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Pathophysiology > Ch. 9 Gastrointestinal Function > Flashcards

Ch. 9 Gastrointestinal Function Flashcards

0
Q

what are the accessory organs?

A

salivary glands, liver, gallbladder, bile ducts, and pancreas

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1
Q

what is the alimentary canal?

A

the canal through which food is passed. consists of the oral cavity, pharynx, esophagus, stomach, small intestine, large intestine, and anus

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2
Q

what is the liver, gallbladder, and pancreas collectively referred to? why is this?

A

they are collectively referred to as the hepatobiliary system because of their close proximity to each other and their complementary functions

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3
Q

what are the four layers of the GI tract walls from inner to outer?

A

mucosa, submucosa, muscle, and serosa

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4
Q

what is the purpose of the mucosa layer of the GI tract walls?

A

it secretes mucus which facilitates the movement of GI contents and protects the GI tissue from the extreme pH conditions of the GI tract

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5
Q

why do the epithelial mucosa cells have a high turnover rate?

A

because of erosion associated with food passage and the highly acidic environment

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6
Q

what does the submucosa layer of the GI tract walls consist of?

A

connective tissue. includes blood vessels, nerves, lymphatics, and secretory glands.

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7
Q

what does the muscle layer of the GI tract consist of?

A

circular and longitudinal smooth muscle layers that function in peristalsis

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8
Q

what is peristalsis?

A

the wavelike motion of muscle contractions that propels food through the GI tract

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9
Q

large serous membrane that lines the abdominal cavity

A

peritoneum

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10
Q

are the two layers of the peritoneum and what is the difference?

A

the outer parietal peritoneum layer overs the abdominal wall and the top of the bladder and uterus. the inner visceral peritoneum layer encases the abdominal organs.

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11
Q

what is the peritoneal cavity?

A

the space between the parietal and visceral layers of the peritoneum.

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12
Q

what does the peritoneal cavity contain serous fluid?

A

to decrease friction and facilitate movement

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13
Q

what is the mesentery?

A

a double layer peritoneum that supplies the intestinal wall. it supports the intestines while allowing flexibility to accommodate peristalsis and varying content volumes

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14
Q

what structures make up the upper GI tract?

A

the oral cavity, pharynx, esophagus, and stomach

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15
Q

what does mastication do?

A

(chewing) it pulverizes the food into small pieces so that saliva can break down the food further

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16
Q

what is the function of saliva?

A

it is secreted from the salivary glands to moisten and further break down food. it contains enzymes and antibodies that can kill or neutralize bacteria

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17
Q

what is the function of the tongue in digestion?

A

it pushes the semisolid food mass to the back of the throat where it is swallowed.

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18
Q

what cranial nerves initiate the swallowing reflex?

A

food passing over the trigeminal and glossopharyngeal nerves initiate it

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19
Q

how do the trigeminal and glossopharyngeal nerves initiate the swallowing reflex?

A

they relay info to the swallowing center in the medulla and then the swallowing center coordinates the movement of food from the mouth through the esophagus to the stomach with cranial nerves V, IX, X, and XII

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20
Q

what is the purpose of the lower esophageal sphincter?

A

it relaxes to allow food from the esophagus to enter the stomach and then prevents the contents in the stomach from refluxing back into the esophagus

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21
Q

what are rugae?

A

wrinkles formed by the stomach wall when it is empty and shrinks. when it fills, they unfold and the wall stretches

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22
Q

how much content can the rugae stretch and accommodate for in the stomach?

A

2-4 L

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23
Q

what digestion occurs in the stomach?

A

in the stomach, hydrochloric acid and enzymes further chemically digest food and the peristaltic churning mechanically digests the food

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24
Q

what is the food mixture in the stomach called

A

chyme

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25
Q

what does the highly acidic nature of chyme do?

A

it aids in digestion and the destruction of bacteria

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26
Q

how does the stomach’s inner lining protect itself from its acidity?

A

epithelial cells are densely packed to prevent tissue damage and there are numerous glands located in the stomach that coat the inner lining with a thick layer of mucus

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27
Q

are nutrients absorbed in the stomach?

A

no, they are just prepared for absorption

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28
Q

what can be absorbed in the stomach?

A

alcohol

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29
Q

how does chyme leave the stomach?

A

through the pyloric sphincter in small (1-3mL), intermittent amounts

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30
Q

as chyme passes through the pyloric sphincter, into the duodenum, what things are added to the mixture?

A

liver and pancreatic secretions to continue the digestion process

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31
Q

what are some of the liver’s primary functions that are vital for homeostasis?

A

metabolize carbs, proteins, and fats; synthesize glucose, protein, cholesterol, triglycherites, and clotting factors; store glucose, fats, and micronutrients and release them when needed; detoxify the blood of potentially harmful chemicals; maintain intravascular fluid volume through the production of circulating proteins; metabilize medications and prepare them for excretion; produce bile; inactivate and prepare hormones for excretion; remove damaged or old erythrocytes from blood to recycle iron and protein; serve as a blood resevoir; convert fatty acids to ketones

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32
Q

about how much blood does the liver store?

A

approximately 450 mL

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33
Q

what is the tough membrane that protects the liver called?

A

Glisson’s capsule

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34
Q

where does the liver get its blood supply from?

A

the hepatic artery and the portal vein

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35
Q

what does the hepatic artery do?

A

carries oxygenated blood from general circulation to the liver at a rate of approximately 300 mL per minute to nourish the liver

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36
Q

what does the portal vein do?

A

carries partially deoxygenated blood from the stomach, pancreas, and spleen, as well as from the small and large intestines to the liver at an approximate rate of 1000 mL per minute so that the liver can process nutrients and digestion by-products

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37
Q

as much as ….% of the liver’s tissue can be lost or removed and the liver can still regenerate its tissue

A

75%

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38
Q

why can the liver regenerate?

A

primarily due to certain liver cells (hepatocytes) that act as stem cells

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39
Q

what do hepatocytes do in addition to providing the liver with regeneration capabilities?

