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Comps - Mod 2 > Module 4 GI PC 617 - Sheet1 > Flashcards

Module 4 GI PC 617 - Sheet1 Flashcards

1
Q

Abdominal pain

A

Can be self-limiting or life threatening

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2
Q

First step in managing abdominal pain

A

Rule out “hot abdomen”

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3
Q

Challenge of treating abdominal pain

A

Design a safe and cost effective plan for work up that will distinguish among many causes

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4
Q

Exam for patients with acute abdominal pain

A

Assess for evidence of obstruction, peritoneal irritation, and vascular problems

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5
Q

If “hot abdomen” suspected

A

Patient should not be sent home who may have an emergency condition that might require urgent surgery

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6
Q

Past treatment for traveler’s diarrhea

A

No longer uses doxycycline and bactrim

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7
Q

Current recommendation for traveler’s diarrhea

A

Cipro, Levoquin, Rifaximin, and Axithromycin. If patient is pregnant, Zithromax

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8
Q

Viral hepatitis

A

A systemic infection that primarily affects the liver cells

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9
Q

Determining type of hepatitis with assessment only

A

Can not be done until blood work examined

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10
Q

Hepatits A or infections hepatitis

A

Spread by fecal-oral route, usually by infected food or water or shellfish grown in infected water

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11
Q

Incubation time of Hepatitis A

A

2-7 weeks

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12
Q

Prodromal symtpoms of Hepatitis A

A

Malaise, anorexia, nausea, low-grade fever, and right upper quadrant pain caused by swellinf of the liver in the liver capsule

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13
Q

Length of illness

A

Usually self-limiting disease that is not severe and will go away in time

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14
Q

Diagnosis of previous infection of Hepatitis A

A

Presence of anti-HAV imune globulin G (IgG)

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15
Q

Diagnosis of acute infection of Hepatitis A

A

Anti-HAV IgM (IgM is first antibody produced after exposure)

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16
Q

First diagnostic tests if patient exhibits signs or symptoms of liver problems

A

LFTs (AST, ALT, and alk phos). If this indicates acute viral infection, then hepatitis panel would be drawn.

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17
Q

Hepatitis panel includes…

A

Hepatitis A, B, and C.

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18
Q

Hepatitis A vaccine

A

Inactivated whole virus - prevents HAV for life. Immunoglobulin may be given to those exposed to the virus - gives passive immunity that lasts 4-6 months

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19
Q

Hepatitis B or serum hepatitis

A

Spread by contact with infected blood or blood products and sexual contact. Maternal transfer to the fetus occurs during birth process or during close contact in the postpartum period, such as breast feeding. Fetus not at risk during pregnancy.

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20
Q

Incubation period of Hepatitis B

A

2-6 moths

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21
Q

Prodromal symptoms of Hepatitis B

A

Longer and worse than Hep A and may include urticaria, rash, arthralgias, angioedema, serum sickness

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22
Q

Jaundice phase of Hepatitis B

A

After prodrome, lasts about 2 weeks. Hep B more likely to cause jaundice than Hep A

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23
Q

Diagnosis of Hepatitis B

A

LFTs; HBV core antigen (HBcAg) appears first,; core antibody (HBcAb) is next to appear (IgM) after exposure and indicates infectious state; HBV surface antigen (HBsAg) shows up early and indicates active infection; HBV surface antibody (HBsAb) indicates resolution with immunity (IgG)

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24
Q

Labs to screen for Hepatitis B

A

HBsAg, HBsAb, and HBcAb

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25
Q

Hepatitis B Vaccine

A

Protects for about 5 years - retest in persons at high risk. Now routine for infants in most states. Also protects against hepatitis cancer

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26
Q

Vaccination when exposure to hepatitis B and not vaccinated

A

Give HBIG (immunoglobulin G) and vaccine as soon as possible after exposure (within 7 days) lasts 4-6 months

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27
Q

Lab test to determine status post immunization

A

Anti-HBsAB. Want to see this be positive.

