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DEXA scan (dual-energy X-ray absorptiometry). Measures bone mineral density to evaluate bone strength and diagnose conditions like osteoporosis and osteopenia. The machine passes two distinct low-energy X-ray beams through your body; as these beams hit your skeleton, denser bones block more radiation while thinner bones let more pass through. By calculating the difference in radiation blocked between your soft tissue and bone, the detector precisely calculates your Bone Mineral Density (BMD) in g/cm2g/cm squared. T-Score Range -1.0 or higher = Normal bone density Between -1.0 and -2.5 = Osteopenia (low bone density, indicating a risk of developing osteoporosis) -2.5 or lower= Osteoporosis (significant bone thinning that requires medical evaluation and treatment). Z-Score Range Above -2.0: This is considered within the expected range for your age group. -2.0 or lower: This indicates below the expected range for your age group, meaning your bone density is significantly lower than your peers. .T-ScoreCompared to a healthy 30-year-old adult of your same sex (peak bone mass).Used to diagnose osteopenia and osteoporosis in postmenopausal women and men over 50.Z-ScoreCompared to an average person of your same age, sex, and weight/ethnicity.Used to identify unusual bone loss in children, premenopausal women, and younger men.The machine passes two distinct low-energy X-ray beams through your body; as these beams hit your skeleton, denser bones block more radiation while thinner bones let more pass through. By calculating the difference in radiation blocked between your soft tissue and bone, the detector precisely calculates your Bone Mineral Density (BMD) in g/cm2g/cm squared. (BY: PRESCRIPTIONCRACKER.COM & PHARMACO-STUDY) — DEXA SCAN FLASHCARD BY PRESCRIPTIONCRACKER.COM

NASH Clinical Research Network (CRN) – Fibrosis Staging: Component Stage Definition / Histologic Features Fibrosis (F) 0 No fibrosis 1a Mild perisinusoidal fibrosis in zone 3 (delicate, fine collagen) 1b Moderate perisinusoidal fibrosis in zone 3 (dense collagen) 1c Portal or periportal fibrosis only (without perisinusoidal fibrosis) 2 Combined perisinusoidal (zone 3) and portal/periportal fibrosis (corresponds to patient’s report) 3 Bridging fibrosis (portal–portal and/or portal–central) 4 Cirrhosis — NASH Clinical Research Network (CRN) – Fibrosis Staging (By: prescriptioncracker.com)

Component Score Definition / Extent Steatosis (S) 0 < 5% of hepatocytes involved 1 5–33% of hepatocytes involved 2 >33–66% of hepatocytes involved (corresponds to patient’s report) 3 >66% of hepatocytes involved Lobular Inflammation (L) 0 No inflammatory foci 1 4 foci per 200× field Hepatocellular Ballooning (B) 0 None 1 Few ballooned hepatocytes 2 Many ballooned hepatocytes / prominent ballooning (corresponds to patient’s report) NAS = Steatosis (0–3) + Lobular inflammation (0–3) + Ballooning (0–2) (Total range: 0–8.) Interpretation of total NAS: • ≤2 → Most consistent with no NASH. • 3–4 → Borderline / uncertain NASH. • ≥5 → Probable or definite NASH. — NAFLD Activity Score (NAS): by: Prescriptioncracker.com

Grading Feature Description Grade 1 (mild) Steatosis Up to 66% Ballooning Occasional in zone 3 Inflammation Intralobular inflammation: scattered polymorphs ± lymphocytes Portal inflammation Portal inflammation: no or mild Grade 2 (moderate) Steatosis Any degree Ballooning Obvious, predominantly zone 3 Inflammation Polymorphs and chronic inflammation noted Portal inflammation Mild to moderate Grade 3 (severe) Steatosis Panacinar Ballooning Ballooning and disarray obvious, predominantly in zone 3 Inflammation Scattered polymorphs ± mild chronic inflammation Portal inflammation Mild or moderate Staging Feature Description Stage 1 — Zone 3 perisinusoidal/pericellular fibrosis, focal or extensive Stage 2 — Zone 3 perisinusoidal/pericellular fibrosis + focal or extensive periportal fibrosis Stage 3 — Zone 3 perisinusoidal/pericellular fibrosis + portal fibrosis + bridging fibrosis Stage 4 — Cirrhosis — Brunt grading and staging criteria: (By: Prescriptioncracker.com)