A

they produce bile and perform most of the liver’s activities

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40
Q

what is the rate at which hepatocytes produce bile?

A

600-1200 mL per day

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41
Q

what is bile?

A

a green or yellowish liquid that contains water, bile salts, conjugated bilirubin, cholesterol, and electrolytes.

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42
Q

what are bile salts necessary for?

A

emulsifying fats and fat-soluble vitamins so that they can be absorbed by the small intestine

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43
Q

what does the distal ileum do?

A

it reabsorbs most of the bile and returns it to the liver through the portal vein for recycling

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44
Q

what component of the bile helps to neutralize the acidic gastric contents so that the intestinal and pancreatic enzymes can function?

A

bicarbonate ions

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45
Q

what are the two places bile can go after it leaves the liver?

A

straight to the duodenum or to the gallbladder for storage

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46
Q

in addition to storing bile, what does the gallbladder do?

A

it concentrates it by removing water

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47
Q

what triggers the gallbladder to contract and release bile?

A

the presence of chyme in the small intestine

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48
Q

where is the pancreas located?

A

it is nestled under the small intestine and the liver?

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49
Q

what two functions does the pancreas have?

A

endocrine and exocrine

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50
Q

what is the exocrine function of the pancreas?

A

it produces enzymes, electrolytes, and water necessary for digestion and secretes these into a duct that delivers them to the duodenum to join chyme

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51
Q

what is the endocrine function of the pancreas?

A

includes producing hormones to help regulate blood glucose and thereby maintaining homeostasis

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52
Q

what are the structures of the lower GI tract?

A

the small intestine, large intestine, and anus

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53
Q

what is the longest section of the GI tract?

A

the small intestine

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54
Q

what is the importance of the length of the small intestine?

A

it allows for adequate absorption

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55
Q

what digestion occurs in the small intestine?

A

enzymes that were excreted into the small intestine break the large food molecules into smaller molecules which are then absorbed and transported to the circulatory and lymphatic system

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56
Q

what is the purpose of the villi and microvilli in the small intestine?

A

they increase the surface area for absorption of nutrients

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57
Q

about how long is the large intestine?

A

about 5 feet

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58
Q

does the large intestine have villi?

A

no

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59
Q

cecum

A

the pouch in which the small intestine ends. this is where the appendix is attached

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60
Q

what makes up most of the large intestine?

A

the colon

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61
Q

what are the three sections of the colon?

A

the ascending, transverse, and descending

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62
Q

what does the mixture entering the large intestine contain?

A

water, unabsorbed food molecules, indigestible food remnants, and electrolytes

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63
Q

how does the colon further participate in digestion?

A

it absorbs 90% of the water and electrolytes, and E. coli feeds off the undigested or unabsorbed food remains

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64
Q

when does chyme become feces?

A

when if move through the colon

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65
Q

what is feces comprised of?

A

the remaining undigested or unabsorbed remnants along with bacteria

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66
Q

why does feces introduce approximately 300 mL of mucus?

A

to aid in bowel movements, even in times of decreased dietary intake

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67
Q

a resevoir to store feces

A

rectum

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68
Q

how does the rectum elicit the defecation reflex?

A

it expands when feces enters the area, stimulating the stretch receptors in the rectal wall which send an impulse through the spinal cord to elicit it

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69
Q

why does feces become more difficult to expel as it stays in the large intestine for longer periods of time?

A

more water is absorbed from it the longer it remains in the large intestine

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70
Q

how do the sympathetic and parasympathetic nervous systems affect digestive activity?

A

stimulation of the sympathetic nervous system slows digestive activity while stimulation of the parasympathetic speeds it up

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71
Q

what are age related changes to the stomach?

A

stomach lining may shrink and become inflammed leading to atrophic gastritis. achlorhydria occasionally because of atrophic gastritis, and achlorhydria can cause b12 deficiency and slow digestion

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72
Q

achlorhydria

A

decreased stomach acid production

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73
Q

what are liver changes associated with age?

A

decreased blood flow, delayed drug clearance, and a diminished capacity to regenerate damaged liver cells

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74
Q

changes in the metabolism and absorption of what nutrients can occur with age?

A

lactose, calcim, and iron

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75
Q

decreased calcium absorption can lead to what in the older adult?

A

bone mineral loss and osteoporosis

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76
Q

why is the older person at risk for constipation?

A

decreased peristalsis

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77
Q

what are the two underlying pathological issues that affect the GI tract?

A

altered nutrition and impaired elimination

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78
Q

what are conditions that alter nutrition?

A

issues with consuming, digesting, and absorbing food

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79
Q

regardless of the cause of altered nutrition what is the similar end result for almost all cases?

A

inadequate nutritional states in which individuals may be underweight and vitamin deficient

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80
Q

what are conditions impairing elimination?

A

constipation and diarrhea

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81
Q

can conditions that cause altered nutrition cause problems with elimination?

A

yes

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82
Q

what are congenital defects of the upper GI tract?

A

cleft lip and palate and pyloric stenosis

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83
Q

relatively common congenital defects of the mouth and face that are apparent at birth

A

cleft lip/cleft palate

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84
Q

when do cleft lip/palate conditions usually develop?

A

between the 4th and 9th week (2nd and 3rd month) of gestation

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85
Q

what things have cleft lip/palate been linked to?

A

genetic mutations, maternal diabetes, drugs, toxins, viruses, vitamin deficiencies, and cigarette smoking

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86
Q

who are most likely to be affected by cleft palate/lip?

A

children of Native American, Hispanic and Asian descent. African Americans are the least likely to have it.

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87
Q

what gender is most likely to have cleft palate? cleft lip?

A

women are 2x as likely to have cleft palate, men are 2x as likely to have cleft lip

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88
Q

what problems can a cleft lip/palate lead to?

A

feeding issues - decreased sucking ability and increased risk for aspiration, speech problems, ear infections, and hearing problems

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89
Q

what other malformations may be present with cleft lip/palate?

