slide1
Download
Skip this Video
Download Presentation
Disorders of Nutrition

Loading in 2 Seconds...

play fullscreen
1 / 69

Gastrointestinal - PowerPoint PPT Presentation


  • 381 Views
  • Uploaded on

Gastrointestinal Disorders . Disorders of Nutrition. Alterations in: Ingesting Digesting Absorbing Eliminating. Anorexia Pica

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Gastrointestinal ' - Gideon


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
disorders of nutrition
Disorders of Nutrition

Alterations in: Ingesting Digesting Absorbing Eliminating

ingestion
Anorexia

Pica

Nausea & Nausea

Esophageal Atresia

Tracheoesopheal fistula

Cleft lip/palate

Anorexia Nervosa

Pyloric Stenosis

Projectile Vomiting

Ingestion
maldigestion
Maldigestion
  • Lactic Deficiency
  • Pancreatitis
  • Cystic Fibrosis
malabsorption
Malabsorption
  • Intestinal Parasites
  • Gastrectomy Loss of Stomach as Reservoir for Food Dumping Syndrome Loss of Intrinsic Factor
  • Celiac Disease (Sprue)
  • Cholecystitis/Cholelithiasis
  • Regional Enteritis (Crohn’s Disease)
elimination
Elimination
  • Diarrhea Osmotic Changes Secretory Changes Mucosal Damage Altered Motility
  • Crohn’s Disease
  • Ulcerative Colitis
basic structure of the gi tract
Basic Structure of the GI tract

PSNS

SNS

longitudinal

muscle

Myenteric

plexus

Circular muscle

Submucosal

plexus

Submucosa

Lumen

enteric nervous system influenced by ans
Enteric Nervous System Influenced by ANS

PSNS

SNS

Pelvic

nerves

NE

Ach

ENTERIC NERVOUS SYSTEM

Myenteric Submucosal

Smooth

muscle

Secretory

Cells

Endocrine

Cells

Blood

Vessels

gastric motility
Gastric Motility

LES

fundus

pylorus

receptive

relaxation

Antrum

approx 3 contractions

per minute

control of gastric emptying
Control of Gastric Emptying

PSNS

SNS

+

-

GASTRIC EMPTYING

-

-

secretin

-

CCK

Duodenal

acid

Duodenal

fats

Duodenal

hypertonicity

small and large bowel motility
Small and Large Bowel Motility
  • Small Intestine
    • 2-4 hours to traverse
    • Segmental contractions to mix
    • Peristaltic waves to move forward
  • Large Intestine
    • Slow progression at 5-10 cm per hour
    • Segmental contractions produce haustra
    • 1-3 mass movements per day
secretion in the stomach
Secretion in the Stomach
  • Parietal Cells
    • HCL
    • Intrinsic Factor
  • Chief Cells
    • Pepsinogen
  • Surface epithelia and mucous cells
    • HCO3- and mucus
control of acid secretion
Control of Acid Secretion

VagusMast CellsG cells

Ach Histamine Gastrin

muscarinic

receptor

H2 receptor

gastrin

receptor

Gastric Parietal Cell

Acid Secretion

secretion in the small intestine
Secretion in the Small Intestine
  • Secretions from Pancreas
    • HCO3-, Proteases, Lipases, Amylases
  • Secretion from Gallbladder
    • Bile acids, pigment, phospholipid
  • Secretions from intestinal epithelia
    • Brush border enzymes
brush border enzymes
Brush Border Enzymes

