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Micro week 1 mini 2
Micro - GI (week 1)
| Question | Answer |
|---|---|
| What kind of motility is exhibited by H. pylori? | Corkscrew motility. |
| What agar does H. pylori grow on ? (list non-selective and selective media) | Non-selective: Chocolate agar, blood agar, brain-heart infusion. **Selective: Thayer-martin, Pylori, Dents** |
| What temp does H. pylori optimally grow at ? | 42 degrees C. Microaerophillic (reduced O2) |
| What are the key identifying characteristics of H. pylori? | Gram (-) Catalase (+). Oxidase (+), **UREASE (+)**. NON-HEMOLYTIC. Also: nalidixic acid resistant and nitrate reducing... thid differentiates it from other helicobacters |
| How is helicobacter differentiated from other species of helicobacter | **It is nalidixic acid resistant and nitrate reducing** |
| What is the most common human infection | H. pylori. Present in more than 1/3 of people. Often asymptomatic. Fecal oral route |
| What is the route of H. pylori transmission | Fecal oral (rarely oral-oral) |
| What role to mucinase and phospholipase play in H. pylori? | Helps with motility |
| What adhesins does H. pylori use? What does it bind? | Uses *sialic acid and lewis X* to bind gastric epithelial surface |
| What kind of tranmission system is used by H. pylori ? | type IV |
| How does H. pylori infection lead to increased acid production ? | via platelet activating factor |
| What is the function of urease production by H. pylori | To defend itself against gastric acid. H. pylori IS NOT an acidophile. |
| What is the function of arginase in H. pylori | Protection against NO produced by the immune system |
| List the factors produced by H. pylori to protect it from immune response. | SOD, Catalase, Arginase, O-antigen mimicry,acid inhibitory protein, urease, modiffied lipid A, flagellin structure also prevents inflammation |
| How is H. pylori dx'd | Biopsy, brush, gastric juice, serology, stool, BREATH |
| How does the rapid urease test work? | cells from biopsy are added to a small card containing urease and indicator. The pH change will result in a color change |
| What stains are used for H. pylori? | Giemsa and Warthin-Starry Silver stain |
| Why serology not a good indicator of treatment progress with H. pylori? What is the best method? | Because antibodies will remain long after the infection is cleared up, rseulting in a positiev result despite a cured infection. Measurement of antigens in stool is the best method. |
| Almost of duodenal ulcers are caused by | H. pylori |
| What is the most common upper GI fungal pathogen? | Candida albicans |
| What agar is candida commonly grown on | Can grow on many types. Sabourauds and potato yeast agar are commonly used |
| How is candida identified? | KOH preparation or PAS stain |
| List the normal flora of the GI tract | 99.9% are anaerobes: Bacteroides, Clostridium, and Anaerobic cocci. 0.1% are anaerobes: E. coli, Klebsiella, Proteus, and enterococci |
| What is the normal fecal fluid excretion / day | <150 mL/day |
| Most fluid absorption takes place in the: | Small intestine (90% of fluid absorption). Net absorption is >8L/day |
| What is dysentary ? | severe inflammatory diarrhea with mucus and blood in the feces (inflammation or cytotoxic destruction of colonic mucosa |
| Describe the 3 major mechansisms by which enteric infxon can occur: | 1)shift in fluid balance (non-inflammatory diarrhea [watery]), 2)Inflammation/cytotoxic destruction of colonic mucosa (Dysentary), 3)penetration though intact mucosa of distal small intestine -->then it mutliplying in RES/lymphatic cells (enteric fever) |
| What are the common symptoms of gastroenteritis? | Nausea, vomiting, diarrhea, and abdominal discomfort. |
| Diarrhea is due to a problem in what region of the GI tract? Dysentary? | Enterocolitis? Diarrhea: Small intestine. Dysentary: colon, enterocolitis: SI AND COLON |
| Penetrating enteric infections are most commonly caused by what bacteria? | Salmonella typhi |
| What is used for quantitative measurement of leukocytes present in stool ? | Lactoferrin. |
| Increased fecal lactoferrin is seen in what type of enteric infections | Inflammatory. May or may not be present in pentrating infections. |
| What is the most common bacterial agent involved in enteric infections in the US? | Salmonella. |
| Pt presents with nausea, vomiting, abdominal cramps, and diarrhea *1-8 hours* following ingestion of meal. What is the likely mechanism of the symptoms? | Pre-formed toxins. (1-8 = short incubation period = pre-formed toxin mediated symptoms) resolves w/i 12 hours |
| Pt presents with nausea, vomiting, abdominal cramps, and diarrhea *8-16 hours* following ingestion of meal. What is the likely mechanism of the symptoms? | Toxins produced in body AFTER ingestion. Resolves in 24 hours |
| Pt presents with nausea, vomiting, abdominal cramps, and diarrhea 16-48 hours hours following ingestion of meal. What is the likely mechanism of the symptoms? | infection by the organism. |
