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Microbio /Immunology
UWORLD Round 1 2021
| Question | Answer |
|---|---|
| What is the mode of action of Hepatitis B virus vaccine? | Recombinant HBsAg to generator anti-HBs antibodies |
| How do anti-HBs antibodies provide immunity to HBV infection? | Antibodies prevent infection by binding o the envelope of circulating virus and inhibiting viral entry |
| Anti-HBs antibodies binding to circulating virus what causes? | Prevents or inhibits viral entry |
| What feature of diabetic patients induce to poor wound healing? | Chronic elevated blood glucose levels |
| How do elevated blood glucose levels contribute to poor wound healing? | Induces the release of ROS and proinflammatory cytokines from neutrophils while also inhibiting production anti-inflammatory cytokines (IL-10) and growth factors needed for fibroblast proliferation and reepithelization |
| What products are inhibited from release in patients with elevated blood glucose levels that lead to persisten inflammation and poor would healing? | Inhibition of anti-inflammatory cytokines (IL-10) and growth factors needed for fibroblast proliferation and re-epithelization in healing wounds |
| What are some anti-inflammatory cytokines? | Interleukin (IL)-1 receptor antagonist, IL-4, IL-6, IL-10, IL-11, and IL-13 |
| Sirolimus first directly binds to which protein in the cytoplasm? | FKBP |
| What does the complex formed by Sirolimus and FKBP in the cytoplasm bind to later? | mTOR |
| Common inmjusuprevive drug that binds and inhbits to mTOR after forming a complex with another protein in the cytoplasm? | Sirolimus |
| What does the inhibition of mTOR causes? | Blocks IL-2 signal transduction and prevents cell cycle progression and lymphocyte proliferation |
| Which interleukin transduction is invited or halted by mTOR inhibition? | IL-2 |
| IL-2 signal transduction is inhibited by mTOR inhibition caused by which common immunosuppressive medication? | Sirolimus |
| What is Rituximab mode of action? | Chimeric antibody directed against CD20+ antigen, specific to B-cells |
| What does the primary response to a new viral antigen results in? | In plasma cells that only produce IgM |
| What immunoglobulin is produced in the primary response to a new antigen? | IgM |
| Where does Isotype switching occur? | Germinal centers of lymph nodes |
| What is required to initiate Isotype switching in the Germinal center of the lymph nodes? | Interaction of the CD40-receptor on B-cells with the CD40-Ligand expressed by activated T-cells |
| Which T cell type has the CD40 receptor expressed? | B cells |
| Which T -cell type has the CD40-Ligand? | Activated T-cells |
| What is CD154 classified? | CD40-Ligand on activated T-cells |
| What is an important immune process that takes place in the Germinal centers of the lymph nodes, due to CD40--CD40L interaction? | Isotype switching |
| What is the main serum immunoglobulin of secondary immune responses? | IgG |
| Which immune response is mediated mainly by IgM, primary or secondary? | Primary immune response |
| Which immune response is mainly mediated by IgG, primary or secondary? | Secondary immune response |
| Where is FcERI found? | Surface of mast cells and basophils |
| FcERI normally binds to: | Fc portion of the circulating IgE antibodies |
| What receptor commonly binds to circulating IgE antibodies? | FcERI |
| What is an high-affinity IgE receptor found in surface of mast cells and basophils? | FcERI |
| What causes the aggregation of FcERI receptors in mast cells and basophils? | Cross-linking of multiple membranes-bound IgE antibodies by a multivalent antigen |
| What are preformed mediators released by degranulation of mast cells and basophils due to FcERI aggregation? | Histamine and Tryptase |
| What conditionis to be suspected in increase release of Histamine and Tryptase? | Allergic reaction |
| What are two common hookworms? | Necator americanus and Ancylostoma duodenale |
| What type of worms are N. americanus and A. duodenale? | Hookworms |
| What regions are more common to find hookworm infections? | Tropical and Subtropical regions with poor sanitation |
| What is the most severe complication of a hookworm infection? | Chronic iron deficiency anemia (microcytic anemia) |
| Where do adult hookworms live in the human body? | Small intestine and feed on human blood |