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28
Q

Hepatitic C or non-A, non-B

A

Transmitted primarily via IV drug use and blood products

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29
Q

Prodromal symptoms of Hepatitis C

A

None - many are asymptomatic. Clinical illness - if it occurs, it is mild with changes in LFTs. Chronic disease - will progress to cirrhosis in about 20 percent of cases. About 20-40% of seropositive patients will convert to negative during the first 6 months

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30
Q

Treatment of Hepatitis C during first 6 months

A

Not usually done during this time secondary to negative conversion of seropositive patients

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31
Q

Screening for hepatitis C

A

Enzyme immunoassay (EIA)

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32
Q

Diagnosis of Hepatitis C

A

LFT first; Anti-HCV antibody - not detectable until weeks or months into disease (97%) will be detectable after 6 months in the body; HCV RNA is detectable in serum at about 1-2 weeks after infection (this is really expensive)

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33
Q

Vaccination for Hepatitis C

A

No vaccine or immunoglobulin because hepatitis C has a high rate or mutation

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34
Q

Replication of Hepatitis D

A

Requires Hepatitis B

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35
Q

Hepatitis E

A

Most common in developing countries - spread by fecal oral route

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36
Q

Transmission of hepatitis D

A

Parenteral and sexual contact

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37
Q

Incubation of Hepatitis E

A

Incubation 2-9 weeks and like Hep A may be very serious for pregnancy women Killing about 21% of pregnant women who are infected

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38
Q

Jaundice

A

Green-yellow staining of skin and mucous membranes by bilirubin

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39
Q

Bilirubin

A

By-product of lysis (can be due to aging or various diseases) of RBC and is transported to liver for metabolism bound to protein in plasma, converted, and excreted thtough the bowel or kidney

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40
Q

Types of jaundice

A

Pre-hepatitc (Unconjugated), hepatic (Conjugated), and posthepatic (Conjugated)

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41
Q

Pre-jaundice

A

Unconjugated - most common cause hemolysis. Hemolysis is most common cause

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42
Q

Hepatitc jaundice

A

Conjugated - Immaturity (newborn) or dysfunction of hepatocyte in bilirubin metabolism

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43
Q

Posthepatic

A

Conjugated - obstruction of bile ducts - pancreatitis, gallbladder stasis

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44
Q

Lab evaluation of jaundice

A

Total bilirubin; direct bilirubin; and indirect bilirubin

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45
Q

Total bilirubin measures

A

Does not differentiate between conjugated and unconjugated

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46
Q

Direct bilirubin

A

Measures conjugated bilirubin - indicates hepatocellular disease, cholestasis, etc

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47
Q

Acute abdominal pain

A

Recent onset of severe pain (sudden)

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48
Q

Chronic abdominal pain

A

Occurs over weeks or months

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49
Q

Nature of abdominal pain

A

In part a result of mechanism responsible

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50
Q

Distention or spasm of hollow viscus causes what type of pain

A

“Visceal” type pain originating from pain receptors located in the organs (viscera) of the abdomen. Pain poorly localized and described as dull.

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51
Q

Paritoneal irritation causes what type of pain

A

“Parietal pain”, sharp, adn well localized

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52
Q

Mechanisms of abdominal pain

A

Any given pain can have more than 1 mechanism

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53
Q

Organs that may cause right upper quadrant abdominal pain

A

Chest cavity, liver, gallbladder, stomach, bowel, right kidney

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54
Q

Organs that may cause left upper quadrant abdominal pain

A

Pancreas, left kidney, spleen, heart or chest cavity

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55
Q

Organs that may cause right lower quadrant abdominal pain

A

Appendix, bowel, right ureter, pelvis

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56
Q

Organs that may cause left lower quadrant abdominal pain

A

Bowel (Diverticulitis), ureter, pelvis

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57
Q

Classic presentations

A

Example is appendicitis. Not all patients have classic presentaitons

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58
Q

Patients that do not typically present with classic symptoms

A

Infants, elderly, and debilitated patients

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59
Q

History of abdominal pain

A

OLDCARTS

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60
Q

Management of abdominal pain

A

Depends on cause

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61
Q

Obtain a consult or refer GI disorders

A

Disorders that present with BWAD - Blood in the stool; Weight loss; Anemia; and Dysphagia

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62
Q

Common causes of nausea and vomiting

A

GI - PUD, CNS - motion sickness, Systemic - pregnancy and food poisoning, Iatrogenia - meds and bulemia

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63
Q

Labs associated with nausea and vomiting

A

No labs if no systemic signs and symptoms and duration less than 24 hours

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64
Q

Therapy of nausea and vomiting

A

Determined by cause - no solids for 4 hrs after vomiting ceases; clear liquids, gradually increase; pharm - may need rectal suppositories (phenergan, bismuth subsalicylate, transdermal scope)

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65
Q

Nausea and vomiting medications safe during pregnancy

A

Reglan - class B; zofran - class B

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66
Q

Complimentary therapy for nausea and vomiting

A

Ginger and vitamin B6

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67
Q

When to consult for nausea and vomiting

A

If the symptoms persist for more than 24 hours.

