Pathoii Digestive

Front 1

d/o of motility-dysphagia-what is it?

Back 1

dysphagia is difficulty swallowing.

Front 2

What are the general causes of dysphagia?

Back 2

mechanical obstruction of the esophagus or a functional d/o that impairs esophageal motility

Front 3

How are mechanical obstructions classified?

Back 3

Intrinsic or extrinsic

Front 4

Describe intrinsic mechanical obstructions in dysphagia

Back 4

-intrinsic obstructions originate in the wall of the esophageal lumen. Tumors, strictures, and diverticular herniations (outpouchings) are all causes of intrinsic mechanical obstructions

Front 5

Describe extrinsic mechanical obstructons

Back 5

extrinsic mechanical obstructions originate outside the esophageal lumen and narrow the esophagus by pressing inward on the esophageal wall. The most common cause of extrinsic mechanical obstruction is tumor

Front 6

What is functional dysphagia?

Back 6

caused by neural or muscular disorders that interfere with voluntary swallowing or peristalsis

Front 7

functional dysphagia and voluntary phase of swallowing- what is it and give examples?

Back 7

disorders that affect the striated muscles of the upper esophagus interfere with the oropharyngeal (volunteer) phase of swallowing.
-typical causes of functional dysphagia in the upper esophagus are dermatomyositis (a muscle diseases) and neurological impairments by cerebrovascular accidents, Parkinson disease, or achalasia

Front 8

What is achalasia? r/t dysphasia?

Back 8

achlasia is a rare d/o r/t
1) denervation of smooth muscle in the middle and lower portions of the esophagus, and..
2) failure of the lower esophageal sphincter (LES) to relax causing functional obstruction of the lower esophagus

Front 9

Achalasia results from..

Back 9

achalasia results from an unknown cause of the autoimmune destruction of myenteric ganglion cells and atrophy of smooth muscle cells
-food accumulates above the obstruction, distends the esophagus, and causes dysphagia
-as hydrostatic pressure increases, food is slowly forced past the obstruction into the stomach

Front 10

clinical manifestations of dysphagia vary according to..

Back 10

clinical manifestations of dysphagia vary accoding to the cause and location of the obstruction

Front 11

Dysphagia and pain while eating/drinking

Back 11

-distention and spasm of the esophageal muscles during eating or drinking may cause a mild or severe stabbing pain at the level of obstruction
-retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, and weight loss are common manifestations of all types of dysphagia
-aspiration of esophageal contents can lead to pneumonia

Front 12

Dysphagia-pain with obstructions of upper esophagus

Back 12

-discomfort occuring 2-4 seconds after swallowing is more common in obstructions of the upper esophagus

Front 13

If the cause of obstruction is a growing tumor, dysphagia and swallowing..

Back 13

-if the cause of obstruction is a growing tumor, dysphagia begins with difficulty swallowing solids and advances to difficulty swallowing semisolids and liquids

Front 14

If the source of dysphagia is neuromotor function, swallowing..

Back 14

-dysphagia is experienced with both solids and liquids if the cause is loss of neuromotor function

Front 15

Dysphagia-pain and lower esophagus

Back 15

discomfort occuring 10-15 seconds after swallowing is more common in obstruction of the lower esophagus

Front 16

Common clinical manifestations of all types of dysphagia

Back 16

-retrosternal pain
-regurgitation of undigested food
-unpleasant taste
-vomiting
-weight loss
above are common manifestations of all types of dysphagia

Front 17

Aspiration of esophageal contents..

Back 17

can lead to pneumonia

Front 18

How to manage sx of dysphagia?

Back 18

eating slowly, eating small meals, taking fluid with meals, and sleeping with head elevated to prevent regurgitation and aspiration
-mechanical dilation of the esophageal sphincter w/ surgical separation of the lower esophageal muscles with a longitudinal incision (myotamy-which widens the passage into the stomach)

Front 19

What is GERD?

Back 19

gastroesophageal reflux disease (GERD) is the reflux of chyme from the stomach to the esophagus

Front 20

In GERD-effect on LES

Back 20

LES (lower esophageal sphincter) may relax spontaneously and transiently 1-2 hrs after eating, permitting gastric contents to regurgitate into the esophagus

Front 21

GERD-how is acid after regurgitation usually neutrolized

Back 21

-the acid is usualy neutralized and cleared from the esophagus by peristaltic action within 1-3 minutes, and sphincter tone is restored.

Front 22

What is physiologic reflux?
What is NERD?

Back 22

-gastroesophageal reflux that does not cause sx is known as physiologic reflux
-in nonerosive reflux disease (NERD), ppl have symptoms of reflux disease but no visible esophageal mucosal injury

Front 23

What is reflux esophagitis?

Back 23

esophageal hypersensitivity is common. In some individuals, however, a combo of factors cause injury and an inflammatory response to reflux called reflux esophagitis

Front 24

Risk factors for GERD?

Back 24

include obesity and Helibacter pylori
-GERD may be a trigger for asthma or chronic cough

Front 25

GERD causes

Back 25

-dysfunction of LES
-hiatal hernia
-delayed gastric emptying
-increased acidity of gastric contents
-increased intraabdominal pressure
Patho: infl response of esophagus-->reflux esophagus

Front 26

LES in normal persons vs those with reflux esophagitis

Back 26

-normally the resting tone of the LES maintains a zone of high pressure that prevents gastroesophageal reflux
-in those with reflux esophagitis, this pressure tends to be lower than normal f/ either transient relaxation or weakness of the sphincter

Front 27

What can cause the development of reflux esophagitis?

Back 27

vomiting, coughing, lifting, bending, or obesity increases abdominal pressure contributing to the development of reflux esophagitis
-delayed gastric emptying contributes to reflux esophagitis by (1) lengthening the period during which reflux is possible and (2) increasing the acid content of chyme

Front 28

D/o that delay emptying include..

Back 28

include gastric or duodenal ulcers, which can cause pyloric edema; strictures that narrow the pylorus; and hiatal hernia, which can weaken the LES

Front 29

Do contents of gastric contents affect severity of esophagitis?
-How does strength of esophageal peristalsis affect severity of esophagitis?

Back 29

yes-if the chyme is highly acidic, or contains pepsin, bile salts, and pancreatic enzymes, reflux esophagitis can be severe
-In ppl with weak esophageal peristalsis, refluxed chyme remains in the esophagus longer than usual and inc amt of time the esophageal mucosa is exposed to acids, pepsin, bile, and enzymes

Front 30

complications of reflux esophagitis

Back 30

reflux esophagitis causes inflammatory responses in the esophageal wall, such as hyperemia, inc capillary permeability, edema, tissue fragility, erosion, and ulcerations.
-fibrosis, basal cell hyperplasia, and elongation of papillae are common
-precancerous lesions can be a long term consequence

Front 31

clinical manifestations of reflux esophagitis..

Back 31

the clinical manifestations of reflux esophagitis are heartburn, regurgitation of acidic chyme, and upper abdominal pain w/in 1 hr of eating

Front 32

The symptoms worsen if the individual..
sx can be present even if..

Back 32

lies down or if intra-abdominal pressure increases-ie as a result of coughing, vomiting, or straining at stool

Front 33

Heartburn may be experienced as..

Back 33

-heartburn may also be experienced as chest pain, which requires ruling out cardiac

Front 34

What is a related complication that may result?

Back 34

-edema, fibrosis (strictures), esophageal spasm, or decreased esophageal motility may result in dysphagia

Front 35

Most common treatment for reflux esophagitis?

Back 35

-proton pump inhibitors
-others..HOB elevation, weight reduction, smoking cessation

Front 36

What is a hiatal hernia?

Back 36

Hiatal hernia, a type of diaphragmatic hernia, is the protrusion (herniation) of the upper part of the stomach through the diaphragm and into the thorax

Front 37

What are the two types of hiatal hernia?

Back 37

1) sliding (direct) hiatal hernia
2) paraesophageal (rolling) hiatal hernia

Front 38

In sliding hiatal hernia, the stomach..

Back 38

In sliding hiatal hernia (90% of cases), the stomach slides or moves into the thoracic cavity through the esophageal hiatus, an opening in the diaphgragm for the esophagus and vagus nerves

Front 39

In sliding hiatal hernia, what contributes to the hernia?

Back 39

a congenitally short esophagus, trauma, or weakening of the diaphragmatic muscles at the gastroesophageal junction contributes to the hernia

Front 40

Why is it called sliding hiatal hernia?

Back 40

While the individual is in the supine posn, the lower esophagus and stomach are pulled into the thorax
-standing causes the stomach to "slide" back into the abdomen

Front 41

Sliding hiatal hernia is exacerbated by..

Back 41

sliding hiatal hernia is exacerbated by factors that increase intra-abdominal pressure. Therefore, coughing, bending, tight clothing, ascites, obesity, or pregnancy accentuates the hernia.

Front 42

What is sliding hiatal hernia associated with ?

Back 42

this type of hernia is associated is associated with gastoesophageal reflux and esophagitis b/c the hernia diminishes the resting pressure of the LES.

Front 43

Pregnant women with sliding hiatal hernia

Back 43

progesterone and estrogen may lower the resting pressure of the LES further

Front 44

What is paraesophageal hiatal hernia?

Back 44

Paraesophageal hiatal hernia (or rolling hiatal hernia) is herniation of the greater curvature of the stomach through a secondary opening in the diaphragm

Front 45

The entire stomach can..
and as the stomach..

Back 45

In paraesophageal hiatal hernia, the entire stomach can pass into the thorax

Front 46

As the stomach..

Back 46

-as the stomach protrudes through the opening into the thorax, it lies alongside the esophagus
-the gastroesophageal junction remains below the diaphragm

Front 47

Is reflux common with paraesophageal hiatal hernia?

Back 47

No. Reflux is uncommon with this type of hernia. The position of a portion of the stomach above the diaphragm, however, causes congestion of mucosal blood flow and can lead to gastritis and ulcer formation

Front 48

What is a major complication of paraesophageal hiatal hernia?

Back 48

a mechanical strangulation of the hernia is a major complication, and surgical correction is requred
-strangulation occludes blood vessels and causes vascular engorgement, edema, ischemia, and hemorrhage

Front 49

Hiatal hernias of both types tend to ccur..

Back 49

in conjunction with several other diseases, including reflux, peptic ulcer, cholecystitis (gallbladder inflammation), cholelithiasis (gallstones), chronic pancreatitis, and diverticulitis

Front 50

Why are manifestations of hiatal hernia difficult to distinguish?
-even so, what are they?

Back 50

-hiatal hernias are often asymptomatic
-generally a wide variety of sx develop later in life and are associated with other GI d/o as well
-manifestations of the various types of hiatal hernia are difficult to distinguish and include..gastroesophageal reflux, dysphagia, heartburn, vomiting, and epigastric pain
-regurgitation and substernal discomfort after eating are common

Front 51

Tx for hiatal hernia

Back 51

is usually conservative
-the individual can diminish reflux by eating small, frequent meals and avoiding the recumbent position after eating
-abdominal supports and tight clothes are avoided, and wt control is rec for obese ppl
-antacids alleviate reflux esophagitis
-Anticholinergic drugs are CONTRAindicated b/c they relax the LES and delay gastric emptying
-ppl who are uncomfy at night benefit from sleeping in semi-Fowler posn, surgery may be performed if other measures fail

Front 52

Intestinal obstruction can be caused..

Back 52

intestinal obstruction can be caused by any condition that prevents the normal flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstruction lesion (ileus).