What is the difference between NAFL, NASH and NAFLD? NAFL: Presence of ≥5% hepatic steatosis without evidence of hepatocellular injury in the form of: ·ballooning of the hepatocytes or ·evidence of fibrosis. Difference between NAFL, NASH & NAFLD: NAFL (non-alcoholic fatty liver) Presence of ≥5% hepatic steatosis without evidence of hepatocellular injury in the form of: • ballooning of the hepatocytes or • evidence of fibrosis. There is a low risk of progression of NAFL to cirrhosis and liver failure. NASH (non-alcoholic steatohepatitis) Presence of ≥5% hepatic steatosis with: • Inflammation and • hepatocyte injury (ballooning) • with or without fibrosis. This can progress to cirrhosis, liver failure, and rarely liver cancer. NAFLD (Non-alcoholic fatty liver disease) NAFLD is an umbrella term that includes the whole spectrum of fatty liver disease in the individuals without significant alcohol consumption, ranging from fatty liver to hepatic steatosis to cirrhosis. It means that NAFLD includes both NAFL and NASH. — What is the difference between NAFL, NASH and NAFLD? (BY: Prescriptioncracker.com)

Types of moisturizers (by: prescriptioncracker.com) 1. Emollients: use in Daily skin care routine, dry and rough skin, papulosquamous skin disease. Examples Dry emollients Isopropyl palmitate, isostearyl alcohol, decyl oleate Fatty emollients Propylene glycol, octyl stearate, glyceryl stearate, jojoba oil, castor oil Astringent emollients Dimethicone, cyclomethicone, octyl octanoate, isopropyl myristate Protective emollients Isopropyl isostearate, diisopropyl dilinoleate 2. Humectant: Used to attract water into stratum corneum. Frequently used with other compounds which may retain the water content. Often used with other ingredients in daily skin care products. other indications includes: Xerosis, ichthyosis. EXAMPLES Honey, sorbitol, glycerin, panthenol, urea, gelatin, hyaluronic acid, alpha hydroxy acids (glycolic acid, lactic acid, sodium pyrrolidine, carboxylic acid), propylene glycol and butylene glycol. 3. OCCLUSIVES: Consist of oils and waxes, forming an inactive layer on the skin surface to physically block water evaporation from the skin (transepidermal water loss). INDICATIONSPrevention of contact dermatitis, xerosis, atopic dermatitis eXAMPLES Petroleum jelly, paraffin, mineral oil, squalene, caprylic/capric triglyceride Stearic acid, lanolin acid Lanolin, cetyl alcohol, stearyl alcohol Lecithin Propylene glycol Cholesterol Candelilla, carnauba Beeswax, lanolin, stearyl stearate — Types of Moisturizers (by: prescriptioncracker.com)

Seven type of eczema observed in eczema patient: Atopic Dermatitis:Also known as atopic eczema, characterized by the presence of dryness, inflammation and itchiness (most common sign). Nummular Eczema Also known as discoid eczema, presents as single or multiple coin-shaped coin-shaped erythematous patches or plaques on the skin. Which can be dry, scaly, and itchy, and may ooze or crust over. Often confused with ringworm (fungal infection) but ring worm presents as ring like appearance with central clearance and unlike discoid eczema, spreads to other body parts as well. Contact Dermatitis Caused by contact of some allergen/irritant with the skin, leading to inflammation and itchiness . Seborrheic Dermatitis: Seborrheic dermatitis is characterized by the presence of red, greasy and inflamed skin covered with white or yellowish scales, affecting mostly oily areas of the body, such as the scalp, face (around the nose and eyebrows) and/or upper chest. often known as cradle cap in infants. Dyshidrotic Eczema: Also known as pompholyx, is a type of eczema characterized by the presence of small fluid filled itchy blisters on the edges of finger of hands and feet. Stress, allergens, excesive moisture due to improper working of immune system, improper sweating meachanism and seasonal allergies can be a reason behind dyshidrotic eczema. Neurodermatitis: Neurodermatitis is characterized by one or two patches of itchy skin that becomes more irritated when scratched, starting a cycle of itching and scratching often leading to thick, leathery patches of skin which can be triggered by stress or localized irritation. Stasis Dermatitis: Occur as a result of poor circulation in the legs which leads to the development of swelling, redness and itchiness with the skin turning dry, scaly and discolored over time. Ulcer may also develop in severe cases (Information by: Prescriptioncracker.com) — Seven type of eczema observed in eczema patients (By: Prescriptioncracker.com)

