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MOD1 > CH2 > Flashcards

CH2 Flashcards

1
Q

What pathway in cardiac hypertrophy is exercised-induced?

A

PI3K/AKT pathway

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2
Q

What pathway in cardiac hypertrophy is GF-induced and considered pathologic?

A

GPCR

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3
Q

What xcript factors are activated via the cardiac hypertrophy pathways? What tx is available here?

A

GATA4, NFAT, MEF2

Xcript factor inh’s

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4
Q

What factor is expressed in the embryonic heart, and not in adults unless cardiac hypertrophy occurs? What does it cause?

A

Atrial natriuretic factor

Salt wasting (water follows), reduced hemodynamic load

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5
Q

What are some examples of hyperplasia?

A

Warts, benign protastic growth, too much estrogen during menstrual cycle

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6
Q

What are normal examples of atrophy?

A

Thyroglossal duct, notochord, decreased uterus size postpartum

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7
Q

What are the different ways atrophy can occur?

A

Disuse, denervation, ischemic, poor nutrition, loss of endocrine stimulation, chronic pressure

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8
Q

What deficiency can induce metaplasia of the respiratory epithelium?

A

Vit A (retinoic acid)

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9
Q

What CA is likely to develop from Barrett esophagus?

A

Adenocarcinoma

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10
Q

What are the hallmarks of reversible injury?

A

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

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11
Q

What are the possible morphological nuclear changes that occur during necrosis?

A

Karyolisis: basophilia of chromatin fades, DNA degradation via endonucleases
Pyknosis: increased basophilia, nuclear shrinkage and DNA condenses
Karyorrhexis: pyknotic nucleus fragments then disappears

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12
Q

What does the coagulative pattern of necrosis present like?

A

Tissue architecture initially preserved/digestion of dead cells blocked, caused by ischemia or infarct

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13
Q

What does the liquefactive pattern of necrosis present as?

A

Tissue degraded into liquid viscous mass, pus present, digestion of cells has occured (unlike coagulative)

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14
Q

What does the gangrenous pattern of necrosis present as, and where?

A

LEs, combo of liquefactive (d/t secondary bacterial infection) and coagulative (primary cause is ischemia)

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15
Q

What does the caseous pattern of necrosis present like?

A

Cheese-like, white appearance of necrotic area, granuloma (distinct inflammatory border)

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16
Q

What does the fat pattern of necrosis present like?

A

Fat destruction leaving chalk-white areas from Ca of fatty acids, common of pancreatitis (enzymatic destruction of acinar cells)

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17
Q

What does the fibrinoid pattern of necrosis present as?

A

Antigen + antibody complexes deposited on vasculature walls, seen in immune reactions

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18
Q

What important cellular components are affected by a wide range of biochemical mechanisms?

A

Mitochondria, cell membrane, protein synthesis machinery

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19
Q

What are the causes of ATP depletion? What percentage of ATP depletion do significant side-effects begin?

A

hypoxia/ischemia, mitochondria damage, nutrient deprivation, cyanide (and other toxins)

5-10%

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20
Q

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?

A

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

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21
Q

What’s associated with the transition metal generation of ROS?

A

Fenton reaction

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22
Q

What are the different ways in which free radicals are made?

A

Ox phos, radiation (UV, x-ray), inflammation, metabolism of xenobiotics, via transition metals (Fe, Cu), NO

23
Q

What is HIF-1? What does it do? Is it expressed in all mammalian cells?

A

Hypoxia-inducible-factor-1, promotes angiogenesis and enhances anaerobic glycolysis in response to hypoxia

Yes

24
Q

How does cyanide disrupt ox phos?

A

Binds and disrupts cytochrome oxidase (complex IV of the ETC)

25
Q

What class of proteins control mitochondria apoptotic activity? What are the pro, anti, and sensory proteins? What is the activity of the sensory proteins?