Front 53

intestinal obstruction-what is the more common site of obstruction and why?

Back 53

the small intestine is more commonly obstructed b/c of its narrower lumen

Front 54

intestinal obstruction is classified by cause as...

Back 54

simple or functional
-simple obstruction: is mechanical blockage of the lumen by a lesion
-functional obstruction is a failure of motility (paralytic ileus) and is common after gastrointestinal or abdominal surgery...ie anesthesia, local inflammatory rxn, and hyperactivity of sympathetic NS contribute to postop ileus

Front 55

What is the most common type of intestinal obstruction?

Back 55

simple obstruction of the small intestine from fibrous adhesions is the most common type of intestinal obstruction

Front 56

acute obstructions usually have ___ causes

Back 56

acute obstructions usually have mechanical causes, such as adhesions or hernias

Front 57

chronic or partial obstructions are more often associated with..

Back 57

tumors or inflammatory d/o, particularly of the large intestine

Front 58

intussescption? what is it and what population is it common in?

Back 58

intussescption is when a part of the intestine invaginates into another section of intestine, like a collapsable telescope. It's usually non-emergent, sx N/V, abd pain, bloody stool. Tx-us. an enema is sufficient

-intusception is rare in adults compared to the more frequent occurence in infants

Front 59

the consequences of intestinal obstruction are related to..

Back 59

its onset and location, the length of intestinal tract proximal to the obstruction, and the presence and severity of ischemia

Front 60

PATHO of intestinal obstruction

Back 60

page 1463 in book

Front 61

the most common causes of small intestin obstruction..

Back 61

are intra-abdominal adhesions, hernias, and neoplasms

Front 62

Small intestine obstruction leads to..(long patho)

Back 62

the accumulation of fluid and gas inside the lumen proximal to the obstruction (can't get past it)
-fluids accumulate from impaired water and e- absorption and enhanced secretion with net movement of fluid f/ the vascular space to the intestinal lumen
-gas from swallowed air, and to a lesser extent f/ bacteria overgrowth, contributes to the distention
-distention begins almost immed, as gases and fluids accumulate proximal to the obstruction
-distention decreases the intestine's ability to absorb water and electrolytes and increses the net secretion of these substances into the lumen

Front 63

What is the result of this increase of secretion into the lumen? in small intestine obstruction

Back 63

-within 24 hours, up to 8 L of fluid and electrolytes enter the lumen in the form of saliva, gastric juice, bile, pancreatic juice, and intestinal secretions
-copious vomiting or sequestration of fluids in the intestinal lumen prevents their rreabsorption and produces severe fluid and electrolyte disturbances
-extracellular fluid volume and plasma volume decrease, causing dehydration
-hemoconcentration (decreased plasma volume (elevates hematocrit, decreases central venous pressure, and cauess tachycardia.
-severe dehydration --> hypovolemic shock

Front 64

in what case does metabolic alkalosis develop, and why?

Back 64

if the obstruction is at the pylorus or high in the small intestine, metabolic alkalosis develops initially as a result of excessive loss of hydrogen ions that would be reabsorbed from the gastric juices

Front 65

metabolic acidosis-in what case does it develop and why?

Back 65

with prolonged obstruction or obstruction lower in the intestine, metabolic acidosis is more likely to occur b/c bicarbonate f/ pancreatic secretions and bile cannot be reabsorbed
-metabolic acidosis may also be accentuated by ketosis, the result of declining CHO stores caused by starvation

Front 66

Effect of hypokalemia

Back 66

Hypokalemia (K is reabsorbed in the small intestine) can be extreme, promoting acidosis and atony (loss of muscle strength) of the intestinal wall

Front 67

If pressure from the distention is severe enough, it..

Back 67

If pressure from the distention is severe enough, it occludes the arterial circulation and causes ischemia, necrosis, perforation, and peritonitis

Front 68

Fever and leukocytosis are often associated with..

Back 68

loss of intestinal motility, overgrowth of bacteria, strangulation, and bowel necrosis

Front 69

Lack of circulation permits the buildup of..worsening..

Back 69

significant amounts of lactic acid, which worsen the metabolic acidosis.

Front 70

Bacterial proliferation and translocation across the mucosa to the ... causes ...

Back 70

bacterial proliferation and translocation across the mucosa to the mesenteric lymph nodes or systemic circulation cause periotonitis or sepsis
-the release of inflammatory mediators into the circulation causes remote organ failure

Front 71

The most common causes of large bowel obstruction are..

Back 71

malignancy, volvulus (twisting), and strictures r/t diverticiulitis

Front 72

consequences of colonic or large bowel obstruction are r/t..

Back 72

the competence of the ileocecal valve, which normally prevents reflux of colonic contents into the small intestine

Front 73

When the ilieocecal valve is competent..

Back 73

the cecum cannot decompress into the small intestine resulting in distention. Ischemia occurs when the intraluminal pressure exceeds capillary pressure in the lumen

Front 74

What is Ogilvie syndrome?

Back 74

Acute colonic pseudo-obstruction (Ogilvie syndrome) is a massive dilation of the large bowel that occurs in critically ill patients, and immobilized older adults. It is characterized by significant dilation of the cecum and absence of mechanical obstruction

Front 75

S/sx of small intestine obstruction are consistent with the pathophysiology. What is colicky pains caused by?

Back 75

Colicky pains caused by distention followed by vomiting are the cardinal sx. Typically the pain occurs intermittently. Pain intensifies for seconds or minutes as a peristaltic wave of muscle contraction meets the obstruction. The passing of the wave is followed by a pain-free interval. Pain may be continuous with severe distention and then diminish in intensity. if strangulation occurs, the pain loses its colicky character, becoming more constant and severe as ischemia progresses to necrosis or perforation. Sweating, nausea, and hypotension occurs as an autonomic NS response.

Front 76

Vomiting and distention with intestine obstruction in proximal small intestine

Back 76

-obstruction in the proximal small intestine causes mild distention and vomiting of bile-stained fluid

Front 77

Obstruction in the pylorus causes..

Back 77

obstruction at the pylorus causes early, profuse vomiting of clear gastric fluid

Front 78

obstruction lower in the small intestine and distention

Back 78

obstruction lower in the small intestine causes more pronounced distention because a greater length of intestine is proximal to the obstruction. In this case, vomiting may not occur or may occur later and contain fecal material.

Front 79

Partial obstruction can cause.. complete obstruction causes..

Back 79

Partial obstruction can cause.. diarrhea or constipation, but complete obstruction usually causes constipation only.

Front 80

Complete obstruction increaes..

Back 80

complete obstruction increases the number of bowel sounds, which may be tinkly and accompanied by peristaltic rushes and crampy, abdominal pain

Front 81

Complete obstruction other complications

Back 81

signs of dehydration, hypovolemia, and metabolic acidosis may be observed as early as 24 hrs after the occurence of complete obstruction. Distention may be severe enough to push against the diaphragm and decrease lung volume. This can lead to atelectasis and pneumonia, particularly in debilitated individual.

Front 82

Explain colonic obstruction

Back 82

colonic obstruction usually presents as hypogastric pain and abdominal distention. Pain can vary from vague to excruciating, depending on the degree of ischemia and the development of peritonitis. Colon cancer is the most common cause, followed by diverticular strictures or volvulus.

Front 83

treatment for intestinal obstruction..

Back 83

replacement of fluid and electrolytes and decompression of the lumen with gastric or intestinal suction are essential forms of therapy
-immediate sx intervention is required for strangulation and complete obstruction.

Front 84

What is gastritis?

Back 84

gastritis is an inflammatory disorder of the gastric mucosa

Front 85

Is gastritis acute or chronic? What can it affect?

Back 85

Gastritis can be acute or chronic and can affect the fundus or antrum or both

Front 86

What does acute gastritis do?

Back 86

acute gastritis erodes the surface epithelium in a diffuse or localized pattern. The erosions are usually superficial

Front 87

What usually causes acute gastritis?

Back 87

usually injury of the protective mucosal barrier by drugs, chemicals, or H pylori infection. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, naproxen, indomethacin, are known to cause erosive gastritis b/c they inhibit prostaglandins, which normally stimulate the secretion of mucus. Alcohol, histamine, digitalis, and metabolic d/o such as uremia are contributing factors. H pylori infection causes inflammation, pain, n/v

Front 88

The clinical manifestations of acute gastritis can include..

Back 88

vague abdominal discomfort, epigastric tenderness, and bleeding.

Front 89

When does healing usually occur with acute gastritis?

Back 89

usually occurs spontaneously within a few days

Front 90

What promotes healing in acute gastritis?

Back 90

discontinuing injurious drugs, using antacids, or decreasing acid secretion with a histamine H2 receptor antagonist and proton pump inhibitor also promote healing

Front 91

Who does chronic gastritis tend to affect?

Back 91

chronic gastritis tends to occur in older adults and causes chronic inflammation, mucosal atrophy, and epithelial metaplasia.

Front 92

how is chronic gastritis usually classified?

Back 92

usually classified as type A, or immune (fundal), or type B, nonimmune (antral), depending on the pathogenesis and location of the lesions

Front 93

What is the most rare and severe type?

Back 93

chronic fundal gastritis is the most rare and severe type

Front 94

What happens in chronic fundal gastritis?

Back 94

the gastric mucosa degenerates extesnsively in the body and fundus of the stomach, leading to gastric atrophy
-loss of chief cells and parietal cells diminishes secretion of pepsinogen, hydrochloric acid, and intrinsic factor
-b/c acid secretion is insufficient, the feedback mechanism that normally inhibits gastrin secretion is impaired, causing elevated plasma levels of gastrin

Front 95

What can these mechanisms of chronic fundal gastritis cause?

Back 95

pernicious anemia can develop b/c intrinsic factor is less available to facilitate Vitamin B12 absorption

Front 96

What do a significant number of individuals with chronic fundal gastritis have?

Back 96

antibodies to parietal cells, intrinsic factor, and gastric cells in their sera, suggesting that an autoimmune mechanism is involved in the pathogenesis of the disease

Front 97

What does chronic fundal gastritis often co-occur with?

Back 97

other autoimmune diseases, ie diabetes, addisons disease, and thyroid disease..strengthening the association that an autoimmune mechanism is involved

Front 98

chronic fundal gastritis is a risk factor for?

Back 98

for gastric carcinoma, particularly in individuals who develop pernicious anemia

Front 99

chronic antral gastritis generally involves..

Back 99

the antrum only and is approximately four times more common than funda gastritis

Front 100

As opposed to chronic fundal gastritis, chronic antral gastritis is NOT associated with..

Back 100

decreased hydrochloric acid secretion, pernicious anemia, or presence of parietal cell antibodies

Front 101

several factors are associated with chronic antral gastritis, including..

Back 101

use of alcohol, tobacco, and NSAIDs. H pylori is a major causative factor associated with chronic atrophic antral gastritis and peptic ulcer disease

Front 102

The host response to H Pylori is..

Back 102

activation of T and B lymphocytes with infiltration of neutrophils. Release of inflammatory cytokines, ie interleukin damage the gastric epithelium

Front 103

What may contribute to gastritis?

Back 103

chronic reflux of bile, disrupting the mucosal barrier

Front 104

The presence of antiparietal cell antibody is specific for..

Back 104

type A gastritis

Front 105

H. Pylori infection secretion confirms..

Back 105

achlorhydria (diminished secretion of hydrochloric acid)

Front 106

The gastric secretions can also be evaluated for the presence of..