Lactase: lactose glucose, galactose

Sucrase: sucrose fructose, glucose

Dextrinase: cleaves amylose branch points

Glucoamylase: maltose glucoses

Only Monosaccharides are Absorbed

digestion and absorption of proteins
Digestion and Absorption of Proteins
  • Pepsin: 15% of peptide bonds broken
  • Pancreatic proteases
    • Trypsin
    • Chymotrypsin
    • Carboxypeptidases
  • Brush Border
    • Peptidases cleave into 1 to 4 aa chains
digestion and absorption of fat
Digestion and Absorption of Fat
  • Bile salts are amphipathic molecules that break up large fat globs into droplet
  • Lipase are water soluble - only work at surface of droplet
    • Triglycerides --------> FFA and glycerol
  • Bile forms micelles with FFA to keep soluble.
  • FFA are lipid soluble so absorb directly
reabsorption of bile
Reabsorption of Bile
  • Bile is reabsorbed at terminal ileum
  • Passive diffusion and active transport
  • Transported to liver via portal blood
  • ALL reabsorbed bile is taken up on first pass by liver
  • Entire bile pool circulates 2 to 5 times per meal. 5-10% lost per day in stool
dysphagia
Dysphagia
  • Neuromuscular: pharynx
  • Stricture or tumor: Progressive solid food dysphagia
  • Achalasia: esophageal motility disorder, loss of peristalsis in lower 2/3 plus impaired LES relaxation
  • Mallory-Weiss syndrome: mucosal tears at distal esophagus, bleeding, pain
oropharyngeal vs esophageal
Nasal regurgitation

Airway obstruction with eating

Coughing when swallowing

Immediate regurgitation

Hoarse voice

No airway distress

Late regurgitation

Chest pain @ meals

Frequent heartburn

Presence of collagen disease

Presence of Left supraclavicular node

Oropharyngeal vs Esophageal
dyspepsia
Dyspepsia
  • Present with heartburn, indigestion, epigastric distress
  • Up to 2/3 will have no identifiable cause
  • One-half will have relief from placebo
  • Symptom profile does not differentiate between GERD, PUD, and non-ulcer dyspepsia (functional)
  • Physical exam is rarely helpful
diagnosis
Diagnosis
  • NSAID: suspect PUD and treat
  • Helicobacter pylori: urea breath test or biopsy during endoscopy
  • GERD: Trial of H2 therapy
  • Functional: may improve with agents that increase motility
  • Zollinger-Ellison syndrome: gastrin level
pud with h pylori
PUD with H. pylori
  • H. pylori is nearly always a factor in non-NSAID peptic ulcer disease
  • Conventional therapy with H2 blockers or H+ pump inhibitors has a 75-80% one-year recurrence rate
  • Treatment for H. pylori reduced recurrence rate to less than 5%
acute infectious diarrhea
Acute Infectious Diarrhea

High fever?

Bloody diarrhea?

NO

YES

Noninflammatory

Inflammatory

watery

large volume

periumbilical

pain

small volume

LLQ pain

+ fecal leukocytes

Shigella, Salmonella,

C. difficile, E. coli (bad)

Campylobacter, HIV-

associated

Viral: rotavirus, Norwalk

S. aureus food poisoning

Giardia

Rehydrate, symptomatic

Culture and treat

chronic diarrhea stool studies
Chronic Diarrhea: Stool Studies
  • Stool Osmolality: normal gap < 50
  • Laxative screen: Mg, PO4, SO4
  • Fecal leukocytes: Inflammatory disease
  • Ova and parasites: Giardia, cryptosporidium
  • Fecal Fat analysis: > 10 g/24 hrs indicates malabsorption
  • Fecal weight: > 1000 g is secretory
osmotic diarrhea lactase def
Osmotic Diarrhea: Lactase Def.
  • Incidence
    • 90% of Asian Americans
    • 95% of Native Americans
    • 50% of Mexican Americans
    • 60% of Jewish Americans
    • 25% of other Caucasians
  • DX: empiric trial of lactose-free diet for two weeks
inflammatory bowel disease
Inflammatory Bowel Disease
  • Ulcerative Colitis
    • Involves only the colon and rectum
    • Mucosal layer is affected
    • Hallmark is bloody diarrhea and lower abdominal cramps
    • Associated with increased cancer risk after 8-10 years of disease
assess uc disease severity
Assess UC Disease Severity
  • Number of stools per day
  • Hematocrit
  • Sed rate
  • Albumin level
crohn disease
Crohn Disease
  • Intermittent bouts of fever, diarrhea, and RLQ pain
  • May have RLQ mass, tenderness
  • Can affect any portion of GI tract
    • 30% are small bowel only
    • 50% are small and large bowel
    • 15-20% are large bowel only
crohn disease31
Crohn Disease
  • Transmural process in the intestinal wall predisposes to fistula formation
  • If suspected, obtain upper GI series with small bowel follow through plus either colonoscopy or barium enema
  • Suggestive findings are ulcerations, strictures, and fistulas
  • RX: stop smoking, drugs similar to UC
compare and contrast cd uc
Crohn’s Disease “Skip” Lesions (granulomatous) Terminal ileum Diarrhea/Constipation Alternates – Less Bloody Malignant Potential(not totally determined)

