NURS 206 Quiz 1 -> Quiz 2

Common clinical presentations of the GI system

1. acidity

2. Transition time

3. Nausea and vomiting

Too slow transition time

increased re-absorption of water

• Constipation

• obstruction

Too fast transition time

Decreased absorption of nutrients and water

decreased removal of waste product (i.e. nausea)

Functions of the GI

Digest food into usable nutrients

Eliminate waste products

Food

Calories per gram of protein and fat

Protein 4cal/g

Fat 9 cal/g

BMR (Basal Metabolic Rate) in adults

Adults → 10 cal/lb

What is BMR and what increases it

Minimum requirement for body to operate at rest

increase BMR

• Fever

• High Thyroid hormones

• More muscle mass

Types of diet

Full diet

Clear liquid

Soft

Specialized (low sodium)

Where does the majority of absorption occur in the small intestine

duodenum + jejunum

What is the upper GI

Mouth + Esohagus + stomach

Stomach anatomy

Indented depressions

lined with mucous cells and specialized gastric cells

pH in the stomach

1.3-3.5

Parietal cells

Secrete HCL

located at opening of gastric pit

requires a stimuli to secrete HCL

What is also activated when parietal cells secrete HCL

a H/K-ATPase (hydrogen, potassium) proton pump

each hydrogen that leaves the parietal cell, a potassium enters

What receptors is for gastrin from G cells

Choleycystokinin receptros

What receptors are for histamine from endocrine cells

H2 receptors

What receptors are for acetylcholine from PSNS

Ach receptors

What do cheif cells do

create pepsinogen

HCL activates it to pepsin

Benefits of HCL (3)

1. Chemical digestion of food

2. destruction of pathogens

3. Nutrient absorption

Nutrient absorption benefit of HCL

instrinsic factor synthesis → vitamin B12 GI absorption

Ferric iron → ferrous iron for better GI absorption

Benefit of ferric iron

doesn’t need to be activated

What does prostaglandin E2 stimulate

Mucous (foveolar) cells

Mucous cell function and make

bicarbonate and mucous secretions

protective mucosal barrier

Gastric mucosa vs duodenum and jejunum (4)

alkaline pancreatic juice and bile

alkaline serous fluid produced by intestinal mucosa

brush border enzymes → nutrient absorption

More protection at duodenum then gradually decreasing

Sphinctors (2)

pyloric sphincter → holds everything in the stomach (at bottom)

Esophageal sphincter → protects esophagus (at top)

HCL control is required for

1. reflux and gastroesophageal reflux disease (GERD)

2. Peptic ulcer disease (PUD)

Acid Reflux

Reflux of gastric contents into the esophagus

burning sensations

HCL only present in esophagus when food is there

GERD definition

persistent acid reflux

Pathophysiology of reflux and GERD

1. Transient (begins and ends, cycle) relxations of esophageal sphincter allows reflux

2. Delayed gastric emptying → when GI function is decreased

Delayed gastric emptying is caused by

stress, immobility, over-eating, congenital syndromes

Suppressed parasympahetic NS

Clinical Presentation of GERD

1. Pain

2. Decreased appetite

3. Bleeding

   1. mucosal erosion

   2. low RBCS

   3. blood in vomit

   4. old blood in stool

4. Respiratory s&s if inhaled

What is black colour in stool (blood) called

Melina

GERD complications

1. weight loss

2. reflux esophagitis

   1. erosion, inflammation

   2. risk of esophageal cancer

3. respiratory/airway erosion

GERD diagnosis

tissue biopsy

GERD can lead to

Barrett’s esophagus

esophageal cancer

GERD treatment

avoid irritants

• adjunct: patient positioning, smaller meals

Decrease acidity: 3 drug classes

Fundoplication → Surgery

3 drug classes that help with GERD

1. Antacids

2. H2 receptor antagonists

3. Protein pump inhibitors

Antacids (4) treatment

1. Alkaline agents → increase stomach pH

2. do not decrease HCL secretion

3. symptom relief only

4. not recommended for persistent reflux

Antacid drug example

Bismuth Subsalicylate (pepto bismal)

Bismuth Subsalicylate

part of more classes → anti-infective (decreases adhesion → more elimination), anti-diarrheal

Antacid mineral content side effects (4)