| S. aureus and B. cereus ingestion are likely to have what major presenting sx? | vomitting 1-6 hours after a meal. (incubation period = 1-6 hours) |
| Pt with major presenting sx of vomiting 1-6 hours after a meal. What are the likely bacterial agents that can cause this? | S. aureus and B. Cereus. |
| Pt presents with watery diarrhea 1-3 days after a meal. What bacterial agent? | E. coli (ETEC) (C. perfringens has a shorter incubation period (8-16 hours) so it would have occured sooner. |
| Pt with water diarrhea 8-16 hours following a meal. Bacteria? | C. perfringens |
| Pt with inflammatory diarrhea 2-48 hours after a meal. Bacteria? | V. parahaemolyticus |
| List the common bacterial agents of inflammatory diarrhea: | V. parahaemolyticus, L. monocytogenes, shigella, non-typhoidal salmonella, Campylobacter, E.coli (EHEC[aka STEC], SPEC, EIEC, EAEC) |
| What type of food intoxication (poisening due to the exotoxin of the bacteria) does not produce enterotoxin? | C. botulinum (produces neurotoxin) |
| What is the mode of action by which Staphlococcal bacteria cause vomitting? | Via binding of enterotoxins to neural receptors in upper GI that in turn, stimulate the vomitting center in the brain. |
| What is the most common staphylococal toxin? What is it produced? | SE-A toxin (MC toxin). It is acquired from a bacteriophage |
| Sx of Staphylococcal food poisening ? | vomiting +/- diarrhea (1 in 3) 1-6 hours after a meal. |
| Mayonaise is a common carrier of what bacteria ? | S. aureus. |
| Staph toxin vs botulism toxin: which is heat stable / which is heat labile? | toxins produced by staph (i.e. SE-A toxin) are heat stable, whereas botulism toxins are heat labile |
| What botulism toxins are asso with human disease? What is the mechanism? | A, B, and E. Only one toxin is produced per isolate. It's mechanism of action is inhibition of Ach at the NM junction causing a decending flacid paralysis |
| Symptoms of botulism toxin poisening? | decending paralysis starting at eye muscles. Begins with nausea, dry mouth +/- diarrhea. After 18-24 hours pt will be weak and dizzy with diplopia and dysphagia, dysarthria * constipation and abdominal pain. *no fever* death due to resp. paralysis |
| What is the most common form of botulism in the US? | Infant botulism. Ingestion of spores found in environmental dust (can also come from honey, but this is a minor reservoir.This is NOT food-borne botulism as it is not the toxin that is ingested, but instead: the spores are ingested. |
| "floppy baby" indicates what kind of poisening ? | infant botulism. |
| What tx is absolutely contraindicated in adult and infant botulism | ANTIBIOTICS SHOULD NEVER BE USED |
| Would botulism is most commonly caused by source | Injection of heroine / inhalation of cocaine. |
| What is the tx for wound botulism | antitoxin antibiotics (penicillin G), surgical debridement, tetanus booster. (as opposed to adult and infantile infectious botulism where antibiotics are NEVER indicated) |
| How is botulism diagnosed? | Based on clinical impression and history, with confirmation by cutlure or toxin activity in food, serum, or stool. TX INITIATED IMMEDIATELY ON SUSPICION (don't wait for labs!) |
| How is botulism treated? | Trivalent antitoxin: human derived for babies, equine derived for >1 yo (only bind free toxin, arresting progression) along with Gastric lavage if food exposure was recent, ICU support with venitllation if needed. |
| What are the sx of C. perfringens food poisening ? | Nausea, watery diarrhea and abdominal cramps ****NO VOMITING!**** |
| What symptom is never present with C. perfringens? | vomitting |
| Common sources of C. perfringens food poisening? | Beef, chicken, gravy dishes prepared for banquets. Foods cookers earlier w/o adequate reheating |
| What is the mechanism of C. perfringens food poisening? (origin of toxin) | *enterotoxin produced in the body after ingestion of vegetative cells in the food*. |
| What is the mechanism of TYPE A exotoxin of C. perfringens? | A: damages brush borders in SI -> alters permeability in ilium ->loss of fluid / IC proteins. |
| How is Bacillus differentiated from clostridium in a lab? | Bacillus = Catalase (+), clostridium = Catlase (-) |
| What are the two types of bacillus cereus food poisoning ? | 1) short incubation (emetic) form: Nasusea, vomiting, ab cramps *NO DIARRHEA*. Resembles staph in sx and incubation period. (CASUSED BY ETE toxin aka CERULIDE 2) long incubation (Diarrheal form) Resembles C. perfringens. |
| Rice dishes held at room temperature are common sources of what type of food poisening ? | Short incubation bacillus cereus food poisoning |
| What bacteria is associated with cereulide toxin? What is the MOA of this toxin? | Cereulide (AKA ETE Toxin) is associated with bacillis cereus. It causes short incubation form of B. cereus poisening. It binds to 5-HT receptor of the vagus nerve and forms ion channels and holes in the cell membrane. |
| What is the MOA of the long incubation form of bacillus cereus food poisening ? | heat labile enterotoxins produced in body AFTER INGESTION cause activation of intestinal adenylate cyclase -> increases fluid secretion into small intestine. |
