Examthree

Front 1

physical - mucus, sloughing epithelium , saliva, peristalsis
chemical - enzymes in saliva, mucus
cellular - phagocytes (PMN), normal microbiota

Back 1

oral cavity (mouth), pharynx (throat), esophagus

Front 2

physical - mucus, sloughing epithelium, peristalsis
chemical - HCl (pH ~2), pepsin (digestive enzyme)

Back 2

Stomach

Front 3

physical - mucus, sloughing epithelium, peristalsis
chemical - digestive enzymes (pancreas), bile (gall bladder)

Back 3

small intestine

Front 4

physical - mucus, sloughing epithelium, peristalsis
chemical - anaerobic conditions
cellular - phagocytes; normal microbiota (100 billion bacteria per gram of fecal material in large intestine)

Back 4

large intestine - includes colon, rectum and anus

Front 5

gastrectomy, achlorlydria, antacid therapy; intestinal obstructions, antimicrobial agent therapy, malnutrition, immaturity (infants)

Back 5

predisposing factors

Front 6

pathogenesis: dental plaque accumulation leads to punched-out ulcers in gingival (gum) tissue (spreads to soft palate, tonsilar areas) which leads to decay of gingiva (foul odor, vile taste) which causes loosening and loss of teeth as a result of bone resorption

Back 6

Acute Necrotizing Ulcerative Gingivitis (ANUG) (bacterial)

Front 7

treatment: surgery, antimicrobial agent treatment
prevention: reduce plaque accumulation by brushing and flossing teeth as well as by reducing dietary sugar content

Back 7

Acute Necrotizing Ulcerative Gingivitis (ANUG) treatment and prevention:

Front 8

is transmitted by direct oral contact and most people are infected as children. pathogenesis: recurrent chronic lesions ("cold" sores or fever blisters) near junction between lip and facial tissue

Back 8

Oral Herpes and Herpes Labialis (viral)

Front 9

treatment: acyclovir, famvir, or valtrex shorten disease episodes, slow recurrence, but don't cure
prevention: avoid contact with cold sores on other people

Back 9

Oral Herpes and Herpes Labialis treatment and prevention

Front 10

epidemiology: Candida albicans, a fungal member of normal microbiota, is an opportunistic fungus that frequently infects immunocompromised patients
pathogenesis: throat inflammation with superficial damage ... unless the patient is immunocompromised, then infection is chronic and damaging

Back 10

Thrush (fungal)

Front 11

treatment: nystatin or clotrimazole for routine infections; fluconazole or itraconazole for systemic therapy, particularly in immunocompromised people
prevention: avoid broad spectrum antibiotics and immunocompromise

Back 11

Thrush treatment and prevention

Front 12

epidemiology: Virus is transmitted via respiratory secretions or saliva before symptoms appear; ~6500 cases reported in the US each year (most age 5-10)
pathogenesis: parotid salivary gland infection causes fever, accumulation of saliva (parotid swelling, tenderness) after 16-18 days; complications - infection of ovaries, testes, thyroid, pancreas, CNS (meningitis, encephalitis, deafness)

Back 12

Mumps (viral)

Front 13

teatment: TLC
prevention: MMR vaccine, avoid contact with respiratory secretions or saliva of infected persons

Back 13

Mumps treatment and prevention

Front 14

epidemiology: Streptococcus mutans - other acidogenic normal microbiota, including S. sanguis, S. mitis and S. salivarius (bacteria)
pathogenesis: Streptococci adhere to tooth surface via glucans and levans produced from carbohydrates such as sucrose (develops into plaque as salts are incorporated);) generated as lactic acid (produced during sugar catabolism) dissolves tooth enamel

Back 14

Dental Caries (bacterial)

Front 15

treatment: physical removal of brownish-black "rotted" material, then "filling" with dental amalgam (problem: amalgam contains mercury)
prevention: tooth brushing and flossing; fluoride treatment (toothpaste, drinking water, dentist's office); reduction of simple sugar content of diet

Back 15

Dental Caries treatment and prevention

Front 16

Dental Caries:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 16

Bacterial

Front 17

Acute Necrotizing Ulcerative Gingivitis (ANUG)
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 17

Bacterial

Front 18

Oral Herpes and Herpes Labialis
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 18

