Module 4 GI PC 617 - Sheet1 Flashcards
(177 cards)
1
Q
Abdominal pain
A
Can be self-limiting or life threatening
2
Q
First step in managing abdominal pain
A
Rule out “hot abdomen”
3
Q
Challenge of treating abdominal pain
A
Design a safe and cost effective plan for work up that will distinguish among many causes
4
Q
Exam for patients with acute abdominal pain
A
Assess for evidence of obstruction, peritoneal irritation, and vascular problems
5
Q
If “hot abdomen” suspected
A
Patient should not be sent home who may have an emergency condition that might require urgent surgery
6
Q
Past treatment for traveler’s diarrhea
A
No longer uses doxycycline and bactrim
7
Q
Current recommendation for traveler’s diarrhea
A
Cipro, Levoquin, Rifaximin, and Axithromycin. If patient is pregnant, Zithromax
8
Q
Viral hepatitis
A
A systemic infection that primarily affects the liver cells
9
Q
Determining type of hepatitis with assessment only
A
Can not be done until blood work examined
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
11
Q
Incubation time of Hepatitis A
A
2-7 weeks
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
13
Q
Length of illness
A
Usually self-limiting disease that is not severe and will go away in time
14
Q
Diagnosis of previous infection of Hepatitis A
A
Presence of anti-HAV imune globulin G (IgG)
15
Q
Diagnosis of acute infection of Hepatitis A
A
Anti-HAV IgM (IgM is first antibody produced after exposure)
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.
17
Q
Hepatitis panel includes…
A
Hepatitis A, B, and C.
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
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.
20
Q
Incubation period of Hepatitis B
A
2-6 moths
21
Q
Prodromal symptoms of Hepatitis B
A
Longer and worse than Hep A and may include urticaria, rash, arthralgias, angioedema, serum sickness
22
Q
Jaundice phase of Hepatitis B
A
After prodrome, lasts about 2 weeks. Hep B more likely to cause jaundice than Hep A
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)
24
Q
Labs to screen for Hepatitis B
A
HBsAg, HBsAb, and HBcAb
25
Hepatitis B Vaccine
Protects for about 5 years - retest in persons at high risk. Now routine for infants in most states. Also protects against hepatitis cancer
26
Vaccination when exposure to hepatitis B and not vaccinated
Give HBIG (immunoglobulin G) and vaccine as soon as possible after exposure (within 7 days) lasts 4-6 months
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Lab test to determine status post immunization
Anti-HBsAB. Want to see this be positive.
28
Hepatitic C or non-A, non-B
Transmitted primarily via IV drug use and blood products
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Prodromal symptoms of Hepatitis C
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
30
Treatment of Hepatitis C during first 6 months
Not usually done during this time secondary to negative conversion of seropositive patients
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Screening for hepatitis C
Enzyme immunoassay (EIA)
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Diagnosis of Hepatitis C
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)
33
Vaccination for Hepatitis C
No vaccine or immunoglobulin because hepatitis C has a high rate or mutation
34
Replication of Hepatitis D
Requires Hepatitis B
35
Hepatitis E
Most common in developing countries - spread by fecal oral route
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Transmission of hepatitis D
Parenteral and sexual contact
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Incubation of Hepatitis E
Incubation 2-9 weeks and like Hep A may be very serious for pregnancy women Killing about 21% of pregnant women who are infected
38
Jaundice
Green-yellow staining of skin and mucous membranes by bilirubin
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Bilirubin
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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Types of jaundice
Pre-hepatitc (Unconjugated), hepatic (Conjugated), and posthepatic (Conjugated)
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Pre-jaundice
Unconjugated - most common cause hemolysis. Hemolysis is most common cause
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Hepatitc jaundice
Conjugated - Immaturity (newborn) or dysfunction of hepatocyte in bilirubin metabolism
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Posthepatic
Conjugated - obstruction of bile ducts - pancreatitis, gallbladder stasis
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Lab evaluation of jaundice
Total bilirubin; direct bilirubin; and indirect bilirubin
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Total bilirubin measures
Does not differentiate between conjugated and unconjugated
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Direct bilirubin
Measures conjugated bilirubin - indicates hepatocellular disease, cholestasis, etc
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Acute abdominal pain
Recent onset of severe pain (sudden)
48
Chronic abdominal pain
Occurs over weeks or months
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Nature of abdominal pain
In part a result of mechanism responsible
50
Distention or spasm of hollow viscus causes what type of pain
"Visceal" type pain originating from pain receptors located in the organs (viscera) of the abdomen. Pain poorly localized and described as dull.
