Med-IQ 2nd Year

Feel free to check out the discussion on how you can start your preparation for FMGE, what are some realistic strategies and the best resources. I have shared some of my strategies and ideas on how to approach it. Hope it helps! ❤️ https://youtu.be/K0wRvdIVvyM?si=YFn7BQbJf073_DTe

https://youtu.be/B9K2AooO94o?si=xCV0KdbAzRDS7ttY

Learn the basics of pharmacokinetics! ADME!💊 The ADME (Absorption, Distribution, Metabolism & Excretion) of drugs is one of the crucial concepts that you will need to understand to transition from biochemistry to pharmacology. This concept helps you understand the various biochemical factors that affect a drug's behaviour in the human body. It helps one decide the dosage, administration and factors that one must consider before giving a drug. I hope this video helps✨ https://youtu.be/Oi7uDTNH4EE?si=V6PCDHSG-9d3crsH

PATHOLOGY OF ISCHEMIC HEART DISEASE: https://youtu.be/Cq39-_yF6GQ?si=dX73t9I5RDnERApv

https://youtu.be/Vg6-0a7y4aE?si=yqAIU90w5TLs7hMD

Good evening, Here's the link to the 3rd year IMD 25 (Med-IQ) resources/mcqs/notes group. https://t.me/+0VL2Z1kyYe82YTJl We'll be continuing the trend of posting mcqs, notes etc whenever possible. But this time we need many to participate as we all have different subjects/modules at different times. The group has separate topics according to our section wise modules in which we can post content related to your module. So for ex. Sec A people can post in pedia, Sec B people in commed etc, Sec C in ob/gyn and Sec D in Surgery. And when module changes we can use the other already created topics and add more. Let's help each other out like we've all been doing for the past 2 years. Feel free to share notes, tips, mcqs from your module whenever you can ❤️ Thank you 😇

And the year comes to an end...✨ Thank you for your constant support medicos!!! ❤️ Here's to being Happy, Learning every step of the way and Working together in the following year. Let's strive to become the best version of ourselves every single day. 🔥 Wishing you all a blessed and a very Happy New Year!!! ✨❤️

Pharmacokinetics & Pharmacodynamics Basics Pharmacokinetics - ADME of drugs Modes of transport - active & passive Passive transport - m/c route for drugs (simple diffusion) Ionized drug - has charge - cannot enter cell - non absorbable Non-ionised drug - neutral - can enter cell - absorbable Lipophilic - lipid loving - can enter cell through lipid bilayer membrane Polar compounds - ionic compounds - non absorbable -> easily excreted Weak acid best absorbed in acidic medium - stomach Weak base best absorbed in basic medium - intestine Tx of drug poisoning - excretion of drug is hastened by alkalinization (if acidic drug poisoning) or acidification (if basic drug poisoning) of urine Bioavailability (F) - fraction of unchanged drug that enters systemic circulation after administration and becomes available to produce action (F) IV = 1 (F) SQ/IM = 0.75 to 1 (F) Oral = 0.05 to 1 Bioequivalence - two related drugs that have comparable bioavailability and similar times to achieve peak blood conc Therapeutic equivalence - two similar drugs that have comparable efficacy and safety Drug receptor interaction: 1. Agonist - primary (same site), allosteric (diff site) 2. Partial agonist - submaximal effects 3. Antagonist - syntopic (same site), allosteric (diff site), chemical (combines with agonist), functional (indirect) 4. Competitive antagonist - reversible binding 5. Non competitive antagonist - irreversible binding ED50 - dose of drug required to produce a specified effect in 50% of the population LD50 - dose of drug required to cause death in 50% of the population; experimental animals Therapeutic index = LD50/ED50

Complete GI pharmacology short notes Topics: 1. GERD 2. Peptic ulcer 3. IBD - Crohn’s, UC 4. Motility disorders

📍Endocrine Androgens 1. Testosterone - principal secreted androgen Leydig cells - majority Androstenedione, dehydroepiandrosterone - weak androgens 2. 1st trimester - fetal testes 3. DHT - binds with higher affinity to androgen R compared w/testosterone 4. Testosterone —-> DHT = 5alpha reductase Type 1 - nongenital skin, liver, bone Type 2 - urogenital tissue in men, genital skin 5. Testosterone —-> estradiol = Aromatase 6. Ingestion of testosterone - not an effective means of replacing testosterone deficiency 7. Alkylated androgens - hepatotoxicity 8. Blood dyscrasias - Danazol 9. Androgen receptor antagonists - Flutamide - treat hirsutism in women Bicalutamide Nilutamide 10. Spironolactone - weak inhibitor of aldosterone, androgen R Gynecomastia - s/e 11. 5 alpha reductase inhibitor Finasteride - type II Dutasteride - both type I and II 12. PDE5 inhibitors - erectile dysfunction Sildenafil, vardenafil - blue green tinting of vision - inhibition of retinal PDE6 CI - patients receiving organic nitrates

