GI (Exam 3) Flashcards
Cleft lip
failure of the maxillary processes and nasal elevations or upper lip to fuse during development
MALES TWICE AS LIKELY
Cleft palate
failure of the hard and soft palate to fuse in development, creating an opening between the oral and nasal cavity
COMMON MULTIFACTORIAL CONGENITAL DEFECTS OF THE MOUTH AND FACE THAT ARE APPARENT AT BIRTH AND VARY IN SEVERITY; USUALLY DEVELOP AT 4-7 WEEKS GESTATION
What can cleft lip and cleft palate lead to?
feeding issues, speech problems, ear infections, hearing problems
Cleft palate demographics
associated with GENETIC MUTATIONS, DRUGS, TOXINS, VIRUSES, VITAMIN DEFICIENCIES, CIGARETTE SMOKING
most frequent in NATIVE AMERICANS, HISPANICS, AND ASIANS; AAs least likely
FEMALES TWICE AS LIKELY
Esophageal atresia
incomplete formation of the esophagus; fairly common congenital defect (Type C)
rarest and most severe is Type D
Possible causes of esophageal atresia?
EXACTLY CAUSE UNKNOWN
VACTERL (Vertebral anomalies, Anal atresia, Cardiac malformations, Tracheoesophageal fistula, Renal anomalies, Limb anomalies)
heart defects
mental/physical developmental delays
genital hypoplasia
ear abnormalities
Risk factors of esophageal atresia?
increased paternal age
maternal use of assisted reproduction
Manifestations/complications of esophageal atresia
excessive secretions
coughing
vomiting
cyanosis after feeding
C: aspiration pneumonia
Pyloric stenosis (infantile hypertrophic pyloric stenosis)
narrowing and obstruction of the pyloric sphincter
muscle fibers become thick and stiff, making it difficult for the stomach to empty food into small intestine
MAY BE PRESENT AT BIRTH/DEVELOP LATER, MOST CASES PRESENT AT 3 WEEKS OLD
Causes/demographics of pyloric stenosis
EXACTLY CAUSE UNKNOWN (MULTIFACTORIAL), MOST COMMON IN MALES AND WHITES
EXPOSURE TO MACROLIDES (ANTIBIOTICS) IN EARLY INFANCY THOUGHT TO INCREASE RISK
Manifestations of pyloric stenosis
hard mass in abdomen
regurgitation
projectile vomiting
wavelike stomach contractions
small and infrequent stools
failure to gain weight
dehydration
irritability
Esophageal abnormality Causes of dysphagia
congenital atresia
esophageal stenosis/stricture
esophageal diverticula
tumors
Neurological Causes of dysphagia
stroke
cerebral damage
parkinson’s
alzheimer’s
muscular dystrophy
huntingtons
cerebral palsy
MS
ALS
Guillan-Barre
Manifestations of dysphagia
sensation of food being stuck in throat
choking
coughing
pocketing food in cheeks
difficulty forming a food bolus
delayed swallowing
Hiatal hernia
a section of the stomach protrudes upward through opening in diaphragm
RISK FACTORS ARE ADVANCING AGE AND SMOKING
Causes of hiatal hernia
weakening of diaphragm muscle
increased intrathoracic pressure (coughing, vomiting, straining during BM)
increased intra-abdominal pressure (pregnancy, obesity)
trauma
congenital defects
Hiatal hernia manifestations
indigestion
heartburn
frequent belching
nausea
chest pain
strictures
dysphagia
soft upper abdominal mass (protruding stomach pouch)
WORSENS WITH RECUMBENT POSITIONING, EATING ESPECIALLY AFTER LARGE MEALS, BENDING OVER, AND COUGHING
Gastroesophageal Reflux Disease (GERD)
chyme or bile periodically backs up from the stomach into the esophagus, irritating the esophageal mucosa
often confused with angina and may warrant ruling out cardiac disease
Causes of GERD
certain foods (chocolate, caffeine, carbonated beverages, citrus, tomatoes, spicy or fatty foods, peppermint)
alcohol or nicotine
history of hiatal hernia
obesity
pregnancy
certain medications (corticosteroids, beta blockers, calcium-channel blockers, anticholinergics)
delayed gastric emptying
Manifestations of GERD
heartburn
epigastric pain (usually after meal or when recumbent)
dysphagia
dry cough
laryngitis
pharyngitis
regurgitation of food
sensation of lump in throat
Complications of GERD
esophagitis
strictures
ulcerations
esophageal cancer
chronic pulmonary disease
Gastritis
inflammation of the stomachs mucosal lining (may involve the entire stomach or region)
Acute gastritis
can be a mild transient irritation or it can be severe ulceration with hemorrhage
usually develops suddenly and likely to be accompanied by nausea and epigastric pain
Chronic gastritis
develops gradually; may be asymptomatic but usually accompanied by a dull epigastric pain and a sensation of fullness after minimal intake
can be further categorized as erosive or nonerosive
