Molecular/Cell Bio Flashcards
What is alternative splicing?
Exons of a gene are reconnected multiple ways during post transcriptional processing, creates diff mRNA sequences and contributes to biodiversity
What elements are needed for PCR?
DNA template that includes target region, flanking sequences adjacent to target region ( the oligotide sequences of flanking must be known to make primers)
What happens to tRNA that is mischarged with the wrong amino acid and not corrected by aminoacyl-tRNA at the tase proofreading?
It will incorporate into the growing polypeptide chain
What Is DNA laddering a marker of?
Is a sensitive marker for apoptosis and refers to DNA fragments in multiples of 180 base pairs
In bacteria, what functions to remove RNA primers and replace them with DNA?
DNA polymerase I
What refers to gene exchange that occurs through the crossing over of 2 double stranded DNA molecules?
Recombination
Nonsense mutations tend to move ______ in electrophoresis due to their dec size
further
trinucleotide expansions tend to move ____ in electrophoresis due tot heir inc sezie
less
Speed of hemoglobin in gel electrophoresis between HbgA, HgbS, HgbC
Hgb A>HgbS>HgbC
Explain the intrinsic pathway mitochondrial pathway of apoptosis
- mitochondria become more permeable and pro-apoptotic substances are released in the cytoplasm under stress/ cessation of survival signals
- the anti-apoptotic proteins Bcl-2 and Bcl-x that reside in the mitochondrial membranes and cytoplasm are replaced with pro-apoptotic proteins such as Bax, Bak, and Bim
- The proapoptotic proteins allow for the inc permeability of the mitochondria which results in release of caspase activating substances like cytochrome C (can see many shrunken eosinophilic cells in the tumor b/c nucleus condensed and made it all pink)
Explain the extrinsic receptor ligand pathway of apoptosis
This requires engagement of death receptors on the cell surface. These death receptors are in the tumor necrosis family (TNFR1 and Fas=CD95).
- After cross linking of Fas with ligand, multiple molecules of Fas come together to form a binding site for a death domain containing adapter protein called FADD
- FADD then binds an inactive caspase bringing multipole caspases together–> activates caspases
Caspases are a family of proteins that cause?
apoptosis
The _______ is the site of ribosomal subunit maturation and assembly. What enzyme functions exclusively in this area? Howdoes it stain?
nucleolus, RNA polymerase I, basophilic
What is the hallmark of initial phase of injury and is it reversible?
cellular swelling (membrane blebbing,loss microvilli, swelling of RER), yes -b/c build up of Na in cell-->water follows
When membrane damage occurs cell injury is
irreversible
- ex: why we do troponin tests in MI is to basically see if enzymes leaked into the blood=irreversible myocyte damage
- ex: ETC is in INNER mitochondrial membrane and once its damaged can’t go back and giving O2 wouldn’t help, cytochrome C can lead out–> apoptosis
Causes of damage for FiO2–>PAO2—>PaO2–>SaO2
FiO2: high altitude
PAO2: anything that inc PACO2= COPD, hypoventilation
PaO2: affected by previous
SaO2: CO poisoning, Methehemoglobinemia(Fe3+ binding Hgb) (normally FeTWO binds O2)
Morphologic sign of cell death is loss of _____
nucleus
-pyknosis(nucleus shrinks), karryohexis (nucleus breaks up into small pieces)< karyolysis
In ______ necrosis, tissue remains firm, cell shape/organ are preserved and the nucleus disappears. This is characteristic of ____infarction of any organ except the _______
coagulative necrosis, ischemic, brain
In _________necrosis, tissue becomes liquified through enzymatic lysis of cells. What 3 situations do you see it in?
liquefactive
-brain infarction(mediated by microglia), abscesses(neutrophils mediate), pancreatitis(enzymes in pancreas digest itself)
_______necrosis resembles mummified tissue, and is characteristic of lower limb and GI tract. Can be superimposed with what other necrosis
Gangrene, liquefactive
________ is a combo of liquefactive and coagulative necrosis, it has a ______ like appearance, and is characteristic of __________ inflammation
Caseous, cottage cheese, granulomatous (from fungal or TB infection)
______necrosis has adipose tissue with chalk white appearance due to deposition of ____?
fat, calcium (fatty acids bind to Ca=saponification)
- ex: trauma to breast, damage of peripancreatic fat
- see giant cells, fat, calcifications
saponification is an example of ________ calcification
dystrophic
-ex: psammoma bodies
_______ necrosis is from damage to the blood vessel walls and leads to ______ of proteins into vessel wall with a ______ stain.
Fibrinoid, leakage, bright pink
-malignant HTN, vasculitis, preeclampsia (fibrinoid necrosis of placenta)
Apoptotic bodies are removed by ______ and is there subsequent inflammation?
macrophages,no
In the _________ pathway, performs create pores in membrane of target cell. Granzyme enters pores and activates caspases
cytotoxic CD8+ T cell mediated pathway
Which 3 enzymes are important for the removal of free radicals?
superoxide dismutase, catalase, glutathione peroxidase
O2-, H2O2, OH-
OH is most damaging
CCl4 is metabolized to what by what organ? What happens to hepatocyte
CCl3 by liver
hepatocytes have dec protein synthesis from cellular damage and apolipoproteins can’t work–> fatty change in liver
Amyloid is a ______ protein that deposits in the _______ space. It tends to deposit around? How does ti stain?
misfolded, extracellular, blood vessels, congo red and apple bifringence
Primary amyloidosis is systemic deposition of __________ derived from ____ light chain. What is it associated with?
AL amyloid, Ig, plasma cell dycrasias: overproduce light chain that leaks out and deposits everywhere
Secondary amyloidosis results from systemic deposition of ________ derived from SAA. SAA is an _______ reactant that is increased in ________ inflammatory states, malignancy, familial Mediterranean fever
AA amyloid, acute phase, chronic
Familial Mediterranean fever is a dysfunction of _______ and presents with fever and acute ______ inflammation. High _____ during attacks deposits as __ amyloid
neutrophils, serosal, SAA, AA
Amyloid depositing in kidneys leads to _______ syndrome
nephrotic
Amyloid depositing in heart leads to ________ and _______
restrictive cardiomyopathy(heart becomes less compliant and bendable) and arrhythmia
Diagnose amyloidosis through _______. Damage organs must be ______ because amyloid can’t be removed
abdominal fat pad and rectum, transplanted
In senile cardiac amyloidosis, _____ deposits in heart. It’s typically asymptomatic
non-mutated transthyretin,
In familial amyloid cardiomyopathy, _________ deposits in the heart. This leads to _______
mutated serum transthyretin, restrictive cardiomyopathy
In type 2 diabetes, _______ deposits in islets of pancreas
amylin (derived from insulin)
Alzheimer’s disease has _____ amyloid deposits in brain. This is derived from Beta-amyloid precursor protein on what chromosome?
AB, 21
Dialysis associated amyloidosis has _____ deposits in joints. This provides structural support for which MHC molecule?
Beta2 microglobulin, MHC class 1
-in CKD, beta2 isn’t filtered well so builds up in blood and deposits
Tumor cells with an amyloid background in the thyroid suggests
medullary thyroid carcinoma
With acute inflammation, how are these all affected: endothelial intracellular cGMP, blood velocity, RBC concentration, arteriolar resistance, endothelial transcytosis
increased cGMP, decreased velocity(b/c as you dilate/inc cross section–> dec vel), increased concentration, decreased resistance, increased transcytosis (collects fluid from vascular side and releases it on interstitial side)