Revised Midterm Review
1. Structure and function of the cellular components (p.28-37)
a.
A. Nucleus: The nucleus contains the genomic DNA, which contain nuclear genes that
code for the synthesis of proteins.
b. Cytoplasmic organelles:
B. Plasma membranes: protects internal cell contents from the external environment,
transports nutrients and waste products, generates membrane potentials, and provides cell
recognition, communication, and growth regulation.
2. Cellular receptors: binding receptors for hormones and neurotransmitters to
relay information.
a. Nucleolus: contains genetic info (DNA) of the cell inside the nucleus (sm ball),
assembles ribosomes, rRNA synthesis, and formation of spindles.
a. Mitochondria: powerhouse of the cell that creates the ATP/Krebs cycle
b. Ribosomes: there are smooth and rough ER. Rough ER has ribosomes;
this is where protein synthesis takes place.
c. Lysosomes: membrane-bound bags of digestive enzymes that degrade
intracellular debris. The “cleaners” of the cell.
d. Lipid bilayer: two lipid layers, outside is HYDROPHILIC water soluble,
and between the layers is hydrophobic, non-water soluble.
3. In regards to cells, what is the function of proteins? They are carrying out a
vast array of tasks that are essential for life, including the structure, function, and
regulation of tissues and organs, as well as acting as enzymes, structural
components, and transporters, messengers, and antibodies among other roles.
4. Gap junctions: specialized structures that directly connect the cytoplasm of
adjacent cells, allowing for the exchange of ions, sm molecules, and electrical
signals. They act as channels between cells, facilitating communication dn
coordination of cellular activity.
5. CELLULAR CHANGES/ADAPTATION (p.66)
a. Atrophy: cells shrink and reduce their differentiated fxn in response to a variety
of normal and injurious factors (disuse, denervation, ischemia, nutrient starvation,
interruption of endocrine signals, persistent cell injury). SMALL CELLS
, b. Hypertrophy: increased in cell mass accompanied by an augmented functional
capacity (response to increased physiologic or pathophysiologic demands) caused
by increased demand or hormones. BIGGER SIZE
i. PHYSIOLOGICAL: muscle (workout)
ii. PATHOPHYSIOLOGICAL: hypertrophy-HEART
c. Hyperplasia: caused by an increased rate of cellular division. Causes: increased
physiological demands or hormonal stimulation, persistent cell injury, MORE
CELLS
i. PHYSIOLOGICAL: menses/uterine lining.BPH. Allows organs to
REGENERATE. Hormonal: replaces lost tissue or supports new growth.
ii. PATHOLOGICAL: TUMOR
d. Metaplasia: the reversible replacement of one mature cell by another less mature
cell type. Causes: adaptation to persistent injury, replacing a cell type better suited
to tolerate injurious stimulation. **FULLY REVERSIBLE when injurious
stimulation is removed. It’s a reprogramming of stem cells.
i. Ex: replacement of columnar ciliated epithelial cells by stratified
squamous epithelial cells. **SKIN CELLS** scrape off and replaced-
epithelial cells.
e. Dysplasia: refers to abnormal changes in the size, shape, and organization of
mature cells and can be called atypical hyperplasia. Cause: adaptive effort gone
astray. Deranged cellular growth is not an accurate cellular adaptation but rather
an atypical hyperplasia. Significant potential to transform into cancerous cells
(preneoplastic lesions), NON-REVERSIBLE, PRECANCEROUS.
f. Anaplasia: a condition where cells lose their normal characteristics and become
primitive or undifferentiated. They lose their normal arrangement and structure,
divide rapidly and abnormally, has variations in size, shape and appearance.
CONSIDERED HALLMARK FOR CANCER AND POOR PROGNOSIS.
g.
6. DNA replication:
i. Bases: nucleotide bases that are further divided in 2 groups: pyrimidines:
C/T, and purine: A/T. They are attached to a repeating sugar-phosphate
chain in which they are specific and complimentary, called
complementary bases. A and T go together, and G and C go together.
a. Apple in the Tree and Car in the Garage
, b.
c. HELICASE UNZIPS the two strands of DNA. It breaks the hydrogen bond
bases that hold the DNA bases together; it usually starts at the origin of the DNA
chosen by the initiator protein and it allows HELICASE to star the replication
origin.
i. Single -Stranded Binding Proteins (SSB proteins) bind to the proteins
that are separated to prevent the bases from binding together again.
ii. Topoisomerase: keeps the DNA from super coiling, needs to be
controlled during replication.
d. PRIMASE: the INITIALIZER, makes the primer (made of RNA) so that the
DNA polymerase can figure out where to go to start to work.