Helicobacter pylori
MOST COMMON CAUSE OF CHRONIC GASTRITIS
embeds itself in the mucous layer, activating toxins and enzymes that cause inflammation
genetic vulnerability and lifestyle behaviors like smoking or stress may increase susceptibility
Other causes of gastritis
food and water contamination
long term use of NSAIDs
excessive alcohol use
severe stress
autoimmune conditions
Gastritis manifestations
indigestion
heartburn
epigastric pain
abdominal cramping
nausea
vomiting
anorexia
fever
malaise
hematemesis and dark, tarry stools can indicate ulceration and bleeding
Complications of chronic gastritis
peptic ulcers
gastric cancer
hemorrhage
Gastroenteritis
inflammation of the stomach and intestines, usually because of an infection or allergic reaction
Peptic Ulcer Disease (PUD)
erosive lesions affecting stomach lining or duodenum; develops from an imbalance between destructive forces and protective mechanisms
vary in severity from superficial erosions to complete penetration
Risk factors for PUD
male
advancing age
NSAIDs
H. Pylori infections
certain gastric tumors
risk factors for GERD (smoking, alcohol, etc.)
Duodenal ulcers (PUD)
MOST COMMON (associated with excessive acid or H.Pylori)
typically present with epigastric pain that is relieved in the presence of food
Gastric ulcers (PUD)
LESS FREQUENT BUT DEADLIER (associated with malignancy and NSAIDs)
pain typically worsens with eating
Stress ulcers (PUD)
develop because of a major physiological stressor on the body due to local tissue ischemia, tissue acidosis, bile salts entering the stomach and decreased GI motility
curlings and cushing’s ulcers
Curlings ulcers
stress ulcers associated with burns
Cushing’s ulcers
stress ulcers associated with head injuries
Stress ulcers complications
GI hemorrhage
obstruction
perforation
peritonitis
Stress ulcers manifestations
epigastric or abdominal pain
abdominal cramping
heartburn
indigestion
nausea
vomiting
Cholelithiasis (gallstones)
common condition that varies in severity based on size of stone but affects both genders and all ethnic groups equally
may instruct bile flow and cause gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma
cholecystitis
Cholecystitis
inflammation or infection in the biliary system caused by calculi
Risk factors for cholelithiasis
advancing age
obesity
diet
rapid weight loss
pregnancy
hormone replacement
long-term parenteral nutrition
Manifestations of cholelithiasis
biliary colic
abdominal distention
nausea
vomiting
jaundice
fever
leukocytosis
Hepatitis
inflammation of the liver
can be acute, chronic or fulminant; active or nonactive
can result in hepatic cell destruction, necrosis, autolysis, hyperplasia, scarring
Hepatitis causes
infections (usually viral)
alcohol
medications (acetaminophen, antiseizure agents, antibiotics)
autoimmune disease
Nonviral hepatitis
noncontagious and most will recover (toxicity related to meds)
may develop liver failure, liver cancer or cirrhosis
Viral hepatitis
contagious but most will recover with sufficient time
advancing age and comorbidity increase the likelihood that liver failure, liver cancer or cirrhosis will develop
Hepatitis A (HAV)
spread through food, drink, and close contact with infected person
Hepatitis B (HBV)
spread from mother to baby, sexual transmission, sharing needles and contact with the blood of an infected person
Hepatitis C (HCV)
spreads through childbirth, sharing needles, tattoos in unregulated shops
Hepatitis D (HDV)
can only be contracted if you have HBV
Hepatitis E (HEV)
transmitted via food or water
Acute hepatitis
four phases; asymptomatic incubation phase, 3 symptomatic phases
Chronic hepatitis
continued hepatic disease lasting longer than 6 months
symptom severity and diseases progression vary depending on degree of liver damage; can quickly deteriorate with declining liver integrity
Cirrhosis
chronic, progressive, irreversible, diffuse damage to the liver resulting in decreased liver function; may develop after 40 yrs even if underlying cause is addressed
leads to fibrosis, nodule formation, impaired blood flow, bile obstruction that can result in liver failure
Cirrhosis causes
HCV
chronic alcohol abuse
Cirrhosis manifestations
portal hypertension
ascites
jaundice
varicosities
enlarged organs
slow/severe bleeding
clotting changes
muscle wasting
hyperlipidemia
hyper/hypoglycemia
toxin and bile accumulation
clay-colored stools and dark urine
