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305 Cards in this Set

  • Front
  • Back
uncontrolled growth and spread of abnormal cells
Cancer
altered cell differentiation and growth
Cancer
2 Rare Cancers:
male breast cancer, eye cancer
Primary Cancer
Cancer formed in the tissue of origin
Secondary Cancer
formed in a different site by cells that have metastasized from the primary
Tumor
An abnormal mass of cells as a result of uncoordinated cell growth
Neoplasia
process of the creation of a tumor
Neoplasm
AKA Tumor
_____Tumors have slow and limited growth, are well differentiated, resemble the cells in the tissue of origin and are localized.
Benign
T/F Benign tumors can be life threatening
True but only if they are located in the brain.
T/F Benign tumors do not interfere with normal functioning
False. Pressure on tissues, blood vessels and nerves (interfere with normal functions)
_____ tumors are less differentiated and have rapid and uncontrollable growth. They are different than the cells in the tissue of origin and invade surrounding tissues causing tissue damage.
Malignant
T/F Malignant tumors are life threatening.
True
T/F Malignant tumors cause ischemia and tissue damage via dilation of blood vessels.
False. Malignant tumors cause ischemia and tissue damage via compression of blood vessels.
What tumors secrete proinflammatory and toxic substances which result in inflammation and tissue damage?
Malignant Tumors
Can benign tumors turn malignant?
Yes.
An example of a benign tumor turning malignant?
Benign fibrous mesothelioma : lungs (can progress to mesothelioma)
Mucinous cysladernoma: pancreas (can lead to malignant invasive pancreatic cancer)
Pre-malignant tumors are
tumors that have a high propensity to become malignant.
An example of a pre-malignant tumor is...
Colon Polyp: Larger and villous benign polyps have a higher chance of becoming cancerous. Risk doubles with family history.

Actinic keratosis: UV damaged skin may develop into squamous cell carcinomas in fair skinned individuals.
What is a Non-solid (“liquid”) tumor? example?
Single genetic abnormality (Leukemia)
What is the fraction of cancer cells that can survive in the blood stream?
1/10,000
Intravasation
Gaining access to the vasculature
Matrix Metalloproteases (MMPs)
Cancer cells use MMPs to digest extra cellular matrix proteins.
MMPS are zinc-dependent endopeptidases.
Collogenases are also members of the MMP family.
Cathepsins
A type of lysosomal endopeptidase that tumor cells secrete in order to degrade matrix proteins.
How do cancer cells gain motility?
Cytoskeleton rearrangement by secreting factors that retract the endothelial lining.
How do cancer cells evade immune surveillance?
By secreting soluble prostacyclins (PGI2) to induce platelet aggregation around the cancer cell.
What do cancer cells use integrin for?
Integrin is a surface cell receptor that can be upregulated in order to better bind to platelets.
What helps a cancer cell "settle" against the force of the blood stream?
Thrombosis and its ability to increase adhesiveness to the endothelium allowing it to "flatten out".
Metastasis
A secondary tumor that went through the blood stream and broke endothelial walls with MMPs & cathepsins to get there.
What are SEM proteins?
Sub-endothelial matrix proteins that a cancer cell must digest in order to create a secondary tumor.
4 Routes of Metastasis
1. Body Cavities
2. Lymphatic Spread
3. Hematogenic Spread
4. Mechanical Transfer
Types of Body Cavities in which Metastsis can occur
1. Peritoneal Cavity: space between parietal peritoneum (attached to abdominal wall) and visceral peritoneum (wrapped around organs).
2. Pleural Cavity: around lungs
3. Pericardial Cavity: around heart
4. Subarachnoid Space: in the brain
5. Joints
Lymphatic Spread
Route of Metastasis that is commonly observed for lung & breast.

Cancer cells first enter lymph nodes that receive drainage from the site of tumor. They can spread to distal lymph nodes, and gain access to the vasculature through thoracic ducts.
Hematogenic Spread
Route of Metastasis that is commonly observed for sarcomas of soft tissues.

Cancer cells enter vasculature through the peripheral vein or through infiltrating blood vessels.
Mechanical Transfer
Route of Metastasis that is RARE. Cancer cells being transferred during operation or diagnostic procedures.
What are potential factors that influence sites of Metastasis?
- Lymph or vasucular drainage
- Local environment suitability: availability of growth factors and cytokines that facilitate secondary growth.
Breast Cancer common sites of metastasis:
Bones, Lungs, Liver, Brain
Prostate Cancer common site of metastasis:
Bones
Lung Cancer common sites of Metastasis:
Brain and Bones
Colon Cancer common sites of Metastasis:
Liver
How do you identify a metastatic tumor?
Histological: Resemblance to the cells in the tissue of origin

Immunological: with antigenic profile
T/F Metastatic tumors may be detected before the discovery of primary tumor
True! Occasionally, a metastatic cancer is detected and primary tumor can not be found.
T/F Most cases of cancer are genetic.
False! Most cases of cancer are sporadic (idiopathic). There are some cancers that are associated with specific clusters of mutated genes.
BRCA1 and BRCA2 Gene mutations
account for 5-10% of breast and ovarian cancers.
Autosomal Dominant.
Normally they suppress tumor growth.