Back 106

intrinsic factor

Front 107

Symptoms of chronic gastritis

Back 107

vague symptoms-anorexia, fullness, n/v, epigastric pain, gastric bleeding may be the only clinical manifestation of gastritis. There is increased risk for gastric carcinoma with chronic H pyloris infection

Front 108

Symptom relief for chronic gastritis

Back 108

usually be managed with smaller meals, a soft bland diet, and avoidance of alcohola nd nsaids, combo of antibiotics used to treat h pylori, gitamin B12 is administered to correct pernicious anemia

Front 109

peptic ulcer disease-what is a peptic ulcer?

Back 109

a peptic ulcer is a break, or an ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum

Front 110

What are two major risk factors for peptic ulcer disease?

Back 110

H. pylori infections of the gastric mucosa and habitual use of NSAIDs
-alcohol and smoking may influence susceptibility to ulcer disease
-some chronic diseases also associated with its development, ie emphysema, RA, cirrhosis
-psychological stress may be, although inconclusive
-exact causation not known

Front 111

Are peptic ulcers acute or chronic?

Back 111

-can be acute or chronic, and superficial or deep

Front 112

What are erosions with peptic ulcers?

Back 112

-superficial ulcerations are called erosions b/c they erode the mucosa but do not penetrate the muscularis mucosae

Front 113

What are true ulcers with peptic ulcer disease?

Back 113

true ulcers extend through the uscularis mucossae and damage blood vessels causing hemorrhage or perforate the GI wall

Front 114

Why are chronic use of NSAIDs a cause of peptic ulcer disease?

Back 114

chronic use of NSAIDs suppress mucosal prostaglandin synthesis resulting in decreased bicarbonate secretion and mucin production and increased secretion of hydrochloric acid

Front 115

What does disruption of the mucosa do?

Back 115

disruption of the mucosa exposes submucosal areas to gastric secretions and autodigestion causing erosion and ulceration

Front 116

What is h. pylori? What are some bad effects of it? **this box given in class to refer to..long, also see pictures in slide Digestive 1

Back 116

H pylori is a gram negative spiral bacterium with a flagella and is a major cause of acute chronic gastritis, peptic ulcer disease in the duodenum and sstomach, gastric adenocarcinoma, and gastric mucosa associated lymphoid tissue (MALT)
-h pylori is transmitted thru the fecal oral route and is usually acquired in childhood, infection is asymptomatic in about 70% of cases.
-in other cases, inflammation and immune responses promote mucosal ulcerations or prevent healing of injured tissue. Pathogenic and virulence factors include:
-an ability to colonize and adhere to gastric epithelial cells
-the possession of flagella that allows movement through the luminal mucous layer to a site of a higher pH
-an ability of adherent strains to suppress acid secretion to improve their survival
-secretion of urease that produces ammonia results in a more alkaline environment
-release of vacuolating cytotoxin (VacA) that promotes bacterial survival and causes epithelial injury
-the presence of cytotoxin-associated gene (CagA) strains that can escape normal immune responses and cause inflammation with release of inflammatory cytokines and reactive oxygen metabolites that damages mucosal epithelial cells and loss of the protective mucosal barrier
-recruitment and activation of neutrophils, macrophages, and mast cells with release of inflammatory cytokines (tumor necrosis factor alpha TLF-alpha, interleukin, (IL)-1,6,8, histamine) that promotes cellular injury
-down-regulation of antral somastatin leading to increased gastrin, increased acid, impaired mucosal bicarbonate production, and increased mucosal exposure to acid and pepsin
-activation or inhibition of T and B cell immune responses that may contribute to mucosal injury
-release of cytokines and chemokines that promote gastric epithelial cell death (apoptosis) and cell proliferation that can result in atrophy, ulcers, or malignant growht


-gene-environment interaction and different pathogenic strains of h pylori increase risk for disease
-patterns of gastritis and disease progression vary by site of infection and strain of h pylori.

Front 117

What is peptic ulcer an "umbrella" term for?

Back 117

A break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. Such breaks expose submucosal areas to gastric secretions and autodigestion. Normally, the gastric and duodenal mucosa are protected from acid and pepsin by mucus and bicarbonate that are secreted by surface epithelial cells. Also, cellular tight junctions prevent back-diffusion of acid

Front 118

duodenal ulcers and frequency

Back 118

occur with greater frequency than other types of peptic ulcers, and affect 10-15% of the population, younger persons, type O blood

Front 119

Factors that are associated with duodenal ulcer include:

Back 119

factors other than H pylori and use of NSAIDs that may be associated with duodenal ulcer:
-increased mass of gastric parietal cells
-serum gastrin levels that remain high longer than normal after eating and continue to stimulate secretion of acid and pepsin (may be caused by H pylori in gastric antrum)
-failure of the feedback mechanism whereby acid in the gastric antrum inhibit gastric release
-rapid gastric emptying, which overwhelms the buffering capacity of the bicarbonate0rich pancreatic secretions
-acid production stimulated by cigarette smoking
-decreased duodenal mucosal bicarbonate secretion

Front 120

all these factors..

Back 120

all these factors, singly or in combo, cause acid and pepsin concentrations in the duodenum to penetrate the mucosal barrier and lead to ulceration

Front 121

Thec haracteristic manifestation of duodenal ulcer..

Back 121

chronic intermittent pain in the epigastric area, pain begins 30 min to 2 hrs after reating, when the stomach is empty, middle of the night often and disappear by morning, pain results from sensorineural stimulation by acid, muscle spasm, or both,
-relieved by food or antacids

Front 122

Is there a link of H Pylori and duodenal cancer?

Back 122

no, and it's not clear why there is not

Front 123

How can acid secretions be suppressed?

Back 123

with drugs that block H2 receptors and inhibit the secretion of acid, proton pump inhibitors inhibit acid production
-anticholinergic drugs may be used to inhibit gastric secretion, suppress gastric motility, and delay gastric emptying

Front 124

gastric (peptic) ulcer what happens to as a result of decreased mucosal protection?

Back 124

decreased mucosal protection = increased hydrogen permeable
-normal to low gastric secretions
-h pylori
-posisble decrease in prostaglandins
-duodenal reflux of bile

Front 125

duodenal ulcer (peptic ulcer) what happens?

Back 125

-h pylori
-increased of acid and pepsin at duodenum
-inadequate secretion of bicarbonate
-mucosa damage

Front 126

Cleft lip..what is it? causes it?

Back 126

-cleft lip is caused by incomplete fusion of the nasomedial or intermaxillary process during the second month of embryonic development

Front 127

Does cleft lip occur with cleft palate?

Back 127

-cleft lip may occur with or without cleft palate

Front 128

The defect in cleft lip is usually where?

Back 128

beneath one or both nostrils and may involve the external nose, the nasal cartilages, the nasal sputum, and the alveolar processes. It may also be associated with a flattening and broadening of the facial features.

Front 129

What is cleft palate, what is it often associated with?

Back 129

-cleft palate is frequently associated with cleft lip, but it can occur alone. The defect may affect only the uvula and soft palate, but it may extend forward through the nostrils thru the hard palate.

Front 130

Cleft palate: if the defect extends thru the hard palate, what are possible complications?

Back 130

If the defect extends thru the hard palate, open communication b/w the structures of the nasopharynx and the oral cavity leads to frequent sinusitis and otis media. Children with orofacial cleft are at risk for S. mutans and Lactobacillus colonization, which can increase caries in the primary dentition.

Front 131

What usually causes cleft lip and cleft palate?

Back 131

usually caused by genetic and environmental factors, and each contributes only a minor developmental defect

Front 132

In cleft lip and palate, what do the genetic and environmental factors do?

Back 132

-these factors reduce the amt of neural crest mesenchyme that migrates into the area that will develop into the embryo's face

Front 133

What is feeding like with cleft lip or palate? Which is more problematic

Back 133

-another major difficulty seen with cleft lip or palate is poor feeding
-b/c suckling involves both the tongue and pressure against the palate, the infant with isolated cleft lip but an intact palate may be breast or bottle fed without great difficulty
-on the other hand, cleft palate may significantly interefere with both. Bottle feeding may require large, soft nipples with an oversized opening. Breast feeding may be impossible for some infants with cleft palate without a prosthesis for the roof of the mouth

Front 134

What is treatment for cleft lip or palate?

Back 134

tx is sx correction, often done in stages. Supportive therapy may include prosthodontics and orthodontics, otolaryngology procedures, and speech and occupational therapy

Front 135

What is pediatric GERD?

Back 135

gastroesophageal reflux disease (GERD) is the return of gastric contents into the esophagus b/c of poor function of the lower esophageal sphincter, which relaxes.

Front 136

Differences in pediatric GER vs GERD: weight

Back 136

GER: regurgitation with normal weight gain
GERD: regurgitation with poor wt gain

Front 137

Differences in pediatric GER vs GERD: esophagitis/pain

Back 137

GER: no s/sx of esophagitis
GERD: persistent irritability, pain in infants, lower chest pain, dysphagia, pyrosis in kids, hematemesis and iron deficiency anemia, esophagitis f/ exposure of esophagus to acidic gastric contents that may cause either strictures or anemia f/ prolonged occult blood loss

Front 138

Differences in pediatric GER vs GERD: respiratory sx

Back 138

GER: no significant respiratory sx
GERD: apnea and cyanosis, wheezing, aspiration or recurrent pneumonia, chronic cough, stridor

Front 139

Differences in pediatric GER vs GERD: neurobehavioral sx

Back 139

GER: no neurobehavioral sx
GERD: neck tilting in infants (Sandifer's syndrome)

Front 140

Clinical manifestations of pediatric GERD:

Back 140

-forceful vomiting with an 85% occurence within the first week of life, aspiration pneumonia in one third of those affected, and poor weight gain

Front 141

pediatric GERD: is some reflux normal?

Back 141

yes, b/c neuromuscular control of the gastroesophageal sphincter is not fully developed. The frequency of reflux is highest in premature infants and decreases during the first 6-12 months of life

Front 142

pediatric GERD is especially troubling in kids with..

Back 142

cerebral palsy and cystic fibrosis

Front 143

What is eosinophilic esophagitis?

Back 143

pediatric disease, atopic disease involving both immediate and delayed hypersensitivity rx to food indigestion

Front 144

What are common manifestations of eosinophilic esophagitis?

Back 144

-dysphagia, food impaction, and vomiting are common

Front 145

Patho of eosinophilic esophagitis?

Back 145

esophagus is infiltrated with eosinophils, associated with inflammation of the entire esophagus that is nonresponsive to acid-suppression therapy

Front 146

Tx of eosinophilic esophagitis?

Back 146

-tx includes elimination diets and corticosteroids.

Front 147

What can eosinophilic esophagitis cause?

Back 147

-the eosinophilic inflammation may lead to progressive subepithelial fibrosis with esophageal strictures, narrowing, and dysphagia

Front 148

What is pyloric stenosis?

Back 148

peds d/o: obstruction of the pyloric sphincter caused by hypertrophy of the sphincter muscle.

Front 149

Is pyloric stenoisis common?

Back 149

it is one of the most common d/o of early infancy and affects infants b/w the ages of 1-2 weeks or 3-4 months. More common in males. More common in white, full term infants. Genetic link, more common in down syndrome infants.

Front 150

What is the cause of pyloric stenosis?:

Back 150

The cause is unknown but increased gastrin secretion by the mother in the last trimester of pregnancy increases the likelihood of pyloric stenosis in the infant.

