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Block 5 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

When chyme moves into jejunum (BLANK) levels go down and this induces the pyloric tone to diminish and allow more chyme to go into duodenum

A

CCK

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2
Q
  1. When does the function of migrating motor complex occur?
  2. What stimulates them? (hormone)
A
  1. during fasting- purpose is to clear indigestible residues from lumen of stomach and small intestine and prevent bacterial overgrowth
  2. motilin
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3
Q

Does peristalsis occur at the same time as segmentation does?

A

No, peristalsis increases as segmentation decreases. Peristalsis is when proximal portions contract and distal portions of GI tract relax to propel bolus through GI tract

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4
Q

What causes the formation of haustra in colon?

A

myenteric plexus

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5
Q

what contraction/relaxation has to happen to open or close ileocecal sphincter?

A
  • Distention of ileum relaxes ileocecal sphincter (open)
  • Distention of cecum contracts the ileocecal sphincter (closes)
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6
Q

What is the function of colonic phase of digestion?

A
  1. reabsorption of remaining fluid, electrolytes, and storage of waste before defecation
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7
Q
  1. What ions are absorbed in the colonic phase of digestion?
  2. How are they absorbed (hint: two ways)
A
  1. Na is absorbed so water can follow and water reabsorption occurs
  2. proximal part of colon (image)→ coupled function of Na/H exchanger and Cl/HCO3- exchanger (electroneutral) - this happens between meals
  3. distal part of colon → through ENaCs (electrogenic))
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8
Q

What ions are secreted in the colonic phase of digestion?

A
  1. Chloride secretion - occurs via CFTR channel - this determines water content of feces → increased Cl secretion means increased H2O secretion (diarrhea)
  2. K+ secretion → can occur paracellular/passive or active/transcellular (image)

note: for K+ secretion this can be increased via aldosterone because aldosterone increases presence of ENaC

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9
Q

In colon - short duration contractions

  1. Their purpose
  2. Their length
  3. What conducts these contractions
A
  1. used for mixing
  2. 8 seconds
  3. produced by circular muscle
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10
Q

In colon - long duration contractions

  1. Their purpose
  2. Their length
  3. What conducts these contractions
A
  1. For mixing
  2. 20-60 seconds
  3. taeniae coli
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11
Q

In colon - high amplitude propagating contractions

  1. Their purpose
A
  1. used to clear colonic contents - pushes aborally (away from mouth) - occurs about 10 times a day - 20+ cm segment of colon loses haustrations and contracts as a unit to propel fecal matter forwards
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12
Q
  1. What needs to contract or relax (for internal and external anal sphincter) in order to defecate?
  2. What nerve system innervates the internal anal sphincter (IAS)
  3. What nerve system innervates the external anal sphincter (EAS)
A
  1. simultaneous relaxation of IAS (involuntary) and relaxation of EAS (voluntary) → (along with relaxation of puborectalis muscle + contraction of abdominal muscle )
  2. pelvic nerves (parasympathetic) - involuntary
  3. pudendal nerves (somatic) - voluntary
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13
Q
  1. (Blank A) stimulation stops colonic movement
  2. (Blank B) stimulation causes segmental contractions in colon
A
  1. sympathetic
  2. vagal
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14
Q
  1. What is gastrocolic reflex?
  2. What is orthocolic reflex?
A
  1. increased colonic motility shortly after ingestion
  2. When you wake after sleep, stretching and sitting and then standing, the orthocolic reflex excites nerves that stimulate muscular contractions in the large intestine (to help produce a bowel movement).
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15
Q

What do dilated intestines due to small bowel obstruction look like in x-ray?

A

step ladder appearance - can be caused by adhesions, hernias, malignancy, crohn’s etc

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16
Q

What is this an imaging of ?

A
  1. Diverticulosis - small pouches that arise along colon
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17
Q

What radiology findings can be associated to ulcerative colitis and crohn’s disease? (3)

A
  1. Transmural inflammation
  2. Luminal narrowing
  3. Skip lesions (A skip lesion is a wound or inflammation that is clearly patchy, “skipping” areas that thereby are unharmed)
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18
Q

Late cancer shows apple core or saddle lesions in radiology but what does early colorectal cancer show?

A

sessile (flat) or pedunculated (image) polyps

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19
Q

What is a toxic megacolon?

A

Toxic megacolon occurs when swelling and inflammation spread into the deeper layers of your colon. As a result, the colon stops working and widens. In severe cases, the colon may rupture.

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20
Q
  1. What is microscopic colitis?
  2. What are the two types of microscopic colitis
A
  1. Microscopic colitis is an inflammation of the large intestine (colon) that causes persistent watery diarrhea. - chronic, watery diarrhea (w/out weight loss) w/ normal appearing mucosa
  2. lymphocytic colitis and collagenous colitis
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21
Q

Differentiate between lymphocytic colitis and collagenous colitis (both are microscopic colitis)

A
  1. Lymphocytic colitis - increased epithelial lymphocytes (associated with celiac and autoimmune disease)
  2. Collagenous colitis - thickened sub-epithelial collagen in older women (normal appearing mucosa)
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22
Q

Irritable bowel syndrome

  1. what part of intestine does it affect?
  2. Symptoms?
A
  1. large intestine
  2. relapsing abdominal pain, bloating, changes in bowel habits
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23
Q

What pattern is necessary to dx someone with irritable bowel movement?

(Hint: it is a pattern of symptoms + 2 of 3 criteria)

A
  1. 3 days/moth of recurrent abdominal pain over 3 MONTHS w/at least 2 criteria
  • improvement with defecation
  • onset associated with change in frequency in stool
  • onset associated with a change in form of stool
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24
Q
  1. What are some extraintestinal manifestations of irritable bowel syndrome?
  2. How is IBS treated
A
  1. painful menstruations, painful intercourse, urinary symptoms
  2. diet modification (avoiding short-chain carbs), stool softeners, anti-diarrheals
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25
Q

Differentiate between visceral, somatic, and referred pain

A
  1. Visceral pain - vague, dull, and nauseated - poorly localized pain bc there is low nerve density (autonomic nerve fibers) in abdominal viscera
  2. Somatic pain - sharp and localized pain - comes from parietal peritoneum that is innervated by somatic nerves
  3. Referred pain - comes from distant source due to convergence of nerve fibers at spinal cord
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26
Q

Digestive tract pain is usually localized where?

