NAME: Eleonor M. Olaybal DATE:January 23, 2018SECTION: BCASE TITLE: Baby, Shots Fired DIFFERENTIAL DIAGNOSIS The patient most likely suffered ahypersensitivity reaction, specifically, a type III hypersensitivity reaction. Afew syndromes or sicknesses that can be associated with this hypersensitivityreaction are Arthus reaction, serum sickness, and systemic lupus erythematosus,based on the clinical findings. What is the diagnosis of this case? This type of hypersensitivityreaction is an adverse effect of the vaccination, specifically Arthus reaction,which occurs after administering vaccines of tetanus or diphtheria withtoxoids.
Symptoms such as swelling, redness and pain begin 6-12 hours aftervaccination. The reaction is categorized as a ‘localized reaction’ as it onlyoccurred in the site of injection. What is Acetaminophen and why did Dr. Demanarigadvised you to prescribe the drug? Acetaminophenis a drug that is used to relieve mild to moderate pain. It can be used torelieve conditions such as muscle pain, fever, and reactions to shots. It isprescribed as it can be used to lessen the hypersensitive reaction, as it wasmentioned that the cause of the hypersensitivity reaction was the vaccination.
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How many kinds of hypersensitivity are generallyrecognized? Four types of hypersensitivity are generallyrecognized, namely Anaphylactic (Type I), Cytotoxic (Type II), Immune Complex(Type III) and T-Cell Dependent or Cell Mediated (Type IV). What are the basic principles of the reactionsand give some clinical examples? Anaphylactic– Vasoactive mediators are released due to activation of basophils and mastcells by IgE antibodies. EX: Anaphylaxis, Hay Fever, Asthma Cytotoxic– The reaction mediates cell destruction through complement activation or ADCC.This type involves the antibodies binding to cell surface antigens.
EX:Transfusion reactions, Hemolytic Disease of the Newborn ImmuneComplex – Immune complexes are deposited locally or systematically and causecomplement activation and an overactive neutrophil response. EX: Arthusreaction, Serum sickness T-CellDependent – This type involves cellular damage, as T-cells are involved. In heresensitized helper T cells activate macrophages or cytotoxic T cells. EX:Contact dermatitis, Tubercular lesions What is the pathophysiological basis of thispresumed type III hypersensitivity reaction? Thereaction involves immune complexes, specifically antibody and soluble antigencomplexes. Normally, phagocytes can clear up these immune complexes but theyare too small to be noticed. Later on, these complexes are attracted to thebasement membrane of blood vessels and cause conditions such as vascularpermeability, which leads to the effusion of fluid into the tissues, causingedema.
Furthermore, it leads to the activation of the complement system, whichis used in large amounts. In addition, neutrophils are also attracted to thesite and generate a continuous inflammatory response. This type of reaction canoccur systematically or locally, depending on where the immune complexes aredeposited.
What could be done to further investigate thereaction? Laboratorytests such as determination of erythrocyte sedimentation rate, C-reactiveprotein, immune complexes and complement studies can be helpful in trackingand/or monitoring the hypersensitivity reaction. What might be learned from this reaction thatmight inform the location for administration of booster doses? Learning from the reaction and itscauses, further administration of booster doses should not be injected at thesame site as the initial vaccination site. It should be administered at theupper extremities instead, in order to avoid a condition that may cause thepatient to stop walking. What might you advise the patients regarding further boosters? Boosters can still be taken as thesymptoms are only the side effects of the vaccine.
The reaction/s that occurredmean that the vaccine is working and the body is responding. But they havelimitations on being administered such vaccines as they experienced ahypersensitive reaction. They should not receive the vaccine more frequentlythan every ten years, as recommended by the Advisory Committee on ImmunizationPractices. NAME: Eleonor M. Olaybal DATE:January 23, 2018SECTION: BCASE TITLE: Mr.
Land Dee’s Cauliflower DIFFERENTIAL DIAGNOSIS Thepossible diseases that correlate with the symptoms of the patient are:HIV/AIDS, HPV Infection, as it was stated that the patient is sexually active,so the disease could be sexually transmitted. Also, the disease is somehowleaning towards HIV as the clinical findings include a positive ELISA and adecreased CD4 count, as well as the genital wart presented in the beginning. What is the diagnosis? Thedisease is most likely related to human papillomavirus infection. Aside from itbeing the most commonly transmitted pathogen through sexual contact, its mainand distinguishing symptom is the presence of warts. In this case, the patient wasalso positive for the biopsy of wart and PCR biopsy for Buscke Lowenstein tumorand HPV, respectively. Therefore, the diagnosis for this case is GCBL or GiantCondyloma of Buscke and Lowenstein.
What are the most common presenting signs andsymptoms of GCBL? Themost common presenting sign and symptom of GCBL is the presence of a wart whichis described as ‘locally destructive’ and is a ‘verrucous plaque’. It typicallyoccurs on the penis but can also occur in the anogenital region. What are the risk factors and predisposingfactors which promote HPV infection resulting in GCBL? Thefactors included are: chronic phimosis and poor penile hygiene.
The incidenceis higher in males who are uncircumcised or immunosuppression secondary to HIV infection. What is the pathophysiology of HPV? HPVtargets the squamous epithelial cells and infects it possibly through skindisruptions. The deepest epidermal layer, the basal epithelial cell, serves asan important location for the replication of the virus.
Afterward, the viruscan be shed the same time as keratinocytes. This is due to the fact that theHPV takes advantage of the differentiation pathway of keratin cells. Thekeratinocytes differentiate and affects the HPV by making their early genesmore expressed, amplifying the viral episome and is able to shed at the sametime with the keratinocyte. In addition, HPV does not cause viremia as it isnot a cytolytic virus. How does HPV promote the development of carcinoma? Thereare actually specific types of HPV that are labeled as oncogenic orcarcinogenic. When infections with these types become persistent, they cancause cell abnormalities that lead to possible malignant transformation, thuscausing the development of carcinoma.
This is dependent with the inactivationof cellular tumor suppressor proteins and subsequent DNA damages by the virus. What are the immune evasion strategies used byHPV? Theimmune system cannot be activated as there is no viremia, as stated above. Also,specific proteins and oncoproteins of HPV affect different immune responsessuch as: HPV E6 and E7 interfering type 1 interferon responses (no initation ofintracellular antiviral cascades) and escape from virus specific cells (e.g.CD8 positive cytotoxic T cells) due to HPV E5 entrapment of peptide loaded HLAclass I receptor. Furthermore, its location is avascular, meaning there is alack of blood vessels, so it evades the immune system easier by being inaccessibleto the cells participating in the immune system.
Why is that the disease is positive for HIV butnegative in RPR? Thedisease might have caused a false positive result in HIV, after all, the ELISAtest for HIV is a screening test and may be prone to false positives due to theviral load of other infections. Furthermore, RPR tests can only produce falsepositives from diseases like malaria, lupus erythematosus, infectiousmononucleosis.