Front 151

What may cause overproduction of gastric secretion in mom in pyloric stenosis infants?

Back 151

may be caused by stress-related factors.

Front 152

Prostaglandin and pyloric stenosis?

Back 152

-exogenous administration of prostaglandin E is associated with an increased incidence of pyloric stenosis

Front 153

What causes hypertrophy of the sphincter muscle in pyloric stenosis? Patho..

Back 153

the circular muscle of the pylorus is grossly enlarged b/c of an increase in cell size (hypertrophy) and an increase in cell number (hyperplasia). Transforming growth factor-alpha plays a role in stimulating this increase in muscle mass. The mucosal lining of the pyloric is folded and the lumen is narrowed by the encroaching muscle. B/c of the extra peristaltic effort necessary to force the gastric contents thru the narrow pylorus, the muscle layers of the stomach may become hypertrophied as well.

Front 154

Clinical manifestations of pyloric stenosis?

Back 154

2-3 week old infant begins vomiting, gradually projectile
-weight loss, hungry, irritability, constipation, vomit is new food plus retained food f/ previous feeding
"olive" bump at upper right quadrant

Front 155

What is failure to thrive (FTT)? How does it manifest?

Back 155

FTT is the inadequate physical development of an infant or a child. It is manifested as a deceleration in weight gain, a low wt/ht ratio, or a low wt/ht/head circumference ratio.

Front 156

When does FTT present?

Back 156

FTT is a common problem and can present anytime in childhood

Front 157

What is organic FTT?

Back 157

has a pathophysiological cause, such as GERD, pyloric stenosis, gastroenteritis, malabsorption syndromes, infection by intestinal parasites, congenital anomalies, very low birth wt, or chronic diseases of major body systems. All these factors either reduce the availability of nutrients for maintenance and growth or increase nutrient requirements, particularly when there is chronic infx.

Front 158

Weakness and problems in FTT

Back 158

a chronic disease or congenital anomaly that causes weakness or reduced stature can create developmental, psychosocial, and emotional problems for the child

Front 159

What is nonorganic FTT?

Back 159

dx of exclusion, absence of GI, endocrine, chronic diseases. Usually associated with psychosocial deprivation, altho behavioral problems can contribute to occurence in the absence of maternal patholic findings
-behavioral and psychosocial problems may be compounded by inadequate economic resources and lack of knowledge
-often due to unwanted pregnancy/PPD/family stress/crisis/maternal mental illness

Front 160

What is NEC?

Back 160

pediatric EMERGENCY
-Necrotizing enterocolitis (NEC) is an ischemic, inflammatory condition of the bowel that causes necrosis, perforation, and death if untreated

Front 161

Frequency of NEC? Mortality rate?

Back 161

-most common gastrointerestinal emergency in newborn
-overall mortality b/w 12-30%
-biggest risk factor is prematurity, reduce risk if preemies are breastfed, increased risk of fatality with decreased gestational age

Front 162

What is thought to be the cause of NEC?

Back 162

reduced mucosal blood flow leading to hypoxic injury to intestinal mucosa is thought to be the cause
-cause unknown but injury to mucosa of bowel and immune response to inflammation may contribute

Front 163

When is NEC likely to occur?

Back 163

within 2 weeks of birth, with earlier sx in full term infants, the more premature the infant, the greater the incidence of NEC

Front 164

Tx of NEC?

Back 164

remove dead colon, put in ostomy

Front 165

Pediatric bowel obstruction-what is the most common cause of acquired intestinal obstruction in infants?

Back 165

intussusception-ped EMERGENCY

-problem b/c vessels get compressed leads to dec blood flow and engorgement of cessels and bleeding into colon
-infants w/ this have abd pain (crying), draw legs up to red pressure in abd, currant jelly stool and is bloody,

Front 166

What is intussusception

Back 166

the telescoping or invagination of one portion of the intestine into the another, causing intestinal obstruction. Usually, the ileum invaginates the cecum, pushing into the colon
-80-90% of intestinal obstructions in infants and kids are caused by intussusception, more common in females

Front 167

What age is intussusception most common?

Back 167

before 1 year, b/w 4-7 months, infrequent after 36 months, except it occurs in kids of all ages after abdominal sx

Front 168

Clinical manifestations of intussusception?

Back 168

affected infant suddenly develops abdominal pain, becomes irritable (colicky), and draws up the knees.
-vomiting occurs soon afterward
-a single normal stool may be passed, evacuating the colon distal to the apex of the intussusception
-after that, 60% of infants pass "currant jelly" stools, dark and jelly from blood and mucus content
-tender, sausage shaped abdominal mass
-infants often cry f/ pain and draw legs in toward abdomen to reduce abd pressure

Front 169

patho of intussusception

Back 169

the telescoping bowel obstructs blood and lymphatic flow in the direction of peristaltic flow, which causes rapid edema and tissue exudation, gangrene may follow

Front 170

What is childhood diarrhea?

Back 170

Common GI problem during infancy and early childhood, and infectious diarrhea is the leading cause of death worldwide, primarily in young children in developing countries

Front 171

Is prolonged diarrhea more dangerous in adults or kids?

Back 171

more dangerous in kids, b/c they have much smaller fluid reserves than adults. Therefore, dehydration can develop rapidly if any disturbance increases fluid secretion into the GI lumen (secretory diarrhea), draws fluid into the lumen by osmosis (osmotic diarrhea), or prevents fluid absorption in the intestine

Front 172

Diarrhea in ___ is of special concern, and why?

Back 172

Diarrhea in infants is of special concern b/c its cause may be a congenital or metabolic anomaly.
-infants have low fluid reserves and relatively rapid peristalsis and metabolism. Therefore, the danger of dehydration is great

Front 173

acute diarrhea in infants causes

Back 173

-common causes of acute diarrhea in infants include infections, congenital aganglionic megacolon, milk-protein allergies, and NEC.

Front 174

infectious diarrhea in newborns is usually associated with..

Back 174

nursery epidemics like E. coli, Klebsiella, staphylococci, salmonella, and shigella.
-diarrhea caused by these agents has a rapid onset,

Front 175

What is chronic diarrhea considered in children?

Back 175

chronic diarrhea persists for more than 4 weeks

Front 176

What is chronic diarrhea typically caused by?

Back 176

caused by abnormal colonic motility, lactose intolerance, parisitic infection, impaired absorption, and antibiotic use

Front 177

Irritable bowel syndrome-what is it?

Back 177

functional d/o characterized by intermittent episodes of diarrhea, constipation, and pain

Front 178

Is there a cure for IBS?

Back 178

no. Symptomatic tx includes laxatives and fiber, antidiarrheals, antispasmodics, antidepressants, analgesics, and serotonin agonists or antagonists

Front 179

What is the dx for IBS?

Back 179

IBS is not well understood. Dx is pain pattern and bowel pattern, occurence of abdominal pain and GI dysfunction for at least 3x/month for 3 consecutive months

Front 180

What are some theories of IBS?

Back 180

-altered motility (ie diarrhea, constipation)
-alteration in innervation -brain-gut-axis (altered response to stimulus to stool in colon-too much or too little response)
-post infection-often have low grade chronic infection
-overgrowth of flora
-food intolerance/allergy-sometimes a change in diet can help-ie avoid gluten/wheat and symptoms improve
-hormone flunctuation in women-often have increased sx before menses
psychological-in crisis situations have to use BR

Front 181

what are diverticulae?

Back 181

diverticulae are hernations or saclike outpouchings of mucosa through the muscle layers of the colon wall

Front 182

What is diverticulosis?

Back 182

asympomatic diverticular disease

Front 183

What is diverticulitis?

Back 183

represents symptomatic inflammation of diverticular disease, trapped feces (nuts very common) leads to localized infx at the diverticula

Front 184

What are the problems with pouches in diverticulits?

Back 184

problem with pouches is something can stuck

Front 185

Cause behind diverticulitis and physiology behind it

Back 185

-habituatl consumption of low residue (fiber) diet reduces fecal bulk and reduces the diameter of the colon
-according to the law of laplace, wall pressure increases as the diameter of the lumen decreases
-pressure within the narrow lumen can increase enough to rupture the diverticula and cause abscess formation or peritonitis.

Front 186

Tx for diverticulitis

Back 186

-increase of dietary fiber intake frequently relieves sxs
-usually antibiotics outpatient are sufficient
-avoiding nuts/seeds is recommended but some say it doesn't matter, will happen anyway
-surgical resection may be required if there are severe complications

Front 187

Where does diverticulitis most often occur?

Back 187

can occur anywhere in GI tract, most common site the left colon. The diverticula form at weak points in the colon wall, usually where arteries penetrate the tunica muscularis to nourish the mucosal layer

Front 188

Other contributing factors to diverticulitis?

Back 188

abnormal colonic motility with intraluminal hypertension.

Front 189

What herniates in diverticulitis?

Back 189

the colonic mucosa herniates thru the smooth muscle layers

Front 190

What is a common associated finding with diverticulitis?

Back 190

thickening of the circular and longitudinal (teniae coli) muscles surrounding the diverticula. Hypertrophy and contraction of these muscles increase intraluminal pressure and degree of herniation.

Front 191

Law of Laplace

Back 191

wall pressure increases as the diameter of a cylindrical structure decreases. Therefore, pressure within the narrow lumen can increase enough to rupture the diverticula.

Front 192

Fiber and diverticulitis?

Back 192

insoluble dietary fiber deficiency also may change the intestinal microflora, decreasing the immune response in the colon and permit low grade inflammation.

Front 193

Complications of diverticulitis?

Back 193

diverticulitis can cause abscess formation, fistula formation, peritonitis, or obstruction

Front 194

circular/longitudinal muscle in small and large intestine and diverticulitis

Back 194

-circular muscle goes around lumen
-longitudinal muscle in large intestine goes length of it not all the way around
-in small intestine it goes all the way around

Front 195

what is peritonitis?

Back 195

Peritonitis is an inflammation (irritation) of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs.

Front 196

Malabsorption syndromes-in general what it is?

Back 196

malabsorption is failed or faulty digestion b/c of deficiencies of chemical enzymes

Front 197

What are the malabsorption syndromes?

Back 197

pancreatic insufficiency, lactose deficiency, bile salt deficiency

Front 198

Malabsorption syndromes: pancreatic insufficiency: what are pancreatic enzymes and what is pancreatic insufficiency?

Back 198

the pancreatic enzymes (lipase, amylase, trypsin, chymotrypsin) are required for the digestion of proteins, carbs, and fats.
-pancreatic insufficiency is the deficient production of these enzymes by the pancreas

Front 199

Malabsorption syndromes: pancreatic insufficiency: what are some causes?

Back 199

causes of pancreatic insufficiency include chronic pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis

Front 200

Malabsorption syndromes: pancreatic insufficiency: what must occur before the maldigestion?

Back 200

significant damage to or loss of pancreatic tissue must occur before enzyme elvels decrease sufficiently to cause maldigestion

Front 201

Malabsorption syndromes: pancreatic insufficiency: what is the chief problem?

