This document discusses anticancer drugs and their mechanisms of action. It notes that anticancer drugs are increasingly important in veterinary practice and are often used in combination with surgery and/or radiotherapy. The document then provides details on the cell cycle, types of anticancer drugs including cytostatics, and their various mechanisms of action such as inhibiting DNA synthesis, disrupting mitosis, and incorporating false building blocks. It also discusses mechanisms of resistance that tumors can develop.
Definition
Anticancer, or antineoplastic, drugs are used to treat malignancies, or cancerous growths. Drug therapy may be used alone, or in combination with other treatments such as surgery or radiation therapy.
Purpose
Anticancer drugs are used to control the growth of cancerous cells. Cancer is commonly defined as the uncontrolled growth of cells, with loss of differentiation and commonly, with metastasis, spread of the cancer to other tissues and organs. Cancers are malignant growths. In contrast, benign growths remain encapsulated and grow within a well-defined area. Although benign tumors may be fatal if untreated, due to pressure on essential organs, as in the case of a benign brain tumor, surgery or radiation are the preferred methods of treating growths which have a well defined location. Drug therapy is used when the tumor has spread, or may spread, to all areas of the body.
Anticancer Drug, also called Anti-Neoplastic drug, that is effective in the treatment of malignant, or cancerous, disease. There are several major classes of anticancer drugs; these include Alkylating Agents, Anti-metabolites, Plant Alkaloids and Hormones.
ANTI CANCER DRUGS[ANTI-NEOPLASTIC DRUGS] MEDICINAL CHEMISTRY BY P. RAVISANKAR.Dr. Ravi Sankar
what is cancer?, History,Malignent tumor, non-malignent tumor(benign tumor),Largest tumor ever removed, tumour growth kinitics, doubling tume, angiogenesis, causes of cancer, drugs, treatment of cancer, classification of anti-cancer agents, mechanism of actions,alkylating agents,anti metabolites, vinka alkaloids, best ways to reducing cancer.
BY P. RAVISANKAR
VIGNAN PHARMACY COLLEGE
VADLAMUDI
GUNTUR
ANDHRA PRADESH
INDIA.
Shortened description of STATURAL ACTIVITY RELATIONSHIP OF ANTIMETABOLITES & its MECHANISM OF ACTION - ANTINEOPLASTIC AGENTS (folate antagonist, purine antagonist & pyridine antagonist)(MEDICINAL CHEMISTRY)
quite useful for B PHARMACY & Pharm D Students.
Definition
Anticancer, or antineoplastic, drugs are used to treat malignancies, or cancerous growths. Drug therapy may be used alone, or in combination with other treatments such as surgery or radiation therapy.
Purpose
Anticancer drugs are used to control the growth of cancerous cells. Cancer is commonly defined as the uncontrolled growth of cells, with loss of differentiation and commonly, with metastasis, spread of the cancer to other tissues and organs. Cancers are malignant growths. In contrast, benign growths remain encapsulated and grow within a well-defined area. Although benign tumors may be fatal if untreated, due to pressure on essential organs, as in the case of a benign brain tumor, surgery or radiation are the preferred methods of treating growths which have a well defined location. Drug therapy is used when the tumor has spread, or may spread, to all areas of the body.
Anticancer Drug, also called Anti-Neoplastic drug, that is effective in the treatment of malignant, or cancerous, disease. There are several major classes of anticancer drugs; these include Alkylating Agents, Anti-metabolites, Plant Alkaloids and Hormones.
ANTI CANCER DRUGS[ANTI-NEOPLASTIC DRUGS] MEDICINAL CHEMISTRY BY P. RAVISANKAR.Dr. Ravi Sankar
what is cancer?, History,Malignent tumor, non-malignent tumor(benign tumor),Largest tumor ever removed, tumour growth kinitics, doubling tume, angiogenesis, causes of cancer, drugs, treatment of cancer, classification of anti-cancer agents, mechanism of actions,alkylating agents,anti metabolites, vinka alkaloids, best ways to reducing cancer.