Viral

Front 19

Thrush
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 19

Fungal

Front 20

Mumps
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 20

Viral

Front 21

Helicobacter Peptic Disease Syndrome (Ulcers):
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 21

Bacterial

Front 22

Botulism:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 22

Bacterial

Front 23

Staphylococcal Intoxication:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 23

Bacterial

Front 24

Mycotoxicosis:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 24

Fungal

Front 25

Enteritis:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 25

Bacterial

Front 26

Giardiasis:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 26

Protozoan

Front 27

Cryptosporidiosis:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 27

Protozoan

Front 28

Bacillary Dysentery (Shigellosis)
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 28

Bacterial

Front 29

Amebic Dysentery (Amebiasis)
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 29

Protozoan

Front 30

Cholera
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 30

Bacterial

Front 31

Typhoid Fever
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 31

Bacterial

Front 32

Poliomyelitis
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 32

Viral

Front 33

Hepatitis A and E
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 33

Viral

Front 34

Toxoplasmosis
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 34

Protozoan

Front 35

Pinworm (Enterobiasis)
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 35

Helminth

Front 36

Trichinosis:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 36

Helminth

Front 37

Tapeworm:
Bacterial?
Fungal?
Viral?
Protozoan?
Helminth?

Back 37

Helminth

Front 38

pathogenesis: bacterium lives in gastric mucus, moves toward gastric epithelial cells using its flagella, adheres to these cells by binding proteins or glycoproteins (especially Lewisb antigens on type O cells), produces urease (neutralizes stomach acid; induces inflammation) and vacuolating cytotoxin (damages gastric cells); infiltrating phagocytes secrete cytokines that augment and prolong inflammation, leading to formation of ulcers, which generate a gnawing or burning pain in the abdomen ... from the navel upwards to the breastbone; less common signs and symptoms include: belching, nausea, vomiting, poor appetite, weight loss, feeling tired and weak; complications include perforated ulcers and an up to 12-fold increased rate of gastric adenocarcinoma (a form of cancer); possible link with sudden infant death syndrome (SIDS)

Back 38

Helicobacter Peptic Disease Syndrome (Ulcers)

Front 39

treatment: two combination drug therapy approaches are:
Two-week, triple therapy - 90% effective in curing it, but hard for patients to accomplish and causes a number of unpleasant side-effects (yeast infection in women, stomach upset, nausea, vomiting, bad taste, loose or dark bowel movements, and dizziness):
Metronidazole (or clarithromycin) 4 times/day
Tetracycline (or amoxicillin) 4 times/day
Bismuth subsalicylate (active ingredient in PeptoBismol) 4 times/day
Rantidine (Zantac) may also be used to block acid production (optional)
Two-week, dual therapy - 80% effective in curing it, and is simpler for patients with fewer side-effects:
Amoxicillin 2-4 times/day (or clarithromycin 3 times/day)
Omeprazole (Prilosec) 2 times/day to block acid production

prevention: avoidance of contact with feces or vomitus (which may contain H. pylori);diminished smoking, caffeine intake, use of nonsteroidal anti-inflammatory drugs (NSAIDs) and stress may also help, because these all seem to be cofactors in prolonging or worsening ulcers

Back 39

Treatment for Helicobacter Peptic Disease Syndrome (Ulcers) and prevention:

Front 40

(bacterium) - foods contaminated with spores (from soil) and improperly canned;
pathogenesis: after 12-36 hour incubation period, exotoxin causes flaccid paralysis of neck and chest, which can cause death (up to 70% of untreated cases; ~5% of treated cases) due to cardiac and/or respiratory failure

Back 40

Botulism

Front 41

treatment: antitoxin (available from CDC)
prevention: avoid ingestion of contaminated foods via better food washing and canning techniques (sanitation)

Back 41

Botulism treatment and prevention

Front 42

(bacterium) in foods contaminated with it by food handlers with lesions, then "incubated" before serving; millions of cases each year in the US
pathogenesis: 2-6 hours after ingestion, enterotoxin causes emesis (vomiting) and accumulation of water in small intestine, which causes abdominal cramps and hypermotility, that results in diarrhea

Back 42

Staphylococcal Intoxication

Front 43

treatment: TLC; self-limiting disease (antimicrobial agents generally not necessary . . . nor recommended)
prevention: avoid ingestion of contaminated foods (sanitation, hygiene)