Back 201

although pancreatic insufficiency causes poor digestion of all nutrients, fat maldigestion is the chief problem.
-salivary amylase and enzymes secreted by teh intestinal brush border assist in carb and protein digestion, but these enzymes do not digest fats

Front 202

Malabsorption syndromes: pancreatic insufficiency: pH associations

Back 202

Absence of pancreatic bicarbonate in the duodenum and jejunum causes an acidic pH that worsens maldigestion by preventing activation of pancreatic enzymes that are present

Front 203

Malabsorption syndromes: pancreatic insufficiency: clinical manifestations

Back 203

maldigestion, a large amt of fat in the stool (steatorrhea) and weight loss are the most common signs of pancreatic insufficiency

Front 204

What is a common tx for Malabsorption syndromes: pancreatic insufficiency:

Back 204

lipase supplementation is usually successful

Front 205

malabsorption syndromes: lactose deficiency: what does it inhibit, and what then happens

Back 205

Lactose deficiency inhibits the breakdown of lactose (milk sugar) into monosaccharides and therefore prevents lactose digestion and absorption across the intestinal wall

Front 206

malabsorption syndromes: lactose deficiency: defect in lactase gene?

Back 206

deficiency of disaccharidase at the villus brush border of the small intestine is caused by a congenital defect in the lactase gene

Front 207

malabsorption syndromes: lactose deficiency: most common in..

Back 207

blacks

Front 208

malabsorption syndromes: lactose deficiency: infants

Back 208

congenital lactase deficiency causes watery diarrhea in breast milk or lactose-containing formulas in infants

Front 209

malabsorption syndromes: lactose deficiency: adult-type lactose intolerance

Back 209

lactase expression is lost before adulthood in adult type lactose intolerance and is genetically determined

Front 210

malabsorption syndromes: lactose deficiency: secondary lactase deficiency

Back 210

secondary (acquired) lactase deficiency can be caused by several diseases of the intestine, including gluten sensitive enteropathy, enteritis, and bacteria overgrowth

Front 211

malabsorption syndromes: lactose deficiency: what happens to the undigested lactose?

Back 211

remains in the intestine, where bacterial fermentation causes gas to form. undigested lactose also increases the osmotic gradient in the intestine, causing irritation and osmotic diarrhea

Front 212

malabsorption syndromes: lactose deficiency: clinical manifestations:

Back 212

bloating, crampy pain, diarrhea, and flatulence.

Front 213

malabsorption syndromes: lactose deficiency: avoiding sx, and one thing to keep in mind b/c of this

Back 213

avoiding milk products and adhering to a lactose free diet, maintian adequate calcium intake decreases osteoporosis risk

Front 214

malabsorption syndromes: bile salt deficiency: what are bile salts?

Back 214

bile salts are conjugated in the bile that is syntehsized from cholesterol and secreted from the liver

Front 215

malabsorption syndromes: bile salt deficiency: why are bile salts necessary?

Back 215

conjugated bile acids (bile acids) are necessary for teh digestion and absorption of fats

Front 216

malabsorption syndromes: bile salt deficiency: what are micelles? what do they do?

Back 216

When bile enters the duodenum, teh bile salts aggregate with fatty acids and monoglycerides to form micelles.
-micelle formation solubilizes fat molecules and allows them to pass thru the unstirred layer at the brush border

Front 217

malabsorption syndromes: bile salt deficiency: what may cause insufficient bile salts and thus micelle formation?

Back 217

-advanced liver disease (which decreases the production of bile salts)
-obstruction of the common bile duct (which decreases flow of bile into the duodenum)
-intestinal stasis (lack of motility, which permits overgrowth of intestinal bacteria that deconjugate bile salts
-and diseases of the ileum, which prevent the reabsorption and recycling of bile salts (enterohepatic circulation)

Front 218

malabsorption syndromes: bile salt deficiency: clinical manifestations, results of fat soluble vit def

Back 218

clinical manifestations r/t poor intestinal absorption of fat and fat-soluble vitamins (ADEK)
-increased fat in stools (steatorrhea) leads to diarrhea nd decreased plasma proteins
-the loss of fat soluble vitamins and their effects include the following:
-Vit A def --> night blindness
-Vit D def --> decreased calcium absorption with bone demineralization (osteoporosis), bone pain, fx
-Vit E def --> uncertain effects may cause testicular atrophy and neurological defects in kids
-Vit K def --> prolongs prothombin time, leading to spontaneous development of purpura (bruising) and petechiae

Front 219

malabsorption syndromes: bile salt deficiency: tx

Back 219

increase medium chain triglycerides in the diet, ie using coconut oil for cooking. Vit A, D, K given parenterally

Front 220

Inflammatory bowel disease: three diseases, how are two they similar?

Back 220

-IBD: 3 are: ulcerative colitis, crohn disese, and diverticular disease

-Ulcerative colitis and Crohn disease are chronic relapsing inflammatory bowel diseases (IBDs) of unknown origin
-both associated with genetic factors, alterations in epithelial cell barrier functions, and immunopathology r/t abnormal T cell reactions to commensal microflora and other luminal antigens

Front 221

IBD: of the two which is more limited in where it occurs?

Back 221

-UC is limited to the mucosa of the colon and rectum, mucosa
-Crohn can involve any part of the GI tract f/ mouth to anus and involves transmural granulomatous inflammatory lesions

Front 222

IBD: UC-what is it?

Back 222

US is a chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon

Front 223

IBD: UC- risk factors, causes, when does it show up?

Back 223

-lesions appear in susceptible ppl b/w 20-40
-risk factors include a family hx of disease or jewish descent, and higher prevalence among white populations and N Europeans
-less prevalent among smokers
-cause is unknown, dietary, infectious, genetic (often ID twins), and immunological factors suggested causes

Front 224

IBD: UC- immunological factors

Back 224

-humoral and cellular immunological factors associated with UC
-colonic epithelial antibodies of teh immunoglobulin G (IgG) class have been identified of individuals with UC and a large number of plasma cells are found in the inflamed colon
-lymphocytes (T cells) in ppl with UC may have cytotoxic effects on the epithelial cells of the colon, as well as damage caused by inflammatory cytokines (IL # and TNF-alpha)
-activated macrophages also contribute cytokines that cause fever and the acute phase response
-autoimmune d/o ie lupus and erythema nodosum may accompany UC

Front 225

IBD: UC- lesions

Back 225

-the primary lesions of UC are continuous with no skip lesions (not bubbly like with Crohn), limited to the mucosa, and not transmural
-the mucosal layer is thinner than normal and there is impairment of the epithelial barrier
-the rectum is almost always involved

Front 226

IBD: UC- where does inflammation begin?

Back 226

inflammation begins at the base of the crypt of Lieberkuhn, in the large intestine, primarily the left colon, with infiltration and relase of inflammatory cytokines from neutrophils, lymphocytes, plasma cells, macrophages, eosinophils, and mast cells
-immune cells at base of Lieberkuhn, cross section of colon, large folds of colon that help increase surface area and villi stick out, make colon look like a carpet, at bottom of villi is crypts b/w villi, that's where increase in leukocytes re, leads to inflammation of that tissue, can be mild or severe

Front 227

IBD: UC- where is it most severe

Back 227

rectum and sigmoid colon

Front 228

IBD: UC- mild inflammation

Back 228

mucosa is hyperemic, edematous, and may appear dark red and velvety

Front 229

IBD: UC- severe inflammation

Back 229

-mucosa becomes hemorrhagic, and small erosions form and coalesce into ulcers.
-Abscess formation occurs in the crypts.
-necrosis and ragged ulceration of teh mucosa ensue
-edema and thickening of the muscularis mucosae (underneath) may narrow the lumen of the involved colon, colon size narrows

Front 230

IBD: UC- chronic disease

Back 230

inflammatory polyps (pseudopolyps) develop in teh colon from rapidly regenerating epithelium

Front 231

IBD: UC- sumamry of patho

Back 231

Immune cells (neutrophils, lymphocytes, macrophages, etc) at base of crypt of Lieberkuhn

-->

Inflammation
mild-mucosa hyperemic, edematous, dark red, velvety
severe-mucosa hemorrhagic, erosive, ulcerated

--->

edema and thickening of muscularis mucosae

--->

decreased lumen size

Front 232

IBD: UC- clinical manifestations

Back 232

-intermittent periods of remission and exacerbation
-vary with severity and extent of disease
-large volumes of watery diarrhea f/ loss of absorptive mucosal surface and decreased colonic transit time
-mucosal destruction causes bleeding, cramping pain, and an urge to defecate
-frequent diarrhea w/ blood and mucus
-mild UC-involves less mucosa and may be limited to proctitis-so frequency of bm, bleeding, pain is minimal
-severe may involve whole colon-fever, high pulse rate, frequent diarrhea, urgency, bloody stools, continuous crampy pain, dehydration, wt loss, anemia, fever

Front 233

IBD: UC- tx-

Back 233

-mesalazine
-steroids and salicylates suppress inflammatory response and help alleviate cramping
-immunosuppressive agents for chronic active disease
-antibiotics, probiotics
-nicotine has protective effects
-dehydration, malnutrition tx
-surgical resection of colon or colostomy if all else fails

Front 234

IBD: UC- immunological factors

Back 234

-humoral and cellular immunological factors associated with UC
-colonic epithelial antibodies of teh immunoglobulin G (IgG) class have been identified of individuals with UC and a large number of plasma cells are found in the inflamed colon
-lymphocytes (T cells) in ppl with UC may have cytotoxic effects on the epithelial cells of the colon, as well as damage caused by inflammatory cytokines (IL # and TNF-alpha)
-activated macrophages also contribute cytokines that cause fever and the acute phase response
-autoimmune d/o ie lupus and erythema nodosum may accompany UC

Front 235

IBD: UC- lesions

Back 235

-the primary lesions of UC are continuous with no skip lesions (not bubbly like with Crohn), limited to the mucosa, and not transmural
-the mucosal layer is thinner than normal and there is impairment of the epithelial barrier
-the rectum is almost always involved

Front 236

IBD: UC- where does inflammation begin?

Back 236

inflammation begins at the base of the crypt of Lieberkuhn, in the large intestine, primarily the left colon, with infiltration and relase of inflammatory cytokines from neutrophils, lymphocytes, plasma cells, macrophages, eosinophils, and mast cells
-immune cells at base of Lieberkuhn, cross section of colon, large folds of colon that help increase surface area and villi stick out, make colon look like a carpet, at bottom of villi is crypts b/w villi, that's where increase in leukocytes re, leads to inflammation of that tissue, can be mild or severe

Front 237

IBD: UC- where is it most severe

Back 237

rectum and sigmoid colon

Front 238

IBD: UC- mild inflammation

Back 238

mucosa is hyperemic, edematous, and may appear dark red and velvety

Front 239

IBD: UC- severe inflammation

Back 239

-mucosa becomes hemorrhagic, and small erosions form and coalesce into ulcers.
-Abscess formation occurs in the crypts.
-necrosis and ragged ulceration of teh mucosa ensue
-edema and thickening of the muscularis mucosae (underneath) may narrow the lumen of the involved colon, colon size narrows

Front 240

IBD: UC- chronic disease

Back 240

inflammatory polyps (pseudopolyps) develop in teh colon from rapidly regenerating epithelium

Front 241

IBD: UC- sumamry of patho

Back 241

Immune cells (neutrophils, lymphocytes, macrophages, etc) at base of crypt of Lieberkuhn

-->

Inflammation
mild-mucosa hyperemic, edematous, dark red, velvety
severe-mucosa hemorrhagic, erosive, ulcerated

--->

edema and thickening of muscularis mucosae

--->

decreased lumen size

Front 242

IBD: UC- clinical manifestations

Back 242

-intermittent periods of remission and exacerbation
-vary with severity and extent of disease
-large volumes of watery diarrhea f/ loss of absorptive mucosal surface and decreased colonic transit time
-mucosal destruction causes bleeding, cramping pain, and an urge to defecate
-frequent diarrhea w/ blood and mucus
-mild UC-involves less mucosa and may be limited to proctitis-so frequency of bm, bleeding, pain is minimal
-severe may involve whole colon-fever, high pulse rate, frequent diarrhea, urgency, bloody stools, continuous crampy pain, dehydration, wt loss, anemia, fever

Front 243

IBD: UC- tx-

Back 243

-mesalazine
-steroids and salicylates suppress inflammatory response and help alleviate cramping
-immunosuppressive agents for chronic active disease
-antibiotics, probiotics
-nicotine has protective effects
-dehydration, malnutrition tx
-surgical resection of colon or colostomy if all else fails

Front 244

IBD: CD- what is it?

