Quick Hints - Medical Notes PDF

Dr Atif Afzal Quick Hints (FCPS 1)  Derivatives  Extraembryonic mesoderm derived from - Epiblast  Extraembryonic coelom derived from- Hypoblast  Intraembryonic coelom derived from -Lateral plate mesoderm  Adrenal cortex derived from - Mesoderm  Adrenal medu...

Dr Atif Afzal Quick Hints (FCPS 1)  Derivatives  Extraembryonic mesoderm derived from - Epiblast  Extraembryonic coelom derived from- Hypoblast  Intraembryonic coelom derived from -Lateral plate mesoderm  Adrenal cortex derived from - Mesoderm  Adrenal medulla derived from - Neural crest cell  Dura matter derived from - Mesoderm  Pia and arachnoid matter derived from -Neural crest cell  Schwan cell Derived from -Neural crest cell  Oligodendrocytes derived from - Neural Tube  Renal agenesis result from -Failure of ureteric bud to reach metanephric mesoderm(Langman)  Two kideny with two ureter and pelvis Result from-Early division of ureteric bud(Langman)  Hepatocyte Derived from – Endoderm  Kuffer Cell Derived from – Mesoderm  Transitional epithelium bladder derived from -- Endoderm Ulcer  Curling ulcer by Inhalation burn  Cushing Ulcer by Brain injury(Raised ICP)  Marjolin Ulcer by External Burn(Squamous cell carcinoma of Skin)  Mortorells Ulcer by Hypertension  Most Common location of Duodenal Ulcer 1st part of Dudenum  Perforation of posterior wall of duodenum Bleed by Gastroduodenal artery  Most common location of gastric ulcer near incisura angularis on Lessure curvature..  Perforation of lesser curvature Bleed by Left gastric artery  Perforation of posterior wall of stomach Bleed by Splenic artery Micturation/Defecation  Initiation of Micturition reflex - Stretch receptors in bladder wall   Micturition centre (stimulatory )- Pons  Micturition centre (Inhibitory ) - Midbrain  Processing of micturition - Cerebral cortex  Micturition reflex / integration - Sacral segments of spinal cord  Voluntarily Inhibition -Activation of Pudendal nerve  Pain and filling sensations of bladder are carried by –Sympathetic(Guyton)  Defecation is initiated by -- Mass Movement  Defecation is Carried out by -- Sacral Parasympathetic  Defecation Reflex- RectoAnal  Defecation Reflex in Baby- Gastrocolic  Bulbar Urethra Rupture(Below Urogenital Diaphram) urine into -Superficial Perineal Pouch  Membranous Urethra Rupture(At Urogenital Diaphram) urine into -Deep Perineal Pouch  Prostatic Urethra Rupture(Above Urogenital Diaphram) urine into -Retropubic Space  Penile Urethra Rupture Urine into -Scrotum> Anterior Abdominal Wall  Injury above Sacral Segment Cause -Spastic Bladder -Automatic Bladder -Urge Incontinence  Injury at Sacral Segment Cause -Atonic Bladder -Autonomous Bladder -Overflow Incontinence Note: Neurogenic is common term for both spastic and Atonic Bladder AIDS/HIV  Initial Test- ELISA  Confirmatory Test -Western Blot  In children Confirmatory- PCR  Hall mark of HIV- Proliferation of Virus in T Cell  Hall mark of AIDS- Progressive Immunodeficiency(Decrease CD4 Count)  Most common opportunistic infection in-HIV is TB  Most common opportunistic infection in- AIDS Pneumocystic Jiroveci  Follow up is done by -CD4 Count  Progression from asymptomatic to Symptomatic stage can be assessed by PCR GIT  Pancreatic Secretion Increased by – CCK(First Aid)  HCO3 secretion Increased by – Secretin  CCK increase Calcium by -- IP3 mechanism  Gastric Motility Increased by – Gastrin  Gastric Motility Decreased by – Somatostatin  Increase Salivary Flow – Cranial Nerve 7 > 9  Increase Small intestine Motility and Decrease Gastric motility -- CCK  Fundus removed=⬇Gastric compliance>>⬇Receptive relaxation  Antrum removed=⬇ Gastric acid production  Pylorus removed➡Solids pass easily  Intrinsic factor released by Fundus of Stomach  Colostomy Result in Secretory Diarrhea  Jejunostomy Result in Osmotic Diarrhea  illeostomy Result in Osmotic Diarrhea  Jejunostomy+illeostomy Result in Secretory+Osmotic Diarrhea  Iron and Calcium absorption – Duodenum  Max water + electrolytes absorption – Jejunum  Passive(Aldosteron independent) water absoprtion -Jejunum  Absorption of LONG chain FA-Jejunum  Vitamin B12 and Bile Salts Absorption -Terminal ileum  For B12 Absorption Needed – Intrinsic Factor  For B12 Transport Needed – Transcobalamin 2  Absorption of SHORT chain FA -COLON  Active(Aldosteron Dependent) water absoprtion -Colon  Max Fluid loss -Colon   Part of Gut removed that cause Fluid loss-illium  illium Resection—Increase water content of feces > Decrease Bile salt absorption Explanation: Though Max absorption occur in Jejunum but Fluid loss will always from Colon and part of Gut remove which cause Fuid loss is illium as when Jejunum is removed no Fluid loss will occur because illium will Start absorbing Fluid but when illium removed then Colon will be over loaded so illium Removal will cause fluid loss through Colon (Bailey and Love)  Carcinoid syndrome – most common site is small intestine (ileum) > lungs , Trachea and bronchi  Most common tumor of appendix – Carcinoid Syndrome  Most common site of Carcinoid syndrome overall GIT > Respiratory system  Sympathetic is always – Adrenergic  Sympathetic is Cholinergic only in – sweat glands  Sympathetic is for Fight and Flight ( Pupillary dilation + Bronchodilation +Decreased GIT Motility )  Parasympathetic effect on GIT -Relaxation of fundus + Contraction of body of stomach +Relaxation of sphincter + Increasead GIT motility  Posterior Deudenal Wall and Pancreatic Rupture Fluid Leaks into -Lesser Sac  Anterior Deudenal Wall Rupture Fluid Leaks into -Right Posterior Subphrenic Space -Right Paracolic Gutter -Greater Sac and RIF Thyroid  Maximum concentration of thyroid hormone -T4  Thyroid harmone Enter in Circulation-T4  Thyroid harmone cause fetal Brain development-T3  Active form of thyroid hormone - T3 (Free form or Unbound is Active)  Thyroid gland is enclosed by -Pretracheal fascia  Metabolism of TSH in liver - Demethylation  Metabolism of Thyroid Harmones In Liver -De-iodination  Dyspnea on lying down – Retrosternal Goiter  Superior Thyroid artery Related to- ELN  Inferior Thyroid atery Related to-RLN  Superior Laryngeal Artery Related to-Internal Laryngeal Nerve  Most Common Nerve injured during Thyroidectomy-ELN  Most Common Nerve injured during Tracheostomy-RLN  Most Common Cause of Bleed During Thyroidectomy- Inferior Thyroid Vein  Most Common Cause of Heavy Bleed During Thyroidectomy- Anterior Jugular vein> Isthmus  During Tonsillectomy Bleed due to Tonsilar arterty , Palatine vein and ascending Pharyngeal Artery Buffer  Major blood/Extracellular/Interstitium/Plasma Buffer - Bicarbonate  Major RBCs buffer -Hemoglobin  Major Intracellular Buffer- Proteins  Major Renal/Renal Tubular Buffer- Phosphate  Major Urinary Buffer(Quantitatively)- Ammonium  Major Bone Buffer- Calcium Carbonate Malignancy Microscopic feature of Malignant tumor :  Metastasis > Invasion of adjacent tissues > pleomorphism > increasead N/C ratio  Histologically Invasion Diagnostic For Malignancy  Grading -- Nuclear differentiation / degree of differentiation / Mitosis  Staging -- Extent of spread / Lymph nodes involvement  Pre-malignant lesion -- Pleomorphism Diagnostic  Pre-malignant condition -- Increased N/C ratio Diagnostic  Most Common Pre-malignant lesion --Leukoplakia  Most Lethal Pre-malignant lesion --Erythroplakia  Most Common Pre-malignant Condition--Submucosal Fibrosis  Most Lethal Pre-malignant Condition--Lichen Planus  Locally Malignant- BCC> Ambleoblastoma  Most common skin CA -BCC (nodular type )  Most common site of BCC is -Upper lip  Most common after Basal CA -Squamous CA  Most common site of SCC - Lower lip  Pre-malignant lesion which must be excised -Actinic keratosis ( on cheeks)  Blue cell tumor in children + releasing catecholamine + gene Amplification -Neuroblastoma  Most Aggressive CA- Melanoma  Most Common Naveus In Children- Junctional  Most Common Naveus In Adult is-Intradermal  Highest Malignant Potential- Dysplastic Naveus  Male age Less than 40 - Seminoma  Male age more than 50 + increased LDH - Lymphoma  Tumor containing mature cells -Teratoma  AFP raised +Schiller Duval Bodies – Yolk Sac Tumor  Call Exner Bodies – Granulosa Cell Tumor  Giant cell tumor (Soap bubble appearance )- Epiphysis  Osteosarcoma (Codman triangle sunburst appearance ) + osteochondroma (most common benign )- Metaphysis  Ewing sarcoma (onion skin )-Diaphysis  Osteoblastoma occurs in - Vertebrae  Osteoid osteoma -- cortex of long bones + has radiolucent osteoid core  Radio sensitive Phase --G2-M Phase(M>G2)  Radio Resistant Phase-- S Phase  Chemo Sensitive-- S Phase  Angiosarcoma in Plastic Factory Worker –Vinyl chloride  Angiosarcoma in Farmer – Arsenic  Plastic Factory Worker – Liver Angiosarcoma  Plastic Factory worker + Smoking – Lung CA > Angiosarcoma  Hydrocarbon(Tyre Factory) +Aromatic Amines – Bladder CA  Smoking + Hydrocarbon – Lung CA > Bladder  Liver CA –Acohol >Aflatoxin >Smoking  Transitional Bladder CA – Smoking >Amines >Hydrocarbon  Squamous Cell Bladder CA –Schistostoma >Stones > Indwelling Catheter  Acute Effect of Radiotherapy--Desquamation  Chronic Effect of Radiotherapy -- Endarteritis Obliterans  Late Effect of Radiotherapy -- Lymphoproliferative Disorder  Common method to detect Tumor -Tumor marker  Common method to detect Tumor cells - Peripheral smear  Regarding sensitivity to radiotherapy : -Lymph node tumor > Seminoma > Glioma > Craniopharyngioma  Least Radio Sensitive Blood Cell – Platlets  Most Radio Sensitive Organ – Skin  Least Radio Sensitive Organ – Vagina  Most Radio Sensitive Mucosa -- Intestinal  Radiation induced Brain malignancy -Meningioma  Overall radiation induced CA- Leukemia  Chemotherapy caused cell death -Apoptosis  Chemotherapy induced vomitting is treated by - Ondansetron  Virus cause malignancy by -Alteration in protein synthesis -Alteration in proto-oncogene - Have /By Using– Oncogene  Radiation cause malignancy by -They Have Proto oncogen -By Producing Free radicals TB  Initial - Chest X ray  Definitive –Sputum Culture(Harrison)  Diagnostic – PCR > AFB  Microscopic - Caseous necrosis  Histological -Epitheliod Cells with Caseating granuloma  Type of Hyper Sensitivity -Delayed Type 4 T Cell Mediated  Margins -Undermined  Antibodies-Cell Bound  Energy  Carbs/Protien Give- 4kcal  Fats Give- 9kcal  Alcohol Give- 7kcal  Carbs Required- 50-60%  Fats Required- 25-35%  Protiens Required- 10-20%  Major source of energy-Adipose Tissue  Max glycogen - Skeletal Muscles  Max glycogen concentration/ per 100 gms-liver.  