intense itchiness
altered hormone regulation (decreased estrogen absorption)
esophageal varices
Pancreatitis causes
cholelithiasis
alcohol abuse
biliary dysfunction
hepatotoxic drugs
metabolic disorders
trauma
renal failure
endocrine disorders
pancreatic tumors
penetrating peptic ulcer
Pancreatitis
pancreatic injury causes enzymes to leak into pancreatic tissue and initiates autodigestion, resulting in edema, vascular damage, hemorrhage, and necrosis
pancreatic tissue is replaced by fibrosis which causes exocrine and endocrine changes and dysfunction of the islets of Langerhans
Acute pancreatitis
medical emergency; mortality increases with advancing age and comorbidity
Complications of acute pancreatitis
acute respiratory distress syndrome
diabetes mellitus
infection
shock
disseminated intravascular coagulation
renal failure
malnutrition
pancreatic cancer
pseudocyst
abscess
Acute pancreatitis manifestations
usually sudden and severe
upper abdominal pain that radiates to the back, worsens after eating and is somewhat relieved by leaning forward of pulling knees to chest
nausea and vomiting
mild jaundice
low grade fever
BP and pulse changes
Chronic pancreatitis manifestations
insidious
upper abdominal pain
indigestion
losing weight w/o trying
steatorrhea
constipation
flatulence
Intestinal obstruction
sudden or gradual and partial or complete blockage of intestinal contents in intestines; mechanical and functional obstructions
chyme and gas accumulate at site of blockage; saliva, gastric juices, bile, and pancreatic secretions begin to collect as blockage lingers and can cause abdominal distention and pain
Mechanical obstructions (intestinal)
foreign bodies
tumors
adhesions
hernias
intussusception
volvulus
strictures
IBS
fecal impaction
Functional obstructions (paralytic ileus) (intestinal)
neurologic impairment
intra-abdominal surgery complications
chemical, electrolyte, and mineral disturbances
infections
blood supply impairment (strangulation, necrosis, contents seep into abdomen)
meds (narcotics)
Intestinal obstruction complications
perforation
pH imbalance
fluid disturbances
shock
death
Manifestations of intestinal obstruction
abdominal distention
abdominal cramping and colicky pain
nausea and vomiting
constipation or diarrhea
intestinal rushes
decreased/absent bowel sounds
restlessness
diaphoresis
tachycardia progressing to weakness
confusion and shock
Appendicitis
inflammation of the vermiform appendix, most often caused by infection
Appendicitis pathogenesis
- inflammation triggers local tissue edema, which obstructs small structure
- as fluid builds up inside appendix, microorganisms proliferate
- appendix fills with purulent exudate and area blood vessels become compressed
- ischemia and necrosis develop; bacteria and toxins leak out to surrounding structures
Complications of appendicitis
abscesses
peritonitis
gangrene
sepsis
death
Appendicitis manifestations
vary from asymptomatic to sudden and severe
nausea, vomiting, abdominal distention, bowel pattern changes
indications of inflammation and infection (fever, chills, leukocytosis)
indications of peritonitis (abdominal rigidity, tachycardia, hypotension)
sharp abdominal pain develops, gradually intensifies (over 12-24 hrs) and becomes localized to LRQ of abdomen (McBurney point)
pain may occur anywhere in abdomen and will temporarily subside when appendix ruptures then return and escalate
Peritonitis
inflammation of the peritoneum that activates several protective mechanisms
Peritonitis: Protective mechanisms
- thick, sticky exudate that bonds nearby structures and temporarily seals them off
- abscesses may form to wall off infections
- peristalsis may slow down in response to inflammation, decreasing spread of toxins
Causes of peritonitis
chemical irritation (ruptured gallbladder or spleen)
direct organism invasion (appendicitis, peritoneal dialysis)
Peritonitis manifestations
usually sudden and severe
ABDOMINAL RIGIDITY
abdominal tenderness and pain
decreased peristalsis
intestinal obstruction
nausea and vomiting
large volumes of fluid leak into peritoneal cavity
indicators of infection, sepsis or shock
Celiac disease
celiac sprue or gluten sensitivity enteropathy; inherited, autoimmune, malabsorption disorder
most common in whites and women, a childhood disease but can develop any time
Celiac disease causes
- combination of immune response to an environment factor (gliadin) and genetic predisposition
