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Block 4a: GI > Wk 2: IBD/Digestion & Absorption > Flashcards

Wk 2: IBD/Digestion & Absorption Flashcards

1
Q

Acarbose

A

Alpha Glucosidase Inhibitor: slows down CHO digestion, requiring less insulin activity

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2
Q

Beano

A

Alpha Galactosidase (enzyme that humans lack) required to break down “Raffinose” and “Stachyose”

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3
Q

SGLT2 Inhibitors

A

Inhibit glucose uptake, specifically in kidneys “gliflozin” suffix Ex’s: Canagliflozin, Dapagliflozin, Empagliflozin

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4
Q

What are 2 tests to assess CHO metabolism?

A

Breath Test & Reducing sugars in feces

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5
Q

How does the breath test work to assess CHO metabolism?

A

Measure unabsorbed CHO by measuring H2, methane (CH4) & other gases and acids

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6
Q

What are some examples and exceptions to reducing sugars in feces that can assess CHO metabolism?

A

Reducing sugars: fructose, glucose/galactose, lactose NOT sucrose nor starch

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7
Q

What are 3 stimulants of parietal cells?

A

Ach, Gastrin, Histamine

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8
Q

How are zymogens from the pancreas activated by the small intestine for protein digestion?

A

Enteropeptidase in duodenum’s microvilli activate Trypsinogen into Trypsin

Trypsin cleaves more Trypsinogen & protease precursors: chymotrypsinogen, procarboxypeptidase, & proelastase into their active forms

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9
Q

What substances (& their sources!) pass through the Ampulla of Vater to reach the small intestine?

A

Bile salts (from the common bile duct) & protease precursors (from the pancreatic duct)

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10
Q

How do peptides & amino acids enter epithelial cells?

A

PEPT1 at the microvilli surface bring in peptides, which are then broken down into AA’s

Peptidases [AA Transporter] bring in AA’s directly from Na/aa gradient

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11
Q

What is Hartnup Disorder & how might it present?

A

Deficiency of neutral AA transporter: SLC6A19=B(0)AT1

Mostly asymptomatic bc neutral aa’s can be taken up as di/tri peptides, although condition can progress…

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12
Q

What is Hartnup Disorder?

A

Insufficient neutral aa transport, especially w/ Tryptophan which can then lead to Niacin deficiency

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13
Q

How does Hartnup Disorder present?

A

3D’s: Dementia, Diarrhea, Dermatitis (C3/C4 dermatome) w/ a circumferential “broad collar rash”-Casal Necklace

3D’s also described as “Pellagra” disease

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14
Q

What is the Tx of Hartnup Disorder?

A

High protein diet & nicotinic acid

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15
Q

How does the pancreas digest phospholipids?

A

Pancreas-> Prophospholipase A2 which is then cleaved by Trypsin into Phospholipase A2

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16
Q

What can patients lacking a pancreas take to help digest macronutrients?

A

Pancrelipase

Each capsule w/ 5000 USP units of lipase, 17,000 USP units of protease & 27,000 USP units of amylase

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17
Q

What are the 3 transport pathways in the GI system?

A

Pumps (active)

Channels (passive)

Carriers (passive); “exchangers:” move in opp directions vs. “cotransporters:” move in same direction

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18
Q

What are 2 ex’s of neurocrine effectors that stimulate Cl secretion?

A

Ach & VIP

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19
Q

What are the 2 main classes of endogenous regulators in ion transport? (Give ex’s)

A

Cyclic Nucleotide Dependent (i) & Ca Dependent (ii)

i) VIP, Prostaglandins, Guanylin (cGMP) & 5’AMP/Adenosine
ii) Ach, Histamine, 5-Hydroxytryptamine & Bile Acids

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20
Q

How is absorption affected by GI motility?

A

Dependent on rate of fluid/nutrients across epithelium

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21
Q

How do reflexes control motility & blood flow in the GI?

A

Secondary activation of nerves & myofibroblast sheaths

Long Reflex: vagovagal reflex activates stretch receptors

Short Reflex: activates cholinergic efferents-> Cl as brushing mucosa induces 5-HT from eterochromaffin cells

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22
Q

How does food move in the small intestine post-prandially? Which region is the exception?