| What is the most common initial event in the transmission of Hookworm infection? | Human skin comes into contact with soil contaminated with human feces |
| Once a hookworm enters the skin, it travels to the _____ immediately and eventually is coughed up. | Lungs |
| What is Histoplasma capsulatum? | Dimorphic fungus, that excitis as a small, ovoid yeast at tissue temperatures |
| Where do Histoplasma capsulatum replicates? | In macrophages |
| How is Histoplasma capsulatum spread thought he body? | Lymphatic and Reticuloendothelial system |
| What is the danger of H. capsulatum infection in immunocompromised? | Develop disseminated disease to liver, spleen and bone marrow |
| What is the Reticuloendothelial system? | Mononuclear phagocyte system |
| What is the function role of the Reticuloendothelial system? | Removes immune complexes from the circulation in healthy persons, and is formed of phagocytic cells that are found in the circulation and in tissues |
| What are common markers positive in a patient with chronic Hepatitis B virus with low infectivity? | HBeAg and anti-HBe Ag |
| What are some characteristic or features of anti-HBeAG? | 1. Appears shortly after HBe Ag vanishes 2. Suggest subsiding viral activity, which means the transition from high infectivity to low infectivity |
| What serum marker indicates transition from high to low infectivity statues in a Hep B viral infection? | Anti-HBe Ag |
| What is the main source of rabies in the United States? | Bats |
| What are the clinical features of Rabies encephalitis? | Agitation and spasms progressing to coma within weeks from initial exposure |
| What the type of vaccination is for Rabies? | Inactivated vaccine |
| Rabies vaccine is it a toxoid, inactivated or live vaccination? | Inactivated vaccine |
| Where does the HSV latent infection develop? | Latent infection of the sensory ganglion |
| HSV and VZV latent infection site: | Sensory ganglion neurons |
| EBV latent infection site: | B lymphocytes |
| What viral infections cause latent infection in the Myeloid cells? | CMV and Human herpesvirus 6 & 7 |
| HIV latent viral infection site: | CD4+ T lymphocytes |
| Where do HPV produce latent viral infection? | Stratified Squamous epithelial cells |
| Latent site: Renal tubular epithelial cells. Virus? | BK virus |
| JC Virus produces latent infection in the: | Neuroglial cells |
| What are common encoded structural genes associated with HIV replication cycle? | gag, pol, and env |
| Which of the HIV cycle polyproteins is the only Glycosylated? | env gene |
| What is the product of env gene? | gp160 |
| What are the products of cleaved env gene (gp160) in the Golgi apparatus? | Glycoproteins gp120 and gp41 |
| Glycosylation of env gene produces is crucial for? | 1. Immune evasion 2. Host cell binding |
| What is Ehrlichia chaffeensis? | Harbored in white-tailed deer and transmitted to humans by tick bite |
| What are histological features of Ehrlichia chaffeensis? | Replicates in vacuoles within monocytes and forms mulberry-shaped, intraleukocytic inclusions (morulae) |
| What is the most important lab feature in Ehrlichia infection? | Lymphopenia |
| What is the common term used for Primary Varicella Zoster infection? | Chicken-pox |
| How is Primary varicella zoster infection presented clinically? | Prodromal illness (fever, malaise) followed by pruritic, vesicular lesions that appears in successive crops in different states |
| What infection is characterized by rash with pruritic, vesicular lesions, that appear in successive crops in different stages? | Primary Varicella Zoster infection |
| What is Chagas disease? | Protozoal illness that is endemic to Latin America |
| What is the main complication of chronic Chagas disease? | Chagas cardiomyopathy |
| What is seen with Chagas cardiomyopathy? | Heart failure, ventricular arrhythmias, and ventricular aneurysms |
| What is a Delayed Hemolytic Transfusion reaction? | A mild, hemolytic reaction that occurs > 24 hours after blood transfusion |
| What type of patients tend to develop a Delayed Hemolytic transfusion reaction? | Those exposed to a minor RBC antigen previously |
| What are examples of conditions that may cause a previous exposure to a minor RBC antigen? | Previous blood transfusion and pregnancy |
| What pathogen causes Primary Amebic Encephalitis? | Naegleria fowleri |
| What cranial nerves provides passage or "transport" of Naegleria fowleri to reach the brain? | Olfactory nerve |