- defect in intestinal enzymes that prevents further digestion of gliadin (a product of gluten digestion)
intestinal villi with atrophy and flatten, causing decreased enzyme production, decreasing surface area available for nutrient absorption
Celiac disease manifestations
in infants, generally appear as cereals are added to diet (4-6 months)
abdominal pain/distention
bloating
gas
indigestion
constipation
diarrhea
lactose intolerance
nausea
steatorrhea
weight loss
irritability
lethargy
malaise
behavioral changes
Complications of celiac disease
anemia
arthralgia
myalgia
bone disease
dental enamel defects and discoloration
intestinal cancers
depression
growth and development delays in kids
hair loss
hypoglycemia
mouth ulcers
increased bleeding tendencies
neurologic disorders
skin disorders
vitamin/mineral deficiency
endocrine disorders
Inflammatory Bowel Disease (IBD)
chronic inflammation of the GI tract, usually intestines; exacerbations and remissions and can be painful, debilitating, and life-threatening
women, whites, jewish people, and smokers
thought to be caused by genetically associated autoimmune state that has been activated by infection
immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the function and neural activity of the secretory and smooth muscle cells
FLUID, ELECTROLYTE, pH IMBALANCES DEVELOP
Crohn’s disease (IBD)
insidious, slow developing, progressive condition often develops in adolescence
patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations (skip lesions); wall is thick/rigid and lumen is narrowed
Crohn’s disease pathogenesis
- form fissures developed by nodules, giving the intestinal wall a cobblestone appearance
- granulomas develop on intestinal wall and nearby lymph nodes
- damaged intestinal wall loses ability to digest and absorb
- inflammation also stimulates intestinal motility, decreasing digestion and absorption
Crohn’s disease manifestations
abdominal cramping and pain (RLQ)
diarrhea
steatorrhea
constipation
palpable abdominal mass
melena
anorexia
weight loss
indications of inflammation (fever, fatigue, arthralgia, malaise)
Complications of crohn’s disease
malnutrition
anemia (iron deficiency)
fistulas
adhesions
abscesses
intestinal obstruction
perforation
anal fissure
delayed growth and development
fluid, electrolyte, pH imbalances
Ulcerative colitis (IBD)
progressive condition of the rectum and colon mucosa, usually developing in 20s-30s
ulcers merge = inadequate surface area for absorption
Ulcerative colitis pathogenesis
- inflammation triggered by T cell accumulation in colon mucosa which causes epithelium loss, surface erosion, and ulceration that begins in rectum and extends to entire colon
- mucosa becomes inflamed, edematous, and frail
- necrosis of the epithelial tissue can result in abscesses; granulation tissue formed is fragile
Ulcerative colitis manifestations
diarrhea (frequent, as many as 20x daily)
watery stools (with blood and mucus)
proctitis
abdominal cramping
nausea and vomiting
weight loss
indications of inflammation (fever, fatigue, arthralgia, malaise)
Ulcerative colitis complications
malnutrition
anemia
hemorrhage
perforation
strictures
fistulas
toxic megacolon
colorectal carcinoma
liver disease
fluid, electrolyte, and pH imbalances
Irritable bowel syndrome (IBS)
chronic, noninflammatory GI condition with exacerbations associated with stress
includes alterations in bowel pattern and abdominal pain not explained by structural or biochemical abnormalities
less serious than IBD and doesn’t cause permanent intestinal damage; MORE COMMON IN WOMEN
3 theories of IBS etiology
- altered GI motility
- visceral hyperalgesia (increased sensitivity to pain)
- psychopathology
intensified response to stimuli with increased intestinal motility and contractions means low tolerance for stretching and pain in intestinal smooth muscle
Complications of IBS
hemorrhoids
nutritional deficits
social issues
sexual discomfort
Manifestations of IBS
stress, mood disorders, food, and hormone changes often worsen symptoms
abdominal distention, fullness, flatus, and bloating
intermittent abdominal pain exacerbated by eating and relieved with shitting
chronic and frequent constipation or diarrhea usually with pain
non bloody stool that may contain mucus
bowel urgency
intolerance to certain foods (gas-forming; sorbitol, lactose, gluten)
emotional distress
anorexia