A

Midline due to bilaterally symmetric innervation

lateralized pain - usually unilateral, somatic innervation

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27
Q
  1. Epigastric may indicate issues with what structures? (3)
A
  1. heart, stomach, pancreas
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28
Q

Describe the current tools and methods used in determining gut microbiota composition?

  1. DNA-based approaches
  2. RNA-based approaches
  3. Protein-based approaches
  4. Metabolite-based approaches
A
  1. Determining what microbiota are present and what can they do
  2. Determining how microbiota respond and what pathways are activated (metatranscriptomics)
  3. How are they interacting with host and/or what proteins are being produced (metaproteomics) - considered best way!
  4. what are the chemical outcomes of their activity (metabolomics) -not the best because if substrate of bacteria is not present then metabolite will not be present
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29
Q

What is the structural function of microbiota of gut?

A
  1. they form a barrier fortification to more harmful pathogens
  2. induces formation of IgA that neutralize pathogens
  3. Regulate immune system development
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30
Q

What is the metabolic function of microbiota of gut?

(hint: what molecule(s) can we not make but gut microbiota can)

A
  1. gut microbiota provides enzymes that we can’t make ourselves.
  2. Provide SCFAs (butyrate) - products of bacterial fermentation of fiber → preferential energy source of colonocytes
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31
Q

In obese humans the (Blank:Blank) ratio is increased

A

firmicute:bacterioidetes

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32
Q

difference between probiotics and prebiotics?

A
  1. Probiotics- live active microorganisms that have beneficial effects to the host - displace the harmful bacterial species in gut (good for IBD, IBS, acute infectious diarrhea)
  2. Prebiotics - nonliving, non-digestible special form of fiber or carbohydrate - nourishes the bacteria that live in intestine (good for obesity, IBD, constipation, traveler’s diarrhea, diabetes)
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33
Q
  1. What are the types of carbohydrates? (4)
  2. Where are these carbs absorbed? (part of GI tract)
A
  1. starch (includes polysaccharides), disaccharides, monosaccharides, indigestible fibers (cellulose and pectin)
  2. Small intestine
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34
Q

Explain how starch (polysaccharides) are digested before being absorbed in small intestine? (2)

A
  1. Starch is digested/broken down in the lumen of the small intestine by amylase enzyme
  2. After initial digestion some products are still not able to be absorbed because they are terminal linkages or branching linkages. Special amylase enzymes break these down AT THE BRUSH BORDER MEMBRANE and then they can be absorbed
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35
Q

Function of

  1. Amylose
  2. Amylopectin
  3. Glucoamylase
  4. Isomaltase
A

these are all enzymes meant to digest/break down starch

  1. amylose works on polysaccharides of straight chain polymers
  2. amylopectin works on branched chain polymers
  3. Glucoamylase breaks down maltotriose and maltose (products that were part of starches but not able to be absorbed until further break down at brush border membrane)
  4. Isomaltase breaks down alpha-limit-dextran (product that was part of starches but not able to be absorbed until further break down at brush border membrane)
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36
Q

Explain how disaccharides are digested before being absorbed in small intestine?

A
  1. Digested AT THE BRUSH BORDER MEMBRANE and then absorbed.
    * disaccharide examples are lactose, sucrose, etc
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37
Q

Explain how monosaccharides are digested before being absorbed in small intestine? (2)

A
  1. Monosaccharides are freely absorbable. Glucose can go directly through intestinal epithelial cells via SGLT1 - no need for digestion. (SGLT1 relies on Na concn to move along with monosaccharide through SGLT1)
  2. Then capillaries and then liver

monosaccharides include glucose, fructose, galactose

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38
Q
  1. Where are proteins absorbed?
  2. Function of endopeptidases?
  3. function of aminopeptidases and carboxypeptidases?
  4. where does these peptidases come from?
A
  1. small intestine
  2. cleave peptide bonds except terminal peptide bonds
  3. cleave peptide bonds at terminal ends (either amino or carboxyl end)
  4. pancreas
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39
Q

Explain how proteins are digested before being absorbed in small intestine? (6)

A
  1. Protein digestion starts in the stomach with pepsin
  2. At small intestine proteins get broken down in the lumen → broken into amino acids
  3. the amino terminal ends get further digested AT THE BRUSH BORDER MEMBRANE because this is where aminopeptidase is found
  4. These amino acids get absorbed (image) in di or tripeptides via active transport (using Na+ gradient)
  5. Di and tripeptides are further digested within the epithelial cells of small intestine
  6. Then go to capillaries and eventually liver
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40
Q

Function of

  1. GLUT5
  2. GLUT2
A
  1. Absorbs fructose from intestinal lumen
  2. Secretes glucose, galactose, fructose from basolateral membrane of epithelial cells of small intestine into blood
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41
Q
  1. Explain process of endocytosis of proteins in small intestine
  2. When does endocytosis of proteins occur?
A
  1. this is when entire proteins are absorbed directly into epithelial cells without digestion
  2. this allows transfer of passive immunity from mother to child postnatal.
  3. Once full protein is in inside epithelial cells then it can be transferred to M-cells on basolateral side with is endocytosis by M cells
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42
Q

What are the types of lipids we ingest? (3)

A
  1. triglycerides, phospholipids, cholesterol
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43
Q
  1. Why are lipids trickier to digest in the GI tract?
  2. Explain how lipids are digested before being absorbed in small intestine?
A
  1. Need to emulsify lipids bc they do not easily mix with aqueous environment
  2. starts in stomach - lingual and gastric lipases digest lipids
  3. Lipases from pancreas do majority of lipid digestion in small intestine
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44
Q

Triglyceride (lipid)

  1. Where in the small intestine are they digest (lumen or brush border)
  2. What are triglycerides broken up into and absorbed?
A
  1. lumen
  2. broken down into glycerol and fatty acids. Then in the epithelial cells they are reformed inside the cell before leaving the cell on the basolateral side
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45
Q

Phospholipids (lipid)

  1. What enzyme digests these?
A

Phospholipase A2

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46
Q

Cholesterol (lipid)

  1. What enzyme digests these?
  2. Through what channel is cholesterol absorbed into epithelial cells?
  3. What drug can inhibit this channel?
A
  1. cholesterol ester hydrolase digests cholesterol
  2. NPC1L1
  3. ezetimibe
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47
Q

What two techniques are used for emulsification of lipids in GI tract?