BY P. RAVISANKAR
VIGNAN PHARMACY COLLEGE
VADLAMUDI
GUNTUR
ANDHRA PRADESH
INDIA.
Shortened description of STATURAL ACTIVITY RELATIONSHIP OF ANTIMETABOLITES & its MECHANISM OF ACTION - ANTINEOPLASTIC AGENTS (folate antagonist, purine antagonist & pyridine antagonist)(MEDICINAL CHEMISTRY)
quite useful for B PHARMACY & Pharm D Students.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. • The use of antineoplastic drugs is
becoming increasingly important in
veterinary practice.
• These drugs are often used in combination
with surgery and /or radiotherapy.
• Generally ,they are prescribed and
adminsitered in combination drugs having
different mechanisms of action to get
greater tumor cell kill.
3. Cancer
Cancer is a disease of cells characterized by
• Progressive
• Persistent
• Perverted(abnormal)
• Purposeless
• Uncontrolled Profileration of tissues
4. Chemotherapy of Malignant Tumors
• A tumor (neoplasm) consists of cells that
proliferate independently of the body’s
inherent “building plan.”
• A malignant tumor (cancer) is present
when the tumor tissue destructively
invades healthy surrounding tissue or
when dislodged tumor cells form
secondary tumors (metastases) in other
organs.
5.
6. Cell cycle
• Both normal as well as cancerous cells
must pass through phases of cell cycle
• G1 Phase(Presynthetic Phase):synthesis
of enzymes and other cellular components
needed for DNA synthesis
• Synthetic Phase(S phase): DNA synthesis
takes place
7. Cell cycle
• G2 phase (premitotic phase): Synthesis of
cellular components for mitosis (pro-
teins and RNA synthesis).
• M phase: Mitotic cell division takes place.
• Go phase (resting phase): Cells stop
dividing temporarily or permanently.
8.
9. Chemotherapy of Malignant Tumors
• A cure requires the elimination of all
malignant cells (curative therapy). When
this is not possible, attempts can be made
to slow tumor growth and thereby prolong
the patient’s life or improve quality of life
(palliative therapy).
10. Chemotherapy of Malignant Tumors
• Chemotherapy is faced with the problem
that the malignant cells are endogenous
and are not endowed with special
metabolic properties.
12. Cytostatics
• are cytotoxic substances that
particularly affect proliferating or dividing
cells. Rapidly dividing malignant cells are
preferentially injured.
• Damage to mitotic processes not only
retards tumor growth but may also initiate
apoptosis (programmed cell death).
13. Cytostatics
• Tissues with a low mitotic rate are largely
unaffected; likewise, most healthy tissues.
This, however, also applies to malignant
tumors consisting of slowly dividing
differentiated cells. Tissues that have a
physiologically high mitotic rate are bound
to be affected by cytostatic therapy.
14. Cytostatics
• Thus, typical adverse effects occur:
Loss of hair results from injury to hair
follicles; gastrointestinal disturbances,such
as diarrhea, from inadequate replacement
of enterocytes
whose life span is limited to a few days;
nausea and vomiting from stimulation of
area postrema chemoreceptors ;and
lowered resistance to infection from
weakening of the immune system .
15.
16.
17. Cytostatics
• In addition, cytostatics cause bone marrow
depression. Resupply of blood cells
depends on the mitotic activity of bone
marrow stem and daughter cells.
18. Cytostatics
• When myeloid proliferation is arrested,the
short-lived granulocytes are the first to be
affected (neutropenia), then blood
platelets (thrombopenia) and, finally, the
more long-lived erythrocytes
(anemia).Infertility is caused by
suppression of spermatogenesis or follicle
maturation.
19. Cytostatics
• Most cytostatics disrupt DNA metabolism.
• This entails the risk of a potential genomic
alteration in healthy cells (mutagenic effect).
Conceivably, the latter accounts for the
occurrence of leukemias several years after
cytostatic therapy (carcinogenic effect).
Furthermore, congenital malformations are to
be expected when cytostatics must be used
during pregnancy (teratogenic effect).