📍Endocrine Estrogen & Progesterone 1. Naturally occurring - Progesterone 2. Drosperinone - derived from spironolactone 3. Estrogen produced by - developing follicles in ovaries, corpus luteum (2nd half of menstrual cycle), placenta Other tissues - liver, adrenal glands, breasts 4. Principal source of circulating estrogen - ovary Main secretory product in - - Premenopausal women - Estradiol - Postmenopausal women - Estrone 5. Estrogen - Control amplitude of gonadotropin pulses Rebuilding of endometrium Increase HDL, decrease LDL and lipoprotein A Decrease number and activity of osteoclasts Progesterone - Predominant control of frequency of LH surge Decreases firing rate of hypothalamic pulse generator Important for maintenance of pregnancy Suppresses menstruation and uterine contractility Increase LDL 6. GnRH suppression - major MOA of progestin-containing contraceptives 7. Lactation begins once levels of Estrogen and progesterone decrease at parturation 8. 2 estrogen receptor genes- ESR1 - ER alpha ESR2 - ER beta Er-alpha - Most abundant in female reproductive tract Predominant in breast cancer Er-beta- Prostate and ovaries does not contain AF-1 domain 9. PR-B - longer with additional AF-3 stimulatory activities of progesterone PR-A - inhibits action of PR-B 10. Estrogen SERM - Tamoxifen, Raloxifene, Toremifene Anti-estrogens - Clomiphene, Fulvestrant Estrogen synthesis inhibitors - Steroidal - Formestane, Exemestane Non-steroidal - Anastrozole, Letrozole, Vorozole 11. Clomiphene - treatment of infertility Fulvestrant - treatment of breast cancer 12. All oral except - Fulvestrant (IM depot) 13. early and advanced Breast cancer - Tamoxifen Osteoporosis - Raloxifene Tamoxifen resistant breast cancers - Fulvestrant 14. PRM- Mifepristone - competes with both progesterone and glucocorticoids for binding with their respective receptors Used to terminate pregnancy w/ misoprostol Ulipristal - selective PR modulator, partial agonist at PRs inhibit ovulation 15. Monophasic contraceptive - fixed amounts of P and E 21 days followed by a 7 day pill free period 16. Endometriosis First line - combined oral contraceptives 17. Add back therapy - low dose synthetic estrogen, or a high dose progestin 18. Finasteride - inhibitor of type 2 isoenzyme of 5alpha reductase Danazol - rarely used due to hirsuitism

Pharmacology Short Notes (Drug tabulation) Drugs affecting renal excretory function 💧 All the best ❤️

Pharmacology Hypnotics and Sedatives 😴😵‍💫 1. Major therapeutic use — relieve anxiety or induce sleep 2. Sedatives/Anxiolytics — among the most prescribed substances worldwide 3. Pathophysiology of anxiety — autonomic balance, decreased GABA-ergic tone, allelic polymorphism of COMT gene, increased adenosine receptor function, increased cortisol, decreased benzodiazepine receptor function, disturbances in serotonin 4. Anxiety stimulants — Amphetamines, cocaine, TCAs, caffeine 5. Miscellaneous cause — Baclofen, cycloserine, hallucinogens, indomethacin 6. Strategy for treatment — reduce anxiety without causing drowsiness 7. Hypnotics should produce a state of sleep that resembles normal sleep 8. Hypnotics in sleep - latency of sleep decreased (time to fall asleep) stage 2 NREM increased REM decreased Slow wave sleep - decreased Tolerance - after 1-2 weeks 9. Benzodiazepines - FAT Short action - Triazolam Intermediate - Alprazolam Long - Flurazepam 10. Barbiturates - Ultra short - Thiopental Short - Secobarbital Long - Phenobarbital 11. Hypnotics -- depress CNS to stage III of anesthesia 12. MOA - Barbiturates - Activate GABA a receptor complex, increase duration of GABA R channel opening Benzodiazepines - Increase receptor affinity for GABA, increase frequency of openings of GABA R channel. Safer than Barbs. 13. GABA-A receptor Cl- channel 14. Barbiturates - more potential for abuse Benzodiazepines - most important sedative/hypnotic 15. Preferred drug for short term insomnia - Benzodiazepines 16. Diazepam, Lorazepam - used to control life threatening seizures in status epilepticus, tetanus, drug induced convulsion, febrile convulsion 17. Clonazepam - absence seizures 18. All benzodiazepines cross placenta 19. Benzodiazepines overdose treated with - Flumazenil (BDZ receptor antagonist) Flumazenil not effective against barbiturates overdose 20. Phenobarbital is excreted unchanged 21. Phenobarbital and meprobamate - autometabolism by induction of liver enzymes 22. Barbiturates contraindication - Porphyria 23. Melatonin - circadian signalling molecule produced by pineal gland MT1 receptor - sleep MT2 receptor - shifts timing of circadian rhythm Ramelteon - binds to both MT1 and MT2 - chronic and transient insomnia Tasimelteon - blinds pts w/circadian rhythm disorder 24. Most selective anxiolytic - Buspirone Partial agonist at 5-HT1A receptor - inhibit serotonin release presynaptically 25. Meprobamate Bis carbamate ester - may cause gastric bezoars 26. Inhibitor of orexin 1 and 2 receptor - Suvorexant 27. Agomelatine - melatonin receptor agonist, 5HT2C receptor antagonist