| Which nerve is involved in the pathogenesis of Primary Amebic encephalitis reaching the brain? | Olfactory nerve |
| What is the description of Naegleria fowleri? | Free-living, motile protozoan causative of amebiasis |
| How does Naegleria fowleri infection reach the brain? | Penetrates the olfactory mucosa and migrates in retrograde fashion thought olfactory nerve |
| What is X- linked agammaglobulinemia? | Immunodeficiency characterized by low circulating B lymphocytes and immunoglobulins. |
| When should agammaglobulinemia be suspected? | In an infant with severe life-threatening enteroviral infection |
| What is the inheritance mode of Agammaglobulinemia? | X-linked recessive |
| What is the flow cytometry findings of X-linked agammaglobulinemia? | Decreased CD19+ B cells and normal T cells |
| What are the lab findings of Agammaglobulinemia? | 1. Decreased immunoglobulins and a decreased antibody response to vaccines 2. Decreased CD19+ B cells and normal T cell in flow cytometry |
| What are common conditions caused by Enteroviruses? | Herpangina, Hand-Foot-and-Mouth disease, or in some cases Aseptic meningitis. |
| What is Herpangina? | Acute viral illness in children most commonly caused by Coxsackie A or B viruses |
| What are symptoms of Herpangina? | Common symptoms are small blister-like bumps or sores (ulcers) in the mouth and fever. It is caused by a virus |
| What is the earliest morphological change of a thermal burn? | Erythema |
| What is erythema? | A type of skin rash caused by injured or inflamed blood capillaries. It usually occurs in response to a drug, disease or infection |
| What causes the erythema in thermal burns? | Release of preformed mediators (eg. histamine) from mast cells |
| What cells release mediators in thermal burns that cause erythema? | Mast cells |
| What is the most common mediator released by Mast cells in burns that cause erythema? | Histamine |
| What produces the symptoms and changes in deep (partial-thickness) burn wounds from blisters? | Fluid extravasation through gaps between damaged venule endothelial cells |
| In partial-thickness burns, what cells usually are damaged that cause blistering? | Venule Endothelial cells |
| Which poliovirus vaccine is the Live attenuated? | Sabin |
| What is the route of administration of Sabin poliovirus vaccine? | Oral |
| Which poliovirus vaccine is administered via oral administration? | Sabin |
| Salk or Sabin poliovirus vaccine. Inactive poliovirus Vaccine? | Salk |
| The Salk poliovirus vaccine is: | Inactivated Poliovirus vaccine |
| Which immunoglobulin difference would be the greatest in a person with live attenuated vaccination and other with Inactivated (silent) vaccination? | Increased in mucosal IgA by the live vaccination |
| Which vaccine produces a stronger mucosal secretory IgA immune response, the Sabin poliovirus or Salk poliovirus vaccine? | Sabin |
| What immune response is seen greatly stronger in Sabin poliovirus vaccine compared to Salk poliovirus vaccine? | Mucosal secretory IgA immune response |
| How is it that the Sabin (live) poliovirus vaccine produces a stronger mucosal secretory IgA immune response than Salk vaccine? | Increase in mucosal IgA offers immune protection at the site of viral entry by inhibiting attachment ot intestinal epithelial cells |
| What endogenous human (GI-associated) characteristic is vital for protection of V. cholerae infection reaching small intestine and causing disease? | Gastric acid secretion |
| Vibrio cholerae survives in acidic or alkalotic environments? | Alkalotic |
| What actions produce better changes of V. cholerae causing disease? | Any action the inhibits the release of gastric acid, due to medication or illness. |
| A person that consumes antacids in a constant form due to gastritis, may increase the risk of infection by what diarrhea-producing toxin? | Cholera toxin |
| What pathogen is the MCC of bacterial prostatitis? | E. coli |
| What is the pathogenesis of Bacterial prostatitis? | Caused by reflux of urine and organisms from the bladder and urethra |
| What condition is due to reflux of urine and pathogens from the bladder and urethra in men? | Bacterial prostatitis |
| What are risk factors that provoke Bacterial prostatitis? | Anatomic abnormalities and/or bladder catheterization |
| What feature of E. coli causes acute bacterial prostatitis? | Adhesins on its fimbriae that promote adherence to urothelial or mucosal cells |