Back 43

Staphylococcal Intoxication treatment and prevention

Front 44

epidemiology:
Aspergillus flavus (fungus) grows on food (especially peanuts) stored in moist places and produces aflatoxin
Aminita, Clitocybe, and Psilocybes (fungi) are poisonous mushrooms due to their production of one or more of these toxins ... phalloidina, amatoxin, ibotenic acid, muscimol, muscarine, psilocybin
pathogenesis:
ingestion of aflatoxin along with food damages intestines and liver; complications - liver cancer
ingestion of various toxins when one eats poisonous mushrooms can cause damage to certain portions of the body

Back 44

Mycotoxicosis

Front 45

one of the various toxins ingested from eating poisonous mushrooms:
causes kidney and liver toxicity followed by violent vomiting, bloody diarrhea, and severe abdominal cramps, and can cause death if the dose is high enough

Back 45

amanitin (amatoxin)

Front 46

one of the various toxins ingested from eating poisonous mushrooms:
cause nausea and vomiting, together with CNS effects including confusion, visual distortion, a feeling of greater strength, delusions, convulsions and drowsiness (may fall asleep and cannot be roused)

Back 46

ibotenic acid and muscimol

Front 47

one of the various toxins ingested from eating poisonous mushrooms:
causes excessive salivation, sweating, tears, lactation (in pregnant women), plus severe vomiting and diarrhea

Back 47

muscarine

Front 48

one of the various toxins ingested from eating poisonous mushrooms:
causes hallucinations

Back 48

psilocybin

Front 49

treatment: TLC, supportive therapy aimed at eliminating toxins, possible liver transplant for amanitin poisoning
prevention:
avoid eating aflatoxin by preventing fungal contamination of foods that will be ingested (low-moisture storage conditions for peanuts, etc.)
avoid eating wild (noncommercial) mushrooms

Back 49

Mycotoxicosis treatment and prevention

Front 50

Bacteria:pathogenesis: enterotoxin or LPS (bacteria) or viral cell damage lead to accumulation of water in small intestine, which causes abdominal cramps and hypermotility, resulting in diarrhea (~accompanied by fever, nausea and vomiting); complications - dehydration, electrolyte loss; death (rare) ... E. coli O157:H7 (4847 cases in US during 2007) causes more severe disease, often complicated by hemolytic-uremic syndrome that leads to kidney damage

Back 50

Enteritis

Front 51

treatment: replace water and salts as needed; antimicrobial agent therapy (sulfa drugs, ampicillin) is used in life-threatening cases only
prevention: rotavirus vaccine; avoid contamination and ingestion of foods and water ... maintain adequate sewage treatment and drinking water purification

Back 51

Enteritis treatment and prevention

Front 52

(protozoan) - fecal/oral transmission via contaminated water; 19,417 cases in US during 2007 ... most commonly detected protozoan disease in US
pathogenesis: cyst survives stomach, develops into trophozoite in the intestines where it adheres and proliferates rapidly, causing maladsorption and tissue damage leading to nausea, abdominal cramps, flatulence, foul-smelling watery diarrhea; complications - chronic disease; carrier state

Back 52

Giardiasis

Front 53

treatment: furazolidone or metronidazole (due to side-effects of these drugs, physicians sometimes prefer to let disease run its course without treatment)
prevention: avoid ingestion of contaminated water (cysts are not killed by chlorine and must be removed from drinking water by filtration

Back 53

Giardiasis treatment and prevention

Front 54

(protozoan) grows in GI tract of calves, pigs, chickens and other poultry; transmitted to humans via improperly treated drinking water; disease first recognized in US in 1976; 11,170 cases in US during 2007; ~one-third of all surface waters contain these cysts
pathogenesis: protozoal damage causes headache, low-grade fever, sweating, nausea, anorexia, vomiting, severe abdominal cramping and diarrhea of short duration in normal, healthy humans; but causes chronic severe (sometimes uncontrollable) diarrhea in immunosuppressed people and may cause death in addition to wasting syndrome

Back 54

Cryptosporidiosis

Front 55

treatment: TLC, replace lost fluids and electrolytes; effective antiparasitic drugs have not been discovered yet
prevention: sanitation (these oocysts are not killed by chlorine and must be removed from drinking water by filtration

