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50 Cards in this Set
- Front
- Back
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Botulism |
Cause: toxin Mechanism: Blocks Ach release in NMJ by cleaving some of the SNARE proteins Effect: skeletal muscle weakness-->paralysis (total blockage of EPP) |
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Tetanus |
Cause: toxin Mechanism: blocks release of inhibitory NT in spinal cord by cleaving synaptobrevin Effect: lose inhibition on spinal motor neurons |
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Lambert-Eaton Myasthenic Syndrome (LEMS) |
Cause: autoimmune disorder Mechanism: increase # of antibodies against presynaptic voltage gated Ca channels Effect: muscle weakness of the limbs |
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Curare |
Action: competes with ACh for receptors on motor end plate Effect: Decreases size of EPP; large dosage causes paralysis of respiratory muscles and death |
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Neostigmine |
Action: inhibits acetylcholinesterase Effect: prolongs and enhances action of Ach at muscle end plate (causes consistent contractions, similar to tetanus), increases chances of ACh to binding to nicotinic receptors |
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Hemicholinium |
action: blocks reuptake of choline into presynaptic terminal Effect: depletes Ach stores from presynaptic terminal |
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Duchenne Muscular Dystrophy |
genetic disorder marked by progressive degeneration of skeletal and cardiac muscle fibers found in boys by age of 4, they die young because of cardiac and respiratory are affected |
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muscle hypertrophy |
actual size is bigger, # of fibers is not changed, can be genetic or caused by working out a lot (body builders) |
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Amytrophic Lateral Sclerosis (ALS) |
causes death of somatic motor neurons -> loss of muscle function/ paresis (muscle weakness) -> paralysis --> death |
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Spinal cord injury (both above and below L1) |
Above L1: spastic bladder, lose cortical control, return to infant like state, constant urination Below L1: flaccid bladder, reflexes are lost, you store too much urine and can't micturate (requires an inbound catheter) |
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blood transfusion incompatibility |
Type II hypersensitivities Foreign antigen induced blood is given that the recipient has antibodies against (e.g type B donor gives to a type A recipient) |
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Drug Induced reaction |
Type II hypersensitivity Foreign antigen induced aspirin and penicillin conjugate an erythrocyte membrane protein, induces synthesis of IgG Ab with attack the drug-coated erythrocytes and damage them. |
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Myasthenia gravis |
Type II hypersensitivity Auto antigens induced IgG Ab attack acetylcholine receptor on the motor end plate. affects skeletal muscles, symptoms: weakness in muscles that control eye movement (e.g. levator palpebrae superioris causing ptosis, can't focus eye but can still constrict pupil to react to light), weakness in arms and legs difficulty swallowing |
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Graves' disease |
Type II hypersensitivity Auto antigens induced IgG antibody becomes agonist to TSH receptor that stimulate thyroid hormone production, results in increase levels of T3 and T4 levels and low TSH (T3 and T4 has negative feedback on pituitary gland) causes Hyperthyroidism |
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Autoimmune hemolytic anemia |
Type II hypersensitivity auto antigens induced patients own Ab (IgM and IgG) attacks their own erythrocyte membrane proteins, destroying RBC |
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Allergies |
Type I hypersensitivity Foreign harmless insoluble proteins Caused by IgE and mast cells |
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What does Corticosteroids do? |
blocks phospholipase A (PLA2), stops production of all newly synthesized mediators (prostaglandins and leukotrienes) (prevents inflammations) |
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what does Aspirin do? |
blocks prostaglandins production, doesn't stop full inflammation since leukotrienes are still produced |
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What does Anti-histamines do? |
Blocks Preformed mediators (histamine, heparin, and chemotactic factor) (lessens all allergy symptoms except inflammation) |
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Arthus reaction |
Type III hypersensititivity Foreign antigen induced local reaction, already immunized (redundancy), e.g. Tetanus |
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Serum Sickness |
Type III hypersensitivity Foreign antigen- systemic response to passive immunization with foreign antiserum (snake bite --> Snake venom --> Horse Ab that attack venom--> you produce Ab again Horse IgG Ab) |
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Rheumatoid Arthritis |
Type III hypersensitivity Autoantigen induced Autoimmune disease, own IgM antibodies attack own IgG antibodies causes joint inflammation patients require anti-inflammatory medication for rest of life |
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Lupus |
Type III hypersensitivity auto antigen induced own IgG Ab attack own DNA and histone proteins causes nephritis, arthritis, and butterfly rash |
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PPD test |
Type IV hypersensitivity foreign antigen induced Tuberculosis screening test sensitization to prior tuberculosis causes memory Th1 cells against bacterial protein. When tuberculin injected, Th1 secrete cytokines attract macrophages and granulocytes and cause induration and erythema |