Back 244

Crohn disease (CD) (granulomatous colitis, ileocolitis, or regional enteritis) is an idiopathic inflammatory d/o that affects any part of the GI tract from the mouth to the anus

Front 245

IBD: CD- most commonly affeted area

Back 245

distal small intestine and proximal large colon

Front 246

IBD: CD- risk factors

Back 246

-family history (ID twins not uncommon), tobacco use, Jewish ethnicity, urban residency, and CARD/NOD/IR gene mutations

Front 247

IBD: CD- pathogenesis

Back 247

may be associated with an overly aggressive response to normal flora bacteria in genetically predisposed ppl
-inflammation with activation of leukocytes and cytokines (TNF, IFN, interleukins) cause injury
-recruited leukocytes release proinflammatory substances, including prostaglandins, leukotrienes, proteases, reactive oxygen species, and nitric oxide, which cause further injury and inflammation
-elevations in IgG are associated with severity of disease

Front 248

IBD: CD- patho where does in begin in body

Back 248

the inflammatory process of CD begins in the intestinal submucosa and spreads across the intestinal wall to involve the mucosa and serosa in areas overlying lymphoid tissue
-progression of the disease involves neutrophil infiltration of the crypts resulting in abscess formation and crypt destruction

Front 249

IBD: CD- are there skip lesions? Why or why not?

Back 249

Yes. the inflammation can affect some segments but not others, creating a pattern called skip lesions (bubbly look),
-one side of intestinal wall may affected but not the other

Front 250

IBD: CD- lesiosn

Back 250

the ulcerations of CD produce longitudinal and transverse fissures that extend inflammation into lymphoid tissue
-the typical chronic lesion is a granuloma having cobblestone projections of inflamed tissue surrounded by aresas of ulceration
-the lumen can narrow with inflammation, edema, and fibrotic strictures
-fistulae may form in the perianal area b/w loops of intestine or extend into bladder

Front 251

IBD: CD- sum of patho

Back 251

inflammation of submucosa then across intestine wall

--->

skip lesions

-->

longitudinal and transverse lesions with ulceration

Front 252

IBD: CD- clinical manifestations

Back 252

may just have "irritable bowel" for several years
-vary and are associated with disease location
-abd pain and distention most common sx, with passage of blood and mucus
-weight loss common
-long term, at risk for intestinal adenocarcinoma (but not in UC, although cancer risk inc for both)
-also younger onset..10-30 most common

Front 253

appendicitis- what is it

Back 253

appendicitis is an inflammation of the verniform appendix, which is a projection from the apex of the cecum

Front 254

appendicitis-how common

Back 254

most common surgical emergency of the abdomen and affects 7-12% of population
-most common b/w 20-30, but can occur at any age

Front 255

appendicitis- cause

Back 255

controversial
-obstruction of the lumen with stools, tumors, or foreign bodies with consequent, increased intraluminal pressure, ischemia, bacterial infx, and inflammation is a common theory

Front 256

appendicitis- what does obstruction lead to

Back 256

the obstructed lumen does not allow drainage of the appendix, and as mucosal secretion continues, intraluminal pressure increases
-the resultant increased pressure decreases mucosal blood flow, and the appendix becomes hypoxic
-the mucuosa ulcerates, promoting bacterial or other microbial invasion with further inflammation and edema
-inflammation may involve the distal or entire appendix
-gangrene develops from thrombosis of teh luminal blood vessels, followed by peroration

Front 257

appendicitis- sum of patho

Back 257

unclear..but has little tube into it, can get stool, food in it, inc pressure in lumen leads to ischemia, infx, more edema etc..rupture can cause peritonitis, contents into abd

Front 258

appendicitis- clinical manifestations

Back 258

epigastric and RLQ pain, rebound tenderness, don't always get that though
-pain can be vague, increase in intensity, intermittent, shift of location
-n/v/anorexia/fever/diarrhea/constipation

Front 259

appendicitis- tx

Back 259

antibiotics or appendectomy

Front 260

ACCESSORY ORGANS IN GI TRACT...
What is a biliary tree?

Back 260

ducts of gallbladder

Front 261

What are the most common general disorders of the gallbladder?

Back 261

obstruction and inflammation

Front 262

What is obstruction of the gallbladder caused by?

Back 262

gallstones (cholelithiasis) which are aggregates of substances in the bile

Front 263

Where do the gallstones go?

Back 263

gallstones may remain in the gallbladder or be ejected, with bile, into the cystic duct. Gallstones that become lodged in the cystic duct obstruct the flow of bile into and out of the gallbladder and cause inflammation

Front 264

What is the difference b/w cholelithiasis and cholecystis?

Back 264

Gallstone formation is termed cholelithiasis

Inflammation of the gallbladder or cystic duct (the short duct that joins the gallbladder to the common bile duct) is known as cholecystitis

Front 265

What are the two different types of cholelithiasis?

Back 265

gall stones in gallbladder

Front 266

Explain most common type of cholelithiasis?

Back 266

Cholesterol gallstones –
aggregation of cholesterol crystals
from bile that is supersaturated
with cholesterol
-Bile supersaturated with cholesterol, bile then starts to form stone
-Decreased motility of gall bladder
-Increased mucus secretion in gall
bladder
-cholesterol more common-super saturation of cholesterol in bile, bile then starts to form the stone, usually decrease motility of gallbladder and increased secretion, green color

Front 267

Less common type of cholelithiasis?

Back 267

-pigmented-occur later in life, less common, associated with cirrhosis, black color
Pigmented gallstones –
cholesterol, calcium, bilirubin
-Increase risk when hemolytic
syndromes ( unconjugated bilirubin)
-associated with biliary tree obstruction and infection

Front 268

What may contribute to stone formation?

Back 268

impaired gallbladder motility and gallbladder stasis

Front 269

Are stones always symptomatic and problematic?

Back 269

No. Stones may lie "silent" or become lodged in the cystic or common duct, causing pain and cholecystitis.
--not nec a problem if u have stones just sitting in gall bladder, is a prob when it blocks ducts

Front 270

What problems may result when gallstones are in specific ducts?

Back 270

stone blocking:

-the cystic duct-can lead to infl of gallbladder itself

-common bile duct-prob with galbladder and liver potentialy b/c of bile

-common bile and pancreatic-no movement of bile or pancreatic enzymes into duodenum

Front 271

gallstones and jaundice?

Back 271

jaundice indicates that the stone is located in the common bile duct

Front 272

gallstones in ducts: change in liver function labs?

Back 272

if stone cystic duct may no change in liver function
-but common bile and panc duct yest very likely

Front 273

What are risk factors for cholesterol stones?

Back 273

-demography-N European, N and S Americans, Native Americans, Mexican Americans
-advancing age
-female sex hormones
-female gender
-the pill
-pregnancy
-obesity and metabolic syndrome
-rapid weight reduction
-gallbladder stasis
-inborn d/o of bile acid metabolism
-hyperlipidemia syndromes

Front 274

What risk factors for pigment stones?

Back 274

-demography-asians more than westerners, rural more than urban
-chronic hemolytic syndrome
-biliary infections
-GI d/o: ileal disease (e.g. Crohn disease), ileal resection or bypass, cystic fibrosis with pancreatic insufficiency

Front 275

What is cholecystitis? What causes it?

Back 275

cholecystitis-gall bladder inflammation

-obstruction causes infection and inflammation
-gallbladder obstruction causes gallbladder to become distended and inflamed
-almost always caused by lodging of a gallstone in teh cystic duct

Front 276

What are possible complications of cholecystitis?

Back 276

obstruction causes the gallbladder to become distended and inflamed
-pressure against the wall of the gallbladder decreases blood flow
-ischemia, necrosis, and perforation of the gallbladder are possible

Front 277

pancreatitis - what is it

Back 277

pancreatitis is inflammation of the pancreas, r/t pancreatic enzymes auto digesting the pancreas it can be both acute and chronic,

Front 278

pancreatitis - what is the pancreas, what is its function

Back 278

the pancreas is a tucked in accessory organ, it has both endocrine (insulin) function and exocrine (r/t digestive system)

Front 279

What are some causes of pancreatitis?

Back 279

obstructive biliary tract disease (particularly cholelithiasis, can also lead to edema..ischemia..cellular injury), peptic ulcers, trauma, hyperlipidemia, and certain drugs, cause unknown in 15-25% duct obstruction
-cell damage causes realease of pancreatic enzymes

Front 280

pancreatitis and pancreatic enzymes

Back 280

inflammation of the pancreas
-leakage of pancreatic enzymes into the pancreatic tissue
-these enzymes cause autodigestion of pancreatic tissue and leak into the bloodstream to cause injury to blood vessels and other organs

Front 281

ACUTE pancreatitis caused by duct obstruction patho..

Back 281

Duct Obstruction:
f/ cholelithiasis ampullary obstruction
f/ chronic alcoholism and ductal concretions

--->

Interstitial edema

-->

Impaired blood flow

-->

Ischemia

-->

Acinar Cell Injury

Front 282

Acute pancreatitis caused by acinar cell injury patho..

Back 282

Acinar cell injury
f/ alcohol
f/ drugs
f/ trauma
f/ ischemia
f/ viruses

-->

release of intracellular proenzymes and lysosomal hydrolases

-->

activation of enzymes (intra or extra cellular)

-->

acinar cell injury

Front 283

Acute pancreatitis caused by defective intracellular transport..

Back 283

Defective intracellular transport
f/ metabolic injury
f/ alcohol
f/ duct obstruction

-->

delivery of proenzymes to lysosomal compartments

-->

intracellular activation of enzymes

-->

acinar cell injury

Front 284

All causes of acute pancreatitis lead to ...and what does this do..

Back 284

acinar cell injury..activates enzymes

Front 285

acute pancreatitis..what do activated enzymes do?

Back 285

Produce lesions caused by:
-interstitial inflammation and edema
-proteolyses (proteases)
-fat necrosis (lipase, phospholipase)
-hemmorhage (elastase)

Front 286

acute pancreatitis..what do these lesions produce?

Back 286

ACUTE PANCREATITIS

Front 287

Acute pancreatitis..so waht are acinar cells?

Back 287

pancreas is made of acinar cells, they secrete digestive enzymes
-pancreatitis develops b/c of an injury or disruption of pancreatic acinar cells, which permit leakage of pancreatic enzymes (trypsin, chymotrypsin, and elastse) into pancreatic tissue

Front 288

acute pancreatitis, are pancreatic enzymes bad?

Back 288

enzymes good..digest proteins, CHO, and fats we eat, but can also digest our own cells..so having exposure to digestive enzymes leads to trouble

Front 289

What does pancreatitis look like, the actual organ?

Back 289

red, inflammed, lesions

Front 290

What are clinical manifestations and concerns of acute pancreatitis?

