Edit Game
UNIT 3 Sigs Part 2
 Delete

Use commas to add multiple tags

 Private  Unlisted  Public



 Save


Get beautiful free images


Delimiter between question and answer:

Tips:

  • No column headers.
  • Each line maps to a question.
  • If the delimiter is used in a question, the question should be surrounded by double quotes: "My, question","My, answer"
  • The first answer in the multiple choice question must be the correct answer.

 Import questions


Get beautiful free images






 Save   24  Close
Pertinent physical exam findings in progeria
alopecia, prominent scalp pain, skin discoloration, reduced subcutaneous adipose tissue, abnormal dentition, beaked nose,
Describe typical characteristics of a peripheral blood smear in a CML patient
leukocytosis, thrombocytosis, myleocytes, neutrophils
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
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
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)
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


Get beautiful free images

Your experience on this site will be improved by allowing cookies.