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Kidney Disease > Upper G.I. > Flashcards

Upper G.I. Flashcards

1
Q

Esophagitis define

A

inflammation or infection in the esophagus

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2
Q

Who experiences esophagitis?

A

Immuno-compromised People
–> Opputunistic Infection such as Candidiasis

  • Immunodeficiency disorders
  • HIV/AIDs
    Immunosupression due to cancer tx
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3
Q

Most common caus eof irritation and inflammation in esophagus

A

gastro esophageal reflux disease (GERD)

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4
Q

Medication Induced GERD Example

A

bisphosphonates can irritate the esophagus if the patient does not remain upright after administration (HAVE TO STAY UPRIGHT TO AVOID ESOPHAGEAL IRRITATION

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5
Q

Swallowing disorders are a result of….

A
  • a lack of neuromuscular coordination of the voluntary or involuntary muscles associated with swallowing, such as from neuromuscular disease
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6
Q

Describe the pathology of GERD

A

The esophagus meets the stomach at the lower esophageal sphincter (LES)

Should have tension in the valve, if relaxed or a lot of pressure in stomach can have reflux into the esophagus

The esophageal surface is not protected by thick mucous, unlike the stomach.

Thus, it is vulnerable to acid irritation, causing pain and erosion.

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7
Q

GERD can eventually lead to….

A

Eventually inflammatory changes can occur (metaplasia).

Metaplasia –> Cell changes that are not normal; but not cancer

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8
Q

GERD Pathology

A

GERD is caused by a lax cardiac sphincter at the gastroesophageal juncture, such that acid irritates the esophageal epithelium, which does not have the productive thick mucous which the gastric lining has.

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9
Q

GERD can affect….

A

uncomfortable and affects quality of life and of sleep.

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10
Q

GERD can mimic….

A

May mimic a heart attack with intense chest pain.

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11
Q

GERD carries the risk for….

A

Barrett’s esophagus: metaplasia, pre-cancerous, must monitor because Barrett’s is a risk for esophageal cancer.

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12
Q

NOn-Pharm Tx of GERD

A

weight loss, extra pillow for sleep, earlier supper, avoiding trigger foods (may vary).

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13
Q

Pharmacological TX for GERD

A

H2 receptor antagonists

Proton pump inhibitors

Traditional antacids may cause rebound acidity but are still a good choice to try (once calm the acid, may stimulate more acid production)

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14
Q

H2 Receptors Antagonist MOA and Example

A

Bind to H2 receptors in gastric parietal cells, reducing H+/K+ ATPase activity (makes the H+ that passes into lumen, Cl- enters as well)

“Idines”

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15
Q

H2 Uses

A

GERD and Peptic Ulcers

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16
Q

H2 in comparison to PPI

A
  • Duration is shorter
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17
Q

PPI MOA

A

Bind to the H+/K+ ATPase of the gastric parietal cell, thereby preventing acid secretion

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18
Q

PPI Uses

A

GERD, peptic ulcers, H. pylori-related ulcers, duodenal ulcers and Zollinger-Ellison disorder (acid hypersecretion)

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19
Q

PPI Examples

A

“azoles”

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20
Q

Parietal Cells do what?

A

secrete acid into the stomach

21
Q

ECL Cells do what

A

Enterochromaffin-like cells, secrete histamine and peptide hormones

22
Q

Muscarinic Receptors do what?

A

binds acetylcholine (Ach) from nerve cells, and they are located on both parietal and ECL cells

23
Q

What stimulates ECL cells? What happens?

A

When ECL cells are stimulated by ACh, they secrete histamine (H2)which stimulates parietal cells to secrete acid.

When the parietal cell is stimulated via both its muscarinic receptors and its H2 receptors, it secretes a lot of acid.

24
Q

H2 antagonists bind to…

A
  • Histamine receptors
25
Q

Proton Pump Inhibitors act at…

A

the site of acid production, blocking the effect of simulation by both histamine receptors and muscarinic receptors.

26
Q

Are PPI’s designed for long term use?

A

NO

27
Q

Gastritis

A

Infection or inflammation of the stomach
Acute or chronic

28
Q

Gastritis can be caused by…..

A

Infection: H. pylori infection is associated with gastric ulcers.

