Intro to Pathology Flashcards
Understand basic pathological processes.
1
Q
What is cell adaptation?
A
The ability of cells to respond to various types of stimuli and adverse environmental changes.
2
Q
What are the four main types of cellular adaptations?
A
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
3
Q
Define hypertrophy and give an example.
A
An increase in the size of individual cells. Example: enlargement of skeletal muscle cells due to exercise.
4
Q
Define hyperplasia and give an example.
A
An increase in the number of cells. Example: increase in the number of epithelial breast cells during pregnancy.
5
Q
Define atrophy and give an example.
A
A reduction in cell size and number. Example: muscle atrophy due to disuse.
6
Q
Define metaplasia and give an example.
A
Transformation from one type of epithelium to another. Example: Barrett’s esophagus due to chronic gastric acid exposure.
7
Q
What are the two main types of cell injury?
A
- Reversible cell injury
- Irreversible cell injury
8
Q
What characterizes reversible cell injury?
A
The cell can recover if the damaging stimulus is removed.
9
Q
What characterizes irreversible cell injury?
A
The cell cannot recover and will die.
10
Q
List some causes of cell injury.
A
- Hypoxia (oxygen deprivation)
- Physical agents (trauma, temperature extremes, radiation)
- Chemical agents (toxins, drugs)
- Infectious agents (viruses, bacteria, fungi)
- Immunologic reactions
- Genetic factors
- Nutritional imbalances (deficiencies or excesses)
- Aging
11
Q
What are the features of reversible cell injury?
A
- Cellular swelling due to failure of the sodium-potassium pump
- Accumulation of fatty acids in the cytoplasm
- Cellular functions are altered but can be restored
12
Q
What are the features of irreversible cell injury?
A
- Severe mitochondrial damage
- Inability to synthesize ATP
- Massive influx of calcium into the cell
- Activation of enzymes that break down cell components
- Rupture of cellular membranes
13
Q
What marks the transition from reversible to irreversible injury?
A
The inability to reverse mitochondrial dysfunction and extreme disturbances in membrane function.
14
Q
List the cellular features of reversible injury.
A
- Cellular swelling (cloudy swelling)
- Fatty change
- Plasma membrane blebbing
- Mitochondrial swelling
- Myelin figure formation
15
Q
List the cellular features of irreversible injury.
A
- Severe mitochondrial damage
- Extensive damage to plasma membrane
- Nuclear changes (pyknosis, karyorrhexis, karyolysis)
- Cytoplasmic blebs rupture
- Lysosomes rupture and release hydrolytic enzymes
16
Q
True or False: In reversible injury, the basic cell structure remains intact.
A
True
17
Q
What happens to cellular organelles and membranes in irreversible injury?
A
There is a breakdown leading to cell death.
18
Q
What is necrosis?
A
A form of cell death characterized by cellular swelling, breakdown of organelles, and rupture of cell membranes.
19
Q
What is coagulative necrosis?
A
Most common type of necrosis caused by ischemia, preserving the tissue architecture.
20
Q
What characterizes liquefactive necrosis?
A
Occurs in infections or in the brain, where enzymes digest dead cells resulting in a liquid mass.
21
Q
What is caseous necrosis associated with?
A
Seen in tuberculosis, combining coagulative and liquefactive necrosis for a cheese-like appearance.
22
Q
What causes fat necrosis?
A
Occurs in pancreatic damage or trauma to fatty tissues.
23
Q
What is fibrinoid necrosis?
A
Seen in immune-mediated vascular damage.
24
Q
What is gangrenous necrosis?
A
Occurs in extremities due to loss of blood supply.
25
Describe the morphological features of coagulative necrosis.
Cells retain their outline but appear homogeneous and eosinophilic; includes nuclear changes like pyknosis, karyorrhexis, and karyolysis.
26
What does liquefactive necrosis appear like?
A viscous liquid mass with completely destroyed cell structures, often containing neutrophils and debris.
27
How does caseous necrosis appear macroscopically?
As a white, soft, cheese-like material.
28
What are the characteristics of fat necrosis?
Shadowy outlines of fat cells and calcium soap formation.
29
What does fibrinoid necrosis show?
Eosinophilic fibrin-like material in vessel walls.
30
What are the two types of gangrenous necrosis?
* Dry gangrene
* Wet gangrene
31
What is apoptosis?