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68
Q

Causes of constipation

A

Slow transit; pelvic floor dysfunction; primary diseases of the colon - stricture, tumor; Endocrine - hypothyroidism, DM; Neuro - parkinson, spinal cord lesion; Medications - anticholinergics, calcium channel blockers, diuretics, antacids

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69
Q

Most common cause of constipation

A

Functional with no underlying pathology

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70
Q

Management of constipation

A

Increase fluid, fiber, exercise; bulk forming agents; stool softeners - short term; avoid chronic laxative use

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71
Q

Consultaiton or referral of constipation

A

If changes in bowel pattern, unresponsive to treatment, or blood in stool

72
Q

Differential diagnoses of diarrhea

A

Medications; toxins; environemntal exposures; osmotic disorders - lactulose; bile salt malabsorption, diabetes; celiac disease, malnutrition - pernicious anemia; Crohn’s; diverticulitis; malignant neoplasms; fistulas; NSAIDs; IBS; alcohol; carcinoma

73
Q

Lab studies and diarrhea

A

No studies is no signs and symptoms and episode less than 48 hours

74
Q

Treatment of diarrhea

A

Stop all solids 12-24 hours, rehydrating solution, may ue Kaopectate or Pepto Bismol for symptomatic relief, Donnatol - cramping

75
Q

Antibiotics use and diarrhea

A

Use if fecal leukocytes, occult blood, fever with watery diarrhea or symptoms >1 week (usually Salmonella, Shigella, or Campylobacter)

76
Q

Antimotility drug use and diarrhea

A

No antimotility drugs if fecal leukocytes or blood in stools

77
Q

Peptic ulcer disease (PUD)

A

Ulceration of the GI mucosa in areas bathed by acid pepsin; stomach, duodenum and esophagus are common sites

78
Q

Etiology of peptic ulcer disease

A

H. pylori requisite factor in 80-90% of cases, NSAID usage

79
Q

Aggravating factors of peptic ulcer disease

A

Physiological stress - severe trauma, burns, shock; psychological stress; alcohol and nicotine use; presence of alcoholic liver cirrhosis, chronic pancreatitis, chronic lung disease, hyperparathyroidism, rheumatoid arthritis; family history

80
Q

Population affected by peptic ulcer disease

A

10% approximately

81
Q

Types of peptic ulcers

A

80% are duodenal, about 5% of gastric ulcers are malignant

82
Q

Signs and symptoms of peptic ulcer disease

A

Intermitent epigastric pain - gnawing, burning, boring, nagging pain begins 1-3 hrs after eating, frequently awaken person at night; pain relieved by food or antacids; some foods; weight loss frequent with gastric ulcer; dyspepsia

83
Q

Dyspepsia

A

Bloating, nausea, anorexia, excessive flatulence

84
Q

Diagnosis of duodenal ulcer

A

History of typical pain-food-relief pattern is important criteria for diagnosis of duodenal ulcer

85
Q

Physical findings of peptic ulcer disease

A

Usually limited to epigastric tenderness; include rectan exam and testing for occult blood through triple testing by patient with take home kit

86
Q

Diagnostic tests for peptic ulcer disease

A

Stool for occult blood - triple at home test; CBC with diff; H. pylori; serum culture or C-urea breath test; fecal antigen test; endoscopy

87
Q

Fecal antigen test and PPIs

A

Can not use test is patient taking PPI

88
Q

Inclusion criteria for endoscopy use in diagnosis of peptic ulcer disease

A

Patient over 50; indicated after 2 weeks of treatment if no improvement; to locate bleeding site in those with diagnosed or suspected blood loss

89
Q

Goals of treatment of peptic ulcer disease

A

Relief of symptoms, healing, prevention of recurrence

90
Q

Nonpharmacological management of peptic ulcer disease

A

Stop smoking; avoid NSAIDs and steroids; reduce stress; reduce alcohol and caffeine

