High Anion Gap Acidosis ‘© Common cause: Ketoacidosis (Starvation, Diabetic, Metabolic) keto acids are anionic ‘© Lactic acidosis (accumulation of lactate) © Uremia ‘© Toxins (Salicylate, Ethylene Glycol, Methanol) © Rare causes: Hypomagnesaemia, hypokalemia, hypocalcemia Decreased Anion Gap Acidosis ‘© Hypoalbuminemia, Multiple myeloma Gibbs Donnan Equilibrium/Donnan membrane equilibrium Unequal distribution of diffusible ions across a selectively permeable membrane because of presence of non- diffusible ion (proteins) in one of the compartments. CSF chloride concentration is higher than plasma chloride Protein concentration of CSF is lesser than that of plasma. To maintain the donnan membrane equilibrium [CI is increased. Increased CSF protein seen in TB meningitis is associated with decreased CSF chloride levels. Buffer systems of blood (Aug 2008) Buffer system constituents (conjugate base/conjugate acid) Bicarbonate bulfer HCO; 7H,C0,(CO,)pKa= 6.1 Plasma protein buffer | Protei/Protein-H Haemoglobin buffer To/Hb-H Phosphate buffer HPO PO; Plasma oncotic pressure Oncotic pressure or colloid osmotic pressure is the osmotic pressure exerted by plasma proteins. Normal value:280-295 mosmolkg Clinical significance: Albumin is the major plasma protein and major determinant (80%) of oncotic pressure, Albumin retains water and electrolytes in vascular compartment. Hence Hypoalbuminemia leads to edema. Structure of Amino Acids and Proteins Dietary) Essential Amino Acids (Feb 10, 14) (Aug 05, 10) ‘These amino acids can’t be synthesized in our body and should be provided in diet 3 Branched chain AA~+ LIV — Leucine, Isoleucine & Valine 3 Basic AA (Feb /2)HAL—Histidine®, Arginine®& Lysine © 2 Aromatic —+ Phenylalanine & Tryptophan Threonine © Methionine * Histidine & Arginine are semi-essential amino acids. Aysiweyso0ig4. Gas chromatography: mobile phase is gas, b, iquid chromatography: mobile phase is liquid, In High Performance Liquid Chromatography (APLC), stationary phase used is small diameter finely divided particles IL Based on the mechanism of separation: |. Partition chromatography 2, Adsorption chromatography 3. Ion — Exchange chromatography Gel filtration chromatography Affinity chromatography High performance liquid chromatography Affinity Chromatography % 12) Affinity chromatography is @ purification technique based on the highly specific interactions such as Antigen-Antibody, Enzyme-Substrate, Receptor-ligand interactions. Reversible nature ofthis interaction is helpful in elution, Substance to be purified is in the mobile phase. Stationary phase contains the affinity ligand for the substance to be separated a Mobile phase Stationary phase 3 . sacoary 8 Lectins Carbohydrates a Receptor Ligand a Enzymes Subscats, substrate analogues cofactors, nkibitors 3, Hindi tagged recombinant protein “NE a ugged recombinant protein Glutathione 3 DNA cDNA GST tag affinity chromatography uses the affinity between glutathione & the enzyme Glutathione S-transferase (GS1), Recombinant proteins tagged with GST can be easily separated from cel extract, GST tagged proteins bind tothe glitathione ligand covalently attached to the agarose beads. Elution is done by adding ‘Sorat msn, excess ghitathione Sina se oot rase Electrophoresis (Aug 09, 12, 14) (Feb 11, 12, 13) St @ suntine 6 a Soy SS" @- ete os 6 Electrophoresis is movement of charged particles insolation . ander the influence of an electric ied Q Formula for velocity () of migration ofthe molecule i, Seer V=Eqit ctoin | gators = electric field in volts/em " q=net electric charge on the molecule I~ frictional coefficient which depends upon the size & shape of the molecule sannon-cst_2 sion oyFirst MBBS Solved Question Papers 24 ‘Negatively charged 2, 3 BPG binds to positively charged amino acid residues (Histidine H21, Lysine EF6) ‘of B chain in the central cavity of deoxyHb. This stabilises the deoxyHb in ‘T” slate & shifts the ODC curve to right favouring unloading of oxygen to tissues. In lung, 1 pO,tesults inT R transition & release of 2, 3 BPG from central cavity. 