Back 290

generally painful, hunched over guarding belly..pain management, hydration imp b/c of accumulation of fluids in the peritoneal cavity

Front 291

Chronic pancreatitis concern

Back 291

chronic pancreatitis is a risk factor for pancreatic cancer

Front 292

Manifestations of liver disorders-general list

Back 292

Of all the acessory organ d/o, acute or chronic liver disease leads to the most systematic, life-threatening complications.
-portal HTN
-ascites
-hepatic encephalopathy
-hepatorenal syndrome
-jaundice

Front 293

Portal HTN-what is it?

Back 293

abnormally high blood pressure in the portal venous sytem primarily caused by resistance to portal blood flow

Front 294

How can portal HTN be characterized?

Back 294

can be broken down into location of problem
-Prehepatic: (looks like it's below the liver), the hepatic portal veins carry blood from the GI tract, pancreas, and spleen to the liver
-Intrahepatic-In the liver the blood flows through the sinusoids and..
Posthepatic: carries the blood into the inferior vena cava

Front 295

Portal HTN-general

Back 295

portal HTN is caused by disorders that obstruct or impede blood flow through any component of the portal venous system or vena cava

Front 296

portal HTN-intrahepatic

Back 296

-something going on inside liver ie infl, blood clot, cirrhosis, hepatitis=intrahepatic cause of portal HTN

Intrahepatic causes result from vascular remodeling with intrahepatic shunts, thrombosis, inflammation, or fibrosis of the sinusoids, as occurs in cirrhosis of the liver or viral hepatitis

Front 297

portal HTN-posthepatic

Back 297

-posthepatic cause-prob with hepatic vein or with the heart, rt sided heart failure can lead to this

Front 298

portal HTN-prehepatic

Back 298

ie thrombosis or something causes narrowing of hepatic portal vein-can cause prehaptic

Front 299

What is the most common clinical manifestation of portal HTN?

Back 299

esophageal varices-vomiting of blood from bleeding esophageal varices is the most common clinical manifestation of portal HTN
-slow, chronic bleeding f/ varices causes anemia or melena
-usually the bleeding develops slowly over years

Front 300

portal HTN-rupture of esophageal varices

Back 300

rupture of esophageal varices causes hemorrhage and voluminous vomiting of dark blood
-usually painless
-rupture caused by combo of erosion by gastric acid and elevated venous pressure
-mortality 30-60%, most die in 1 year

Front 301

What can occur to spleen as result of portal HTN

Back 301

can also have splenomegaly if no blood flow thru splenic vein

Front 302

can ascites occur with portal HTN?

Back 302

ascites can occur with portal HTN or cirrhosis of liver

Front 303

What is ascites?

Back 303

ascites is the accumulation of fluid in the peritoneal cavity
-ascites traps body fluid in a "third space" from which it cannot escape
-the effect reduces the amount of fluid available for nml physiologic functions

Front 304

Most common cause of ascites?

Back 304

cirrhosis is the most cause of ascites. Likewise, ascites is the most common complication of cirrhosis

Front 305

ascites patho

Back 305

cirrhosis of liver (hepatocyte failure)

--->

Portal HTN

-->

Water retention (increased Na retention)

-->

increased fluid in peritoneal cavity

-->

decreased blood volume to kidney

-->

then furthers then water and Na retention..vicious cycle

Front 306

Hepatic encephalopathy-what is it?

Back 306

Brain exposed to substances
usually removed by the liver

-hepatic encephalopathy-when our liver is working it helps purify our blood, removes amonia and fatty acids, when decreased blood flow thru liver or decreased function of liver, blood bypasses liver and not be cleaned and chemicals can reach brain which can lead to neuro changes-decreased cognition/coma, tremor, ECG changes

Front 307

Hepatic encephalopathy -what is the most hazardous to reach to brain? STARRED in notes

Back 307

The most hazardous substances are end products of intestinal protein digestion, particularly ammonia

-the digestion of blood from leaking or ruptured varices adds to the amount of ammonia present in systemic blood, as does the action of ammonia-forming bacteria in the colon
-the astrocyte is the most vulnerable because it is the site of ammonia detoxification
-ammonia that reaches the brain is metabolized to glutamine with osmotic disturbances and alterations in cerebral blood flow that interfere with neurotransmitters, cause astrocyte edema and oxidation, and can result in brain herniation and death

Front 308

What can be a cause of -hepatic encephalopathy?

Back 308

portal HTN, acute fulminant hepatitis, or can be result of liver disease where the function of the liver is altered

Front 309

Manifestations of hepatic encephalopathy?

Back 309

A neurologic syndrome of impaired
cognitive function, flapping tremor (asterixis),
and electro-encephalogram EEG changes

Front 310

What is jaundice?

Back 310

Jaundice (icterus) is a yellow or greenish pigmentation of the skin caused by hyperbilirubinemia.

Front 311

What can cause hyperbilirubinemia and jaundice?

Back 311

hyperbilirubinemia and jaundice can result from:

1) extrahepatic obstruction to bile flow (gallstones)
2) intrahepatic obstruction (hepatocellular disease such as cirrhosis or hepatitis)
3) excessive production of bilirubin (excessive hemolysis or RBCs)

Front 312

What is unconjugated (indirect) bilirubin? Is it water or lipid soluble? How is it excreted?

Back 312

Erythrocytes (red blood cells) generated in the bone marrow are disposed of in the spleen when they get old or damaged. ..turned into unconjugated bilirubin in the reticuloendothelial cells of the spleen. This unconjugated bilirubin is not soluble in water, It is then bound to albumin and sent to the liver.

LIPID SOLUBLE

NOT excreted in urine..not sure how it is

Front 313

What is conjugated (direct) bilirubin? IS it water or lipid soluble?

Back 313

Unconjugated bilirubin plus glucuronic acid

WATER SOLUBLE

Excreted in urine and in stool via bile

Front 314

First cause of jaundice.. give an example

Back 314

Prehepatic/hemolytic jaundice

-a.k.a. hemolytic jaundice
Too much RBC breakdown.liver not able to keep up with breakdown of rbc, and liver tries to process it and cant, ie sickle cell you might see this

Front 315

What lab result will you see with prehepatic jaundice?

Back 315

ELEVATED INDIRECT (UNCONJUGATED BILIRUBIN)

hepatocytes can't keep up and conjugating blirubin so end up with elev unconj bilirubin, causes indirect bilirubin to go up

Front 316

What is the second cause of jaundice? 2 main causes

Back 316

Intrahepatic Obstruction
-hepatocyte dysfunction
-obstructed/blockage of bile caniculi

Front 317

What abnormal lab test will you see with jaundice f/ intrahepatic obstruction?

Back 317

ELEVATED CONJUGATED AND UNCONGUATED BILIRUBIN

dec processing of bilirubin, not too much bilirubin but liver is unable to process it b/c hepatocytes arent working as well, so liver cant conj bilirubin and leads to elev of conjug and uncon-why both? some are still working

Front 318

What is the third cause of jaundice? Cause?

Back 318

Extrahepatic obstruction jaundice

-occlusion of common bile duct

Front 319

What is the patho of extrahepatic obstruction jaundice?

Back 319

extrahepatic obst-blockage of common bile duct ie gall stone-liver working, conjugating bilirubin properly, but b/c duct is blocked no movement of conjugated bilirubin into intestine and outside of body, leads to light colored stool (bilirubin gives it the color, bilirubin may not be getting into int), conj bilirubin has to go somewhere-inc exretion in urine (dark urine)

Front 320

What lab result will you see with extrahepatic obstruction jaundice?

Back 320

ELEVATED CONJUGATED BILIRUBIN..

even though it is being excreted in the urine...still can't keep up with the elevated levels in bloodstream

Front 321

What is viral hepatitis?

Back 321

relatively common systemic disease that affects primarily the liver

Front 322

Where is hepatitis A mainly found?

Main transmission?

Associated with chronic hepatitis?

Back 322

Hepatitis A Virus (HAV)

Found in feces, bile, sera of infected individuals

-usual mode of transmission is fecal-oral route (contaminated food or water), infected blood possible but less common

Not associated with chronic hepatitis

Front 323

Hepatitis B **focus on this one for test**

Where is it found in infected individuals?

How is it transmitted?

Associated with liver diseases?

Back 323

Hepatitis B virus (HBV)

-found in blood and body fluids of infected individuals, also an STD

-Transmitted through blood, body fluids, maternal (in 3rd trimester)

-Yes, HBV is a major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma

Front 324

What are common co-infections of Hepatitis B?

Back 324

Coinfection with HCV, HDV, and HIV is common b/c these viruses share the same routes of transmission

Front 325

What is acute heptatitis B?

Back 325

Acute hepatitis B refers to newly acquired infections. In most people with acute hepatitis, symptoms resolve over weeks to months and they are cured of the infection. However, a small number of people develop a very severe, life-threatening form of acute hepatitis called fulminant hepatitis.

Front 326

What is chronic hepatitis B?

Back 326

Chronic hepatitis B is an infection with HBV that lasts longer than 6 months. Once the infection becomes chronic, it may never go away completely.

Front 327

Hepatitis B antibodies what are they

Back 327

antibodies (A protein produced by lymphoid tissue in response to the presence of an antigen.)

Front 328

Hepatitis B has unique structures..what are they?

Back 328

virus has unique structures-

have surface protein (outer layer of circle, double layer): HBsAg: we test for these antigens

Core proteins (underneath surface protein): HBeAg & HBcAg: usually not detectable in serum

and genetic material: DNA and DNA polymerase if you imagine a circle

Front 329

What do you see in chronic hepatitis?

Back 329

elevation of surface antigen, increased liver function tests/infl in liver, lasts greater than 6 months

Front 330

What is anti-HB?

Back 330

Hepatitis B surface antibody (anti-HBs)

Used to detect previous exposure to HBV; can also be acquired from successful vaccination. This test is done to determine the need for vaccination (if anti-HBs is absent) or to determine if a person has recovered from an infections and is immune (cannot get the infection again).

Front 331

Hepatitis B incubation phase?

Back 331

incubation period (avg 90 days) not much serologically happening with hep b

Front 332

Hepatitis B prodromal phase?

Back 332

symptomatically fatigue, malaise, n/v, low grade temp, HA, URQ discomfort, this is when virus is replicating and causing problems in hepatocytes

Front 333

Hepatitis B indric phase?

Back 333

Indric phase-about month 4, when you see jaundice, increase in liver functions, dark urine, enlargement of liver, as you progress and convalesce (gradually return to health) sx reduce, wont see as much antigen present and will start seeing more antibodies present
-by about 7 weeks of elevation of surface antigen-about 50% of ppl resolve sx and have decline of antigen, and almost everyone does by 15 wks, if extends beyond that considered more chronic hepatitis b

Front 334

Hepatitis B recovery phase?

Back 334

about month 4.5 on..antibodies to HBV rise

-IgG anti-HBs
-IgG anti-HBc
-IgM anti..

Front 335

What happens during the indric phase?

Back 335

Acute sx: jaundice, high ALT, high AST

Front 336

General overview of Hep B

Back 336

virus introduces self to hepatic cells, triggers immune response which leads to infl, can have necrosis of hepatocyte and virus itself damaging hepatocytes, also damage/obst of bile -chole dec movement of bile flow and can lead to obstructed jaundice ..more severe immune response and sx also have good resolution of disease

Front 337

Hepatitis C

most common cause?

associated with chronic hepatitis?