Discovered @ UCLA.
Tumor Suppressor genes
Encode for proteins that are important in regulating cell growth and differentiation. Mutation-induced loss of function promotes tumor formation.
APC Gene Mutation
Familial Adenomatous Polyposis (FAP)
RARE disease.
polyps develop into colon cancer later on in life
Autosomal Dominant

APC is normally a tumor suppressor gene that targets beta catenin from entering nucleus and initiating transcriptional activity.
Proto-oncogenes/ Oncogenes
Encode for proteins that are important in regulating cell growth and differentiation. Certain mutations in proto-oncogenes or over-expression turn them into oncogenes resulting in over activity of the gene product leading to tumor formation.
RAS
proto-oncogene that was first isolated from a rat sarcoma. Encodes a GTPase important for cell growth.
Mutation in GGC (glycine) to GTC (valine) makes RAS constitutively.

Found in 20-30% of tumors.
HRAS
KRAS
NRAS (neuroblastoma)
KRAS
Type of RAS gene that is high in leukemias, colon cancer, pancreatic cancer, & lung cancer.
HRAS
Type of RAS gene that is high in bladder cancer
WNT gene
proto-oncogene found in wingless drosphila that encodes a family of proteins that frees up cytoplasmic beta-catenin and initiates cell proliferation activity.

SFRP-1 affects WNT availability.
SFRP-1 loss occurs in the following cancers
bladder cancers, breast cancers, & colorectal cancers.

(in increasing order)
Rb Gene
Retinoblastoma protein.

Tumor Suppressor Gene

When Rb is damaged, ATM cycle cannot produce p21. p21 stops CDK which tells the cell to stop proliferation (from G1 to S phase)

Autosomal Dominant.
increased
TP53
Tumor Suppressor Gene that encodes p53, “Guardian of the genome”. P53 is involved in cell cycle regulation, DNA repair and apoptosis.

- activates p21 which stops G1/S cell cycle
- activates GADD45, XP which repairs DNA damage
- activates Bax,Bak activates apoptosis for cells that can't be fixed.
Li-Fraumeni syndrome
a very rare autosomal dominant disorder, individuals who inherit one copy of mutated TP53 are at much higher risk to develop cancer at a young age, develop multiple cancers including breast cancer, osteosarcoma and soft tissue sarcoma. Brain tumors and leukemia are also found.
Human Papillomavirus (HPV)
Repeated infection by Types 16 and 18 HPV of the >120 types of HPV is associated with increased incidence of cervical cancer.
HPV infects host cells and produces:
early proteins (E1-E7) and late proteins (L1 and L2)
Cancer Risk Factors
Genetic
Exposure
Radiation
Chemical Carcinogens
-Direct: alkylating agents
-Indirect: become active after biotransformation = aflatoxin B1
-Polycyclic Aromatic Hydrocarbons: benzo(a)pyrene

Hepatitis B & C AND Alcohol Consumption (liver cancer due to hepatocyte damage)
Benzo[a]pyrene (BaP)
CYP450 metabolizes to epoxide and converted to diols that react with DNA.
What is Imaging in Cancer Diagnosis?

Types of Imaging for Cancer Diagnosis
Determining the presence and size of cancerous tissue in normal tissues.

Transmission
Reflection
Emission
Transmission Imaging:
X-rays, Computed Tomography scan (X ray), bone scan (radio isotope), mammograms (X ray) , lymphoangiogram (dye based imaging for lymphatic system)
Reflection Imaging
Ultrasound sonography (detect tumors in abdomen, liver and kidney)
Emission Imaging
Magnetic Resonance Imaging (heart, brain, liver, pancreas, reproductive organs), Positron Emission Tomography (radio isotope, function and anatomy of tisseu/organ)
What are Cytologic and histologic diagnosis methods for Cancer?
Determining whether cells in the tissue preparation are cancerous; determine if it is a primary or mestastasized tumor.

Examples: Pap smear, biopsy, immunohistochemical analysis following immunostaining for protein markers
What are Genetic Diagnosis methods for Cancer?
Determining the presence of specific mutations. Only useful in cancers known to be associated with genetic mutations.

Examples: PCR analysis specific mutations, DNA arrays
What are Biomarker methods for Cancer Diagnosis?
A handful of biomarkers are available. However, they are not specific to malignant form of the tumors and not generally elevated in pre-symptomatic stage. At the moment, they may be more useful for assessing prognosis in response to treatment.

