GI Flashcards

1
Q

What is the role of serotonin in the gut?

A

stimulates gut motility

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2
Q

What is the primary cause of GERD?

A

LES malfunction

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3
Q

What tissue is damaged from exposure to stomach acid in GERD?

A

squamous cell lining of the lower esophagus

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4
Q

What causes Esophagitis?

A

GERD (most common cause)
Allergies
Meds (NSAIDS and Antibiotics)
Smoking, excessive ETOH
Obesity

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5
Q

What cell changes occur in Barretts Esophagus?

A

squamous cells turn into metaplasic columnar epithelium

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6
Q

Barretts esophagus is a precursor to…

A

adenocarcinoma of the esophagus

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7
Q

What are the complications of GERD?

A

Esophagitis
Barrett’s Esophagus
Esophageal CA
Strictures

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8
Q

What is Odynophagia

A

painful swallowing

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9
Q

Why is Barrett’s Esophagus often diagnosed late?

A

early symptoms are subtle; leads to poor prognosis

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10
Q

What happens in the GI tract when cells are damaged?

A

inflammation, ulceration

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11
Q

Major risk factors for esophageal CA?

A

Smoking
ETOH
Obesity
Barretts Esophagus/GERD

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12
Q

Most common cause of peptic ulcer disease

A

H. Pylori infection

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13
Q

How do NSAIDS damage the mucosa in gastritis?

A

inhibits production of prostaglandins which maintain mucus production and protective barrier against stomach acid

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14
Q

How does autoimmune gastritis affect the hematological system?

A

Causes B12 deficiency, leading to pernicious anemia

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15
Q

How does autoimmune gastritis cause B12 deficiency?

A

destroys parietal cells in stomach lining, which are responsible for producing intrinsic factor

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16
Q

Major risk factors of gastric CA…

A

Chronic gastritis
H pylori
Epstein Barr Virus
poor diet
pernicious anemia

17
Q

What sub-type of gastritis is H pylori associated with?

18
Q

Epigastric pain with duodenal ulcer is typically ______ by eating

19
Q

Epigastric pain with gastric ulcer is typically _____ with eating

A

increased or worsened

20
Q

Basic Pathophysiology of Chron’s disease

A

immune system mistakenly attacks the GI tract lining and causes chronic inflammation

21
Q

What cells from the innate immune system are involved in Chrons

A

Dendritic cells and Macrophages
-antigen presenting cells constantly sense bacterial antigens d/t impaired mucosal barriers=constant T1H cell activation

22
Q

What cells from the adaptive immune system are involved in Chrons?

A

-T1H produce interferon gamma= activates macrophages and continues inflammation loop
T17 releases cytokines that sustain/escalate inflammation

23
Q

What happens with cytokine storm in Chrons?

A

Excessive release of cytokines = tissue damage, which worsens symptoms

24
Q

Transmural inflammation in Chrons leads to what?

A

thickening/scarring of the intestinal wall as it tries to heal
-causes fibrosis/strictures=obstructions

25
Q

What is the hallmark of Chrons?

A

Granulomas form and cause skip lesions-Cobblestone appearance

26
Q

What is dybiosis?

A

an imbalance in the gut microbiota that contributes to immune system misfire in the gut

27
Q

Where in the GI tract is Ulcerative Colitis (UC) found?

A

large intestine and rectum

27
Q

Where in the GI tract is Chrons found

A

Can be found anywhere in the GI tract but commonly in the ileum and beginning of the lrg intestine

28
Q

What are the lab values for Chrons

A

-Elevated CRP (higher than in UC)
-Elevated fecal calprotectin (indicate
inflammation)
-Anemia, Leukocytosis,
Thrombocytosis

29
Q

Patho of UC

A

-genetic predisposition-
disruption of the epithelial barrier fxn of the colon (starts in rectum) = abnormal immune response causing inflammation and ulceration in the mucosal lining

30
Q

Epithelial barrier dysfunction leads to…

A

decreased goblet cell production which = decrease in protective mucus which leaves lining vulnerable to bacteria and toxins
-Leaky gut d/t tight junctions btween cells weaken and allow bad things to pass through

31
Q

What does chronic ulceration of the lrg intestine do in the long run?

A

exposes deeper tissue layers over time, which attracts more immune cells that cause further damage (neutrophils and lymphocytes)

32
Q

What is the hallmark of UC?

A

Crypt abscess formation (clusters of neutrophils w/in colonic crypts)
-indicates severe inflammation and bacterial invasion

33
Q

How does dysbiosis contribute to UC?

A

Short Chain Fatty Acids(SCFA’s) are produced by beneficial bacteria; loss in this=decreased SCFA production =impaired mucosal barrier

34
Q

Lab values in UC

A

-Elevated CRP (lower than in Chrons)
-Elevated fecal calprotectin (indicate
inflammation)
-Anemia, Leukocytosis,
Thrombocytosis

35
Q

What is IBS?

A

chronic functional GI disorder- altered bowel habits with an identifiable cause

36
Q

How does IBS differ from IBD?

A

IBS does not cause inflammation or cause permanent harm to the GI tract
IBS DOES cause inflammation and damage to the

37
Q

Characteristics of IBS

A

abd pain accompanied by change in bowel habits (diarrhea, constipation, or both), bloating

38
Q

Triggers of IBS

A

Changes in routine
Stress
certain foods