Diverticular Disease
conditions related to the development of diverticula, outwardly bulging pouches of intestinal wall that occur when mucosa secretions or large intestine submucosa layers herniate through a weakened muscular layer; may be congenital or acquired
Diverticular disease causes
low-fiber diet and poor bowel habits resulting in chronic constipation (muscular wall can become weakened from the prolonged effect of moving hard stools)
more common in developed countries with shitty diets
Diverticulosis
asymptomatic diverticular disease, multiple diverticula present
Diverticulitis
diverticula become inflamed, usually because of retained fecal matter (often asymptomatic until it becomes serious)
potential for fatal obstruction, infection, abscess, perforation, peritonitis, hemorrhage, shock
Diverticular disease manifestations
abdominal cramping
passing frank blood
low-grade fever
abdominal tenderness (LLQ)
abdominal distention/mass
constipation
obstipation
nausea
leukocytosis
Oral Cancer
most cases involve squamous cell carcinomas of the tongue and mouth floor; very treatable if caught early but most cases are advanced upon diagnosis
usually appears as one or more painless, whitish thickenings that develop into a nodule or an ulcerative lesion that persists, doesn’t heal and bleeds easily
a lump, thickening or soreness in the mouth, throat, or tongue as well as difficulty chewing or swallowing
Risk factors of oral cancer
smoked and smokeless tobacco
alcohol consumption
viral infections (HPV)
immunodeficiency
inadequate nutrition
poor dental hygiene
chronic irritation
exposure to UV light
often metastasizes to neck lymph nodes and esophagus
Esophageal cancer
usually squamous cell carcinoma in distal esophagus; most common in men and associated with chronic irritation
tumors grow the circumference of the esophagus, creating a stricture, or they can grow out into the lumen of the esophagus creating an obstruction
Complications of esophageal cancer
esophageal obstruction
respiratory compromise
esophageal bleeding
Manifestations of esophageal cancer
usually asymptomatic early, delaying treatment
dysphagia
chest pain
weight loss
hematemesis (vomiting blood)
Gastric cancer
occurs in several forms but adenocarcinoma (an ulcerative lesion) is most frequent
incidence and mortality rates declined in US but very prevalent in Japan
Risk factors of gastric cancer
STRONGLY ASSOCIATED WITH INTAKE OF SALTED, CURED, PICKLED, PRESERVED, AND SMOKED FOOD
low fiber diet
constipation
family history
H.Pylori infections
smoking
pernicious anemia
chronic atrophic gastritis
gastric polyps
Manifestations of gastric cancer
asymptomatic early stages delay diagnosis and treatment
abdominal pain/fullness
epigastric discomfort
palpable abdominal mass
melena
dysphagia that worsens over time
excessive belching
anorexia
nausea
vomiting
hematemesis
premature abdominal fullness after meals
unintentional weight loss
weakness
fatigue
Liver Cancer
most commonly occurs as a second tumor that has metastasized from breast, lung or other GI structures; rates in US have tripled since 1980
causes of primary tumors are chronic cirrhosis and hepatitis
Liver cancer manifestations
anorexia
fever
jaundice
nausea
vomiting
abdominal pain (RUQ)
hepatomegaly
splenomegaly
portal hypertension
edema
third spacing
ascites
paraneoplastic syndrome
diaphoresis
weight loss
Pancreatic cancer
aggressive malignancy that quickly metastasizes, usually adenocarcinoma
most frequent in men and AA’s
Pancreatic cancer risk factors
family history
obesity
chronic pancreatitis
long-standing diabetes mellitus
cirrhosis
alcohol abuse
tobacco use
Pancreatic cancer manifestations
often asymptomatic until well advanced
progressive upper abdomen pain that may radiate to back
jaundice
dark urine
clay-colored stools
indigestion
anorexia
weight loss
depression
malnutrition
hyperglycemia
increased clotting tendencies
Colorectal cancer
very common and fatal
associated with fatty, caloric, low fiber diets with red meat, processed meal, and alcohol
Risk factors for colorectal cancer
male
AA
family history
advancing age
obesity
tobacco use
physical inactivity
IBD
Colorectal cancer manifestations
asymptomatic until advanced
lower abdominal pain and tenderness
blood in stool (occult or frank)
diarrhea
constipation
intestinal obstruction
narrow stools
unexplained anemia (usually iron deficiency)
unintentionally weight loss