A

teeth and nose malformations

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90
Q

what does cleft lip result from?

A

failure of the maxillary processes and nasal elevations or uppper lip to fuse during development. can be unilateral or bilateral

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91
Q

what does cleft palate result from?

A

failure of the hard and soft palates to fuse in development, creating an opening between the oral and nasal cavities

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92
Q

by what age is cleft lip repair recommended? when is cleft palate?

A

by 3 months for cleft lip and by 1 year for cleft palate

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93
Q

what is pyloric stenosis?

A

a narrowing and obstruction of the pyloric sphincter because muscle fibers become thick and stiff, making it difficult for the stomach to empty food into the small intestine

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94
Q

when does pyloric stenosis usually present itself?

A

may be present at birth, or may develop later in life, but development after 6 months is rare

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95
Q

what is the cause of pyloric stenosis?

A

the exact cause is unknown, but genetics are thought to play a role

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96
Q

who is pyloric stenosis most likely to effect?

A

caucasians and men

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97
Q

when do the clinical manifestations of pyloric stenosis usually appear?

A

within several weeks after birth

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98
Q

in this form of pyloric stenosis, the hypertrophied pyloric muscle can be palpated as a hard, olive shaped mass in the abdomen and vomiting is usually the first symptom.

A

the congenital form

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99
Q

what are manifestations of pyloric stenosis?

A

regurgitation, vomiting - usually after every feeding and it’s usually projectile, belching, wavelike stomach contractions, small infrequent stools, abdominal pain, failure to gain weight, dehydration, irritability

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100
Q

why do wavelike stomach contractions present theirselves with pyloric stenosis?

A

because there is an increased peristaltic effort to pass food through the narrowed areas

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101
Q

why does irritability occur with pyloric stenosis?

A

because of persistent hunger

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102
Q

difficulty swallowing

A

dysphagia

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103
Q

how does dysphagia usually develop?

A

secondary to a condition that causes mechanical obstruction of the esophagus or impaired esophageal motility

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104
Q

what are some conditions that may lead to dysphagia?

A

mechanical obstructions, neurologic disorders, muscular disorders

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105
Q

what are some mechanical obstructions that can cause dysphagia?

A

congenital atresia (separation of the upper and lower esophagus), esophageal stenosis or stricture, esophageal diverticula (outpouching of the esophageal wall), tumors (esophageal or of nearby structures)

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106
Q

what are some neurological disorders that can cause dysphagia?

A

stroke, cerebral damage, achalasia (failure of the LES to relax because of loss of innervations), Parkinson’s disease, Alzheimer’s disease

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107
Q

what are clinical manifestations of dysphagia?

A

sensation of food being stuck in the throat, choking, coughing, ‘pocketing’ of food in the cheeks, difficulty forming bolus, delayed swallowing, painful swallowing (odynophagia)

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108
Q

what is there an increased risk of with dysphagia?

A

aspiration

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109
Q

what is a muscular disorder than can cause dysphagia?

A

muscular dystrophy

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110
Q

voluntary or involuntary forceful ejection of chyme from the stomach up through the esophagus and out the mouth

A

vomiting or emesis

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111
Q

what are causes of vomiting?

A

protection from infection, drug or alcohol overdose, food poisoning, etc; reverse peristalsis from an intestinal obstruction; increased intracranial pressure - projectile; severe pain

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112
Q

what area of the brain coordinates vomiting, and what things can stimulate this center?

A

the medulla; drugs, toxins, and chemicals can stimulate it

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113
Q

what is the sequence of involuntary vomiting?

A

a deep breath is taken, the glottis closes and the soft palate rises, respirations cease in order to minimize the risk for aspiration, the gastro esophageal sphincter relaxes, abdominal muscles contract, squeezing the stomach against the diaphragm and forcing the chyme upward toward the esophagus, reverse peristaltic waves eject chyme out the mouth

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114
Q

vomiting may be preceded by what two things?

A

nausea - the subjective urge to vomit

retching - strong unproductive effort to vomit

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115
Q

what can recurrent vomiting lead to?

A

fluid, electrolyte, and pH imbalances. also exhaustion due to the strong muscle contractions needed

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116
Q

when is an individual at risk for aspiration while vomiting?

A

when supine or unconscious, when the vomiting or cough reflex is suppressed

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117
Q

what is the name for the contents vomitted?

A

vomitus

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118
Q

what can aspiration of vomitus cause?

A

serious damage and inflammation to lung tissue

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119
Q

what can the characteristics of vomitus tell us?

A

the underlying cause/specific problems

120
Q

hematemess

A

condition of blood in the vomitus

121
Q

describe the appearance of hematemesis. why does this happen? what can it indicate?

A

characteristic brown, granular appearance similar to coffee grounds resulting from proteins in the blood being digested in the stomach. blood in the stomach is irritating to the gastric mucosa so the stomach attempts to expel it. occurs due conditions that cause upper GI bleeding

122
Q

what can yellow or green colored vomitus indicate? why does it usually occur?

A

indicates the presence of bile. can occur as a result of a GI tract obstruction

123
Q

what can a deep brown colored vomitus indicate? why does this usually occur?

A

may indicated contents from the lower intestine, possibly fecal. usually occurs with intestinal obstruction.

124
Q

what can it indicate when there is undigested food in the vomitus?

A

conditions that impair gastric emptying

125
Q

a section of the stomach protrudes upward through an opening in the diaphragm toward the lung and into the thorax

A

hiatal hernia

126
Q

what can cause a hiatus to develop?

A

the weakening of the diaphragm muscle, frequently from increased intrathoracic pressure (coughing, vomiting, straining to defecate) or from trauma and congenital defects

127
Q

what are risk factors for developing a hiatal hernia?

A

advancing age and smoking

128
Q

small hiatal hernias typically go undetected and rarely cause problems. what can large ones cause?

A

chyme to reflux into the esophagus, irritating the mucosa. when the stomach protrudes through the diaphragm, it creates a pouch where chyme can become stuck and cause mucosa inflammation.

