Diabetes Discussion Dr. Shriniwas Kashalikar
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Dr. Shrinivas Kashalikar raises several questions about diabetes diagnosis and treatment: 1. He asks why intracellular glucose levels are not measured instead of plasma glucose levels, and how intracellular levels correlate with plasma levels. 2. He questions whether high blood glucose could cause intracellular glucose starvation due to defective utilization. 3. He also asks if reducing carbohydrates and fat would disproportionately increase protein intake, and if that could harm the kidneys. 4. Finally, he inquires about the effects of variable absorption and excretion on blood glucose, the impact of energy output changes, and why moderate sweet foods and stress management are not more integrated into diabetes education and treatment.
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1)HIGHLY SEDATIVE-DIPHENHYDRAMINE,DIMENHYDRINATE,PROMETHAZINE,HYDROXYZINE 2)MODERATELY SEDATIVE- PHENARIMINE,CYPROHEPTADINE, MECLIZINE,CINNARIZINE
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TRIPROLIDINE,CLEMASTINE
SECOND GENERATION ANTIHISTAMINICS-FEXOFENADINE,
LORATADINE,DESLORATADINE,CETIRIZINE,LEVOCETIRIZINE,
AZELASTINE,MIZOLASTINE,EBASTINE,RUPATADINE. Mechanism of action of 2nd generation antihistaminics-
These drugs competitively antagonize actions of
histamine at the H1 receptors.
Pharmacological actions-
Antagonism of histamine-The H1 antagonists effectively block histamine induced bronchoconstriction, contraction of intestinal and other smooth muscle and triple response especially wheal, flare and itch. Constriction of larger blood vessel by histamine is also antagonized.
2) Antiallergic actions-Many manifestations of immediate hypersensitivity (type I reactions)are suppressed. Urticaria, itching and angioedema are well controlled.3) CNS action-The older antihistamines produce variable degree of CNS depression.But in case of 2nd gen antihistaminics there is less CNS depressant property as these cross BBB to significantly lesser extent.
4) Anticholinergic action- many H1 blockers
in addition antagonize muscarinic actions of ACh. BUT IN 2ND gen histaminics there is Higher H1 selectivitiy : no anticholinergic side effects
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Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
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Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
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Diabetes Discussion Dr. Shriniwas Kashalikar
- 2. KASHALIKAR
- 3. 1. Why intracellular glucose concentration is not determined instead of plasma glucose concentration? 2. If it is measured in experiments how does it correlate with the plasma glucose levels or what are the corresponding values? 3. Is not there intracellular starvation of glucose, if blood glucose is increased because of defective utilization?
- 4. 4. If there reduction in the carbohydrate and fat intake, would not it mean that there is proportionate increase in proteins? Would not it be detrimental to kidney? 5. What is the assurance that plasma glucose is not affected by variable absorption and variable excretion in faeces? 6. Would not the variable energy output affect the blood glucose (Without deterioration of glucose metabolism)?
- 5. 7. If the glucose intake is reduced, would not it deprive the normal stimulation of insulin secretion? Would it not be alright therefore to include normal (not excessive) sweet items in diet? 8. Why is the scientific stress management (pivotal in prevention and management of hundreds of disease conditions including diabetes ) not taught in all the education courses and on electronic media? 9. How many studies have correlated the stress and diabetes mellitus
- 6. quantitatively? 10. How many studies have correlated diabetic complications with the blood glucose levels? 11. Why don't the practitioners of allopathy study and use Ayurvedic remedies and pranayama in diabetes? DR. SHRINIWAS KASHALIKAR