PUD, Pancreatitis, and Gall Stones (Test 1)

peptic ulcer disease (PUD)

is characterized by discontinuations in the inner lining of the GI tract (ulcers)

peptic ulcers

open sores > or = to 5 mm caused by gastric acid and/or pepsin secretion

-usually occurs in the stomach and duodenum and extend deep into the muscularis mucosa

parietal cells

secretes gastric acid

increased

Acid secretion is __________ in patients with duodenal ulcers.

normal or reduced

Acid secretion is ______________ in patients with gastric ulcers.

pepsinogen

-the inactive precursor of pepsin and is secreted by the chief cells in the gastric fundus and duodenum

-breaks down food and hydrolyzes mucus

peptic ulcers

Alterations in mucosal defense promote formation and expansion of _______________

mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow

What protects the gastroduodenal mucosa from noxious endogenous and exogenous substances?

prostglandins are secreted to facilitate mucosal integrity and repair to prevent expansion to deep mucosal injury

What happens when the gatroduodenal mucosa is injured?

-upper GI bleeding

-perforation

-obstruction

What can happen if the gastroduodenal mucosa is injured and unresolved?

-H. pylori infections

-NSAIDs

-cigarette smoking

-varying sensitivity and specific of detection methodology

What causes PUD?

1 in 6

What is the estimate of people who have peptic ulcers in the US?

PUD symptoms

-abdominal pain (peaks after you eat)

-bloating, fullness

-N/V

-weight loss/weight gain

-progressive dysphagia

-GI bleeding in vomit or stool

hematemesis

vomiting blood

melena

dark, tarry stool containing partially digested blood

presence of ulcers seen in scope

What is the sign of PUD?

Helicobacter pylori

What is the most common cause of PUD?

H. pylori

-are spiral, microaerophilic, gram-neg bacteria with flagella that can survive in and attempt to neutralize the acidic environment of the stomach

-primarily transported gastro-oral or fecal-oral contact

-close contact within households

-low income status

-country of origin

What are the risk factors for acquiring H. pylori?

flagella

What facilitates the initial infection of H. pylori and allow for colonization of the gastric mucosa? (starts in stomach and expands to duodenum)

cytotoxin

associated gene protein (CagA)

vacuolating cytotoxin (VacA)

a vacuolating toxin

-cytotoxin

-vacuolating cytotoxin

What are the toxins that are produced by H. pylori that deter phagocytes allowing the H. pylori to thrive in place?

urease

H. pylori produces __________ which converts urea to ammonia which neutralizes gastric acid alkalinizing their microenvironment. Ammonia may also be toxic to gastric epithelial cells.

microenvironment alkalinization

can lead to hypochlorhydira (low gastric acid) or achlorhydria

hypersecretion of gastric acid which damages the mucosa (epithelial cells die)

How do nearby parietal cells compensate when the H. pylori alkalizes their microenvironment?

-damaging epithelial cells directly

-breaking down mucus barrier so H+ damages the epithelial cells

-altering the pH of the stomach

-altering the host inflammatory response, and recruiting nearby neutrophils and macrophages

H. pylori induces chronic gastric mucosal inflammation by:

NSAIDs

-block prostaglandin synthesis by inhibiting cyclooxygenase COX enzymes leading to a decrease in gastric mucous and bicarbonate production and mucosal blood flow

-they also cause superficial mucosal damage and petechiae

petechiae

pinpoint hemorrhages

-dose

-duration of use

-type of drug

NSAID-induced ulcers are due to what?

COX-1

NSAID induced PUC has an increased risk when more selective for __________ vs COX-2.