A
  1. mechanical disruption by mechanical movements in stomach
  2. Use of detergent like bile acids. colipase anchors pancreatic lipase to the bile salts to allow for lipid digestion
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48
Q

How are lipids absorbed in the small intestine? (3)

A
  1. Lipid digestion products are transported to the enterocytes in mixed micells and then absorbed into the epithelial cell
  2. Inside the epithelial cell they are reformed inside the cell before leaving cell via chylomicrons
  3. chylomicrons go to lacteals before going into blood (too big for blood capillary) → by going to lacteals (lymphatic system) they can bypass the liver and enter circulation from thoracic duct
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49
Q

where in small intestine are bile acids reabsorbed?

A
  1. Distal ileum
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50
Q
  1. What minerals are absorbed in the small intestine (2)
  2. In what part of the small intestine?
A
  1. calcium and iron
  2. proximal part of the small intestine (calcium can also be absorbed in the rest of the small intestine)
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51
Q
  1. How is calcium absorbed in the small intestine?
A
  1. Diffusion through paracellular gaps (only occurs if there is low calcium in blood such as in pregnancy)
  2. Actively absorbed via transporters on epithelial cells (transporters are regulated by vitamin D)
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52
Q
  1. What are the two forms iron is absorbed through?
  2. How is each absorbed/what changes need to happen to each form?
A
  1. heme (more efficient_ and non-heme
  2. Heme - taken up and degraded inside cell ;;; Non-Heme : iron is in ferric (Fe3+) form and needs to be converted to ferrous (Fe2+) form and then it can be absorbed
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53
Q

Vitamin B12 is absorbed in the small intestine but what part of the small intestine?

A
  1. distal ileum
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54
Q

Duodenum of small intestine

  1. villi are [long/short] and [thin/fat]
  2. [A lot or few] goblet cells
  3. [Adventitia or serous] covering
  4. Marker of duodenum (structure)?
A
  1. long and thin
  2. a few goblet cells
  3. adventitia
  4. Brunner’s glands are found in submucosa- secrete bicarbonate to neutralize stomach acids
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55
Q

Jejunum of small intestine

  1. villi are [long/short] and [thin/fat]
  2. [A lot or few] goblet cells
  3. [Adventitia or serous] covering
  4. Marker of jejunum? (structure)
A
  1. Villi are long and thin
  2. more goblet cells than duodenum but less than ileum
  3. Serosa covering
  4. Paneth cells - produce antimicrobial compounds (defensins and lysozyme)
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56
Q

Ileum of small intestine

  1. villi are [long/short] and [thin/fat]
  2. [A lot or few] goblet cells
  3. [Adventitia or serous] covering
  4. Marker of ileum (structure)
A
  1. villi are short and fat
  2. a lot of goblet cells
  3. serosa covering
  4. Peyer’s patches are marker of ileum
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57
Q

Large intestine

  1. Main roles
  2. goblet cells are [present/absent]
  3. how do villi look?
  4. What types of cells are found here? (hint: one of them is enterocytes obviously)
  5. How does the large intestine make vitamin K and B12?
A
  1. absorption of water, electrolytes and gases and feces compaction
  2. HIGH number of goblet cells
  3. no villi in large intestine
  4. enterocytes, DNES cells, and stem cells
  5. there is a lot of microorganisms that make and release vitamin K and B12
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58
Q

What is glycocalyx?

A
  1. specialized mesh of glycoproteins, carbs, and enzymes. this is found on the apical parts of microvilli of the small intestine. Essential for nutrient absorption.
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59
Q

How are enterocytes bonded close together?

A
  1. bound via tight junctions and adherens junctions - prevents fluid leakage but in duodenum this is leaky
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60
Q
  1. What parts of the colon are surrounded by serosa and adventitia?
A
  1. serosa covers cecum, transverse, and sigmoid colon - adventitia covers ascending and descending colon
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61
Q
  1. The appendix contains high amount of what type of tissue?
A
  1. lymphoid tissue - may act as storage for normal gut microbes during severe GI infections
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62
Q
  1. Differentiate what epithelial types are found in the colorectal zone and the anal transition zone?
A
  1. colorectal zone: simple columnar epithelium with goblet cells, lymphoid follicles, blood vessels
  2. anal transition zone: stratified squamous epithelium (w/keratinization more distally)
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63
Q
  1. What does the endoderm create in the abdomen?
  2. What does the mesoderm create in the abdomen?
A
  1. GI tract epithelium and glands + abdominal organs
  2. Surrounding GI structures like stroma, muscles, peritoneum, spleen, mesentery
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64
Q
  • Pharynx
  • Thoracic esophagus
  • Abdominal esophagus
  • Stomach
  • Superior half of duodenum (1st and 2nd parts)
  • Liver parenchyme and hepatic duct epithelium
  • Gallbladder, cystic duct, and common bile duct
  • Dorsal and ventral pancreatic rudiments (exocrine cells, pancreatic duct epithelium, endocrine cells)

WHAT DERIVES THIS? (foregut, midgut, hindgut)

A

Foregut

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65
Q
  • Inferior half of the duodenum (3rd and 4th parts)
  • Jejunum
  • Ileum
  • Cecum and its appendix
  • Ascending colon
  • Right ⅔ of transverse colon

WHAT DERIVES THIS? (foregut, midgut, hindgut?)

A

Midgut

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66
Q
  • Left ⅓ of the transverse colon
  • Descending colon
  • Sigmoid colon
  • Rectum
  • Anorectal canal to the pectinate line

WHAT DERIVES THIS? (foregut, midgut, hindgut)

A

Hindgut

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67
Q

How does the esophagus develop in an embryo? (2)

A
  1. a small diverticulum (bulging pouch) appears in the ventral wall of pharynx (4th week)
  2. A tracheoesophageal septum separates what will be esophagus and trachea
68
Q

How does the stomach develop in an embryo? (2)

A
  1. originally begins as a tube. this tube rotates so dorsal side is on the left and ventral side is on right. The right/ventral side starts growing more than the left (BECOMES GREATER CURVATURE OF STOMACH)
  2. the stomach rotates 45 degrees clockwise to have the slanted position in abdomen
69
Q
  1. What is esophageal atresia (EA)?
  2. What symptoms does it present with
A
  1. esophagus does not connect to stomach (deviation of TE septum)
  2. polyhydramnios (too much amniotic fluid around baby), drooling, choking, vomiting, failure to pass NG tube into stomach
70
Q
  1. What is tracheoesophageal fistula (TEF)?
  2. What symptoms does it present with
A
  1. Abnormal connection between esophagus and trachea.
  2. Gastric distention (air in stomach on CXR), aspiration pneumonia, distress
71
Q

what is gastroschisis?