A programmed cell death process characterized by activation of caspase enzymes and formation of apoptotic bodies.
32
What are the main pathways of apoptosis?
* Extrinsic pathway
* Intrinsic pathway
33
What triggers the extrinsic pathway of apoptosis?
External signals binding to death receptors on the cell surface.
34
What initiates the intrinsic pathway of apoptosis?
Internal cellular stress leading to mitochondrial release of cytochrome c.
35
What are examples of physiologic apoptosis?
* Embryonic development (e.g., formation of digits)
* Hormone-dependent involution
* Cell turnover in continuously renewing tissues
* Immune system regulation
36
What are examples of pathologic apoptosis?
* Viral infections (e.g., HIV-induced T cell depletion)
* Neurodegenerative diseases (e.g., Alzheimer's, Parkinson's)
* Ischemic injury (e.g., myocardial infarction)
* Toxic insults (e.g., radiation-induced cell death)
* Cancer (e.g., tumor cell death induced by chemotherapy)
37
What are the causes of inflammation?
* Microbial infections
* Physical trauma
* Chemical agents
* Tissue necrosis
* Foreign bodies
* Immune reactions
## Footnote
These causes can trigger the inflammatory response in the body.
38
List the cardinal signs of inflammation.
* Rubor (redness)
* Calor (heat)
* Tumor (swelling)
* Dolor (pain)
* Functio laesa (loss of function)
## Footnote
These signs are used to identify inflammation in affected tissues.
39
What is vasodilation in the context of inflammation?
Increased blood flow to the affected area
## Footnote
Vasodilation is one of the key vascular events that occur during inflammation.
40
What does increased vascular permeability allow during inflammation?
Allows plasma proteins and fluid to enter tissues
## Footnote
This process is crucial for the inflammatory response as it helps deliver necessary components to the site of injury.
41
What is margination in the cellular events of inflammation?
Leukocytes line up along vessel walls
## Footnote
This is an important step that facilitates the movement of leukocytes to the site of injury.
42
Describe the process of chemotaxis.
Directed movement of leukocytes towards the site of injury
## Footnote
Chemotaxis is essential for the effective response of the immune system.
43
What are the mediators of inflammation?
* Vasoactive amines (e.g., histamine)
* Plasma proteins (e.g., complement, kinins)
* Lipid mediators (e.g., prostaglandins, leukotrienes)
* Cytokines (e.g., TNF-α, IL-1)
* Chemokines
* Nitric oxide
## Footnote
These mediators play various roles in regulating the inflammatory response.
44
What are the possible outcomes of acute inflammation?
* Resolution
* Fibrosis
* Abscess formation
* Chronic inflammation
## Footnote
These outcomes determine the long-term effects of the inflammatory response on tissue health.
45
What are the morphological features of acute inflammation?
* Vascular changes (vasodilation, increased blood flow, vascular congestion)
* Edema (accumulation of fluid in extracellular spaces)
* Cellular infiltrate (predominance of neutrophils)
* Fibrin deposition (formation of fibrin networks)
* Tissue necrosis (localized tissue destruction)
## Footnote
These features help in diagnosing and understanding the severity of inflammation.
46
What is serous inflammation?
Protein-rich fluid exudate
## Footnote
This type of inflammation is characterized by the presence of a clear, yellowish fluid.
47
What characterizes fibrinous inflammation?
Exudate rich in fibrin
## Footnote
Fibrinous inflammation indicates a more severe inflammatory response and is associated with tissue damage.
48
True or False: Suppurative inflammation is characterized by the formation of pus.
True
## Footnote
This type of inflammation often occurs in bacterial infections.
49
Fill in the blank: In severe cases of acute inflammation, localized tissue destruction is referred to as _______.
[tissue necrosis]
## Footnote
Tissue necrosis can complicate the inflammatory process and lead to further health issues.
50
What are the main causes of chronic inflammation?
Persistent infection, prolonged exposure to toxic agents, autoimmune reactions, recurrent acute inflammation
51
List the morphological features of chronic inflammation.
* Cellular infiltrate: Predominance of mononuclear cells
* Tissue destruction: Ongoing damage due to inflammatory mediators
* Repair: Attempts at healing through fibrosis and angiogenesis
* Granulation tissue formation: New blood vessels and fibroblasts
* Fibrosis: Excessive collagen deposition leading to scarring
52
What characterizes granulomatous inflammation?