Example: PSA-prostate specific antigen.
Most common Cancers
Skin cancer
Breast (female)
Prostate
Colorectal
Gynecologic
Most common Cancers in Men? Women?
Men: Prostate, Lung & Bronchus

Women: Breast, Lung & Bronchus
Which Cancer Causes the highest number of deaths each year?
Lung Cancer
What are the cancers with the highest survival rate?
Prostate, Melanoma, Breast
What is Cancer?
Uncontrolled growth and spread of abnormal cells or “altered cell differentiation and growth”
Tumor
An abnormal mass of cells as a result of uncoordinated cells growth. The process is call neoplasia (new growth) and product, neoplasm.
Benign Tumor
slow and limited overgrowth, cells well differentiated and resemble cells in tissue of origin, localized (encapsulated).
Pre-malignant tumor
Malignant tumor in pre-invasion state
Malignant tumor
Cancerous tumor with rapid and uncontrollable growth, cells much less differentiated and maybe very different of cells in tissue of origin, invade surrounding tissues, metastasize to distal organs.
Benign Tumor Suffix?
Malignant Tumor Suffix?
Benign: -OMA

Malignant: -COMA/TOMA
Non-Solid (“liquid”) Tumors
Example: Leukemia

Can be the result of a genetic abnormality
T/F All benign tumors are not life threatening.
False! Brain tumors can sometimes be fatal (glioma) due to the pressures they cause on the brain and tumors affect the normal functioning of other tissues w/ the pressures they exert.
T/F All malignant tumors are life threatening
True! Because they invade the surrounding tissues and cause tissue damage, ischemia and tissue injury as well as inflammation.
Benign fibrous mesothelioma
An example of a benign tumor becoming malignant and causing lung cancer.
Mucinous cystadenoma
An example of a benign tumor becoming malignant and causing pancreatic cancer.
Pre-malignant Tumor
high tendency to become malignant tumors.
Colon polyp
Example of a pre-malignant tumor: Larger and villous adenomatous (benign) polyps have a higher chance of becoming cancerous. Risk doubles with family history of colon cancer.
Actinic keratosis
Example of a pre-malignant tumor:
very common in fair skinned individuals, UV damaged skins may develop into squamous cell carcinomas.
What is Cell Proliferation?
Cell reproduction.
What is Cell Differentiation?
When the cell becomes a specialized cell and cannot "differentiate" into another cell type.
Self-renewal
able to divide without differentiation
Potency
differentiation potential
Totipotent stem cell
first few cells in a fertilized egg, able to generate entire organism
Pluripotent stem cells
formed from totipotent stem cells and can develop into any of the 3 germ layers of an embryo to form specific organs
Multipotent stem cells (progenitor cells)
can only develop into a limited number of cells types.

Example, hematopoietic stem cells.
Unipotent stem cells (precursor cells)
can only develop into only one cell type.

Example: Skin cells and hepatocytes.
T/F Can all cells be Totipotent under specific conditions?
True! New research shows that its possible that all cells can be totipotent under the correct conditions.
S Phase
DNA Synthesis & Chromosome Duplication
Cyclin A
Protein that helps start G2 from S Phase
G2 Phase
Protein Synthesis
Cyclin B
Protein that begins the M phase from the G2 phase.

Checkpoint for DNA damage.
M Phase
Mitosis Phase where nuclear division & cytoplasmic division takes place.
Cyclin D
Protein that helps transition from the M phase to the G1 phase.
G0 Phase
No reproduction will occur this is the dormant state of the cell. Its highly dependent on resources and nutrients.
G1 Phase
Protein synthesis occurs here.
Cyclin E
Protein that helps transition from the G1 phase to the S phase.

Checkpoint for DNA damage
How do Cyclins regulate the Cell Cycle?
Specific Cyclin will dimerize with CDKs to phosphorylate target proteins. This process controls cell cycle entry and progression
Benign Tumor Cell Characteristics
--Well-differentiated cells; But still able to proliferate
Malignant tumor cells
---poorly differentiated and highly proliferative cells

come from progenitor cells
Grade I malignant cells vs Grade IV malignant cells
Grade I: closet to well differentiated normal cells

Grade IV: closest to undifferentiated progenitor cells
What is the Detection Limit of conventional radiography for Cancer Cells?
10^9
What is a potentially lethal number of cancer cells?
10^12
What kinds of genetic abnormalities do cancer cells have?
chromosome abnormalities (number and structure), point mutations (addition, deletion & amplification)
Do cancer cells need growth factor to proliferate?
No, but they can also encourage autocrine production of growth factors if they need to or they can alter pathways/receptors of growth factors to stim. proliferation.
What are some altered cell-cell/cell-environment interactions in Cancer cells?
1. Loss of Normal cell-cell contact inhibition - keep growing even after they are packed together.
2. Reduced ability to adhere to sister cells in tissue - a way they can leave to other places of the body
3. Can survive without other cells
4. "Free" tumor cells and can adhere to other cells and dislodge at will.
How do cancer cells live so long?
Cancer cells are essentially immortal due to high levels of telomerase that adds a TTAGGG sequence, elongating its length after each division.
Do cancer cells have the ability to present antigens?
Yes. Tumor cells may express antigens that are different from neighboring cells in the tissue.
What is angiogenesis and do cancer cells have the ability to do this?
Angiogenesis is the creation of vasculature (blood vessels) in an area.

