receptor is cleaved and released IgA into lumen. IgA is tethered within mucosal layer and stays there to neutralize toxins/microbes
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9
Q
  1. When is fluoroscopy utilized?
  2. When is barium swallow (esophogram) used?
  3. When is video swallow test used?
A
  1. evaluates morphology and motility of internal organs using real time X-rays
  2. Evaluates upper GI tract (pharynx and esophagus)
  3. Modified barium swallow - used to evaluate swallow reflex after CNS injury
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10
Q

What does hiatal hernia look like in imaging?

A

image

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11
Q

What does reflux esophagitis look like in imaging?

A
  1. Reflux esophagitis is defined as inflammation of the esophageal mucosa secondary to gastroesophageal reflux disease (GERD)
  2. image
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12
Q

What does barrett’s esophagus look like in imaging?

A
  1. Barrett’s esophagus is a condition in which the flat pink lining of the swallowing tube that connects the mouth to the stomach (esophagus) becomes damaged by acid reflux, which causes the lining to thicken and become red
  2. image
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13
Q

What does esophageal carcinoma look like in imaging?

A
  1. looks like bitten apple - showing apple core
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14
Q

Function of these papillae in tongue

  1. filiform papillae
  2. foliate papillae
  3. Fungiform papillae
  4. Circumvallate papillae
A
  1. break up foods and move food towards throat
  2. have taste buds
  3. have taste buds
  4. have taste buds + has salivary glands that help flush taste buds
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15
Q

Differentiate how the filiform, foliate, fungiform, and circumvallate papillae of tongue look like under microscopy

Description: rounded/very large+rounded/columnar/spiky+keratinized

A

image

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16
Q
  1. What is the difference between serous and mucous glands?
  2. how do they look differently under microscopy?
A
  1. serous glands secrete a protein-containing solution, which is involved in digesting starch and protecting oral cavity from pathogens like bacteria - stain darker (blue arrow)
  2. mucous glands secrete a thick solution with mucus, which is involved in lubricating food and oral cavity - stain lighter
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17
Q

label the layer of the GI wall

A
  1. mucosa - blue bracket (closest to lumen)
  2. submucosa - black bracket
  3. muscularis externa - dotted bracket (closer to lumen - circular muscle that can create sphincters → then Myenteric/Auerbach plexus → then outer longitudinal muscle)
  4. Adventitia/serosa -brown bracket
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18
Q
  1. What layers/structures are found within the mucosa?
  2. Function of each
A
  1. Epithelium, lamina propria, muscularis mucosa
  2. epithelium protects - lamina propria is loose connective tissue with blood vessels, nerve fibers, lymphatics, immune cells, etc - muscularis mucosa is thin strip of smooth muscle
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19
Q
  1. What important plexus is found in submucosa?
  2. What important plexus is found in muscularis externa?
A
  1. Meissner’s nerve plexus- controls GI secretions and local blood flow
  2. Auerbach’s/Myenteric plexus - coordinates peristalsis
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20
Q
  1. Function of submucosa
  2. Function of muscularis externa
  3. Function of adventitia and serosa
A
  1. more connective tissue with glands, vasculature, and lymphatics - has meissner’s plexus to regulate secretions and blood flow
  2. help with peristalsis
  3. Adventitia- attaches organs to body wall and contains blood vessels, lymphatics, and nerves — serosa - produces lubricant to prevent friction
  • organs can have adventitia and serosa or just one
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21
Q
  1. where are parotid, sublingual, and submandibular glands found?
  2. What does each secrete (serous acini vs mucous acini)
A
  1. image
  2. Parotid - serous acini only
  3. Sublingual - mucous acini only
  4. Submandibular - both serous and mucous acini
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22
Q
  1. What are the types of cells that line the esophagus epithelium?
  2. identify the structure pointed out by blue arrow
A
  1. non-keratinized stratified squamous epithelium
  2. esophageal glands that secrete lubricating mucus
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23
Q

Differentiate between these cells of the stomach

  1. surface mucous cells
  2. parietal cells
  3. mucous neck cells
  4. chief cells
  5. diffuse neuroendocrine (DNES) cells
A
  1. produce thick ALKALINE mucus to prevent autodigestion
  2. produce HCl and Intrinsic factor
  3. secrete fluid mucus for lubrication
  4. secrete pepsinogen and lipase
  5. secretes hormones like (gastrin, serotonin, ghrelin, somatostatin)
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24
Q

Indicate what cells are found in these parts of the stomach

  1. Cardia
  2. Fundus (body)
  3. Pylorus
    4.
A
  1. high number of mucous cells - no chief cells
  2. mix of every cell type - very thick mucosa
  3. high number of mucous cells - no chief cells

gastric glands are found throughout stomach but what cells they have within can depend on the area of the stomach (for example cardia has gastric glands but there are no chief cells found within

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25
Q
  1. Describe where the gastric pit, neck, and gastric gland is
  2. Describe what cells are typically found within each region
A
  1. image
  2. Gastric pit- has surface mucous cells
  3. Neck - parietal, DNES, Stem, and Mucous neck cells (4)
  4. Gastric gland (at the base) - chief cells and G cells
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26
Q
  1. What hormones/signal induce the parietal cells to secrete HCl and intrinsic factor? (3)
A
  1. Gastrin, Histamine, and Parasympathetic activity (ACh)
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27
Q

The small intestine has villus and crypts. when the epithelial cells slough off how do you regenerate epithelium?