Appearance of eczema according to skin color of eczema patientslight to medium skin tones (it may appear as pink or red rashes with bumps and crust) medium to dark skin tones ( It may appear to be dark brown, gray or purple with dry, small bumps.) By: prescriptioncracker.com — Appearance of eczema according to skin color by: prescriptioncracker.com

Table describing ranges of C-reactive protein (CRP) levels and their associated clinical conditions, along with hsCRP cardiovascular risk categories. CRP < 0.3 mg/dL: Normal; typically seen in healthy adults CRP 0.3 to 1.0 mg/dL: Normal or minor elevation; may occur in obesity, pregnancy, depression, diabetes, common cold, gingivitis, periodontitis, sedentary lifestyle, cigarette smoking, and genetic factors CRP 1.0 to 10.0 mg/dL: Moderate elevation; associated with systemic inflammation such as rheumatoid arthritis, systemic lupus erythematosus, other autoimmune diseases, malignancies, myocardial infarction, pancreatitis, and bronchitis CRP > 10.0 mg/dL: Marked elevation; commonly seen in acute bacterial or viral infections, systemic vasculitis, and major trauma CRP > 50.0 mg/dL: Extreme elevation; typically indicates severe acute bacterial infection hsCRP (high-sensitivity CRP) for cardiovascular risk: < 1 mg/L: Low risk 1 to 3 mg/L: Moderate risk > 3 mg/L: High risk DO YOU KNOW WHY DOES CRP INCREASES BUT EST REMAINS NORMAL? FOR ANSWER VISIT: PRESCRIPTIONCRACKER.COM — Ranges of CRP as per conditions (by PRESCRIPTIONCRACKER.COM)

Erythrocytes Sedimentation Rate (ESR): The erythrocyte sedimentation rate (ESR) test is defined as test in which the time taken by red blood cells to settle at the bottom of the tube, is measured. ESR test is used for the detection of the inflammation in the body as during the inflammation the level of blood proteins increases such as fibrinogen (most prominent), beta-globulins, alpha-globulins, gamma-globulins and albumin (less prominent). High level of blood protein (particularly fibrinogen, accounts for 60-70% of the increase in ESR) promotes the aggregation of red blood cell which cause them to settle rapidly at the bottom of the tube. Table showing normal erythrocyte sedimentation rate (ESR) ranges by age and sex: Men under 50 years: 15 mm/hr or lower Women under 50 years: 20 mm/hr or lower Men over 50 years: 20 mm/hr or lower Women over 50 years: 30 mm/hr or lower Children: 10 mm/hr or lower. Table showing conditions associated with increased and decreased erythrocyte sedimentation rate (ESR). Elevated ESR values: Anemia; arteritis (e.g., giant cell arteritis); infections (including bone or joint infections, tuberculosis, endocarditis, and abscess); kidney disease; low serum albumin; systemic lupus erythematosus; lymphoma (including lymphoplasmacytic lymphoma); multiple myeloma and metastatic cancer; polymyalgia rheumatica; red blood cell abnormalities; rheumatoid arthritis and other inflammatory arthritis; systemic vasculitis; thyroid disease; vasculitis; crystal arthropathies Decreased ESR values: Polycythemia (increased red blood cells causing thicker blood); sickle cell disease; leukocytosis (increased white blood cells); heart failure; liver and kidney disorders. Medications can also affect ESR for example, both the oral contraceptive pill (OCP) and heparin increase sedimentation. — ESR (All about ESR) (BY PRESCRIPTIONCRACKER.COM)