Highest energy compound -ATP  Highest energy molecule - ATP  Highest energy content -Starch  Highest Quantity of Unsaturated Fatty Acid-Sun Flower  Highest Quality of Unsaturated Fatty Acid- Soya Bean  In Fasting -Upto 48hours -- Glucose -From 48 hours till 72 hours -- Fatty acids/TGs -After 72 hours -- Proteins /amino acids Prostate  Median-Structurally largest lobe  Lateral-Anatomically largest lobe  Peripheral-Largest zone  CA prostate - Peripheral zone / Posterior lobe + Metastasize to Vertebral column and brain by Anterior Intervertebral venous plexus  BPH - Median lobe / Transitional zone  Hepatitis  Orofecal Route- Hep A >Hep E  Most lethal Hepatitis -Hep D  Most common in pregnancy - Hep A  Most lethal/Remote Area in pregnancy -Hep E  Most lethal/Common virus after blood transfusion / Transplant – CMV >Hep B > Hep C  Most common sexual spread – Hep B  HCC- Hep B > Hep C  Cirhosis- Hep C > Hep B  Needle Stick injury Risk – Hep B(30%) > C(3%) > HIV(0.3%)  Hep A & E -Naked Viruses Pelvis  Finger couldn't reach sacral promontory -- Android pelvis  If Finger reaches Sacral promontory -- Contracted Pelvis  Pelvis in males -- Android (Heart shaped )  Pelvis is females -- Gynecoid (Rounded shape)  Most favourable pelvis for delivery -- Gynecoid pelvis  Reference point for head during labour --Ischial spine  Bony landmark for Pudendal nerve block -- Ischial spine Cranial Nerve Palsy  In CN3 palsy – pupils dilation occurs + Ptosis  In Hornor syndrome – Damage to cervical Sympathetic chain + pupil constriction + Ptosis and Anhydrosis  In CN 4 palsy – Vertical Diplopia ( Superior oblique )  In CN 6 palsy – Horizontal Diplopia ( lateral rectus )  In CN3 palsy – both Vertical and Horizontal Diplopia  HB/ Anemias  Hemoglobin synthesis starts in -- Proerythroblast or Early Normoblast  Hemoglobin First appears in -- Intermediate Normoblast  RBC Nuclei disappear in -- Late Normoblast >Reticulocytes  Max Production--Late Normoblast  Maximum concentration -- Reticulocytes  Iron Transport form --- Transferrin  Iron Excess storage form --Hemosiderin  Iron Normal Storgae Form-- Ferritin  Iron Fe2+ in reduced form binds to --Hemoglobin  Heme binds with --Hemopexin  Hemoglobin binds with -- Haptoglobin  Iron is absorberd from -- Duodenum  Diagnostic for IDA -- Serum Ferritin  Diagnostic For B12 Deficiency-- B12 Assay  Diagnostic For Folate Deficiency--RBC Folate Level  Diagnostic For Pernicious Anemia-- Anti Intrinsic Factor Antibodies  Diagnostic feature of Aplastic anemia -- Fatty marrow > Pancytopenia  Acute Intravascular Hemolysis-- Decrease Hepatoglobin > Reticulocytosis  Chronic Intravascular Hemolysis-- Hemosidrinuria >Hemoglobinuria Defense Lines  Tissue -- Macrophages  Blood -- Neutrophils  Surface --Skin  Major scavengers --Macrophages  Phagocytosis done by --Neutrophils  Opsonization -- C3b  Phagocytosis by -- C5a  Most potent Chemo tactic Factor--LTB4 > C5a  Pain--Bradykinin > Prostaglandins E2  IL-1 and TNF – Fever mediator  Prostaglandins F2, E2 and D2 – Vasodilation  Late mediator of Inflammation – PG & Leukotriens  Initial mediator of inflammation – Histamine Lesions  Dopamine loss in Substantia nigra and Striatum -- Parkinson Disease  GABA loss in Substantia Nigra and Globus Pallidus -- Huntington Disease  GABA loss in Caudate Nucleus --Chorea  GABA loss in Globus Pallidus-- Athetosis  GABA loss in Subthalamic Nuclei –Hemiballismus Embolism/DVT  Most common source of emboli – femoral vein  Most common site of DVT –Popliteal vein  Most common cause – Immobilization  D dimers – Sensitive for DVT  FDP –Specific for DVT Neural Tube Defect(NTD)  AFP raised in-- Anencephaly  AFP Decreased in--Down syndrome  Specific For NTD --Acetylcholinesterase  Senstive For NTD--AFP  NTD in early Pregnancy Diagnose--USG  NTD in Late Pregnancy Diagnose--Amniocentesis  Neural tube defects-- most common is Meningo-myelocele  Neural tube defects occur due to --Folic acid Deficiency and vitamin A toxicity Collagen/Wound  Type 1 Collagen -Fibrocartilage + bone + tendons + fascia + Skin  Type 2 -- Elastic and Hyaline cartilage + vitreous body  Type 3 -- Blood vessels + uterus+Reticulin+Skin  Type 4 -- Basement membrane + Lens  Early wound healing + granulation tissue-- Type 3 collagen  Late wound healing + wound strength -- Type 1 collagen  Hyaline cartilage --Larynx + articular surfaces of Synovial joints + Trachea  Elastic cartilage -- Ear pinna + nose  Sesamoid cartilage--Ala of nose > Larynx  Sesamoid bone --Patella  Diet Deficient in fruits and vegetables -- Decreased tensile strength  Diet having Complete absence of fruits and vegetables-- Decreased collagen synthesis..  