* Formation of granulomas: Focal collections of activated macrophages
* Epithelioid cells: Modified macrophages with abundant pink cytoplasm
* Multinucleated giant cells: Fusion of epithelioid cells
* Lymphocyte cuff: Surrounding the granuloma
* Central necrosis: In some cases (e.g., tuberculosis)
* Fibrosis: Surrounding the granuloma in later stages
53
What are the types of granulomas?
* Foreign body granulomas
* Immune granulomas (e.g., tuberculosis, sarcoidosis)
54
Enumerate the complications of wound healing.
* Excessive scarring or keloid formation
* Wound dehiscence (separation of wound edges)
* Infection
* Chronic non-healing wounds
55
What local factors affect wound healing?
* Infection
* Poor blood supply
* Foreign bodies
* Mechanical stress
56
What systemic factors affect wound healing?
* Age
* Nutrition
* Diabetes
* Medications (e.g., steroids)
* Smoking
* Obesity
* Stress
57
What are the stages of wound healing?
* Hemostasis (immediate)
* Inflammatory phase (1-4 days)
* Proliferative phase (4-21 days)
* Remodeling phase (21 days to 1 year)
58
What occurs during the hemostasis stage of wound healing?
* Vasoconstriction
* Platelet aggregation
* Fibrin clot formation
59
What happens during the inflammatory phase of wound healing?
* Neutrophil and macrophage infiltration
* Removal of debris and bacteria
60
What processes occur during the proliferative phase of wound healing?
* Angiogenesis
* Fibroblast proliferation
* Collagen synthesis
* Granulation tissue formation
* Re-epithelialization
61
What occurs during the remodeling phase of wound healing?
* Collagen reorganization
* Scar maturation
* Gradual regain of tissue strength
62
What is a neoplasm?
An abnormal mass of tissue resulting from uncontrolled, excessive growth of cells that persists even after the initial stimulus is removed.
63
Classify neoplasms by behavior.
* Benign
* Malignant (cancer)
* Potentially malignant (in situ)
64
Classify neoplasms by tissue of origin.
* Epithelial (carcinomas)
* Mesenchymal (sarcomas)
* Hematopoietic and lymphoid
* Germ cell tumors
* Nervous system tumors
65
List the features of benign neoplasms.
* Slow growth rate
* Well-circumscribed and often encapsulated
* Resemblance to tissue of origin (well-differentiated)
* Lack of invasion into surrounding tissues
* No metastasis
* Limited effect on host (unless in a critical location)
* Generally good prognosis
* Often can be surgically removed with low risk of recurrence
66
List the features of malignant neoplasms.
* Rapid, uncontrolled growth
* Poorly circumscribed and invasive
* Loss of differentiation (anaplasia)
* Invasion of surrounding tissues
* Ability to metastasize
* Significant effect on host health
* Poor prognosis if untreated
* High risk of recurrence after treatment
67
Give examples of carcinomas.
* Lung cancer
* Breast cancer
* Colorectal cancer
68
Give examples of sarcomas.
* Osteosarcoma
* Leiomyosarcoma
69
Give examples of hematologic malignancies.
* Leukemias
* Lymphomas
70
What is an example of a brain tumor?
Glioblastoma multiforme
71
List the differences between benign and malignant neoplasms.
72
What are the genetic factors that act as risk factors for cancer?
Inherited mutations (e.g., BRCA1/2 in breast cancer)
## Footnote
Genetic factors can significantly increase the likelihood of developing certain types of cancer.
73
How does age influence cancer risk?
Increased risk with advancing age
## Footnote
Age is a significant risk factor due to the accumulation of mutations over time.
74
What types of cancer are associated with tobacco use?
Lung, mouth, throat cancers
## Footnote
Tobacco use is one of the leading preventable causes of cancer.
75
List the types of cancer associated with alcohol consumption.
Liver, esophageal, breast cancers
## Footnote
Alcohol consumption can increase cancer risk through various mechanisms, including damage to DNA.
76
What chronic infections are known to increase cancer risk?
HPV (cervical cancer), Hepatitis B/C (liver cancer)
## Footnote
These infections can lead to significant cellular changes that promote cancer development.
77
Identify environmental toxins that are risk factors for cancer.
Asbestos (mesothelioma), UV radiation (skin cancer)
## Footnote
Exposure to these toxins can lead to serious health consequences, including cancer.