129
Q

does a hiatal hernia by itself usually cause symptoms?

A

rarely

130
Q

what are manifestations of hiatal hernia?

A

vary depending on the size: indigestion, heartburn (pyrosis), frequent belching, nausea, chest pain, stricutres, dysphagia. may have soft upper abdominal mass because of the protruding stomach pouch.

131
Q

what do symptoms of hiatal hernias reflect? what can make these symptoms worse and what can make them better?

A

reflect inflammation of the esophagus and stomach due of reflux of gastric acid, air, or bile. worsen when in the dorsal recumbent position, eating, bending over and coughing. improve upon standing.

132
Q

condition where chyme periodically backs up from the stomach into the esophagus. occasionally bile can back up as well.

A

gastroesophageal reflux disease (GERD)

133
Q

why does GERD occur?

A

the gastric back flow occurs because the LES opens from decreases in LES pressure or increases in stomach pressure. the presence of gastric secretions irritates the esophageal mucosa.

134
Q

what are causes of pressure changes that may cause GERD?

A

certain foods (chocolate, caffeine, carbonated beverages, citrus fruit, tomatoes, spicy or fatty foods, peppermint), alcohol consumption, smoking, hiatal hernia, obesity, pregnancy, certain medications, nasogastric intubation, delayed gastric emptying

135
Q

what does the severity of GERD depend on and what are some manifestations?

A

varies in severity depending on the weakness of the LES. clinical manifestations: heart burn, epigastric pain (usually after a meal or when recumbant), dysphagia, nausea (usually after eating), dry cough, laryngitis, pharyngitis, regurgitation of food, and sensation of a lump in the throat

136
Q

what is GERD often confused with?

A

angina - may warrant ruling out cardiac disease

137
Q

what can GERD result in?

A

esophagitis, strictures, ulcerations, esophageal cancers, and chronic pulmonary disease (asthma)

138
Q

an inflammation of the stomach’s mucosal lining that may be either acute or chronic

A

gastritis

139
Q

acute gastritis

A

can be a mild, transient reaction or a severe ulceration with hemorrhage. usually develops suddenly and is likely to be accompanied with nausea and epigastric pain

140
Q

chronic gastritis

A

develops gradually and can last for months. may be asymptomatic. likely to be accompanied by a dull epigastric pain and sensation of fullness after minimal intake

141
Q

inflammation of the stomach and intestines usually resulting from allergy or infection

A

gastroenteritis

142
Q

what is the most common cause of chronic gastritis? how is this spread? what does it do? and why do some people get chronic gastritis with it, but not others?

A

helicobacter pylori. spreads from person to person. erodes the stomach’s protective mucosal barrier, causing inflammation. genetic vulnerability and lifestyle behaviors may increase susceptibility and explain why only a small amount of people develop chronic gastritis due to the organism.

143
Q

what are some other organisms that can cause gastritis aside from H. pylori.

A

E. coli, Salmonella, rotavirus, and amoebas, long-term use of NSAIDs (reduce cyclooxygenase which helps preserve mucosal lining), excessive alcohol, severe stress that may cause ischemia and decreased gastric motility, autoimmune conditions, other chronic diseases

144
Q

what are the clinical manifestations of gastritis?

A

indigestion, heartburn, epigastric pain, abdominal cramping, nausea, vomiting, anorexia, fever, and malaise. hematemesis and dark stools may indicate ulcerations and bleeding

145
Q

what does chronic gastritis increase the risk for?

A

peptic ulcers, gastric cancer, anemia, and hemorrhage

146
Q

break in the protective mucosal lining of the lower esophagus, stomach, or duodenum?

A

peptic ulcers

147
Q

who is peptic ulcer disease (PUD) most common in?

A

males, african americans, and hispanics

148
Q

what are risk factors for the development of PUD?

A

advancing age, NSAID use, H. pylori infections, chronic disease, and certain gastric tumors

149
Q

why does PUD develop?

A

due to an imbalance between destructive forces and protective mechanisms

150
Q

ulcers that are most commonly associated with excessive acid or H. pylori infections. epigastric pain is relieved in the presence of food. most common type.

A

duodenal ulcers

151
Q

ulcers that are often associated with malignancy and NSAID use, pain worsens when eating, less frequent but more deadly form of ulcer

A

gastric ulcers

152
Q

term used to describe PUD that develops because of a major physiological stressor

A

stress ulcers

153
Q

ulcers associated with burns

A

curling’s ulcers

154
Q

stress ulcers associated with head injuries

A

cushing’s ulcers

155
Q

why do stress ulcers develop, and where do they develop most frequently?

A

develop due to local tissue ischemia, tissue acidosis, entry of bile salts into the stomach, and decreased GI motility. most often develop in the stomach

156
Q

what is often the first indicator of a stress ulcer and why?

A

hemorrhage is the first indicator because of the ulcer’s rapid development and the tendency to be masked by the primary problem

157
Q

what are complications of PUD?

A

GI hemorrhage, obstruction, perforation, peritonitis

158
Q

what are clinical manifestations fo PUD and what do they resemble?

A

resemble other conditions of GI inflammation; epigastric or abdominal pain, abdominal cramping, heartburn, indigestion, chest pain, nausea and vomiting, dark tarry stools, fatigue, weight loss

159
Q

common condition in which calculi of varying sizes and shapes from inside the gallbladder

A

cholelithiasis

160
Q

who is cholelithiasis more common in and what are some risk factors for its development?

A

more common in fair-skinned women. risk factors: advancing age, obesity, rapid weight loss (bariatric surgery), pregnancy, hormone replacement, certain chronic diseases (diabetes mellitus and liver disease), and long-term parenteral nutrition

161
Q

inflammation or infection in the biliary system due to calculi

A

cholesystitis

162
Q

in what ways do small calculi and large calculi affect the biliary system differently?

A

small calculi are usually asymptomatic and are excreted with bile while large calculi usually obstruct bile flow and cause clinical manifestations

163
Q

what can prolonged obstruction of bile flow lead to?