A

Via low amplitude, irregular contractions; mixing

EXCEPT in distal ileum: forceful bolus contractions
->emptying (giving an added pause to salvage fluids/nutrients)

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23
Q

Describe the 2 motor activities of the GI system; which is the main motor reponse to eating?

A

1) Propagation: moving out (HAPC/LAPC)
2) Segmental: mixing (single/bursts) *majority*

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24
Q

Contrast High Amplitude Propagated Contractions (HAPC) vs. LAPC

A

HAPC:
amplitude >100 mmHg
frequency: 3-6x/day
function: mass mvt of colonic contents
defecation

LAPC:
amplitude <50 mmHg
>100x/day
transport fluid
assoc w/ abdominal distension & flatuluence

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25
Q

What are the 2 intestinal ion transport mechanisms that the small intestine and colon share?

A

Cl secretion & Electroneutral NaCl absorption

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26
Q

What are intestinal ion transport mechanisms unique to the small intestine?

A

HCO3- secretion

Na (& bile acid) coupled nutrient absorption

Proton coupled nutrient absorption

Ca (throughout) & Fe absorption (proximal)

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27
Q

What are intestinal ion transport mechanisms unique to the colon?

A

Electrogenic Na absorption

Short chain FA absorption

K absorption/secretion

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28
Q

Where are indigestible fibers and carbohydrates degraded? Effects?

A

In colon by bacteria, generating short chain FA’s->
colonocyte fuel

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29
Q

Describe 2 mediators involved in Cl secretion

A

Guanylin & 5’ AMP/Adenosine

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30
Q

Describe the source of Guanylin & its effects

A

Source: enteroendocrine cells

Stimulates epithelial Cl secretion & affects kidney salt mgmt

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31
Q

Describe the source of 5’AMP/Adenosine & its effects

A

Released by neutrophils & micro-organisms & cytokines (largely in setting of infection)

Endogenous cyclic nucleotide dependent regulator of ion transport that activates Cl- secretion

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32
Q

Where is most bile reabsorbed & what is its main effect?

A

Ileum, via nutrient coupled mechanisms

Act as laxative, inducing diarrhea

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33
Q

How is the type of diarrhea determined?

A

Stool Gap: 290 mmol/kg-2[Na+K of stool]

Secretory gap <50
Osmotic gap>100

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34
Q

Describe osmotic diarrhea

A

H2O absorbed passively, dependent on luminal substance absorption

Lactose can remain behind undigested
Poorly absorbed salts (ie: MgSO4)
Sorbitol

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35
Q

Describe secretory diarrhea & 1 classic source

A

Excess Cl- secretion (ie: Vibrio Cholera: non-invasive but potent toxin)

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36
Q

Describe the drug class & MOA of the anti-diarrhealLoperamide

A

Opioid Agonist, acts on colon’s myenteric plexus
Long reflex ↓ mass movements & SM tone

↑ time of material in colon & fluid absorption

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37
Q

Describe the drug class & MOA of the anti-diarrheal Diphenoxylate-Atropine

A
  • Diphenoxylate:* opioid-agonist that ↓ propagation & ↑ absorption
  • Atropine*: added to ↓ risk of dependence bc high doses causes anticholinergic AE’s (ie: tachycardia)
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38
Q

Describe the class & MOA of the constipation drug Bisacodyl

A

Stimulant laxative

Stimulates enteric nerves->colonic contractions

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39
Q

Describe the class & MOA of the constipation drug Polyethylene Glycol

A

Osmotic Laxative

Osmotic gradient used to draw H2O into lumen

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40
Q

Describe the class & MOA of the constipation drug Lubiprostone [Amitiza]

A

Bicyclic Fatty Acid

Selectively activates Type II Cl channel in apical membrane, ↑ intestinal fluid secretion

Activates Prostaglandin receptors, mediating intestinal fluid secretion, ↑ tight junction integrity & function

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41
Q

Describe the class & MOA of the constipation drug Linaclotide [Linzess]

A

Oligopeptide agonist of guanylate cyclase 2C

↑ HCO3- and Cl- secretion via ↑ CGMP & induction of PKGII and Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)

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42
Q

What are the induction therapies for active mild-moderate, severe & refractory Ulcerative Colitis?

