CH2 Flashcards
What pathway in cardiac hypertrophy is exercised-induced?
PI3K/AKT pathway
What pathway in cardiac hypertrophy is GF-induced and considered pathologic?
GPCR
What xcript factors are activated via the cardiac hypertrophy pathways? What tx is available here?
GATA4, NFAT, MEF2
Xcript factor inh’s
What factor is expressed in the embryonic heart, and not in adults unless cardiac hypertrophy occurs? What does it cause?
Atrial natriuretic factor
Salt wasting (water follows), reduced hemodynamic load
What are some examples of hyperplasia?
Warts, benign protastic growth, too much estrogen during menstrual cycle
What are normal examples of atrophy?
Thyroglossal duct, notochord, decreased uterus size postpartum
What are the different ways atrophy can occur?
Disuse, denervation, ischemic, poor nutrition, loss of endocrine stimulation, chronic pressure
What deficiency can induce metaplasia of the respiratory epithelium?
Vit A (retinoic acid)
What CA is likely to develop from Barrett esophagus?
Adenocarcinoma
What are the hallmarks of reversible injury?
Cellular swelling, membrane blebbing, lost microvilli, mitochondrial swelling with densities, dilation of ER, polysome detachment, myelin figures –> FAs –> calcium soaps, disaggregation of chromatin, fatty change
What are the possible morphological nuclear changes that occur during necrosis?
Karyolisis: basophilia of chromatin fades, DNA degradation via endonucleases
Pyknosis: increased basophilia, nuclear shrinkage and DNA condenses
Karyorrhexis: pyknotic nucleus fragments then disappears
What does the coagulative pattern of necrosis present like?
Tissue architecture initially preserved/digestion of dead cells blocked, caused by ischemia or infarct
What does the liquefactive pattern of necrosis present as?
Tissue degraded into liquid viscous mass, pus present, digestion of cells has occured (unlike coagulative)
What does the gangrenous pattern of necrosis present as, and where?
LEs, combo of liquefactive (d/t secondary bacterial infection) and coagulative (primary cause is ischemia)
What does the caseous pattern of necrosis present like?
Cheese-like, white appearance of necrotic area, granuloma (distinct inflammatory border)
What does the fat pattern of necrosis present like?
Fat destruction leaving chalk-white areas from Ca of fatty acids, common of pancreatitis (enzymatic destruction of acinar cells)
What does the fibrinoid pattern of necrosis present as?
Antigen + antibody complexes deposited on vasculature walls, seen in immune reactions
What important cellular components are affected by a wide range of biochemical mechanisms?
Mitochondria, cell membrane, protein synthesis machinery
What are the causes of ATP depletion? What percentage of ATP depletion do significant side-effects begin?
hypoxia/ischemia, mitochondria damage, nutrient deprivation, cyanide (and other toxins)
5-10%
What does MPTP stand for? What protein is key in its formation and what’s an inh for it? What does it do? What opens it?
Mitochondrial permeability transition pore
Cyclophilin D, Cyclosporine
Opens up outer membrane of mitochondria allowing H to leak out which disrupts the H gradient along the inner membrane necessary to make ATP
Ca
What’s associated with the transition metal generation of ROS?
Fenton reaction
What are the different ways in which free radicals are made?
Ox phos, radiation (UV, x-ray), inflammation, metabolism of xenobiotics, via transition metals (Fe, Cu), NO
What is HIF-1? What does it do? Is it expressed in all mammalian cells?
Hypoxia-inducible-factor-1, promotes angiogenesis and enhances anaerobic glycolysis in response to hypoxia
Yes
How does cyanide disrupt ox phos?
Binds and disrupts cytochrome oxidase (complex IV of the ETC)
