CANCER: A group of disease involving abnormal cell growth with the potential to invade or spread to other part of the body.
CHEMOTHERAPY: the term chemotherapy is describe as the use of chemicals or drugs to treat cancer.
CYTOTOXIC DRUG: lysis both normal and cancer cells
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.
CANCER: A group of disease involving abnormal cell growth with the potential to invade or spread to other part of the body.
CHEMOTHERAPY: the term chemotherapy is describe as the use of chemicals or drugs to treat cancer.
CYTOTOXIC DRUG: lysis both normal and cancer cells
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.
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.
Modern Prospecting Techniques for Connecting with Prospects (from Sales Hacke...HubSpot
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While buyers have evolved and become more sophisticated, sales reps and training programs have been slow to adapt to that change.
Learn actionable modern prospecting techniques you can apply immediately from two best selling authors and sales experts: Max Altschuler CEO of Sales Hacker, and Mark Roberge CRO of HubSpot.
3 Proven Sales Email Templates Used by Successful CompaniesHubSpot
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The lack of visible female role models is pervasive in the tech industry, particularly on Wikipedia, where just under 17% of Wikipedia biographies were on women. That's why HubSpot wrote fourteen Wikipedia entries for remarkable women in tech to help inspire young women to reach positions at the highest levels of STEM.
ANTI-CANCER DRUGS: All you need to know by RxVichuz!RxVichuZ
This is my 49th powerpoint....gives a precise insight into the theories behind anti-cancer agents, their actions on specific cell-cycles & important ADRs
Also, insight into newer molecules, monoclonal antibodies & management of anticancer ADRs.
Helpful for precise brush-up on antineoplastic agents!!
Vishnu.R.Nair.
CLASSIFICATION OF ANTI - CANCER DRUGS.pptxAnupam32727
This presentation shows the classification of ANTI-CANCER drugs.
It includes the introduction and classification of anticancer drugs with their mechanism of action and drug of choice in the treatment of various cancer diseases.
Exercise Testing in Cardiology : Dr. Akif Baigakifab93
The testing modality and protocol should be selected in accordance with the patient’s estimated functional capacity based on age, estimated physical fitness from the patient’s history, and underlying disease
Several exercise test protocols are available for both treadmill and stationary cycle ergometers
Patients who have low estimated fitness levels or are deemed to be at higher risk because of underlying disease (e.g., recent MI, heart failure) should be tested with a less aggressive exercise protocol
Treadmill and cycle ergometers may use stepped or continuous ramp protocols
Work rate increments (stages) during stepped protocols can vary from 1 to 2.5 METs
Ramp protocols are designed with stages that are no longer than 1 minute and for the patient to attain peak effort within 8 to 12 minutes
The natriuretic peptide system works antagonistically to the RAAS and has favorable effects on the pathogenesis of heart failure
Natriuretic peptides are broken down by an enzyme called neprilysin
Neprilysin is also responsible for the breakdown of other substances, including bradykinin and angiotensin II
Sacubitril/valsartan is a combination product
Sacubitril is a pro-drug that, upon activation, acts as a neprilysin inhibitor
It works by blocking the action of neprilysin, thus preventing the breakdown of natriuretic peptides
This leads to a prolonged duration of the favorable effects of these peptides
Coronary heart disease (CHD) remains a leading cause of death worldwide, accounting for 16% of total deaths globally .
Atherosclerosis plays a central role, with early fatty streaks progressing to late complex atheromas
Vascular calcification, the pathogenic and process of ectopic bone production, specifically was shown to strongly correlate with degree of atherosclerosis (both calcified and noncalcified)
Vascular calcification was shown independently to predict cardiovascular morbidity and mortality
These associations, combined with the radio-opaque appearance of calcium hydroxyappatite on CT images, have led to extensive investigation of the quantification, or scoring, of coronary artery calcium (CAC).
CAC scoring has emerged as a widely available and powerful tool for stratifying cardiovascular risk, predicting patient outcomes, and guiding preventive therapy
A coronary bifurcation consists of a flow divider (carina) and three vessel segments:
The proximal main vessel (PMV)
The distal main vessel (DMV) and
The side branch (SB).
A bifurcation lesion is a major epicardial coronary artery stenosis next to and/or including the ostium of a significant side branch
A significant SB is a branch whose severe narrowing or acute occlusion before or during intervention can cause considerable ischemia or a new infarction area that will worsen the clinical course of a particular patient.