A

mild-mod: Aminosalicylate & consider topical application for L sided disease, if local to rectum/sigmoid colon

severe: Glucocorticoids
refractory: Biologic (Anti-TNF); Cyclosporine (rare)

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43
Q

What are maintenance therapies for Ulcerative Colitis?

A

Aminosalicylates->Azathioprine (steroid sparing)

->Biologic *reqs regular IV infusion*

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44
Q

When is surgery indicated in Ulcerative Colitis? Prognosis?

A

Refractoriness, Toxic Megalon, Obstruction, Hemorrhage, Dysplasia/Cancer

~30% of patients will have proctocolectomy
UC doesn’t recur post-surgery

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45
Q

What are the induction therapies for active mild-moderate & severe Crohn’s Disease?

A

mild-mod: Aminosalicylate & Budesonide
severe: Glucocorticoids & Biologics

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46
Q

What are the maintenance therapies for Crohn’s Disease?

A

Azathioprine (purine analogue) & MTX (folate analogue) & Biologics

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47
Q

When is surgery indicated in Crohn’s Disease? Prognosis?

A

Stricture, Perforation, Hemorrhage & Cancer

60-70% of patients w/ >1 surgeries over lifetime

48
Q

Describe fts of the IBD drug class: 5-Aminosalicylate

A

MOA: ↓ Cyclooxygenase & Lipoxygenase
↑ Prostaglandins & Leukotrenes

Ex’s: Sulfasalazine & Mesalamine

Sulfasalazine AE’s: anemia & oligospermia

49
Q

Describe fts of the IBD drug class: Antibiotics

A

MOA: changes microbiome

Ex’s & AE’s: Ciprofloxacin (-) tendon rupture

Metronidazole (-) dysgeusia [taste alteration]
(-) peripheral neuropathy

Rifaximin

50
Q

Describe fts of the IBD drug class: Glucocorticoids

A

MOA: ↓ WBC activity & cytokine production

AE: HTN, DM, Osteoporosis, Infection, Cataracts

Ex’s: Prednisone, Budesonide

51
Q

Describe fts of the IBD drug class: Purine Analogue

A

MOA: ↓ nucleic acid synthesis, WBC anti-proliferative effect

AE’s: ↓ WBC, pancreatitis, hepatotoxicity, Lymphoma

Ex’s: 6-MP, Azathioprine

52
Q

Describe fts of the IBD drug class: Folate Analogue

A

MOA: ↓ DNA synthesis, anti-inflammatory effects

AE’s: BM supression, Hepatotoxicity, Pneumonitis

Ex: MTX

53
Q

Describe fts of the IBD drug class: Biologics

A

MOA: Inhibits TNF-alpha & adhesion molecules

Ex: Infliximab, Natalizumab

AE’s: Opportunistic Infections, Lymphoma *shared (-) w/ Purine Analogues*

54
Q

Describe fts of the acid relief drug class: Antacids

A

MOA: neutralizes gastric acid

Ex’s: Magnesium/Aluminum Hydroxide, Calcium Carbonate

AE: Mg(OH)2: diarrhea
AlOH: constipation

55
Q

Describe fts of the acid relief drug class: Sucralfate

MOA
AE
Ex

A

MOA: coats injured mucosa

AE: can bind concomitant medications

Ex: Sulfated Sucrose w/ AlOH

56
Q

Describe fts of the acid relief drug class: H2 Receptor Antagonists

A

MOA: competitive antagonist of parietal cell H2R

Ex’s: Ranitidine, Famotidine, Nizatidine,
Cimetidine (-) gynecomastia [man boobs]

(-) inhibition of P450

57
Q

Describe fts of the acid relief drug class: Proton Pump Inhibitors

A

MOA: Irreversibly inhibits parietal cell H+/K+ ATPase

Well tolerated but associations w/ (-) C Diff, Dementia, Osteoporosis, Pneumonia

Ex’s: Omeprazole, Lansoprazole, Rabeprazole, Pantoprazole, Esome_prazole_

58
Q

What does this upper endoscopy reveal?

A

Erosive Esophagitis (GERD)

Erosion: linear white line, which enters mucosa but not submucosa

59
Q

What are symptoms of GERD?