Irritation: foods (acidic or spicy)

Medications: NSAIDS (by blocking prostaglandin synthesis, they reduce production of protective mucous in the stomach), certain antibiotics –> Cuts down on the ability to produce thick mucous –> needs prostaglandins for mucous production  Chronic NSAID use
Alcohol: direct irritant
Atrophy of old age: achlorhydria, reduced acid production, greater risk of infections
Major stress: surgery, major burns, severe illness –>Risk of ulcers  Be put on an H2 antagonist to prevent ulcer
Autoimmune (+pernicious anemia with B 12 deficiency)  attack intrinsic factor

29
Q

Gastritis Signs and symptoms

A

Pain (around belly button)
Bloating
Burning sensation
Heavy feeling in stomach
Belching or flatulence
Nausea/vomiting
Loss of appetite - If long term
Weight loss (chronic)
Blood in vomit or stool
Coffee-grounds emesis  someone throws up and looks like coffee grounds, actually blood (coagulation)
Melena (tarry stool)  Black and sticky stool  presence of blood that has gone through G.I. tract

30
Q

Tx of H. Pylori

A

Triple antibiotic therapy +PPI is typical

31
Q

Gastric Ulcer Tx and length

A

One or two antibiotics (amoxicillin, tetracycline, metronidazole or clarithromycin). Choice depends on allergies, sensitivity
And bismuth (coats and helps with healing)
And H2 antagonist or PPI
2-3 weeks of treatment
Surgery only if perforated or nonhealing

32
Q

Gastric Ulcers present a risk of

A

Anemia

33
Q

Main causes of gastric ulcers

A

NSAIDS
H. Pylori

34
Q

Gastric cancer rates are highest in countries with….

A

high rates of H. pylori infection and a diet high in salt and smoked food

35
Q

Gastric cancer is mainly what type?

A

Most are adenocarcinomas (glandular tissue).

36
Q

Tx of Gastric Cancer

A

Treatment is surgery in the early stages, plus radiation and chemotherapy for later stages.

37
Q

Pancreas has how many parts

A

The pancreas has 3 parts: tail, body and head.

38
Q

The pancreas function

A

It has endocrine and exocrine functions

39
Q

Pancreas Exocrine Function

A

Its exocrine functions are to produce acid-neutralizing bicarbonate and digestive enzymes such as lipase, amylase and protease to break down fats, carbohydrates and proteins.

40
Q

Acute Pancreatitis Definition

A

Acinar cell injury and duct obstruction results inappropriate extracellular leakage of activated digestive enzymes and thus autodigestion of pancreatic and extra-pancreatic tissues

41
Q

Sverity of Acute Pancreatitis

A

Spectrum of severity from self-limiting, mild disease to fatal hemorrhagic pancreatitis with massive necrosis

42
Q

Damage to Pancrease in Acute Pancreatitis is due to….

A

Necrosis of acinar cells leads to inflammation; Inflammation releases oxygen free radicals which damage tissue. Patchy areas with necrotic adipocytes occur (fat necrosis); fibrosis upon healing (which will impair pancreas function)

43
Q

Symptoms of acute pancreatitis

A

Severe epigastric pain that radiates to the upper back, nausea & vomiting

44
Q

Diagnosis of acute pancreatirtis

A

: serum amylase and lipase become elevated (suppose to be contained in pancreas and ducts).

hock and collapse may occur

45
Q

Management of Acute Pancreatis

A

Supportive care, avoid alcohol, pain management

46
Q

Chronic Pancreatitis

A

Chronic pancreatitis (80% due to alcoholism) presents as recurrent or persistent epigastric pain with signs of pancreatic insufficiency

47
Q

Chronic Pancreatitis Signs

A

– poor digestion, pain upon eating, greasy/smelly stools, malnutrition

48
Q

How does alchol cause chronic pancreatitis?

A

Alcohol is a pancreatic “secretagogue” meaning it stimulates secretion, however, these extra proteins can clog up the pancreatic ducts, leading to obstructions. (extra proteins can clog up the ducts)
The areas of fat necrosis can also be come calcified. “saponification”

49
Q

Chronic Pancreatitis Tx

A

As pancreatic function declines, the patient may need pancreatic enzyme supplements (pancreatin)

Kidney Disease (3 decks)

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