Nervous System
anterior horn of spinal cord (cell body) -> ventral rootlets -> ventral root -> mixed spinal nerve -> dorsal rami -> unnamed nerve
a) the Iliocostalis is part of what group of muscles?
b) dorsal rami vs. ventral rami?
c) the efferent cell body is in the anterior horn. Where is the afferent cell body?
A standard pregnancy test uses ___. What is this?
hCG. It is a hormone that is crucial for sustaining progesterone output from the corpus luteum.
Bonus:
a) At one point, the corpus luteum progesterone output is taken over by what? When?
b) When might an OB calculate DOB to a mother who has just gotten a pregnancy positive test?
Starting from smallest structure and ending with a full turn, describe the structure of DNA, incl. the bonds that hold different levels of structure together.
Nitrogenous base: Can be pyrimidine (6 carbon ring, C, T, U) or purine (5,6 carbon dicyclic ring, A, G).
Nucleoside: nitrogenous base + pentose (ribose or deoxyribose), formed with N-glycosidic Bond
Nucleotide: Nucleoside + phosphate groups (1-3, phosphodiester bond
DNA double helix: sugar-P backbone, 5'-3' directionality on strands, strands run antiparallel to eachother. Nucleotides base pair, base stack, and are in the inside (hydrophobic) while phosphate-sugar backbone is on outside (hydrophilic). Double helix has major groove and minor groove.
Bonus: Why is the major groove important for something like glucocorticoid receptor activation?
What is the guardian of the genome? What is it's function? How does the guardian get activated and what does it do in the cell?
p53. It's function is to halt cell-cycle progression in the face of DNA Damage.
DNA Damage activates Chk1/Chk2 and ATM/ATR. MDM2, a ubiquitin ligase that targets p53, is inhibited by ATM, causing p53 to be free, allowing it to activate p21, inhibiting Cdk2 and upregulating BRCA1 & BRCA2. p53 may also just cause apoptosis.
Bonus. How does p53 activate apoptosis? (General pathway of activation)
What are the 4 types of powers to view slides at? What can each power see?
Low Power: Anatomic Structures
Medium Power: Tumor architecture, Pathological changes
High Power: Cell types, Cytomorphology
Very High Power: Only in Electron Micrscopy, can view individual cellular structure
Generally, higher power provides greater resolution
How is the organization of spinal nerves important diagnostically? What could they diagnose?
Bonus: What is a common cause of spinal nerve compression and how does it happen (describe relevant anatomical structures) ?
Describe gametogenesis.
At week 2, epiblasts give rise to primitive germ cell and settle in yolk sac. Around 4th and 5th week primordial germ cells migrate to embryo.
Oogenesis: Once they reach ovary in 6th week, they form follicles and devide by mitosis. At 7th MONTH they enter prophase I and are arrested by OMI.
Spermatogenesis: Once they reach embryo, they stay there until puberty, where spermatogonia will differentiate into sperm cells.
Take a ride! The Central Dogma of Biology States that DNA becomes RNA which becomes Proteins. As much as you can, write the process of replication, transcription, and translation from beginning to end. Highlight differences between Eukaryotes and Prokaryotes, including structural & functional differences.
A good answer would talk about the mechanisms and differences between prokaryotes and eukaryotes. Some things to highlight would be the differences in compaction of DNA, organization of the nucleus, sequences for initiation/recognition, and more. Bonus points for highlighting places along the central Dogma where diseases may occur.
Name and describe the function of all learned TSGs. (If possible, order them for where they would be activated/effect the cell cycle)
p16/Ink4 - inhibits Cdk4/6
RB - inhibits release of E2F when hypophosphorylated
p27 - inhibits Cyclin E, after activation by contact inhibition at E-Cadherin Cadherens junctions.
p53 - halts cell cycle progressing past S phase, causes p21 activation (inhibit Cdk2, activate BRCA1/2) or apoptosis
Wee1 kinase - doesn't allow cell to go from G2 to M until DNA stability is checked (technically a TS, but also a key protein to prevent mitotic catastrophe)
APC/C Complex - degrades Cyclin B if metaphase has been done properly.
