DR MANISH-2.pdf laser proctology piles and fistula

Jan 27, 20250 likes19 views

Get the best piles and fistula treatment in Jaipur with advanced laser proctology techniques. Dr. Manish Rajput, a renowned specialist, provides painless, quick, and highly effective treatments for piles, fissures, and fistula. Using cutting-edge laser technology, the procedures ensure minimal discomfort, no stitches, and faster recovery, helping patients return to their daily lives with ease. Dr. Rajput is committed to offering personalized care and long-term solutions, ensuring lasting relief and improved quality of life. With his expertise and modern facilities, you can expect safe and reliable treatment for all proctological conditions.

D R M A N I S H
RAJPUT
ht t ps://dr manishr ajput .com
Bookan appointment!

IN T R O D U C T IO N
Dr
. Manish Rajput is an I
nterventional
Radiologist & Team Lead, Team I
R
Jaipur
. They are the biggest team of
I
nterventional Radiologists. They are
trained from Tata Memorial Center
,
Mumbai, I
ndia. They have worked in so
many government and corporate
hospitals across the country.

Medical school (MBBS):2005-2011: -People’s
Medical College, Bhopal(MP)
DNB (Radio diagnosis):
- Apollo hospital,
Hyderabad(Telangana)
FVIR (PDCC):- Tata Memorial Centre,
Mumbai(Maharashtra)
Senior Resident: Hinduja Hospital Mumbai, SMS
Hospital Jaipur
Past Visiting Doctor:Leelavati Hospital Mumbai,
Breach Candy Hospital Mumbai, Wockhardt
Hospital Mumbai, Hinduja Hospital Mumbai
Ex Assitant Professor:JNU Medical College, Jaipur
Currently Working as Senior Consultant
Interventional Radiologist in various corporate
hospitals of Rajasthan based in Jaipur
HIS
EDUCATION

S T R E N G T H S
Ilead the biggest I
R team in the state.
Vast portfolio for I
R services.
All the team members are from Tata
Memorial Hospital, Mumbai.
Extensive experience in performing and
interpreting basic Radio-Diagnosis.
Gained experience in performing
I
nterventional Radiologic procedures.
Ipossess oratory skill by speaking at
numerous industry events.
Ability to teach complex concepts in a basic
manner
.

Varicose Veins Prostate Artery Embolization PRG
Biopsy and
fNAC
Angioplasty & Venoplasty PCN & DJ Stenting
O
U
R
S
E
R
V
I
C
E
S

+91 7729021111
dr.manish@infinityintervention.com
O-5-A, Adinath Marg, Near Surya
Hospital, C Scheme, Ashok Nagar,
Jaipur, Rajasthan 302001
C ON TA C T
US!