Vitamin C -- Hydroxylation of glycine and proline residues  LOCAL factor for delayed wound healing -- Infection  SYSTEM factor for delayed wound healing -- Anemia > malnutrition  Old age Decreased wound healing -- Harmonal and endocrinological changes Coagulation Disoder  Factor V mutation(Laden ) leads to--Thrombosis  Factor V deficiency leads --Bleeding  Factor 12 deficiency leads --Thrombosis.  Most common acquired thrombotic disorder is-- Anti-phospholipid syndrome  Most common Inherited coagulopathy -- VWBD  Most common inherited Thrombotic disorder is -- Factor V Mutation (Laden)  Natural anticoagulant and anti-thrombotic --Heparin  Natural thrombolytic --Plasmin > plasminogen  Extrinsic and intrinsic pathway converge on -- Stuart factor (Factor 10)  Factor 8 is produced by -- Endothelium  Clotting factor not completely synthesized in liver is --Factor 8  Activation of extrinsic path way by--Thromboplastin(Tissue Factor)  Activation of Intrinsic Pathway by--Factor12  Vitamin k dependent factor with Shortest half life is -- Factor 7  Vitamin k dependent factor having Longest half life is --Factor 2  APTT raised only--Hemophilia(Intrinsic Pathway)  APTT and BT raised --VWBD(Intrinsic Pathway)  APTT and PT raised -- Vit K deficiency or liver disease  All 3 raised -- DIC  Only BT raised – ITP(Low Platlets) or Platlets Function Defect ( Platlets count normal )  Heparin Inhibit -- Factor Xa  Heparin Act by-- Anti-thrombin 3  Antidote of heparin is-- Protamine sulphate  Heparin monitoring is done by--APTT(Intrinsic Pathway)  Heparin is given --IV  Warfarin acts on and inhibits -- Vitamin K Epoxide reductase  Warfarin antidote is -- FFP(Immediate )  Warfarin action is reversed by --Vitamin k (long acting )  Warfarin monitoring is --INR > PT(Extrinsic Pathway)  Warfarin in given --Orally End Arteries  Functional End Arteries -- Heart  Anatomical / True End Arteries --Retinal Artery  END arteries are present in -- Central Retinal Artery >> Spleen >> Heart Neonates  C- shaped Vertebral column  Has Circular abdominal cavity  Liver has 5% of body weight ( largest organ )  Sample taken from Radial Artery> posterior tibial artery > Dorsalis  Blood volume is 85ml/kg  Myasthenia Gravis  Myasthenia gravis-- Antibodies’ against postsynaptic voltage gated cannels  Diagnostic test --ACH receptor antibodies  Most accurate/confirmatory/gold standard--EMG  Initial drug for Mysthenia gravis--Neostigmine  DOC For maintained therapy -- Pyridostigmine  Physostigmine – Crosses BBB immediately and Increase Acetylcholine  In Lambert eaten Syndrome – Antibodies are directed against Calcium channels Exercise  During Exercise blood flow increased to -- Exercising skeletal muscle  During Exercise decreased blood flow to--Kidneys > Splanchnic Vessels  During Strenous Exercise decreased blood flow to--Skin  During Exercise blood flow to Exercising muscles is maintained by -- Local Metabolites  During Exercise blood flow to Non-Exercising Muscle is maintained by – Sympathetic Cholinergic(Guyton)  During Exercise there is an increase in --Ventricular contractility  During Exercise subjective feelings of getting tired is due to – Increased Heart rate  After Exercise feeling of getting tired is due to – Increased Lactic acid Pregnancy Respiratory Changes Remain Same  Respiratory rate  Vital Capacity Increase   Tidal volume  Minute ventilation  Inspiratory Capacity Decrease  TLC  Residual Volume Other Changes  Increase GFR – Decrease BUN and  Increase Cardiac output  Dilutional Anemia  Hyper coagubility  Increase Lipolysis  HCG maintain Pregnancy upto 8-10 Weeks  After 10 weeks by Estriol and Progesterone of Placenta  HCG In blood – Upto10 days  HCG In Urine – After 10 days  Labour Initiated by Fetal Cortisol > Fetal ACTH(Pituitry) CVS  R ventricle Pressure during Systole-- 25  R ventricle Pressure during Diastole – 0-8  R ventricle Pressure at which Pulmonary Valve Open-- 8mmhg  L ventricle Pressure at which Aortic Valve Open-- 80mmhg  Max Aortic Pressure -- Reduced Ejection  Min Aortic Pressure-- Isovolumetric Contraction  Max Ventricular Pressure --Rapid Ejection  Min Ventricular Pressure -- Rapid Filling  Max Ventricle Filled-- Atrial Systole  Max Ventricle Filling-- Rapid Filling  Max Pulse Pressure – Dorsalis pedis > Femoral > Popliteal > Aorta  Highest Systolic Presuure – Renal Artery  Max O2 – Pulmonary Capillaries  Low O2 – SVC > Pulmonary Artery > Umblical artery  Highest O2 Saturation – Umblical Vein  Cardiac output unchanged in – Sleep  Pace Maker activity of SA Node due to – Sodium Chanells  Action Potential of Pace Maker due to – Calcium Chanells  Action Potential of Cardiac Muscle