exam 2- gastro Flashcards
digestion
the process that takes substances in one form and breaks them down into molecules small enough to pass through the intestinal wall into the blood
mouth
beginning point with ingestion of food. major functions: chewing, saliva secretion
what is salivary amylase
ptyalin starts carbo breakdown in the saliva
how much saliva is made in a day
leter to a leter and a half
pharynz
food is swallowed and moved into esophagus at this time the trachea is closed off
esophagus
muscular tube that lies behind the trachea, initiates peristalsis
pyloric sphincter
allows stomach to empty and prevents blackflow into stomach from the small intestine
small intestine
includes the
duodemun, jejunum, ilieum
major function:
absorption of nutrients 90%
large intestine
includes:
ascending, transverse, descending and sigmoid colin
major function:
absorption of water and electrolytes and formation of wastes
rectum and anal canal
function is excretion of waste
cleft lip/palate
genetic structural disorder 1/600-1/5000 births
what causes a cleft lip/palate
decrease in mesenchyme (forms connective tussue migrating to area)
incomplete fusion of the nasomedial or intermaxillary process
cleft lip
incomplete fusion of uvula, soft palate or hard palate
fleft palate
cleft lip and cleft palate can occur separately or together and can be minor to severe
yep.
esophageal atresia
cells of embryonic foregut fail to develop. .. leads to a puch at the end of eh esophagus and no connection to the stomach (1-3000/4500 births)
who is at risk for esophageal atresia
premi and low birthwate babies
tracheo-esopheageal fistula
the foregut fails to seperate into a totally seperate esophagus and trachea resulting in a patent fistula (open connection)between the two structures
what are the manifestations for both esophageal atresia at TEF
unable to handle oral secretions
coughing/choking/spitting up
aspiration into lungs
abdominal distention with air swallowed
pyloric stenosis
genetically influenced abnormal narrowing of pyloric sphincter
1-200/1000 males more
what is the patho of pyloric stenosis
sphincter muscle hypertrophies during development which narrow opening– delayed stomach emptying
what is the manifestation of pyloric stenosis
vomiting (primary)
constipation
how is pyloric stenosis diagnosed
ultrasound
where is the vommiting center located
the medulla of brain
what is the first pathway for vomiting
cortical stimulation: direct
all senses exposure to noxious stimuli or emotional stress
what is the second pathway for vomiting
chemoreceptor trigger zone: direct
located in the brain
responds to impulses of motion (inner ear) and chemicals (drugs)
what is the third pathway for vomiting
Visceral receptors (sympathetic afferents) receptors in many organs and are irritated with inflammation, menstruation, obstruction or spasms
what is the fourth pathway for vomiting
receptors of stomach itself
receptors respond to distention, gas, inflammation, irritation, ischemia and stimulate vomiting center through the vagus nerve
what are the four component of actual vomiting
esophageal sphincter opens
pyloric sphincter closes
glottis closes off airway
diaphragm, intercostal muscles and abd muscles contract
what are the clinical manifstations of vomiting
nausea/vomiting sympathetic stim and para (perspiration, salvation, pallor, decreaded Bp and HR) presence of underlying cause dehydration electrolyte imbalance
what two types of cells are found in the crypts of lieberkuhn
cells that secrete intestinal juices
absorptive cells
malabsorption
impared absorption of fats, carbos, proteins, vitamins, minerals, water into bloodstream
ulcerative colitis
chronic inflammatory disease that causes ulceration of the colonic mucosa ulually in the rectum and sigmoid colin (20-40 yoa)
what are the etiologies of UC
genetic infectious immunologic psychosomatic dietary
where does UC usually start
in rectum and extend into sigmoid colon
inflammatory process begins at bases of crypts of lieberkuhn
leads o ulceration and mucosal destruction
what is the patho chain for UC
inflammatory process mucosa becomes hyperemic and edematous mucosal hemorrhages ulceration/mucosal destruction cloughing
clinical mani of UC
cramping abdominal pain bloody mucousy diarrhea fluid and electrolyte imbalances weight loss anemia
how is evaluation done for UC
sigmoidoscopy or barium enema looking for ulcerations of sigmoid and rectal areas
chrohn’s disease (regional enteritis)
chronic, inflammatory disorder that can affect both large and small intestine
etiology of chron’s
same as UC
patho chain of chrohn’s
inflammatory process in submucosa spreads inward and outward "skip lesions" "transmural" (entire width of wall) strictures fissures can extend inflammation
clinical manifestations of Crohn’s
nonspecific diarrhea for several years non-bloody diarrhea abominal pain (LRQ) fluid/electrolyte imbaance vitamin deficiencies weight loss obstruction fissures
stress ulcers
caused by shock, burns, drugs, infections acute related to ischemia (sock shunts blood) superficial gastric erosiions occure in stomach or duodenum do not penetrate the muscularis layer
two different peptic ulcer disease
gastric ulcers
duodenal ulcers
gastric ulcers
ulcers of gastric mucosa 55-65yoa
which is more common gastric or doudenal ulcers
doudenal
gastric ulcer risk factors
smoking NSADS alcoho chronic diseases psychologic stress infection (helicobcter pylori)
what is the patho change of gastric ulcers
mucosal barrier has increased permeabiity to H+
back dffusion of acid
ulceration
clinical mani of gastric ulcers
pain upper abd pain
hemorrhage/perforation
tend to be more chronic
evaluation for gastric and duodenal ulcers
barium x rays or endoscopy
duodenal ulcers affect
affect younger people, men
risk factors for doudenal
similar to gastric except
hypersecretion of acid or pepsin
patho chain of duodenal ulcers
increased acid concentrations
penetrate the mucosal barrier
ulceration
clinical mani of duodenal ulcers
chronic intermittent epigastric pain (pain, food, relief)
pain reoccurs 2-3 hrs after eating
hemorrhage/perferation
megacolon (hirshprung disease)
congential functional obstruction of colon caused by inadequate motility usually the distal end of sigmoid colon where a malformation of the para affects motility
patho chain of hirshprung disease
absence of autonimic para ganglion calls in colon
lack of peristalsis
obstruction
clinical mani of hirshprung disease
sonstipation
small volume diarrhea (first sign)
inflammation/inflectin
eval of hirshprung
rectal biopsy which show absence of ganglion cells
xray
adult intestinal obstruction etiology/patho
hernia
torsion or twisting of bowel
diverticulosis (outpouching of bowel)
ileus (decreased motility of bowel)
clinical mani of adult intestinal obstruction
distention abd pain loss of bowel sounds fluid/electrolyte imbalances vomiting
eval of adult intestinal obstruction
based on clinical mani and xrays