A

At bottom of crypt you have undifferentiated stem cells - these regenerate villous epithelial cells

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28
Q

GI regulatory substances: GASTRIN

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
  3. Direct and indirect effects of gastrin?
A
  1. G cells in the stomach antrum and duodenum
  2. increase gastric H+ secretion ( plus increase in growth of gastric mucosa and gastric motility)
  3. direct- gastrin directly stimulates parietal cells to secrete substances
  4. Indirect - gastrin stimulates ECL cells in stomach to release histamine which also stimulates parietal cells
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29
Q

GI regulatory substances: CCK (cholecystokinin)

  1. what cells secrete this? Where are these cells found?
  2. released in response to what?
  3. Action of this substance?
A
  1. I cells of duodenum and jejunum
  2. a meal rich in fat and lipids
  3. increased pancreatic secretion, increased gallbladder contraction and relaxation of sphincter of Oddi PLUS decrease gastric emptying (all in the effort to metabolize food in small intestine)
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30
Q

GI regulatory substances: Somatostatin

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
  3. In what instances is this used therapeutically?
A
  1. D cells in pancreatic islets and GI mucosa
  2. DECREASE HCl and pepsinogen secretion, decrease pancreatic and small intestine secretion, decrease gallbladder contraction, decrease insulin and glucagon release [INHIBITS MOST GI HORMONES]
  3. Used to reduce overactive GI system (in carcinoid serotonin secreting tumor/diarrhea)
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31
Q

GI regulatory substances: SECRETIN

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
A
  1. S cells in duodenum
  2. INCREASED pancreatic bicarbonate (HCO3-) secretion, increase bile secretion + DECREASED gastric acid secretion
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32
Q

GI regulatory substances: Glucose dependent insulinotropic peptide (GIP) - type of incretin

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
A
  1. K cells in duodenum and jejunum
  2. decreases H+ secretion and increases insulin release
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33
Q

GI regulatory substances: MOTILIN

  1. Where are these cells found?
  2. Action of this substance?
  3. What disorder is it typically used in therapeutically?
A
  1. stomach and small intestine - increased in fasting state
  2. produces migrating motor complexes (MMCs) -a cyclic, recurring motility pattern that occurs in the stomach and small bowel during fasting
  3. Gastroparesis (delayed gastric emptying)
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34
Q

GI regulatory substances: Vasoactive intestinal peptide (VIP)

  1. Where are these cells found?
  2. Action of this substance?
A
  1. parasympathetic ganglia in sphincters, gallbladder, and small intestine
  2. increases intestinal water and electrolyte secretion + increases relaxation of intestinal smooth muscle and sphincters, limiting intestinal muscle contractions -can cause diarrhea
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35
Q

GI regulatory substances: Peptide YY

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
A
  1. L cells in terminal ileum and colon
  2. decreases intestinal motility - this is bc fat reaches terminal ileum after not being efficiently absorbed - meal will be retained longer to allow for more digestion+absorption
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36
Q

GI regulatory substances: Glucagon like peptide (GLP-1/GLP-2) - type of incretin

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
  3. What disorders is GLP1 or GLP2 used for as therapeutic?
A
  1. L cells in terminal ileum and colon
  2. stimulates insulin secretion (GLP1) and epithelial proliferation (GLP2)
  3. GLP1 - used for diabetes ;;; GLP2 is used for short bowel syndrome to increase absorptive capacity
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37
Q

GI regulatory substances: Serotonin

  1. what cells secrete this? Where are these cells found?
  2. Action of this substance?
A
  1. EC cells (in intestinal lining)
  2. Stimulates gastric motility (reduces appetite)

99% of body serotonin is made in GI tract

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38
Q

Small intestine epithelium

Small intestine has villi and crypts.

  1. What cells are found in the crypt, neck, and tip of villi?
A
  1. bottom of crypt- has undifferentiated stem cells and paneth cells
  2. neck has absorptive cells, goblet cells, enteroendocrine cells (EEC)
  3. tip of villi have absorptive cells and goblet cells
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39
Q

How are the linings of colon different than in small intestine?

