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Patho: Nursing > exam 2- gastro > Flashcards

exam 2- gastro Flashcards

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1
Q

digestion

A

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

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2
Q

mouth

A

beginning point with ingestion of food. major functions: chewing, saliva secretion

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3
Q

what is salivary amylase

A

ptyalin starts carbo breakdown in the saliva

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4
Q

how much saliva is made in a day

A

leter to a leter and a half

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5
Q

pharynz

A

food is swallowed and moved into esophagus at this time the trachea is closed off

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6
Q

esophagus

A

muscular tube that lies behind the trachea, initiates peristalsis

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7
Q

pyloric sphincter

A

allows stomach to empty and prevents blackflow into stomach from the small intestine

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8
Q

small intestine

A

includes the
duodemun, jejunum, ilieum
major function:
absorption of nutrients 90%

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9
Q

large intestine

A

includes:
ascending, transverse, descending and sigmoid colin
major function:
absorption of water and electrolytes and formation of wastes

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10
Q

rectum and anal canal

A

function is excretion of waste

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11
Q

cleft lip/palate

A

genetic structural disorder 1/600-1/5000 births

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12
Q

what causes a cleft lip/palate

A

decrease in mesenchyme (forms connective tussue migrating to area)

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13
Q

incomplete fusion of the nasomedial or intermaxillary process

A

cleft lip

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14
Q

incomplete fusion of uvula, soft palate or hard palate

A

fleft palate

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15
Q

cleft lip and cleft palate can occur separately or together and can be minor to severe

A

yep.

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16
Q

esophageal atresia

A

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)

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17
Q

who is at risk for esophageal atresia

A

premi and low birthwate babies

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18
Q

tracheo-esopheageal fistula

A

the foregut fails to seperate into a totally seperate esophagus and trachea resulting in a patent fistula (open connection)between the two structures

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19
Q

what are the manifestations for both esophageal atresia at TEF

A

unable to handle oral secretions
coughing/choking/spitting up
aspiration into lungs
abdominal distention with air swallowed

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20
Q

pyloric stenosis

A

genetically influenced abnormal narrowing of pyloric sphincter
1-200/1000 males more

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21
Q

what is the patho of pyloric stenosis

A

sphincter muscle hypertrophies during development which narrow opening– delayed stomach emptying

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22
Q

what is the manifestation of pyloric stenosis

A

vomiting (primary)

constipation

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23
Q

how is pyloric stenosis diagnosed

A

ultrasound

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24
Q

where is the vommiting center located

A

the medulla of brain

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25
Q

what is the first pathway for vomiting

A

cortical stimulation: direct

all senses exposure to noxious stimuli or emotional stress

26
Q

what is the second pathway for vomiting

A

chemoreceptor trigger zone: direct
located in the brain
responds to impulses of motion (inner ear) and chemicals (drugs)

27
Q

what is the third pathway for vomiting

A 
Visceral receptors (sympathetic afferents)
receptors in many organs and are irritated with inflammation, menstruation, obstruction or spasms
28
Q

what is the fourth pathway for vomiting

A

receptors of stomach itself
receptors respond to distention, gas, inflammation, irritation, ischemia and stimulate vomiting center through the vagus nerve

29
Q

what are the four component of actual vomiting

A

esophageal sphincter opens
pyloric sphincter closes
glottis closes off airway
diaphragm, intercostal muscles and abd muscles contract

30
Q

what are the clinical manifstations of vomiting

A 
nausea/vomiting
sympathetic stim and para (perspiration, salvation, pallor, decreaded Bp and HR)
presence of underlying cause
dehydration
electrolyte imbalance
31
Q

what two types of cells are found in the crypts of lieberkuhn

A

cells that secrete intestinal juices

absorptive cells

32
Q

malabsorption

A

impared absorption of fats, carbos, proteins, vitamins, minerals, water into bloodstream

33
Q

ulcerative colitis

A

chronic inflammatory disease that causes ulceration of the colonic mucosa ulually in the rectum and sigmoid colin (20-40 yoa)

34
Q

what are the etiologies of UC

A 
genetic
infectious
immunologic
psychosomatic
dietary
35
Q

where does UC usually start

A

in rectum and extend into sigmoid colon
inflammatory process begins at bases of crypts of lieberkuhn
leads o ulceration and mucosal destruction

36
Q

what is the patho chain for UC

A 
inflammatory process
mucosa becomes hyperemic and edematous
mucosal hemorrhages
ulceration/mucosal destruction
cloughing
37
Q

clinical mani of UC

A 
cramping abdominal pain
bloody mucousy diarrhea
fluid and electrolyte imbalances
weight loss
anemia
38
Q

how is evaluation done for UC

A

sigmoidoscopy or barium enema looking for ulcerations of sigmoid and rectal areas

39
Q

chrohn’s disease (regional enteritis)

A

chronic, inflammatory disorder that can affect both large and small intestine

40
Q

etiology of chron’s

A

same as UC

41
Q

patho chain of chrohn’s

A 
inflammatory process in submucosa
spreads inward and outward
"skip lesions" "transmural" (entire width of wall)
strictures
fissures can extend inflammation
42
Q

clinical manifestations of Crohn’s

A 
nonspecific diarrhea for several years
non-bloody diarrhea
abominal pain (LRQ)
fluid/electrolyte imbaance
vitamin deficiencies 
weight loss
obstruction 
fissures
43
Q

stress ulcers

A 
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
44
Q

two different peptic ulcer disease

A

gastric ulcers

duodenal ulcers

45
Q

gastric ulcers

A

ulcers of gastric mucosa 55-65yoa

46
Q

which is more common gastric or doudenal ulcers

A

doudenal

47
Q

gastric ulcer risk factors

A 
smoking
NSADS
alcoho
chronic diseases
psychologic stress
infection (helicobcter pylori)
48
Q

what is the patho change of gastric ulcers

A

mucosal barrier has increased permeabiity to H+
back dffusion of acid
ulceration

49
Q

clinical mani of gastric ulcers

A

pain upper abd pain
hemorrhage/perforation
tend to be more chronic

50
Q

evaluation for gastric and duodenal ulcers

A

barium x rays or endoscopy

51
Q

duodenal ulcers affect

A

affect younger people, men

52
Q

risk factors for doudenal

A

similar to gastric except

hypersecretion of acid or pepsin

53
Q

patho chain of duodenal ulcers

A

increased acid concentrations
penetrate the mucosal barrier
ulceration

54
Q

clinical mani of duodenal ulcers

A

chronic intermittent epigastric pain (pain, food, relief)
pain reoccurs 2-3 hrs after eating
hemorrhage/perferation

55
Q

megacolon (hirshprung disease)

A

congential functional obstruction of colon caused by inadequate motility usually the distal end of sigmoid colon where a malformation of the para affects motility

56
Q

patho chain of hirshprung disease

A

absence of autonimic para ganglion calls in colon
lack of peristalsis
obstruction

57
Q

clinical mani of hirshprung disease

A

sonstipation
small volume diarrhea (first sign)
inflammation/inflectin

58
Q

eval of hirshprung

A

rectal biopsy which show absence of ganglion cells

xray

59
Q

adult intestinal obstruction etiology/patho

A

hernia
torsion or twisting of bowel
diverticulosis (outpouching of bowel)
ileus (decreased motility of bowel)

60
Q

clinical mani of adult intestinal obstruction

A 
distention
abd pain
loss of bowel sounds
fluid/electrolyte imbalances
vomiting
61
Q

eval of adult intestinal obstruction

A

based on clinical mani and xrays

Patho: Nursing (4 decks)

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