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GI > GI Review Deck 1- Upper GI and Malabsorption > Flashcards

GI Review Deck 1- Upper GI and Malabsorption Flashcards

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1
Q

Describe the Meissner’s plexus and Auerbach’s plexus

A

Messiner’s is sensory, in submucosa. Auerbach’s is myenteric between muscle layers (between inner circular and outer longitudinal)

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2
Q

The GI tract has which layers, and which parts don’t have which layers?

A

Outer epithelia, lamina propria, muscularis mucosa, submucosa, submucosal plexus, circular muscle, myenteric plexus, longitudinal muscle, serosa.
Esophagus does not have serosa (Strength in GI tract, connective tissue).

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3
Q

What is the ora serrata

A

Z- line, where the squamous cell turns into columnar epithelia above the stomach

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4
Q

What tissue makes up the bulk of the GI tract

A

Columnar epithelium (Squamous at anus and esophagus)

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5
Q

Types of dysphagia

A

1) Deglutition- oropharyngeal dysfunction
- Disruption of transfer of food to mouth to esophagus. No trouble chewing or swallowing, but can’t get the food down. Coughing, choking during meals, saliva, aspiration pneumonia, drooling

2) Transit- Esophageal disruption of material from esophagus to stomach
-Solid or liquid gets stuck in retrosternal area, unable to eat, discomfort

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6
Q

Symptoms and treatment for disorders of deglutition

A

Oropharyngeal dysfunction
Coughing, drooling, aspiration pna, choking

Tx: G-tube feeding, speech therapy

Examples: ALS, stroke, Muscular dystrophy, Parkinson’s, Scleroderma

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7
Q

Describe achalasia

A

Destruction of ganglia in myenteric plexus, leads to abscent peristalsis in esophagus, failure of LES to relax.

Tx: Nitroglycerin, smooth muscle relaxant, Botox, surgery to divide LES muscles.

Sx: Full quickly, regurgitation, weight loss

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8
Q
A

Achelasia X-ray– shows LES inability to open
Image taken from Barium X-ray

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9
Q
A

Esophageal spasm
Diffuse esophageal spasm
Corckscrew esophagus

TX: NTG, Ca blockers, botox, myomectomy

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10
Q
A

Zenker’s diverticulum
Sx: Dysphagia
Mucosa protrudes through killans triangle, increased risk of SCC

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11
Q

Describe Zenker’s Diverticulum

A

Increased pressures in pharynx leads to mucosa protrusion though killian’s triangle.
Increased risk of SCC

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12
Q

Describe Plummer Vinson syndrome

A

Dysphagia secondary to proximal esophageal web

Middle aged women

Triad: Iron deficiency anemia, glossitis, dysphagia

Highewr risk of SCC

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13
Q

Which 2 esophageal disorders increase risk of SCC

A

Plummer vinson syndrome, Zenker’s Diverticulum

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14
Q

Demographic for plummer vinson syndrome

A

Middle aged women, associated with IDA

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15
Q
A

Plummer Vinson syndrome
Associated with IDA, SCC, Glositis

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16
Q

Where are squamous cell carcinoma vs adenocarcinomas located in the esophagus

A

SCC: Proximal and mid esophagus
Adenocarcenoma: Distal Esophagus

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17
Q

Causes of SCC vs Adenocarcinoma of esophagus

A

SCC: Tobacco, Alcohol
Adenocarcinoma: GERD, Barretts

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18
Q
A

Schatzki ring

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19
Q

pathophys and tx

A

Schatzki ring
Mucosal membrane ring at squamocolumnar junction, relationship with GERD, common, cause dysphagia most common with MEAT consumption

Treated with balloon dilation

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20
Q

Tx for Schatzki ring

A

Balloon Dilation

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21
Q

Cause and Tx

A

Peptic stricture
Caused by GERD
Tx with Gerd Rx and dilation

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22
Q
A

Eosinophilic Esophagitis
Unknown cause (food allergy, GER, genetics?)
Dysphagia, food impaction, chest pain symptoms
Biopsy: >15 eosinophils (Gerd Esophagitis <15)
Tx: PPI, allergy testing, food elimination, budesonide, dupixent