A
  1. small intestine has villi and crypts but colon has surface cells and crypts (image is of colon)
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40
Q
  1. What is crypt of Lieberkuhn?
  2. What is the purpose of paneth cells in small intestine?
A
  1. crypt between villi in small intestine
  2. secrete antimicrobial peptides, called defensins, thereby contributing to host defense against microbes in the small intestine
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41
Q

What is each of the salivary glands innervated by?

  1. parotid gland
  2. submandibular gland
  3. sublingual gland
A
  1. IX - glossopharyngeal (parasympathethic)
  2. VII - facial (parasympathetic)
  3. VII - facial (parasympathetic)
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42
Q

what is in the composition of saliva? (6)

A
  • water
  • mucin - for lubrication
  • glycoproteins - solubilization of food which allows for taste
  • salivary amylase - for carb digestion
  • lingual lipase - for lipid digestion
  • electrolytes including bicarbonate (for neutralization of gastric secretions in esophagus)
  • and more
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43
Q

In salivary glands what are the different roles of acinar cells vs ductal cells?

A
  1. Acinar cells - these are at the base of salivary glands and produce initial form of salivary fluid (isotonic solution) (can be serous or mucus)
  2. Ductal cells - line the salivary glands and do secretion or absorption of ions to make saliva a hypotonic solution
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44
Q
  1. What are the functions of the ductal cells to make saliva a hypotonic solution? (4 movements)

(think of Na, K, HCO3-, Cl, Water, H+)

A
  1. NaCl are taken out of saliva (this occurs with Na/H and Cl/HCO3- exchanger protein - absorption)
  2. K and HCO3- are put into saliva (this occurs with Cl/HCO3- exchanger protein AND H/K exchanger - excretion)
  3. water is impermeable in ductal epithelium so none is reabsorbed or secreted
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45
Q

What happens to saliva concn with high flow rate and low flow rate through the salivary glands?

A
  1. With high flow rate you get concn closer to the original isotonic solution because there is less time to change concn within gland
  2. With low flow rate you get greater modification (very hypotonic saliva) because more time is spent in gland
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46
Q

How does sympathetic vs parasympathetic input affect saliva secretion?

A
  1. sympathetic - induces scant amylase rich saliva
  2. parasympathetic - leads to voluminous saliva secretion (parasympathetic is mainly regulatory system) → Muscarinic antagonists = dry mouth, muscarinic agonists = drooling / salivation
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47
Q

What salivary gland is responsible for most of the saliva we make?

A

submandibular gland (makes both serous and mucus saliva)

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48
Q

What are the steps to swallowing (5)

A

Image

For step 2: pharyngeal mechanoreceptors are activated when food is pushed back and this sends afferents to swallowing center in medulla which sends efferent impulses via cranial nerves and vagus nerve to finish swallowing reflex

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49
Q

what is primary peristalsis vs secondary peristalsis

A
  1. moves bolus down into stomach- after food passes through UES
  2. initiated by distention of esophagus - this is meant to clear esophagus from remaining bolus and refluxed acid
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50
Q

What is the receptive relaxation reflex?

A
  • This is when bolus is pushed through to the stomach. The stomach has to dilate and there is relaxation of lower esophageal sphincter and proximal part of the stomach.
    • To receive the bolus more easily
  • This uses extrinsic innervation of the stomach (vagal fibers)
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51
Q

What are the different functions of the proximal and distal parts of the stomach?

A
  1. proximal - storing food
  2. distal - mixing and grinding food
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52
Q

Describe the different patterns of gastric motility (indicate special cells or hormones or molecules that are involved in the steps)

  1. Accommodation (reservoir)
  2. Segmentation (mixing)
  3. Propulsion (peristalsis)
A
  1. proximal stretch of stomach - relaxation when food is entering from esophagus (release of NO and VIP cause relaxation)
  2. some regions of stomach contract and some relax in distal stomach to mix - does this via interstitial cells of Cajal that generate slow waves of spontaneous depolarization
  3. pushes food down close to pyloric sphincter by contracting stomach and relaxing pyloric sphincter - (decreased CCK from duodenum allows for gastric emptying)
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53
Q

What is gastric accommodation reflex?

A

When the stretching of the stomach body due to food and presence of nutrients in duodenum induces relaxation of stomach → this causes food to be stored in stomach and slow down passage of any more food since there is already food present that needs to be digested

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54
Q

When proximal stomach contracts and pyloric sphincter relaxes what happens?

A

gastric emptying

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55
Q

What is found within gastric juice and their functions (4)

A
  1. HCl - initiates digestion, activates pepsin
  2. Pepsinogen - aids in protein digestion
  3. Intrinsic factor - for B12 absorption
  4. Mucus - protects gastric mucosa from HCl and gastric contents
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56
Q

How does parietal cells secrete H+ (HCl) when originally they have H2CO3?