due to – Sodium Chanells  Becks Triad (Cardiac temponade)--Muffled Heart sounds Hypotension and Raised JVP  Rustling Sound /Pericardial Rub--Pericarditis  Pain unrelated to Respiration--Myocarditis  SA node located in--Upper one third Sulcus terminalis  SA node located in--Sub Epicardium  AV node located in--Endocardium  Conducting System--Sub Endocardium  Heart rate and location of pacemaker: -SA node--60-80 -AV node--40-60 -Purkinje fibers --20-40  SA node – Slowest pre-potential / Works as synctium as it is able to generate impulses at a faster rate  Purkinje Fibers have highest speed of conduction due to -Wide diameter > large no of gap junctions > Large no of sodium Channel >Less no of myofibril > Short refractory period  Speed of conduction : -Purkinje fibers > Bundle of His > Atria > Ventricles > SA node> AV node  Speed of Rate -SA Node > AV Node > Purkinji fibers  First Heart Sound --Isovolumetric contraction ( Closure of mitral and tricuspid valve )  Second Heart Sound-- Isovolumetric relaxation ( Closure of aortic and Pulmonary valve )  Third Heart Sound--Rapid ventricular filling (Normal in children, pregnancy and athletes )  Fourth heart sound--Atrial Systole  Inferior wall MI ( RCA )--Leads 2, 3 and AVF   Anterior wall MI (LAD ) --Leads V1-V6  Lateral wall MI ( LCX ) -- Leads 1 , AVL , V5 and V6  Best Initial – ECG  1-2 hr – Myoglobin  Within 4hr – CK MB  After 4hr – Trop  Senstive – Trop T  Specific – Trop I  4h Post MI – Arrhythmia  4-24h Post MI – Arrhythmia  1-3 Days Post MI – Fibrinous Pericarditis  4-7 Days Post MI – Cardiac Temponade  Month Post MI -- Aneurysm  Most Common Congenital/Acyanotic Disorder Child-- VSD  Most Common Acyanotic Disorder in Adults -- ASD  Most common Congenital Cyanotic Disorder – TOF  Most Congenital Cyanotic anomaly at birth-- TGA  Female living at Hill or if baby is premature -- PDA  Cyanotic Heart Disease in Which Shunt in Necessary for Survival –TGA  Preload determine by -- EDV (Depends on Venous return)  After load determine by-- MAP  TPR determine by-- Diastolic BP ECG  Hypokalemia --U wave + inverted T Waves  Hyperkalemia -- Tall T Waves  Normal ECG is unable to record--Electrical activity of SA node  ECG changes can be seen in the following conditions Except -- Sleep  Saw tooth appearance on ECG -- Atrial flutter  P wave absent + Irregular RR Interval in --Atrial fibrillation  QRS complex shows -- Ventricle Depolarization  ST Segment shows -- Complete Ventricular Depolarization / Plateau phase  Isoelectric line --PR segment  Isoelectric period-- ST segment  TP segment --Relaxation of Ventricles  Hypoglycemia increase --QT interval  Most specific finding of Pericarditis --PR depression  Time taken by the impulse to travel from Endocardium to Epicardium – QRS Complex  Time taken by the impulse to travel from Epicardium to Endocardium – QT Interval  Absent p waves Pacemaker In-- AV node(Also R Ventricle-Moderator Band)  PR Segment on ECG coincides with --A wave of JVP  Large A wave-- Tricuspid Stenosis  Cannon A wave --3rd Degree Heart Block & AV dissociation  Tall QRS complex --Hypertrophy of Ventricles  Low voltage QRS complex --Obesity , Old MI , COPD & Constrictive pericarditis  P-Mitrale occurs in-- Mitral stenosis Endocrinology  Immediate action of Insulin -- Entry of potassium into cells  Intermediate Action of Insulin -- Protien Synthesis  Late Action of Insulin-- Lipogenesis  Action of insulin at Cellular level is -- Entry of glucose into cells  Insulin Independent Glucose uptake – Excercising Skeletal Muscle > Brain(Guyton)  Anti Ketotic – Insulin  Ketogenic – Glucagon  Hypoglycemia increaseas -Glucagon > Gastrin > Secretin ( Ganong)  GH is increased In  -Hypoglycemia > Exercise > NREM (Guyton + Ganong)  Potent stimulant of Aldosterone – Hyperkalemia & Hyponatremia  Potent stimulant of Renin – Sympathetic > Hyponatremia > Hypokalemia  Potent Stimulant For ADH -- Nausea > Increase Plama Osmolarity  Renin is Inhibited by – Increased Angiotensin 2  Thirst centre is stimulated by – Angiotensin 2  Renin Increase by Hypokalemia and Decrease by Hyperkalemia (Ganong)  Angiotensin 2 cause -- Vasoconstriction > Thirst Stimulation( Ganong)  Cortisol main function – Gluconeogenesis  Glucagon main function -- Glycogenolysis  Cortisol Increase Neutrophil and Decrease Lymphocytes  ACTH effectively control -- Cortisol(Hydrocortisone) > Androgens ( Guyton)  Excessive Exercise causes – Hyperkalemia  Early Pregnancy Endometrium Sensitive to -- Progesterone  Late Pregnancy Endometrium Sensitive to – Oxytocin  In Pregnancy Lactation inhibited by – Estrogen + Progesterone > Estrogen >Progesterone  During Lactation Amonorrhea due to – Decrease GnRH  Milk Production -- Prolactin  Milk Ejaculation – Oxytocin  In Pre menopausal Breast Atrophy – Decrease Estrogen +Progesterone  In Post menopausal Breast Atrophy – Decrease Estrogen  Most Common Cause of Breast Atrophy – Decreased Estrogen  Most Potent Anabolic – Testosterone  Potency – DHT > Testosterone  Potency – Estradiol > Estron >Estriol  Increase Estriol – Indicates Fetal Well Being  Osteoporosis – Thin and wide trabeculae + long term use of Steroid  Osteoclasts in -- Howhship lacunae  Osteoblast -- Bone making cells + Produce ALP+ Laid Bone Matrix  Osteoclast – Bone Resorption  Osteocytes – Maintain Bone Matrix & Integrity  Demineralization of bone done by – PTH  Bone Remineralization – Vit D  Bone Remodeling – Vit C  PTH directly Regulates – Vitamin D levels  PTH Indirectly Regulates – Calcium Absorption from intestine By Vitamin D  Osteon Has -- Concentric lamellae  Patient has cast applied now has Decreased muscle mass -- Disuse atrophy + Decreased no of actin and myosin  Estrogen Function – Breast Duct Development + Endometrial Proliferation  Progesterone Function – Maintain Endometrial Thickness(Proliferation) > Secretory phase > Alveoli and lobule development Respiratory  Central Chemoreceptor Respond to( Sequence wise) 1-CSF PH or Interstitial PH( Increase H ions) 2-Increase CO2 In Arterial Blood  Peripheral Chemoreceptor(Carotid and Aortic body) Respond to 1-Decrease O2 2-Arterial PH(H ions)  Increase A-a Gradient Seen in 1-Fibrosis 2-V/Q Defect 3-R-L Shunt  A-a Gradient Normal Value – 0 -10mmhg  A/a Ratio Normal – 0.8(>0.75)  In Airway Obstruction 1-V/Q is Less than Normal(Guyton) called R-L Shunt 2-Composition of Systemic arterial blood approaches Mixed Venous Blood 3-Increase A-a Gradient  In Pulmonary Embolism 1-V/Q is Infinite Called Dead Space 2-Composition of Alveolar Air approaches Inspired Air  At High Altitude 1-Survival due to – Increase Hb Concentration 2-Pulmonary Vasoconstriction(Due to Hypoxia) 3- Hb-O2 Curve Shift to Right 4- Increase 2,3 DPG Concentration  Exercise Increase 1-O2 Consumption 2-CO2 Production  Small Cell CA associated with 1-ACTH(CUSHING Syndrome) 2-SIADH 3- Lambert Eaton 4-Poor Prognosis  Squamous Cell CA Associated with 1-Smoking 2-Hypercalcemia(PTHrP) 3- Keratin Pearls and Intracellular Bridges  Chloride Shift occur by – Band 3  Venous Blood have more – HCO3 & PCV(PCV >HCO3)  RBC Venous Blood Have more – Chloride Ions  Erythropoietin Produced By – Hypoxia  Erythropoietin Inhibited By – Theophylline  R Shift of O2 Curve – Bohar Effect  L Shift of O2 Curve – Haldane Effect  O2 100 Percent in -- L-R Shunt  Pulmonary Blood flow and Ventilation Highest at -- Base  Pulmonary Blood flow and Ventilation Lowest at – Apex  V/Q and Arterial PO2 Highest at – Apex  V/Q and Arterial PO2 Lowest at – Base  Pulmonary Vasoconstriction Caused By – Hpoxia  Pulmonary Vasoconstriction Accentuated by – Increase CO2  Asthma Most Imp Diagnosed By -- FEV1/FVC  In Fibrosis FEV1/FVC Remain -- Normal  In Asthma and COPD FEV1/FVC – Decreased  Lung CA –Smoking >Radon >Asbestos  Asbestos – Lung CA >Mesothiloma  Primary Tb -- Ghone Complex + Lower Lobe  Secondary Tb -- Cavitation + Upper Lobe  Activated in Lung – Angiotensin 2  Inactivated in Lung – Bradykinin( By ACE) & Serotonin  Sarcoidosis Characteristic – Erythma Nodosum (Davidson)  Sarcoidosis Diagnosed Histologically by – Non Caseating Granuloma(Robins)  Hydrocorisone differ from Dexamethasone Because they – Retain Na Renal  Dilute Urine(Decrease Osmolarity)-- Early DCT(Macula Densa ) > Thick Limb  Dilute Urine(Decrease Osmolarity)-- Thick Limb >> DCT Note : Difference between Early DCT and Only DCT  In Dehydraion(ADH) Concentrated Urine(Increase Osmolarity) –CD(Vasa Racta)  Erythropoeitin secreted by -- Peritibular capillaries > Mesangial Cells  Kidney Podocytes -- At visceral layer of bowman capsule  Cresents -- formed by parietal cells lining bowman capsule  GFR measure Clinically / Best Estimated -- Creatinine clearance  GFR best Way to Measure -- Inulin  Best way to Measure RPF -- PAH  Best test for renal failure -- Creatinine clearance  Clearance -- PAH >K >Inulin >Urea > Sodium> Amino acid and Glucose  Concentrating urine in summer or during fasting-- ADH  Loop diuretics act on -- Thick ascending limb  Thiazide diuretics act on -- Early DCT  Osmotic diuretics act on -- PCT  Renal columns contain—Interlobar Artery  Capsule Contain – Interlobular Artery  Glomerulus Contain – Interlobular Artery  Hilum Contain – Segmental Artery  Medullary rays contain -- Collecting ducts  Prone to Ischemia-- PCT  Maximum water & sodium absorption -- PCT  Maximum water & sodium absorption with any hormone --PCT  Maximum potassium absorption -- PCT  Potassium loss due to dietry irregularities -- Distal tubules  ADH-- Increase Urea transport to DCT  ADH -- Inhibited by alcohol  ADH -- Regulates plasma volume / urine osmolarity  ADH --V1 receptors cause vasoconstriction  ADH -- V2 receptors act on kidney  Highest Tubular transport maximum – Glucose >PAH > Lactate  Threshold for Glucose –200(Guyton)  Sodium Absorption -- Aldosterone  Sodium excretion -- ANP  Net SODIUM Absorption -- Aldosteron & ANP  Renin -- Produced by JG cells  Renin -- Long term B.P regulation  Baroreceptor respond