Other important elements to consider that are not inherent in the bifurcation classifications include:
Extent of disease on the SB (limited to the ostium or involving the vessel beyond the ostium)
Its size (over 2.5mm in reference diameter)
Bifurcation angle, and
Disease distribution
Left ventricular (LV) dysfunction remains one of the
best prognostic determinants of survival in patients
with coronary artery disease (CAD)
⚫ It was originally thought that dysfunctional
myocardium after an infarction was irreversibly
damaged
⚫ However, it was later recognized that some of the
involved tissue remained viable and contractility may
be restored with revascularization
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
Tetralogy of Fallot (TOF) is a congenital heart defect, which has four anatomical components:
Anterior malalignment ventricular septal defect (VSD)
Aortic override over the muscular septum
Variable degrees of subvalvar, valvar, and supravalvar pulmonary stenosis
Right ventricular (RV) infundibular narrowing and RV hypertrophy
Ventricular septal defects occur either as an isolated defect or as a component of a more complex lesion
It occurs in 50 percent of all children with CHD and in 20 to 30 percent as an isolated lesion
Most common congenital cardiac anomaly in children
Second most common congenital abnormality in adults, second only to bicuspid aortic valves
They are more common in premature infants and those born with low weight
VSDs are slightly more common in females (56%)
Patients with peripheral artery disease who have undergone lower-extremity revascularization are at high risk for major adverse limb and cardiovascular events
The efficacy and safety of rivaroxaban in this context are uncertain
Most common cyanotic heart defect seen in children beyond infancy, accounting for a third of all congenital heart disease (CHD) in this age group
Tetralogy of Fallot (TOF) is a congenital heart defect, which has four anatomical components:
Anterior malalignment ventricular septal defect (VSD)
Aortic override over the muscular septum
Variable degrees of subvalvar, valvar, and supravalvar pulmonary stenosis
Right ventricular (RV) infundibular narrowing and RV hypertrophy
Bentracimab (also known as PB2452) is a neutralizing recombinant human immunoglobulin G1 monoclonal antibody antigen-binding fragment that binds ticagrelor and its major active circulating metabolite with high affinity and specificity
Chlorthalidone for hypertension in advanced ckdakifab93
Chlorthalidone, a thiazide-like diuretic, reduces cardiovascular morbidity, such as the incidence of stroke and heart failure, and cardiovascular mortality
However, its efficacy and safety among patients with advanced chronic kidney disease remain poorly understood
An acute illness caused by an autoimmune response to infection with group A Streptococcus, leading to a range of possible symptoms and signs affecting any or all of heart, joints, brain, skin and subcutaneous tissues
Amyloidosis is a group of protein-folding disorders in which >1 organ is infiltrated by proteinaceous deposits known as amyloid. Amyloid involvement of the heart (cardiac amyloidosis) carries the worst prognosis of any involved organ, and light-chain (AL) amyloidosis is the most serious form of the disease
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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2. Anti cancer drugs acts on
1) Bone marrow : causes Bone marrow suppression
2) GIT : causes Nausea and vomiting
3) Hairs: Alopecia
4) Causes increase in Serum Uric Acid : Due to lysis of tumor cells
This Side effects are common to all anticancer drugs.
5. -M.O.A : It attaches to N7 of Guanine of DNA dimer and destroys DNA
-Side effects :
1) Bone marrow : causes Bone marrow suppression
2) GIT : causes Nausea and vomiting
3) Hairs: Alopecia
4) Causes increase in Serum Uric Acid : Due to lysis of tumor cells
5) Secondary Leukemias : MC : AML
6) Infertility
12. NITROSUREAS
Carmustine = Causes Persistent Neutropenia
Lomustine
Semustine
- Can cross Blood Brain Barrier. Hence used in Brain Tumors
13. -Treatment of Choice : CHOP +/- R
C - Cyclophosphomide
H - Hydroxyrubocin
O - Oncovin
P -Prednisolone
R -Rituximab
14. FOLFOX or FOLFIRI regimen
FOL - Folinic Acid
F - 5-FU
OX - Oxyplatinum
FOL - Folinic Acid
F - 5-FU
IRI - Irinotecan
15. Cisplatin -Most emitogenic Anticancer drug
-Most important side effect :
Nephrotoxicity
-Other S/E : Ototoxicity
-Marrow sparing drug
Carboplatin Maximum Bone marrow suppression
(Most hematotoxic)
Oxaliplatin Used for Colorectal cancers
16. 1) Nephrotoxicity is seen with: (DNB Dec 2010)