Simple Squamous, one layer of flat, oval cells.
Renal medulla, Renal Corpuscle, serosa of urinary bladder
Simple Cuboidal, one layer of cuboidal cells
Ovarian surface, bile duct lining
Simple Columnar, One layer of columnar cells
Gallbladder lining, apical surface of intestinal epithelium
Pseudostratified Columnar Epithelium
Simple columnar cells with varying nucleus location
Respiratory epithelium (paired with cilia and goblet cells)
Stratified squamous epithelium, multiple layers of squamous cells
Keratinized (epidermis) or nonkeratinized (oral cavity)
Stratified Cuboidal, multiple cuboidal layers
sweat gland duct, esophageal mucous gland duct
Stratified columnar, multiple columnar layers
male urethra, conjunctiva
Transitional Epithelium, multiple different cell layers
Bladder tract
Bonus: What are all the types of glands?
Bonus x 2: Epithelial cells have domains. What are they and how can they be modified?
Generally, the sympathetic and parasympathetic nervous system are antagonistic systems that make use of both pre and post ganglionic neurons. The sympathetic nervous system uses NE postganglionically and the parasympathetic uses Ach.
Name as many exceptions to the above as you can (sympathetic-only innervations, non-canonical neurotransmitter use, ganglion positioning). Most done is winner.
Sympathetic-Only: cells of adrenal medulla, arterial blood vessels, sweat glands, piloerector muscles
Non-canonical NT: (only sympathetic) Dopamine in Renal Blood Vessels, Ach in sweat glands, Ach in adrenal medulla
Ganglion positioning: (only sympathetic) preganglionic directly innervate adrenal medulla. preganglionic innervate preveterbral ganglia in abdomen.
What causes gastrulation? What arises from gastrulation? What are the deriviatives of the things that arise from gastrulation?
Surface Ectoderm: Skin
Neural Crest: two pathways
- Ventral: Dorsal Root Ganglia (DRG), Parasympathetic ganglia, Sympathetic & Enteric Neurons, Schwann Cells, Cells of Adrenal Medulla
- Dorsal: Melanocytes & Hair Follicles
Neural Tube: CNS
Mesoderm:
Notochord becomes nucleus pulposus of IV discs
Cardiogenic Mesoderm gives rise to heart tube -> heart
Paraxial Mesoderm is para-neural tube gives rise to somites, which gives rise to somatocoeles
Sclerotomes - vertebrae and ribs
Myotomes - skeletal muscle
Dermatomes - dermis of skin
Intermediate mesoderm - urogenital system
Lateral Mesoderm
Gives rise to somatopleures and splanchnopleures (body walls) (specifics later)
Endoderm
comes from primitive streak
Give rise to foregut, midgut (communicates with yolk sac via vitelline duct to create primitive umbilical ring later), and hindgut
Gives rise to GI tract, Respiratory system (lung buds), and bladder + urethra lining
Give the following pathways for each repair mechanism, highlighting important/named proteins.
Short Patch Base Excision
Long Patch Base Excision
Nucleotide Excision Repair
Non Homologous End Joining
Homologous Recombination
Non-Homologous Recombination/Transposition
Short Patch: DNA Glycosylase Recognition, AP Endonuclease Excision, DNA Polymerase removal & filling nucleotide, DNA Ligase sealing
Long Patch: DNA Glycosylase Recognition, AP Endonuclease Excision, DNA Polymerase removal & filling nucleotide, FEN1 cutting flag, DNA Ligase sealing
Nucleotide Excision Repair: Recognition (Independent proteins, RNA polymerase), XPB/XPD Helicase, excision nucleases, DNA Polymerase fills gap, DNA ligase seals
Non Homologous End Joining: Ku protein recognition, ends tethered by XRCC4, excision nucleases excise, DNA polymerase fills gap, DNA ligase seals
Homologous Recombination: DSB recognized & turned into single strands, Rad51 creates D-loop, DNA polymerase creates Holiday junctions, DNA Ligase seals single strands. (crossing over may occur)
Non Homologous Recombination: Use endonucleases to cut themselves out of DNA, use Reverse Transcriptase to insert them in other DNA parts.