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polydactylism |
individuals have an extra digit or digits on hands or feet autosomal dominant has incomplete penetrance and variable expressivity. |
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Phenylketonuria (PKU) |
individuals have mutate phenylalanine hydroxylase and can not metabolize phenylalanine autosomal recessive (polygenic) |
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Rett syndrome |
X-linked dominant mutated MECP2 gene, acts as a transciptional repressor in the nervous system during development |
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Hemophilia A |
X-linked Recessive Mutated factor VIII gene affected individuals can not clot blood efficiently |
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Leigh syndrome |
mitochondrial inherited disorder Neurodegenerative disorder, usually an early onset disease but adult onset forms do exist |
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Huntington's disease |
Autosomal dominant Insertion (frameshift) CAG repeat at the end of the 1st exon of gene HTT produced HTT protein that maintains neuronal transmission, mutated proteins form clusters at the synaptic junctions eventually initiates cascade 3--> apoptosis Normal gene contains <29 repeats Carrier contains 29-36 repeats, (late onset) affected individuals have >36 repeats symptoms: trouble remembering, and have trouble with muscle control (swallowing) |
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Fragile X syndrome |
X-linked Dominant Insertion (frameshift) CGG repeat in the FMR1 gene Normal individuals have 6-50 copies mutant individuals have >230 repeats repeats in non-transcribed region of gene, but cause methylation of gene, thus turning gene off |
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Xeroderma Pigementosum |
Caused by defective nucleotide excision repair (too many pyrimidine dimers) unable to repair UV damage= skin cancers |
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Down Syndrome |
Trisomy of autosomal chromosome 21 affects males or females usually caused by problems in mitotic division 1, affected by mother's age affects mental abilities, looks affected |
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Turner's syndrome |
(XO) all females, but sterile (ovaries not developed) have neck flaps very sporadic and not hereditary |
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Klinefelter Syndrome |
(XXY) or (XXXY) only affects males, testes very large, sterile and usually very tall, and have long faces |
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Robertsonian translocations |
only occurs with acrocentric chromosomes (13, 14, 15, 21, 22) Phenotypically normal Short arms of 2 different chromosomes are lost and the remaining long arms fuse to form a single chromosome |
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Philadelphia chromosome |
present in 95% of individuals with CML and ALL (leukemia) ( forms an oncogene) new gene formed Abl gene from Chromosome 9 and Bcr from Chromosome 22 are fused (chromosome 9 and 22 switch parts of their q arms) |
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Alzheimer's disease |
localized amyloidosis; caused by deposits of beta amyloid protein deposits in the brain. caused by mis-folded proteins (specifically Beta-sheets) |
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Creutzfeldt-Jakob Disease (CJD) |
form of spongiform encephalopathy can be sporadic (new mutation causing it), hereditary, or acquired (eating contaminated beef) caused by misfolding prion proteins (PrPc) into an infectious PrPsc. (causes chain reaction) |
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Maple syrup Urine Disease |
Autosomal recessive, caused by BckD not breaking down Valine, isoleucine, and leucine |
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Ciguatoxin |
lowers threshold for voltage gated sodium channel activation--> AP is produced more readily |
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Lidocaine |
blocks voltage gated sodium channels --> prevent depolarization and AP (common anesthetic) |
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Tetrodotoxin (TTX) |
blocks voltage gated sodium channels ---> prevent depolarization and AP |
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Dendrotoxin |
blocks voltage gated potassium channels ---> blocks repolarization |
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Tetraethylammonium (TEA) |
blocks voltage gated potassium channels---> blocks repolarization |
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Acute lymphoproliferate syndrome (ALPS) |
caused by the lack of expression of FasL, causes T cells that would usually be deactivated, so stay activated |
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Severe combined immunodeficiency disease (SCID) |
No adaptive immune system, caused by not having RAG |
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Bare Lymphocyte syndrome |
a partial or complete deficiency in MHC I and MHC II proteins symptoms range from none to severe combined immune deficiency, depending on the number of MHC loci that are expressed. (e.g. blocking only 1 gene may be asymptomatic, while blocking both ABC of both parent alleles can be severe.) |
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Hyper IgM syndrome |
can only use T cell Independent B cell activation Symptoms: blood becomes very viscous, blue color in extremities |
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Hemolytic disease of the Newborn (erythroblastosis fetalis, or Hydrops fetalis) |
occurs only when mother is Rh - and baby is Rh +. Mother gets sensitized during birth and produces IgG against Rh + factor, resulting in future Rh + babies being killed by lack of RBCs. Treated with Rhogam, which is a modified IgG that targets Rh factor. prevents mom from producing antibodies against the babies blood cells. |