Cytostatics possess different mechanisms of
action.
20. Cytostatics
• Damage to the mitotic spindle (B).
• The contractile proteins of the spindle
apparatus must draw apart the replicated
chromosomes before the cell can divide. This
process is prevented by the so-called spindle
poisons that arrest mitosis at metaphase by
disrupting the assembly of microtubules into
spindle threads.
• The vinca alkaloids, vincristine and
vinblastine (from the periwinkle plant, Vinca
rosea) exert such a cell-cycle-specific effect.
21. Cytostatics
• Paclitaxel, from the bark of the pacific yew
(Taxus brevifolia), stabilizes microtubules
and as a result, interferes with the normal
breakdown of microtubules during cell
division. Docetaxel is a semisynthetic
derivative. Together with docetaxel, it
forms the drug category of the taxanes.
22.
23. (A)Inhibition of DNA and RNA synthesis
• Mitosis is preceded by replication of
chromosomes (DNA synthesis) and
increased protein synthesis (RNA
synthesis). Existing DNA serves as a
template for the synthesis of new DNA or
RNA.
24. De novo synthesis may be inhibited by:
• Damage to the template (1).
• Alkylating cytostatics are reactive
compounds that transfer alkyl residues into
a covalent bond with DNA. For instance,
mechlorethamine (nitrogen mustard) is able
to cross-link double-stranded DNA on giving
off its chlorine atoms. Correct reading of
genetic information is thereby
rendered impossible.
25.
26. • Other alkylating agents are chlorambucil,
melphalan,, cyclophosphamide, ifosfamide,
lomustine, and busulfan.
• Specific adverse reactions include
irreversible pulmonary fibrosis due to
busulfan and hemorrhagic cystitis caused by
the cyclophosphamide metabolite acrolein
(preventable by the uroprotectant mesna).
Cisplatin binds to (but does not alkylate) DNA
strands.
27.
28.
29. • Cystostatic antibiotics insert
themselves into the DNA double strand;
this may lead to strand breakage (e.g.,
with bleomycin). The anthracycline
antibiotics daunorubicin and adriamycin
(doxorubicin) may induce cardiomyopathy.
Bleomycin can also cause pulmonary
fibrosis.
30. • The epipodophyllotoxins, etoposide
and teniposide, interact with
topoisomeraseII, which functions to split,
transpose, and reseal DNA strands ; these
agents cause strand breakage by
inhibiting resealing.
31. (2) Inhibition of nucleobase synthesis
• Tetrahydrofolic acid (THF) is required
for the synthesis of both purine bases and
thymidine. Formation of THF from folic
acid involves dihydrofolate reductase .
32. Inhibition of nucleobase synthesis
• The folate analogues aminopterin and
methotrexate (amethopterin) inhibit
enzyme activity as false substrates. As
cellular stores of THF are depleted,
synthesis of DNA and RNA building blocks
ceases. The effect of these antimetabolites
can be reversed by administration of folinic
acid (5-formyl-THF, leucovorin, citrovorum
factor).
33.
34. (3). Incorporation of false building
blocks
• Unnatural nucleobases (6-mercaptopurine;
5-fluorouracil) or nucleosides with
incorrect sugars (cytarabine) act as
antimetabolites. They inhibit DNA/RNA
synthesis or lead to synthesis of missense
nucleic acids.
35.
36. • 6-Mercaptopurine results from
biotransformation of the inactive precursor
azathioprine .
• The uricostatic allopurinol inhibits the
degradation of 6- mercaptopurine such
that co-administration of the two drugs
permits dose reduction of the latter.
37. • Frequently, the combination of cytostatics
permits an improved therapeutic effect
with fewer adverse reactions.
38.
39. Mechanisms of resistance are
multifactorial
• Initial success can be followed by loss of
effect because of the emergence of
resistant tumor cells.
• Diminished cellular uptake may result from
reduced synthesis of a transport protein
that may be needed for membrane
penetration (e.g., methotrexate).