maximally to – Increasing BP(Ganong)  Most Rapid Response to Decrease BP – Baroreceptor  Most Potent Response to Decrease BP – CNS Ischemic  CNS Ischemic Activate at – 60 or Below 60 mmhg(Guyton)  Maintain During Shock – Baroreceptor  Maintain as a Whole – RAAS  Long Term BP Regulation – RAAS  Over all most important – RAAS  SubENDOthelial deposits -- SLE, Diffuse proliferated GN ,Membrane proliferated GN  Sub EPIthelial deposits -- PSGN  Intramembranous Deposits -- Diffuse Proliferated GN , Membrane Proliferated GN type 2  Focal segmental Glomerulonephritis -- Massive Protienuria  Mild Hypomagnesemia Stimulate Parathyroid -- Hypercalcemia  Severe Hypomagnesemia suppress Parathyroid – Hypocalcemia  Hypermagnesemia Cause -- Hpocalcemia  Hypokalemia is associated with – Metabolic Alkalosis  Hyperkalemia associated with –Metabolic Acidosis  Hypokalemia – Decrease Nerve Excitability In RMP  Hyperkalemia – Increase Nerve Excitability In RMP  Hyponatremia – Decrease Hight of Action Potential  Hypernatremia – Increase Hight of Action Potential  Hypocalcemia – Increase Excitability  Hypercalcemia – Decrease Excitability Micro  Ascetic Tap – E-coli  Peritonitis – E-coli  Pyogenic Peritonitis – Bacterioides  Peurperal Sepsis – Group B streptococcus > E coli > Bacterioides  Nasopharyngeal CA – EBV  Oropharyngeal CA – HPV  Lung CA – CMV  Respiratory Symptoms – Ascaris  Fisherman With Anemia +Echymosis -- Vitamic C deficiency  Fisherman With Anemia – B12 Deficiency – Diphyllobothrium  Microcytic Anemia – Ankylostoma  Conjuctival Swelling – Loa Loa  Global Blindness – Cataract > Chlymydia > Glucoma  Rectal Prolapse – Trichuris Trichura  Muscle(Myalgia) – Trichinella Spiralis  Portal HTN – Schistosoma Mansoni + Japonicum(Lateral Spine)  Pulmonary HTN – Schistosoma Haematobium(Terminal Spine)  Cholangiocarcinoma – Clonorchis Sinesis  Hydatid Cyst – Echinococus  Neurocysticercosis(Brain Cyst) – Tenia Solium Malaria  Plasmodium malarie can lead to--Nephrotic syndrome (Membranous GN)  Plasmodium Vivax and ovale has-- Hypnozoite stage (means sleep)  Primaquine is DOC to kill-- Hypnozoites.  Shortest pre-erythrocytic phase is seen in -- Plasmodium Falciparum.  Longest pre_erythrocytic phase is in -- Plasmodium Malariae  Species that cause relapse are --Vivax and ovale  Most common non falciparum malaria is --Plasmodium Vivax.  DOC for non falciparum malaria is --Chloroquine.  Malignant tertian malaria is caused by --Plasmodium falciparum  Benign tertian malaria (48 hours) is caused by --Ovale/vivax  Quartan malaria (72 hours ) caused by --Plasmodium Malariae  Quotidian malaria caused by -- plasmodium Knowlesi > Falciparum  Anemia in malaria is --normocytic normochromic.  Dormant phase of malaria--Hypnozoite  Malaria enter into human body as --Sporozoite  Sporozoite divide in liver as --Merozoite  New specie of malaria is –Knowlesi  STD by – Chlymydia > Gonorrhea > Syphlis  Tubuovarian mass – Gonorrhea  Honymoon Cystitis – E coli Biochemistry Vitamins  B1 Deficiency --Dry Beri ber ,,Wet Beri beri ,Wernicke korsakoff Measured by Transketolase activity  B2 Deficiency – Corneal Vascularization  B3 Deficiency – Pellagra( Diarrhea,, Dementia , Dermatitis )  B5 Required – Co factor for Co enzyme A  B5 Deficiency – Adrenal Insufficiency   B7(Biotin) – Bind Avidin in egg and Carrier of One carbon  B7 -- Role in liver Metabolism  B9(Folic acid) – One Carbon Transfer  B9 Deficiency – NTD  B12 Deficiency -- Megaloblastic Anemia  Vit A deficiency Early Sign -- Night Blindness(Lipincot)  Vit A Toxicity – Scaly Dermatitis > Jaundice,, NTD  Optic Neuritis – B12 > B6  Peripheral Neuritis -- B1 >B6 >B12  Carbohydrate Metabolism – Thiamine  Protien Metabolism – Riboflavin  Lipid Metabolism -- Biotin Amino Acids  Ketogenic – Leucine and Lysine  Postive charge – HAL( Histidine ,, Arginine & Lysine)  Negtive Charge – Aspartate and Glutamate  DNA has – Histidine  Amino Acid deficiency causes cell injury -- Glycine  Amino acid cause injury to cell -- Choline  Amino Acid causing renal stones – Lysine(COLA)  Amino acid in abnormal metabolism -- Tryptophan Cell Cycle  INTERPHASE....Chromosomes REPLICATE  INTERPHASE....DNA REPLICATE  INTERPHASE....Barr Bodies are studied  INTERPHASE is divided into...  1.G1  2.S (SYNTHESIS Phase)  3.G2  4.Mitosis ( also called M phase & cytokinesis is a part of it )  G1...Primary Growth , Protiens , Organelles , mRNA Synthesis )  G1...Also Called growth phase  G1... Longest phase ( 8to 10 Hours)  G1 Check point...To check if DNA is damaged  S....DNA Replicate  S....Cytotoxic & cancer drugs act here to destroy DNA  S.....5 to 6 hours  G2...Secondry growth ( between S phase & Mitosis)  G2...Short ( 3 to 4 hours)  G2 Check point... To check if DNA has replicated properly  MITOSIS / M Phase  M...Shortest (2 hours)  M... To see spindle assembly and allignment  M...Nuclear content divide  M...genetic material is Chromosome (Genetic material is chromatid when NOT in M phase)  