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Pathophys 2 > Peptic Ulcer disease at home > Flashcards

Peptic Ulcer disease at home Flashcards

1
Q

3 possible locations of peptic ulcers

A

1) Lower esophagus
2) Antrum of stomach
3) Duodenum

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2
Q

What is the most common location for peptic ulcers? Why?

A

The Duodenum
*Because it’s particularly vulnerable: Its mucosal lining is not covered in an alkaline covering, but it is exposed to acidic contents from the stomach.

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3
Q

Three ulcer types (severity)

A

1) Superficial (erosions)
2) Deep (“true ulcers”)
3) Perforating ulcer

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4
Q

What is a superficial ulcer?

A

An ulcer that affects the mucosal lining, but leaves underlying blood vessels and muscle layers intact /unaffected.

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5
Q

What is a deep ulcer?

A

Ulceration penetrates through the submucosal layer and into the muscle layer.

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6
Q

When would pain occur with an ulcer?

A

When it is deep enough so that the gastric acid has contact with nerves.

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7
Q

What is a perforating ulcer?

A

When the wall is penetrated: Exposes body cavity to the content of the tract.

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8
Q

Risk factors for ulcers (6)

A
  • Smoking
  • H. pylori infection
  • Habitual use of NSAIDs
  • Habitual use of alcohol
  • Psychological stress
  • Chronic diseases
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9
Q

Three chronic diseases that increase the risk for ulcers

A
  • Emphysema
  • Rheumatoid arthritis
  • Cirrhosis
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10
Q

Five contributing factors to duodenal ulcers

A

(1) Hypersection of gastric acid and pepsin
(2) Elevated plasma gastrin levels
(3) Inadequate secretion of pancreatic sodium bicarbonate
(4) Excessively rapid gastric emptying
(5) Immune reaction to H. pylori infection

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11
Q

What causes a hypersection of gastric acid and pepsin (2)

**Ultimately due to _________

A
  • Smoking
  • Excess parietal cells (produce HCl)

**Due to excess gastrin

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12
Q

What is the role of gastrin? What happens when a person has excess gastrin?

A
  • Gastrin stimulates the release of GASTRIC ACID and PEPSIN

- Excess gastrin –> Hypersection of gastric acid and pepsin

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13
Q

What is the mechanism for neutralizing acid in the duodenum? Damage to what organ would affect this?

A
  • Sodium bicarbonate

- Damage to the exocrine pancreas would affect this

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14
Q

How would an immune reaction cause an ulcer?

A

The immune reaction could damage the duodenal lining –> Duodenal ulcer

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15
Q

Two clinical manifestations of ulcers

A
  • Chronic intermittent pain in the epigastric region

- Food-relief pattern

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16
Q

Food-relief pattern: GASTRIC ULCER

A
  • No immediate pain: Food gets between acid and ulcer
  • Pain is 20-30 minutes after a meal
  • Consuming more food 20-30 minutes after first meal relieves pain
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17
Q

Food-relief pattern: DUODENAL ULCER

A
  • Pain occurs about an hour after meal (when acid hits duodenum)
  • Pain is relieved if you eat again 20-30 minutes later, as it then blocks the acid from the ulcer.
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18
Q

Why does the food-relief pattern ultimately not work?

A

Because the more food you consume, the more gastric acid you stimulate.

19
Q

Three types of meds for ulcers

A
  • Antacids (histamine blockers, proton pump inhibitors
  • Antibiotic (for H. pylori)
  • Anti-cholinergic drugs
20
Q

Mechanism of antacids (2 types)

A
  • Histamine blockers block histamine release or histamine receptors (histamine in stomach stimulates acid production)
  • Proton pump inhibitors directly block the production of HCl by blocking the pumps that move hydrogen ions out of the parietal cells into the stomach where they bind with Chloride to make hydrochloric acid
21
Q

How do antibiotics treat duodenal ulcers?

A

To treat an H. pylori infection

22
Q

How do anti-cholinergic drugs work to treat duodenal ulcers?

A
  • Inhibit secretion
  • Suppress gastric motility
  • Delay gastric emptying
23
Q

What is usually the ultimate cause of stress ulcers?

Explain this mechanism

A

ISCHEMIA

(sympathetic stimulation -->
decreased mucosal blood flow -->
mucosal metabolism declines -->
decreased mucous production -->
exposes mucosa to gastric acid -->
autodigestion, ulcer formation)
24
Q

What is a cushing ulcer? Where does trauma occur

A
  • A type of ulcer that is especially severe

- Trauma involves a part of the brain where the vagal nerves originate

25
Q

Mechanism of a cushing ulcer

A

Stress response + Intense activation of the vagus nerves (stimulated gastric acid production) = lots of ulceration

26
Q

Presence of food & acid in the duodenum triggers duodenal mucosal cells to release what two hormones? What do these two hormones act on?

A

1) CCK
2) Secretin

**Act on the pancreas and liver to release bile and digestive jucies

27
Q

Role of secretin

What does it act on? What does it do? What is secreted as a result?

A
  • Acts on the exocrine pancreas
  • Binds to duct cells
  • Stimulates the release of sodium bicarbonate solution
28
Q

What organ is our only source of Lipase?

A

PANCREAS

29
Q

Enzymes:
Fat (1)
Carbs (1)
Protein (3)

A

Fat: Lipase
Carbs: Amylase
Protein: Tripsin, Chymotripsin, Carboxypeptidase

30
Q

What is the cause of pancreatic insufficiency?

A

Usually a pancreatic disease – can be endocrine or exocrine disease

31
Q

Losing _______ pancreatic enzymes can be especially devistating

A

Exocrine

32
Q

Clinical manifestations of pancreatic insufficiency (2)

A

1) The presence of a large amount of fat in the stool (Steatorrhea)
2) Weight loss

33
Q

What causes bile salt deficiency? (2)

A
  • Advanced liver disease (cirrhosis)

- Obstruction of bile ducts

34
Q

Clinical manifestations of bile salt deficiency (2)

A
  • Gray colored stool

- Deficiencies in fat-soluble vitamins

35
Q

Why does stool appear gray or clay colored?

A

Absence of excreted bile means no bilirubin –> NO BROWN POOP

36
Q

Why does bile salt deficiency result in deficiencies in fat-soluble vitamins?

A

Because it’s bile’s role to EMULSIFY fat. In the absence of bile fat, we can still digest some fat, but we can’t access all parts of the fat –> Can’t access all vitamins.

37
Q

Result of a VITAMIN A deficiency

A

NIGHT BLINDNESS

38
Q

Result of a VITAMIN D deficiency (4)

A
  • DECREASED CALCIUM ABSORPTION
  • Bone demineralization (osteoporosis)
  • Bone pain
  • Fractures
39
Q

Result of a VITAMIN K deficiency

A
  • Prolonged prothrombin time –> Leads to bleeding, spontaneous brusing
40
Q

Result of a VITAMIN E deficiency

A

May cause neurological effects, esp in children.

41
Q

What breaks down glucose, fructose and lactose? Where?

A

DISACCHARIDES clinging to brush border enzymes

42
Q

What races are more likely to have lactose intollerence?

A

African, middle-eastern

43
Q

What happens with lactose intolerance?

2 symptoms and the physiological reasons why

A

Lactose is not digested by lactase, so it enters the colon.

  • Consumed by bacteria of colon –> Fermentation occurs –> PAINFUL GAS CRAMPS
  • Presence of lactose in colon elevates osmolarity, draws water into colon –> OSMOTIC DIARRHEA

Pathophys 2 (9 decks)

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