A

Burning chest, dysphagia & regurgitation

60
Q

What are atypical (extra-esophageal) GERD symptoms?

A

Chest pain, cough, asthma flares, hoarse voice

61
Q

Which receptor binds gastrin on the surface of the parietal cell?

Which receptor binds Ach on the surface of the parietal cell?

A

CCK receptor binds Gastrin

Muscarinic M3 receptor binds Ach

62
Q

What dx can follow this upper endoscopy biopsy?

A

Barrett’s Esophagus: intestinal metaplasia from stratified squamous->columnar

Note: no longer stratified squamous epithelium & presence of goblet cells

63
Q

What is the only known precursor lesion for esophageal adenocarcinoma?

A

Barrett’s Esophagus

64
Q

What are RF’s for Barrett’s Esophagus? What is NOT a RF that distinguishes it from squamous cell cancer?

A

Older age >50 y/o, M, Caucasian, Central Obesity, Long standing GERD, Tobacco

Alcohol is NOT a RF unlike in squamous cell

65
Q

How is nondysplastic Barrett’s Esophagus treated & managed?

A

Tx: Omeprazole (PPI) vs. reflux but also to ↓ risk of progression from nondysplastic->dysplastic cancer

Repeat endoscopy in 3 yrs for surveillance

66
Q

Why would Barium swallow not be recommended in pt w/ Barrett’s Esophagus that has progressed?

A

Ba can end up in lungs if pt cannot even handle food or her own saliva

Structural/motility dysphagia can handle Ba but NOT oropharyngeal type

67
Q

What does this upper endoscopy reveal? & What risk does this carry?

A

Food impaction; if left for >24 hours, can cause perforation/ischemia

68
Q

What does this upper endoscopy reveal?

A

Erosion

69
Q

What can cause food impaction & is described as “chronic reflux esophagitis?”

A

Peptic Stricture: 90% benign esophageal strictures, occurs in 7-23% of patients w/ GERD

Although may be ↓ bc of improved GERD Tx

70
Q

Following dilation for peptic stricture, how soon should pt F/U for repeat endoscopy? What other surveillance measure is required?

A

1 mo or even sooner if dysphagia continues

Repeat endoscopy in 3 yrs for Barrett’s esophagus surveillance

71
Q

What type of metastatic disease has a predilection for the GI tract & is often pigmented?

A

Metastatic Melanoma

72
Q

What type of tumor is in this upper endoscopy?

A

Esophageal Adenocarcinoma

73
Q

Compare the 2 main types of esophageal cancer re area of impact, RF’s & epidemiology

A

Squamous Cell Carcinoma:
Upper/middle 1/3 of esophagus
RF: Smoking, Alcohol
EPI: most common in E Eur & Asia

Adenocarcinoma:
Lower 1/3 of esophagus
RF: Smoking, Caucasian race, M, Obesity

EPI: Most common type in N. America & W hemisphere, incidence still rising

74
Q

When is manometry used as a diagnostic test?

A

Only after structural disease is ruled out, which is why upper endoscopy is done 1st

75
Q

Describe what you observe in this upper endoscopy:

A

Trachealization or “felinization” of esophagus

76
Q

What does this Barium Swallow reveal?

A

Ridges can be seen, consistent w/ esophageal ridges or strictures

77
Q

What would you expect to see in biopsy of Eosinophilic Esophagitis?

A

Acute mucosal inflammation w/ >15 eosinophils/high powered field (HPF) *doesn’t meet criteria if any fewer eosinophils*

Blue circle: Nucleus
Red circle: Eosinophil

78
Q

What is the EPI, associations & symptoms of EOE?

A

EPI: Young, Caucasian men

Associated w/ Atopic Triad: Asthma, Seasonal allergies & Eczema (often w/ family Hx)

Sx: esophageal dysfunction: dysphagia, odynophagia, chest pain, reflux “burning”

79
Q

What are some secondary causes of EOE & how would these present histologically?

A

<15 eosinophils/HPF

Celiac Disease, Crohn’s Disease, Infection, Hypereosinophilic Syndrome, Achalasia, Drug Hypersensitivity, Vasculitis, Pemphigus, CT Diseases, Graft vs. Host Disease

80
Q

What is the 1st line Tx of EOE? What if that fails? In severe cases?