A

a birth defect where there is a hole in the abdominal wall beside the belly button. The baby’s intestines, and sometimes other organs, are found outside of the baby’s body, exiting through the hole

72
Q
  1. What is volvulus?
  2. What symptoms does it present with
A
  1. intestine twists around itself and the mesentery that supports it, creating an obstruction
  2. vomiting, sepsis, bowel necrosis
73
Q
  1. What is meckel’s diverticulum?
A
  1. A true diverticulum, containing all layers of the small bowel wall (mucosa, submucosa, muscular layers). They arise from the antimesenteric surface of the middle-to-distal ileum.
  2. Rule of 2s: 2% of population / 2x rate in males / 2 inches in size / 2 feet from ileocecal valve
74
Q
  1. what is vitelline duct?
  2. What is vitelline cyst?
  3. What is vitelline fistula?
A
  1. an embryonic structure providing communication from the yolk sac to the midgut during fetal development. Normally, it obliterates spontaneously and separates from the intestine between approximately the 5th and 9th weeks of gestation.
  2. when the midportion of the vitelline duct remains patent and each end is obliterated, and mucus then accumulates within the cyst
  3. a completely patent vitelline duct. It may be an opening from the umbilicus to the intestine - can show feces in umbilicus
75
Q

What syndrome is duodenal atresia associated with?

A

Down syndrome

  • duodenal atresia is when the recanalization of the epithelium fails so duodenum is not created or underdeveloped
76
Q
  1. What is Hirschsprung disease?
  2. some symptoms
  3. What is always involved in this disease?
  4. What does imaging show for this?
A
  1. Hirschsprung disease is a birth defect in which there is malformation of myenteric (Auerbach’s) / submucosal (Meissner’s) plexus → lack of peristalsis → obstruction
  2. presents with abdominal distention, failure to pass meconium
  3. RECTUM
  4. (transition zone imaging- cone shaped portion where proximal part is normal and distal bowel is narrow)
77
Q

What is annular pancreas

A

a rare congenital abnormality characterized by a ring of pancreatic tissue surrounding the descending portion of the duodenum

78
Q
  1. What is inflammatory bowel disease
  2. What are the two types?
A
  1. recurrent episodes of abdominal pain, bloody diarrhea → chronic autoimmune disease w/relapsing, remitting course
  2. Ulcerative and Crohns disease
79
Q

Inflammatory bowel disease

  1. typical age
  2. female vs male
  3. race or ethnicity prevalence
  4. extraintestinal manifestations
A
  1. 15-40
  2. female
  3. white and jewish populations
  4. ankylosing spondylitis (bone in the spine fuse) and uveitis (inflammation inside eye)
80
Q
  1. smoking cigarettes improves outcomes in (BLANK A) and worsens outcomes in (BLANK B)
A

BLANK A - ulcerative colitis

BLANK B - Crohns disease

81
Q

Since inflammatory bowel disease is an autoimmune disease - what antibodies does ulcerative colitis and crohn’s each show respectively?

A
  1. Ulcerative colitis shows - p-ANCA
  2. Crohn’s shows - anti-saccharomyces cerevisiae antibodies
  • not reliable for clinical use in dx IBD but can be used to differentiate between UC and Crohn’s
82
Q

IBD: Ulcerative Colitis

  1. where does UC start/always show up in the GI tract?
  2. Where does it never show up in?
  3. Granulomas present in inflammation of mucosa/submucosa?
  4. What cells mediate this autoimmune reaction?
A
  1. Rectum (presents w/LLQ pain
  2. never involves the small intestine
  3. No granulomas
  4. Th2 mediated disorder
83
Q

IBD: Crohn’s Disease

  1. where does UC start/always show up in the GI tract?
  2. Where does it never show up in?
  3. Granulomas present in inflammation of mucosa/submucosa?
  4. What cells mediate this autoimmune reaction?
A
  1. occurs in any portion of the GI tract but most commonly occurs in terminal ileum of small intestine.
  2. N/a - it can occur anywhere
  3. Yes, non-caseating granulomas present
  4. Th1 mediated disorder
84
Q

IBD: Ulcerative Colitis vs Crohn’s Disease

  1. Which shows pseudo polyps? - also describe what pseudo polyps are
  2. Which has inflammation transmurally (throughout whole intestinal wall) vs. limited to mucosa/submucosa?
  3. Which shows cobblestone mucosa (and what is this?)
A
  1. ulcerative colitis → A form of healing practice of the body to heal lesions of UC. (image)
  2. Crohn’s has transmural inflammation - UC has limited to mucosa/submucosa
  3. Crohn’s disease - cobblestone mucosa is due to the formation of ulcers. At times, these ulcers can appear close together in the intestines and resemble the appearance of cobblestones.
85
Q

IBD: Ulcerative Colitis vs Crohn’s Disease

  1. Which shows a “lead pipe” appearance on x-ray and which shows a “string” appearance on x-ray?
  2. Which shows crypt abscesses (and what are they)?
  3. Which shows creeping fat (and what is this)?
A
  1. UC - lead pipe (due to mucosal regeneration after injury) ;;;; Crohn’s string sing (due to strictures that form due to inflammation that heals)
  2. UC - the accumulation of inflammatory cells within the crypts of the gastrointestinal tract (image)
  3. Crohn’s - When transmural inflammation heals mesenteric fat, the kind that naturally develops in the abdominal area, wraps around the bowel wall, causing it to thicken
86
Q

IBD: Ulcerative Colitis vs Crohn’s Disease

  1. which is more indolent and which is more abrupt with onset?
  2. Which more commonly has extraintestinal manifestations
A
  1. UC is more indolent and Crohn’s is more abrupt onset
  2. Crohn’s disease - migratory polyarthritis, erythema nodosum, kidney stones, etc (UC also has extraintestinal manifestations but less that Crohn’s)
87
Q

For mild irritable bowel syndrome

  1. What is given as treatment regimen (3) - also give reason for each
A
  1. Sulfasalazine - used to treat and prevent acute attacks of mild to moderate ulcerative colitis
  2. Synthetic glucocorticoid - to lower activity of immune system
  3. Antibiotics for a short period - They have a well-established role in helping to treat complications of Crohn’s Disease such as abscesses and fistulas
88
Q

