Exam 3: GI Pathophysiology Flashcards

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
Q

Parietal cells produce:

A

Stomach acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Chronic gastritis/PUD usually caused by:

A

H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

H. pylori survives in stomach by:

A

Secreting ammonia as buffer against gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

S/s of H. pylori:

A

Upper abdo discomfort
N/V
Ulcers

29
Q

Peptic ulcers are:

A

Chronic lesions anywhere in the GI tract exposed to acid, although 98% are in proximal duodenum/stomach (4:1)

30
Q

Causes of peptic ulcers:

A
H. pylori
NSAIDs
Smoking
Alcohol
Corticosteroids
Stress
31
Q

S/s of peptic ulcers:

A

Epigastric pain
N/V
Hemorrhage
Perforation

NOT cancer

32
Q

Acute gastritis is:

A

Acute, usually transient, mucosal inflammation

33
Q

Causes of acute gastritis:

A
Just about anything
NSAIDs
ETOH
Smoking
Chemo
Uremia
Sepsis
Ischemia, shock, stress
Ingestion
Trauma to stomach
34
Q

S/s of acute gastritis:

A

Epigastric pain
N/V
Hematemesis
Melena

35
Q

Most common type of stomach cancer:

A

Gastric carcinoma (> 90%)

36
Q

Causes of intestinal-type adenocarcinoma:

A
Nitrites/nitrates
Smoked, pickled, salty food
↓ in fruit/veg consumption
Chronic gastritis
H. pylori
37
Q

Causes of diffuse carcinoma:

A

Not well understood

38
Q

Four layers of intestine from outermost to innermost:

A

Serosa
Muscularis
Submucosa
Mucosa

39
Q

If starches are not absorbed or broken down:

A

Bacteria will eat them, leading to cramps and bloating

40
Q

Non-digested proteins in the bloodstream cause:

A

Inflammation and the creation of antibodies/immune response

41
Q

Monosaccharide uptake is aggressive due to:

A

Glucose and galactose being taken in via Na+ cotransporters

42
Q

Most at-risk blood supply in the GI system:

A

Splenic flexure

43
Q

Developmental problem behind Hirchsprung’s:

A

Aganglionic segment of distal colon lacks Meissner & Auerback plexuses and thus has no peristalsis

44
Q

Sequelae of Hirchsprung’s:

A

Obstruction
Enterocolitis
Perforation

After removal of large segment: chronic diarrhea d/t minimal H2O absorption

45
Q

Tx of Hirchsprung’s:

A

Removal of aganglionic segment

46
Q

Worst case scenario for ischemic bowel disease:

A

Transmural infarction - 90% mortality rate

47
Q

Five causes of ischemic bowel disease:

A
Arterial thrombosis
Arterial embolism
Venous thrombosis
Non-occlusive ischemia
Mechanical obstruction
48
Q

Cause of hemorrhoids:

A

Straining during defecation
Pregnancy (caval obstruction backs up to portal-caval anastamoses)
Hepatic portal hypertension

49
Q

Secretory diarrhea:

A

Caused by bacterial infections
Ex. cholera
Can lose 1L/hr!

50
Q

Cholera causes diarrhea by:

A

Causing epithelium to lose Cl- into the lumen, which inhibits Na+ uptake and H2O uptake

51
Q

Osmotic diarrhea:

A

Due to non-digestible agents in the lumen that act as osmotic agents
Ex. GoLytely

52
Q

Exudative diarrhea:

A

Due to destruction of epithelial layer - not enough viable tissue, poor absorption
Ex. shigella, salmonella, campylobacter, etc

53
Q

Malabsorption diarrhea:

A

Ex. lactose intolerance, giardia, lympatic obstruction d/t fat buildup
Bacterial feeding on ingested food causes bloating, gas, diarrhea

54
Q

Deranged motility diarrhea:

A

D/t surgery or hyperthyroidism

Usually ↓ motility but can sometimes be ↑

55
Q

Dx’ing CD vs UC:

A

Colonoscopy - UC will be in the colon with pseudopolyps

X-ray - can show wall thickening

56
Q

Distribution of ulcerative colitis:

A

In the colon in one continuous section, starting at anus and going backwards

57
Q

Distribution of Crohn’s disease:

A

Anywhere from mouth to anus, usually in intestines

Skip lesions

Deep fissures, not ulcers

58
Q

Diverticula are:

A

Pouches protruding out of the bowel

59
Q

Diverticulitis is:

A

When diverticula get inflamed

60
Q

Sequelae of diverticulitis:

A

Perforation

Fistula formation

61
Q

S/s of diverticulitis:

A

LLQ pain

Bleeding

62
Q

Tx of diverticulitis:

A

Fiber

63
Q

Types of mechanical bowel obstruction:

A

Herniation
Adhesions
Intussception
Volvulus

64
Q

Types of pseudo-obstructions:

A

Paralytic ileus
Bowel infarction
Myopathies/neuropathies

65
Q

Colonic tumor becomes invasive when:

A

Penetrates the muscularis mucosae and enters submucosal layer

66
Q

S/s of colorectal carcinoma:

A

Pain
Obstruction
Changes in bowel habits

67
Q

S/s of left-sided colorectal CA:

A

Visible blood in stool, LLQ pain

68
Q

S/s of right-sided colorectal CA:

A

Fatigue
Weakness
Iron deficiency anemia