Table showing changes in acute-phase proteins during inflammation, categorized by functional groups with proteins that increase or decrease. Complement proteins: Increased: C3, C4, C9, Factor B, C1 inhibitor, C4b-binding protein, mannose-binding lectin, properdin Decreased: Properdin Coagulation system proteins: Increased: fibrinogen, plasminogen, tissue plasminogen activator, factor VIII, urokinase, protein S, vitronectin, plasminogen-activator inhibitor 1 Decreased: factor XII Proteinase inhibitors: Increased: alpha-antitrypsin, alpha-antichymotrypsin, inter-alpha-trypsin inhibitors Decreased: none listed Transport proteins: Increased: ceruloplasmin, haptoglobin, haemopexin, ferritin Decreased: transferrin, transthyretin, thyroxin-binding globulin Other proteins: Increased: C-reactive protein (CRP), serum amyloid A, secreted phospholipase A, lipopolysaccharide-binding protein, interleukin-1-binding protein, interleukin-1 receptor antagonist, granulocyte colony-stimulating factor, alpha-acid glycoprotein, fibronectin, angiotensinogen Decreased: albumin, alpha-fetoprotein, insulin-like growth factor (BY: PRESCRIPTIONCRACKER.COM) — Acute-phase protein changes observed with inflammation (BY: PRESCRIPTIONCRACKER.COM)

unexplained hair loss and brain fogg (explained by prescriptioncracker.com) Causes of hair loss: Telogen effluvium-The most common form of hair loss occur 2-3 months post body stress due to serious infection, inflammation, prolong illness, surgery, and hormonal changes espcially after child birth Hair loss can be due to certain medications like: lithium, beta-blockers, warfarin, heparin, amphetamines, levodopa and especially anti-cancer medication like doxorubicin/adiramycin Hair loss can be due to medical illness such as : systemic lupus erythematosus (lupus), syphilis, a thyroid disorder (such as hypothyroidism or hyperthyroidism). it may also be due to nutritional deficiencies like: deficiency of protein, iron, zinc or biotin, occurs especially in people with dietary restriction or in female who suffers from heavy menstrual flow Tinea capitis is the fungal infection of scalp. it causes patchy hair loss and is most common in childen Alopecia areata is an autoimmune disorder that causes patchy hair loss in one or more areas. When this process causes complete loss of hair from the scalp it is known as alopecia totalis. — Causes of hair loss by prescriptioncracker.com