For moderate to severe irritable bowel syndrome

  1. What is given as treatment regimen (3) - also give reason for each
A
  1. Glucocorticoids, biologics - to suppress immune activity and induce a person into remission
  2. biologics, immunosuppressant (like azathioprine and methotrexate) - maintain the remission of the patient
  3. infliximab - a monoclonal antibody of TNF has quick disease activity reduction and IBD patient life quality improvement. (effective in 40-50% of patients) →to induce remission in patients who are sick

The drug you use to induce remission is also same drug you use in maintenance of remission

89
Q

For severe to fulminant irritable bowel syndrome

  1. What is given as treatment regimen
A
  1. aggressive therapy and hospitalization
  2. IV steroids, bowel rest and parenteral nutrition, fluid resuscitation
  3. Maybe surgery if #2 fails or if obstruction, mass, large abscess
90
Q
  1. What is the mechanism of action of metoclopramide?
  2. What is the purpose of this drug?
  3. In what patient conditions is this used in?
  4. contraindications?
A
  1. DOPAMINE (D2) RECEPTOR ANTAGONIST - in the CTZ (chemoreceptor trigger zone (CTZ) for emesis) and peripherally in GI tract
  2. to prevent nausea
  3. When pt has CHEMO, MIGRAINE, POST OP
  4. parkinson’s disease
91
Q

What other drugs work like metoclopramide as dopamine receptor antagonists in CTZ?

A
  1. Prochlorperazine
  2. Promethazine
  3. Chlorpromazine
92
Q
  1. What is the mechanism of action of Ondansetron (drugs ending in -setron)?
  2. What is the purpose of this drug?
  3. In what patient conditions is this used in?
  4. side effects?
A
  1. Serotonin (5-HT3) receptor antagonists
  2. prevents nausea and vomiting
  3. POST OP, CHEMO INDUCED N/V, morning sickness
  4. QT prolongation can occur
93
Q
  1. What receptors are found in the chemoreceptor trigger zone (CTZ) for emesis which induce nausea and vomiting?
  2. Where is the CTZ located?
A
  1. Serotonin (5-HT3) receptor
  2. Dopamine (D2) receptor
  3. NK1 receptor
  4. located in the area postrema of brain - does not have BBB
94
Q

What receptors are activated to induced motion sickness via the vestibular system? (2)

A
  1. H1 receptors
  2. ACh muscarininc receptors
95
Q
  1. What is the mechanism of NK1 Antagonists?
  2. List names of drugs in this category
  3. What is the purpose of this drug?
  4. In what patient conditions is this used in?
  5. side effects/contraindications?
A
  1. Block activation of NK1 receptors in vomiting center by substance P
  2. Aprepitant (end in -pitant)
  3. To stop/diminish nausea and vomiting (used in combo w/ondansetron/dexamethasone)
  4. CHEMO INDUCED
  5. contraindicated in nursing mothers, also inhibits CYP3A4
96
Q
  1. What is the mechanism of action of Scopalamine?
  2. What is the purpose of this drug?
  3. In what patient conditions is this used in?
  4. side effects?
A
  1. Muscarinic Receptor Antagonists (block activation of vestibular system)
  2. to prevent or stop motion sickness
  3. N/A - not useful for chemo nausea
  4. dry mouth, blurred vision, etc
97
Q
  1. What is the mechanism of action of H1 antagonists??
  2. What is the purpose of this drug?
    3.
A
  1. blocks H1 receptors in vestibular system
  2. prevents motion sickness
98
Q

What is the drug regimen for chemo induced N/V (CINV) - when patient is low risk?

A
  1. 5-HT3 antagonist (end in -serton) OR Dexamethasone (a corticosteroid)
99
Q

What is the drug regimen for chemo induced N/V (CINV) - when patient is medium risk?

A
  1. 5-HT3 antagonist (end in -serton) AND Dexamethasone (a corticosteroid)
100
Q

What is the drug regimen for chemo induced N/V (CINV) - when patient is high risk?

A
  1. 5-HT3 antagonist (end in -serton)
  2. Dexamethasone (a corticosteroid)
  3. Olanzapine (antipsychotic that antagonizes 5-HT3, D2, muscarininc, H1, and adrenergic receptors)
101
Q
  1. Dexamethasone and methylprednisone are (BLANK) - these have unknown MOA but they treat nausea and vomiting
  2. What indications are they used for?
A
  1. Corticosteroids
  2. Prevent or treat POST OP N/V, CHEMO N/V, RADIATION N/V
102
Q
  1. What is the mechanism of action of a bulk forming laxative
  2. What are examples of this laxative type?
  3. Onset (slow/fast)?
  4. Must be taken with (BLANK)
A
  1. Poorly absorbed substance which causes water to be absorbed into the substance and form soft fecal mass in colon which leads to distention of colon and initiation of peristalsis
  2. psyllium, methylcellulose
  3. slow onset (12-72 hours)
  4. lots of water
103
Q
  1. What is the mechanism of action of a osmotic laxative
  2. What are examples of this laxative type?
  3. Onset (slow/fast)?
  4. contraindication
A
  1. These laxatives are poorly absorbed salts or sugars which cause an osmotic effect to hold water in intestinal tract → induces peristalsis
  2. polyethylene glycol / sorbitol / milk of magnesia / lactulose
  3. Fast if given rectally (15-30 min); Slow if given orally (30-96 hours)
  4. renal impairment
104
Q
  1. What is the mechanism of action of a stimulant laxative
  2. What are examples of this laxative type?
  3. Onset (slow/fast)?
  4. contraindication
  5. What types of patients especially require this?
A
  1. Stimulates colonic neurons and irritate mucosal lining of colon. This leads to colonic electrolyte and fluid secretion into GI tract. (reduces water and electrolyte absorption)
  2. senna and bisacodyl
  3. Slow (6-10 hours)
  4. Stomach pain, appendicitis
  5. chronic opioid users - bc opioids reduce peristalsis
105
Q
  1. What is the mechanism of action of a surfactant laxative
  2. What are examples of this laxative type?
  3. Onset (slow/fast)?
  4. What types of patients especially require this?
A
  1. Stool softener - exerts a detergent effect to break and soften the fecal mass - may also stimulate secretion of fluid
  2. docusate
  3. slow if orally (12-72 hours);; fast if rectally (2-15 min)
  4. When straining should be avoided like post partum or hemorrhoid
106
Q
  1. What is the mechanism of action of a lubiprostone?
  2. In what situations should this be used?
A
  1. activates Chloride channels in gut leading to increased fluid retention in lumen
  2. in chronic idiopathic constipation, IBS-C in women
107
Q
  1. What is the mechanism of action of a linaclotide?
  2. In what situations should this be used?
  3. contraindications
A
  1. Agonist of guanylate cyclase - increases Cl-/HCO3- secretion into intestinal lumen which leads to water coming into lumen
  2. chronic idiopathic constipation, IBS - C
    not for children!
108
Q
  1. What is the mechanism of action of a peripherally acting mu-opioid receptor antagonists?
  2. drug names under this category (4)
A
  1. blocks peripherally acting mu-opioid receptors - used for opioid induced constipation
  2. alvimopan, methylnaltrexone, naloxegol, naldemedine
109
Q