Aluminum → constipation

Magnesium → diarrhea

Clacium → kidney stones

Sodium → BP

H2 receptor antagonists (3)

gastric histamine 2 receptor antagonism

• selective blockade (H2 specific)

• Decreases HCL (other stimuli present)

H2 receptor antagonist drugs (4)

1. Rantidine (Zantac)

2. Cimetidine

3. Famotidine

4. Quick relief

Rantidine (Zantac) (3)

H2 receptor antagonist

Does not cross BBB (IV, titrated to effect)

• most popular because not crossing BBB

Protein pump inhibitors (PPIs)

binds and inhibits H+ K+ -ATPase proton pump

inhibits hydrogen H+ binding with chloride

• Prevents HCL acid formation

• reduce HCL all around

• Reserved for patients with ongoing GERD

Protein Pump inhibitor drugs

1. Omeprazole (Losec)

2. Iaonsoprazole (Prevacid)

3. Pantoprazole (Pantoloc)

Clinical applicaition for protein pump inhibitors

efficacy → higher than H2 recap

long term presciripiotn

• onset and t ½ longer than H2 receptor blockers → chronic relief

Zollinger-Ellison syndrome

Too much gastrin and HCL

treatment with PPI

Result of tumours

Peptic Ulcer Disease (PUD) pathophysiology

1. Failure of endogenous protection (tight mucosal-cell junction and mucous/bicarbonate layer)

2. Mucosal inflammation and erosion of stomach or duodenum

   1. Duodenal ulcers are 4X more common → no natural protecetion

   2. erosion may extend into/thru deep layers of mucosa

Clinical presentation of PUD (4)

Pain → depending on ulcerations

Anorexia → decreased nutrients, malnourishment

Bleeding

Anemia

What condition is it if food makes the pain better or worse?

Better → PUD

• because of bicarbonate and mucous secretions with food

Worse → Duodenal ulcer

Common causes of PUD (4)

1. Stress

2. H-pylori infection

3. NSAID overuse

4. Risk for complications

   1. perforation

   2. obstruction

   3. cancer

Why does NSAID overuse cause PUD (4)

NSAID → COX-1 prostaglandin inhibitors

• decreased clotting → bleeding

• Decreased mucosal protection

• decreased GI overall

H (helicobacter)-pylori infection classification (2)

gram- bacteria

present in 90% of duodenal and 75% of gastric ulcers

Diagnosis of a H-pylori infection

Serology → anti IGG antibodies

Stool test → Stool collection over 24 hours

Breath test → CO2 capture

How does a breath test and CO2 capture detect a H-pylori infection

Urea in prescence of H pylori becomes ammonia and CO2

Treatment of PUD (3)

1. deecrease acidity

2. Treatment infection

3. stop causitive agents (NSAIDS)

Treatment of H-pylori

Amoxicillin 1g PO bid

PPI

Peptobismol

Prevention

Peritonitis classification (2)

Mucosal perforation

Inflammation of the peritoneum (lining of abdominal cavity)

Clinical presentation of peritonitis (6)

1. evolves fast, becomes life threatening

2. Pain

3. Fever

4. N&V

5. SNS symptoms

6. CBC → lymphocytes and leukocytes increase

Causes of peritonitis

1. perforated PUD

2. other perforations e.g. diverticulitis, ruptured appendix

3. injury e.g. stab wound

Retching definition

rhythmic movement of abdominal muscles/diaphragm/chest wall

Emesis

vomiting (expulsion of GI contents)

Dysphagia

difficult swallowing

Colonoscopy

viewing of lower GI tract

Endoscopy

viewing of upper GI tract

What are some types of congenital malformations in the upper GI? (2)

1. TEF (TE fistula)
   Tracheoesophageal fistula

2. sophagel trachea

Tracheoesophageal fistula

• connection between trachea and esophagus

congenital anomaly

• food can’t enter stomach

• choking, vomiting

Small intestine basics (4)

1. 20 feet long, 1 inch in diameter

2. 3 parts → duodenum, jejunum, ileum

3. Absorption of nutrients

4. Digestion (duodenum + jejunum)

what does the gall bladder produce

bile → from CCK

Chyme prescence causes bile secretions and pancreaic juice

Protein digestion (2)

1. first digested in stomach from pepsinogen

2. pancreatic juice breaks it down into AA chains

what activates pepsin to pepsinogen

HCL

Carbohydrate Digestion and absorption (2+1)