A Azathioprine
B Leflunomide
C Mycophenolate mofetil
D Tacrolimus
17. Ans. D) Tacrolimus
I. It is a Macrolide Antibiotic
II. Tacrolimus (FK 506) inhibits IL-2 transcription like cyclosporine does.
II. The drug is more potent than cyclosporine and requires therapeutic drug
monitoring.
III. Patients treated with the calcineurin inhibitors cyclosporine and tacrolimus
are at high risk of developing renal injury.
Side Effects
1) Nephrotoxicity
2) Neurotoxic
3) Precipitates DM
4) Hepatotoxic but not Ototoxic
Inhibits IL-2 transcription
IL-2 activates T cell
Thus Tacrolimus decreases T-cell
activity
18. -Prodrug of Anti Cancer drug 6-Mercaptopurine
- Drug of choice for Steroid Resistant Ulcerative Colitis
Side effects :
1) Bone marrow suppression ; Most Important
2) Hepatotoxicity
3) Nephrotoxicity : Rare
19. Leflunomide is an immunomodulator and is used in severe
rheumatoid arthritis.
SIDE EFFECTS
1) severe liver injury
2) interstitial lung diseases,
3) myelosupression and anemia.
20. -Mycophenolate is a prodrug
-It is an inosine monophosphate dehydrogenase inhibitor.
-Common Side Effect :
1) gastrointestinal upset
2) bone marrow depression.
21. -Immunomodulator
-Side Effects : SPORT Channel
S - Sedation
Po -Phocomelia /Peripheral Neuropathy
R - Rash
T - Thrombosis
Channel - Constipation
Phocomelia
Limb bud formation defect
22. 2. Cerebellar ataxia is caused by (DNB June 2012)
A Arabinofuranosyl cytidine
B Bleomycin
C Cisplatin
D Busulfan
23. Ans. A Arabinofuranosyl cytidine
Cytarabine (Arabinofuranosyl cytidine) is used intrathecally for meningeal
leukemia.
This can cause cerebellar toxicity – ataxia & slurred speech as well as cerebral
toxicity – seizures, dementia, coma etc.
The other side effects are potent myelosuppression, GIT & mucosal side effects,
dermatitis, reversible rise in LFT & pulmonary side effects.
24. Anti Folate Anti PyramidinesAnti Purines
-Methotrexate
-Pemetrexed
-Pralatrexate
-6-mercaptopurine
6-thioguanine
Cladribine
Fludrabine
-5-FU
-Capecitabine
-Gemcitabine
-Cytarabine
(Arabinofuranosyl
cytidine)
26. C - Choriocarcinoma
A - Autoimmune diseases
N -Non Hodgkin Lymphoma
C - Crohn’s Disease
E - Ectopic Pregnancy
R -Rheumatoid Arthritis
27. 1) Bone marrow : causes Bone marrow suppression
2) GIT : causes Nausea and vomiting
3) Hairs: Alopecia
4) Causes increase in Serum Uric Acid : Due to lysis of
tumor cells
5) Megaloblastic Anemia
6) Hepatotoxicity
28. -Methotrexate resistance is due to overproduction of Dihydrofolate
Reductase(DHFRase)
-Methotrexate is a weak acid and hence its excretion is increased by
Alkalinisation
29. Weak- Warfarin
A - Aspirin/ Antiepileptics
C -Chlorthiazide
I - Ibuprofen
D - Dopa (Levodopa)
30. Drug Feature
6-mercaptopurine -Metaboliosed by Xanthine Oxidase
- S/E : Hepatotoxicity
6-thioguanine S/E : Hepatotoxicity
Cladribine DOC in Hairy cell Leukemia
Fludrabine DOC in CLL
-Purines : Adenine and Guanine
31. 5-FU S/E: Hand and foot Syndrome
Capecitabine -Prodrug and is metabolised to 5-FU
-S/E: Hand and foot Syndrome
Gemcitabine DOC in Pancreatic Cancers
Cytarabine S/E: Cerebellar ataxia
-Pyramidines : Cytosine, Thymine and Uracil.