51
Paritoneal irritation causes what type of pain
"Parietal pain", sharp, adn well localized
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Mechanisms of abdominal pain
Any given pain can have more than 1 mechanism
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Organs that may cause right upper quadrant abdominal pain
Chest cavity, liver, gallbladder, stomach, bowel, right kidney
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Organs that may cause left upper quadrant abdominal pain
Pancreas, left kidney, spleen, heart or chest cavity
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Organs that may cause right lower quadrant abdominal pain
Appendix, bowel, right ureter, pelvis
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Organs that may cause left lower quadrant abdominal pain
Bowel (Diverticulitis), ureter, pelvis
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Classic presentations
Example is appendicitis. Not all patients have classic presentaitons
58
Patients that do not typically present with classic symptoms
Infants, elderly, and debilitated patients
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History of abdominal pain
OLDCARTS
60
Management of abdominal pain
Depends on cause
61
Obtain a consult or refer GI disorders
Disorders that present with BWAD - Blood in the stool; Weight loss; Anemia; and Dysphagia
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Common causes of nausea and vomiting
GI - PUD, CNS - motion sickness, Systemic - pregnancy and food poisoning, Iatrogenia - meds and bulemia
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Labs associated with nausea and vomiting
No labs if no systemic signs and symptoms and duration less than 24 hours
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Therapy of nausea and vomiting
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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Nausea and vomiting medications safe during pregnancy
Reglan - class B; zofran - class B
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Complimentary therapy for nausea and vomiting
Ginger and vitamin B6
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When to consult for nausea and vomiting
If the symptoms persist for more than 24 hours.
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Causes of constipation
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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Most common cause of constipation
Functional with no underlying pathology
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Management of constipation
Increase fluid, fiber, exercise; bulk forming agents; stool softeners - short term; avoid chronic laxative use
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Consultaiton or referral of constipation
If changes in bowel pattern, unresponsive to treatment, or blood in stool
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Differential diagnoses of diarrhea
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
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Lab studies and diarrhea
No studies is no signs and symptoms and episode less than 48 hours
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Treatment of diarrhea
Stop all solids 12-24 hours, rehydrating solution, may ue Kaopectate or Pepto Bismol for symptomatic relief, Donnatol - cramping
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Antibiotics use and diarrhea
Use if fecal leukocytes, occult blood, fever with watery diarrhea or symptoms >1 week (usually Salmonella, Shigella, or Campylobacter)
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Antimotility drug use and diarrhea
No antimotility drugs if fecal leukocytes or blood in stools
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Peptic ulcer disease (PUD)
Ulceration of the GI mucosa in areas bathed by acid pepsin; stomach, duodenum and esophagus are common sites
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Etiology of peptic ulcer disease
H. pylori requisite factor in 80-90% of cases, NSAID usage
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Aggravating factors of peptic ulcer disease
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
Population affected by peptic ulcer disease
10% approximately
81
Types of peptic ulcers
80% are duodenal, about 5% of gastric ulcers are malignant
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Signs and symptoms of peptic ulcer disease
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
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Dyspepsia
Bloating, nausea, anorexia, excessive flatulence
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Diagnosis of duodenal ulcer
History of typical pain-food-relief pattern is important criteria for diagnosis of duodenal ulcer
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Physical findings of peptic ulcer disease
Usually limited to epigastric tenderness; include rectan exam and testing for occult blood through triple testing by patient with take home kit
86
Diagnostic tests for peptic ulcer disease
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
Fecal antigen test and PPIs
Can not use test is patient taking PPI
88
Inclusion criteria for endoscopy use in diagnosis of peptic ulcer disease
Patient over 50; indicated after 2 weeks of treatment if no improvement; to locate bleeding site in those with diagnosed or suspected blood loss
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Goals of treatment of peptic ulcer disease
Relief of symptoms, healing, prevention of recurrence
90
Nonpharmacological management of peptic ulcer disease
Stop smoking; avoid NSAIDs and steroids; reduce stress; reduce alcohol and caffeine
91
Pharmacological management of peptic ulcer disease
PPIs most potent but most expensive; H2RAs - 4-6 weeks then nightly pm x 2 yr
92
Treatment options for H. pylori
Use of 2 antibiotics most efficacious, PPI, clarithromycin, amoxicillin or flagyl x 14 days
93
Patient education and peptic ulcer disease
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
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Reporting symptoms of peptic ulcer disease
Lack of response to medications, rectal bleeding, weight loss, increased weakness or dizziness, increasing pain
95
Follow up for peptic ulcer disease
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
Gastroesophageal reflux disease (GERD)