| What aids in the attachment of E. coli to urothelial cells in Bacterial Prostatitis pathogenesis? | Adhesins on fimbriae of E. coli |
| Common cause of life-threatening secretory (watery) diarrhea in the immunocompromised (advanced AIDS)? | Cryptosporidium |
| How is the diagnosis of Cryptosporidium-induced diarrhea made? | Visualizing oocysts with modified acid-fast stain in stool or basophilic organisms lining the brush-border in a biopsy |
| What is found in stool in a patient with Cryptosporidium cause diarrea? | Oocytes with modified acid -fast stain |
| What is the biopsy finding of patient with Cryptosporidium-induced diarrhea? | Basophilic organisms lining the brush-border |
| What are common risks that increase possibilities of developing Candidemia? | Presences of central vascular catheter and recipient of parental nutrition |
| What is the morphology of Candida? | Branching pseudohyphae with blastoconidia |
| Morphology: Pseudohyphae with blastoconidia. Organism? | Candida |
| What is the morphology of Blastomyces? | Yeast with broad-based budding |
| Morphology. Yeast with broad-based budding. Organism? | Blastomyces |
| What is the clinical presentation of Candida infection? | Mucocutaneous or invasive infections |
| How does Blastomyces enter the body? | Inhaled, then traveling to skin and bone |
| Which yeast is known to be acquired via inhalation? | Blastomyces |
| What is the morphology of Coccidioides?? | Spherules with endospores |
| What organism is often seen as spherules with endospores, when describing its morphology? | Coccidioides |
| What are the clinical features of Coccidioides infection? | Transient pulmonary syndrome ---> meninges and bone |
| What yeast is known to cause Transient Pulmonary syndrome? | Coccidioides |
| Which opportunistic pathogenic yeast is known to cause Meningitis in immunocompromised? | Cryptococcus |
| What is the morphology of of Cryptococcus? | Encapsulated yeast |
| What is the morphology of Histoplasma? | Small, oval yeast within macrophages |
| Which pathogenic yeast would be described as small, oval yeast within macrophages? | Histoplasma |
| What is the rare clinical manifestation of Histoplasma (yeast) infection? | Community-acquired pneumonia that may cause dissemination |
| What is a severe, rare, dermatological condition in infants and children due to St. aureus infection? | Staphylococcal Scalded Skin syndrome |
| Who and how is Staphylococcal Scalded Skin syndrome produced? | Occurs in infants and children due to the production of exfoliative exotoxins by S. aureus |
| What condition is due to the production of Exfoliative by S. aureus? | Staphylococcal Scalded Skin syndrome |
| The Exfoliative exotoxins produced in Staph Scalded Skin syndrome ---> | Cleave Desmoglein in Desmosomes, leading widespread epidermal blistering and shedding, especially with gente pressure |
| What condition may be suspected in a child with fever, and a acute skin condition that produces release of dermis upon minimal touch? | Staphylococcal Scalded Skin syndrome |
| What protein is cleaved by Exfoliative exotoxins of SSSS? | Desmoglein in desmosomes |
| What gram (+) coagulase (+) and catalase (+) infection is associated with a condition with a (+) Nikolsky sign? | Staph aureus; condition Staph Scalded Skin syndrome |
| List of organisms known to cause diarrhea illness in HIV-AIDS patients: | 1. CMV 2. Cryptosporidium 3. Microsporidium 4. MAC |
| What pathogen is known to be a common cause of colitis in advanced AIDS patients? | CMV |
| What is the most common (#1) cause of reactivation of CMV in advance AIDS patients? | CMV retinitis |
| What is the second most common causes of CMV reactivation in advanced AIDS patients? | CMV-colitis |
| What is the histological findings of CMV colitis biopsy? | Large cells with prominent basophilic intranuclear inclusions |
| What are findings of colonoscopy of CMN-colitis? | Erythema, erosions, and ulcerations |
| What are the two major categories of the 3 major HIV structural genes? | 1. Host protease (env gene products) 2. Viral protease (gap-pol gene products) |
| What protease cleaves HIV associated env gene? | Host protease |
| What is the role of Protease inhibitors? | Block viral protease from cleaving gap-pol polyproteins, which results in the formation of immature virions that are noninfectious. |