Proned to Develop Abcesses & Fistula formation

Ulcerative ColitisContinuous ulcerationof mucosa of colonColon, rectum – distalWatery diarrhea – has mucus/pus – may be bloody – commonProned to develop colon carcinomarare abcess/fistula formation

Compare and Contrast – CD & UC
motility diarrhea ibs
Motility Diarrhea: IBS
  • Irritable bowel syndrome is a chronic (>3months) functional disorder with no identifiable pathology
  • Fluctuations in stool frequency and consistency (no nocturnal diarrhea)
  • Perceived abd distention, bloating, pain
  • Often associated with anxiety or depression
slide34
IBS
  • It is not IBS if fever, bloody stools, nocturnal diarrhea, or weight loss are present
  • Consider checking CBC, sed rate, albumin, and stool for occult blood to rule out inflammatory disease, consider lactose-free trial.
  • RX: restrict caffeine, gas producing food, high fiber. Rx depression
occult gi bleeding
Occult GI Bleeding
  • Detected by FOBT: worry colorectal CA
  • Indicated for iron deficiency anemia in males or postmenopausal females
  • Unless S&S suggest Upper GI etiology (heartburn, dyspepsia PUD) start with colonoscopy (or barium enema)
  • If no source, follow with endoscopy
acute abdominal pain
Acute Abdominal Pain
  • Tension: spasm, associated with intense peristalsis (irritant, infection, obstruction)
  • Ischemia: intense constant pain (bowel strangulation, volvulus adhesion)
  • Inflammation: first localized to serosa covering inflamed part then extends to abdominal wall causing reflex muscle spasms (rigidity, involuntary guarding)
assessment of the pain
Assessment of the Pain
  • Is it nongastric? consider aortic aneurysm, ectopic pregnancy, PID, kidney
  • Is it an acute surgical abdomen?
    • Involuntary guarding, rigidity
    • Absent bowel sounds
    • Is there shock
localization of abdominal pain
Localization of Abdominal Pain
  • Stomach, duodenum: mid epigastric
  • Small bowel: periumbilical
  • Colon: low abdomen, midline
  • Rectum: sacrum and perineum
  • Gallbladder: mid epigastric radiates to RUQ or right scapula
  • Pancreas: mid epigastric radiate to back
  • Appendix: RLQ, but variable
bowel obstruction
Bowel Obstruction
  • Presentation
    • Pain, distention, vomiting, obstipation
  • Evaluation
    • Flat and upright abdominal film
  • Small bowel: less urgent
    • intestinal tube, decompression
  • Large bowel: urgent, danger of cecal perf
    • immediate surgical consult
types of bowel obstruction
Mechanical Obstruction * Adhesions * Tumors * Impaction * Strangulated Hernia * Volvulus “Twisting” * Intussusception (telescoping)

Functional Obstruction * Bowel Manipulation (surgery) * Narcotic Anesthesia * Peritonitis