What drug categories are used for constipation? (7)

A
  1. bulk forming laxative
  2. osmotic laxative
  3. stimulant laxative
  4. surfactant laxative
  5. lubiprostone
  6. linaclotide
  7. peripherally acting mu-opioid receptor antagonist
110
Q

What drug categories are used for diarrhea (anti-motility drugs)? (5)

A
  1. opioid derivatives
  2. Atropine
  3. bismuth subsalicylate
  4. eluxadoline
111
Q
  1. What is the mechanism of action of opioid derivatives when treating for diarrhea?
  2. name of drugs in this category? (2)
  3. How are the two drugs in this category different?
A
  1. binds to the opiate receptor in the gut wall. Consequently, it inhibits the release of acetylcholine and prostaglandins, thereby reducing propulsive peristalsis, and increasing intestinal transit time. Loperamide increases the tone of the anal sphincter
  2. Diphenoxylate and loperamide
  3. Diphenoxylate cross BBB so it is combined with atropine to prevent abuse;;; loperamide does not cross BBB
112
Q
  1. How does atropine help as an antidiarrheal?
A
  1. only for short term use - relieves muscle spasms in gut - paired with diphenoxylate (opioid derivative) to prevent abuse
113
Q
  1. What is the mechanism of action of Bismuth Subsalicylate when treating for diarrhea?
  2. Used in what situations?
  3. side effects?
A
  1. Absorbs excess water (antisecretory) - also has antimicrobial effects
  2. Nonspecific diarrhea like traveler’s diarrhea
  3. black tongue/stool
114
Q
  1. What is the mechanism of action of Eluxadoline when treating for diarrhea?
  2. Used in what situations?
A
  1. peripherally acting Mu-opioid receptor agonist (remember opioids cause less peristalsis which is good in this case because you need more time in GI to form more solid stool - stop diarrhea)
  2. IBS-D
115
Q

Alosetron Hydrochloride

  1. For what syndrome is this used for?
  2. MOA?
A
  1. IBS-D
  2. 5-HT3 antagonist, inhibits hyperactivity of large intestine
116
Q

Dicyclomine

  1. For what syndrome is this used for?
  2. MOA?
A
  1. IBS-C and IBSD
  2. anticholinergic antispasmodic, relaxes muscles of gut / bladder + ↓ gastric acid
117
Q

Rifaximin

  1. For what syndrome is this used for?
  2. MOA?
A
  1. IBS-D
  2. Decreases bacterial load - w/low system absorption
118
Q

Hyperplastic Polyp

  1. Where is found
  2. Characteristic of these polyps?
  3. Benign/Cancerous/pre-cancerous?
  4. What structure does it have under microscopy imaging
A
  1. rectosigmoid colon
  2. proliferation of goblet cells - these goblet cells have normal cellular structure and no dysplasia
  3. benign
  4. “Saw tooth” - serrated pattern (image)
119
Q

what is the most common type of polyp?

A

Hyperplastic polyp

very common in adults >60 years old

120
Q

Adenomatous Polyp

  1. Where is found
  2. Characteristic of these polyps?
  3. What structure does it have under microscopy imaging (4)
A
  1. Can be found throughout large intestine
  2. These polyps have the potential to become malignant/cancerous - bc it has some dysplasia
  3. there can be sessile, pedunculated, tubular (most common - adenomatous epithelium forming tubules), villous (long projections extending from surface - high malignancy risk)
121
Q

Juvenile Polyp (most common)

  1. Where is found
  2. Typical patient
  3. Characteristic of these polyps? (3)
  4. Risk of malignancy?
  5. Mutations?
A
  1. Rectum - can lead to painless rectal bleeding
  2. children younger than 5 years old
  3. These are hamartomatous polyps usually pedunculated with - (ONE) dilated cystic glands with retention of mucus and lined by tall columnar epithelium, (TWO) a markedly expanded lamina propria, and (THREE) diffuse chronic infiltration of inflammatory cells.
  4. they do have risk of adenocarcinoma if >10 polyps so screen
  5. SMAD4 or BMPR1A mutations
122
Q

Peutz-Jegher Polyp

  1. Where is found
  2. Typical patient
  3. Characteristic of these polyps?
  4. Risk of malignancy?
  5. Mutations?
A
  1. throughout GI tract but most common small bowel
  2. Patient presents with spots on lips and buccal mucosa (lining inside mouth)
  3. Hamartomatous polyps - large pedunculated polyp with tree like projections
  4. Has some risk for malignancy
  5. Loss of function mutations in LKB1/STK11 gene
123
Q
  1. What are hamartomatous polyps?
A
  1. Hamartomatous polyps are composed of the normal cellular elements of the gastrointestinal tract, but have a markedly distorted architecture.
  2. Hamartomatous Polyposis Syndromes (HPS) are genetic syndromes, which include Peutz-Jeghers syndrome, Juvenile polyposis syndrome, PTEN hamartoma tumour syndrome (Cowden Syndrom, Bannayan-Riley-Ruvalcaba and Proteus Syndrome) as well as hereditary mixed polyposis syndrome.
124
Q

What is CEA (carcinoembryonic antigen) used for in colon cancer?

A
  1. to detect if there is recurrence in patients
125
Q

How does right sided colon cancer present differently than left sided?

A
  1. Right sided - iron deficiency and weight loss - non-obstructive because lesions grown out from lining (not into lumen)
  2. Left sided - comes with LLQ pain, bleeding in stool - circumferential lesions which grow outwards from lumen of colon leads to pencil thin stool
126
Q

When should colorectal cancer screening begin and every how many years?

A
  1. age 45 and every 10 years after that + fecal occult blood testing
127
Q

What bacteria is strongly associated with colon cancer?