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Autocoids mcq.ankush goyal gmc patiala punjab by Dr Ankush goyal, has 54 slides with 276 views.Lipid Autocoids: A Comprehensive Overview Introduction Lipid autocoids, also known as eicosanoids and related lipid mediators, are bioactive molecules derived from polyunsaturated fatty acids (PUFAs). These molecules play crucial roles in inflammation, immunity, hemostasis, cardiovascular function, and various physiological and pathological processes. Unlike classical hormones, lipid autocoids act locally, exerting their effects at or near their site of synthesis. This document provides an in-depth analysis of lipid autocoids, covering their biosynthesis, classification, physiological roles, and clinical significance. Classification of Lipid Autocoids Lipid autocoids are broadly classified into the following categories: 1. Eicosanoids (Derived from Arachidonic Acid) Prostaglandins (PGs) Thromboxanes (TXs) Leukotrienes (LTs) Lipoxins (LXs) 2. Specialized Pro-resolving Mediators (SPMs) Resolvins Protectins Maresins 3. Endocannabinoids Anandamide (AEA) 2-Arachidonoylglycerol (2-AG) 4. Platelet-Activating Factor (PAF) 5. Sphingolipid-Derived Mediators Sphingosine-1-Phosphate (S1P) Ceramides Biosynthesis of Lipid Autocoids Lipid autocoids are derived from membrane phospholipids through enzymatic pathways: 1. Phospholipase A2 (PLA2) Activation: PLA2 catalyzes the release of arachidonic acid (AA) from membrane phospholipids. 2. Cyclooxygenase (COX) Pathway: Converts AA into prostaglandins and thromboxanes. COX-1: Constitutive enzyme (housekeeping functions). COX-2: Inducible enzyme (inflammation and pain response). 3. Lipoxygenase (LOX) Pathway: Converts AA into leukotrienes and lipoxins. 5-LOX: Leads to leukotrienes (inflammation, bronchoconstriction). 12-LOX & 15-LOX: Lead to lipoxins (anti-inflammatory action). 4. Cytochrome P450 (CYP) Pathway: Converts AA into epoxyeicosatrienoic acids (EETs), which regulate vascular tone. 5. Endocannabinoid Biosynthesis: Derived from membrane phospholipids via enzymatic reactions. Degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Physiological Roles of Lipid Autocoids 1. Inflammation and Immune Response Prostaglandins (e.g., PGE2) modulate fever and pain. Leukotrienes mediate allergic responses and asthma. Lipoxins and resolvins promote resolution of inflammation. 2. Cardiovascular System Thromboxanes (TXA2) induce platelet aggregation and vasoconstriction. Prostacyclin (PGI2) inhibits platelet aggregation and promotes vasodilation. EETs regulate blood pressure and vascular homeostasis. 3. Pulmonary Function Leukotrienes (LTC4, LTD4, LTE4) are potent bronchoconstrictors. PGE2 has bronchodilatory effects. 4. Renal Function Prostaglandins regulate glomerular filtration rate and sodium excretion. EETs contribute to natriuresis. 5. Neurotransmission and Pain Endocannabinoids modulate pain perception and neuroprotection. Prostaglandins contribute to central pain sensitization. 6. Reproductive System P

Autocoids mcq.ankush goyal gmc patiala punjabDr Ankush goyal

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Lipid Autocoids: A Comprehensive Overview Introduction Lipid autocoids, also known as eicosanoids and related lipid mediators, are bioactive molecules derived from polyunsaturated fatty acids (PUFAs). These molecules play crucial roles in inflammation, immunity, hemostasis, cardiovascular function, and various physiological and pathological processes. Unlike classical hormones, lipid autocoids act locally, exerting their effects at or near their site of synthesis. This document provides an in-depth analysis of lipid autocoids, covering their biosynthesis, classification, physiological roles, and clinical significance. Classification of Lipid Autocoids Lipid autocoids are broadly classified into the following categories: 1. Eicosanoids (Derived from Arachidonic Acid) Prostaglandins (PGs) Thromboxanes (TXs) Leukotrienes (LTs) Lipoxins (LXs) 2. Specialized Pro-resolving Mediators (SPMs) Resolvins Protectins Maresins 3. Endocannabinoids Anandamide (AEA) 2-Arachidonoylglycerol (2-AG) 4. Platelet-Activating Factor (PAF) 5. Sphingolipid-Derived Mediators Sphingosine-1-Phosphate (S1P) Ceramides Biosynthesis of Lipid Autocoids Lipid autocoids are derived from membrane phospholipids through enzymatic pathways: 1. Phospholipase A2 (PLA2) Activation: PLA2 catalyzes the release of arachidonic acid (AA) from membrane phospholipids. 2. Cyclooxygenase (COX) Pathway: Converts AA into prostaglandins and thromboxanes. COX-1: Constitutive enzyme (housekeeping functions). COX-2: Inducible enzyme (inflammation and pain response). 3. Lipoxygenase (LOX) Pathway: Converts AA into leukotrienes and lipoxins. 5-LOX: Leads to leukotrienes (inflammation, bronchoconstriction). 12-LOX & 15-LOX: Lead to lipoxins (anti-inflammatory action). 4. Cytochrome P450 (CYP) Pathway: Converts AA into epoxyeicosatrienoic acids (EETs), which regulate vascular tone. 5. Endocannabinoid Biosynthesis: Derived from membrane phospholipids via enzymatic reactions. Degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Physiological Roles of Lipid Autocoids 1. Inflammation and Immune Response Prostaglandins (e.g., PGE2) modulate fever and pain. Leukotrienes mediate allergic responses and asthma. Lipoxins and resolvins promote resolution of inflammation. 2. Cardiovascular System Thromboxanes (TXA2) induce platelet aggregation and vasoconstriction. Prostacyclin (PGI2) inhibits platelet aggregation and promotes vasodilation. EETs regulate blood pressure and vascular homeostasis. 3. Pulmonary Function Leukotrienes (LTC4, LTD4, LTE4) are potent bronchoconstrictors. PGE2 has bronchodilatory effects. 4. Renal Function Prostaglandins regulate glomerular filtration rate and sodium excretion. EETs contribute to natriuresis. 5. Neurotransmission and Pain Endocannabinoids modulate pain perception and neuroprotection. Prostaglandins contribute to central pain sensitization. 6. Reproductive System P