| How is Granulomatous inflammation defined? | Chronic inflammation characterized by aggregates of activated macrophages that assume an epithelioid appearance. |
| What is the MCC of viral gastroenteritis? | Norovirus infection |
| Norovirus is the most common cause of: | Viral gastroenteritis |
| What are instances that tend to cause outbreaks of Norovirus gastroenteritis? | Schools, cruise ships, and nursing homes |
| What are the symptoms of Norovirus-induced gastroenteritis? | Vomiting and Watery diarrhea |
| What are the minor RBC antigens? | Non-Rh D antigens expressed on erythrocytes |
| What infection or condition is diagnosed or tested by the INF-gamma assay test? | Latent Tuberculosis infection |
| What test is used to diagnose laten tuberculosis infection? | INF-gamma assay test |
| How does INF-gamma assay test works? | Measures the amount of INF-gamma released by T-lymphocytes when exposed to antigen unique to Mycobacterium tuberculosis |
| What cells are involved in INF-gamma assay test? | T helper 1 lymphocytes (Th1) |
| What pathogen infection is the MCC of skin and soft-tissue abscesses (furuncles)? | Staph aureus |
| What is an furuncle? | Painful, necrotic, purulent center skin or soft-tissue abscess, surrounded erythema |
| How is a furuncle caused by S. aureus treated? | Incision and drainage and antibiotics to eliminate the local infection |
| What is the histological and common term to describe the histological view of colonies of S. aureus ? | Grape-like clusters |
| What pathogen in vitro or cultured growth described as "Grape-like clusters"? | Staph aureus |
| What are Scabies? | A human mite infection associated with pruritic papular rash with excoriations and burrows |
| Human mite infection producing an "itchy" rash, with excoriations and burrows. | Scabies |
| What is the treatment for Scabies? | Permethrin and/or Ivermectin is generally effective |
| What human mite infection is treated with topical Permethrin or with Ivermectin? | Scabies |
| What is "Sensitization" to aeroallergens? | Inhaled antigens induce Th1 cells to differentiate into Th2 |
| What is the name of the process which describes how inhaled antigens induce Th1 cells to differentiate into Th2 cell? | Sensitization |
| Once a Th1 is differentiated into a Th2 cell by inhaled antigens, it causes: | Th2 cell promote B-cell maturation and isotype class switching to IgE antibodies |
| How are IgE antibodies which are cross-linked in allergic reaction pathogenesis, produced? | Isotype class switching into IgE antibodies, caused by Th2 cell promoting B-cell maturation. |
| On which cell those IgE antibodies cross link in an allergic reaction? | Mast cells |
| What is secreted by Mast cell degranulation? | Histamine and Tryptase (and other vasoactive proteins) to then produce an allergic response |
| What is the most severe complication of untreated group A strep pharyngitis? | Acute rheumatic fever |
| Acute Rheumatic Fever is often due to an untreated: | Group A Strep pharyngitis |
| What is the empiric treatment for group A streptococcus pharyngitis? | Penicillin |
| What is the MCC of acquired valvular heart disease and cardiovascular death? | Rheumatic heart disease |
| What condition is developed in INF-gamma signaling pathway defects? | Disseminated Mycobacterial disease |
| What is the usual cause of Disseminated Mycobacterial disease in infancy or early childhood? | INF-gamma signaling pathway deficits |
| What is the host defense Mycobacterial infections? | Depend on the ability of macrophages to sequester mycobacteria in granulomas and directly kill the bacteria in phagosomes |
| What are signs and symptoms that should raise suspicion of group A streptococcus infection as the cause of pharyngitis? | Acute-onset sore throat, exudative tonsillopharyngitis, and no evidence of viral symptoms (coryza, cough, and conjunctivitis) |
| What provides the quickest form of identifying a group A streptococcus pharyngitis? | In office throat swabs |
| What is the primary mediator of tissue tropism in viruses? | Viral surface glycoproteins |
| What occurs upon mutations to viral surface glycoprotein? | Alter tropism and cause non-infective viruses to become infectious. |
| The change of tropism leading to a virus to be non-infective, and then transform into an infective form, is very likely due to: | Mutations to the viral surface glycoproteins |
| Rotavirus is: | Common cause of self-limited childhood diarrhea in unvaccinated individuals |