Back 55

Cryptosporidiosis treatment and prevention

Front 56

(bacteria); transmitted via fecally-contaminated drinking water or food;
pathogenesis: damages epithelial cells of intestine, causing nausea, abdominal cramping, diarrhea (leads to dehydration and electrolyte loss), mucosal ulceration, rectal bleeding, blood and "sheets" of PMNs in stools (S. dysenteriae may produce a neurotoxin that causes vomiting and/or Shiga toxin that can lead to hemolytic uremic syndrome); may last 3-6 weeks; complications - death (10-15%) due to circulatory collapse in severe cases

Back 56

Bacillary Dysentery (Shigellosis)

Front 57

treatment: replace water and salts; trimethoprim-sulfamethoxazole, norfloxacin, ciprofloxacin, or furazolidone if patient is very young or very old and at risk of death
prevention: avoid ingestion of contaminated water ... maintain adequate sewage treatment and drinking water purification

Back 57

Bacillary Dysentery (Shigellosis) treatment and prevention

Front 58

(protozoan) transmitted via cysts ingested with food or water contaminated with human fecal material. pathogenesis: cysts develops into trophozoites in small intestine, then penetrate the colon, causing ulcerations, sharp abdominal pain, colitis, diarrhea, dysentery; complications - recurrent attacks, carrier state; invades bloodstream, causes fatal brain, liver and/or lung abscesses

Back 58

Amebic Dysentery (Amebiasis)

Front 59

treatment: metronidazole or paromomycin
prevention: avoid ingestion of contaminated water ... maintain adequate sewage treatment and drinking water purification

Back 59

Amebic Dysentery (Amebiasis) treatment and prevention

Front 60

(bacterium) - present in water throughout world. pathogenesis: after 2-3 days' intestinal colonization, these bacteria produce enough cholera toxin to cause massive accumulation of water in small intestine leading to "explosive" diarrhea (rice-water stools) and vomiting, which leads to dehydration and electrolyte loss; complications - coma (poor blood flow to brain) and death due to shock (mortality rate is 60% in untreated cases, ~1% in treated cases)

Back 60

Cholera

Front 61

treatment: replace water and salts (i.v. and/or oral); tetracycline
prevention: new oral cholera vaccine; avoid ingestion of contaminated food or water ... maintain adequate sewage treatment and drinking water purification

Back 61

Cholera treatment and prevention

Front 62

epidemiology: Salmonella typhi (bacterium); transmitted via fecally contaminated food or water; ~400 cases per year in the US
pathogenesis: invades via intestinal epithelium, multiplies in lymph nodes, spreads systemically (bacteremia; rose spots); proliferates in (and damages) liver, then reinfects small intestine (via bile secreted by gall bladder); results in fever (104 degrees F), lethargy and delirium; complications include carrier state (10-15%) and death (severe cases)

Back 62

Typhoid Fever

Front 63

treatment: ampicillin or chloramphenicol
prevention: vaccine; avoid ingestion of contaminated foods and water ... maintain adequate sewage treatment and drinking water purification

Back 63

Treatment and prevention Typhoid Fever

Front 64

(virus) is transmitted via water (summer); fewer than 10 cases per year in the US; ~270,000 cases (~25,000 deaths) per year, worldwide; polio costs ~$1.5 billion per year ($230 million in the US)
pathogenesis: intestinal infection leads to infection of motor neurons, damage causes paralysis; complications include muscle atrophy, paralysis, death (*blank* syndrome, which only affects those who had polio earlier in their lives, and for which there is some help)

Back 64

Poliomyelitis

Front 65

treatment: TLC, supportive measures ... such as braces, wheelchairs or iron lungs
prevention:
sanitation ... adequate treatment of drinking water and prevention of its contamination with sewage
vaccines
injectable vaccine
inactivated viruses - doesn't cause disease, but induces production of neutralizing antibodies (only)
Jonas Salk developed the oral vaccine
attenuated, infectious viruses - can cause disease in immunocompromised children, but induces CTLs as well as neutralizing antibodies
Albert Sabin developed this vaccine
CDC recently decreed that only IPV should be used for vaccinating infants in the US
World Health Organization (WHO) is spearheading a move to eradicate this disease, and good progress is being made in this effort

Back 65

Treatment and prevention Poliomyelitis

Front 66

(virus) cases per year in US; transmitted via raw shellfish, produce, other fecally-contaminated foods, especially in institutions
pathogenesis: intestinal infection with this virus leads to anorexia, nausea, vomiting, low-grade fever; systemic distribution leads to liver damage, which causes jaundice; some people are asymptomatic, however; complications - chronic disease, relapses are common;

