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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
Pertinent physical exam findings in progeria
alopecia, prominent scalp pain, skin discoloration, reduced subcutaneous adipose tissue, abnormal dentition, beaked nose,
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
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
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 clinical features of TTP
Purpura, Confusion, Arrhythmia, Proeinuria, increase serum indirect bilirubin + LDH, decrease haptoglobin
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
What are common symptoms of anemia you see in patients with CML?
Anemia -> lower oxygenation of blood->body compensates = pallor, dyspnea, tachycardia
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
Describe typical characteristics of a peripheral blood smear in a CML patient
leukocytosis, thrombocytosis, myleocytes, neutrophils
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
What are the guidelines for breast cancer screening
Women aged 50-74, riskier screen ages 40+; mammogram only
Outline the steps of a clinical breast exam
Inspection (skin, nipples, retraction views); palpation (vertical strip pattern, nipple, areola); Lymph nodes (supra/infra clavicular, axillary)
Identify common risk factors for breast cancer
genetics (BRCA1/2, HER2); Demographics (female, older); prolonged estrogen exposure; Previous cancers/radiation; Lifestyle (alcohol, BMI, smoking)
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
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
Describe how 5-flurouracil (5-FU) produces its chemotherapeutic effect
Inactive (parent drug)-> metabolized-> metabolites FdUMP block TS=interfere with DNA/RNA/protein formation
Describe different screening and diagnostic test for colorectal cancer
Physical exam, digital rectal exam, Fecal Occult (stool based tests), Colonoscopy
Explain the mechanism behind the APC/β-catenin pathway in the development of colorectal cancer
Loss APC function->β-catenin accumulates->complex w DNA->increases MYC->proliferation
why do patients with Ewing sarcoma present with generalized pain?
immune cells trigger inflammation->cytokines->inflammatory markers->activate nociceptors throughout body
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
What is the role of CD99 stain in developing diagnosis in Ewing Sarcoma?
Cell-surface transmembrane protein that is highly expressed in Ewings Sarcoma
What are common radiological findings in Ewing Sarcoma?
Interrupted periosteal reaction; Moth-eaten bone destruction; ill-defined border; soft tissue mass accumulation around bone tumor
Discuss the role of specific mutations in cell signaling genes in the development of cutaneous melanoma: BRAF, RAS, C-KIT
BRAF-V600E mutation=proliferation; RAS-cell cycle kinetics (proliferative/survival); C-KIT-tyrosine kinase receptor=growth factor bind site-turn on cascade
Discuss the process of melanoma cancer from a Benign nevus to Metastatic melanoma (mentioning skin layers or biologic events)
Benign nevus (epidermis)->Dysplastic nevus (basement membrane)->radial growth (dermis)->vertical growth (dermis)->metastatic (lung/liver/brain)
Describe the general appearance of cutaneous melanoma with the ABCDE criteria
A: Assymetrical; B: blurry border; C: more than 1 color; D: diameter>6mm; E: evolution of mole sudden change in shape/size/color
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 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
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
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 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
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
what are the classic signs and symptoms someone with vWF will present with?
Nosebleeds (epistaxis); Bleeding from mucosal surfaces; Easy bruising; heavy menstural bleeding; longer bleeding after dental work/surgery/injury
What will the lab findings be for a patient with vWF disease and why: Bleeding time, PT, aPTT
Bleeding time- prolonged (impaired platelet plug formation; PT: normal (extrinsic fine); aPTT: prolonged (reduced VII->impaired intrinsic)
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
Explain why these lab findings are abnormal in a patient with HS: Hb, Hct, MCV, total bilirubin, LDH, HPV B19
Hb-low, lifespan HS erythrocytes; Hct-low,insuff RBC; MCV-low, sphere RBC; T. bilirubin-up, breakdown RBC; LDH-up, hemolysis; HPV B19-pos, infect bone marrow
Explain the main 3 factors in the pathophysiology behind Normocytic Anemia (where does TTP, HS, SCD fit within a factor)
1. Defects in RBC environment (TTP); 2. Defects in RBC membrane (HS); 3. Defects in RBC internal contents (SCD)
Explain the role of parvovirus B19 in the development of acute anemia (aplastic) crisis with chronic spherocytosis
Parvovirus infects and destroys RBC progenitors in the bone marrow, can halt production of RBCs for 1-2 weeks until immune system controls the infection
What is the pathophysiology of hereditary spherocytosis?
Primary membrane defect (akryin gene-> spectrin protein)-> membrane loss-> spherocyte forms-> splenic trap->erythrostasis = phagocytosis extravascular hemolysis
why do we treat sickle cell disease with Hydroxyurea?
increases fetal hemoglobin to retard gelation and sickling of RBCs
What are 3 prominent features preseent on the peripheral blood smear of a patient with Sickle Cell disease?
Howell-Jolly Bodies (hyposplenia), Sickled red cells, polychromasia (reticulocytotic)
Rationalize the vital signs in a child with Sickle Cell disease: Fever + Tachypnea + Tachycardia + Pain + Hypotensive
Fever (chest infection) + Tachypnea (RR, low o2 stat); Tachycardia (HR, low o2 stat) + Pain (bone infarction) + hypotensive (hypovolemia, pulmonary edema)
Explain the pathophysiology behind Sickle Cell Disease
RBC is sickled->vaso-oclusion->splenic sequestration + Acute chest pain + Infections; Extravascular hemolysis-> Jaundice + Aplastic crisis
In reference to anabolic and catabolic, what is Glycogenesis? What is Glycogenolysis?
Glycogenesis - anabolic (create glycogen to be stored); Glycogenolysis- catabolic (break down glycogen to useable glucose)
Explain the rationale for use of HMG-CoA reductase inhibitors in the management of FH
inhibit conversion HMG-CoA to Mevalonate-> reduce cholesterol uptake ->increase synthesis LDL hepatic receptors ->re-uptake LDL = decrease plasma LDL
What is the most distinguished clinical feature you would see on a patient with FH?
Xanthomas
Describe the pathophysiology of FH
Elevated LDL at birth due to lack of LDL clearance from plasma (absent/disorder LDL receptors)
What are foamy macrophages and their role in FH?
Lipoproteins sequestered -> pro inflammatory -> phagocytes -> cholesterol -> foamy = LDL filled macrophage
Why is there an increase in serum lactate acid in infants with Von Gierk's disease
glucose-6-phosphate is also the substrate for glycolysis and produces lactate
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)


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