Reflux of stomach and duodenal contents into the esophagus leading to a spectrum of clinical manifestations predominated by inflammation of the esophagus
97
Etiology of GERD
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
Drugs that cause inappropriate relaxation of the lower esophageal sphincter (LES)
Narcotics, benzos, calcium channel blockers, alcohol, nicotine, chocolate, peppermint
99
Esophageal motility and GERD
Deflects normal motility
100
Heartburn and GERD
Daily prevalence symptom and 10% of normal adult population is affected
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Signs and symptoms of GERD
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
Physical findings of GERD
Epigastric tenderness; stool for occult blood - triple home testing; dysphagia with weight loss; loss of dental enamel
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Diagnostic tests of GERD
Usually diagnosed by history; endoscopy
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Endoscopy indicated as diagnostic for GERD for...
>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
Treatment for GERD
Lifestyle modification - helpful but unlikely to control symtpoms. Follow-up in 2-4 weeks
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Cholecystitis
Acute or chronic inflammation of the gallbladder
107
Cause of cholecystitis
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
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Pathophysiology of cholecystitis
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
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Risk factors for cholesterol stone formation
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
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Gallbladder hypomotility
Prolonged fasting, pregnancy, oral contraceptive use
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Signs and symptoms of cholecystitis
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
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Biliary colic
Sudden appearance of severe pain in the epigastrium or right hypochondrium which subsides relatively slowly (1-6 hrs)
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Physical findings of cholecystitis
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.
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Positive Murphy's sign
Inspiratory arrest secondary to extreme tenderness when subhepatic area is palpated during deep inspiraiton
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Diagnostic tests of cholecystitis
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
Appendicitis
Inflammation of the vermiform appendix
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Etiology of appendicitis
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
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Leading cause of abdominal surgery
Appendicitis
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Signs and symptoms of appendicitis
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
McBurney's point
Shifting of pain to right lower quadrant from unbilical area associated with appendicitis
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Elderly patient's presentation of appendicitis
May present with mild symptoms of unexplained weakness, anorexia, tachycardia, and abdominal distention with little pain
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Signs and symptoms of appendicitis perforation
Sudden cessation of pain; abdominal rigidity; generalized abdominal tenderness; high fever; vomiting; dehydration; decreased bowel sounds; shock
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Physical findings of appendicitis before perforation
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
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Diagnostic tests of appendicitis
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
Treatment of appendicitis
Refer when suspected
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Diverticulitis
Inflammation of one or more diverticula in the bowel wall with microperforation and abscess formation in the pericolic fat
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Etiology of diverticulitis
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
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Most common occurrance of diverticulitis
Most often occurs in the sigmoid colon, but can occur anywhere in the GI tract
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Percentage of complications with diverticulitis
15% will develop complications; perforations; and abscesses
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Signs and symptoms of diverticulitis
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
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Physical findings of diverticulitis
Mild fever, tachycardia; guarding, rebound tenderness, rigidity especially over LLQ; if abscess has formed, a tender palpable mass may be noted
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Diagnostic tests for diverticulitis
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
Management/treatment of diverticulitis
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
Patient education regarding diverticulitis
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
Follow up regarding diverticulitis
Return visit 24-48 hrs after initial therapy and again after completion of antibiotic therapy
136
Acute gastroenteritis
Acute inflammation of the GI mucosa
137
Etiology of gastroenteritis
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
Types of gastroenteritis
Inflammatory vs noninflammatory (does not invade bowel tissue) vs penetrating (invades lymphatics) and bacterial vs viral vs parasitis
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Signs and symptoms of gastroenteritis
Abrupt onset of N/V; explosive flatulence; crampy abdominal pain; frequent watery diarrhea; myalgia; headache; fever; generalized weakness
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Physical findings of gastroenteritis
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
Diagnostics of gastroenteritis
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
Management/treatment of gastroenteritis
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
Antisecretory meds and antibiotics
They may decrese effectiveness of antibiotics
144
Diarrhea > 2 weeks indicates...