12,3 BPG levels 12,3 BPG levels Hypoxic conditions: ‘Stored blood High altiude Diabetes Melitus Severe anaemia Hypophosphat Congenital Heart diseases Smokers ‘Chronic lung diseases Buffering action of hemoglobin — Haldane effect Carboxy group of Hb binds to H° and buffer their levels. When Hb lases 02, it becomes a stronger base or weaker acid, making more sites available to buffer H°-This ability of Ho to neutralize (buffer) more H’, as it releases oxygen is termed the Haldane effect. Chloride shift(Hamburger phenomenon) (Aug 08) In the venous side of capillaries, CO, enters the RBCs from tissues + Production of H,CO, inside RBCs —> Dissociation into H'& HCO3—> His buffered by deoxyHb —HCOS- comes out of the RBCs to blood via band 3 protein —>To maintain electrical neutrality most abundant anion (chloride) of ECF goes inside RBCs via the same band 3 anion exchanger of RBC membrane, (Draw a diagram..) Importance: As a result of chloride shift, total number of ions increases inside RBCs causing osmotic absorption of fluid inside RBCs. Adaptation to high altitude (Feb 15) The fraction of ©, in inhaled air is same in high altitude as that of sea level. But the density of ai is lesser This leads to reduced partial pressure of oxygen in alveolar air(pAO,) —> | hemoglobin saturation. Short-term acclimatisation: ‘© Hyperventiation © 12,3.BPG levels due to 7 pd ‘hemoglobin saturation—+ 1 deoxy Hb —-more binding of H’— 1 pH Longeterm acclimatisation: © erythropoietin —+ Polycythaemia Molecular basis of high oxygen affinity of HbF 21 residue of helix H of y chain is non-polar serine instead of histidine. As a result, 2,3 BPG can’t bind to y chain of HDF. So affinity of HDF to oxygen is high and P., value is low. This is why oxygen is transported in placenta from maternal circulation to fetal circulation not the vice versa ‘Thalassemia(Feb 12) ‘Thalassemia isa disorder of quantitative defect in globin chains. Defect in a chain gene in chromosome 16 leads to « thalassemia, Defect in B chain gene in chromosome 11 leads to thalassemia, Instead of usual of 2 copies, « chain is coded by 2 copies of gene. Therefore 4 alleles are present for « chain. Fetal hemoglobinGlutamate is the actual source of all the nitrogen of urea Glutamate on oxidative deamination by glutamate dehydrogenase produces NH, Transfer of amino group of glutamate to oxaloacetate produces aspartate. So it is glutamate which isthe actual source of al the nitrogen of urea, CPS Tvs. CPS II (Feb 10) [ rst [Eocation Mioctondia [Pathway vor Urseeele Pyrimidine Bonies Souee oi Ni Free NH icatcd om aaa dei rones® | Gaming [ Regataed by NAcc Gita [ es Ne Arginine can be synthesised in our body to some extent Partial urea cycle that operates in nonshepatic cells can synthesize arginine to some extent. This is not sufficient during growth burst, pregnancy & breast feeding and itis necessary to supplement arginine in diet So arginine isa semicessential amino aci. NH, is toxic to brain (Aug 05) ‘© Excess NH, shifts the equilibrium of glutamate dehydrogenase reaction towards formation of slutamate, This depletes «KG and impairs TCA cycle ‘© Glutamate binds to NH, to produce glutamine by glutamine synthetase. © This reaction causes depletion of ATP. © Reducesbrainpoolof Glutamate which leadsto decreased formation ofinhibitory neurotransmitter GABA. Aysiweyso0ig Fate of Carbon Skeleton Sources & Fate of Acetyl-coA (Apr 01) (Feb 05, 09) ei | ketogei inte Ft act dton src i / [Acetyicok] ——+ entre / worn fla meh \ = Malonylcon orl Kelone bodies (Fatty acid synthesis), 206,Methanol poisoning is treated by ethanol Formaldehyde produced from methanol is highly toxic. Ethanol competes with methanol for the enzyme alcohol dehydrogenase and inhibit HCHO production. Vitamins Ring structures present in vitamins A Beionone D CPP ring of roids E Tocopherol K Nephthoguinone ‘Alle rings oF A, D. BE & K ae derivatives of prone B, thiazole ring 2, isoalloxazine Folate Peidine ring + glutamate 3, Contin oD Vitamer 8 Simi frms of same vain having biologi ivi, z Vit K:Menaquinone, Menadione 3 Certain vitamins are synthesised by the body a Vit D&Niacin él Certain vitamins are synthesised in the body by intestinal flora Vit K& Biotin Wald’s visual cycle (Feb 08, 09) desi Rhodopsin (opsined-cis-rtinal Z /- coin = ~~ RPE Ancistetinal Sel,» _albtrans-etinal a (Wc) mee 2 ene liver 1cistetinol ES —+ alttransretinl 89 ‘Wald’s visual