Cancer cells can induce Angiogenesis.
VEGF
vascular endothelial growth factor. cancer cells secrete this in order to stimulate new blood vessel formation and sustain tumor growth.
What role does Hypoxia play in angiogenesis of cancer cells?
Hypoxia induces HIF which stimulates VEGF.
What are factors that increase VEGF?
1. Oncogenes & tumor suppressor genes.
2. EGF, HER-2, IGF-1
3. COX-2 and PDGF
Criteria of a central neurotransmitter must be _____ and stored in the presynaptic terminal & neuron, must be released in accordance with neuronal _______ (Ca2+ dependent, vesicular), must activate target tissue identical to neuronal stimulation.
synthesized; stimulation
Excitation (EPSP)
depolarize postsynaptic neuron
Inhibition (IPSP)
hyperpolarize postsynaptic neuron
ligand gated ionophores are what speed?
FAST
This receptor is composed of 4-5 subunits.
ligand gated ionophores
Subunits are selective-drug targeting subunits so there are many types of subunits especially with ___________ receptors.
ligand-gated ionophore
T/F Ligand-gated Ionophores only control ionic composition
False.
They also control membrane potential.
Membrane-bound enzymes and G-protein coupled receptors are _____ in terms of their speed.
Slow
What types of receptors can change between hyperpolarization and depolarization?
Membrane-bound enzymes and G-protein coupled receptors
What kinds of receptors can regulate transcription & translation but are not intracellular?
Membrane-bound enzymes and G-protein coupled receptors
only have 1 Membrane spanning region
Membrane-bound enzymes
Membrane-bound enzymes activate intracellular enzymes such as:
1. Tyrosine Kinase
2. Serine/Threonine Kinase
3. Guanylyl cyclase
4. Tyrosine phosphatase
Tyrosine Kinase is a _________________ that ______ tyrosine to activate it.
Membrane-bound enzyme; phosphorylates
Serine/Threonine Kinase is a _________________ that ______ serine/threonine to activate it.
Membrane-bound enzyme; phosphorylates
Guanylyl Cyclase is a _________________ that converts ____ ---> ____ which activates protein kinases to activate/inactivate other proteins.
Membrane-bound enzyme; GTP; cGMP
Tyrosine phosphatase is a ________ that ________ tyrosine to inactivate it.
Membrane-bound enzyme; dephosphorylates
In the ______ family the protein has 7 membrane spanning regions with the ____ subunit determining the effector. When the receptor binds to the protein, ___ ---> ___.
G-protein superfamily; alpha; GDP; GTP
Go
inhibits calcium channels (influx)
Gs
activates calcium channels (influx)
Gi
activates potassium channels (efflux)
In Phospholipase C, ____ activates PLC to make ___ & ___. ____ binds to the calcium storage vesicle which causes a release of calcium. The calcium will bind to the ____-Protein kinase C complex and activates ____, which will activate other proteins.
Gq; IP3; DAG; IP3; DAG; PKC (protein kinase C)
In Adenylate Cyclase, ___ activates AC to increase ___ production while ___ inhibits it. The new product activates _____ which will in turn activate other proteins.
Gs; Gi; PKA (protein kinase A)
________ goes into the nucleus where it modulates transcription and translation in Adenylyl Cyclase.
CREB
T/F in Adenylate Cyclase, the protein is a dual regulator.
True. because it causes activation and inhibition!
In Phospholipase A2, ____ activates PLA2 to liberate ______ ____ from the membranes. That will then combine with ____ & ____ to yield prostaglandins, prostacyclins, and thromboxanes as well as _______ to yield leukotrienes.
Gi; Arachidonic Acid; COX1; COX2; Lipoxygenase.
The really slow receptors are the...
intracellular receptors.
_______ receptors regulate transcription and translation by forming a dimer at the receptor to activate or inactivate mRNA transcription.
intracellular receptors
Remove NTs with two things:
metabolism or reuptake.
What is the normal target of drug treatment?
the precursor
What is the rate limiting step (usually)
enzyme
Exitatory Amino Acids?
Glutamate, Aspartate
What is the rate limiting step in Glutamate synthesis?
enzyme: glutaminase

glutamine --> glutamate
For Glutamate, uptake occurs with ____ dependent transporters are located on neuron and ____ cells.
Na+; glial
Metabolism of Glutaminate:
Glutamine synthase in glia

Glutamate ----> Glutamine
Kainate Receptors are found in the _________ terminal and are _______ receptor types. They produce _____ effects by increasing Na+ and decreasing K+ in the cell.
glutamatergic; ionophore; excitatory
NMDA Receptors are found in the _________ terminal and are _______ receptor types. They produce excitatory effects by increasing ____ and decreasing ____ in the cell. Sometimes increase ____.
glutamatergic; ionophore; Na+; K+; Ca+
_____ Receptors are found in the glutamatergic terminal and are ligand-gated ion channel receptor types. They produce excitatory effects with K+, Na+ and Ca++.