A

1st line: PPI, helps gauge responsive eosinophilia *if you stay on PPI-don’t require steroids*

If PPI’s fail: Topical Steroids (topical for esophagus): Budesonide/Fluticasone inhaler that is swallowed rather than inhaled

Severe: Systemic Steroids

81
Q

What can be done for food elimination in EOE? What specific diet can a patient stick to?

A

Allergy Testing

6 Food Elimination Diet: Milk, Wheat, Soy, Eggs, Nuts, Seafood *primary pediatric Tx & adult EOE but difficult to follow*

82
Q

What does this upper endoscopy reveal?

A

Candida Esophagitis

83
Q

When should CMV Esophagitis be suspected?

A

Ulcers in immunocompromised setting (ie: Chemo/HIV)

84
Q

Describe a biopsy of Candida Esophagitis:

A

Up to only about 3 eosinophils/HPV

Numerous fungal forms w/ pseudohyphae

85
Q

What is the best Tx option for Candida Esophagitis?

A

Fluconasole: antifungal

86
Q

In setting of Candida Esophagitis, what complication can arise w/ steroid Tx? What if Fluticasone is tapered?

A

Candida can still be a risk w/ steroid Tx w/ chance of recurrence w/ tapering of Fluticasone

87
Q

What type of dysphagia is diagnosed most accurately for when a patient points to “where it gets stuck?”

A

Proximal Dysphagia

88
Q

When would a Ba swallow be preferred over upper endoscopy?

A

If pt has many comorbidities

89
Q

How does a Barium Swallow appear in Achalasia?

A

“Bird’s Beak” w/ little contrast passing through esophagus into stomach but not complete obstruction

90
Q

What do these endoscopies reveal & what condition is it associated with?

A

(L) Dilated esophagus

(R): Residual food particles

91
Q

What are the symptoms of Achalasia? What is its pathophysiology?

A

Difficulty swallowing (S) AND (L) bc motility problem
Chest Pain
Regurgitation
Weight Loss (in severe cases)

PATH/PHYS: Lack of inhibitory neurons in LES

92
Q

What test confirms the dx of Achalasia after a Barium Swallow? What other tests might be helpful?

A

Esophageal Manometry

To rule out pseudoachalasia from obstruction (ie: tumor) at lower esophagus-CT scan or endoscopic US/upper endoscopy may be helfpul

93
Q

What manometric findings are consistent w/ Achalasia?

A

Failure of LES relaxation, aperistalsis & high resting LES pressure

94
Q

How does manometry present in setting of Scleroderma?

A

Low LES pressure & hypotensive LES

95
Q

What is a good Tx option for Achalasia in a patient w/ many comorbidities? Give an ex of a more invasive option & why it wouldn’t be as strongly considered

A

Botulinum toxin injection into LES

More invasive Heller Myotomy cuts LES & wraps stomach around it; may induce acid reflux

96
Q

What is a concern for performing esophageal dilation to treat Achalasia in a patient w/ many comorbidities?

A

May require stopping medications like bloodthinners (Clopidogrel [Plavix])

97
Q

Describe the treatment outcomes for Achalasia short & long term:

A

Short Term: Dilation & Botox work well but don’t do as well as time goes on & may req repeat procedures

Long term: Heller Myotomy best

98
Q

What is the best diagnostic test in a patient presenting w/ melena?

A

CBC (may reveal ↓ Hb)

99
Q

What does this upper endoscopy reveal?

A

“Clean-based” duodenal ulcer: no visible blood vessels nor bleeding

100
Q

What are the 2 types of ulcers in Peptic Ulcer Disease & how do their presentations differ?

A

Gastric Ulcer: pain worsens after eating

Duodenal Ulcer: pain improves after eating

101
Q

What are RF’s for PUD?

A

NSAID’s

H Pylori

Systemic Diseases: CD

  • Zollinger Ellison’s Syndrome* (hypergastrinemia from neurogastrin tumor)
  • Behcet’s Disease*: blood vessel inflammation-possibly autoimmune
102
Q

W/ suspicion of PUD & the following biopsy, what is the best Tx?