91
Q

Pharmacological management of peptic ulcer disease

A

PPIs most potent but most expensive; H2RAs - 4-6 weeks then nightly pm x 2 yr

92
Q

Treatment options for H. pylori

A

Use of 2 antibiotics most efficacious, PPI, clarithromycin, amoxicillin or flagyl x 14 days

93
Q

Patient education and peptic ulcer disease

A

Disease and therapeutic management; purpose, dosage, side effects of meds; diet - encourage avoidance of known gastric acid stimulants - coffee, cola. No evidence to support need for bland diet or small frequent meals; avoid triggers; avoid eating within 3 hrs of bedtime to avoid nocturnal stimulation of acid secretion; stress reduction

94
Q

Reporting symptoms of peptic ulcer disease

A

Lack of response to medications, rectal bleeding, weight loss, increased weakness or dizziness, increasing pain

95
Q

Follow up for peptic ulcer disease

A

1-2 weeks check - symptom response to meds; GI bleeding; side or toxic effects of meds; for those with gastric ulcers, document healing and is unnecessary in uncomplicated duodenal ulcers

96
Q

Gastroesophageal reflux disease (GERD)

A

Reflux of stomach and duodenal contents into the esophagus leading to a spectrum of clinical manifestations predominated by inflammation of the esophagus

97
Q

Etiology of GERD

A

Most often related to inappropriate relaxation of the lower esophageal sphincter (LES) which allows reflux of gastric acid and pepsin into the distal esophagus; low resting pressure of the sphincter; poor esophageal clearance

98
Q

Drugs that cause inappropriate relaxation of the lower esophageal sphincter (LES)

A

Narcotics, benzos, calcium channel blockers, alcohol, nicotine, chocolate, peppermint

99
Q

Esophageal motility and GERD

A

Deflects normal motility

100
Q

Heartburn and GERD

A

Daily prevalence symptom and 10% of normal adult population is affected

101
Q

Signs and symptoms of GERD

A

Retrosternal aching or burning occurring 30-60 minutes after eating associated with large meals and aggravated by lying down or bending over; chest heaviness, pressure radiating to neck, jaws, or shoulders (can mimic angina); regurgitation of fluid or food; nocturnal aspiraiton; recurrent pneumonia or bronchospasm

102
Q

Physical findings of GERD

A

Epigastric tenderness; stool for occult blood - triple home testing; dysphagia with weight loss; loss of dental enamel

103
Q

Diagnostic tests of GERD

A

Usually diagnosed by history; endoscopy

104
Q

Endoscopy indicated as diagnostic for GERD for…

A

> 50 with sudden onset of symptoms; does not respond to therapy; alarm symptoms (bleeding, anemia, dysphagia, odynophagia); longstanding symptoms at risk for Barrett’s esophagus

105
Q

Treatment for GERD

A

Lifestyle modification - helpful but unlikely to control symtpoms. Follow-up in 2-4 weeks

106
Q

Cholecystitis

A

Acute or chronic inflammation of the gallbladder

107
Q

Cause of cholecystitis

A

90% related to presence of pigmented or cholesterol calculi which vary in diameter from 1mm - 4 cm; occurs subsequent to bile stasis, bacterial infection, or ischemia

108
Q

Pathophysiology of cholecystitis

A

When a stone becomes impacted in the cystic duct, inflammation develops behind the obstruction; if not relieved, pressure builds up in the gallbladder and leads to distention, ischemic changes, gangrene, and perforation with subsequent abscess formation and less frequently generalized peritonitis

109
Q

Risk factors for cholesterol stone formation

A

Cholesterol hypersecretion in bile related to age, gender - female, maternal family history, obesity, high triglycerides and other metabolic diseases, rapid weight loss, estrogen therapy, oral contraceptive use, Pima Indian descent/Scandinavians

110
Q

Gallbladder hypomotility

A

Prolonged fasting, pregnancy, oral contraceptive use

111
Q

Signs and symptoms of cholecystitis

A

Episodic occurrence of postparandial fullness, heartburn, nausea, flatulence, regurgitation of bitter fluid, vomiting often precipitated by a large or fatty meal; anorexia (inability to finish an average size meal); recurrent episodes of biliary colic; tenderness in the same area may persist for days; accompanied by vomiting in 75% of the cases; constant aching pain or pressure in the right upper quadrant or epigastrium that radiates to the back or right shoulder

112
Q

Biliary colic

A

Sudden appearance of severe pain in the epigastrium or right hypochondrium which subsides relatively slowly (1-6 hrs)

113
Q

Physical findings of cholecystitis

A

Unremarkable between attacks. During attack; mild temperature elevation, tachycardia, and increased respiratory rate. Mild jaundice occurs in 20% of cases. Abdomen: guarding, rebound tenderness in R hypochondrium, palpable tender sausage shaped mass in RUQ during acute attack in 20-30% of cases. + Murphy’s signs. Hypoactive bowel sounds. Dehydration rare.