32. Cute - Chloroquine
P - Penicillamine
A - Azathioprine
G -Gold Salts
L - Leflunomide
I - Immunosuppresant drugs
Malika - Methotrexate (DOC)
Sherawat - Sulfasalazine
TNF-@ Inhibitors
1) Adalizumab
2) Etanarcept
3) Infliximab
IL-1 Receptor Antagonist
Anakinra
IL-6 Inhibitor
Tocilizumab
Disease Modifying Anti Rheumatoid Drugs
33. 3. Which of the following is highly emetogenic:
A Cisplatin
B High dose methotrexate
C High dose cyclophosphamide
D Carboplatin
34. Ans. A) Cisplatin as well as option
C. High dose Cyclophosphamide
Nausea & vomiting is a prominent feature of many of cytotoxic drugs.
This is due to CTZ stimulation as well as generating the emetogenic stimuli from
upper GIT as well as other areas.
A. High emetogenic – cisplatin, mustine,cyclophosphamide, actinomycin D,
dacarbazine, lomustine.
35. -Located in Area Postrema
- Remember its location: Can come in exam.
36. Drugs which are effective in
chemotherapy induced vomiting:
A. 5-HT3 receptor antagonists – granisetron, palanocetron, ondansetron
etc.
B. NK1 antagonists (Substance P antagonist): Aprepitant
C. Dexamethasone
CHEMOTHERAPY INDUCED VOMITING DOC
Early Onset Ondansetron
Late Onset Aprepitant
37. 4. Which is not a alkylating agent
A Cyclophosphamide
B Chlorambucil
C 5-FU
D Melphalan
38. Ans. C 5-FU
5-FU( 5 Fluro Uracil) is a antimetabolite – classified as anti-pyrimidine
compound.
Rest all are alkylating agents – act by formation of active carbonium ion which
damages DNA.
The alkylating agents are further classified as
Nitrogen mustards – mechlorethanamine, cyclophosphamide’s, ifosfamide,
melphalan &chlorambucil
Ethyleneimine & methylmelamines – altretamine & thiotepa
Methyl hydrazine derivatives – procarbazine.
Alkyl sulfonates – busulfan
Nitrosoureas – carmustine, lomustine.
Triazenes – Dacarbazine, temozolomide
Platinum co-ordination complexes – cisplatin, carboplatin and oxiliplatin.
39. 5. Ifosfamide is a (DNB Dec 2012)
A Alkylating agents
B Antimetabolite
C Folate antagonists
D Plant Alkaloids
40. Ans. A alkylating agent
Ifosfamide is a synthetic isomer of cyclophosphamide.
Importantly, it is not a metabolite of cyclophosphamide.
It causes greater neurotoxicity and cystitis than cyclophosphamide
42. 6. All of the following are side effects of thalidomide except (AIIMS Nov 2009)
A Hypothyroidism
B Diarrhea
C Teratogenicity
D Deep Vein Thrombosis
43. Ans. B Diarrhea
Thalidomide causes constipation and not diarrhea
The most common adverse effects are sedation and constipation
the most serious one is treatment-emergent peripheral sensory
neuropathy.
44. -Immunomodulator
-Side Effects : SPORT Channel
S - Sedation
Po -Phocomelia /Peripheral Neuropathy
R - Rash
T - Thrombosis
Channel - Constipation
Phocomelia
- Teratogenic S/E
- Limb bud formation defect
45. 7.
Which of the following is cell cycle specific
A Ifosfamide
B Bleomycin
C Vinblastine
D Cyclophosphamide
46. Ans. C Vinblastine
Vinblastine is a M phase specific vinca alkaloid.
It blocks the mitotic spindles and produces metaphase arrest.
Since it produces an interference with chromosomal segregation it is useful in
tumors that are rapidly dividing.
The drug is used in blood and reproductive cancers.
Side effects
nausea, vomiting, myelosupression and bone marrow depression.