cycle explain the mechanism of regeneration of active 11-cis retinal from inactive all-trans retinal, Regeneration ean happen either of the 2 mechanism 1. Isomerisation in the Retinal pigment epithelium itselfFirst MBBS Solved Question Papers 96 FIGLU excretion test (Histidine load test¥) for folate deficiency (Aug 10, 11*) (Feb 13) sm aie termina (leet il) Mee zed aca THA Sermo TW ‘-formimino glutamate (FIGLU) is @ molecule formed during the catabolism of Histidine, one ofthe donors of one carbon groups. Tetrahydro folate (THEA) isthe acceprorof formimino group from histidine. I folic acid is deficient, this one earbon transfer won't happen & FIGLU will be exereted inthe urine. ‘ FIGLU excretion following a load of histidine indicates folate deficiency. Now a days exact measurement of serum folate levels are done by methods like eletrochemilumines- Deficiency of one vitamin can lead to deficiency of the other Essential amino acid tryptophan can be converted into the vitamin Niacin (B,) in our body. Kynureninase, ‘one of the enzyme involved in this pathway is PLP dependant, Thus deficieney of B6 can lead to deficiency ofB, Coenzyme role of Pyridoxine Pyridoxal 5'-phosphate (PLP) is the coenzyme form of pyridoxine. It is usually tightly attached (prosthetic group) tothe enzyme via Schiff base formed between the aldehyde group of PLP and c-amino group of lysine of the enzyme. PLP serves in a wide variety of chemical reactions like decarboxylation, transamination, racemization, elimination, replacement, and f-group interconversion. In addition to its maia role in amino acid metabolism, PLP plays a role in carbohydrate & Lipid metabolism also. Aldehyde group of PLP forming a Schiff base is the basis of cofactor in catalysis. But in Glycogen, Phosphorylase reaction, itis the phosphate group that plays te role, ‘Therapeutic role of Pyridoxine Treatment of pellagra Prevention & treatment of INH (isoniazid) toxicity Copper chelating agent penicillamine increases the risk of pyridoxine deficiency. So itis supplemented in patients of Wilson’s disease treated with penicillamine. 4, High doses of B, may help to activate cystathionine B synthase enzyme in patients of homocystinuria tain cases of X-linked sideroblastic anemia respond to B, Pyridoxine dependent seizures in infants won't respond to any anticonvulsant therapy except Pyridoxine Causes of Pellagra 1, Decreased intake of B, 2. Maize (com) is used as staple food — Niacin isin bound form, and hence unavailable. 3, Songhum (jowar) is used as staple food -» High amount of leucine inhibits the uptake of tryptophanLactic Acidosi Lactic acidosis is accumulation of lactate and protonsas lactic acid dissociates in physiological pH. Tapes ‘Type A: duct to tissue hypoxia and consequent anaerobic glycolysis ‘Type B: Hereditary & acquired causes ‘© Diabetes, renal failure, sepsis, leukemia Glycogen storage disorders Methyl malonic academia Drugs: Biguanide drugs (Phenformin & metformin), salieylates Poisons: Methanol, ethanol ‘Treatment: coreet the underlying defect Metabolic Alkalosis (Feb 14) Increase in blood pH1>7.4S due to primary inerease in bicarbonate levels Alkalosis may develop due to, © Addition of base Exogenous — NaHCO, administration, Citrate in transfused blood © Endogenous excess regeneration of HCO during recovery from organic acidosis © Loss of acid © Via kidney ~ diuretics, © Via GIT—Loxs of HCI by vomiting, Nasogastrie aspiration Chloride depletion leads to alkalosis: Chloride and bicarbonate are the major anions of ECF, Deficiency of one lead to an inerease in the other to maintain the electrical neutrality. So chloride deficiency leads to excessive reabsorption of HCO,; by renal tubules. Potassium depletion leads to alkalosis: Bicarbonate reabsorption in both the proximal and distal tubules is increased in the presence of potassium depletion, Therapeutic classification of metabolic alkalosis: ‘CHLORIDE RESPONSIVE ‘CHLORIDE UNRESPONSIVE. (urinary chloride 20 mEq/L) ‘Gastric losses (vomiting/ Nesogastrie aspiration) _ | 1° & 2° hyperaldosteronism (mineralocorticoid excess) Diets ~ Loop & Thiazide ‘Cushing's syndrome ‘Chloride losing diarrhoea (villous adenoma) Bartter Syndrome Cystie fibrosis Giteiman syndrome Liddle syndrome