The answer is not NMDA
AMPA
Metabotropic receptors found in the glutamatergic pathway use ____ and ____ in order to decrease cAMP and increase IP3 & Ca+.
Gi, Gq
Glutamatergic pathways in the brain: _____ to _____. Many short interneurons in all parts of brain.
cortex; striatum
Spondee
A poetic foot consisting of two accented syllables.
What are the inhibitory amino acids?
GABA, Glycine, Taurine
Ballad
A simple narrative poem, often incorporating dialogue that is written in quatrains, generally with a rhyme scheme of ABCD.
For GABA, uptake occurs with ____ dependent transporters are located on neuron and ____ cells.
Na+; glial
Metabolism of GABA:
GABA-transaminase after glial uptake

GABA ---> glutamate
_____ Receptors are found in the GABAergic terminal and are ligand-gated ion channel receptor types. They produce inhibitory effects by increasing ____ ions.
GABA-A; Cl-
______ receptors are metabotropic type of receptors using ____ to inhibit AC, decreasing ___ & ___ ions and decreasing cAMP.
GABA-B; Gi; K+;Ca++
The CNS effects of GABA include:
Anxiety
Sedation
Epilepsy
Motor Function

T/F
True.
Increased GABA function decreases locus ______ output and inhibits ______ and hippocampus causing anxiety.
ceruleus; amygdala.
Epilepsy with GABA is caused by Inhibition of neuronal hyperactivity in ____ while Serotonin inhibits colliculi.
foci
In motor function, Caudate/putamen inhibits _____ _____ and Serotonin via GABA.
globus pallidus
Huntington’s Chorea
degeneration of striatal GABA neurons
GABA neurons are all over the brain BUT one of the important pathways are _______ to substantia nigra to ______.
striatum; colliculi
superior colliculi
visual
inferior colliculi
hearing
What is the rate limiting step in Norepinephrine synthesis?
tyrosine hydroxylase

tyrosine -----> DOPA
There are no glial cells helping in norepinephrine pathway. T/F
True
How is norepinephrine synthesized?
tyrosine ----> DOPA ----> Dopamine ----> Norepinephrine

enzymes: tyrosine hydroxylase, AADC, DBH (Dopamine beta Hydroxylase)
For Norepinephrine, uptake occurs with ____ dependent transporters which are located on _____ cells.
Na+; neuronal.

NO GLIAL INVOLVEMENT
Metabolism of Norepinephrine:
neuronal MAO-A (MOST)

glial MAO-B (some)

COMT: leads to inactive metabolite
Alpha-1 receptors are found in the _________ terminal and are _______ receptor types. They are liked to ____ which activates PLC. This increases ____ and DAG.
Noadrenergic; metabotropic; Gq; IP3
Alpha-2 receptors are found in the _________ terminal and are _______ receptor types. They are liked to ____ inhibit adenylyl cyclase. This decreases levels of _____. It is also linked through ____ to inhibit Ca2+ levels. Also increase _______ reflex for blood pressure control.
Noradrenergic; metabotropic; Gi; cAMP; Go; baroreceptor
_____ Receptors are found in the Noradregnergic terminal and are metabotropic receptor types. They produce stimulatory effects with Gs to stimulate _____ and increase cAMP levels.
Beta; Adenylyl Cyclase
Norepinephrine increases _____ in the CNS via the pathway of ____ ____ ____ (RAS) to cortex to the _________.
arousal; Reticular Activating System; hypothalamus.
T/F Alpha 1 receptors in brain stem regulate blood pressure.
False. Alpha 2 receptors
_______ neurotransmitters assist in memory from the RAS to hippocampus & cortex pathway.
Norepinephrine
_______ neurotransmitters assist in pain inhibition from the RAS to descending pathways to spinal cord.
Norepinephrine
______ cell bodies are located in the locus ceruleus.
Norepinephrine
Norepinephrine cell bodies are located in....
locus ceruleus
________ travels from LC to hippocampus, cortex, hypothalamus, cerebellum
Norepinephrine
What is the rate limiting step in Serotonin synthesis?
Rate-limiting step is dietary tryptophan levels
How is serotonin synthesized?
Tryptophan ----> 5-OH-Tryptophan ---> 5HT
Uptake in serotonin happens in the.... by....
neuronal cells by the Na+ dependent channels. NO GLIAL INVOLVEMENT.
How is Serotonin Metabolized?
Neuronal MAO-A (100%)
5HT-1 Receptors are found in the serotonergic terminal and are _______ receptor types. They produce _____ effects by decreasing cAMP and K+ in the cell. It is liked with the protein ____ to inhibit adenylyl cyclase. Pathway used in anti-________ drugs.
metabotropic; inhibitory; Gi; anxiety
__________ receptors deal with anti-depression and anti-psychotic behaviors. They are linked by ____ to activate PLC and produce ______ effects.
5HT-2; Gq; Excitatory
What is the receptor in serotonin that is a ligand-gated ionophore?
5HT-3 receptors.
5HT-3 receptors are ____________ receptor types and produce excitatory effects.
ligand-gated ionophore
5-HT 4, 6, 7 are _____________ receptor types and use ____ to increase cAMP.
metabotropic; Gs
In terms of sensory, less serotonin will cause an _________ of the senses.
arousal
Serotonin neurons that travel from the RAS to the cortex & hypothalamus deal with:
Sleep & Arousal
Serotonin receptors that deal with migraine are....
5HT1D receptors on cranial blood vessels
Serotonin receptors that deal with emesis are....
5HT3 receptors in area postrema
Serotonin neurons that travel from the RAS to the cortex & thalamus deal with:
Inhibit Sensory Transmission
Serotonin neurons that travel from the RAS to the lamina II spinal cord deal with:
Pain Inhibition
What is the rate limiting step in Dopamine synthesis?
Tyrosine Hydroxylase