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Disorder of Parathyroid Gland Hyperparathyroidism Hyperparathyroidism is hypersecretion of PTH. Classification Hyperthyroidism is classified in to two 1. Primary hyperparathyroidism. 2. Secondary hyperparathyroidism. Primary Hyperparathyroidism • Primary hyperparathyroidism is a relatively common disorder, affecting approximately 2% of the population over 55 years of age. • It most commonly affects post-menopausal women, with women having a 2 to 3 times greater risk of developing primary hyperparathyroidism than men. Cause:  It typically results from a single adenoma, but may also result from multiple adenomas, hypertrophy of the parathyroid glands, carcinoma, radiation to the neck, lithium use.  Hereditary factors: such as multiple endocrine neoplasia (MEN) types I and II.  The autonomous hypersecretion of PTH in primary hyperparathyroidism results in hypercalcemia, which, together with elevated or sometimes normal PTH levels without an underlying stimulus is diagnostic for this disease.  Other common causes of hypercalcemia, such as cancer, would result in depressed PTH levels. • Primary hyperparathyroidism is usually incidentally found in the early stages of the disease on routine bloodwork, demonstrating an increased serum calcium level. • Most patients are asymptomatic at diagnosis or have non-specific symptoms such as weakness, fatigue, mental fogginess, anxiety, depression, gastroesophageal reflux, or bone pains. Patients who present at later stages may have symptomatic hypercalcemia with severe bone disease, nephrolithiasis, neuromuscular dysfunction, gastrointestinal problems, or cardiovascular disease. • Rarely, a volume-depleted patient with primary hyperparathyroidism may present in hypercalcaemic crisis secondary to a rapid spike in serum calcium level that may lead to dangerous cardio and neurotoxicity, renal impairment, and gastrointestinal dysfunction Secondary Hyperparathyroidism • Unlike primary hyperparathyroidism, which is characterized by inappropriate secretion of PTH, secondary hyperparathyroidism occurs as an appropriate reaction to a stimulus that induces the secretion of PTH from the parathyroid glands. • In secondary hyperparathyroidism, PTH is synthesized and secreted in response to chronically low serum calcium levels, which may result from malabsorption of calcium from the GI tract, vitamin D deficiency, renal insufficiency, or medications such as thiazide diuretics. • On bloodwork, this would appear as a low to normal serum calcium level with an elevated PTH level; this differentiates secondary from tertiary hyperparathyroidism, which results when secondary hyperparathyroidism progresses, and the parathyroid become overwhelmed and start producing PTH semi-autonomously without proper stimulation. • When this occurs, hypercalcemia ensues, and bloodwork results appear similar to those with primary hyperparathyroidism. • The difference between primary and tertiary hyperparathyroidism is that tertiarHypoparat

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