Licorice ingestion (Compensation; Respiratory acidosis by hypoventilation Effects of metabolic Alkalosis: ‘© Tbinding of free Ca" to albumin —» | ionised Ca''~» Tetany & cardiac depression ‘© Shift of hemoglobin oxygen dissociation curve to left—+ decreased release of O, to tissues © Depression of respiratory system Aysiweyso0ig 113First MBBS Solved Question Papers 18 Purine & Pyrimidine bases ate salvaged(Feb 10, 12 paper I & II, 13, 15) (Aug 04, 05, 07, 10, 11, 12) (Sep 02) De novo Synthesis of bases isan energy expensive process and hence all the cells reeycle purine & pyrimidine bases by converting them into nucleotides. RBC & Brain are entirely dependent upon purine salvage pathway as they lack PRPP-amido transferase ‘© Hypoxanthine Guanine Phosphoribosyl Transferase enzyme can act on both hypoxanthine & guanine. ‘© It transfers phosphoribosy! group to form mononucleotides. ‘© Adenine Phosphoribosyl ‘Transferase acts in the similar manner to produce AMP. Pyrimidine phosphoribosy| transferase salvages pyrimidine bases. Hypoxanthine + Papp "=" ype pp, Gusnines prep =" Gap sp, Adenine + PRPP ana +P, «dback competitive inhibition by end products IMP & GMP ‘© Lack of bases for salvage + PRPP — stimulation of PRPP amido transferase —rde novo synthesis, Lesch Nyhan Syndrome (Feb 10, 12) (Aug 08, 13) X-linked recessive disorder with complete absenceof HGPRTase enzyme of purine salvage pathway Enzymes of de novo synthesis of purines are absent in brain. Therefore brain is dependant entirely upon salvage pathway. Reason for hyperuricemia: (Aug 11) HGPRTase enzyme reutilises (salvages)purine bases. When these enzyme is deficient, guanine, xanthine or hypoxanthine are not salvaged and therefore degraded to uricacid resulting in hyperuricemia, Clinical Features: ‘© Alfected children are usually male, © Hyperuricemia Spasticity, Mental retardation Self-mutilation — biting tongue, fingers, chewing lips ~ striking feature ofthis disease ‘Treatment: ‘© No curative treatment is available. Removal of deciduous teeth is done to avoid injury. Other ‘managements are symptomatic. # Geneti counselling & carir testing for prevention. Orotic acidusia(Aug 08, 10, 13) (Feb 09, 11) Disorder of pyrimidine metabolism associated with excessive excretion of orotic acid in urine, (OMP isthe ’pyrimidine nucleotide to be synthesised.)First MBBS Solved Question Papers 140 Memory aid: DEAB G,/S check point is controlled by RB Progression from G, to $ phase requires a transcription factor called E2F. RB protein binds to E2F and prevents it from acting. When there is a stimulus for cell cycle, eyelin D/edk or cyclin D/edk6 complex phosphorylates RB. Phosphorylated RB can’t bind to E2F and E2F is free to activate the genes for proteins required for cell eycle progression. Apoptosis vs Necrosis Apoptosis Necrosis Inflammatory reaction | Absent (clean call death) Present Unit of death ingle eels ‘many adjacent cells Call size Call shrinkage Pel swelling initially Cell membrane ‘Cytoplasmic blebs formed ‘Membrane disruption Nucleus ‘Chromatin condensation ‘Nuclear disruption Phagocytosis Phagoytois ofapepttie bodies by macrophages | Phageetosis of ell debris by macrophages Purpose thor physiological as in embryonic life or pathoogeal. [always pathological Necroptosit Necroptosis (inflammatory cell death) is a programmed form of necrosis. Markers of apoptosis (Annexin V) & markers of necrosis both will be present. Medical Genetics Autosomal dominant inheritance All porphyrias except congenital erythrocytic porphyria. © Familial bypercholesterolemia © Most disorders involved with structural proteins e.g. Marfan’s, Achondroplasia, Osteoger imperfecta, Neurofibromatosis, Von-willebrand disease ete. Autosomal recessive inheritance Most ofthe metabolic disorders © Allurea cycle disorders except OTC deficiency © All lysosomal disorders except Fabry & hunter X-linked recessive disorders Fabry, Hunter, Haemophilia, Glucose-6-phosphatase deficiency, color blindness, Lesch-Nyhan ete. X-linked dominant disorders © Vit D resistant rickets © Rett syndrome © Incontinentia pigment Fragile-X-SyndromeFirst MBBS Solved Question Papers 160 Nature of the sample | Only coloured sample can be used Even colourless samples can be used | co compare hespasie cpa | Operave segues ess sled personal reques sled pool } Proteinuria Renal Glomerular ~ Most common. Functional, orthostatic Selective Non-selectve Tubular ~ characterised by low molecular weight proteinuria Overload — Bence jones, Hl, Mb Posterenal — Pus cells, RBC cast Bence-Jones proteins (BJP) are light chains excreted in urine in patients of multiple myeloma (Aug 09, 13) (Feb 12) Multiple myeloma is a neoplastic condition of bone marrow with clonal proliferation of plasma cells Immortalised B-cells produce monoclonal anibodies.Excess light chains are excreted in urine and are known, as Bence-jones proteins. They may of either « or. type, never both as the proliferation is monoclonal Heat precipitation test for BJP: Urine sample is collected from the patients suspected with multiple myeloma. When heated gradually in boiling water bath, Bence-Jones protein precipitates at temperatures between 40” and 60°C but dissolve at and above 100°C. Upon cooling, precipitate will reappear around 60°C only to dissolve again below 40°C, Confirmatory test: ‘© Serum protein electrophoresis for detection of M band is the confirmatory test for multiple mycloma, ‘© Immunofixation is done to find out antibody class (type of heavy & light chain) Benedict’s test(Aug 08, 09) Benedict’s testis used to detect the presence of reducing sugars. Any sugar with fee aldehyde or keto group will give a +Ve Benedict's test. Reducing sugars under alkaline conditions from enediols which are powerful reducing agents Na,CO,#2H,0 -+ 2NaOH +H,CO, 2NaOH CuSO, +Cu(OH),+Na,SO, CuOH),-*Cu0 +H,0 D.Glucose +2Cu0—D-Gluconic acid + Cu,0 | Components of Benedict's reagent: 'Na,CO,—+ provides mild alkaline condition CuSO,-+ provides Cu for reduction Sodium citrate stabilising agent — prevents precipitation of Cu by forming loos complex ‘Semi-quantitative test: By fixing the amount of Benedict's reagent and the sample, benedict’ testis made semi-quantitative, 5 ml of benedict’s solution is heated first to check for auto reduction. Then 8 drops (2 ml) of urine sample is added and heated for 2 minutes.First MBBS Solved Question Papers 170 Siractares under cover of gluteus maximus/Feb 13) GF; 9 muscles, 7 vessels, Serves, 6 bones & joints, 3 ligam 3 bursa Poplital fossa/Feb 13) 76 Enumerate the muscles of foot in each layer with nerve | 115 supply/Feb 13) "Name the muscles of ayer of sole ofthe foot (ng 10) Flexor digitorum brevis, Abductor halluses and abdustor igiiminimnt Muscles of 2 layer of ole of the foot dug 08) ‘Flexor digitorum longus, Flexor Hlallueis Longus, Flexor digitorum accessories, Lumbrical muscles Bursae around the patella (Aug 08) ‘Supra, Pre, infra patellar bursa; pes anserine bursa Housemaid’s knee > prepatellar bursitis; Clergymen > infta patelar bursitis knee ‘Siructures piercing oblique popliteal Tigameni(Feb09) * Medial genicular nerves vessels + Terminal part ofthe posterior division of obturator nerve ‘Arteries forming wochanterie anastomosis(F@b09) 74 ‘Contents of sub sartorial canal/'eb09) Femoral artery, femoral vein, saphenous nerv vastusmedials, branches of obturator nerve “Maseles supplied by the obluator nerve/Aug 09) a ‘Bones forming medial longitudinal arch of foot (Aug 09) “Anterior end — Head of fist, second and third metatarsals Posterior end - Medial tubercle of calcanueum ‘Name 2 asel bones ofthe Fooi(FebI9) Talus, ealeanuem Medial, intermediate and lateral cuneiform, and cuboid Terminal branches of siatie nerve(Fb10) 168 Name the Hamstring mussles(4ug 10) Semmitendinosus, semimembranosus & biceps femoris Muscles within the rectus sheath(Aug 70) 210 Ligamenis present within the knee joint ug 10) [Anterior & posterior rucate ligaments 2. Meniseofemoral ligament 3. Coronal ligament ‘Maseles causing lateral rotation at hip jointug 10) (Feb W “Two obturator, two gemelli, Quadratus femoris Accessory muscles Pirformis, gluteus maximus and Palthi postare/aug 11) “Pah means leg folded posture. Thighs and legs le in a horizontal position in this posture. This is used for doing ‘yopasana & meditai, Anatomical description: Flexion at knees, flexion, abduction & lateral rottion at hips and crossing of legs infront of perineum. Sartorius helps in this posture Muscles attached