Tyrosine ----> DOPA
For Dopamine... uptake on neurons? glia? or both?
ONLY NEURONS
Metabolism for Dopamine?
Neuronal MAO-A,
glial MAO-B
extracellular COMT
D1-like receptors are on the ________ terminal and are _________ types of receptors and produce ________ effects although it increases cAMP via a ____ protein
dopaminergic; metabotropic; inhibitory; Gs
________ receptors are on the dopaminergic terminal and are metabotropic receptors that produce inhibitory effects with ____ protein which decreases cAMP production. They are also linked with ____ to inhibit Ca2+ channels
D2-like; Gi; Go
VTA to nucleus accumbens & frontal cortex describes the pathway of ____________ (NT)
dopamine. this pathway deals w euphoria & addiction.
In dopaminergic pathways, _____ to _____ deals with the motor system that affects parkinson's disease & Huntington's chorea.
substantia nigra; striatum
hypokinesia is.... and is in what disease?
too little dopamine; Parkinson's
excess dopamine causes involuntary movements in this disease....
Huntington's chorea
Schitzophrenia is caused by an imbalance in these 3 receptor subtypes... it inhibits the release of...
D2, D3, and D4 ; prolactin
_____ receptors can cause Emesis in the area prostrema in the dopaminergic pathway.
D2
What pathway do these three relate to?
Substantia nigra to caudate/putamen

Ventral tegmental area to nucleus accumbens

Hypothalamus to pituitary gland (via prolactin release)
Dopaminergic
In the reward pathway....

Dopamine inhibits _______ meanwhile GABA inhibits ______ and movement.
GABA; DA
Too little DA, too much ACh, too much GABA
hypokinesia, rigidity, tremor (Parkinson’s Disease)
Too much DA, too little ACh, too little GABA
hyperkinesias, chorea (involuntary movements)
What is the rate limiting step in Acetylcholine synthesis?
choline uptake
Uptake in Acetylcholine -
Na-dependent neuronal transporter specific for choline
Metabolism of ACh:
Extracellular acetylcholinesterase
___ and ___ receptors in the cholinergic terminal are metabotropic and increase DAG & IP3 with _____ protein to produce an excitatory effect.
M1; M3; Gq
M2 & M4 receptors in the cholinergic terminal are _________ types of receptors that decrease cAMP and K+ with ____ protein to produce an inhibitory effect.
metabotropic; Gi
Nicotinic receptors at the cholinergic terminal increase ___, decrease ___ and increase ___. They produce excitatory effects.
Na+; K+; Ca2+
The two major pathways for ACh in the brain are ______ _____ to frontal, parietal and thalamus

AND

____ ____ to hippocampus
basal nucleus; septal nucleus
Endogenous Opioid Peptides Synthesis:
1. mRNA translated into precursor proteins
2. Precursor proteins transported and stored in vesicles
3. Precursor proteins enzymatically cleaved into products
Rate Limiting step in Endogenous Opiod Peptide Synthesis?
Rate-limiting step: DNA transcription?
What is the type of uptake used in Opioid Peptide Synthesis?
NO UPTAKE!