114
Q

Positive Murphy’s sign

A

Inspiratory arrest secondary to extreme tenderness when subhepatic area is palpated during deep inspiraiton

115
Q

Diagnostic tests of cholecystitis

A

CBC with diff - mild leukocytosis with increased bands; LFTs; serum electrolytes; BUN & creatining; HCG if of childbearing age; ultrasound to show gallstones, thickened gallbladder wal - fast 8 hrs; Technetium Tc99mPIPIDA (HIDA) scan - cystic duct occlusion and non-visualized gallbladder if diagnosis unclear; refer to surgeon

116
Q

Appendicitis

A

Inflammation of the vermiform appendix

117
Q

Etiology of appendicitis

A

Obstruction of appendix with hardened feces, stricture, inflammation, foreign body, or neoplasm; occurs in all age groups, but more common in males 10-30 yrs old, higher mortality rate due to complications in children, adolescents, and people >55

118
Q

Leading cause of abdominal surgery

A

Appendicitis

119
Q

Signs and symptoms of appendicitis

A

Acute onset of periumbilical or epigastric pain which ranges from mildly diffuse to severe; anorexia, nausea, and vomiting; shifting of pain to RLQ after several hrs aggravated by walking or coughing; occasional radiation of pain into testicles; spasms of abd muscles; constipation, usual; diarrhea rare; elderly clients may present differently

120
Q

McBurney’s point

A

Shifting of pain to right lower quadrant from unbilical area associated with appendicitis

121
Q

Elderly patient’s presentation of appendicitis

A

May present with mild symptoms of unexplained weakness, anorexia, tachycardia, and abdominal distention with little pain

122
Q

Signs and symptoms of appendicitis perforation

A

Sudden cessation of pain; abdominal rigidity; generalized abdominal tenderness; high fever; vomiting; dehydration; decreased bowel sounds; shock

123
Q

Physical findings of appendicitis before perforation

A

Fever; abdominal rigidity; point and rebound tenderness in RLQ, decreased or absent bowel sounds; positive psoas and obrurator signs; rectal exam - tenderness in the right perirectal area

124
Q

Diagnostic tests of appendicitis

A

CBC with diff - leukocytosis with increased band cells (shift to left in elderly); C-reactive protein (normal after 24 hrs would indicate NOT appendicitis); urinalysis (bladder/kidney); HCG (r/o ectopic); abdominal ultrasound/CT if diagnosis uncertain

125
Q

Treatment of appendicitis

A

Refer when suspected

126
Q

Diverticulitis

A

Inflammation of one or more diverticula in the bowel wall with microperforation and abscess formation in the pericolic fat

127
Q

Etiology of diverticulitis

A

Inflammatory process similar to etiologic agents in appendicitis; occurs in about 25% of persons with diverticula (estimated to be 5-10% of adult population); indicence increases after age 45; higher incidence in women; low fiber diet

128
Q

Most common occurrance of diverticulitis

A

Most often occurs in the sigmoid colon, but can occur anywhere in the GI tract

129
Q

Percentage of complications with diverticulitis

A

15% will develop complications; perforations; and abscesses

130
Q

Signs and symptoms of diverticulitis

A

Acute LLQ pain - steady and severe lasting for several days or crampy and intermittent; constipation; pain increased with defecation; flatulence; N&V; low grade fever

131
Q

Physical findings of diverticulitis

A

Mild fever, tachycardia; guarding, rebound tenderness, rigidity especially over LLQ; if abscess has formed, a tender palpable mass may be noted

132
Q

Diagnostic tests for diverticulitis

A

CBC - slight leukocytosis; urinalysis - WBCs; stool for occult blood via home testing of 3 stools; plain abd films - look for free abd air, bowel obstruction; if not responsive to treatment - CT of abd and pelvis - shows degree of inflammation; colonscopy AFTER acute phase may be helpful