47. DRUGS INHIBITING
FORMATION OF SPINDLE
FEATURES
VINCRISTINE -Doesn’t cause bone marrow
suppression(marrow sparing
drug)
-S/E : SIADH and Peripheral
Neuropathy
VINBLASTINE S/E; Bone marrow suppression
-M Phase Specific
48. DRUGS INHIBITING BREAK
OF SPINDLE
FEATURES
PACLITAXEL -Stabilises Microtubule
-S/E :
1) Allergy
2) Peripheral Neuropathy
49. TOPOISOMERASE –I Inhibitor TOPOISOMERASE –II Inhibitor
Irinotecan Etoposisde
Anthracyclines
Doxorubocin
Daunorubocin
Used in Colorectal Cancer
(FOLFORI Regimen)
-Etoposide causes Secondary
Leukemias
-Anthracyclines causes Cardiotoxicity
51. 1) ALKYLATING AGENTS
2) ETOPOSIDE
-MC Secondary Leukemia due to Anti cancer drugs is : AML
ALKYLATIN
G AGENTS
ETOPOSIDE
Secondary
Leukemias
Develops long
4-5yrs
1-2yrs
Myelodysplasia Occurs Doesn’t occur
53. 8) Bleomycin toxicity affects which type of cells.
A Type 1 pneumocyte
B Type 2 pneumocyte
C Endothelial cell.
D Alveolar macrophages
54. Ans. A Type 1 pneumocytes
Bleomycin
causes destruction of type 1 pneumocyte thereby causing hyperplasia of
type-II pneumocytes.
-Bleomycin is an Anticancer Antibiotic
-Bone marrow sparing drug
56. 9) ‘Hand Foot’ syndrome can be caused by?
A 5FU
B Vincristine
C Capecitabine
D Mitomycin-C
57. Ans. A 5FU as well as C. Capecitabine
5-FU can cause hand foot mouth disease. It is given I.V.
Generally, this disease affects infants and children.
Adults with immunodeficiency can also be affected.
Capecitabine is a oral 5FU analog, that obviate the need for I.V.
58. 5-FU S/E: Hand and foot Syndrome
Capecitabine -Prodrug and is metabolised to 5-FU
-S/E: Hand and foot Syndrome
Gemcitabine DOC in Pancreatic Cancers
Cytarabine S/E: Cerebellar ataxia
-Pyramidines : Cytosine, Thymine and Uracil.
59. 10) Topical MITOMYCIN-C is used in: (DNB Dec 2009)
A Sturge weber syndrome
B Urinary bladder cancer
C Endoscopic angiofibroma
D Skull base osteomyelitis
60. Ans. B Urinary bladder cancer
I. Mitomycin is an anti-tumor antibiotic with alkylating agent like property. It is
used in superficial cancer of urinary bladder.
II. The drug has radiomimetic effects, and also sensitizes hypoxic tumor cells to
the effects of hypoxia. Hemolytic uraemic syndrome is a known
complication of mitomycin.
III. The drug also produces bone marrow depression.
The drug of choice for superficial cancer of urinary bladder is BCG
given intravesically.
61. 11) Which of the following statement is false regarding vincristine? (AIIMS May 2012)
A It is an alkaloid
B Its use is associated with neurotoxicity
C It does not cause alopecia
D It is useful drug for induction of remission in acute lymphoblastic leukemia
62. Ans. C It does not cause alopecia
(Mnemonics :
Vincristine: CNS side effect;
Vinblastine: Blood/Bone marrow side effect)
a. Vincristine is a vinca alkaloid.
Vincristine is very useful for inducing remission in childhood acute leukemia.
b. It is also used for treatment of chronic lymphocytic leukemia and chronic
myelocytic leukemia.
Prominent adverse effects are peripheral neuropathy and alopecia.
63. DRUGS INHIBITING
FORMATION OF SPINDLE
FEATURES
VINCRISTINE -Doesn’t cause bone marrow
suppression(marrow sparing
drug)
-S/E : SIADH and Peripheral
Neuropathy
VINBLASTINE S/E; Bone marrow suppression
-M Phase Specific
64. 12. Allopurinol should be avoided, or reduced doses should be used if given
with which of the chemotherapeutic agent ?
A Bleomycin
B Cisplatin
C Cyclophosphamide
D Mercaptopurine
65. Ans. D Mercaptopurine
I. Mercaptopurine and other thiopurine are purine antimetabolites that are
metabolically inactivated by xanthine oxidase.