(hah i tricked youu)
Endogenous Opioid Peptides Metabolism?
extracellular peptidases
____ receptors are in the opioid pathway and are linked through ____ & ___ to inhibit AC and Ca2+ channels. They are endorphins ___________. Produce inhibitory effects.
Mu/Delta; Gi; Go; enkephalins
____ receptors are in the opioid pathway and are linked through ____ & ___ to inhibit AC and Ca2+ channels. They are dynorphin. Produce inhibitory effects.
Kappa; Gi; Go
Proopiomelanocortin --> ___-endorphin
______ nucleus to:
o _________ (Stress)
o Preiaqueductal grey, raphe (pain)
o Nucleus tractus solitaries (autonomic reflexes)
o Striatum (motor rigidity)
o Nucleus _______ (euphoria, addiction)
B; Acurate; Hypothalamus; accumbens;
_________ --> met-enkephalin, leu-enkephalin
Interneurons in:
o Hypothalamus (endocrine)
o _________ grey, substantia gelatinosa (pain)
o Nucleus tractus solitaries (Autonomic reflexes)
o ______ (motor rigidity)
o Nucleus accumbens (euphoria, addiction)
o Cortex, hippocampus, limbic system (emotions)
proenkephalin; Periaqueductal; striatum;
Prodynorphin --> dynorphin __ and __
Interneurons in
o Hypothalamus (endocrine)
o ____ spinal cord (pain)
o Striatum, substantia nigra (motor rigidity)
o Nucleus accumbens (dysphoria)
o Limbic system (emotions)
A & B; ventral;
Other peptide relased from dorsal root ganglion
Substance P
Other peptides that deal with the feeding metabolism:
Neuropeptide Y
CCK
VIP
Leptin
Other peptide that acts as a growth hormone & nerve growth factors
BDNF
Primary visual processing area
Occipital cortex
Primary motor processing area
Frontal cortex
Primary sensory (tactile) processing area
Temporal cortex
Primary auditory processing area
Parietal cortex
Stimulates caudate nucleus
Frontal cortex
The “brakes” of the basal ganglia
Putamen
Endocrine center
Hypothalamus
Basal ganglia afferent region
Putamen
Basal ganglia efferent region
Globus Pallidus
Executive function
Frontal cortex
Stimulatory center of the reticular activating system
Locus ceruleus
Inhibitory center of the reticular activating system
Raphe nuclei
Inhibits caudate nuclei
Substantia nigra
Overactivity is implicated in Huntington’s chorea
Dopamine
Overactivity is implicated in drug addiction.
Dopamine
Overactivity is implicated in epilepsy
Glutamate
Underactivity is implicated in epilepsy
GABA
Cell bodies project from ventral tegmental area to nucleus accumbens
Dopamine
Cell bodies project from locus ceruleus to cortex
Norepinephrine
Cell bodies project from raphe nucleus to spinal cord
Serotonin
Cell bodies project from arcuate nucleus to periaqueductal gray
Beta-endorphin
Cell bodies project from cortex to caudate and putamen
Glutamate
Small interneurons are present in the dorsal spinal cord.
Met-enkephalin
Small interneurons are present in the ventral spinal cord.
Dynorphin
Cell bodies project from caudate nucleus to substantia nigra.
GABA
Cell bodies project from septum to hippocampus
Acetylcholine
The rate-limiting step for its synthesis is a Na-dependent transporter
Acetylcholine
The rate-limiting step for its synthesis is the dietary levels of the precursor
Serotonin
Shares almost the same synthetic pathway as glutamate
GABA
Shares almost the same synthetic pathway as dopamine
Norepinephrine
44. Which of the following are true about acetylcholine (ACh)?
a. there is a loss of ACh neurons in the brain of patients with Alzheimer's disease.
b. nicotinic ACh receptors generally cause excitation of postsynaptic cells.
c. short acetylcholine neurons are localized in the striatum and are thought to be the cause of resting tremor in Parkinson’s Disease.
d. cholinergic neurons project from the basal nucleus throughout the cortex.
e. all of the above are true.
e. all of the above are true.
43. Which of the following are true about NMDA-selective glutamate receptors?
a. agents that activate these receptors may increase memory formation and make you smarter.
b. chronic activation of these receptors could cause loss of neurons due to excitotoxicity.
c. activation of these receptors may make you have a seizure.
d. drugs that block these receptors may be useful therapeutic agents for decreasing brain damage in stroke patients.
e. all of the above.
e. all of the above are true.
41. Which of the following are true about agents that increase dopamine D2-like receptor activities?
a. they would worsen the symptoms of Parkinson's disease.
b. they are useful as antiemetic agents.
c. chronic treatment with them could cause male breast development and lactation.
d. they might worsen the symptoms of schizophrenia.
e. all of the above.
d. they might worsen the symptoms of schizophrenia.
40. If intact working norepinephrine pathways in the brain are necessary for transmitting "good mood" thoughts, then which of the following actions of a new drug called
“Ai-ight” would cause an increase in mood?
a. inhibiting dopamine beta hydroxylase activity.
b. increasing norepinephrine transporter activity.
c. increasing the number of presynaptic alpha 2 receptors.
d. increasing the number of postsynaptic beta receptors.
e. all of the above.
d. increasing the number of postsynaptic beta receptors.
39. Which of the following are true about GABA?
a. there is a selective loss of GABA neurons in the striatum of patients with Huntington’s chorea.
b. It is thought that GABA agonists help relieve the symptoms of anxiety because GABA inhibits both locus ceruleus and amygdala activity.
c. GABA receptors always inhibit action potentials of postsynaptic cells regardless of which receptor subtype is involved.
d. GABA-B receptors can form heterodimers which can activate different G-protein coupled second messenger systems.
e. all of the above.
e. all of the above.
38. Endogenous opioid peptides generally have inhibitory cellular effects because they can:
a. inhibit potassium conductance during an action potential thereby inhibiting release of neurotransmitter.
b. increase calcium ion concentrations intracellularly thereby causing hyperpolarization.
c. inhibit cyclic AMP formation via an interaction with Gi.
d. increase sodium ion concentrations extracellularly by opening sodium channels.
e. all of the above.
c. inhibit cyclic AMP formation via an interaction with Gi.
37. Which of the following receptor subtypes does NOT act as an autoreceptor?
a. 5-HT1D
b. D1 dopamine
c. Alpha-2
d. M2 muscarinic
e. GABA-B
b. D1 dopamine
36. High affinity reuptake pumps are:
a. calcium dependent.
b. sodium dependent.
c. temperature dependent.
d. voltage dependent.
e. both b and d are true.
b. sodium dependent.
35. The spinothalamic tract:
a. is a sensory pathway that carries fine sensations for the hands and face.
b. is a sensory pathway that carries pain and temperature sensations for the body.
c. contains both sensory and motor fibers.
d. can be inhibited by descending adrenergic and serotonergic projections.
e. both b and d are true.
e. both b and d are true.
What is responsible for the Blood Brain Barrier? (Cellularly)
The tight junctions of overlapping capillary endothelial cells are responsible for the BBB
CNS-Vascular endothelial Composition:
Have little transcytotic activity- lack both fluid-phase and receptor-mediated _______.
endocytosis
CNS-Vascular endothelial Composition:
Contain specific ______ for glucose (nutrients), amino acids, vitamins, metals, nucleosides
transporters
CNS-Vascular endothelial Composition:
______ enzymes – neurotransmitters and peptidases
catabolic
Non ______ soluble substances cross the BBB with transporters.
lipid.
_______ transports glucose down its concentration gradient in the BBB.
GLUT 1
All 3 _____ _____ carriers in the BBB are Na+ dependent. Only ____ and ____ systems require energy and transport glycine, alanine and serine AND alanine, serine and cysteine (RESPECTIVELY). The ___ system on the other hand transports large neutral AA with branched or ringed side chains (leucine and valine).
Amino Acid; A and ASC; L
_______ is the precursor for dopamine and is used to treat parkinson's.
L-DOPA
MDR Protects brain from circulating neurotoxins
Multiple Drug Resistant
2-aminobicycloheptane-2-carboxylic acid (BCH) is a Experimental inhibitor of which transporter?
L-System
Alpha-methylaminoisobutyric acid (MeAIB) is a Experimental inhibitor of which transporter?
A-System
4 Things that disrupt BBB:
1. Tumors
2. Hypertension
3. Ischemic Events (Stroke)
4. Head Injury
Circumventricular organs are.... (definition)