A

gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma

164
Q

what are the clinical manifestations of cholelithiasis?

A

biliary colic (abdominal cramping and pain that worsens after a fatty meal), abdominal pain (especially in the upper right and middle quadrants that may radiate to the back and right shoulder), abdominal distention, nausea and vomiting, jaundice, clay-colored stool due to lack of bile, fever, leukocytosis

165
Q

what is the hallmark sign of cholelithiasis?

A

colicky pain in the upper right quadrant of the abdomen

166
Q

what are the three types of cholelithiasis?

A

cholesterol (most common), bilirubin (pigmented. multiple, small, black stones), mixed (usually found in large numbers. bilirubin center, surrounded by cholesterol and calcium)

167
Q

what are disorders of the liver most often acquired by?

A

ingestion of hepatotoxic substances or infections

168
Q

an inflammation of the liver that can be caused by infections, alcohol, medications, or autoimmune disease. may be acute, chronic, or fulminant, active or nonactive

A

hepatitis

169
Q

what things increase the likelihood of liver fialure, liver cancer, or cirrhosis in patients with hepatitis?

A

advancing age and comorbidity

170
Q

what can hepatitis result in?

A

hepatic cell destruction, necrosis, autolysis, hyperplasia, and scarring

171
Q

any disease that is fulimant is….

A

rapidly progressing and often fatal

172
Q

what are the four phases of acute hepatitis? what occurs during each one and when do they occur?

A

incubation phase - after initial exposure - 2 weeks. asymptomatic.
prodromal phase - 2 weeks after exposure. viral symptoms: nausea, vomiting, malaise, anorexia, low-grade fever, and headache
icteric phase - 1-2 weeks after prodromal. lasts up to 6 weeks. jaundice, dark tea colored urine, clay-colored stools, hepatomegaly, right upper quadrant pain
recovery phase - resolution of jaundice. 6-8 weeks after exposure. liver may remain enlarged for up to 3 months

173
Q

hepatitis characterized by continued hepatic disease lasting longer than 6 months. symptom severity and disease progression vary depending on degree of liver damage

A

chronic hepatitis

174
Q

an uncommon, rapidly progressing form of hepatitis that can quickly lead to liver failure, hepatic encephalopathy, or death within 3 weeks

A

fulminant hepatitis

175
Q

chronic, progressive, irreversible, diffuse damage to the liver resuling in decreased liver function

A

cirrhosis

176
Q

what are the causes of cirrhosis?

A

hepatitis and the factors that lead to hepatitis. chronic alcohol abuse is the most common factor in the US, while hepatitis is the most common in developing countries.

177
Q

what can the liver damage with cirrhosis eventually lead to?

A

fibrosis, nodule formation, impaired blood flow, and bile obstruction that can result in liver failure

178
Q

how long can cirrhosis take to develop? does development stop with the removal of the underlying cause?

A

it can take up to 40 years to develop and can still develop even with the removal of the underlying cause

179
Q

high blood pressure in the portal vein due ot poor blood flow through the liver. what can this condition lead to?

A

portal hypertension. can cause veins to engorge and variscosities to develop in the esophagus. nearby organs using the same circulation (spleen, pancreas, and stomach) enlarge as pressure rises. bleeding can occur and esophageal bleeding has a high mortality and recurrence rate. fluid accumulates in the peritoneal cavity

180
Q

what are the clinical manifestations of cirrhosis?

A

neurological impairment (hepatic encephalopathy), manifestations of hepatitis, spider nevi (spider veins), variscosities in esophagus and abdomen, bleeding either slow or severe particularly in esophageal varicies, ascites, ulcers and GI bleed, changes in clotting factors

181
Q

ascites

A

when fluid accumulates in the peritoneal cavity

182
Q

what organ is most often affected by disorders of the pancreas?

A

the gallbladder because of the intricate relationship between the two, but all in all the entire body is effected because of the pancreases significant role in maintaining homeostasis through regulating electrolytes, water, and glucose

183
Q

what is the prognosis like for pancreatic disorders?

A

it is frequently grave

184
Q

inflammation of the pancreas that can be either acute or chronic

A

pancreatitis

185
Q

what are the causes of pancreatitis? which one is the most common acute cause and which is the most common chronic cause?

A

cholelithiasis (most common acute), alcohol abuse (common chronic), biliary dysfunction, hepatotoxic drugs, metabolic disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, and penetrating peptic ulcer

186
Q

what happens when the pancreas is injured or function is disrupted?

A

pancreatic enzymes leak into pancreatic tissue and initiate 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

187
Q

which type of pancreatitis is considered a medical emergency?

A

acute pancreatitis, mortality rate is approximately 20%

188
Q

what does acute pancreatitis mortality rate increase with?

A

advancing age and comorbidity

189
Q

what are the serious complications that can develop with acute or chronic pancreatitis?

A

acute respiratory distress syndrome, diabetes mellitus, infection, shock, disseminated intravascular coagulation, renal failure, malnutrition, pancreatic cancer, pseudocyst or abscess

190
Q

how does acute respiratory distress syndrome occur with acute pancreatitis?

A

acute pancreatitis can trigger the release of chemicals that lead to it

191
Q

how can chronic pancreatitis lead to diabetes mellitus?

A

it can damage the insulin-producing cells in the pancreas

192
Q

how can acute pancreatitis lead to shock?

A

infection and the release of miscellaneous immune mediators can trigger shock

193
Q

how can acute and chronic pancreatitis lead to renal failure?

A

sock and activation of the reninangiotensin system lead to decreased renal perfusion

194
Q

how can pancreatitis lead to malnutrition?

A

decrease pancreatic enzyme production. these enzymes are necessary for digestion and absorption. malnutrition may occur even if there is adequate food intake

195
Q

how can pancreatitis lead to pancreatic cancer?

A

long-standing inflammation caused by chronic pancreatitis can initiate cellular mutations

196
Q

how can acute pancreatitis lead to pseudocyst or abscess?