A

Omeprazole & antibiotics in setting of PUD w/ H Pylori

103
Q

Describe H Pylori:
Type of bacteria

Location found

Spread

EPI

Risks

Tx:

A

Microaerophilic gram (-) bacteria

Found adherent to stomach mucosal layer

Fecal-oral spread

EPI: more common in developing countries

Risks: Gastritis, Ulcers (Gastric & Duodenal*), Gastric Adenocarcinoma, Mucosa Associated Lymphoid Tissue (MALT) Lymphoma

Tx: Triple therapy: Omeprazole, Amoxicillin [Metronidazole* if PCN allergic] & Clarithromycin (antibiotic)

104
Q

What test can be performed to see if H Pylori has been eliminated? Is further Tx required?

A

H Pylori Breath Test

Even if asymptomatic, Omeprazole may be continued for 1 more month

105
Q

Describe the criteria to dx Functional Dyspepsia, characteristics & EPI

A

20% w/ sx: major economic impact, resembles ulcer sx
not life-threatening but affects QOL

EPI: F>M, Smokers, NSAID Users

106
Q

What is the 1st step to treat functional dyspepsia in a patient <60 y/o? If >60 y/o?

When is an endoscopy not called for in a patient <60 y/o?

A

If <60 y/o: Check H Pylori stool antigen
If >60 y/o: Endoscopy to test for malignancy

No endoscopy for pt < 60 y/o if “alarm features” absent ex: weight loss, GI bleed, dysphagia

107
Q

W/ suspicion of Functional Dyspepsia & H Pylori stool antigen (-), what is the best Tx option?

A

Omeprazole & lifestyle modifications (ie: caffeine reduction, smoking cessation)

108
Q

In a diabetic patient, what condition might be a concern in setting of dysphagia? What is the best diagnostic test?

A

Diabetic Gastroparesis

Gastric Emptying Test

109
Q

What are the Sx of Gastroparesis? How can it be diagnosed? Etiology?

A

Sx: Early satiety, Nausea, Vomiting, Abdominal pain (although not predominant sx)

Dx: Gastric Emptying Test: gold standard; documented delay in gastric emptying required*
Liquid emptying may be normal but emptying of solids may lag

Etiology: Idiopathic (post-viral) 35.5%, Diabetes (29%)

110
Q

Rank order of gastric emptying time among macronutrients

A

Fats>Proteins>Carbohydrates

111
Q

Following upper endoscopy, what might a video swallow reveal in a Parkinson’s patient w/ dysphagia?

A

Pooling in valleculae (groove), penetration of barium, pyriform sinus residue, no frank aspiration & evidence of cricopharyngeal bar (muscle contour-hypertensive UES; not diverticulum but due to HTN)

112
Q

Describe characteristics of a Cricopharyngeal Bar

Tx?

A

Upper Esophageal Sphincter

Frequent incidental radiological finding: usually asx, so look for other causes of dysphagia

Tx: Refer to ENT for endoscopic dilation & cricopharyngeal myotomy

113
Q

Describe Oropharyngeal Dysphagia

Clinical Px
Causes
Tx

A

Px: coughing during swallow, food sticking in throat, nasal regurgitation

Causes: Neurologic (Parkinson’s, Stroke, ALS), Tumors, Zenker’s Diverticulum (false; herniation)

Tx: Dietary modification, speech therapy, repairing underlying mechanical cause

114
Q

What is an Upper GI Series?

A

Similar to Ba Swallow but looks further & for longer (ie: stomach->small intestine)

115
Q

How might DES spasm present in Ba Swallow, Esophageal Manometry, & pH Impedance Testing?

Among these, what is the gold standard for Dx?

A

Ba Swallow: Corkscrew appearance

Manometry*: sev simultaneous high amplitude contractions; very pink colors-high P *gold standard for Dx*

pH Impedance testing normal on omeprazole

116
Q

What are the Sx of DES? Tx’s?

A

Sx: Esophageal dysphagia to (S) & (L), exacerbated by T extremes, Retrosternal chest pain

Tx: 1st line- CCB (Diltiazem), TCA
2nd line-Botulinum Toxin, Sildenafil (Vasodilator-Viagra)

Block 4a: GI (5 decks)

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