A

Has H2CO3 then split into HCO3- and H+. HCO3- goes into blood but H+ goes into stomach lumen (along with Cl- to make HCl)

57
Q

low intra-gastric pH leads to what changes in the stomach?

A

inhibits the secretion of gastric juices because inside of stomach is already very acidic and pH is just going lower. → does so via somatostatin (which inhibits all GI hormones)

58
Q

What is the zollinger-ellison syndrome?

A

Ulcers of the DUODENUM produced by excessive gastric acid secretions

59
Q

How does H pylori cause ulcers?

A

H. pylori bacterium that reside in GI tract can produce ulcers because it inhibits somatostatin release (which is responsible for inhibiting secretion of all GI hormones and gastric acid secretion)

60
Q

ACHALASIA

  1. What is it?
  2. What causes it? (3 reasons)
  3. How it looks on imaging?
  4. Clinical presentation (3)
A
  1. distention of esophagus and constriction of LES. Constriction of LES bc there is increased LES tone.
  2. first cause: Idiopathic (ganglion cell degeneration resulting in failure of inhibitory neurons responsible for LES relaxation) —– second and 3rd cause: Chaga’s disease and diabetic neuropathy
  3. Birds beak (look at image)
  4. chest pain, regurgitation that leads to aspiration pneumonia, difficulty belching
61
Q

Mallory-Weiss Syndrome

  1. What is it?
  2. What causes it?
  3. Clinical presentation (2)
A
  1. partial thickness, longitudinal lacerations at the gastroesophageal junction
  2. violent coughing or vomitting
  3. hematemesis, severe vomiting/retching
62
Q

BOERHAAVE SYNDROME

  1. What is it?
  2. What causes it?
  3. Clinical presentation (3)
A
  1. severe transmural (across an entire organ or blood vessel) tears of esophagus associated with mediastinitis (swelling of mediastinum) → mediastinitis happens because contents of esophagus fall out and into surrounding area causing pain
  2. forceful vomiting or straining
  3. chest pain, tachypnea, shock [HEMATEMESIS IS NOT A FREQUENT SYMPTOM WHICH IS WHAT DIFFERENTIATES THIS FROM MALLORY-WEISS) +requires surgery
63
Q
  1. What are esophageal varices?
  2. Often seen with what disorder?
A
  1. abnormal, enlarged veins in the esophagus. Can be small ruptures where patient bleeds out from
  2. cirrhosis/portal hypertension - move blood back and one place it increases tension is esophagus vessels
64
Q
  1. What is Barrett’s Esophagus a complication of?
  2. Clinical presentations?
A
  1. GERD - this results in metaplasia of esophageal lining → transforms into lining that is seen in intestine (columnar epithelium and goblet cells)
  2. may be asymptomatic or just GERD symptoms
65
Q
  1. What is a complication of barrett’s esophagus?
  2. What type of cancer can this develop into
A
  1. dysplasia (abnormal looking cells) - this is a step before cells turn cancerous. This is treated as a pre-invasive lesion
  2. Adenocarcinoma
66
Q

Esophageal adenocarcinoma

  1. What does it develop from?
  2. Where is it found in esophagus?
  3. What should you look for in microscopic imaging to know its adenocarcinoma?
A
  1. Barrett’s esophagus
  2. In the distal third of esophagus bc that is where reflux is which causes barrett’s
  3. glandular formation
67
Q

Esophageal Squamous Cell Carcinoma

  1. Risk factors for this?
  2. Where is it found in esophagus?
  3. What should you look for in microscopic imaging to know its adenocarcinoma?
A
  1. squamous dysplasia can lead to this. Alcohol, tobacco, esophageal injury, achalasia
  2. anywhere in esophagus (early on it has a small gray-white plaque thickening and later becomes a mass that obstructs lumen)
  3. Keratin pearls
68
Q

Erosion vs ulceration

A
  1. Erosion - shedding of the superficial mucosa - no deeper than muscularis mucosa (still mucosa)
  2. Ulcer - loss of entire mucosal thickness
69
Q

What is reflux esophagitis?

A

this is also know as GERD - inflammation of epithelial layer

70
Q
  1. What is infectious esophagitis
  2. What is eosinophilic esophagitis
A
  1. Commonly caused be candida/HSV-1/CMV - inflammation of esophagus epithelium
  2. immune mediated allergic reaction with eosinophilic inflammation. Eosinophils on biopsy
71
Q

Acute gastritis

  1. What is it?

Chronic gastritis

  1. What is it
  2. What causes it?
A

Acute gastritis

  1. mucosal damage from too much acid or loss of protection leads to inflammation which has neutrophils

Chronic gastritis

  1. same as acute but because it is chronic can show atrophy, metaplasia, dysplasia, carcinoma
  2. Chronic NSAID use, autoimmune gastritis, H. Pylor
72
Q

Difference between gastritis and gastropathy

A

Gastritis and gastropathy are conditions that affect the stomach lining, also known as the mucosa. In gastritis, the stomach lining is inflamed. In gastropathy, the stomach lining is damaged, but little or no inflammation is present.