A

it can cause pancreatic fluids and necrotic debris to collect in cystlike pockets - if a large pseudocyst or abscess ruptures, it can lead to internal bleeding and infection

197
Q

what are the manifestations for acute pancretatis?

A

sudden and severe; upper abdominal pain that radiates to the back, worsens after eating, and is somewhat relieved by leaning forward or pulling the knees toward the chest; nausea and vomiting; mild jaundice; low-grade fever; blood pressure and pulse changes

198
Q

what are the clinical manifestations of chronic pancreatitis?

A

upper abdominal pain, indigestion, losing weight without trying, steatorrhea (oily, fatty, odorous stools), constipation, flatulence

199
Q

a change in bowel patterns characterized by an increased frequency, amount, and water content of the stool

A

diarrhea

200
Q

what things can diarrhea result from?

A

it can be secretory - due to an increase in fluid secretion
osmotic - due to a decrease in fluid absorption
motility is affected - an alteration in GI peristalsis

201
Q

how long does diarrhea have to last to be considered chronic?

A

longer than 4 weeks

202
Q

what is acute diarrhea often caused by?

A

bacterial or viral infections or by certain medications

203
Q

what are usual causes of chronic diarrhea?

A

inflammatory bowel diseases, malabsorption syndromes, endocrine disorders, chemotherapy, and radiation

204
Q

what are the clinical manifestations of diarrhea originating in the small intestine?

A

stools are large, loose, and provoked by eating. usually is accompanied by pain in the right lower quadrant of the abdomen

205
Q

what clinical manifestations will diarrhea originating in the large intestine have?

A

small, frequent stools accompanied by cramping and pain in the lower left quadrant of the abdomen

206
Q

what are the clinical manifestations of acute diarrhea?

A

generally infectious in origin and accompanied by cramping, fever, chills, nausea, and vomiting. blood, pus, or mucus may be present in the stool which can aid in diagnosis, hyperactive bowel sounds; fluid, electrolyte, and pH imbalance may be present

207
Q

bright, red blood on the surface of the stool

A

frank blood

208
Q

small amounts of blood hidden in the stool

A

occult blood

209
Q

dark, tarry stool from a significant amount of bleeding higher up in the GI tract

A

melena

210
Q

change in bowel pattern characterized by infrequent passage of stool

A

constipation

211
Q

what occurs during constipation?

A

stool remains in large intestine longer than usual. the longer the stool remains there, the more water is removed and absorbed and as a consequence the stool becomes hard and difficult to pass

212
Q

what things can cause constipation?

A

low-fiber diet, inadequate physical activity, delaying the urge to defecate, laxative abuse, stress, travel, diseases of the bowel, pregnancy, certain medications, mental health problems, neurologic diseases, spinal cord injuries, and colon cancer. common in children who are toilet training

213
Q

what are the clinical manifestations of constipation?

A

pain during the passage of a bowel movement, inability to pass stool after straining or pushing for more than 10 mins, no bowel movements for more than three days, hypoactive bowel sounds

214
Q

blockage of intestinal contents in the small intestine or large intestine. (small intestine is the most common)

A

intestinal obstruction

215
Q

what are the two types of intestinal obstructions and what is the difference?

A

mechanical obstructions - physical barriers

functional obstructions result from GI tract dysfunction

216
Q

what can mechanical obstructions occur due to?

A

foreign bodies, tumors, adhesions, hernias, intussusception, strictures, volvulus, Crohn’s disease, diverticulitis, Hirschsprung’s disease, and fecal impaction

217
Q

intussusception

A

telescoping of a portion of the intestine into another portion

218
Q

vovulus

A

twisting of the intestine

219
Q

what can paralytic ileuses (or functional obstructions) occur because of?

A

neurologic impairment, intra-abdominal surgery complications, chemical, electrolyte, and mineral distrubances, intra-abdominal infections, abdominal blood supply impiarment, renal and lung disease, and certain medications

220
Q

what occurs during an intestinal obstruction?

A

chyme and gases accumulate at the site of the blockage. over time, saliva, gastric juices, bile, and pancreatic secretions begin to collect as the blockage lingers. this buildup increases serum electrolytes and protein and causes abdominal distention and pain, intestinal blood flow can become impaired, leading to strangulation and necrosis. intestinal contents will begin to seep into the abdomen as pressure at the blockage increases

221
Q

what can happen if a complete obstruction goes untreated?

A

death can occur within hours due to shock and cardiovascular collapse

222
Q

what are some complications that can arise due to an intestinal obstruction?

A

perforation of the intestines, pH imbalances, fluid disturbances, shock, and death

223
Q

what are clinical manifestations of an intestinal obstruction?

A

abdominal distention, abdominal cramping and colicky pain, nausea and vomiting, constipation, diarrhea, borborygmi, intestinal rushes, decreased or absent bowel sounds, restlessness, diaphoresis, tachycardia progressing to weakness, confusion, and shock

224
Q

inflammation of the vermiform appendix often caused by infection.

A

appendicitis

225
Q

what occurs during appendicitis?

A

inflammation process triggers local tissue edema which obstructs the small structure. fluid build up inside it and microorganisms proliferate. it fills with purulent exudate and stretches. the wall compresses area blood vessels and blood flow is comprimised so ischemia and necrosis occur. the pressure inside esclates, forcing bacteria and toxins to surrounding structures. pressure inside the appendix will continue to intensify until it ruptures or perforates, releasing it’s contents

226
Q

why can abscesses and peritonitis occur with apendicitis? why can gangrene occur?

A

abscesses and peritonitis can occur as the bacteria escape the appendix, gangrene can occur because of worsening necrosis

227
Q

what are the clinical manifestations of appendicitis?