133
Q

Management/treatment of diverticulitis

A

Clear liquids for 2-3 days followed by low-residue diet once symptoms subsided; metonidazole 500 mg tid AND cipro 500 mg bid x7-14 days OR bactrium DS bid x 7-14 days OR augmentin bid x 7-14; if moderate to sever, will require hospitalization and may need surgical management

134
Q

Patient education regarding diverticulitis

A

After acute phase, gradually increase fiber to include bran, whole grains, cereals, raw cooked or dried fruit, raw vegetables; avoid laxatives and enemas; bulk forming agents may help to prevent frequent recurrences

135
Q

Follow up regarding diverticulitis

A

Return visit 24-48 hrs after initial therapy and again after completion of antibiotic therapy

136
Q

Acute gastroenteritis

A

Acute inflammation of the GI mucosa

137
Q

Etiology of gastroenteritis

A

Commonly due to infectious agents - viruses, bacteria, and parasites; second leading cause of morbidity in US; epidemic outbreaks of bacterial enteritis occur in groups who have ingested contaminated food; primarily self-limiting; very young, elderly, and those with chronic disease are at a higher risk of mortality

138
Q

Types of gastroenteritis

A

Inflammatory vs noninflammatory (does not invade bowel tissue) vs penetrating (invades lymphatics) and bacterial vs viral vs parasitis

139
Q

Signs and symptoms of gastroenteritis

A

Abrupt onset of N/V; explosive flatulence; crampy abdominal pain; frequent watery diarrhea; myalgia; headache; fever; generalized weakness

140
Q

Physical findings of gastroenteritis

A

Fever - viral low grade, bacterial higher; abdomen - diffuse tenderness; no spasm or rebound tenderness with salmonella; hyperactive bowel sounds; slight distention; absent or hypoactive bowel sounds common with botulism; dizziness, difficulty swallowing and other neurodeficits are indication of botulism are require immediate referral

141
Q

Diagnostics of gastroenteritis

A

Fecal leukocytes if fever >102, bloody diarrhea, abdominal pain, profuse watery diarrhea and dehydration or frail, elderly or immuno-compromised; CBC with diff, serum electrolytes, BUN and creatinine; if leukocytes - stool culture, O&P, parasites, C-diff culture if suspected; fever, chilld, rigors, night sweats adn weight loss indicate penetrating diarrhea and require blood cultures

142
Q

Management/treatment of gastroenteritis

A

Most can be treated for 24-48 hr without labs; clear liquids 24 hr, hydrate!; antisecretory and antispasmotics - anticholinergic drugs can be used to decrease N/V, cramping, diarrhea; antimotility agents used with noninflammatory diarrhea but not with fecal leukocytosis or blood in stool; antibiotics with fecal leukocytes, occult blood, fever with watery diarrhea; cipro or nonfloxacin until stool cultures return if not pregnant

143
Q

Antisecretory meds and antibiotics

A

They may decrese effectiveness of antibiotics

144
Q

Diarrhea > 2 weeks indicates…

A

Likely indicates Giardia and treatment choice is Fragyl

145
Q

Most common cause of traveler’s diarrhea

A

E. coli

146
Q

Treatment/management of traveler’s diarrhea

A

Self-limiting but antibiotics may shorten course; cipro, rifaximin or z-mycin only if diarrhea lasts more than 1-2 days or if associated with high fever; Pepto-Bismol may be prescribed

147
Q

Prevention of traveler’s diarrhea

A

Avoid untreated water and ice; avoid raw fruits and vegetables; avoid undercooked meat; avoid unpasteurized milk

148
Q

Management/treatment of diarrhea

A

For all cases, assess hydration and provide rehydrating solutions; consult with MD if symptoms not improved in 48 hrs; may want to obtain stool for O&P; report food poisoning to health department; usually self-limiting; return if not improved in 48-72 hrs; diarrhea may continue 1-2 weeks with salmonella

149
Q

Irritable bowel syndrome (IBS)

A

Functional disturbance of intestinal motility marked by a common symptom complex with includes abdominal pain and alternate bouts of constipation and diarrhea; influenced by emotional factors