• converted to monosaccharides

• salivary amylase, pancreatic juice, and brush border enzymes

• carb absorption → simple suger (big sugars cause bloating from movement of water in stool)

Simple sugars examples (3)

Glucose

galactose

fructose (Maybe)

Fat digestion (3)

begin in mouth by bilingual lipase

emulsification through bile + pancreatic juices

break to fatty acids → transported through lymphatics through triglycerides before systemic circulation

Large intestine anatomy (5)

• 5 feet long, 3 inch in diameter

4 parts

• ascending colon

• transverse colon

• descending colon

• sigmoid olon

Large intestine function

1. reabsorption of water (simple columnar cells)

   1. only 100 ml of water excreted in stool

2. host flora → vitamin B & K synthesis

What is GI innervation classified as

intestinal motility affected by the nervous system

GI inervation is affected by (2)

1. ANS

2. Enteric Nervous system

ANS in GI

Sympathetic → stoppage of GI function

Parasympathetic → optimized GI function

Enteric NS input is from (3)

mechanoreceptors: GI stretch → digestion starts

Chemoreceptors: food prescence/osmolality/pH
ANS

Hirschsprung disease classificaiton and cause (3)

1. GI innervation issue (no colon movement)

2. Parasympathetic ganglion cells in wall of large intestine don’t develop before birth

3. Affected segment of colon doesn’t have ability to relax and move bowel contents (peristalsis)

What procedure is for Hirschsprung disease and how does it work

Pull-through procedure

1. Cut diseased section

2. attach healthy section to anus

Inflammatory GI disorders S&S and kinds (4)

Common S&S → anorexia, diarrhea, nausea

1. Chron’s disease

2. Ulcerative colitis

3. Celiac disease

Chron’s disease (3)

can affect any part of the GIT (even mouth)

discountinous patchy inflammation

transmural (affects full thickness of bowel wall)

Ulcerative Colitis (3)

1. affects only large intestine

2. continuous inflammation (Chronic)

3. mucosal and submucosal layers are affected

What is celiac disease (4)

• gluten sensitivty enteropathy

• gluten triggeredimmune response

• overt T-cell mediaed immune response o alpha-gliadin

• Causes inflammation → loss of villi

Signs and symptoms and complications of Celiac disease (5)

S&S

1. anorexia

2. bloating

3. diarrhea

4. malnutration

Complications

malnutrition, malabsorption

Diagnosis and treatment of celiac (3)

Diagnosis

1. serology, biopsy (endoscopic)

2. bloodwork test: tTG-IgA completed on gluten in diet

Treatment

• avoidance of gluten

Naturally gluten-FREE whole grains (9)

1. Quinoa

2. Amaranth

3. Buckwheat

4. Sorghum

5. Rice

6. Millet

7. Teff

8. Corn

9. GF oats

whole grains with GLUTEN (9)

1. Farro

2. Bulger wheat

3. Triticale

4. Durum

5. Rye

6. Barley

7. Spelt

8. Kamut

9. Semolina

Examples of infectious diseases (2)

1. C-diff

2. E-coli

C-diff classifications (3) and development (1)

gram + bacterium

• severly infectious and contagious

• Puss and blood in stool

from altered host flora

TreatmentTreatment of C-diff

1. Stool sample

2. empiric treatment

3. vancomycin

What should you do after C-diff infection antibiotics

restore flora through probiotics

(bio K+)

E-Coli classification, causes and S&S (3+)

1. Gram - bacterium

Causes

1. ingestion of E-coli

   1. undercooked meat

   2. contaminated veggies

   3. water

S&S → diarrhea, pain, fever

Complications with E-coli (3)

bacterial toxin-caused “hemolytic uremic syndrome”

• Toxin: Shiga-toxin destroys endothelial cells, platelets, TBC’s

• can cause renal disease → HUS

Treatment of E-coli infection (2)

Supportive

Rehydration → because of fluid loss through GI

Diarrhea symptoms and cause (3)

1. increased frequency and fluidity of loose or uniformed stool

2. caused by inflammation or infectious organisms

   1. e.g. Food intolerances, intestinal disease, pathogens, drugs

Acute vs chronic diarrhea

Acute < 2 weeks, sudden onset

Chronic >4 weeks, related to long-term disease or drug treatment