78
How does diet contribute to cancer risk?
High red meat consumption (colorectal cancer)
## Footnote
Diet plays a crucial role in cancer risk, with certain foods linked to specific types of cancer.
79
What is the relationship between obesity and cancer?
Increased risk for various cancers including breast and colon
## Footnote
Obesity is linked to inflammation and hormonal changes that can promote cancer.
80
How does lack of physical activity affect cancer risk?
Increased risk for colon and breast cancers
## Footnote
Regular physical activity is protective against several types of cancer.
81
What hormonal factors are associated with increased cancer risk?
Prolonged estrogen exposure (breast cancer)
## Footnote
Hormonal imbalances can lead to increased cell proliferation and cancer.
82
What is the impact of immunosuppression on cancer risk?
Increased risk of various cancers
## Footnote
Immunosuppressed individuals are at a higher risk due to reduced immune surveillance.
83
What occupational exposures can be risk factors for cancer?
Certain chemicals, radiation
## Footnote
Workers in specific industries may face higher risks due to exposure to carcinogenic substances.
84
What are oncogenes?
Genes that promote cell proliferation or survival when mutated
## Footnote
Oncogenes arise from proto-oncogenes through gain-of-function mutations.
85
Give an example of an oncogene and its role in cancer.
RAS: Constitutively active in many cancers, promoting cell growth and survival
## Footnote
RAS mutations are common in various tumor types, making it a key target for cancer therapy.
86
What are tumor suppressor genes?
Genes that prevent uncontrolled cell growth when functioning properly
## Footnote
Mutations in these genes can lead to cancer development.
87
Provide an example of a tumor suppressor gene.
TP53: 'Guardian of the genome,' regulates cell cycle and apoptosis
## Footnote
TP53 mutations are found in many types of cancer, underscoring its importance.
88
What is the function of DNA repair genes?
They maintain genomic stability by repairing DNA damage
## Footnote
Mutations in these genes can lead to an accumulation of genetic errors and cancer.
89
Name a DNA repair gene and its associated risk.
BRCA1/2: Involved in double-strand break repair, mutations increase breast and ovarian cancer risk
## Footnote
These genes are critical in maintaining the integrity of genetic material.
90
What is angiogenesis?
Formation of new blood vessels to supply the tumor
## Footnote
Angiogenesis is essential for tumor growth and metastasis.
91
What role do pro-angiogenic factors play in angiogenesis?
Tumor cells release factors (e.g., VEGF) that activate endothelial cells
## Footnote
These factors stimulate the formation of new blood vessels towards the tumor.
92
What are the steps involved in metastasis?
1. Local invasion
2. Intravasation
3. Survival in circulation
4. Extravasation
5. Colonization
## Footnote
Each step is crucial for the spread of cancer to distant organs.
93
What are the common metastatic sites for cancer?
Lungs, liver, bones, brain
## Footnote
These organs are frequently affected due to their vascular nature and ability to support tumor growth.
94
Classify the types of carcinogens.
1. Chemical carcinogens
2. Physical carcinogens (e.g., radiation, asbestos)
3. Biological carcinogens (e.g., viruses)
## Footnote
Carcinogens can arise from various sources and have different mechanisms of action.
95
What are the two classifications of chemical carcinogens?
1. Direct-acting carcinogens
2. Indirect-acting carcinogens (procarcinogens)
## Footnote
Understanding these classifications helps in assessing cancer risk.
96
What is the initiation phase in the mechanism of action of chemical carcinogens?
Carcinogen interacts with DNA, forming adducts or causing mutations
## Footnote
This is the first step in the carcinogenic process and is crucial for cancer development.
97
What occurs during the promotion phase of chemical carcinogenesis?
Stimulates proliferation of initiated cells without directly damaging DNA
## Footnote
Promotion supports the growth of cells that have already incurred genetic damage.
98
What is the progression phase in carcinogenesis?
Accumulation of additional genetic changes leading to increased growth and invasive potential
## Footnote
This phase marks the transition from benign to malignant tumors.
99
Name an example of a direct-acting carcinogen.
Alkylating agents form DNA adducts
## Footnote
Direct-acting carcinogens have immediate effects on DNA.
100
What is a common example of an indirect-acting carcinogen?
Benzo[a]pyrene, activated by cytochrome P450 enzymes
## Footnote
Procarcinogens require metabolic activation to exert their carcinogenic effects.