e. POLYMORAZE: the BUILDER, this enzyme replicates DNA molecules to
actually build new strand of DNA. However, it can't build anything without a
primer to build new DNA…however It is UNDER A LOT OF PRESSURE; it has
to double-check its work, or it can have the wrong protein or no protein in the
DNA, making it a big mistake.
i. Mutation: any inherited alteration of genetic material
ii. Frameshift mutation: involves the insertion or deletion of one or more
base pairs to the DNA molecule
iii. Mutagens are agents, such as radiation and chemicals, that increase the
frequency of mutations.
f. Replication goes one direction, from 3’ to 5’, because of the antiparallel DNA
replication is ASYMMETRIC
i. Leading strand: is replicated as a continuous polymer
ii. Lagging strand (the one that is being used as the copy) must be
synthesized in short sections in a “backstitching” process.
iii. Okazaki fragments: the backstitching fragments of DNA
g. LIGASE: The GLUER helps glue the OKASAKI fragments together where the
polymerase is on the lagging strand to bridge the gaps.
h. Semi-conservative: the new strand with an old strand of DNA being done
7. RNA vs DNA
a. RNA Sugar molecule is ribose (not deoxyribose=DNA).
b. Uracil replaces Thymine (both can form base pairs with adenine).
c. RNA forms stable single-stranded molecules (DNA double-stranded).
8. Cell growth and proliferation: p.56
a. Must be balanced between birth rate and cell death rate. Two essential strategies
of cell cycle control:
, i. First, a variety of protein mitogens and GFs are required in specific
combinations for the growth and proliferation of particular cell types.
ii. Second, cells respond to spatial signals from the extracellular matrix and
neighboring cells that indicate the available space.
iii. Dormant cells can remain in G1phase indefinitely (called G0). Cycling
cells proceed through G1,S phase (synthesis), G2, M phase (mitosis), and
cell division. S phase is characterized by the duplication of DNA and the
synthesis of intracellular components in preparation for cell division. M
phase, or mitosis, proceeds through six stages, beginning with prophase, in
which the process of cell replication occurs.
iv.
Pro: CONDENSE
Meta: meet in the middle
Ana: away
Telo: so far away youuse a
telephone about tho move
aaway
v.
9. Action potential:CH. 43-46/p.49
a. Action Potential:
i. Stage 1: resting potential (-70mv more negative on the inside of neurons
than outside the neurons)
1. Structure and function of the cellular components (p.28-37)
a.
A. Nucleus: The nucleus contains the genomic DNA, which contain nuclear genes that
code for the synthesis of proteins.
b. Cytoplasmic organelles:
B. Plasma membranes: protects internal cell contents from the external environment,
transports nutrients and waste products, generates membrane potentials, and provides cell
recognition, communication, and growth regulation.
2. Cellular receptors: binding receptors for hormones and neurotransmitters to
relay information.
a. Nucleolus: contains genetic info (DNA) of the cell inside the nucleus (sm ball),
assembles ribosomes, rRNA synthesis, and formation of spindles.
a. Mitochondria: powerhouse of the cell that creates the ATP/Krebs cycle
b. Ribosomes: there are smooth and rough ER. Rough ER has ribosomes;
this is where protein synthesis takes place.
c. Lysosomes: membrane-bound bags of digestive enzymes that degrade
intracellular debris. The “cleaners” of the cell.
d. Lipid bilayer: two lipid layers, outside is HYDROPHILIC water soluble,
and between the layers is hydrophobic, non-water soluble.
3. In regards to cells, what is the function of proteins? They are carrying out a
vast array of tasks that are essential for life, including the structure, function, and
regulation of tissues and organs, as well as acting as enzymes, structural
components, and transporters, messengers, and antibodies among other roles.
4. Gap junctions: specialized structures that directly connect the cytoplasm of
adjacent cells, allowing for the exchange of ions, sm molecules, and electrical
signals. They act as channels between cells, facilitating communication dn
coordination of cellular activity.
5. CELLULAR CHANGES/ADAPTATION (p.66)
a. Atrophy: cells shrink and reduce their differentiated fxn in response to a variety
of normal and injurious factors (disuse, denervation, ischemia, nutrient starvation,
interruption of endocrine signals, persistent cell injury). SMALL CELLS
, b. Hypertrophy: increased in cell mass accompanied by an augmented functional
capacity (response to increased physiologic or pathophysiologic demands) caused
by increased demand or hormones. BIGGER SIZE
i. PHYSIOLOGICAL: muscle (workout)
ii. PATHOPHYSIOLOGICAL: hypertrophy-HEART
c. Hyperplasia: caused by an increased rate of cellular division. Causes: increased
physiological demands or hormonal stimulation, persistent cell injury, MORE
CELLS
i. PHYSIOLOGICAL: menses/uterine lining.BPH. Allows organs to
REGENERATE. Hormonal: replaces lost tissue or supports new growth.