-Allopurinol inhibits Xanthine Oxidase
As a result Xanthine oxidase is not available to degrade Mercaptopurine
Leads to Toxicity of Mercaptopurine i.e Severe hepatotoxicity
Thus decreased dose of Mercaptopurine should be given if co-administered with
Allopurinol.
66. 13. AMIFOSTINE is protective to to all except:
A Salivary gland
B Skin
C CNS
D GIT
67. Ans. C) CNS
-Amifostine is a cytoprotective drug .
-It doesn’t cross Blood Brain Barrier. Hence is not protective to CNS.
-Amifostine is protective to salivary glands (reduces xerostomia) and GIT
(prevents esophagitis).
-Its xerostomia preventing action can also be considered to be protective to
skin.
68. 14. Which of the following causes persistent leucopenia? (AIIMS Nov 2011)
A Cisplatin
B Vinblastin
C Doxorubicin
D Carmustine
70. 15. Temozolomide is a (DNB June 2011)
A Carbonic anhydrase inhibitor
B Alkylating agent
C Anti metabolite
D Tyrosine kinase inhibitor
71. Ans. B Alkylating agents
- Temozolomide is a Newer alkyalting agent
- It can cross BBB , hence used for brain cancer (anaplastic astrocytoma
and glioblastoma multiforme)
- commonly used oral and intravenous
S/E: Nausea, vomiting, headache, constipation , myelosuppression
72. 16. SIADH is caused by the following drugs except?
A Vincristine
B Vinblastine
C Actinomycin D
D Cyclophosphamide
73. Ans. C Actinomycin D
Drugs Causing SIADH
1. Intravenous cyclophosphamide
2. Carbamazepine
3. Vincristine or vinblastine
4. Phenothiazines
5. Haloperidol
6. Tricyclic antidepressants or serotonin-reuptake inhibitors
7. Monoamine oxidase inhibitors
8. Bromocriptine
9. Clofibrate
10. Narcotics, opiate derivatives
74. 17. Alkalinisation of urine ameliorates the toxicity of which of the
following drugs? (AIIMS May 2009)
A Arabinoside-cytosine
B Ifosfamide
C Cisplatin
D Methotrexate
75. -Methotrexate resistance is due to overproduction of Dihydrofolate
Reductase(DHFRase)
-Methotrexate is a weak acid and hence its excretion is increased by
Alkalinisation
76. Weak- Warfarin
A - Aspirin/ Antiepileptics
C -Chlorthiazide
I - Ibuprofen
D - Dopa (Levodopa)
77. 18) Which anticancer drug causes hypercoagulable syndrome?
A 5-FU
B L-asparaginase
C Melphalan
D Carmustine
79. 19. Methotrexate resistance is due to:
A Depletion of Folate
B Overproduction of DHFRase
C Overproduction of Thymidylate kinase
D Decreased DHFRase
80. Ans. B Overproduction of DHFRase
Mechanisms of methotrexate resistance
I. Impaired transport of methotrexate into cells
II. Production of altered forms of DHFR that have decreased affinity for the
inhibitor
III. Increased concentrations of intracellular DHFR through gene amplification or
altered gene regulation
IV. Decreased ability to synthesize methotrexate polyglutamates
V. Increased expression of a drug efflux transporter, of the MRP (multidrug
resistance protein) class.
81. 21. High dose methotrexate is given in:
A Osteosarcoma
B Colon Cancer
C Retinoblastoma
D Ewing's sarcoma
82. Ans. A Osteosarcoma
Drugs effective in osteosarcoma are: .
doxorubicin,
ifosfamide,
cisplatin, and
high-dose methotrexate with leucovorin.
Osteosarcoma is radioresistant; radiation therapy has no role in the routine
management.
84. CML INDia Imatinib (DOC)
Nilotinib
Dasatinib
Lung cancer After ECG we look for
Lungs
After – Afatinib
E-Erlotinib
C- Ceritinib
G - Geftinib
RCC We PASS urine due to
kidney
P -Pazotinib
A - Axitinib
S - Sorafenib
S - Sunitinib
HCC We feel Sorry for Liver
cancer
Sorry - Sorafenib
GIST Imatinib (DOC)
Malignant Melanoma DVT D - Dabrefinib
V - Vemurafenib
T - Trameltenib
Medullary carcinoma thyroid Vandematram Vandetanib
85. 22) Which of the following drug acts by inhibiting tyrosine kinase activated by EGF
receptor as well as HER2
A Imatinib
B Geftinib
C Erlotinib
D Lapatinib
87. 23) Paclitaxel acts by (DNB June 2011)
A Topoisomerase inhibitor
B Inhibition of Microtubule formation
C Mitotic cell inhibitor
D Exaggerates polymerization and causes the stabilization of the microtubules
88. Ans. D Exaggerates polymerization and causes the stabilization of the
microtubules
II. It enhances polymerization of tubulin: a mechanism opposite to that of vinca
alkaloids.