A

strep bovis - perform colonoscopy if identified

128
Q
  1. What is the chromosomal instability pathway in colorectal cancer?
  2. What are the three steps/three mutations that occur via chromosomal instability pathway - in order
  3. What type of colorectal cancer is formed from chromosomal instability pathway? (FAP, HNPCC)
A
  1. The accumulation of a characteristic set of somatic mutations with aging in specific tumor suppressor genes and oncogenes - most common pathway to colorectal cancer generation
  2. step one - loss of APC (increase risk for polyps) , step two - KRAS activation (leads to polyp formation), step three - loss of P53 (leads to tumor cell growth)
  3. FAP (familial adenomatous polyposis) - via the adenoma-carcinoma sequence
129
Q
  1. What is the microsatellite instability pathway in colorectal cancer?
  2. leads to left or right sided tumors?
  3. What type of colorectal cancer is formed from chromosomal instability pathway? (FAP, HNPCC)
A
  1. mutations or methylation of mismatch repair genes
  2. right sided
  3. HNPCC/Lynch Syndrome
130
Q

Familial Adenomatous Polyposis (FAP)

  1. autosomal dominant or recessive
  2. Begins with mutation in what gene?
  3. How many polyps are typical for classic FAP
  4. At what age is this found?
  5. If untreated what does this lead to?
    6.
A
  1. Autosomal dominant
  2. APC
  3. >100 polyps
  4. <30 years old
  5. If untreated this can lead to colorectal cancer - this is a syndrome that predisposes people to cancer
131
Q

HNPCC/Lynch Syndrome

  1. autosomal dominant or recessive
  2. Begins with mutation in what gene?
  3. How many polyps are typical for classic FAP
  4. Leads to what type of colorectal cancer
  5. Can lead to risk of what other cancers?
A
  1. Autosomal dominant
  2. MLH1, MSH2 (mismatch repair proteins)
  3. lower number of polyps than FAP - usually in right colon
  4. Remember this is a condition that if left untreated leads to colorectal cancer - mucinous type of adenocarcinoma
  5. endometrial, ovary, stomach
132
Q
  1. overexpression of COX-2 can lead to what cancer along with microsatellite instability and chromosomal instability pathway?
  2. left or right sided colon cancer?
  3. What can be used to reduce risk of colorectal cancer?
A
  1. colorectal cancer
  2. left sided colon cancer
  3. aspirin use
    4.
133
Q
  1. How is gardner syndrome related to FAP?
  2. What is it?
  3. What symptoms arise with this? (2)
A
  1. A type of FAP
  2. Gardner syndrome is a rare condition that’s characterized by multiple colorectal polyps. People with Gardner syndrome have a high risk of developing colorectal cancer early in life.
  3. bumps all over body (can be bone growths, skin cysts, connective tissue growths) — retinal pigment hypertrophy (CHRPE) (dark spot in retina seen on exam)
134
Q
  1. How is Turcot syndrome related to FAP?
  2. What is it?
A
  1. Turcot syndrome is a type of FAP
  2. characterized by the formation of multiple benign growths (polyps) in the colon that occur in association with a primary brain tumor
135
Q
  1. What are carcinoid tumors?
A
  1. slow growing neuroendocrine tumors commonly found in GI tract
    2.
136
Q
  1. What is carcinoid syndrome?
  2. what are the clinical presentations of this? (4)
  3. What metabolite appears in urine in carcinoid syndrome (diagnostic)
A
  1. occurs when a rare cancerous tumor called a carcinoid tumor secretes certain chemicals into your bloodstream, causing a variety of signs and symptoms. - commonly secretion of serotonin occurs
  2. Cutaneous flushing (if histamine is released), diarrhea (increased GI motility due to serotonin release), bronchospasm (histamine), heart murmur (valvular lesions from fibrogenesis)
  3. 5-HIAA (metabolite of serotonin)
137
Q
  1. What is carcinoid heart disease?
  2. What is treatment of this? (3)
A
  1. fibrous deposits in tricuspid/pulmonic valve leads to stenosis/regurgitation. This process is initiated by carcinoid tumor.
  2. Surgical excision, hepatic resection (to relieve symptoms), octreotide (binds somatostatin receptors on carcinoid tumors to inhibit release of serotonin from carcinoid tumors)
138
Q

In what age range is intussusception most common?

A

<2 years old

139
Q

Appendicitis is acute inflammation of appendix due to obstruction of opening of cecum

  1. what causes obstruction in adults?
  2. What causes this obstruction in children?
A
  1. fecaliths (hard fecal masses)
  2. Lymphoid hyperplasia (due to infection)
140
Q

Acute abdomen is acute onset of abdominal pain caused by peritoneal inflammation

  1. What mechanical technique can be done to determine if there is inflammation in peritoneum
  2. Common life threatening causes of acute abdomen? (3)
A
  1. rebound tenderness
  2. appendicitis, diverticulitis, ectopic pregnancy
141
Q

Difference between true and false diverticulum? (use names of each too)

A

○ True Diverticulum: protrusion of muscular / mucosa / submucosa layers of GI tract (Meckel)

○ False Diverticulum: protrusion of mucosa / submucosa only (Zenker)

142
Q
  1. What can often lead to ischemic bowel disease?
  2. What areas of GI are most prone to this?
  3. Compications?
A
  1. hypoperfusion due to acute arterial occlusions - can occur due to atherosclerosis, aortic aneurysm, hyper coagulable state, thrombi, vasculitis
  2. Watershed areas (splenic flexure and rectosigmoid flexure)
  3. Necrosis of mucosa can occur and perforation of bowel as well
143
Q
  1. Diverticulitis presents with fever, increased WBC, and (BLANK) quadrant pain
  2. Where is diverticulosis → diverticulitis most common?
  3. How is diet involved in development of diverticulosis?
A
  1. Blank - LLQ
  2. sigmoid colon
  3. low fiber diets can cause diverticulosis - usually in western populations
144
Q

Angiodysplasia in colon

  1. What is it?
  2. Where does it most often occur?
  3. what can it cause
A
  1. Nests of tortuous veins, venules, and capillaries that closely approach the luminal surface - malformed submucosa and mucosal blood vessels
  2. cecum or right colon
  3. MAJOR lower intestinal bleeding
145
Q

Where does bowel obstruction commonly occur?

