Cell Injury
What are the mechanisms of cell injury?
Mitochondrial Dysfunction- usually caused by Hypoxia, Ischemia, Radiation, and other injurious agents, causing necrosis. (ATP shortage, ROS, oxygen depletion, increased Ca2+)
Membrane Dysfunction - usually caused by ROS or other injurious agents, causing necrosis (ATP shortage, phospholipid shortage, cytoskeleton, depletion)
DNA damage like that caused by radiation can lead to Apoptosis
Mutations/Cell Stress/Infections can lead to ER unfolded protein accumulation, Apoptosis
What are the two classes of GPCRs?
Heterotrimeric/Monomeric.
Bonus: Give a pathway that uses each.
What hormone is checked in pregnancy tests?
hCG
Compare the Morphology of a Necrotic Cell and Apoptotic cell?
Enlarged, swollen vs. Reduced Shrunken
Pyknosis, Karyorrhexis, or Karyoysis vs. Nuclear Fragmentation
Plasma Membrane disrupted vs. intact
Cell contents are degraded and leak out vs. apoptotic bodies
Pathological vs. Physiological
What phoshphorylation cascade is related with growth factors?
MAPK cascade.
RTK activation -> Grb-2 recruit -> GEF -> RAS -> Ref -> Mek -> Erk.
What are the symptoms of tetralogy of fallot?
Ventricular Septal Defect
Right Ventricular Hypertrophy
Overriding Aorta
Pulmonary Stenosis
What are the intracellular accumulations?
Lipids - accumulation of triglycerides
Cholesterol - cholesterolosis
Protein - proteins in pathological locaitons
Amyloid - misfolded proteins form aggregates
Hyaline Change - may accumulate as a result of intracellular or extra cellular change
Alzhimer’s Disease - amyloid accumulation
Gout - uric acid accumulation in joints
Calcification: deposition of calcium salts, can be dystrophic (normal serum) or metastatic (hypercalcemia)
Glycogen - accumulation of glucose
Pigments - endogenous (lipofuscin) or exogenous (coal, tobacco)
What is the Michaelis-Menten Equation and related variables/constants?
V = Vmax[S]/([S]+Km)
Vmax = k2[E] for S>>>
kcat = k2 for S>>>, catalytic step
kcat/Km = catalytic efficiency
Write the Coagulation Cascade (include factors, different names, and cofactors/mediators)
Primary Hemostasis:
1. Vasconstriction, exposure of VWF
2. Platelet Adhesion
3. Platelet Activaiton
4. Platelet Aggregation
Secondary Hemostasis:
What are all the forms of cellular adaptations in response to injury? Try to name a physiological and pathological example of each.
Hypertrophy - increased size of cells, increased production of intracellular components. Phy: increased functional demand (uterine or muscle growth). Path: cardiac ventricular hypertrophy due to hypertension
Hyperplasia - increased cell division. Phy: breast tissue proliferation at puberty. Path: benign prostatic hyperplasia
Atrophy: initial decrease in cell size and organelles, may follow with apoptosis. Phys: ovaries after menopause. Path: skeletal muscle atrophy after not being uesd
Metaplasia: cell type switching to withstand a stressor. Barrett esophagus (squamous to columnar epithelium)
Dysplasia: abnormal cells within tissue.
What is the mechanism by which the GLUT1 uniporter leads to insulin release?
GLUT1 imports glucose
Glucose import means respiration, increasing ATP and NADH
ATP inhibits K(ATP) channels
K(ATP) channel depolarizes cells
Depolarization of cell leads to voltage-gated Ca2+ channel release
This leads to Ca2+ release from ER
Ca2+ release means Insulin secretion.
What combination of signals can lead to Cell growth? Explain each signaling mechanism.
Outside-In, Inside-Out signals.
Outside-In signals, activate integrins through ECM. This leads to cytoskleton changes that are pro-growth.
Inside-Out signals activate GF-RTKs or GPCRs to lead To integrin activation through talin.
Bonus: If these signals interact with each other to modulate genetic expression to varying levels, what is it called ?