150
Q

Diagnostic criteria of irritable bowel syndrome

A

Abdominal discomfort relieved by passage of stool or associated with diarrhea, constipation or mucus in stool; onset of symptoms in young adulthood; no blood in stool; symptoms present for at least 3x/month for at least 3 months beginning 6 months prior to diagnosis

151
Q

Physical findings of irritable bowel syndrome

A

Abdomen - milk abdominal tenderness, normal or mildly hyperactive bowel sounds; otherwise normal findings

152
Q

Diagnostic tests of irritable bowel syndrome

A

CBC, sed rate, blood chemistry, TSH, stool for occult blood and fecal leukocytes; pts > 50 colonscopy; pts <50 sigmoidoscopy; R/O lactose intolerance

153
Q

Ruling out lactose intolerance

A

2 week lactose free diet or drink quart of milk and check for symptoms/hydrogen breath testing

154
Q

Management/treatment of irritable bowel syndrome

A

High fiber diet especially with constipation; bulking agents; drug therapy should be reserved for those with more severe symptoms that do not respond to conservative treatment (about 1/3 of patients); targeted to dominant symptom (pain, constipation, diarrhea) - antispasmotics, antidiarrheal, anticonstipation, and psychotropics

155
Q

Hepatitis

A

Inflammation of the liver

156
Q

Diagnostics of hepatitis

A

AST/ALT, hepatitis panel

157
Q

Serologic markers - hepatitis A acute infection

A

IgM anti-HAV

158
Q

Serologic markers - hepatitis B acute infection

A

HBsAg, IgM anti-HBc, HBV DNA, HBeAG (suggests greater infectivity)

159
Q

Serologic markers - hepatitis A prior infection

A

IgG anti-HAV

160
Q

Serologic markers - hepatitis B chronic infection

A

HBsAg, IgG antiHBc, HBV DNA, HBeAg (higher infectivity), Anti-Hbe (lower infectivity)

161
Q

Serologic markers - hepatitis B prior infection

A

ant-HBs (if only marker - immunity from vaccination), IgG antiHBc, anti-HBe

162
Q

Serologic markers - hepatitis B acute infection

A

HCV-RNA, anti-HCV (usually within 2 weeks of active infection)

163
Q

Management of hepatitis

A

Treatment of symptoms; educate to abstain from alcohol and any hepatotoxic drugs; no strenous activities or contact sports until recovery; universal precautions

164
Q

Treatment post-exposure to hepatitis A

A

Standard immune globulin

165
Q

Treatment post-exposure to hepatitis B

A

Vaccination plus ep B immune globulin

166
Q

Pancreatitis

A

Inflammation of the pancreas

167
Q

Symptoms of pancreatitis

A

Severe abdominal pain, poorly localized, frequently radiates to back

168
Q

Diagnostics of pancreatitis

A

Serum amylase - elevated 3x normal (secreted in salivary gland disease); serum lipase 3x elevation specific to pancreatitis; abd CT scan most useful

169
Q

Management of pancreatitis

A

Referral to gastoenterologist

170
Q

Jaundice

A

Elevated AST and ALT indicate hepatocyte damage. ALT is usually higher in viral hepatitis. In alcoholic hepatitis, AST may be higher. Alkaline phosphates (ALP-1 and ALP-2)

171
Q

Alkaline phosphates are produced where?

A

ALP-1 found primarily in the liver. ALP-2 found in the bone. Smaller amounts are produced in the intestines, kidney, and placenta.

172
Q

When alkaline phosphates are normally elevated

A

With rapid bone growth (adolescence, fetus). Fetal bone growth may not contribute that much but along with the placental production, you would see elevated levels

173
Q

Gamma-glutamyl transferase (GGT)

A

May be used to determine the cause of an elevated alkaline phosphatase (ASP). Both ALP and GGT are elevated in disease of the bild ducts and in some liver diseases, but only ALP willb e elvated in bone disease

174
Q

Normal GGT and high ALP indicates…

A

Most likely the cause is bone disease

175
Q

Aggravating factors of Hemorroids

A

Constipation, pregnancy, straining

176
Q

Signs and symptoms of hemorrhoids

A

Bleeding and discomfort

177
Q

Treatment of hemorrhoids

A

Increase fiber; increase fluids, bulk forming agents, reguarl exercise, OTC topicals, Tucks, Sitz batha

Comps - Mod 2 (9 decks)

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