Bonus: For each, except Non Homologous Recombination, what can they repair?
Bonus 2: NER has 3 diseases associated with it, what are they and how do they differ?
Explain the significant events that progress through in the four phases of the cell cycle: G1, S, G2, and M.
G1 to G2
Mitogenic signals induce Cyclin D synthesis
Cyclin D binds Cdk4/6, which becomes partially phosphorylated. Full phosphorylation requires additional kinases, such as CAK
Cdk4/6 then hyperphosphorylates Rb, releasing E2F from it.
E2F activates transcription of cyclin E, activating Cdk2/cyclin E complex
Cdk2/Cyclin E phosphorylates more Rb, releasing enough E2F activate DNA replication factors and to produce Cyclin A, which mains DNA synthesis and S phase.
S to G2
Finishing DNA replication begins transcription for Cyclin B, which would bind Cdk1, but it is currently inactivated by CAK and Wee1 kinases.
G2 to M
Once cell is ready to divide, Cdc25 removes inhibitory phosphate from Cdk1, activating it to promote mitosis through various functions
Phosphorylation of condensing to compact chromosomes
Phosphorylation of nuclear lamins to break down nuclear envelope
Phosphorylation of microtubule associating proteins to depolymerize cytoskeletal MTs and organize for mitotic spinde
Phosphorylation of APC/C complex for anaphase and degrading Cyclin B
Name every derivative of Connective Tissue.
3 kinds: Adipose, Cartilage, Bone
Adipose - White & Brown
Cartilage - Hyaline, Elastic, Fibrocartilage
Bone - is bone
2 Broad Classes of Connective Tissue Proper: Loose and Dense.
Loose - lamina propria, mainly transient WBCs
Dense - Irregular (haphazard collagen) and Regular (Dense packing)
Bonus: Structurally, how do all these tissues differ? Where might they may be found?
What neurotransmitter causes vasoconstriction and where would it act on? Vasodilation?
Vasoconstriction is caused by sympathetic innervation of vascular smooth muscle, but vasodilation is caused by parasympathetic innervation of vascular endothelium.
Bonus:
a) Describe the mechanism for both.
b) Describe ALL cholinergic & adrenergic receptors: give a location for each where they are found, cellular function and general function (if possible). For each, highlight which nervous system(s) makes use of them.
What is the placenta? When does it develop? What are it's main functions?
It's main functions are to
- Exchange wastes and nutrients
- allows transmission onf maternal antibodies
- produce progesterone in 3rd-4th month, produces estriol near end of pregnancy
Bonus:
The main goal of the placenta is to supply the fetus. What other structure provides nutrition to the fetus? What are the other functions of this structure? What does this structure wrap around?
What are the 3 major motifs of Transcription Factors? How do they work (if possible) ?
Helix-Turn-Helix: Binds Major Groove of DNA
Zinc-Finger: contains a-helix and b-sheet, 2 Cys and 2His, binds to zinc. Binds Major Groove of DNA
Leucine Zipper: contains 2 a-helix that dimerize in leucine-rich a-helical zipper region. Binds Major Groove of DNA
Bonus: What motif(s) do many steroid transcription factor/receptors use?
Describe the current multi-step molecular model of carcinogenesis, including examples of oncogenes that occur at each stage.
Neoplasia
Early mutations, like Initiator and Driver Mutations occur here, including RAS mutations
Ras mutations lead to constant stream of proliferative signals, are often mutually exclusive to RTK activating mutations (Monomeric G-Protein RAS pathway)
Other Early mutation can be familial retinoblastoma, where person inherits RB mutation
Increasing Dysplasia
Late Mutations occur here, including TP53 mutations, which contribute to genomic instability
Also includes late RB mutations, sporadic retinoblastoma
Malignancy
Signified by transformation from Dysplasia
Malignant tumors frequently have mutated TP53/p53, leading to sporadic or germline tumors (Li-Fraumeni Syndrome)
Treatment Resistance
Treatment related mutations
Name every type of slide presentation and every type of staining.