Types of Bowel Obstruction
itis from top to bottom
“Itis” from TOP to BOTTOM

“itis” Etiology Clinical Findings

esophagitis reflux (GERD) - pain after meals

- “heartburn”

gastritis -PUD ASA, ETOH - epigastric pain

H. pylori

regional enteritis ? Etiology - diarrhea with

(Crohn) blood and mucus

ulcerative colitis ? Etiology - bloody diarrhea

itis from top to bottom42
“Itis” from TOP to BOTTOM

“itis” Etiology Clinical Findings

diverticulitis low fiber diet low abdominal

pain, fever

appendicitis obstruction - RLQ pain, fever

“fecalith” - rebound pain

peritonitis perforation - severe pain, ileus

bowel ischemia - guarding, rigid

pancreatitis biliary disease - pain to back, shock

ETOH - high lipase, amylase

itis from top to bottom43
“Itis” from TOP to BOTTOM

“itis” Etiology Clinical Findings

cholecystitis cholelithiasis - RUQ pain

- steatorrhea

hepatitis viral, acute ETOH - jaundice, big liver

- high AST, ALT

- flu-like symptoms

appendicitis
Appendicitis
  • Etiology:
    • Obstruction by fecalith, inflammation
  • Presentation:
    • RLQ pain (classic, but may be anywhere), N&V, fever, diarrhea, RLQ tenderness
  • Evaluation: CBC, abdominal ultrasound
  • RX: immediate surgical consult
diverticulitis
Diverticulitis
  • Etiology:
    • Microperforation with peridiverticular inflammation
  • Presentation:
    • Elderly with LLQ pain, severe constipation, nausea, fever
  • Evaluation:
    • CBC, abd film, CT if peritoneal signs
  • Rx: NPO, antibiotics, IV fluids
acute pancreatitis
Acute Pancreatitis
  • Etiology: unknown
    • Associated with ETOH, biliary disease
  • Presentation:
    • Severe epigastric and back pain
  • Evaluation:
    • CBC, glucose, calcium, electrolytes, amylase, lipase (renal studies)
    • Severity index
severity scale pancreatitis
During first 48 hours

HCT drop of >10%

BUN rise >5 mg/dl

PaO2 < 60

Calcium < 8 mg/dl

Fluid sequestration of > 6 liters

Severity Scale: Pancreatitis

Initially

  • Age over 55
  • WBC > 16,000
  • Blood glucose > 200
  • Base deficit > 4
  • Serum LDH >350
  • AST > 250
pancreatitis severity
Pancreatitis Severity

Number of criteria

Mortality Rate

0-2

3-4

5-6

7-8

1%

16%

40%

100%

cholecystitis
Cholecystitis
  • Etiology:
    • 95% associated with stone in cystic duct
  • Presentation:
    • Often obese female, fever, RUQ pain with scapular or epigastric pain, colicky, N&V
  • Evaluation:
    • CBC, RUQ ultrasound, HIDA scan
  • RX: Prompt cholecystectomy
steatorrhea
Steatorrhea
  • Pancreatic steatorrhea:
    • > 90% of exocrine function lost
  • Bile salt deficiency:
    • decreased ileal reabsorption (Crohn)
    • blocked secretion (cholestasis)
  • Bacterial overgrowth syndromes:
    • stasis of small bowel contents
  • Mucosal defects: Celiac disease (sprue)
jaundice
Jaundice
  • Jaundice occurs with bilirubin level > 3 mg/dl (normal 0.2-1.2)
  • Increased RBC breakdown
  • Impaired liver uptake of bilirubin
  • Impaired excretion of bilirubin
functions of the liver
Functions of the Liver
  • Nutrient metabolism (glucose, protein, fat, fat soluble vitamins)
  • Production of serum proteins and enzymes (albumin, clotting factors etc.)
  • Detoxification of hormones, drugs
  • Bile synthesis (conjugation of bilirubin)
  • Urea synthesis
manifestations of liver dysfunction
Manifestations of Liver Dysfunction
  • Impaired protein synthesis
    • bleeding (clotting factor deficiency)
    • edema (hypoproteinemia)
    • immune deficiency (substrate for antibody)
  • Accumulation of toxins and hormones
    • feminization (excess estrogens)
    • poor metabolism of drugs
    • spider nevi (estrogen)
manifestations of liver dysfunction56
Manifestations of Liver Dysfunction
  • Inadequate bile synthesis
    • increased bilirubin level
    • jaundice
  • Inadequate urea synthesis
    • increased blood ammonia level (NH3)
    • hepatic encephalopathy
  • Release of marker enzymes into blood
    • AST (SGOT)
    • ALT (SGPT)
high direct bilirubin
High Direct Bilirubin
  • Hepatocellular injury:
    • hepatitis
    • drugs
    • hemochromatosis
    • Alpha-1 antitrypsin deficiency
  • Cholestasis:
    • stones, tumors, strictures
    • cholangitis
acute hepatitis
Acute Hepatitis
  • Etiology: acute liver inflammation and cellular injury: viral, toxic
  • Presentation: jaundice, anorexia, fatigue, diffuse abd discomfort, dark urine
  • Evaluation: History of viral or toxin exposure, AST, ALT, Alk phos, bilirubin, serology for viral hepatitis
viral hepatitis
Viral Hepatitis