Why Triptans Work When Serotonin Fails: A Conflict backed by Magnesium-Driven Model of Migraine” Magnesium is a critical homeostatic ion that maintains vascular, platelet, and neuronal stability. Under physiological conditions, magnesium functions as a natural calcium antagonist, limiting calcium influx into platelets and neurons, stabilizing neuronal membranes, and tonically blocking NMDA receptor channels. It also indirectly supports serotonergic inhibitory tone within the trigeminovascular system. When magnesium deficiency develops, this multi-layered protective barrier is lost, initiating a cascade of interconnected events that culminate in migraine. At the platelet level, magnesium deficiency removes inhibition of calcium entry, leading to platelet hyperreactivity, aggregation, and degranulation. Activated platelets release stored vasoactive mediators, most notably serotonin (5-hydroxytryptamine, 5-HT), into the circulation. This serotonin release is abrupt, unregulated, and occurs primarily within the vascular compartment. Circulating serotonin preferentially activates vascular 5-HT₂ receptors, which are readily accessible from the bloodstream, producing transient vasoconstriction of cerebral and meningeal vessels. This early vasoconstrictive phase corresponds clinically to prodromal migraine features. However, platelet serotonin stores are finite. Following degranulation, serotonin levels rapidly decline due to depletion of platelet reserves, ongoing metabolism, and reuptake. Thus, migraine physiology is marked not by sustained serotonin elevation, but by a sharp rise followed by a pronounced fall in serotonin availability. This decline in serotonin represents a pivotal transition point in migraine pathogenesis. Under normal conditions, a steady background level of serotonin is present around the trigeminal nerves that supply the meninges (the coverings of the brain). This serotonin is not meant to trigger pain or pleasure here; instead, it acts quietly in the background to keep these nerves calm and under control. Serotonin does this by attaching to special receptors called 5-HT₁B and 5-HT₁D receptors, which sit on the endings of trigeminal sensory nerve fibers. These nerve endings are the same ones that release pain-producing chemicals during a migraine. When serotonin binds to these receptors, it sends a “slow down” signal into the nerve. Inside the nerve cell, this signal switches off pathways that normally make the neuron excitable. It lowers the level of chemical messengers that promote firing, reduces the entry of calcium into the nerve ending, and blocks the machinery that releases stored neurotransmitters. In simple terms, the nerve becomes less jumpy and less likely to fire. Because calcium entry is reduced, the nerve cannot easily release pain-related substances like CGRP and substance P. These substances are powerful migraine triggers because they dilate blood vessels, inflame surrounding tissues, and amplify pain signals. By preventing their release, serotonin keeps the trigeminal system quiet and helps stop migraine attacks from starting. So, under healthy conditions, serotonin acts like a protective gatekeeper. It doesn’t eliminate pain completely, but it sets a threshold that prevents harmless stimuli from turning into a full migraine. When serotonin levels drop or its signaling is impaired—as happens in menstrual migraine or magnesium deficiency—this inhibitory brake is lost, and the trigeminal nerves can easily become overactive, leading to CGRP release and migraine pain. When serotonin levels fall after platelet depletion, this inhibitory restraint is removed. Reduced stimulation of 5-HT₁B/₁D receptors leads to disinhibition of trigeminal neurons, allowing calcium channels to open more readily during neuronal activation. The loss of serotonergic control therefore indirectly enhances calcium influx into trigeminal nerve terminals. Simultaneously, magnesium deficiency directly increases neuronal calcium influx through independent mechanisms. Magnesium normally blocks NMDA receptors; its deficiency removes this block, leading to excessive glutamate-mediated excitatory signaling. Enhanced NMDA receptor activity depolarizes neurons and further increases calcium entry. In addition, magnesium deficiency reduces the threshold for activation of voltage-gated calcium channels, amplifying calcium influx during action potentials. Thus, magnesium deficiency promotes neuronal calcium overload through both direct ionic effects and indirect loss of inhibitory serotonergic control. Elevated intracellular calcium is the final common trigger for neurotransmitter and neuropeptide release. Increased calcium facilitates synaptic vesicle docking and fusion, resulting in exocytosis of CGRP and substance P from trigeminal nerve endings. CGRP is a potent vasodilator that produces sustained dilation of meningeal blood vessels, while substance P increases vascular permeability and plasma protein extravasation. Together, these neuropeptides initiate and sustain neurogenic inflammation, mast cell activation, and sensitization of peripheral and central trigeminal pain pathways. Clinically, this stage corresponds to the pain phase of migraine, characterized by throbbing headache, photophobia, phonophobia, nausea, and central sensitization. By this time, serotonin levels are already low, explaining why vasodilation and inflammation dominate rather than vasoconstriction. CGRP becomes the principal driver of migraine pain and associated symptoms. This integrated cascade also explains the apparent paradox between endogenous serotonin and triptan therapy. Platelet-derived serotonin released during magnesium deficiency is non-selective, short-lived, and largely confined to vascular receptors, failing to provide sustained inhibitory control over trigeminal neurons. In contrast, triptans such as sumatriptan are selective 5-HT₁B/₁D receptor agonists that directly restore inhibitory restraint at trigeminal nerve terminals. By re-inhibiting calcium channels and suppressing CGRP and substance P release, triptans abort migraine attacks despite low endogenous serotonin levels. In summary, magnesium deficiency initiates migraine by removing platelet and neuronal calcium regulation, triggering platelet aggregation and serotonin release followed by serotonin depletion, abolishing serotonergic inhibitory restraint on trigeminal neurons, enhancing glutamate-NMDA excitotoxicity, and directly increasing neuronal calcium influx. These converging mechanisms culminate in excessive CGRP and substance P release, producing neurogenic inflammation, vasodilation, and migraine pain. This unified model explains why magnesium supplementation is effective in migraine prevention, while triptans are effective in acute migraine termination. — Why Triptans Work When Serotonin Fails A Conflict backed by Magnesium-Driven Model of Migraine. by prescriptioncracker.com