101
Fill in the blank: Tobacco smoke components include _______.
nitrosamines, PAHs
## Footnote
These components are well-known carcinogens associated with various cancers.
102
What is the role of reactive oxygen species in cancer?
Leads to oxidative DNA damage
## Footnote
Reactive oxygen species can result from environmental exposures and contribute to cancer development.
103
What are epigenetic changes in the context of cancer?
Altered DNA methylation or histone modifications
## Footnote
These changes can affect gene expression and lead to tumorigenesis.
104
List some examples of chemical carcinogens.
1. Tobacco smoke components
2. Aflatoxin B1
3. Vinyl chloride
4. Benzene
5. Arsenic compounds
## Footnote
These substances are linked to an increased risk of developing cancer.
105
What type of necrosis is this?
This is caseous necrosis.
## Footnote
Characterized by a cheese-like appearance, commonly associated with granulomatous inflammation in tuberculosis.
106
What type of necrosis is this?
This is fat necrosis.
## Footnote
Involves the destruction of adipose tissue, often due to pancreatic lipase activity in acute pancreatitis, leading to saponification.
107
What type of necrosis is this?
This is fibrinoid necrosis.
## Footnote
Occurs in immune reactions involving blood vessels, with deposition of immune complexes and fibrin, seen in vasculitis and malignant hypertension.
108
What type of necrosis is this?
This is liquefactive necrosis.
## Footnote
Results from enzymatic digestion of dead cells, common in brain infarcts and abscesses, creating a liquid viscous mass.
109
What type of necrosis is this?
This is coagulative necrosis.
## Footnote
Typically caused by ischemia or infarction, leading to protein denaturation while preserving tissue architecture (e.g., myocardial infarction). This is the most common type of necrosis.
110
What type of necrosis is this?
This is gangrenous necrosis.
## Footnote
Not a distinct pattern but a clinical variant; can be dry (coagulative necrosis due to ischemia) or wet (superimposed infection leading to liquefactive necrosis).
111
Describe the differences between necrosis and apoptosis.
112
What is Pyknosis?
**Definition**: Pyknosis is the irreversible condensation of chromatin in the nucleus of a cell undergoing apoptosis or necrosis.
**Key Features**: Shrunken, dark, basophilic nucleus; nuclear membrane intact.
**Significance**: First step of nuclear degradation in cell death.
113
What is Karyorrhexis?
**Definition:** Karyorrhexis refers to the fragmentation of the pyknotic nucleus into small, dense pieces.
**Key Features**: Irregular, fragmented nuclear material scattered within the cytoplasm.
**Significance**: Follows pyknosis; common in both apoptosis and necrosis.
114
What is Karyolysis?
**Definition**: Karyolysis is the complete dissolution of the nuclear structure due to enzymatic degradation of chromatin.
**Key Features**: Fading of nuclear basophilia, leaving a ghost-like, pale nucleus or absent nucleus.
**Significance**: Final stage of nuclear degradation, typically seen in necrosis.
115
What is reversible cell injury?
**Definition**: A type of cellular injury where the damage can be reversed if the stressor is removed.
**Key Features**: Cell swelling, fatty change, plasma membrane blebbing, ribosomal detachment, and mitochondrial changes without membrane rupture.
**Outcome**: Cells recover if the injury is mild or of short duration.
116
What are common causes of reversible cell injury?
**Hypoxia/Ischemia**: Reduced oxygen leading to decreased ATP production.
**Chemical Agents**: Toxins, drugs, and alcohol causing metabolic disturbances.
**Infections**: Mild bacterial or viral infections causing transient stress.
**Physical Factors**: Mild thermal injury, radiation, or mechanical stress.
117
What is irreversible cell injury?
**Definition**: A type of cellular injury where the damage is permanent, leading to cell death (necrosis or apoptosis).
**Key Features**: Severe mitochondrial damage, membrane disruption, lysosomal rupture, and nuclear changes (pyknosis, karyorrhexis, karyolysis).
**Outcome**: Results in cell death despite the removal of the stressor.
118
What are common causes of irreversible cell injury?
**Severe Hypoxia/Ischemia**: Prolonged oxygen deprivation leading to necrosis.
**Extreme Physical Injury**: Intense heat, cold, or mechanical trauma.
**Toxins:** High concentrations of poisons (e.g., cyanide, heavy metals).
**Infections**: Virulent pathogens causing overwhelming cellular damage
119
How do reversible and irreversible cell injuries differ?
