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Sigs Unit 3 Part 1
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Summarize the two main roles of vWF in the process of clot formation
1.primary hemostasis- PLT adhesion; 2.secondary hemostasis- vWF complexes VIII->prolong half-life VIII (prevent its degradation)->complex IX->activate X
Why does a person with a G6P deficiency need to eat corn starch?
corn starch is a glucose polymer that is broken down slowly = control glucose levels
What is the underlying pathogenesis of Von Gierk's (Type I) disease?
glucose-6-phosphatase deficiency (can't go from G6P to Glucose)
Differentiate the causes and inheritance patterns of the major types of vWD (Type 1, 2, 3)
Type 1: partial deficiency-quantity, autosomal dominant; Type 2: qualitative variant, AD/some AR; Type 3-severe quantitative-missing vWF, Autosomal Recessive
Discuss the role of factor V in blood clot formation (coagulant) & hemostatic (anticoagulant) regulation
Factor V synthesized in liver; Thrombin activates Factor V-> prothrombin to thrombin; Factor V cofactor aPC to degrade VIII/VIIIA= reduce thrombin formation
Discuss the clinical significance of APC-resistance assay and ratio in screening for factor V gene mutation
degree of abnormality of APC-assay correlates to heterozygosity (higher APC ratio) or homozygosity (low APC ratio) factor V Leiden mutation
Discuss how Protein S and C work and their relevance in evaluating thrombophilia
Proteins S & C work together to prevent your blood from clotting too much; if low S&C = clot too much; P&C inactivate factors V/VIII = slow down clot formation
what are 3 drugs that can treat Factor V Leiden and briefly explain their MOA
1. Warfarin-block carboxylation of prothrombin/VII/X & proteins C/S->deactivates Vitamin K; 2. Dabigatran-inhibit thrombin; 3. Rivaroxaban-direct Xa inhibitor
Describe the DNA damage that occurs from ultraviolet (UV) radiation and explain how this damage can lead to cancer
UVB causes thymine base pairs to bind to each other->pyrimidine dimers; UVA->ROS=damage DNA repair proteins=cancer
What is the characteristic translocation associated with Ewing Sarcoma?
location at the chromosome 22 breakpoint of the t(11;22)(q24;q12) translocation; EWS (EWSR1) gene is involved in translocations in Ewing's sarcoma
why do patients with Ewing sarcoma present with generalized pain?
immune cells trigger inflammation->cytokines->inflammatory markers->activate nociceptors throughout body
Describe how 5-flurouracil (5-FU) produces its chemotherapeutic effect
Inactive (parent drug)-> metabolized-> metabolites FdUMP block TS=interfere with DNA/RNA/protein formation
Discuss the TNM classification of malignancy and colorectal cancer
T: extent/size of tumor (how far grown in wall colon-mucosa, muscularis properia, suberosa/serosa); N: spread to nearby lymphs; M: metastasis to distant organs
Identify 3 specific gene mutations which can lead to the development of breast cancer
BRCA2: tumor suppressor, chromosome stability; BRCA1: tumor suppressor,DNA damage response/repair; HER2: proto-oncogene, nonregulated tissue growth
Identify common risk factors for breast cancer
genetics (BRCA1/2, HER2); Demographics (female, older); prolonged estrogen exposure; Previous cancers/radiation; Lifestyle (alcohol, BMI, smoking)
Describe the genetic pathogenesis of Chronic Myeloid Leukemia
Translocation of chromosome 9 segment onto Chromosome 22-> Philadelphia Chromosome w/ BCR-ABL fusion gene= hematopoeitic stem cell division unregulated
Explain the significance of elevated LDH and Uric acid in the presentation of CML
LDH: high turn over of cells-excess cell lysis; Uric Acid-breakdown of cellular nucleic acid contents of leukemia cells
What are common symptoms of anemia you see in patients with CML?
Anemia -> lower oxygenation of blood->body compensates = pallor, dyspnea, tachycardia
Contrast the pathogenesis of TTP with that of HUS
HUS: shiga toxin->ADAMTS 13 inhibition->failure to cleave vWF multimers; TTP: ADAMTS13 antibodies/congenital ADAMTS13 mutation->failure to cleave vWF multimers
Describe the clinical features of TTP
Purpura, Confusion, Arrhythmia, Proeinuria, increase serum indirect bilirubin + LDH, decrease haptoglobin
Describe the process of plasmapheresis
liquid part of the blood, or plasma, is separated from the blood cells. Typically, the plasma is replaced with another solution--> returned to body
Describe the process that leads to microangiopathic hemolytic anemia (schistocyte formation) in TTP
TTP->ADAMTS13 deficient->cleavage down, increase vWG multimers->hypercoagubale->prothombotic->aggregate->obstruct vessel->sheering RBCS=shistocytes
What does LMNA code for in and why is it so important in development of progeria?
LMNA codes for Lamina A-protein that acts as scaffolding on the inner side of the nucleus->farnesyl stays on lamina A->piles on=abnormal nuclear envelop
How does p53 signaling and senescence interact with aging and progeria?
DNA damage->lamina disrupted->chromatin conformation distress->increase p53 signaling->increase cell/tissue senescence= accelerated aging


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