Likely indicates Giardia and treatment choice is Fragyl
145
Most common cause of traveler's diarrhea
E. coli
146
Treatment/management of traveler's diarrhea
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
Prevention of traveler's diarrhea
Avoid untreated water and ice; avoid raw fruits and vegetables; avoid undercooked meat; avoid unpasteurized milk
148
Management/treatment of diarrhea
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
Irritable bowel syndrome (IBS)
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
Diagnostic criteria of irritable bowel syndrome
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
Physical findings of irritable bowel syndrome
Abdomen - milk abdominal tenderness, normal or mildly hyperactive bowel sounds; otherwise normal findings
152
Diagnostic tests of irritable bowel syndrome
CBC, sed rate, blood chemistry, TSH, stool for occult blood and fecal leukocytes; pts > 50 colonscopy; pts <50 sigmoidoscopy; R/O lactose intolerance
153
Ruling out lactose intolerance
2 week lactose free diet or drink quart of milk and check for symptoms/hydrogen breath testing
154
Management/treatment of irritable bowel syndrome
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
Hepatitis
Inflammation of the liver
156
Diagnostics of hepatitis
AST/ALT, hepatitis panel
157
Serologic markers - hepatitis A acute infection
IgM anti-HAV
158
Serologic markers - hepatitis B acute infection
HBsAg, IgM anti-HBc, HBV DNA, HBeAG (suggests greater infectivity)
159
Serologic markers - hepatitis A prior infection
IgG anti-HAV
160
Serologic markers - hepatitis B chronic infection
HBsAg, IgG antiHBc, HBV DNA, HBeAg (higher infectivity), Anti-Hbe (lower infectivity)
161
Serologic markers - hepatitis B prior infection
ant-HBs (if only marker - immunity from vaccination), IgG antiHBc, anti-HBe
162
Serologic markers - hepatitis B acute infection
HCV-RNA, anti-HCV (usually within 2 weeks of active infection)
163
Management of hepatitis
Treatment of symptoms; educate to abstain from alcohol and any hepatotoxic drugs; no strenous activities or contact sports until recovery; universal precautions
164
Treatment post-exposure to hepatitis A
Standard immune globulin
165
Treatment post-exposure to hepatitis B
Vaccination plus ep B immune globulin
166
Pancreatitis
Inflammation of the pancreas
167
Symptoms of pancreatitis
Severe abdominal pain, poorly localized, frequently radiates to back
168
Diagnostics of pancreatitis
Serum amylase - elevated 3x normal (secreted in salivary gland disease); serum lipase 3x elevation specific to pancreatitis; abd CT scan most useful
169
Management of pancreatitis
Referral to gastoenterologist
170
Jaundice
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
Alkaline phosphates are produced where?
ALP-1 found primarily in the liver. ALP-2 found in the bone. Smaller amounts are produced in the intestines, kidney, and placenta.
172
When alkaline phosphates are normally elevated
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
Gamma-glutamyl transferase (GGT)
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
Normal GGT and high ALP indicates...
Most likely the cause is bone disease
175
Aggravating factors of Hemorroids
Constipation, pregnancy, straining
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Signs and symptoms of hemorrhoids
Bleeding and discomfort
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Treatment of hemorrhoids
Increase fiber; increase fluids, bulk forming agents, reguarl exercise, OTC topicals, Tucks, Sitz batha