Dietary fibres are of two types: soluble dietary fibre and insoluble dietary fibre (does not dissolve in water). Insoluble dietary fibre should be avoided during the active disease as they can irritate the already inflamed area of the colon and can also speed up the bowel movements that can aggravate the diarrhoeal condition. While soluble dietary fibre can be taken during active disease and for the maintenance of the remission Following is the list of insoluble dietary fibres that should be avoided during the active disease state. Wholemeal or granary bread Wholemeal rice e.g. brown rice and pasta High fibre cereals Sweetcorn, mushrooms, onions (especially raw), broccoli, cabbage, cauliflower Skins of fruits & vegetables e.g. Jacket potato skins (the edible skin of a potato that's baked or cooked with the flesh inside, acting as a natural "jacket" or vessel), peppers, tomatoes, cherries, grapes, dried fruit. Seed fruits should also be avoided Nuts, seeds and popcorn. Diary food item: Diary item like milk, yogurt, ice cream, custard and cheese are sometime intolerable for some patients especially during the active disease state, due to the presence of lactose in them. Avoiding these dairy items means avoiding major sources of calcium which can create bone health disorders. Thus, it is often recommended, to lactose intolerant patients, to include following food items in their diet as an alternative source of calcium: Low Lactose or Lactose Free milks and milk products. Rice, soya, or Oat milks fortified with calcium. Hard cheese instead of soft cheese may be tolerated better. Fatty and Spicy food: Fatty food (butter, fried food) as well as spicy food can irritate the already inflamed colon and can trigger the symptoms of ulcerative colitis so, such type of food should also be avoided. Other food triggers of ulcerative colitis: Artificial sugars and sugar alcohols like xylitol, sorbitol, mannitol, aspartame, sucralose, and saccharine should be avoid during active state of ulcerative colitis. Alcohol should be avoided Caffeinated beverages like tea, coffee, and energy drinks should be avoided. Processed foods containing certain additives like carboxymethylcellulose (CMC), polysorbate-80, carrageenan, maltodextrin, titanium dioxide, sulfites, and guar gum should also be avoided Eating red meat on daily basis have also shown to increase the risk of inflammation. So, in order to avoid the inflammatory attack, the patient should go for different protein sources like chicken, salmon and tuna fish, eggs and tofu etc. Though red meat can also be taken once in a week.

Soluble fibres are partially digested in the intestine which forms a sticky substance that aid in the formation of soft and formed stool without triggering the inflammatory attack. Soluble fibres include the following: • Oats e.g. Porridge, White rice and and white bread can be taken. • The body of fruits and vegetables e.g. peeled apples and pears, bananas, blended fruits, tinned fruit, peeled root vegetables such as carrots, parsnips, turnip Omega-3 PUFA rich foods like salmon and tuna fish, flaxseed oil and flaxseed meal are also encouraged to eat. Lactose free or low lactose dairy products can be used. Water, broth and low sugar electrolyte drinks can be taken in ulcerative colitis

nutrients required in migraine by prescriptioncracker.com

role of vitamin b12, b9 and iron

Drug (domperidone) Clinical Characteristics Nature Antidopaminergic Therapeutic Class Prokinetic/Antiemetic agents Mechanism of action Block dopamine receptors (D2 and D3) in periphery to produce prokinetic effect and in chemoreceptor trigger zone (CTZ lie just outside the BBB, regulates vomiting) to produce anti-emetic effect. It’s also increase the level of prolactin in the body. Indication Dyspepsia, indigestion, epigastric sense of fullness, epigastric pain, regurgitation, diabetic gastroparesis, nausea, and vomiting. Dosage forms availability Oral, injection, and rectal Dosage and administration guidelines Oral Adult Dose: for all indications 10-20mg orally 3-4 times a day 30 minutes before meal, maximum 80mg/day. Must reevaluate the need for continuation of treatment after every 4 weeks Precautions Renal impairment, Electrolyte disturbance, Elderly (>60yrs) Contraindications Prolactinoma, GI haemorrhage, perforation, obstruction, hepatic impairment or Cardiac Dysfunction Adverse drug reactions Ventricular arrhythmias, QT interval prolongation, Sudden cardiac death, Galactorrhoea, gynecomastia, or menstrual irregularities. Interactions Ketoconazole, ritonavir, erythromycin Facts ● Don’t Cross BBB so, less EPS. ● Not US FDA approved due to high cardiac toxicity. ● Approval in other countries is restricted to short durations and lowest effective doses, with warnings about ECG monitoring in high-risk patients. Common Brands ● Motilium/Pelton (TABLET+SYRUP) ● Motilium V/Domel/Pelton V (Domperidone Maleate) ● Domflash ORO (Oro dispersible tablet) ● Pelton-C (Domperidone + Cinnarizine) — Domperidone