ii. PATHOLOGICAL: TUMOR
d. Metaplasia: the reversible replacement of one mature cell by another less mature
cell type. Causes: adaptation to persistent injury, replacing a cell type better suited
to tolerate injurious stimulation. **FULLY REVERSIBLE when injurious
stimulation is removed. It’s a reprogramming of stem cells.
i. Ex: replacement of columnar ciliated epithelial cells by stratified
squamous epithelial cells. **SKIN CELLS** scrape off and replaced-
epithelial cells.
e. Dysplasia: refers to abnormal changes in the size, shape, and organization of
mature cells and can be called atypical hyperplasia. Cause: adaptive effort gone
astray. Deranged cellular growth is not an accurate cellular adaptation but rather
an atypical hyperplasia. Significant potential to transform into cancerous cells
(preneoplastic lesions), NON-REVERSIBLE, PRECANCEROUS.
f. Anaplasia: a condition where cells lose their normal characteristics and become
primitive or undifferentiated. They lose their normal arrangement and structure,
divide rapidly and abnormally, has variations in size, shape and appearance.
CONSIDERED HALLMARK FOR CANCER AND POOR PROGNOSIS.
g.
6. DNA replication:
i. Bases: nucleotide bases that are further divided in 2 groups: pyrimidines:
C/T, and purine: A/T. They are attached to a repeating sugar-phosphate
chain in which they are specific and complimentary, called
complementary bases. A and T go together, and G and C go together.
a. Apple in the Tree and Car in the Garage
, b.
c. HELICASE UNZIPS the two strands of DNA. It breaks the hydrogen bond
bases that hold the DNA bases together; it usually starts at the origin of the DNA
chosen by the initiator protein and it allows HELICASE to star the replication
origin.
i. Single -Stranded Binding Proteins (SSB proteins) bind to the proteins
that are separated to prevent the bases from binding together again.
ii. Topoisomerase: keeps the DNA from super coiling, needs to be
controlled during replication.
d. PRIMASE: the INITIALIZER, makes the primer (made of RNA) so that the
DNA polymerase can figure out where to go to start to work.
e. POLYMORAZE: the BUILDER, this enzyme replicates DNA molecules to
actually build new strand of DNA. However, it can't build anything without a
primer to build new DNA…however It is UNDER A LOT OF PRESSURE; it has
to double-check its work, or it can have the wrong protein or no protein in the
DNA, making it a big mistake.
i. Mutation: any inherited alteration of genetic material
ii. Frameshift mutation: involves the insertion or deletion of one or more
base pairs to the DNA molecule
iii. Mutagens are agents, such as radiation and chemicals, that increase the
frequency of mutations.
f. Replication goes one direction, from 3’ to 5’, because of the antiparallel DNA
replication is ASYMMETRIC
i. Leading strand: is replicated as a continuous polymer
ii. Lagging strand (the one that is being used as the copy) must be
synthesized in short sections in a “backstitching” process.
iii. Okazaki fragments: the backstitching fragments of DNA
g. LIGASE: The GLUER helps glue the OKASAKI fragments together where the
polymerase is on the lagging strand to bridge the gaps.
h. Semi-conservative: the new strand with an old strand of DNA being done
7. RNA vs DNA
a. RNA Sugar molecule is ribose (not deoxyribose=DNA).
b. Uracil replaces Thymine (both can form base pairs with adenine).
c. RNA forms stable single-stranded molecules (DNA double-stranded).
8. Cell growth and proliferation: p.56
a. Must be balanced between birth rate and cell death rate. Two essential strategies
of cell cycle control:
, i. First, a variety of protein mitogens and GFs are required in specific
combinations for the growth and proliferation of particular cell types.
ii. Second, cells respond to spatial signals from the extracellular matrix and
neighboring cells that indicate the available space.
iii. Dormant cells can remain in G1phase indefinitely (called G0). Cycling
cells proceed through G1,S phase (synthesis), G2, M phase (mitosis), and
cell division. S phase is characterized by the duplication of DNA and the
synthesis of intracellular components in preparation for cell division. M
phase, or mitosis, proceeds through six stages, beginning with prophase, in
which the process of cell replication occurs.
iv.
Pro: CONDENSE
Meta: meet in the middle
Ana: away
Telo: so far away youuse a
telephone about tho move
aaway
v.
9. Action potential:CH. 43-46/p.49
a. Action Potential:
i. Stage 1: resting potential (-70mv more negative on the inside of neurons
than outside the neurons)