Type A B+(D)C E

Transmission oral-fecal blood and blood and oral-fecal

body fluids body fluids

Risk contaminated sexual, IV sexual, IV waterborne

food

Prognosis good more severe 85% chronic ?

5% carrier

B+D more

severe

acute toxic hepatitis
Acute Toxic Hepatitis
  • Etiology: exposure to hepatotoxin or its metabolite
  • Evaluation: No definitive tests:
    • history of exposure is important
    • negative viral serology screen
    • improvement after discontinuing drug
    • if alcohol is the toxin, AST > ALT, 2:1
chronic alcoholic liver disease
Chronic Alcoholic Liver Disease
  • Etiology: chronic, heavy ETOH exposure
    • Only 15-20% of alcoholics develop liver disease
    • Men > 4-6 drinks/day, Women > 3-4/day
  • Pathogenesis: unknown
  • Presentation:
    • fatty liver
    • hepatitis
    • cirrhosis
cirrhosis of the liver
Cirrhosis of the Liver
  • Fibrotic liver
    • loss of hepatocellular functions
    • obstruction to bloodflow from the gut
  • Etiology
    • Chronic alcohol use (most common)
    • Biliary (obstruction in bile drainage)
    • Postnecrotic (viral, toxic hepatitis)
    • Cardiac (right heart failure, liver congestion)
liver cirrhosis
Liver Cirrhosis

cell failure

From GI

tract

jaundice

bleeding

low albumin

-edema

immune deficient

estrogen excess

encephalopathy

Portal vein

To vena

cava

portal hypertension

ascites

esophageal varices

hemorrhoids

anorexia

Hepatic vein

treatment monitoring
Treatment & Monitoring
  • Abstinence from alcohol
  • Restore nutrition: (high protein diet unless hepatic encephalopathy)
  • Monitor PT, AST, ALT, albumin, bilirubin
  • Vitamin K
  • Abnormal PT despite vitamin K indicates a severely compromised liver
treatment monitoring65
Treatment & Monitoring
  • Ascites:
    • caput medusae: flow outward from navel
    • sodium restriction
    • spironolactone
    • monitor for spontaneous bacterial peritonitis
    • If ascites is present, high likelihood of esophageal varices
treatment monitoring66
Treatment & Monitoring
  • Hepatic Encephalopathy
    • Altered mental status due to accumulation of toxins, including ammonia (NH3)
    • Precipitated by GI bleed, drugs, increased shunting of blood around liver
    • Monitor NH3 level
    • lactulose
    • withhold protein
liver cancer
Liver Cancer
  • May and usually does have similar clinical manifestations to cirrhosis. Liver cancer is almost always metastatic. The survival rate s less than 5%.
ad