| How does Rotavirus causes illness? | Infects villous enterocytes in the doudenum and proximal jejunum and results in villous blunting, proliferation on secretory crypt cells, and a loss of brush border enzymes |
| What parts of the small intestine are affected by Rotavirus infection? | Duodenum and proximal jejunum |
| What is the description of diarrhea caused by Rotavirus infection? | Watery diarrhea without fecal leukocytes |
| What pathogen is known to cause watery diarrhea without fecal leukocytes? | Rotavirus |
| Where does Viridians streptococci exists in normal human flora? | Oral cavity |
| What is a possible result of a viridans streptococci infection? | Transient bacteremia after dental procedures |
| Normal inhabitants of the oral cavity and causative of subacute bacterial endocarditis. | Viridans streptococci |
| S. viridans attaches or binds to what in people with pre-existing valvular lesions, leading endocarditis? | Adhere to fibrin - platelet aggregates |
| What is the most common eye-related complication of congenital CMV? | Chorioretinitis |
| What TORCHES infection is known to cause Chorioretinitis? | Congenital CMV |
| List of complications of Congenital CMV: | 1. Chorioretinitis 2. Sensorineural deafness 3. Seizures, jaundice, hepatomegaly, splenomegaly, and microcephaly |
| What is a common cause of congenital cataracts? | In-utero rubella infection |
| What is a common eye-complication of congenital rubella infection? | Congenital cataracts |
| What is the first step of prevention of central venous catheter? | Proper hand hygiene |
| List of Preventive measures of Central Venous Catheter infection: | 1. Proper hand hygiene 2. Full barrier precautions during insertion 3. Chlorhexidine skin disinfection 4. Avoidance of Femoral insertion site 5. Removal of catheter when is no longer needed |
| What site (vessel) is avoided in placing a central venous catheter? | Femoral vein |
| What are the echinocandins? | Antifungal medications that inhibit synthesis of the Polysaccharide glucan, an essential component of the fungal cell wall |
| What part of the fungal cell is destroyed or inhibited by Echinocandins? | Cell wall |
| What part of the cell is destroyed by Azoles, Amphotericin B and Nystatin? | Prevent synthesis of the cell membrane, by inhibiting the synthesis of Ergosterol |
| How is inflammation characterized? | Passage of circulating inflammatory leukocytes into the inflamed tissue |
| Passage of circulating inflammatory leukocytes into the inflamed tissue. | Inflammation |
| What are the steps of inflammation? | 1. Margination 2. Rolling 3. Activation 4. Tight adhesion and crawling 5. Transmigration |
| What protein is associated in Transmigration step of inflammation? | PECAM-1 |
| Which step of inflammation involves PECAM-1? | Transmigration |
| What protein is involved or associated with Tight adhesion and crawling step of inflammation? | ICAM-1 |
| What proteins are involved in Rolling step of inflammation? | E-selectin and P-selectin |
| What inflammation protein binds to CD18 beta integrins? | ICAM-1 |
| Where is PECAM-1 primarily found? | Peripheral intercellular junctions of endothelial cells |
| What is assessed by the Candida Antigen Skin test? | Activity of T-cell mediated immunity through recruitment of macrophages and CD4+ & CD8+ T-cells in a type IV hypersensitivity reaction |
| What cells are involved in the Candida Antigen Skin test? | Macrophages and T-lymphocytes |
| What is anergy? | Failure to respond to candida antigen testing, is typical in patients with severe combined immunodeficiency (SCID) |
| What immunodeficiency is often associated with the Candida Antigen skin test? | Severe Combined Immunodeficiency (SCID) |
| How are the late dermatologic type I hypersensitivity reactions manifested? | Indurated skin lesion hours after exposure to the allergen due to local tissue damage caused by Major Basic Protein (MBP) released from eosinophils |
| What WBC secretes major basic protein (MBP)? | Eosinophils |
| What is the difference between dermatologic hypersensitivity type I reaction late manifestations to those of type IV hypersensitivity? | Type IV develop over days because of the time needed to produce a cell-mediated immune response |
| Why do type IV hypersensitivity reactions of the skin take longer than type I hypersensitivity dermal reaction? | Time needed for a cell-mediated immune response delays the manifestation in type IV hypersensitivity reaction of the skin |