with ioubial tract(Feb 12) ‘Gluteus maximus & Tensor fescialatae “Maseles producing Inversion & Everson of Foot at subtalar joine(Aug 12) Taversion:Tibials anteriordlibials posterior version: Peroneus longus, brevis, and tetiusFirst MBBS Solved Question Papers 180 ‘Oblique fissure of lung(ug 11) 26 Costodiaphragmatie recess(Aug 12) 2 Tricuspid valve(Aug 12) 259 Formation and termination of extemal jugular veinfAug 12) Formation: joining of the posterior division of the retro ‘mandibular vein with the posterior auricular vein Termination: drains into subclavian vein Peculiarities of Ist intercostal nerve(Aug 12) Runs along the intemal surface of 1 rib, No anterior culaneous branch and often no lateral cutaneous branch, Formation and termination of Lent superior intercostal vein(Aug 12) 1 direily drains into Left brachiocephalic vein 29, 386 4 unite and drain into Left brachiocephalic SH t 8° drain into accessory hemiazygos vein, ‘9 11 drain into hemiazygos vein, ‘Supra sternal space of Burns(Peb13) Tm the Suprastemal notch, the investing fascia of neck splits into 2 layers One attaches to the anterior border of the manubrium & the other to the posterior border. This leaves a small suprasteral space called space of burns, Contents 1, Stemal head of stemocleidomastoid 2, Anterior jugular vein anastomoses 5. Lymph nodes 4. Interclaviculr ligament ‘Apex beai(Feb13) Lowermost and outermost point of definite cardiac impulse, Normally located in the left Sintercostl space, about 1 centimeter medial to the mideclavieuler fine, In children, i is located in the 4Mintercostal space, lateral to the mid-clavicular line ‘Contens of posterior Mediastinum(Febi3) 247 Applied aspects of pleura(FebI3 233; Paracentecs, Peurisy, Pneumothorax, Hemothorax, Empyema ets ‘Ligamentum areriosum (Feb09) ‘Remnant of the duclus arteriosus between the aoria and the Teft pulmonary artery. Related to let recurrent laryngeal ‘Sub divisions of mediastinum(Feb09) 2s “Hasal’scorpuseles(F2b09) Concentric, cosinophilicepithelioid cells surounding cxnfound in medulla of thymus, Splanchnie nerves inthe thoracic region(eb09) 296; Greater TT), Lesser (TT), Least (ToL) “Attachment of supra pleural membrane (Feb09) of T7; Base > inner Apex > tip of transverse proc 7 border of IbFirst MBBS Solved Question Papers 190 GIT Essay Different types of salivary glands & composition, functions and regulation of secretion of salivacaug 08) 2, Composition, functions and regulation of secretion of gastric juice¢rebo,11)(Aug 14) 3, Describe the enteric and colonic movements.Discuss the role of the enteric nervous system. Add a note on defecation(Feb10) 4, Composition, functions and regulation of secretion of pancreatic juice. (Feb13) Smarks: “Composition & Functions of salivatag 1) 2s ‘Regulation of salivary secretions (Feb21) 27 ‘Describe the phases of gastric juice secretion Aug 10,11) ‘Components of gastric seeretion® regulation (Feb12) 232-234 ‘Composition & functions of gasrie Juiee(Aug 12) “Mechanism of secretion of HCI in stomachaug 08) 2 Digestive proteases (Feb10) 2D ‘Components and functions of bile (F609) 252 Hepat and gall bladder bile 4ug20) 252 Entero hepatic eirlation of bile(Aug 09) 251 diagram, 252 Deghatton Aug) 270 ‘Micelle formation ugi0) 2S Functions of panereatie juiee(Feb13) 2 ‘Transporters of amino aeids in gut and kidney(Feb10) : ‘Small intestinal movements(Aug 1 12) aT 3/2.5/2 marks Dietary Abredimportance (Feb17, 15) (hug 09) 267 Movements of small intestine(F2b75) 27 [Enterohepatic eirelation(Wov 14) (ug 13)(Feb13) 251 diagram, 252 zymes involved in digestion of faiov 4) 295; ‘Composition of bile and physiologial role (Feb74) 252 Funetions of bile slisug 12) 252 Pathophysiology of peptic uler(Rb14) 240 Gastric emprying(aug 13) 204 Functions of saliva (Aug 09,13) (Feb 09) 225 ‘Cholelithiasis (Feb12) 260 Enterogastic | Vagovagal reflex(affernt & efferent both mediated by CN X) whieh is initiated by presence reflex (eb12) | of acidic chime in duodenum. In respons antrum which in tum decreases HCL se Gastrin release is inhibited from G-cells in pyloric jon & gastric motilityFirst MBBS Solved Question Papers 194 (Tiyroninesymesis ug Tay cniay [SRD Teiany(Augl2 12) 03 Asromesaly (eb7) 38 [Placenta hommones(ag 72) Em Tron dwarf (eb12) [Autosomal recessive dist ‘onder; insensitivity fo growth hormone due to defective GH receptor. Patients ate short statuted & diabetic. Rx: recombinant IGF=2 Progeria(FebI2) Progeris is premature ageing. 