73
Q
  1. What is Cushing ulcers
  2. What is Curling’s ulcers
A
  1. Cushing ulcers: a gastro-duodenal ulcer produced by elevated intracranial pressure caused by an intracranial tumor or head injury. increased intracranial pressure leads to overstimulation of the vagus nerve. As a result, increased secretion of gastric acid may occur which leads to gastro-duodenal ulcer formation known as Cushing’s ulcer.
  2. Curling’s ulcers: a stress-induced ulcer of the stomach or duodenum that occurs in relation to extreme physical stress, such as major surgery
74
Q

What are Type A Chronic Gastritis and Type B Chronic Gastritis?

A
  1. Type A Chronic Gastritis - Pernicious Anemia ;; autoimmune destruction of gastric parietal cells leads to loss of intrinsic factor. You get chronic inflammation in the gastric body/fundus.
  2. Type B Chronic Gastritis - H. Pylori Infection ;; infection that can lead to imbalances in mucosal defenses cause ulcers and leads to chronic inflammation in antrum. H.Pylori is associated with MALT lymphoma and gastric adenocarcinoma
75
Q

What is in the therapy for H. Pylori infection? (4)

A
  1. Proton pump inhibitor
  2. Clarithromycin
  3. Amoxicillin
  4. metronidazole
76
Q
  1. What is peptic ulcer disease
  2. Where is peptic ulcer disease most likely to occur?
  3. Symptoms
A
  1. development of solitary ulcer
  2. Duodenum (as a result of H. Pylori infection)
  3. epigastric pain that improves with eating/food and worse at night. Can should upper GI bleeding. -→ for peptic ulcer disease complications include hemorrhage and obstruction
77
Q
  1. If Peptic Ulcer Disease occurs in stomach (gastric ulcer)…where in the stomach is it most likely to occur?
  2. How to differentiate from duodenal ulcer
A
  1. lesser curvature of stomach
  2. gastric ulcer has epigastric pain that WORSENS with meal and has risk of malignancy (duodenal is usually benign)
78
Q

Gastric carcinoma - Intestinal type

  1. What type of cancer?
  2. Results due to what?
  3. Ulcer description and location
  4. Risk factors
A
  1. adenocarcinoma
  2. from intestinal metaplasia (as a result of H. Pylori autoimmune/chronic gastritis) - gastritis meaning stomach, particularly antrum of stomach
  3. large ulcer with irregular margins found in antrum of stomach
  4. Older men, smoking, H. Pylori
79
Q

Gastric carcinoma - Diffuse type

  1. What type of cancer?
  2. Arises from what cells?
  3. Histology shows what feature?
  4. Risk factors
A
  1. Adenocarcinoma
  2. Thickening of stomach - presents with early satiety. Derived from gastric mucosa cells
  3. signet ring cells
  4. CDH1 mutation, loss of E-Cadherin, TP53 mutation
80
Q

Gastrointestinal Stromal Tumor (GIST)

  1. What is this
  2. What cells does it arise from
  3. mutations in what gene leads to this
A
  1. a type of cancer that begins in the digestive system. GISTs happen most often in the stomach and small intestine (submucosal lesion).
  2. arises from interstitial cells of Cajal (pacemaker cells meant for mixing/stomach movement)
  3. c-KIT gene activating mutation
81
Q

Proton pump inhibitors

  1. mechanism of action
  2. end in what suffix?
  3. disorders it is used in?
A
  1. inhibit the H+/K+ ATPase pump in parietal cells resulting in reduced gastric acid secretion → this is irreversible inactivation of proton pumps (for 24-48 hrs)
  2. end in -prazole
  3. GERD, gastric and duodenal ulcers, in H. Pylori treatment
82
Q

H2 receptor antagonists

  1. mechanism of action
  2. end in what suffix?
  3. disorders it is used in?
  4. adverse effects
A
  1. prevent histamine from binding to H2 receptor on gastric parietal cell which prevents gastric acid secretion
  2. end in -tidine
  3. Mild GERD, gastric reflux that is not chronic
  4. confusion and headache; can lead to vitamin B12 deficiency
83
Q

Acid neutralizers (Antacids)

  1. mechanism of action
  2. Drug names
A
  1. Neutralizes H+ released intro gastric lumen to decrease acid concn
  2. Al(OH)3, milk of magnesium, alka seltzer, tums
84
Q

How does pancreatic juices from from acini to main pancreatic duct? (4 steps)