COMPRE Revision - Additional Pointers Pulmonary edema - excessive interstitial fluid in the alveoli 1. Increased hydrostatic pressure - left sided heart failure (m/c), pulmonary vein obstruction 2. Decreased oncotic pressure - hypoalbuminea, nephrotic syndrome, liver disease 3. Lymphatic obstruction 4. Direct injuries - bacterial pneumonia, liquid aspiration 5. Indirect injuries - systemic inflammatory response syndromes Pulmonary embolism - blood clots obstructing large pulmonary arteries 1. M/c source of blood clot - deep veins of legs 2. Due to thrombophilia 3. Recurrent embolism can cause pulmonary hypertension & cor pulmonale Mallory-Weiss tears, are most often associated with severe retching or vomiting secondary to acute alcohol intoxication. Longitudinal mucosal tears near the gastroesophageal junction. 1. Alcoholism 2. Frequent vomiting 3. Hematemesis Gall bladder disorders 1. Biliary atresia - seen in infants within 2 months of life, presents as jaundice and progresses to cirrhosis 2. Cholelithiasis - gall stones, precipitation of cholesterol or bilirubin 3. Biliary colic - waxing & waning right upper quadrant pain 4. Acute cholecystitis - acute inflammation of gallbladder wall 5. Chronic cholecystitis - rokitansky askchoff sinus herniation of gallbladder mucosa into muscular wall 6. Gall bladder carcinoma - adenocarcinoma from glandular epithelium, gall stones major risk factor

COMPRE revision notes - PART 3 Topics: 1. Inflammation (acute vs chronic) 2. SLE 3. Tissue response to injury

COMPRE revision notes - PART 2 Topics: 1. Tumor suppressor genes 2. HIV 3. Hepatitis 4. Tumors

COMPRE revision notes - PART 1 Topics: 1. Thyroid tumors 2. Cushing’s & addisons 3. Sprue 4. Hodgkin’s lymphoma 5. Kimmelstiel Wilson disease

Genetics 2 - Pediatrics - Important points 🧬 Maple syrup urine disease - AR, defect in branched chain ketoacid dehydrogenase, accumulation of leucine, isoleucine and valine in brain, classic MSUD is most common and severe PKU - AR, defect in phenylalanine hydroxylase or tetrahydrobiopterin metabolism, phenylalanine accumulation, seizures & mental retardation Homocystinuria - AR, cystathionine synthase deficiency, Ectopia lentis, marfanoid habitus Ornithine transcarbamylase deficiency - m/c inborn error of urea synthesis, X linked dominant, hyperammonemia FAOD - fatty acid oxidation disorders - hypoglycemia, hypo ketosis, acidosis, encephalopathy etc MCAD - medium chain acyl coa dehydrogenase deficiency - m/c FAOD GAL - galactosemia - AR, galactose accumulation G6PD - most common enzymopathy, destruction of RBCs, jaundice & kernicteru, normal value > 2U/g Hb, infection -> hemolysis (Hep A, B, CMV, pneumonia & typhoid fever) Only glycogen storage disease that is X linked is Hers disease (type VI) due to liver phosphorylase deficiency. All the other GSD are AR. Only mucopolysaccharidoses that is X linked is Hunter syndrome (type II) due to defect in iduronate sulfatase enzyme. All others are AR. ZWS - Zellweger syndrome - PEX1 gene mutation, cerebrohepatorenal syndrome, high in VLCFA Rhizomelic chondrodysplasia punctata - AR PEX7 gene, GNPAT gene & AGPS gene, normal VLCFA, error in plasmalogen synthesis X lined adrenoleukodystrophy - ABCD1 gene, only in males, high VLCFA