| Why is Hepatitis C virus genetically unstable? | Lacks proofreading 3' ----> 5' exonuclease activity in its RNA polymerase |
| Which hepatitis virus is known to lack proofreading 3'--5' exonuclease activity in its RNA polymerase? | Hepatitis C virus |
| What are some important features of Hepatitis C virus? | 1. Lack of proofreading 3' --> 5' exonuclease activity in tis RNA polymerase 2. Envelope glycoprotein sequences also contain a hypervariable regions prone to frequent genetic mutation |
| What is a severe complication or manifestation following Primary Infection with HSV-1? | Herpetic gingivostomatitis |
| What is herpetic gingivostomatitis? | Severe vesicular or ulcerative disease following primary infection of HSV-1 |
| How is primary HSV-1 infection diagnosed? | Evidence of Multinucleated Giant cells in a Tzanck smear |
| What parts of the oral cavity are involved in herpetic gingivostomatitis? | Gingiva, tongue, palate, and pharynx along with systemic symptoms |
| Herpes reactivation is clinically presented as: | Mild perioral vesicles |
| Where herpes reactivation (HSV-1) occurs? | Trigeminal ganglia |
| What bacteria produce IgA protease? | N. meningitidis, N. gonorrhoeae, Strep pneumonia, and H. influenzae |
| How does IgA protease work? | Cleaves secretory IgA at the hinge region, rendering ineffective bacterium |
| How does secretory IgA function? | Exist on mucosal surfaces and in secretions and acts by binding and inhibits the action of pili as well other cell surface antigens that normally mediate mucosal adherence and subsequent penetration |
| What organism produces Protein A? | Staph aureus |
| How does Protein A work? | Causes impairment of complement-mediated cell lysis, accomplished by binding the Fc portion of IgG, preventing complement fixation |
| What bacterial factor is known to prevent complement fixation by binding to the Fc portion of the IgG? | Protein A |
| How is Coccidioides immitis tissue sample histologically differentiate? | Spherules containing endospores |
| What is the manifestation of Coccidioides immitis infection in a healthy inidcitual? | Pulmonary disease ranging from a flu-like illness to chronic pneumonia |
| What are different ways in which Aspergillus fumigatus can cause illness or disease? | Opportunistic infection, colonizing, and provoking a lung hypersensitivity reaction |
| What is the opportunistic infection caused by Aspergillus fumigatus infection? | Invasive pulmonary aspergillosis |
| What is the result of Aspergillosis as an colonizing agenta? | Aspergilloma, when it forms a ball within a preexisting lung cavity |
| What is the hypersensitivity reaction associated with Aspergillus infection? | Allergic bronchopulmonary aspergillosis |
| What condition promotes the development of Allergic bronchopulmonary aspergillosis? | Patients with asthma |
| What type of patients are at higher risk of opportunist infection by Aspergillus fumigatus? | Immunosuppressed and neutropenic |
| What is the initial step in development of a Primary Tuberculosis infection? | Unchecked Mycobacterium tuberculosis replication within the alveolar space and alveolar macrophages. |
| What T cells release INF-gamma during a M. tuberculosis infection? | CD4+ T cells |
| What cell line is activated by INF-gamma as it is released by CD4+ T cells in the TB infective process? | Macrophages |
| What is blocked by the Botulinum toxin? | Presynaptic exocytosis of ACh vesicles, causing impaired muscarinic and nicotinic neurotransmission |
| What is the result of Botulinum toxin inhibiting or preventing exocytosis of presynaptic ACh vesicles? | Proper muscarinic and nicotinic neurotransmission |
| What are the clinical manifestations or features of Botulism? | Symmetric, descending paralysis that first manifest with cranial nerve abnormalities, often following consumption fo Home-canned products |
| What neuromuscular condition is associated with consumption of home-canned goods? | Botulism |
| Botulinum toxin inhibits the release of which neurotransmitter vesicle formt he presynaptic neuron? | ACh |
| Blocks the presynaptic exocytosis of ACh vesicles, causing impaired muscarinic and nicotinic neurotransmission. | Botulinum toxin |
| How is Ascaris lumbricoides most commonly transmitted? | Contaminated food or water |