Slide Presentations: FFPE, Aspiration, Smear, EM
Stain:
Eosin stains positively charged, basic components (red)
Hematoxylin stains negatively charged, acidic components (blue)
Methenamine silver stains fungi (black)
Brown and Hopps, tissue gram stain stains bacteria (Gram positive bacteria are blue, gram negative bacteria are red, Golden counter stain)
Verhoff van Gieson stains elastin (black brown) and collagen (red)
Trichrome stains collagen (blue/green) with black nuclei and red muscle.
Periodic Acid Schaffer (PAS) stains carbohydrates (red/purple with pink counter)
Take a ride! Starting from one word (randomly selected), try and relate as many things as possible to the word and it's derivatives. Your goal is to try and recreate as much knowledge from the lectures as possible. A good answer includes paths of neural innervation, receptors, example organ innervations, signaling pathways, etc.!
Use LOs for answers :3
What is the process by which the thoracic, abdominal, pericardial, and pleural cavities are created?
Septum Transversum partially separates thoracic and abdominal cavity.
Lung bud grows into the pericardioperitoneal canals, creating pleuroperitoneal folds and membranes.
Pleuropericardal folds form and fuse with each other to make pleuropericardial membrane.
Forms pericardial cavity and pleural cavities.
Pleuropericardial membranes become the fibrous pericardium.
Pleuroperitoneal folds fuse over septum transversum to create start forming diaphragm.
Diaphragm separates thoracic and abdominal cavities.
Bonus: What 5 things contribute to the formation of the diaphragm?
In both prokaryotes & eukaryotes, there are mechanisms of genetic regulation, controlling what genes are encoded and to what level they can be made. Name as many as you can.
Most control is at transcriptional level.
Prokaryotic:
- control with operons, making use of operators and inducer/repressor proteins that respond to environment.
- control with attenuation, making use of environment-sensitive parts of RNA to create pauses in transcription that allows translation (occurring simultaneously) to make different transcripts.
- some RNA editing
Eukaryotic:- Nucleosome compaction, which can be edited through covalent bonds to might it more compact or less compact
- DNA Methylation
-use of enhancers/transcription factors- RNA splicing (w/ Alternative Splicing)
- RNA editing
Bonus: DNA Methylation at what non-coding structure greatly affects transcription? How does DNA methylation change in these regions in these cancers?Explain each of the following potential causes of cancer, and give a prominent cancer that comes from each.
Point Mutations
Indels
Chromosomal Rearrangements
Gene Amplification
Viruses
Chemicals
Radiations
Point Mutations: most common mutation, but not always carcinogenic. Cancer related: RAS/GF-RTK point mutation causing constitutive activation of MYC, leading to many cancers.
Indels: insertion or deletion. Cancer related: Von-Hippel Lindau Syndrome (VHL gene deletion).
Chromosomal Rearrangements: translocation, inversion, deletion, duplication. Cancer Related: 9:22 translocation leading to Chronic/Acute Myeloid Leukemia. (Translocations frequently in leukemia/lymphoma)
Gene Amplification: genes may be mutated to be constantly expressed. Cancer Related: MYCN amplification is prognostic indicator in neuroblastoma.
Viruses: viruses can cause expression of certain cellular mechanisms leading to cancer. Cancer related: HPV can activate E6 and E7, may lead to Cervical Cancer.
Chemicals: chemicals can directly or indirectly (by metabolites) cause cancer. Cancer Related: activated Aflatoxin B1 can cause Hepatocellular Carcinoma
Radiation: radiation can cause bulky DNA lesions leading to cancer. Cancer Related: secondary malignancy after radiation therapy of Hodgkin's Lymphoma can cause breast cancer.
What are the structures in bone?
Articular Cartilage - articulates bones with other bones
Endosteum - within bone cavities of compact and spongy bone
Osteons - Structure for growth, parallel to bone length
Bone Blood Supply - Haversian Canal, Volkmann’s Canals
Bonus: What is the process of bone growth?
Bonus x 2: What is the process of bone healing?