A

often begins as a sharp pain over the umbilicus which gradually intensifies and becomes localized to the lower right quadrant of the abdomen, often have elevated WBC count, pain will temporarily subside if appendix ruptures but will return and escalate. nausea, vomiting, and fever after pain starts, indicaitons of inflammation and infection, indications of peritonitis (right abdominal rigity, tachycardia, hypotension)

228
Q

an inflammation of the peritoneum, the membrane that lines the abdominal wall and organs

A

peritonitis

229
Q

is peritonitis usually acute or chronic?

A

acute

230
Q

what may peritonitis result from? what are examples of each?

A

it may be chemical - ruptured gallbladder or spleen

or direct organism invasion - appendicitis and peritoneal dialysis

231
Q

what will peritonitis lead to if it is not quickly treated and how?

A

chemical irritation can lead to bacterial invasion because the inflammatory response triggered by the chemical increases intestinal wall permeability this allows for passage of enteric bacteria. necrosis or perforation of the intestinal wall also creates an opportunity for enteric bacteria invasion

232
Q

what are some protective mechanisms activated during pertonitis in an attempt to localize the problem?

A

inflammation, a thick sticky exudate is released that bonds nearby structures and temporarily seals them off, abscesses may form, peristalsis slows decreasing the spread of toxins and bacteria.

233
Q

what can happen if the underlying cause is not treated in peristalsis?

A

sepsis and shock can develop

234
Q

what is the classical manifestation/cardinal sign of peritonitis, what is this?

A

abdominal rigidity - a rigid, board-like abdomen develops because of a reflexive abdominal muscle spasm that occurs in response to the peritoneal inflammation

235
Q

what are the clinical manifestations of peritonitis?

A

sudden and severe. abdominal rigidity, abdominal tenderness and pain, nausea and vomiting, decreased peristalsis, intestinal obstruction (due to decreased peristalsis), fever, malaise, leukocytosis, indications of sepsis and shock (tachycardia, hypotesion, restlessness, and diaphoresis)

236
Q

what is third spacing?

A

a phenomenon that occurs with peritonitis where large volumes of fluid can leak into the peritoneal cavity leading to hypovolemic shock

237
Q

chronic inflammation of the GI tract, usually the intestines

A

inflammatory bowel disease (IBD)

238
Q

what diseases are encompassed by IBD?

A

Chrohn’s disease, and ulcerative colitis

239
Q

who is IBD more common in?

A

women, caucasians, persons of Jewish descent, and smokers

240
Q

what are IBD conditions characterized by?

A

periods of exacerbations and remissions that can vary in severity

241
Q

what are IBD disorders thought to be caused by?

A

a genetically associated autoimmune state that has been activated by an 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 int he GI tract

242
Q

what can develop from IBD?

A

fluid, electrolyte, and pH imbalances. it can be painful, debilitating and life threatening

243
Q

insidious, slow-developing, progressive condition that often emerges in adolescence, and may occur anywhere along the GI tract, but usually affects the intestines

A

Crohn’s disease

244
Q

what is Crohn’s disease characterized by, what are these called and why?

A

patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations. they are often called skip lesions because they are secparated by areas of normal tissue

245
Q

what causes the intestinal wall to have a cobblestone appearance in Crohn’s disease?

A

the ulcerations combine to form fissures which are separated by nodules

246
Q

what are granulomas?

A

nodules consisting of epithelial and immune cells

247
Q

what eventually occurs because of the cobblestone like appearance that occurs with Crohn’s disease?

A

the entire intestinal wall becomes thick and rigid, the intestinal lumen becomes narrowed and potentially obstructed. granulomas develop on the intestinal wall and nearby lymph nodes because of the chronic inflammation. over time, the damaged intestinal wall loses the ability to process and absorb food and the inflammation stimulates intestinal motility decreasing digestion and absorption

248
Q

what are complications of Crohn’s disease?

A

malnutrition, anemia, fistulas, adhesions, abscesses, intestinal obstructions, perforation, anal fissues, fluid electrolyte and pH imbalances, and delayed growth and development in children

249
Q

what are the manifestations of Crohn’s disease?

A

abdominal cramping and pain, diarrhea, steatorrhea, constipation, palpable abdominal mass, melena, anorexia, mouth ulcers, weight loss, indications of inflammation

250
Q

a progressive condition of the rectum and colon mucosa that usually develops in the second or third decade of life

A

ulcerative colitis

251
Q

what occurs during ulcerative colitis?

A

inflammation causes epithelium loss, surface erosion, and ulceration. ulceration begins in the rectum and extends in a continuous segment to involve the entire colon. the mucosa becomes inflamed, edematous, and frail. necrosis of the eopithelial tissue can result in abscesses

252
Q

does ulcerative colitis affect the small intestine?

A

rarely

253
Q

what happens with ulcerative colitis as the body attempts to heal?

A

as the body attempts to heal, granulation tissue is formed but the tissue remains fragile and bleeds easily. the ulcers combine, creating large areas of stripped mucosa

254
Q

why do fluid, electrolyte, pH, and nutritional imbalances occur with ulcerative colitis?

A

there is lack of an adequate surface for absorption due to the amount of ulcers stripping away intestinal mucosa

255
Q

what are complications of ulcerative colitis?

A

malnutrition, anemia, hemorrhage, perforation, strictures, fistulas, pseudopolyps, toxic megacolon, colorectal carcinoma, liver disease, fluid electrolyte and pH imbalances

256
Q

life-threatening condition caused by rapid dilation of the large intestine, seen with ulcerative colitis

A

toxic megacolon

257
Q

what are the clinical manifestations of ulcerative colitis?

A

frequent diarrhea containing blood and mucus (as many as 20 daily), tenesmus, proctitis, abdominal cramping, nausea and vomiting, weight loss, indications of inflammation

258
Q

persistent rectal spasms associated with the need to defecate. seen as a manifestation of ulcerative colitis

A

tenesmus

259
Q

chronic, noninflammatory, GI condition characterized by exacerbations associated with stress. includes alterations in bowel patterns and abdominal pain not explained by structural or biochemical abnormalities and does not cause permanent intestinal damage.

A

irritable bowel syndrome (IBS). it is not as serious as IBD.