A

small intestine

146
Q
  1. What causes hemorrhoids?
  2. Which are painful external or internal hemorrhoids?
  3. Risk factors for hemorrhoids (4)
A
  1. dilated anal/perianal collateral vessels due to hemorrhoid plexus hypertension
  2. external
  3. constipation, increased abdominal pressure, pregnancy, cirrhosis
147
Q

differentiate between

(more or less concerning, upper/lower GI source, what it looks like)

  1. Hematemesis
  2. Coffee ground emesis
  3. Hematochezia
  4. Melena
A
  1. Active bleeding - vomiting RED blood - more concerning
  2. Vomiting BROWN blood - granular material - coagulated blood
  3. passage of bright red blood from rectum (can be minor but if larger amounts then this is potentially life threatening due to massive UGI or LGI bleed)
  4. concerning, most likely upper GI source - black tarry foul smelling stool
148
Q

What is occult bleeding?

A

not visible to naked eye, blood loss symptoms (anemia / lightheadedness / etc)

149
Q
  1. upper GI bleeding
  2. lower GI bleeding

Describe each in relation to ligament of treitz

A
  1. upper GI bleed is proximal to ligament of treitz
  2. lower GI bleed is distal to ligament of treitz
150
Q

What general things can lead to upper GI bleeding?

A
  1. peptic ulcers, esophageal varices, mallory weiss tear, gastritis
151
Q

What general things can lead to lower GI bleeding?

A
  1. Hemorrhoids
  2. Diverticulitis
  3. Vascular ectasia (the blood vessels in the lining of the stomach become fragile and become prone to rupture and bleeding)
  4. Intussusception
  5. IBS
152
Q

Celiac Disease - an autoimmune mediated intolerance of gliadin (glutn protein in wheat)

  1. What part of the GI tract does this affect?
  2. What HLAs is this associated with?
  3. the antibodies are against what three things?
  4. What occurs the GI epithelium
A
  1. distal duodenum and proximal jejunum
  2. HLA-DQ2, HLA-DQ8
  3. tTG, endomysial (connective tissue), deaminated gliadin
  4. villous atrophy - flat mucosa → reduction in absorptive surface area and impaired nutrient uptake
153
Q

Lactose intolerance

  1. How do you dx this (via what test)
  2. How does the villi, mucosa change
  3. What symptoms occurs?
A
  1. Lactose hydrogen breath test - pos test is when Hydrogen rises >20 ppm
  2. normal
  3. osmotic diarrhea with low stool pH
154
Q

Pancreatic insufficiency

  1. what is this?
  2. What causes this?
  3. What symptoms occur?
A
  1. malabsorption of fat, Vit B12, and fat soluble vitamins (ADEK) due to the pancreas not making enough of a specific enzyme the body uses to digest food in the small intestine. → seen with HCO3-, decreased duodenal pH, decreased fecal elastase (because pancreas juices/enzymes are decreased)
  2. Chronic pancreatitis, cystic fibrosis, obstructing cancer
  3. bulky/frothy/clay colored stool
155
Q

Whipple disease

  1. What bacteria is involved?
  2. What staining is positive
  3. How does malabsorption happen in whipple disease? What is found in lamina propria?
  4. extraintestinal symptoms? (4)
A
  1. Tropheryma whipplei
  2. PAS
  3. foamy macrophages bc bacteria accumulate here → leads to lymphatic obstruction (this is malabsorption - impairing the breakdown of foods, and hampering your body’s ability to absorb nutrients, such as fats and carbohydrates.)
  4. cardiac symptoms, arthralgias, neruologic symptoms
156
Q

What does decreased D-Xylose test indicate?

A

Decreased D-xylose indicates celiac disease or bacterial overgrowth - d-xylose is passively absorbed without enzymatic activity so if its absorption is diminished then it means mucosa is abnormal/damaged

157
Q

What are some extraintestinal manifestations of celiac disease? (3+)

A
  1. dermatitis herpetiformis
  2. Aphthous stomatitis (image)
  3. arthritis and more
158
Q

How does giardia lamblia cause malabsorption?

A

The parasite attaches itself to the lining of the small intestines in humans, where it causes diarrhea and interferes with the body’s absorption of fats and carbohydrates from digested foods.

159
Q

How does cystic fibrosis lead to malabsorption AND maldigestion?

A
  1. malabsorption - mutation in CFTR channel interferes with luminal hydration → makes viscous luminal contents and prevents nutrient absorption
  2. maldigestion - in pancreas ducts are plugged by thick mucus leading to loss of release of pancreatic enzymes for digestion
160
Q
  1. Glucose-galactose malabsorption is mutation in what glucose transporter?
  2. what patient is this found in?
  3. complication?
A
  1. SGLT-1
  2. pediatric condition where infants present with severe diarrhea shortly after birth
  3. Cause osmotic diarrhea because of remaining glucose/galactose in intestinal lumen → can lead to severe malnutrition
161
Q

What there is an issue with fat/lipid digestion what can this lead to (clinical presentation)?

A

steatorrhea

  • congenital lipase deficiency + pancreatic insufficiency
162
Q
  1. What is hartnups disease?
  2. What is cystinuria
A
  1. Hartnup disease is a condition caused by the body’s inability to absorb certain protein building blocks (amino acids) from the diet. As a result, affected individuals are not able to use these amino acids to produce other substances, such as vitamins and proteins.
  2. Cystinuria is an inherited metabolic disorder characterized by excessive amounts of undissolved cystine in the urine, as well as three chemically similar amino acids: arginine, lysine, and ornithine.
163
Q

What is the difference between omphalocoele and gastroschisis in neonates?

A
  1. Omphalocoele - herniated abdominal viscera through an enlarged umbilical ring - defect is covered by a membrane (amnion+peritoneum)
  2. Gastroschisis - defect in lateral body wall folding- lateral herniation - closed umbilical ring - NO COVERING MEMBRANE
164
Q
  1. What are the six dimensions of health care quality?
  2. And what does each mean?
A

Safe - Avoiding injuries to patients from the care that is intended to help them

Timely - Reducing waits and sometimes harmful delays for patients and providers

Effective - Providing the appropriate level of services based on scientific knowledge

Efficient - Avoiding waste, including waste of equipment, supplies, ideas, and energy

Equitable - Providing care that does not vary in quality because of personal characteristics

Patient-Centered - Providing care that is respectful of and responsive to individual patients

165
Q

What are the three questions in the model for improvement?

A

What are we trying to accomplish?

How will we know a change is an improvement?

What change can we make that will result in an improvement?

166
Q

How do you test changes in the model for improvement?

A
167
Q
A

Block 5 (7 decks)

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