A

BCL2

Pro: BAX, BAK
Anti: BCL2, MCL1, BCL-XL
Sensor (BH3s, arbiters): BAD, BIM, BID, Puma, Noxa

Inh anti and activate BAX and BAK when cell stress senses

26
Q

What does cytochrome c complex with after its release from the mitochondria, and what does it create? What does the creating activate?

A

APAF-1 (apoptosis-activating-factor-1)

Apoptosome

Caspase 9

27
Q

What proteins block caspases? What blocks these blockers?

A

IAPs

Smac & Diablo from the mitochondria

28
Q

What R family do death R’s belong to? What do they contain? What’s an example and what’s an inh?

A

TNF

Death domains

Fas (On self-cells or neighboring lymphocytes), binds FasL on T cells (some CTLs), recruits FADD, activates caspases 8 and 10

FLIP: inh caspase 8

29
Q

Where do intrinsic and extrinsic apoptosis pathways intersect?

A

BH3s, caspase 8 can activate these

30
Q

What are the executioner caspases? What do they activate?

A

3 and 6, DNases

31
Q

What is the purpose of phosphatidylserine?

A

Flips from inside the cell membrane to outside during cell injury and imminent death, “eat me” signal

32
Q

What complement tag is used in the removal of dead cells?

A

C1q

33
Q

Where does p53 arrest the cell cycle?

A

G1

34
Q

When does necroptosis occur?

A

Bone growth plate formation, pancreatitis cells death, reperfusion injury, Parkinson, host defense vs viruses

35
Q

What’s the programmed mechanism for necroptosis?

A

TNFR1 or Fas binds ligand, RIP1 and RIP3 recruited, activates caspase 8.. Morphology follows necrosis though

36
Q

What are the key players in pyroptosis?

A

Cytoplasmic immune R’s, inflammasome, caspase 1, IL-1, inflammatory respose

37
Q

What does an autophagosome originate from?

A

Phagophore

38
Q

What protein is required for autophagosome formation? What gene fam is it from? What’s it’s job?

A

LC3, Atgs, to discriminately acquire targets for autophagy

39
Q

What are “foam cells” associated with? What color are they?

A

Atherosclerosis, yellow

40
Q

What is a xanthoma?

A

Tumorous mass/accumulation of cholesterol in macros inside skin and tendons

41
Q

What is cholesterolosis?

A

Accumulation of cholesterol-filled macros in lamina propria o the gallbladder

42
Q

Where are protein accumulations often found?

A

Proximal renal tubules during proteinuria when glomerulus is damaged

Russel bodies seen in plasma cell ERs

43
Q

List where these kinds of intermediate filaments are found: keratin, neurofilaments, desmin, vimentin, glial

A

Epithelial cells, neurons, muscle cells, connective tissue, astrocytes

44
Q

Where in cells are glycogen stores found?

A

Cytoplasm in clear vacuoles

45
Q

What is the most common exogenous pigment?

A

Coal dust (carbon), air pollutant in urban areas

46
Q

What is lipofuscin?

A

The wear-n-tear pigment that’s a product of free radical injury via lipid peroxidation, turns tissue a yellow/brown color

47
Q

What is melanin derived from? What’s the enzyme involved?

A

Tyrosine

Tyrosinase in melanocytes

48
Q

Why is asbestosis so damaging?

A

Ca and Fe bind to the asbestos spicules in the lungs creating dumbbell formations that irritate the lungs

49
Q

What is Werner Syndrome?

A

Premature aging due to defects in the helicase enzyme

50
Q

What denotes the end of a cell’s replicative life?

A

Senescence, telomere no longer able to protect chromosome ends

51
Q

What tumor suppressors are active between the G1 –> S phase of the cell cycle?

A

P16 and INK4a from the CDKN2A gene locus

52
Q

What tx promotes autophagy? What pathway does this tx target?

A

Rampamycin

IGF-1 –> AKT –> mTOR

53
Q

What are the effects of Sirtuins?

A

Reduce metabolism, reduce apoptosis, stimulate protein folding, limit ROS, increase insulin sensitivity and glucose metabolism

MOD1 (5 decks)

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