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23
Q

Sx of EoE

A

Dysphagia, chest pain, food impaction

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24
Q

Tx for EoE

A

PPI, food elimination, allergy testing

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25
Odynophagia
painful swallowing
26
Candida esophagitis
27
Viral esophagitis
28
Pill esophagitis Kissing ulceration Common with NSAIDs (ibuprofen, aspirin, naproxen), Doxy/Tetracyclein, Bisphosphonates (Aldronate) KCl, Ferrous Sulfate
29
Primary Symptom in EoE
Dysphagia, food impaction, chest pain
30
Esophageal pH
>4 This is relevent in GERD because stomach pH is 1.5, so acid harms mucosal lining
31
GERD Alarm symptoms
IDA Hematemisis or melena dysphagia unexplained weight loss family history of esophageal cancer caucasian male >50 (More prone to Barrett's and esophageal cancer)
32
When to do an endoscopy if suspecting GERD
- Failure to respond to PPI - Alarm symptoms - Exclude Barrett's in at risk populations (Longstanding GERD, Caucasian males >50)
33
GERD
34
What is Barrett's esophagus
Chronic GERD complication Intestinal Metaplasia in esophageal squamous mucosa 10% of people with GERD Increased risk of esophageal adenocarcinoma (Progresses to adenocarcinoma)
35
Risk factors for barrett's esophagus- adenocarcinoma
- Severity/duration of reflux - Length of Barrett's segment - Smoking (NOT ALCOHOL) - Obesity - White male
36
If there are goblet cells in the esophagus, what does this suggest
Intestinal meteplasia from the stomach to the esophagus-- barrett's esophagus
37
Barrett's esophagus treatment
Acid suppression (PPI) Screen at risk groups Ablation or removal of Barrett's tissue
38
First line treatment for GERD
Eliminate factors predisposing to GERD (Weight loss, quit smoking/Alcohol, Reduce foods lowering LES pressure (fats, sweets, pepperment, chocolate, caffine), reduce acidic foods, replace meds that lower LES pressure, NPO 2 hours before bed, Elevate head of bed
39
Second line GERD treatment
Metoclopramide ( Serious SIs) GABA agonist (reduce LESRs) Mucosal protectants ( Sucralfate (Carfate) or alginic acid (alginate) Antiacids (PPIs, H2 blockers)
40
Erosion vs ulcer
5mm or > is an ulcer, less is an erosion. Breaks in the lining of mucosa, iwth submucosal extension
41
Dyspepsia
Pain in upper abdomen
42
Chief cells secrete what
pepsinogen
43
Key epidemiology of H. pylori
- Differences in the subspecies and host factors account for clinical differences in presentation - Cytotoxin- associated gene A(CAG) and VACA play roles in pathogenicity, strains with the factors have more tissue inflammation
44
How to diagnose H pylori
Stop PPIs 2 weeks before test, re-test at least 4 weeks after the last antibiotic is taken
45
H pylori increases risk of which diseases
MALT lymphoma, adenocarcinoma
46
Incidental findings of H pylori should be treated- true or false
TRUE-- all people with evidence of H pylori should be offered treatment
47
First line treatment for H pylori
Quad therapy Treat (tetracycline) My ( Metronidazole) Belly (Bismuth) Pain ( Pantoprozole/PPI)
48
After a patient is treated for H pylori, do you need follow up?
YES-- need testing to confirm eradication Urea breath test, fecal antigen test, upper endoscopy. At LEAST 4 weeks after treatment and withheld PPIs MUST treat with salvage regimine after if quad therapy doesn't work ( Clarithromycin)
49
Zollinger Ellison syndrome
Secretion of gastrin by a Neuro endocrine tumor (Gastrinoma). Excessive gastric acid secretion leads to severe PUD.
50
DX for Zollinger ellison syndrome
High fasting serum gastrin levels (Discontinue PPI before test. Gastrin levels should be low when fasting. If high when fasting, indicates tumor) and secretin stimulation test.
51
Risk factors for PUD
- Alcohol - Tobacco - COPD - Renal insufficiency -Older age
52
Differential Diagnoses for PUD
- Gastritis - Gastric tumors - GERD - Pancreatitis
53
Distribution of types of PUD
Duodenal ulcers: Most common in younger patients (30-55). BETTER with meals, worse 2-5 hours after Gastric Ulcers: Most common in older patients (55-70). WORSE with meals, better much later after
54
Lipases break down which macronutrient
Lipids in mouth
55
Amylases break down which nutrient group
Carbohydrates in mouth
56
Pepsin breaks down which nutrient group
proteins from stomach
57
What is the only nutrient broken down in the stomach
protein via pepsin
58
Where does most carbohydrate digestion occur
intestinal mucosa via brush border enzymes (sucrase, maltase, lactase)
59
Describe bile's pathway
Bile is produced in the liver, stored in the gallbladder, and the gallbladder contracts in the presence of CCK/fat to get the bile into the duodenum
60
Describe what happens with CCK release
CCK stimulates the pacreas to release proenzymes, enterokinase activates trypsinogen to trypsin, which activates other enzymes. If active, the enzymes would destroy pancreas, so have to be inactive in pacnrease and activated outside
61
Where is the majority of water secreted and absorbed
majority absorbed in small intestine (78%) Colon absorbs 20% Stool is 1% water
62
Where are iron and calcium absorbed
duodenum
63
where are carbohydrates absorbed
duodenum and jejunum
64
where are fats and proteins absorbed
duodenum, jejunum, ileum
65
If your ileum is resected, what cannot be absorbed
B12, Bile salts
66
If your duodenum is ressected, which nutrients is your patient likely deficient in
Iron, Calcium
67
Where is iron absorbed
duodenum
68
In reduced brush boarder enzymes, what is the ultamate result
Reduced carbohydrate absorbtion means more starch gets to the colon. This causes gas, bloating, and diarrhea because bacteria can't metabolize so much starch.
69
Causes of flatuance due to carbohydrate malabsorption
Decreased brush boarder enzymes/mucosal damage Pancreatic insufficiency, where carbs are no longer broken down
70
MMA levels are elevtaed in which disease
elevated in B12 deficiency
71
Homocysteine levels are elevated in which disease
B12 deficiency or folate deficiency
72
Folate levels are increased in which disorder
SIBO causes an incrase in folic acid
73
Lactase deficient ethnic groups
US Native americans, middle east and meditaranian, asia
74
Complication of lactose intolerance
osteoporosis
75
Causes of SIBO
- Dismotility (neuropathy in diabetics, hypothyroidism, scleroderma) - Altered anatomy (diverticulosis) - Acid deficiency (pancreatitis) - Immune deficiency (AIDS, severe malnutrition)
76
Consequences of SIBO
Mucosal injury loss of protein and disaccharides Produce Vitamin K and Folate (CAREFUL w Warfarin)
77
Deficiencies in someone who undergoes a roux-en-y procedure
- B12- need gastric acid, disyncronization - B1 (thiamine) - Folate - Iron - Zinc - Copper -Selenium - Calcium All of those abosrbed in duodenum and proximal jejunum

GI (6 decks)

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