260
Q

who is IBS more common in?

A

women

261
Q

what things are thought to trigger IBS?

A

stress, food, hormone changes, and/or GI infections. it is thought to be an intensified response to stimuli that is characterized by increased intestinal motility and contractions

262
Q

what are complications seen with IBS?

A

hemorrhoids, nutritional defecits, social issues, and sexual discomfort

263
Q

what are clinical manifestations of IBS?

A

abdominal distention, fullness, flatus, and bloating; intermittent abdominal pain exacerbated by eating and relieved by defecations; chronic and frequent constipation, usually accompanied by pain; nonbloody stool that may contain mucus; bowel urgency; intolerance to certain foods (especially those that cause gas and those containing sorbitol lactose and gluten); emotional distress; anorexia

264
Q

what are diverticula?

A

outwardly bulging pouches of the intestinal wall that develop when mucosa sections or large intestine submucosa layers herniate through a weakened muscular layer

265
Q

condition related to the development of diverticula

A

diverticular disease

266
Q

is diverticular disease congenital or acquired?

A

it may be either

267
Q

what are the risk factors for developing diverticular disease?

A

poor diet which is low in fiber and poor bowel habits that result in chronic constipation

268
Q

why does diverticular disease occur because of constipation?

A

the muscular wall can become weakened from the prolonged effort of moving hard stools, pressure increases in the intestine in an attempt to propel the stool, forcing the mucosa through areas of weakness

269
Q

where is diverticular disease rare and where is it more common? why?

A

rare in developing countries, but more common in developed countries because the diets in developed countries contain more processed foods and low-fiber diets are more common

270
Q

asymptomatic diverticular disease where there are usually multiple diverticula present

A

diverticulosis

271
Q

state in which diverticula have become inflamed, usually because of retained fecal matter

A

diverticulitis

272
Q

what can diverticulitis result in?

A

potentially fatal obstructions, infection, abscess, perforation, peritonitis, hemorrhage, and shock. often remains asymptomatic until the condition becomes serious

273
Q

when are clinical manifestations seen with diverticulitis? what are they?

A

when the condition becomes serious. abdominal cramping followed by the passing of a large quantity of frank blood. bleeding may last hours to days and then stop spontaneously; low-grade fever; abdominal tenderness (usually lower left quadrant); abdominal distention; constipation; obstipatoin; nausea; vomiting; a palpable abdominal mass; and leukocytosis

274
Q

oral cancer can occur anywhere in the mouth, but most are what?

A

squamous cell carcinomas of the tongue and mouth floor

275
Q

what are risk factors for the development of oral cancers?

A

smoked and smokeless tobacco, alcohol consumption, viral infections (especially with the human papilloma virus), immunodeficiencies, inadequate nutrition, poor dental hygiene, chronic irritation, and exposure to ultraviolet light

276
Q

who is more likely to have oral cancer?

A

men are twice as likely as women, african americans

277
Q

is oral cancer very treatable?

A

yes, in its early stages, but most cases are advanced by the time diagnosis is made because the cancer tends to be hidden

278
Q

how does oral cancer initially appear?

A

as a painless, whitish thickening that develops into a nodule or ulcerative lesion. multiple lesions may become present. these lesions persist, do not heal, and bleed easily

279
Q

what are the manifestations of oral cancer?

A

a lump, thickening or soreness in the mouth, throat, or tongue as well as difficulty chewing or swallowing.

280
Q

where does oral cancer often metastasize to?

A

neck lymph nodes and the esophagus

281
Q

what are the most common types of cancer that cause esophageal cancer?

A

squamous cel carcinoma or adenocarcinoma

282
Q

who does esophageal cancer most often affect?

A

men

283
Q

where is esophageal cancer most common? what is it associated with?

A

most common in the distal esophagus. it is associated with chronic irritation and obesity

284
Q

in what ways can the tumors of esophageal cancer grow?

A

they can grow to match the circumference of the esophagus, creating a stricture or they can grow out into the lumen of the esophagus, creating an obstruction

285
Q

what are complications associated with esophageal cancer?

A

esophageal obstruction, respiratory compromise, and esophageal bleeding

286
Q

why is prognosis poor with esophageal cancer?

A

because it is usually asymptomatic in its early stages, so it is not diagnosed until later in its progression

287
Q

what are the clinical manifestations for esophageal cancer?

A

dysphagia, odynophagia, chest pain, weight loss, hematemesis, and halitosis

288
Q

what type of cancer usually causes pancreatic cancer?

A

adenocarcinoma

289
Q

who does pancreatic cancer occur most frequently in?

A

men and african americans

290
Q

what are risk factors for the development of pancreatic cancer?

A

family history, obesity, chronic pancreatitis, long-standing diabetes mellitus, cirrhosis, alcohol abuse, and tobacco abuse

291
Q

why is prognosis usually bad for people with pancreatic cancer?

A

it is often asymptomatic until it is well advanced and has metastasized

292
Q

what are the clinical manifestations of pancreatic cancer?

A

upper abdominal pain that may radiate to the back, jaundice, dark urine and clay-colored stools, indigestion, anorexia, weight loss, depression, malnutrition, hyperglycemia, increased clotting tendencies

293
Q

what does colorectal cancer most often develop from?

A

an adenomatous polyp

294
Q

where is colorectal cancer common?

A

it is very common and fatal in the US and worldwide

295
Q

incidence and mortality rates for colorectal cancer are most common among….

A

men and african americans

296
Q

what are risk factors for the development of colorectal cancer?

A

dietary factors: excessive intake of fat, calories, red meat, processed meat, and alcohol and a deficient intake of fiber. family history, advancing age, obesity, tobacco use, physical inactivity, and IBD

297
Q

what are the clinical manifestations of colorectal cancer?

A

lower abdominal pain and tenderness, blood in the stool, diarrhea, constipation, or other change in bowel habits, intestinal obstruction, narrow stools, unexplained anemia, unintentional weight loss

Pathophysiology (11 decks)

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