| Two forms of B.cereus food poisening? | emetic (preformed toxins) and diarrheal form (enterotoxins produced in the body following ingestion) |
| What are the two major types of virus that cause gastroenteritis? | Rotavirus (Reoviridae) and Calciviruses (calciviridae) |
| Childhood diarrhea of viral origin is most commonly causes by what virus ? | Rotavirus. |
| Diarrhea due to outbreak of a virus: What virus is most commonly involved? | Calciviruses (noroviruses) |
| compare rotaviruses to calciviruses with regard to epidemiology and pt common affected | Rotavirus is typically seen in childhood diarrhea (or eldery diarrhea) *immunity is usually developed by age 2, but old people gave week immune systems*...Calciviruses are typically seen in adults and outbreaks of diarrhea. |
| What are the key features of rotavirus? | DSRNA, SEGMENTED (11 segments) NAKED. |
| Watery diarrhea of 5 days duration is most likely caused by what virus? | rotavirus. Also presents with sudden onset of vomitting after 2 days. |
| What is the enterotoxin of rotavirus | (NSP4) |
| What Immunoglobulis protects against second infection of rotavirus? | IgA |
| What kind of vaccine is the rotavirus vaccine ? | Live-attenuated vaccination |
| Describe the key features of norovirus: | AKA Calcivirus. (+)ssRNA, Naked, icosahedral. Causative agent of viral gastroenteritis in adults and in outbreaks |
| Norovirus (aka calcivirus) vs rotavirus with regard to duration: | ROtavirus is 5-7 days of diarrhea, usualy in young children and eldery patients. while norovirus is 2-3 days and doesn ot involve a fever, typically seen in adults and in outbreaks |
| What types of hepatitis are waterborne (enteric transmission) ? What types are parenterally xmitted | A and E. Only cause AcutE disease... death is rare. Except for Hep E, which is often fatal in pregnant women. B, C, and D are parenterally xmitted. |
| What are the long term complications chronic hepatitis? | Cirrhosis, decompesated liver dz, and Hepatocellular carcinoma |
| What hepatitis type when present with hep B, causes more severe hepatitis than chronic HBV alone? | Hep B + Hep D together causes more severe hepatitis. |
| What virus(es) when present with Hep B, increase the risk of liver cirrhosis? | Hep D as well as HIV both increase chances of liver cirrhosis when present with Hep B |
| HIV and ____ coinfection increase the risk of liver fibrosis | Hep C |
| What is the only virus that requires coinfection with another type of virus? | Hep D (think "D" for "Defective".) Hep D requires pre-infection with Hep B |
| What is the infection form of E. Histolytica? (cysts or trophozoites) | cysts |
| Tear drop ulcers are symptomatic of what parasite? | Entamoeba histolytica |
| Describe the cellular structure of entamoebas histolytica | multinucleated cell (4 nuclei) with centrally located karysosome. Each nucleas has a cartwheel appearance. |
| What is a common source of giardia lamblia ? | Commonly seen in people who have recently gone camping/hiking who drank from STREAM WATER. Causes fatty, foul-smelling, diarrhea of several days duration. No fever, blood, or pus. |
| Sx of Balantidiasis? Cause (parasite name) | Caused by Balantidium coli. Diarrhea +/- mucus and blood, colitis, no extraintestinal spread |
| What is the main difference between intestinal sporozoa and other sporozoa? | Intestinal sporozoa go through the sexual and asexual life cycles in the same host, while the others go through those cycles in seperate hosts. |
| What is the most important intestinal sporozoa ? | Cryptosporidium parvum |
| Acid fast oocysts in the stool is diagnostic of: | intestinal sporozoa. Most of cryptosporidium parva. (could also be isospora belli or cyclospora) |
| Pt with a hx of camping gets diarrhea after drinking stream water. NO FEVER, NO BLOOD IN STOOL Likely parasitic cause? | Giardia lamblia (giardiasis). |
| Pt with a hx of swimming gets diarrhea. Likely parasitic dx? | Cryptosporidium parvum. Dx'd via acid fast oocysts in the stool |
| Pt with FEVER, diarrhea, vomitting, and right sided pleuritic should pain and tear drop ulcers in intestines. Likely parasitic dx? | Entamoeba histolytica (stage IV ((extraintestinal amoebiasis)) |
| What is the confirmatory dx of Amoebiasis? | specific IgM antibody, ELISA, PCR, etc |
| What is the most important interstinal ciliate? | THere is only one intestinal ciliate. It is Balantidium coli (B.coli). Cause bilantidiasis. |
| What is the most important flagellate of the GI ? | Giardia lamblia |
| Lactose intolerance is a feature of what parasitic GI infection? | giardia lamblia (giardiasis) |
| Dx of giardia lamblia? | fecal cysts or antibody detection |
| What is the clinical presentation of giardiasis? | 4-6 loose, foul smelling, fatty BMs(steatorrhea)/day with weight loss, and *NO FEVER AND NO BLOOD IN STOOL* in a pt with a hx of hiking / drinking water from stream |
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Semester4
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