A
  1. Acini (many acini together make a lobule) - Acini contain zymogen granules containing pancreatic enzymes. Acini synthesize and secrete almost all the digestive enzymes active in the lumen of the small intestine
  2. Acini drain these juices into intercalated ducts
  3. Intercalated ducts drain into intralobar ducts
  4. Intralobar ducts drain into main pancreatic duct
85
Q

Pancreatic secretion

  1. High or low bicarb?
  2. High or low Chloride?
  3. Hypo/Hyper/Iso -tonic?
A
  1. High carbohydrate concn - bicarb neutralizes acidic fluid from stomach and allows pancreatic enzymes to function?
  2. Low chloride in pancreatic secretion
  3. Isotonic
86
Q

What are the functions of the enzymes found in pancreatic secretions?

  1. alpha amylase
  2. pancreatic lipase
  3. phospholipase A2
  4. Trypsin/chymotrypsin/elastase/carboxypeptidase
A
  1. hydrolyzes alpha (1,4) linkages between glucose monomers in starch (secreted in active form so don’t have to be altered)
  2. hydrolyzes 1 and 3 bond triglycerides (fatty acids)
  3. hydrolyzes phospholipids (secreted in inactive for so needs to be activated by trypsin)
  4. protein digestion enzymes (secreted in inactive form and activated by trypsin)
87
Q

Explain the mechanism of bicarbonate secretion form pancreatic ductal cells (remember bicarb is PRESENT in pancreatic secretions- so it is excreted)

A
  1. bicarb enters into ductal epithelial cells on basolateral side via Na/HCO3 cotransporter + along with diffusion of CO2 into ductal epithelial cells
  2. On apical/luminal side of ductal epithelial cells;;; HCO3- is exchanged for Cl- (which is what makes there be bicarb in secretions and less Cl-)
88
Q

What are the 2 functions of bile? (bile is secreted from liver)

A
  1. promote digestion and absorption of dietary lipid and cholesterol
  2. Elimination of waste products
89
Q

How do bile salts hep digestion of lipids?

A

Bile salts act like detergents. They emulsify lipid particles, dissolving particles in water and allowing digestion.

90
Q
  1. What is cholestasis (pay attention to the “stasis” part)
  2. What symptoms are seen (some symptoms indicate how urine and stool look like)
A
  1. Disrupted bile flow to intestines.
  2. Retaining too much bile acids/bile salts - you get hapatocyte injury and pruritus
  3. Retaining too much bilirubin - you get jaundice
  4. Retaining too much cholesterol - you get xanthomas
91
Q
  1. What is cholelithiasis?
  2. What are the two types
A
  1. Gallstones
  2. Cholesterol (supersaturation of cholesterol in bile) and pigment (excess bilirubin production due to hemolytic anemia or excess recycling of bilirubin)
92
Q

What are esophageal webs?

A

An esophageal web is a thin (2-3 mm), eccentric, smooth extension of normal esophageal tissue consisting of mucosa and submucosa that can occur anywhere along the length of the esophagus. Cause is unknown.

93
Q
  1. What is plummer-vinson syndrome? (classic triad)
A

Plummer-Vinson syndrome (PVS) is a rare condition characterized by the classic triad of dysphagia, iron-deficiency anemia, and esophageal web.

Plummer-Vinson syndrome is a condition that can occur in people with long-term (chronic) iron deficiency anemia. People with this condition have problems swallowing due to small, thin growths of tissue that partially block the upper food pipe (esophagus).

94
Q
  1. What is oropharyngeal dysphagia?
  2. What is esophageal dysphagia?
A
  1. Difficulty initiating the swallowing process
  2. Difficulty passing food bolus from upper esophagus to stomach. Food sticks after swallowing.
95
Q
  1. What general issue is occurring if person has esophageal dysphagia with solid foods only?
  2. What general issue is occurring if person has esophageal dysphagia with solid AND liquids?
A
  1. mechanical obstruction
  2. neuromuscular disorder
96
Q

Fill in the blank (3 different disorders)

A

image

esophageal rings- a ring of tissue that forms where esophagus and stomach meet

97
Q

Fill in the blank (3 disorders)

A

image

98
Q
  1. What is scleroderma esophagus
  2. What is herpes esophagitis
A
  1. In the GI tract, scleroderma can affect the smooth muscle of the esophagus, damaging healthy tissue and replacing it with scar tissue. Scleroderma causes strictures, or narrowing, of the esophagus and makes the muscle tissue weaker
  2. Esophagitis is inflammation and irritation of the esophagus, and herpes esophagitis is a rare type that results from an HSV infection. causing inflammation and ulcers of the esophagus
99
Q

When a physician makes a mistake what is the framework for best practice disclosure?

A
  1. acknowledgement, explanation, remorse, reparation
99
Q

What is the difference between invasive and non-invasive bacterial diarrhea?