Aspirin

can be very damaging given its acidic properties because it inhibits prostaglandin signaling

10x

the risk of ulcers is _________ greater when an NSAID is coadmin. with low dose aspirin than when either drug is taken alone

20x

the risk of ulcers is __________ greater when NSAIDs are taken with concomitantly with anticoagulants

6x

the risk of ulcers is _______ greater when NSAIDs are taken with serotonin reuptake inhibitors

stress-induced PUD

develop secondary to systemic stress, and considered a medical emergency

-trauma

-shock

-acute illnesses

-some chronic illnesses

-psychological stress

PUD complications

-upper GI bleeds

-risk of gastric perforation or penetration

-gastric outlet obstruction (delayed emptying)

-gastric cancer

upper endoscopy

visualization of the ulcer and implementation of therapeutic maneuvers to control bleeding

-upper endoscopy

-radiography

-helicobacter tests (urea breath, blood, stool, tissue biopsy)

What can you do to diagnose PUD?

urea breath

swallow a labelled urea and detect urease activity in exhaled air

Hgb, hematocrit and fecal samples for blood

What can you do during a PUC diagnosis to determine extent of bleeding?

-remove the trigger

-lifestyle changs

-OTC antacids, PPIs, histamine-2-receptor blockers

-Gi cytoprotective agents

-endoscopy therapies

What are the treatments plans for PUD?

antibiotics

How should you treat a patient who has PUD and is H. pylori positive?

no more NSAIDs

How should you treat a patient with NSAID induced PUD?

to lower the acidic environment in the stomach

Why do we utilize antacids, PPIs, and H2 blockers for PUD treatment?

pancreatitis

inflammation of the pancreas

acute pancreatitis

sudden onset of inflammation and swelling of pancreas

chronic pancreatitis

repeated acute attacks which leads to inflammatory infiltrates and fibrosis within the pancreas (leading to loss of pancreatic exocrine and endocrine functions)

symptoms of acute pancreatitis

-severe pain in 95% of patients

-quickly reaches max intensity and can persists for hours to days

-n/v

-pain in upper abdomen or back

symptoms of chronic pancreatitis

-can go unnoticed for several years but initial presentation is most often chronic abdominal pain

-n/v

-pain in upper abdomen or back

•Tenderness on palpitation

•Distended abdomen, reduced bowel sounds

•May show hypotension, tachycardia, and low-grade fever as signs of severe inflammation and necrosis

•May show other systemic signs (dyspnea, tachypnea, jaundice, altered mental state)

With chronic pancreatitis, steatorrhea

What are the signs of pancreatitis?

steatorrhea

excess excretion of fat in stools

-elevated serum lipase

-elevated serum amylase

-leukocytosis

-elevated C-reactive protein

-steatorrhea

What are the lab tests used to determine pancreatitis?

•Gall stones

•Blockade of pancreatic duct

•Alcohol misuse, drugs, trauma/injury

•Very high triglycerides

acute pancreatitis is often driven by:

chronic alcohol use

Chronic pancreatitis is most often driven by what?

acinar cells

exocrine (secretin, mucin, ect)

islet of langerhans

endocrine (insulin, glucagon)

acinar

What type of cell is injured with both acute and chronic pancreatitis?

chronic

Complications are more common with _________ pancreatitis.

-steatorrhea

-increased risk of DM

-relieving signs and symptoms

-pancreatic enzyme replacement therapy

-abstain from alcohol and drugs

-eat smaller meals

-reduct diet fat intake

What are the ways to treat pancreatitis?

cholelithiasis

stones that form in the gallbladder composed of cho, bilirubin, bile and /or calcium

when the gallbladder is slow to empty bile and it reaches the limit of solubility

How do gall bladder stones occur?

cholecystitis

inflammation of the gall bladder (stones obstructing the duct can cause this)

cachexia

wasting syndrome

risk factors for gall stones

•Pregnancy- physical restriction and hormones decrease contractility of gallbladder

•Obesity

•Metabolic syndrome

•Bariatric surgery, Crohn’s disease

•Prolonged fasting, rapid weight loss, cachexia (wasting syndrome)

•Genetics

•Higher risk in females

gall stones symptoms

-abdominal pain after eating greasy or spicy foods (right upper quadrant)

-n/v

-fever

-jaundice

jaundice

yellowing of skin and whites of eyes (sign that bile duct is obstructed by stone)

cholecystectomy

removal of the gallbladder