1. Media _______ – hormone/ANS regulation
2. Organum _______ of the lamina terminalis – BP
3. _______ organ – water balance/ BP
4. Sub ______ organ – BP
5. Area ______ – vomiting
areas in CNS that lack BBB

eminence; vasculosum; subfornical; commissural; postrema
The lining of the ventricles and central canal of the spinal cord is called _______.
ependymal
The ependymal lining has special cells called ______ which form tight junctions that prevent the entry of molecules from the blood supply of the _______ organs from entering the CSF.
tanycytes; circumventricular
_______ ____ functions as a one-way valve and blood/CSF barrier.
Arachnoid villi
The _______ are fluid-filled spaces in the brain where the CSF is produced and circulates
ventricles
______ are connective tissue sheaths that are comprised of three membraneous layers: _____ mater (collagenous connective tissue) which contains venous sinuses, _____ mater (Collagenous and elastic fibers) avascular, and the ____ mater (Connective tissue-collagenous and elastic fibers) which is the external layer with tiny blood vessels. They function to pad & protect the brain.
Meninges; Dura; Arachnoid; Pia
The function of the CSF is to do three main things:
1. provide nutrients
2. cushion
3. removal of wastes
What produces CSF?
choroid plexus.
what is the choroid plexus?
choroid plexus-specialized highly vascularized epithelial structures found on the inner lining of all brain cerebral ventricles
How is CSF absorbed?
It is pressure dependent and if the pressure decreases (80-150), absorption stops.

Arachnoid Villi

Dura venous sinuses
meningitis
Inflammation of the meningeal layers
What two layers of the meninges are most often affected in meningitis?
arachnoid & pia
_____ meningitis increases lymphocytes, sugar and protein in CSF. prognosis is generally _______.
Viral; good
_____ meningitis has three major invaders: Haemophilus influenza, Streptococcus pneumonia, Neisseria meningitides. prognosis is generally _______.
bacterial; bad
The most infectious form of bacterial meningitis is...
Neisseria meningitides - meningococcal meningitis
symptoms of meningitis:
Headache
Neck stiffness
Fever
Nausea/vomiting
Photophobia
Lethargy
pneumococcal meningitis
Streptococcus pneumonia
water in the brain
Hydrocephalus
Hydrocephalus can be caused by decreased CSF absorption via the clogging of the _______ ___. It can also be caused by a tumor in the _____ _____ which causes overproduction of CSF. Brain tumors and obstruction of the _____ can cause this by blocking flow of CSF.
arachnoid villi; choroid plexus; ventricles