2 types: Childhood (lutchinson gillfond) & Adult (wermer syndrome. Tslomeric shortening occurs prematurely that results in features of ageing like greying of hair, wrinkling of skin Permissive ation(Febiay Potentiation of eft of one hormone in he presence ofthe other is known as permissive ection. eg. Thyroxin potentiates the ealorigenic action of catecholamines, ‘Gonn’s syndrome (Febi2) 1° hyperaldosteronism due to adrenal adenoma, C= early onset hypertension, hypokalemia, Absence of edema is duc to ANP. Tidosierone | Absense of edema in cor escape(Aug 09,11) | sodium and water retain) rn syndrome is due to Atrial Natriuretic Peptide which overcomes he ing ation of ekdostrone, Houssay snimal(aug 11) _ sensitive to insulin after pancreas reded the insulin sensitivity. Ia humans, similar condition iss Experimenatl animal model with pancreatectomy and hypophysectomy: Animals were abnormally removal of pituitary and died due to hypoglycemia. Removal in Simmonds's Turner's syndrome & 3 Features(Aug 11) “Monosomy of X chromosome in females, 45XO; Py amenorthea, webbed neck, male distribution of pubie hair, shot stature, coarctation of aorta “Hormones involved in growih(fug 77) Growth hormone acts via somatomedin, Somatostatin inhibits GH, Estrogen & Testosterone cause pubertal growth spurt Fetal growth is due to thyroxin, Sesond messengerug 08 1,12) aT Actions ofrelaxindinhibin(aug 10) 504,460 [Leptin eb) 859, 450 ‘Mallerin regression Taetor(Fb70) 46 XY fetus release MRFTantimllarian hormone from seminiferous lubules inthe 9-I1 weeks of gestation which causes regression of molleran duct in eraniocaudal direction, MRE is a member of TGR Composition of semen(FebT0) ‘Actions of Insulin Aug 09) [Estrogen ~Functionsug 5) a8 Physiological basis of pregnancy diagnosing et (Fab 09) SO ‘Actions of prolactin (Aug 08) Established actions: Proliferation & differentiation of mammary epithelium, Inhibition of gonadotropin release (Lactational amenorrhea) Proposed action: mitogenic to lymphocytes “Hormones of hypothalamus (Aug 08) TRH, GaRH, GHRH, CRH, Somatostatin, Dopamine Oxytocin and vasopressin are secreted by hypothalamus and stored in posterior pituitary. [Tigra incon eon) 398 [cates ces) sas1, Define arterial blood pressure, Describe the nervous regulation of arterial blood pressure Au 08,10, 4) 2. Define cardiac cycle. Describe in detail with the help of a diagram. The mechanical changes during cardiac cyele. Add a note on heart sounds. (Feb 09, 13}.Nov 14) 3, Define Cardiac output. Discuss the factors regulating the cardiac output. Adda note on Fick's principle. (bt, 14, 15)(Aug 12) 5 marks Question Pano (Sembulingam) Pacemaker Potential (Aug 08 09)(Peb12, 13) 328 Regulation of coronary cireulaion(ug 08)(Feb13) ol Triple response/Feb 09, 10) (647 (Red reaction Alare(axon reflex) & Wheal) ‘Alia natriuretic peptidefAug 09) 46 ‘Kirchoi?s law and Binthoven's law (FBI) KirchofT law: sum ofall currenis owing nto @ node is zero(ql “q2+q3 0) 552 imhover Excitation contraction coupling im eardiac muscle (Fb10) ‘Chemo receptors(aug 19) 720; central & peripheral Endothelins(aug 10) 611; vasoconstrictor produced by endotheli involved in regulation of BP. ‘Normal BOG in Lead IFebty 12) 350-555 Special Teatures of coronary cireulation(Aagi) Tigh oxygen demand, well developed autoregulation, Adenosine &NO are vasodilators, Functional end [Non progressive shock(Febl2) 655 Hiypovolemic shock(aug 12) 655 Heart Sounds aug 12) i Windkissl effect (Aug 08) Elastic recoiling of sorta; ensures that blood flows t periphery during the ventricular diastole also. Thus continuous blood flow is maintained, Aorta is aka windkessel Phonocardiogram(Aug 08) ‘548; reconding of heart sounds Labelled diagram of arterial pulse and explain (Feb 09) 623 ‘raw a normal E-C.G, and label i (Feb 09) 535 Jugular venous pulse(aug 08) ] 628; @— atrial contraction; v— ventricular contraction; €— cusp bulging, x & y descents ABojoiskud 195,‘Name the functional divisions ofthe cerebellum. Describe the