Back 66

Hepatitis A and E

Front 67

treatment: TLC (prolonged rest)
prevention: Vaccine, sanitation (good food handling techniques, adequate sewage treatment and drinking water purification), gamma globulin injection

Back 67

treatment and prevention of Hepatitis A and E

Front 68

(protozoan) infection occurs via oocysts transmitted via cat feces or tissue cysts transmitted by eating undercooked meat, especially pork, lamb or venison; >20% of adults in US and >30% of world population have been infected
pathogenesis: cysts develop into tachyzoites in intestines, invade the intestinal lining and multiply in the intestinal cells, then spread throughout the body to multiply in other cells, causing disseminated infection that leads to chronic fatigue, fever, malaise, sore throat, headache, muscle pain, swelling of spleen, liver, and lymph nodes; these signs and symptoms last several weeks, then subside as the immune system controls (but does not eliminate) the infection; some people are asymptomatic; complications include chronic latent infection often with neurologic or retinal disease (retinochoroiditis); birth defects if infected during third trimester of pregnancy; this disease is a big problem in AIDS and other immunocompromised patients

Back 68

Toxoplasmosis

Front 69

treatment: pyrimethamine and sulfadiazine, plus folinic acid.
prevention: cook meat to safe temperatures; avoid cat feces (pregnant women should not clean cat litter boxes)

Back 69

Treatment and prevention of Toxoplasmosis

Front 70

is a roundworm (a type of helminth) that is transmitted by fecal/oral contact; pinworm infects 20-50 million people per year in the US ... 10-40% of children under 12, and 16% of adults, have worms at some time in their lives (most prevalent multicellular parasite in US)
pathogenesis: worms proliferate in large intestine (takes 2-4 weeks), causing damage that results in abdominal discomfort, diarrhea, pruritus

Back 70

Pinworm (Enterobiasis)

Front 71

treatment: mebendazole
prevention: avoid ingesting contaminated soil, animal and human feces

Back 71

Treatment and prevention of Pinworm (Enterobiasis)

Front 72

(roundworm ...a type of helminth) is transmitted by ingestion of pork; ~one million cases in the US in 1950 ... currently ~15 cases reported each year; 4% of US population infected
pathogenesis: ingested cysts develop into worms, which mature in intestine (in 2 days), release many larvae (after 5 days) causing nausea, abdominal pain, vomiting, constipation; larvae enter bloodstream (after 7-14 days) causing fever, then localize in muscles and encyst (after 3 weeks) causing myalgia, facial edema, damage throughout body (heart, muscles, CNS); complications - incapacitation, death (~6% - depends on worm burden)

Back 72

Trichinosis

Front 73

treatment: thiabendazole or mebendazole are used in addition to steroids, which reduce severe symptoms ... but no known cure for this chronic disease
prevention: cook pork at 350 degrees F for 45 minutes per pound until internal temperature is 170 degrees F (77 degrees C)

Back 73

treatment and prevention of Trichinosis

Front 74

these flatworms (helminths) are transmitted by ingestion of cysts in poorly cooked meat or fish
pathogenesis: attaches to intestine via scolex, absorbs nutrients directly through their external surfaces (most infestations are asymptomatic, but some patients experience nausea, abdominal cramps, hunger pains, anorexia, weight loss); complications - intestinal obstruction (many worms present); poor absorption of vitamin B12

Back 74

Tapeworm

Front 75

treatment: niclosamide or praziquantel
prevention: avoid soil contamination with human feces; avoid eating raw or poorly cooked beef or pork - cook for 15 min at 131 degrees F (55 degrees C)

Back 75

Treatment and prevention of Tapeworm

Front 76

pathogenesis: prions are taken up from the digestive tract and somehow get into the brain, where they interact with cell receptors, changing their shape or conformation, which causes accumulation of prion molecules as the cells replace the altered receptor molecules; this causes accumulation of fibrils of insoluble prion complexes and results in slow degeneration of the central nervous system with obvious dysfunction, progressive dementia, and vacuolar degeneration of the brain

Back 76

Mad Cow Disease

Front 77

treatment: TLC
prevention: avoid eating beef that may contain prions

Back 77

Treatment and prevention of Mad Cow