III. The microtubules are stabilized and their depolymerization is prevented.
IV. This stability results in inhibition of normal dynamic reorganization of the
microtubule network that is essential for vital interphase and mitotic functions.
V. Abnormal arrays or ‘bundles’ of microtubules are produced throughout the
cell cycle.
89. 24. ATRA is useful in the treatment of which of the following type of AML?
(AIIMS Nov 2012)
A Monocytic leukemia
B Myelomonocytic leukemia
C Promyelocytic leukemia
D Erythro leukemic leukemia
90. Ans. C Acute Promyelocytic leukemia {APL}
Treatment of promyelocytic leukemia is by tretinoin.
It is an oral drug that induces the differentiation of leukemia cells bearing the t
(15,17)
It is not effective in other forms of AML.
91. 25. Leucovorin is used as Rescue therapy for patients who are on one of the
following drug therapies
A Asparagine
B Methotrexate
C 6-mercaptopurine
D Cyclophosphamide
92. Ans. B Methotrexate
a. Methotrexate toxicity: Folinic acid (Leucovorin, citrovorum factor),is an
active coenzyme form which does not need to be reduced by DHFRase before
it can act.
b. Methotrexate is a DHFRase inhibitor; its toxicity is not counteracted by folic
acid, but antagonized by folinic acid.
c. Folinic acid is expensive and not needed for the correction of simple folate
deficiency for which folic acid is good enough.
93. 26. Which phase of the cell cycle is resistant to most chemotherapeutic agents:
A G0
B G1
C G2
D M
94. Ans. A G0
a. The G0 phase is the resting or dormant stage of the cell cycle.
b. No cell division takes place. This phase is, overall, the most resistant to
chemotherapeutic agents because most of the (phase-specific) anti cancer
drugs produce their lethal effects quickest and best on cells that are actively
proliferating, whether synthesizing or preparing to synthesize DNA, or to
undergo mitosis.
Good examples of drugs that are reasonably effective against cells in G0 (or
any other phase) are the alkylating agents (e.g., cyclophosphamide) and
several of the antitumor antibiotics (e.g., dactinomycin, doxorubicin).
95. 27.A cancer patient develops severe, irreversible cardiomyopathy because the
maximum lifetime dose of an anticancer drug was exceeded. Which of the following
is most likely responsible for this patient’s symptoms? (AIPG 2011)
A Asparaginase
B Bleomycin
C Cisplatin
D Doxorubicin
96. Ans. D Doxorubicin
I. Doxorubicin, an antitumor antibiotic, is cardiotoxic, and the risk for and
severity of cardiomyopathy is dose-related.
II. [There is a maximum recommended lifetime (cumulative) dose for this
drug, and if it exceed the risk of cardiac damage rises significantly]
97. 28. Which of the following are the most common and worrisome adverse
responses associated with cyclosporine therapy? (AIPG 2010)
A Cardiotoxicity and hepatotoxicity
B Hepatotoxicity and nephrotoxicity
C Hypotension and pulmonary fibrosis
D Nephrotoxicity and infection risk
98. Ans. D Nephrotoxicity and infection risk
a. Nephrotoxicity; occurs in about 8 of 10 patients receiving cyclosporine. It is
typically dose-dependent and, particularly in renal transplant patients, could
be due to either the drug (too much) or to rejection. Infection occurs about as
often as renal dysfunction.
b. Cyclosporine can cause hepatotoxicity, but the incidence is far lower than that
of renal responses or infection. Blood pressure changes can occur, but with
cyclosporine the change usually involves increased pressure, and it is common.
c. Cardiac or pulmonary toxicities and thromboembolism due to the drug itself
are extremely uncommon. The drug blocks transcription of IL-2 and thus reduces
activity of CD-4 lymphocytes. This increases risk of infections.
