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Diseases - MCB E2

Diseases and Drugs for MCB Exam 2

Novobiocin and Ciprofloxacin antibiotics that target Gyrase, a Topo II found only in prokaryotes that adds negative supercoils
Xeroderma Pigmentosa genetic disease resulting from mutations to the XP genes involved in nucleotide excision repair. Afflicted individuals are highly susceptible to UV-induced damage to DNA
Hereditary Nonpolyosis Colorectal Cancers (HNPCC) caused by mutations in MSH and MLH proteins (human analogs of MutS and MutL) involved in mismatch repair. Germ-line mutation and thus present in every cell type, but presents in colon due to high cell turnover
Huntington's Disease genetic disease caused by a CAG triplet repeat expansion. Considered pathogenic when repeat exceeds ~35 repeats
Rifampicin blocks prokaryotic initiation of transcription by blocking the formation of the first phosphodiester bond
Actinomyocin D inhibits transcription (and replication at high concentrations) by binding DNA to prevent strands from separating and unwinding
HIV Antitermination virus expresses TAT protein that prevents host cell from terminating it transcription to increase viral protein production
Diptheria toxin adds ribose to to dipthamide (modified His) on eEF2 in order to prevent translocation during elongation and thus inhibit translation in eukaryotes
Botulism toxin prevents SNARE complex from forming when synaptic vesicles attempt to dock causing the release of neurotransmitter to be inhibited
Cholera toxin prevents GTP hydrolysis on Gα causing constant activation of Adnenylyl Cylcase. This leads to increased levels of cAMP that causes diaherrea
Albuteral binds 7-transmembrane-domain receptors to increase cAMP and thus activate PKA to cause bronchodilation
Nitroglycerin elicits release of nitric oxide to cause an increase in cGMP in smooth mm cells that leads to vasodilation in coronary arteries
Methotrexate Resistance caused by gene amplification in cancer cells to increase production of methotrexate targets so that a patient requires increasingly larger doses
Pertusis Toxin uncouples heterotrimertic G proteins from interacting with its G-protien coupled receptor
Severe Combined Immunodeficiency (SCID) caused by a RAG 1 and 2 mutation preventing V(D)J site specific recombination from occuring and thus causing compromised immune systems
Food-Poisoning microbe toxins attack tight junction proteins to increase junction permeability of fluid, leading to diarrhea
Pemphigus Folicaeus/Vulgaris antibody mediated destruction of desmoglein in desmosomes leading to blistering in the stritum spinosum (spiney layer of epidermis)
Bullous Pomphigold autoantibody destruction of against BP 230(plaque in hemidesmosomes) or a transmembrane collagen that normally holds cells to the basal lamina. Results in fluid accumulation at the base of epithelium
Ehlers-Danlos Type IV caused by faulty transcription of Type III collagen. Susceptible to aortic and intestinal rupture
Ehlers-Danlos Type VI caused by faulty hydroxylation of collagen. Augmented skin and susceptible to rupture of the eyeball
Ehlers-Danlos Type VII caused by a decrease in procollagen peptidase causing increased articular mobility and frequent dislocations
Scurvy caused by a lack of Vit C, a cofactor for proline hydroxylase. Leads to gum ulceration and hemorrhages
Osteogenesis Imperfecta Caused a Gly substitution mutation in the α1 or α2 polypeptides for type I collagen that is more deleterious if at the C-term. Causes brittle bones and cardiac insufficiency
Epidermolytic Diseases Caused by faulty keratins(IF that hemidesmosomes link α6ß4 integrins to). Causes fluid accumulation at the base of the epithelium
Congential Deafness mutation in Connexon 26. Causes abnormal K+ recirculation in cochlear sensory epithelia
Inherited Cataracts mutation in connexon 46 and 50. Causes a disruption in the pathway for delivering nutrients and removing metabolites in the lens of the eye
Rickettsia tick-bourne bacterium that causes Skin rash, cerebral involvement, and perivascular lymphocytic infiltration. Mainly targets endothelial cells
Lyme's Disease Caused by the bacteria Borrelia burgdorferi. Carrier = rodents. Symptoms = target rash, lethargy, heart palpitations & tachycardia. Vector = black-legged tick at nymph stage. Most common in South-eastern US
Tetracycline used to treat lyme's disease. Mechanism of action is to block IF2 with charged fMET tRNA from binding
Chloramphenicol used to treat lyme's disease - blocks peptide bond formation during translation in bacteria
dysplastic epithelia Stratifies squamous epithelium which lacks a normal pattern of maturation and contains atypical cells
Fanconi anemia aplastic pancytopenia, sensitive to cross-linking agents
Bloom syndrome hypersensitivity to DNA-damaging agents such as ionizing radiation.
actinic keratosis Atypical squamous maturation, Chronic dermal inflammation, Solar elastosis- Breakdown of Elastic & collagen fibers, Keratin ‘pearls’ where keratin debris can’t escape
ataxia Telangiectasia sensitive to gamma radiation, increased risk of lymphomas, symptoms: ataxia, dilated BVs, immune dysfunction
Created by: c.phill