structure, connections, and functions of cerebellum. Mention two signs of cerebellar lesions. (Feb 08) 3, Enumerate the ascending tracts in the spinal cord. Deseribe the pathway for pain in detail. Add a note fon referred pain (Aug 09,12) 4. What are the types of muscular exercise? Discuss the various physiological changes occurring during and after exercise. (6010) Elucidate how pressure vibrations in the air are perceived as sound (Febi0) 6. With the help of a diagram, describe the auditory pathway. Add a note on conduction deafness (Aug 7. ‘Trace the visual pathway and the effects of lesion at various points in the pathway(Feb11) 8, Classify pain. What are the receptors for pain? Describe the dual Pathways for pain. What is Analgesic system in the brain?(Feb12) 9, Describe the connections and Functions of Hypothalamus(Febr3) 10. Describe in detail the photochemical mechanism of vision and mechanism of dark adaptation.(Feb 14) S marks ‘Question Page no (Sembulingam) Taste Pathway ug 08,1, 1)(RebT) 1025 ‘Draw the optic pathway: Depict the lesions at various levels (ug 09) athway-993; lesions 993 [Efects of lesion in opie pathway ug 08) 993 Brown sequard syndrome(Aug 8, 09,11)(Reb 12) (Nov 14) 24 Funetions of Thalamus(aug 08)(Feb11) 851 ‘Neuromuscular transmission/Aug 08) 201 ‘Neuro-muscular junction (Feb 05) 200 ‘Compare REM and noneREM sleep(Feb 09) 952 wble REM sloep(Febrt) 952 Induction of seep(Febi@) : (Feb 09) (Nov 14°) (Feb 159) 39 Formation, circulation and functions* 0 ‘Componenis of vestibular apparatus (ug) 920 ibular pparatus(Feb 08) 323 Functions of ve "Dark Adaptation (Reb 08, 139(auy 11) 983 ‘Organ of eoni(Feb 09) 10H Myasthenia gravis & biological basis ofits teatment (Feb 09)(8ug 11) 22 Blood brain barvier (ug 09) 952 Pupllary Tight relexes(aug 03) 998 {Causes of muscle tone(Febt0) 913 Funetion of palacostriatum(Feb10) : (Climbing, mossy and parallel fibers(F2b10) 866 Control of appetite(Febid) 858; Feeding and satiety ‘Theories of Heating/Aug 10)(Feb11) 1020) ABojoiskud 197First MBBS Solved Question Papers 200 Punetions of prefrontal lobe(Reb1 ug 73) Personality, Registration of shor Execution of planned actions, Seat of intelige Autonomic changes during emotional response do cochlear poteatial (Feb12) 1019 Delia waves in BEG(PebI1) 930 ‘itolith organs(ug 11) 920 Monroe Kellie Doctrine (aug 19) The craniumd it constituents (blood, CSF, an 1d brain issue) are in a sate of volume equilibrium: So any inerease in Volume of one of the cranial constituents must be compensated by a decrease in Volume ‘of another That i why hemiation of uneus of temporal lobe happens in intracranial pressure, ‘Stereognosisa is centerfaug 12) Perception af -D objesis; Parietal lobe Functions of frontal lobe(Aug 11) Contains pre-motor (including broea’s), motor & supplementary motor area > Movement & speech PLUS Functions of prefrontal lobe “Mechanoreceplor & example(4ug 11) Recepiors responding to mechanical tinal. & Pacinian corpuscle ‘Summation & is types(Aug 11, 12)(Feb13) Spatial & Temporal ‘Cholinergic & Adrenergie receplors(aug 12) Draw the structure of rods & Cones(aug 11) 979 ‘Shasticity vs Rigldity(Awg 1) ‘Cog-wheel rigiity(FebI2) Cogwheel rigidity sa combination of lead-pipe rigidity and wemor, Homunculus(Peb12) Inverted representation af body in the cortical precentral (motor) &postcental (sensory) gy ‘Motor homunculus(Nov14) 890 Betz eelis(Feb12) Giant pyramidal neuronal cells located in the Sayer of area 4 (1° motor cortex; origin of pyramidal tract “Anomie aphasia(rebi2) Posterior texporal & inferior parietal gyrus lesion will result in inability to name familie objects Dopamineiug 72) 790 Functions of Basal Ganglia(Febta) (ug 13) 880 ‘Vestibule cerebelium(Febi3) 869 ‘KluverBuey syndrome(Feb13) Bilateral amygladectomy produces hyperphagia, hypersexuality, hyperorality, visual agnosin&e docility Referred pa 23) 840 erimetry(Feb13) Practical book Types of memory (Feb13) 939 Define synapse and deseribe ts properties@lug 13) ‘Synapse is a contiguous jnction between 2 neurons. Delay, Fatigue & Summation (Spatial & Temporal), Plasticity Panetions of thalamus(ug 13) Except olfaction all sensory fibres relay in thalamus, mediates visual (LGB) and auditory (MGB) responses, Memory (pape7 cite)