Drug (ITOPRIDE) Clinical Characteristics Nature Antidopaminergic + Cholinergic agent (decreases AchE) Therapeutic Class Prokinetic/Antiemetic agents Mechanism of action Itopride is basically a dopamine D2 receptor antagonist which by antagonizing D2 receptors, also decreases the inhibitory effects of dopamine on acetylcholine (Ach) release. It also inhibits the enzyme AchE (that break down Ach) which increases the concentration of Ach. Thus, the overall result of the itopride administration is boost up in the level of acetylcholine (Ach) that leads toward the promotion of gastric motility, increases the lower oesophageal sphincter pressure, enhances gastric emptying and improves gastro-duodenal coordination. This dual mode of action of Itopride is exceptional, making it a unique choice among other prokinetic agents. Indication Functional dyspepsia such as nausea and vomiting, non-ulcer dyspepsia (chronic gastritis), sensation of bloating, early satiety, upper abdominal pain, or discomfort, anorexia, and heart burn Dosage forms availability Tablet (50mg or 150mg) and Capsules (150mg) Dosage and administration guidelines Oral Adult Dose: 50mg orally 3 times a day 30 minutes before meal, or 150mg OD (once daily) 30 minutes before meal maximum 150mg/day. Not recommended in children. Precautions As it increases Ach level thus can causes cholinergic effects Contraindications GI haemorrhage, perforation, obstruction, or in cases where GI motility is harmful. Adverse drug reactions Diarrhea, Constipation, increase saliva, nausea, dizziness, headache, tremor, abdominal pain Interactions Anticholinergic Drugs Facts ● Don’t Cross BBB so, less EPS. Itopride is hydrophilic and is a substrate of P-glycoprotein (P-gp), which actively pumps it out of the CNS. ● Not US FDA approved due to lack of manufacturer’s interest ● Approved in other countries for the above-mentioned indication. ● No Cardiac Toxicity. Common Brands ● ITP 50mg OR ITP OD (150mg) ● Emptin-OD 150mg and Emptin 50mg ● Ganaton 50mg and Ganaton OD 150mg ● Tespral 50mg — Itopride

Drug (Levosulpiride ) Clinical Characteristics Drug category Antidopaminergic (Antipsychotic due to BBB penetration) Therapeutic Class Prokinetic/Antipsychotic Mechanism of action Levosulpiride acts as a selective antagonist of dopamine D₂ receptors, both centrally (in the brain) and peripherally (in the gastrointestinal tract) also act on CTZ, thus ● Produces antipsychotic effect, Increases prolactin levels, potential EPS ● increases the acetylcholine level and promote GI motility. ● produces anti-emetic effect Indication Dyspepsia, Nausea, vomiting, vertigo, Inflammatory bowel syndrome (IBS), Schizophrenia, Tourette’s Syndrome, depression with or without anxiety Dosage forms availability Tablet (25mg and 50mg) and Capsules (25,50 and 100mg) Dosage and administration guidelines Oral Adult Dose: 50mg -200mg daily However the dose for CNS disorder may vary depending upon condition: Schizophrenia: 3-5mg/kg daily to children over 14 yr of age. Adults: Initially, 200-400mg twice daily, Maximum 1.2g BD if necessary, especially in the case of patients with positive symptoms and Up to 800mg daily in the case of patient with negative symptoms In case of patient with neither predominating, are given usual dose of 400-600mg bd. Tourette’s Syndrome: Adolescents14-18 yr: 200-400mg bd. Precautions Should be careful while giving it to manic or hypomanic patient, as it can exacerbate the symptoms in such patients. Contraindications Comatose, CNS depression, pheochromocytoma Adverse drug reactions Extrapyramidal effects, cardiovascular effects, hypotension, sleep changes, over stimulation and agitation Interactions Anticholinergic Drugs, Alcohol, CNS depressants, guanethidine, antacids, NSAIDs Facts ● Cross BBB have EPS. ● Not US FDA approved due to lack of manufacturer’s interest ● Approved in other countries for the above-mentioned indication. Common Brands ● Sulvorid 25 and 50mg ● Motivo 25 and 50mg ● Lusell 25 and 100mg ● Scipride 50mg ● Sowel 25, 50 and 100mg — Levosulpiride

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