Exam 3: GI Pathophysiology Flashcards

(68 cards)

1
Q

After a meal, blood pH shifts:

A

More alkaline d/t shift of H+ into lumen of stomach, HCO3- into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Once food enters duodenum, blood pH shifts:

A

Back to normal; HCO3- is dumped into lumen to increased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hiatal hernia is caused by:

A

Stomach moving through opening in diaphragm by esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sequalae of hiatal hernia:

A

Trapping of food in esophagus and heartburn/regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Achalasia is:

A

Loss of inhibitory innervation of LES, leading to food sitting in esophagus instead of moving into stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of achalasia:

A

Aperistalsis
Incomplete relaxation of LES
↑ tone of LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sequlae of achalasia:

A

Dysphagia
Mucosal inflammation/ulceration
Squamous cell carcinoma (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cause of esophageal varices:

A

Impaired hepatic portal blood flow –> portal HTN –> blood backup to esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

% of cirrhosis pts with esophageal varices:

A

2/3rds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sequelae of esophageal varices:

A

Rupture & hemorrhage

Hematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mortality rate of ruptured esophageal varices:

A

20-30% per episode with a 70% recurrence rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Barrett’s esophagus is:

A

Metaplastic change from esophageal cells to stomach cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Contributing causes to GERD:

A

Obesity
Hiatal hernia
Vagal nerve abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cause of Barrett’s esophagus:

A

Long standing GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sequelae of Barrett’s esophagus:

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Two types of esophageal cancers:

A

Squamous cell carcinoma

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Conditions predisposing to SCC:

A

Tobacco use
Alcohol use
Achalasia
Drinking very hot tea??

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Conditions predisposing to adenocarcinoma:

A

Barrett’s esophagus/GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

S/s of esophageal CA:

A

Dysphagia
Obstruction
(Typically late in progression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Chronic gastritis can lead to:

A

Peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acute gastritis can lead to:

A

Acute gastric ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Normal stomach pH:

A

1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Gastric pits are:

A

Depressions in epithelial lining containing gastric glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chief cells produce:

A

Gastric juice enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Parietal cells produce:
Stomach acid
26
Chronic gastritis/PUD usually caused by:
H. pylori
27
H. pylori survives in stomach by:
Secreting ammonia as buffer against gastric acid
28
S/s of H. pylori:
Upper abdo discomfort N/V Ulcers
29
Peptic ulcers are:
Chronic lesions anywhere in the GI tract exposed to acid, although 98% are in proximal duodenum/stomach (4:1)
30
Causes of peptic ulcers:
``` H. pylori NSAIDs Smoking Alcohol Corticosteroids Stress ```
31
S/s of peptic ulcers:
Epigastric pain N/V Hemorrhage Perforation NOT cancer
32
Acute gastritis is:
Acute, usually transient, mucosal inflammation
33
Causes of acute gastritis:
``` Just about anything NSAIDs ETOH Smoking Chemo Uremia Sepsis Ischemia, shock, stress Ingestion Trauma to stomach ```
34
S/s of acute gastritis:
Epigastric pain N/V Hematemesis Melena
35
Most common type of stomach cancer:
Gastric carcinoma (> 90%)
36
Causes of intestinal-type adenocarcinoma:
``` Nitrites/nitrates Smoked, pickled, salty food ↓ in fruit/veg consumption Chronic gastritis H. pylori ```
37
Causes of diffuse carcinoma:
Not well understood
38
Four layers of intestine from outermost to innermost:
Serosa Muscularis Submucosa Mucosa
39
If starches are not absorbed or broken down:
Bacteria will eat them, leading to cramps and bloating
40
Non-digested proteins in the bloodstream cause:
Inflammation and the creation of antibodies/immune response
41
Monosaccharide uptake is aggressive due to:
Glucose and galactose being taken in via Na+ cotransporters
42
Most at-risk blood supply in the GI system:
Splenic flexure
43
Developmental problem behind Hirchsprung's:
Aganglionic segment of distal colon lacks Meissner & Auerback plexuses and thus has no peristalsis
44
Sequelae of Hirchsprung's:
Obstruction Enterocolitis Perforation After removal of large segment: chronic diarrhea d/t minimal H2O absorption
45
Tx of Hirchsprung's:
Removal of aganglionic segment
46
Worst case scenario for ischemic bowel disease:
Transmural infarction - 90% mortality rate
47
Five causes of ischemic bowel disease:
``` Arterial thrombosis Arterial embolism Venous thrombosis Non-occlusive ischemia Mechanical obstruction ```
48
Cause of hemorrhoids:
Straining during defecation Pregnancy (caval obstruction backs up to portal-caval anastamoses) Hepatic portal hypertension
49
Secretory diarrhea:
Caused by bacterial infections Ex. cholera Can lose 1L/hr!
50
Cholera causes diarrhea by:
Causing epithelium to lose Cl- into the lumen, which inhibits Na+ uptake and H2O uptake
51
Osmotic diarrhea:
Due to non-digestible agents in the lumen that act as osmotic agents Ex. GoLytely
52
Exudative diarrhea:
Due to destruction of epithelial layer - not enough viable tissue, poor absorption Ex. shigella, salmonella, campylobacter, etc
53
Malabsorption diarrhea:
Ex. lactose intolerance, giardia, lympatic obstruction d/t fat buildup Bacterial feeding on ingested food causes bloating, gas, diarrhea
54
Deranged motility diarrhea:
D/t surgery or hyperthyroidism Usually ↓ motility but can sometimes be ↑
55
Dx'ing CD vs UC:
Colonoscopy - UC will be in the colon with pseudopolyps | X-ray - can show wall thickening
56
Distribution of ulcerative colitis:
In the colon in one continuous section, starting at anus and going backwards
57
Distribution of Crohn's disease:
Anywhere from mouth to anus, usually in intestines Skip lesions Deep fissures, not ulcers
58
Diverticula are:
Pouches protruding out of the bowel
59
Diverticulitis is:
When diverticula get inflamed
60
Sequelae of diverticulitis:
Perforation | Fistula formation
61
S/s of diverticulitis:
LLQ pain | Bleeding
62
Tx of diverticulitis:
Fiber
63
Types of mechanical bowel obstruction:
Herniation Adhesions Intussception Volvulus
64
Types of pseudo-obstructions:
Paralytic ileus Bowel infarction Myopathies/neuropathies
65
Colonic tumor becomes invasive when:
Penetrates the muscularis mucosae and enters submucosal layer
66
S/s of colorectal carcinoma:
Pain Obstruction Changes in bowel habits
67
S/s of left-sided colorectal CA:
Visible blood in stool, LLQ pain
68
S/s of right-sided colorectal CA:
Fatigue Weakness Iron deficiency anemia