A

Invasive causes bleeding in the diarrhea (hematochezia) - there is blood and leukocytes due to direct damage to the GI tract. You also get fever.

100
Q

Secretory vs osmotic diarrhea?

A
  1. Secretory - when the body secretes electrolytes into your intestines and this causes water to build up in the intestines
  2. Osmotic - involves unabsorbed substances in the intestines that draws water out from plasma and into intestinal lumen.
101
Q

What bacteria cause food borne illness that manifests mainly in vomiting?

A
  1. Staph aureus (enterotoxin producing)
  2. B. Cereus

both do not show person to person spread

102
Q

What bacteria cause food borne illness that manifests mainly in diarrhea?

A
  1. C. perfringens (watery diarrhea)
103
Q

Humans are the only host of what parasite?

A

pinworm (E. Vermicularis)

104
Q
  1. What is the life cycle of the pinworm?
  2. What test is done to check for pinworm infestation?
A
  • Eggs laid by adult female worms at night in the perianal area.
  • These eggs are spread after hosts touches perianal area and then other person ingests this
  • Then larvae hatch in small intestine and migrate to perianal region, lay eggs, and cycle repeats
  • Scotch tape test - seeing eggs on tape laid in perianal area at night and removed in morning
105
Q

Describe the pathogenic strain of E. Coli (EPEC)

  1. presentation
  2. method of infecting
A
  1. shows with pediatric diarrhea in developing countries.
  2. Pili/adhesions allow bacterial attachment to small intestine epithelial cells. (not toxin)
106
Q

Describe the enteroinvasive strain of E. Coli (EIEC)

  1. presentation
  2. method of infecting
A
  1. Dysentery
  2. Penetrates intestinal epithelium through M cells to gain access to submucosa (like shigella)
107
Q

Describe the Toxigenic strain of E. Coli (ETEC) - “traveler’s diarrhea”

  1. presentation
  2. method of infecting (hint: toxins)
  3. Treatment
A
  1. watery diarrhea w/o inflammation
  2. LT (heat labile toxin) - increases cAMP and leads to increased H2O secretion —– ST (heat stabile toxin) - increases cGMP and leads to increased H2O secretion
  3. azithromycin/ciprofloxacin
108
Q

Describe the Hemorrhagic strain of E. Coli (EHEC)

  1. presentation
  2. method of infecting
  3. tx
  4. O:H ratio?
A
  1. shiga-toxin producing e.coli - bloody diarrhea (dysentery)
  2. attach to mucosa of large intestine similar to EPEC (M cells)
  3. ANTIBIOTICS are CONTRAINDICATED - just do supportive tx
  4. O157:H7 ratio
109
Q

Protozoal Diarrhea

Giardia Intestinalis

  1. presentation
  2. treatment
A
  1. foul smelling fatty diarrhea
  2. metronidazole
110
Q

Protozoal Diarrhea

Entamoeba Histolytica

  1. presentation
  2. treatment
A
  1. dysentery, liver abscesses – Trophozoites with RBCs in cytoplasm
  2. metronidazole
111
Q

Protozoal Diarrhea

Cryptosporidium

  1. presentation
A
  1. water, self limited diarrhea in immunocompetent patients → acid fast oocysts
112
Q

Protozoal Diarrhea

Balantidum coli

  1. presentation
A
  1. diarrhea - largest protozoan that infects humans
113
Q

Protozoal Diarrhea

Cyclospora

  1. presentation
A
  1. diarrhea in traveler’s or from contaminated imported foods - more severe in immunocompromised
114
Q

Intestinal Nematodes

Taenia Solium

  1. presentation
A
  1. neurocysticercosis (a preventable parasitic infection of the central nervous system)
115
Q

Differentiate between

  1. Ascaris lumbricoides
  2. Trichinella spiralis
  3. Enterobius Vermicularis
A
  1. thick-shelled eggs that creates very long worms. These long worms can obstruct ileocecal valve
  2. Trichinella spiralis - cause fever, vomiting, MYALGIAS - encyst in striated muscle cells
  3. Remember scotch tape taste - worms migrate to perianal region
116
Q

Viral Diarrhea

Norovirus (A calicivirus)

  1. presentation
  2. How is it spread/infectious dose needed
  3. duration
A
  1. epidemics of diarrhea and vomiting - most common cause of epidemic gastroenteritis worldwide
  2. Low infectious dose - highly infectious
  3. 1-3 days
117
Q

Viral Diarrhea

Rotavirus (A Reovirus)

  1. presentation
  2. prevention?
A
  1. PEDIATRIC (<4 years old) vomiting and fever (uncommon in adults)
  2. vaccine given to kids
118
Q

Viral Diarrhea

Adenovirus

  1. presentation
  2. duration/season of presentation
A
  1. conjunctivitis, hemorrhagic cystitis, pediatric gastroenteritis in summer
  2. peak is during summer
119
Q

Viral Diarrhea

ECHO (enteric cytopathic human orphan) virus

  1. presentation
A
  1. can cause mild gastroenteritis but most manifestations are extraintestinal (like aseptic meningitis)
120
Q

What are the two toxins of clostridium difficile and what do they each do?