**Reversible Injury**: Cell swelling, fatty changes, intact plasma membrane, recovery possible.
**Irreversible Injury**: Membrane rupture, mitochondrial damage, nuclear degradation (pyknosis, karyorrhexis, karyolysis), leading to cell death.
120
What are the key pathways of apoptosis and their main steps?
**Apoptosis Pathways:**
1. **Intrinsic (Mitochondrial) Pathway:**
Triggered by internal stress (DNA damage, oxidative stress, etc.).
**Key Steps:**
* Activation of pro-apoptotic proteins (BAX, BAK).
* Mitochondrial outer membrane permeabilization (MOMP).
* Release of cytochrome c into the cytoplasm.
* Formation of the apoptosome (Apaf-1 + cytochrome c + ATP).
* Activation of caspase-9 (initiator caspase).
* Activation of executioner caspases (caspase-3, -6, -7).
* **Cellular breakdown**: DNA fragmentation, membrane blebbing, apoptotic bodies.
2. **Extrinsic (Death Receptor) Pathway:**
Triggered by external signals (e.g., FasL, TNF-α binding to death receptors).
**Key Steps**:
* Binding of ligand to death receptors (Fas, TNFR).
* Recruitment of FADD (Fas-associated death domain).
* Formation of the DISC (death-inducing signaling complex).
* Activation of caspase-8 (initiator caspase).
* Direct activation of executioner caspases (caspase-3, -6, -7).
* Apoptotic cell death.
## Footnote
Mnemonic for Caspases:
"I 8 too much at the 9th inning, now I’m 3 times sad (apoptotic)."
(Caspase-8 and -9 initiate; caspase-3 executes.)
121
Which of the following is typically associated with necrosis but not apoptosis?
Rupture of the cell membrane.
122
Coagulative necrosis and which of the following are seen in wet gangrene?
In wet gangrene, you typically see a combination of coagulative necrosis and liquefactive necrosis.
**Explanation:
Coagulative Necrosis:**
* Characteristic of ischemic injury (except in the brain).
* The tissue architecture is preserved for a short time after cell death due to protein denaturation.
* Seen in conditions like myocardial infarction and dry gangrene.
**Liquefactive Necrosis:**
* Involves enzymatic digestion of dead cells, leading to a soft, liquid mass.
* Common in infections (due to neutrophilic enzymes) and in brain infarctions.
## Footnote
Mnemonic:
“Wet gets runny” — wet gangrene involves liquefaction due to infection on top of ischemic necrosis.
123
What is the function of the G₁ → S checkpoint?
It restricts entry into the S-phase under certain conditions, preventing poorly controlled cell division if dysregulated.
124
What can result from dysregulation of the G₁ → S checkpoint?
Poorly controlled cell division.
125
How is the G₁ phase regulated?
Cyclins bind CDK4 in the presence of growth factors via tyrosine kinase receptors, leading to phosphorylation of Rb, release of E2F, and initiation of DNA replication.
126
What role does Cyclin D/CDK4 complex play in cell cycle regulation?
It phosphorylates Rb, causing its inactivation and release of E2F, which promotes DNA replication.
127
What happens when Rb is phosphorylated?
t becomes inactivated, releasing E2F transcription factor to initiate DNA replication.
128
What is the role of the E2F transcription factor?
It promotes DNA replication after being released from phosphorylated Rb.
129
What is p53 and its primary role?
p53 is a tumor suppressor that reduces DNA replication and promotes apoptosis via the intrinsic pathway.
130
How is p53 activated?
DNA damage activates p53, leading to the expression of p21, which inhibits CDKs.
131
What happens when p21 is activated?
It inhibits CDKs, reducing CDK-mediated phosphorylation of Rb and causing cell cycle arrest in the G₁ phase.
132
How does p53 contribute to apoptosis?
It increases Bax, Bad, and Bak levels, leading to cytochrome C release from mitochondria and activation of caspases.
133
What is the function of CDKs (Cyclin-Dependent Kinases)?
They phosphorylate target proteins like Rb to regulate cell cycle progression, becoming inactive when inhibited by p21.
134
What triggers the activation of Cyclin D?
Growth factors binding to tyrosine kinase receptors.
135
Describe the events of cell cycle control.