Back 337

Hepatitis C: HVC, also known as non-A, non-B hepatitis

post-transfusion, also common with IV drug users

yes, associated w/ chronic hepatitis, also most common cause of chronic liver disease in the West

Front 338

Hepatitis D

associated with..

associated with chronic hepatitis?

Back 338

Hepatitis D: HDV occurs in ppl with hepatitis B.

-cannot have D without B
-D depends on B for its replication

yes, associated with chronic hepatitis

Front 339

Hepatitis E

transmission

-associated with chronic hepatitis?

Back 339

resembles Hepatitis A, also oral-fecal transmission

-not associated with chronic hepatitis

Front 340

Hepatitis G?

transmission

chronic hep assoc?

Back 340

recently discovered,

parenterally and sexually transmitted

unknown if associated with chronic hepatitis

Front 341

Viral hepatitis (all)..

patho

Back 341

Virus infects liver cell

-->

Immune response – phagocytes, cytotoxic T cells,
natural killer cells

-->

Inflammation

-->

Hepatocyte Necrosis
Damage and obstruction of bile canaliculi

-->

Cholestasis (bile cannot flow from the liver to the duodenum). and obstructive jaundice

Front 342

If you have been vaccinated what should show up?

Back 342

antibodies..if they don't after 3 tests then you are as susceptible as if you didn't get the vaccine

Front 343

If you have the virus what shows up?

Back 343

antigens

Front 344

What is fulminant hepatitis?

Back 344

clinical syndrome resulting in severe impairment or necrosis of liver cellsa nd potential liver failure
-may be a complication to Hep B or C, particularly C
-toxic reactions to drugs and congential metabolic d/o also can cause fulminant hepatitis
-tylenol (aceta..) OD is the leading cause of acute liver failure in the US
-usually develops 6-8 weeks after the initial sx of viral hepatitis or a metabolic liver d/o
-tx is supportive, hepatic necrosis is irreversible
-liver transplant may be life saving

Front 345

What is cirrhosis?

Back 345

Irreversible inflammatory disease that disrupts
liver function and development of fibrosis and
nodular tissue..liver gets bumpy

Front 346

Causes of cirrhosis? several..etoh

Back 346

alcohol: The oxidation of alcohol damages hepatocytes

alcohol does 2 things:

1) can inc liver's fat content
2) as a byproduct Acetaldehyde..breakdown product of alcohol, acetyl can led to changes in protein synthesis in liver and lead to changes in vit/mineral metabolism, also can change cell membrane, and start to damage cytoskeletal (protein scaffolding in cell), decrease oxidation of fatty acids, decrease mitochondrial protein frataxin..both can lead to infl, change in collagen formation..

Front 347

First problem of alcoholic cirrhosis.. fatty liver

Back 347

etoh

-->

fatty liver

-->

inflammation

-->

necrosis and inflammation

-->

change in collagen formation

-->

fibrotic changes

Front 348

Second problem of alcoholic cirrhosis.. Acetaldehyde

Back 348

Acetaldehyde

-->

functional changes:
change in vitamin and mineral metabolism
decreased protein synthesis

-->

cell damage:
change in cytoskeleton
change in membrane frataxin
decrease oxidation of fatty acids
decrease mitochondrial fraxatin

--> follows same patterns of fatty liver from alcoholic cirrhosis from here on

inflammation

-->

inflammation and necrosis

-->

change in collagen formation

-->

fibrotic changes

Front 349

What does a normal liver do?

Back 349

detoxifies, produces coagulation factors, metabolizes, makes bile, involved w/ prot synthesis, glucose regulation and metbolism..bile formation, bilirubin modification, blood clotting factors, albumin synthesis, metabolism of cholesterol, conversion of proteins and fats to glucose, drug toxins metabolized, storage for vit and minerals, hormone metabolism

Front 350

Another cause of cirrhosis..biliary What is it?

Back 350

Biliary (bile canaliculi)
-Cirrhosis begins in the bile canaliculi and ducts, rather than in the hepatocytes as in alcoholic cirrhosis

Front 351

biliary cause of cirrhosis..what are the two types? what is the first?

Back 351

Primary biliary cirrhosis (autoimmune)
-mitochrondiral antibodies hallmark of this
-inflammation and destruction of small intrahepatic bile ducts with portal inflammation and ultimately fibrosis
-often accompanies autoimmune disease
-sx are caused by intrahepatic obstruction of bile flow..steatorrhea, fat soluble vitamin deficiencies, jaundice, light color stools..can worsen into liver failure, death, portal HTN..

Front 352

second cause of biliary cirrhosis?

Back 352

Secondary biliary cirrhosis (obstruction)
-prolonged partial or complete obstruction fo the common bile duct or its branches
-may be caused by gallstones, tumors, fibrotic strictures, chronic pancreatitis
-bile accumulates in centrilobular spaces
-nicrotic areas develop and are followed by proliferation and infl of the portal ducts that result in edema and fibrosis
-sx similar to primary

Front 353

STOPPED AT..

Back 353

what happens when liver doesnt properly function (in gmail notes)

Front 354

What is the patho/hormones of ascites?

Back 354

also ascites have water retention-sets up cycle that perpetuates a cycle

kidney red blood flow-releases renin

-->

inc in renin and renin angiotenison system

-->which leads to aldosterone

-->which leads to sodium retention..also inc in antidiuretic hormone, inc in water and sodium perpetuates this and cycle occurs

Front 355

Why does ascites occur in the abdomen?

Back 355

thats where the blockage is and theres space for it

Front 356

What goes wrong in liver failure?

Back 356

1) jaundice

2) ascites/muscle breakdown

Front 357

Weight regulation is...

Back 357

complicated!

culture revolves around food
Lots of factors including physiological, psychological, social

Front 358

Two sets of neurons from the ___

Back 358

Hypothalamus

Front 359

Think of each set of neuron as a ...

Back 359

volume dial on radio..
change in activity up or down which has influence on hunger and metabolism

Front 360

Set of neurons that promotes body weight gain

Back 360

NPY/AGRP neurons
-Increases appetite and food intake
-Decreases energy expenditure and metabolism

Front 361

Set of neurons that promote body weight loss

Back 361

POMC/CART neurons
-Decreases appetite and food intake
-Increases energy expenditure and metabolism

Front 362

What turns these "volume dials" of neuron activity up or down?

Back 362

Multiple hormones that have been identified in body r/t weight and regulation of neurons

Front 363

Which hormones involved in body weight regulation come from adipose cells?

Back 363

Adiponectin
Leptin
Resistin

Front 364

Which hormone comes from the pancreas?

Back 364

Insulin

Front 365

Which hormone comes from the stomach?

Back 365

Grehlin

Front 366

Which hormones come from the intestines?

Back 366

Peptide YY
Cholecystokinin (CCK)

Front 367

What is the response to:
Ghreliln, CCK

Back 367

NPY/AGRP neurons are MORE active, reminder:
Increases appetite and food intake
Decreases energy expenditure and metabolism

So..Grehlin and CCK promotes obesity and NPY/AGRP neurons

Front 368

What is the response to: Leptin, Insulin, Peptide YY

Back 368

NPY/AGRP neurons is LESS active
-meaning it promotes weight loss

Front 369

What is the response to: Leptin, Insulin

Back 369

POMC/CART neurons (reminder:)
Decreases appetite and food intake
Increases energy expenditure and metabolism

So Leptin and Insulin promote weight loss via the pomc/cart

Front 370

Obesity is considered a BMI..

Back 370

over 30

Front 371

Obesity: resisitence to ___ may cause weight gain

Back 371

Leptin

Leptin Resistance – high levels of leptin but ineffective
-causes weight gain

Front 372

Obesity and resistence to ___ also..

Back 372

Insuline Resistance
-DM risk
-pathology unknown

Front 373

What hormone may also influence obesity?

Back 373

grehlin..but not known for sure

Front 374

So which hormones promote obesity?

Back 374

Grehlin, CCK

activate NPY/AGRP neurons

Front 375

Inefficient ___ hormones promote obesity?

Back 375

Leptin, Insulin, Peptide YY --> decreased activity of NPY/AGRP neurons

Front 376

Which hormones active POMC/CART?

Back 376

Insulin, Leptin activate POMC/CART

Front 377

Bulimia Nervosa-body weight?

Back 377

Body weight remains near normal but with
aspirations for weight loss

Front 378

Bulimia Nervosa-findings

Back 378

-Recurrent episodes of binge eating
-Self-induced vomiting, laxative use
-Two binge-eating episodes per week for at least 3 months
-Fasting to oppose the effect of binge eating, or excessive
exercise

Front 379

bulimia-complications of vomiting

Back 379

Continual vomiting of acidic chyme can cause pitted
teeth, pharyngeal and esophageal inflammation, and tracheoesophageal fistulae

Front 380

complications of bulimia.. laxative use

Back 380

Overuse of laxative can cause rectal bleeding

Front 381

Anorexia-psych

Back 381

A person has poor body image disorder and
refuses to eat with goal to lose weight
-can occur with bulimia or separately

Front 382

anorexia and body weight

Back 382

Anorexic patients can lose 25% to 30% of
their ideal body weight due to fat and muscle
depletion

Front 383

What occurs from weight loss and fat and muscle depletion in anorexia?

Back 383

-electrolyte/dehydration issues
-hormonal hanges lead to menstrual changes, -secondary amenorrhea
-can lead to starvation

Front 384

Body weight regulation-what is MSH associated with?

Back 384

POMC/CART neurons -->

increased MSH expression and release

-->

decreased food intake and increased energy expenditure

Front 385

What is starvation?

Back 385

Starvation is decreased caloric (energy) intake leading to weight
loss

Front 386

What are the two major categories of starvation?

Back 386

Short term and long term

Front 387

What is short term starvation?

Back 387

short term starvation, or extended fasting-within hours after meal (prof)

book: consists of several days of total dietary abstinence or deprivation

Front 388

What happens first in short term starvation?

Back 388

Glycogenolysis-the splitting of glycogen into glucose
-4-6 hours after meal, body in a well-fed state and its energy requirements are met by glucose from recently ingested carbs
-once all available energy has been absorbed from intestine, glycogenolysis occurs-glycogen in the liver is converted to glucose
-the process peaks within 4-8 hours, then the next phase begins

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What is the second step is short term starvation?

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gluconeogenesis-the formation of glucose from noncarbohydrate molecules: lactase, pyruvate, amino acids, and the glycerol portion of fats
-structures not normally used to concert into sugar (think of neo/new), us picks up 4-8 hrs after last meal
-like glycogenolysis, gluconeogenesis takes place within the liver
-both of these processes deplete stored nutrients and thus cannot meet the body's energy needs indefinitely
-proteins continue to be catabolized to a minimal degree, providing carbon for the synthesis of glucose

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What is long term starvation?

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begins after several days of dietary abstinence and eventually causes death

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What does body start out with in long term starvation? What are the complications and reasons for them?

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-starts with glyconeogenesis to maintain glucose levels
-body starts to use fat molecules lipolysis breakdown of fat to make glucose
-when dieting you want lipolysis, but problem is ketones can occur,
-ketoacidosis, after fat used up or gets closure-body breakd down own proteins, problem is when this occurs it doesnt discern protein source (ie lets take leg not heart/diaphragm) so eventually latter happens-resp failure and cardiac arrest, kidney function, electrolyte imbalance

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Very brief patho of long term starvation

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Gluconeogenesis
-->
lipolysis
-->
proteolysis

..Death