A
  1. Toxin A (enterotoxin) - binds to brush border of gut and disrupts normal flora of large intestine
  2. Toxin B (cytotoxin) - cytoskeletal disruption via actin depolymerization → leads to pseudomembranous colitis (swelling or inflammation of the large intestine (colon) due to an overgrowth of C diff bacteria)
121
Q

Clostridium difficile

  1. how is it treated?
  2. symptoms
A
  1. oral vancomycin (MAIN ONE)….fecal transplant
  2. Mild to severe diarrhea that can lead to sepsis or death – antibiotic associated or hospital acquired diarrhea
122
Q

Bacterial Diarrhea

Salmonella spp

  1. How is it transmitted usually
  2. What are the types
  3. unique agar finding
A
  1. Both types are transmitted via contaminated food (poultry or dairy) and also person to person spread
  2. Salmonella typhi and salmonella enteritidis
  3. only on salmonella enteritidis: black colonies on Hektoen agar bc it makes H2S
123
Q

Salmonella typhi vs enteritidis

Differences in symptoms

A
  1. Typhi - constipation then diarrhea but symptoms start 5-21 days after ingestion and improve over weeks or months. Can show fever, rose spots, abdominal pain, intestinal bleeding
  2. Enteritidis - Watery Diarrhea, sometimes bloody (don’t give antibiotics bc this typically prolongs excretion of salmonella)
124
Q

Salmonella typhi

  1. prevention methods?
  2. tx?
A
  1. preventative vaccines against the virulence factors
  2. azithromycin if uncomplicated but ceftriaxone if severe
125
Q

Bacterial Diarrhea

Shigella

  1. presentation
A
  1. watery diarrhea followed by dysentery
126
Q

Bacterial Diarrhea

Vibrio cholera (cholera)

  1. presentation
  2. pathogenesis
  3. tx
A
  1. rice water stools w/no blood or WBCs
  2. overactivation of cAMP which leads to extreme H2O secretion
  3. oral rehydration
127
Q

Bacterial Diarrhea

Vibrio parahaemolyticus

  1. what does it cause?
  2. from what source?
A
  1. gastroenteritis
  2. raw shellfish
128
Q

Bacterial Diarrhea

Campylobacter Jejuni

  1. presentation
  2. how is it spread
  3. complications from this?
A
  1. Bloody diarrhea (#1 cause in USA)
  2. spread via poultry
  3. Guillain-barre syndrome, reactive arthritis
129
Q

Bacterial Diarrhea

Yersinia Enterocolitica

  1. presentation
  2. how is it spread
A
  1. diarrhea, pseudoappendicitis pain
  2. pet feces and pork
130
Q

H pylori

  1. how is it diagnosed?
A
  1. Urea breath test - H. pylori produces an enzyme called urease, which breaks urea down into ammonia and carbon dioxide. During the test, a tablet containing urea is swallowed and the amount of exhaled carbon dioxide is measured.
131
Q
  1. How do chief cells look differently to parietal cells and DNES cells in histology
  2. what do you stain DNES cells with?
A
  1. silver stain
132
Q

What do mucous cells look like - histology?

A
133
Q

The left gastric artery branches directly from the celiac trunk - after which it splits again - one part continues to lesser curvature of the stomach while the other part ascends towards the (Blank)

A
  1. abdominal esophagus
134
Q

omeprazole and esomeprazole (PPI) inhibit CYP2C19 and increases serum concn. of (3)

A
  1. diazepam
  2. citalopram
  3. phenytoin
135
Q
  1. What change to ionic composition of saliva would be achieved with vagal stimulation?
  2. What structure in the esophagus is controlled by efferents from the dorsal motor nucleus?
  3. What pressure change happens immediately after the UES opens during swallowing?
A
  1. High HCO3- content
  2. lower esophagus
  3. a decrease in gastric pressure
136
Q
  1. Vagal stimulation causes what gastric motility pattern?
  2. How does acute gastritis cause excessive acid production?
A
  1. gastric accomodation reflex
  2. increased ECL cell (endocrine cells of the stomach - release histamine) stimulation
137
Q

What is the best way to distinguish between inflammatory and secretory diarrhea with a bacterial etiology?

A

Fecal lactoferrin is a marker of white blood cell presence. released from PMNs. Therefore, presence or absence of fecal indicative of fecal white blood cells and an inflammatory mechanism

Block 5 (7 decks)

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