| How does Ascaris lumbricoides travel or is spread through the body? | After ingestion, the eggs hatch into larvae in the small intestine, penetrate the intestinal walls, and migrate across the lungs into the alveoli |
| What condition or syndrome is associated with an advanced or chronic A. lumbricoides infection? | Loeffler syndrome |
| A person with Loeffler syndrome is most likely infected by which worm infection? | Ascaris lumbricoides |
| What is the most common pathogen infecting burns in patients? | Pseudomonas aeruginosa |
| What are common cephalosporins that treat Pseudomonas aeruginosa? | Ceftazidime and Cefepime |
| What are two common penicillins that treat P. aeruginosa? | Ticarcillin and Piperacillin |
| What is Clostridium septicum? | Spore-forming, exotoxin-producing, gram positive organism that is the MCC of gas gangrene |
| What is the MCC of Spontaneous gas gangrene? | Clostridium septicum infection |
| What are clinical symptoms of Spontaneous Gas Gangrene due to C. septicum infection? | Rapid-onset pain, hemorrhagic bullae, and tissue crepitus. |
| What is the greatest risk factor for C. septicum infection? | Underlying colonic malignancy |
| What infection is commonly developed in a person with an colonic malignancy? | Clostridium septicum infection |
| What is the leading cause of foodborne gastroenteritis? | Nontyphoidal Salmonella |
| What is the clinical presentation of gastroenteritis due to Nontyphoidal salmonella infection? | Marked by 3-4 days of self-limieted fever, nausea, vomiting and watery diarrhea |
| What are symptoms or conditions resulting in invasive disease due to nontyphoidal salmonella infection? | Long bones ---> osteomyelitis Vasculature ----> Mycotic aneurysm Heart ----> Endocarditis |
| Which type of patients have the greatest risk of developing invasive diseases from a nontyphoidal salmonela infection? | Sickle cell disease patients, immunocompromised, and those with advanced age |
| What is the structural composition of Bordetella pertussis? | Small, gram negative coccobacilli |
| What is a common and severe consequence of B. pertussis infection? | Outbreaks of whooping cough in unvaccinated individuals |
| What pathogen infection is associated with Paroxysmal cough and vomiting? | Bordetella pertusis |
| How does B. pertussis cause disease? | Secretion of exotoxins that severely damage ciliated respiratory epithelium |
| What is the result of HIV pol gene mutations? | Responsible for acquired resistance to reverse transcriptase inhibitors, Protease inhibitors, and Integrase strand transfer inhibitors |
| What is a result of HIV env gene mutation? | Enable virus to escape from Host-neutralizing antibodies |
| What is the scientific term for "head lice"? | Pediculus humanus capitis |
| How does Pediculus humanus capitis infection discovered? | Eggs (nits) are attached to the hair shaft and can be identified on inspection |
| What its the first line of treatment for head lice? | Topical Permethrin and Ivermectin |
| What is the use for Transporter Associated with Antigen Processing (TAP) proteins? | Necessary for loading of cytoplasmic proteins onto MHC I |
| What is the direct result of the TAP protein-MHC I complex? | Activate CD8+ cytotoxic T cells through interaction with the T-cell receptor and CD8 co-receptor |
| What genes encode MHC II molecules? | HLA-DP, HLA-DQ, and HLA-DR genes |
| What is the role MHC II molecule role? | Present extracellular antigens processed in acidified lysosomes by APCs (B cells, macrophages) |
| Which immunodeficiency is developed due to deficient MHC II expression? | SCID |
| What condition can be associated with impaired activation of B and T cells, and development of a form of SCID? | Deficiency of MHC II expression |
| What type of immunoglobulin are the antibodies of a mother that is blood type A or B? | IgM |
| What type of immunoglobulin are the antibodies (anti-A and anti-B) of a blood O mother? | IgG |
| Which blood type of a mother would cause an increase risk for Hemolytic disease of the fetus and newborn? | Mother with blood type A or B |
| Does a mother with blood O+ or blood A+, has less risk of developing Hemolytic disease of the newborn? | Mother with blood type O |
| Which immunoglobulin can cross the placenta, IgM or IgG? | IgG |
| Why does IgG blood antibodies are the ones that can cause Hemolytic disease of the newborn? | IgG can cross the placenta |
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rakomi
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