40. • Augmented drug extrusion: increased
synthesis of the P-glycoprotein that
extrudes drugs from the cell (e.g.,
anthracyclines, vinca alkaloids,
epipodophyllotoxins, and paclitaxel) is
reponsible for multi-drug resistance (mdr-1
gene amplification).
41. • Diminished bioactivation of a prodrug, e.g.,
cytarabine, which requires intracellular
phosphorylation to become cytotoxic.
• Change in site of action: e.g., increased
synthesis of dihydrofolate reductase may
occur as a compensatory response to
methotrexate.
42. • Damage repair: DNA repair enzymes may
become more efficient in repairing defects
caused by cisplatin.
Editor's Notes
dislodgedTo move or go from a dwelling or former position
Transmission of pathogenic microorganisms or cancerous cells from an original site to one or more sites elsewhere in the body, usually by way of the blood vessels or lymphatics.
The area postrema is a medullary structure in the brain that controls vomiting.
The area postrema, one of the circumventricular organs,[4] detects toxins in the blood and acts as a vomit-inducing center. The area postrema is a critical homeostatic integration center for humoral and neural signals. Recent studies have implicated its function as a chemoreceptor trigger site for vomiting in response to emetic drugs.
Because cytostatics affect dividing cells, many of the side effects are concentrated on renewable tissue, such as hair, bone marrow and mucous membranes. The type and severity of the side effects depend on the drugs used, dosages, your overall condition and how our body responds to the drugs.
Diarrhoea
Diarrhoea is a common side effect of chemotherapy. It is caused by damage to the intestinal mucous membranes.
The solitary tract and nucleus are structures in the brainstem that carry and receive visceral sensation and taste from the facial (VII), glossopharyngeal (IX) and vagus (X) cranial nerves.[1]
my·e·loid (m-loid) adj. 1. Of, relating to, or derived from the bone marrow
leu•ke•mi•a (luˈki mi ə) any of several cancers of the bone marrow characterized by an abnormal increase of white blood cells in the tissues.n. any of several cancers of the bone marrow characterized by an abnormal increase of white blood cells in the tissues
Microtubules (micro- + tube + -ule) are a component of the cytoskeleton, found throughout the cytoplasm. These tubular polymers oftubulin can grow as long as 50 micrometres and are highly dynamic. They are involved in chromosome separation (mitosis and meiosis), and are the major constituents of mitotic spindles, which are used to pull apart eukaryotic chromosomes.
Pulmonary fibrosis is the formation or development of excess fibrous connective tissue (fibrosis) in the lungs. It is also described as "scarring of the lung".
Mesna (INN) /ˈmɛznə/ is an organosulfur compound used as an adjuvant in cancer chemotherapy involving cyclophosphamide and ifosfamide. It is marketed by Baxter as Uromitexan and Mesnex. The name of the substance is an acronym for 2-mercaptoethane sulfonate Na (Na being the chemical symbol for sodium). It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[1]
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cys·ti·tis (s-stts) n. Inflammation of the urinary bladder.
Cystitis
Definition
Cystitis is defined as inflammation of the urinary bladder.
mesna
[mes´nah]a sulfhydryl compound given orally or intravenously together with a urotoxic antineoplastic agent such as ifosfamide orcyclophosphamide because it inactivates some of their metabolites and thus lessens damage to the bladder.
car·di·o·my·op·a·thy
(kär′dē-ō-mī-ŏp′ə-thē) n. pl. car·di·o·my·op·a·thies A disease or disorder of the heart muscle, especially of unknown or obscure cause.
transpose
To reverse or transfer the order or place of; interchange
To put into a different place or order
mis·sense (mssns) adj. Of or relating to a mutation that changes a codon for one amino acid into a codon for a different amino acid
P-glycoprotein 1 (permeability glycoprotein, abbreviated as P-gp or Pgp)
P-glycoprotein 1 also known as multidrug resistance protein 1 or ATP-binding cassette sub-family B member 1 or cluster of differentiation 243 is an important protein of the cell membrane that pumps many foreign substances out of cells