M... Divided into Prophase, prometaphase, Metaphase, AnaPhase , Telophase, Cytokinesis  PROPHASE....Spindle fibers appear Chromosome Condensation  PROPHASE...Centriole start moving to the oposite end & chromosomes first appear  PROMETAPHASE....Spindle fibers attach to chromosome & chromosome movement  PROMETAPHASE....Nuclear membrane dissolve marking the begining of prometaphase  METAPHASE...Chromosome Allignment at Equatorial Plate  METAPHASE.....Chromosome thickest  METAPHASE......Chromosome begin to divide  METAPHASE...Karyotyping  ANAPHASE.... Division of chromatids & sister chromatids move to opposite side  ANAPHASE....NON Disjunction  TELOPHASE...Spindle fibers disappear & Decondensation of Chromosomes  TELOPHASE...Complete divison  TELOPHASE....Nuclear membrane formation  CYTOKINESIS....Cytoplasm divide  Barr Bodies....Heterochromatin  Barr Bodies....have X chromosome  Barr Bodies....seen under light microscope  Barr Bodies....ABSENT in Turner  Barr Bodies....Scanty In Turner  Barr Bodies....Diagnostic for Turner   One Barr body in Klinfelter  NO. of Barr bodies in OX.....No Barr Bodies  NO. of Barr bodies in XX... 1 Barr Body  NO. of Barr bodies in XXX....2 Barr bodies  Best Test for chromosomal abnormalities is Karyotyping  Cell to Cell – Cadherin  ECM TO ICM – Intermediate Filament  ECM to Cytoskeleton – Integrin  Leukocyte Adhesion to Endothelium – ICAM(CD18 Subunit) Organelles  Detoxification of drugs – SER  Detoxification of Alcohol in Toxic Dose –SER  Detoxification of Alcohol in Normal Dose – Peroxisomes( Oxidase and H2O2 )  Lysosomes Contain – Hydrolytic enzyme  SER Originate from – Peroxisome  Lysosome Originate from – Golgi Body  Continue with Nuclear membrane – RER  Nissle Substance in –RER  Lydeg Cell Has – SER  Mitochondria – power house + self-replicating + Short chains Fatty acids Metabolism  Double membrane bounded organelles – Nucleus and Mitochondria  Golgi bodies – Packaging of cells  Production of proteins – Ribosomes > RER  Centrioles make – Basal body ( basal body makes cilia and flagella )  Hypertrophy – Increased in size ( Increased DNA content)  Hyperplasia – Increased in number  Hypertrophy and Hyperplasia both together – Uterus in Pregnancy Cancer Marker  Cytokeratin – Carcinoma(Epithelial)  Vimentin – Sarcoma (Mesenchymal)  Desmin – Muscle  Pharmacology  DOC for T. Solium – Praziquental > Niclosamide > Albendazole  DOC for C. Difficile – Metronidazole > Vancomycin (Levinson)  DOC for mild C. Difficile – Metronidazole (Levinson)  DOC for Severe and resistant C.Difficile – Vancomycin (Levinson)  DOC for Travller Diarrhea – Norfloxacin > Metronidazole  1st Line in AF -- Beta Blockers (Davidson)  For Rate control in AF -- Beta Blockers & Digoxin (Davidson)  For Rhythm Control in AF with no IHD – Flecainide(Davidson)  For Rhythm Control in AF with IHD – Amidarone( Davidson)  DOC For Cardiogenic Shock – Dopamine & Dobutamine  DOC for Hypotension UnRecordable BP -- Dopamine  DOC for Anaphylactic Shock – Adrenaline(Epinephrine)  DOC for Pseudomonas – Ceftazidime  DOC for UTI by Pseudomonas -- Ciprofloxacin  DOC for OCD – Clomipramine  DOC for SAH – Nimodipine  DOC for acute Pancreatitis – Pethidine > Morphine  DOC for Post Surgery Analgesia in Asthma Patient – Pethidine (Oxford Anasthesia Book)  DOC for Post Surgery Analgesia– Ketorolac > Pethidine  Drug in morning Sickness –Pyridoxine  Drug in motion Sickness – Meclizine  Drug in Mountain Sickness – Acetazolamide  DOC for Meningitis Adults – Ceftriaxone > Cefotaxime  DOC for Meningitis in Baby – Pencillin G  DOC in endometriosis – Medroxy progesterone > Leuprolide > Danazole(Ten Teacher)  DOC for Pregnancy induced HTN – Labetalol >Methyl dopa  DOC for Pregnancy Hypertensive Emergency – Hydralazine > Labetalol  DOC for Eclampsia – MgSO4  DOC in Uterine Atony -- Oxytoxin > Ergometrine(Ten Teacher)  Anti Thyroid in 1st Trimester – PTU  Anti Thyroid in 2nd & 3rd Trimester – Methimazole  Crosses Placenta and affect Fetus – Methimazole > PTU  Don’t Cross Placenta – Thyroxin  Elderly Diabetic – Tolbutamide  Obese Diabetic – Metformin  Non Obese Diabetic – Sulfonylurea  Organophosphate poisning Antidote – Pralidoxime  Organophosphate poisning Symptoms Reversal –Atropine  Drug in Liver Decompensation used – Lorazepam &Oxazepam  Drug in liver Disease Pre operatively – Fentanyle  Drug Contraindicated in Liver Disease – Pentazocin > Paracetamol  Hepatic Encephalopathy Progress by – Diuretic >Paracetamol  NM Blocker in Asthma –Cisatracurium  NM Blocker in Liver disease – Atracurium  Pancuronium Eliminated by -- Kideny (80 percent)  Rocuronium Eliminated by – Liver (75-90 percent) & Kidney  Diazepam Act through -- Interneuron  Morphine Release –Histamine  Terbutaline cause – Fetal Hypoglycemia and Maternal Hyperglycemia  Analgesic effect of TCA – 1-2 weeks (Davidon)  Antidepressent effect of TCA—3-4 weeks  Safe Analgesic dose NO – 25 ppm  Safe Analgesic dose NO In 8h– 25 ppm  Safe Analgesic dose NO In 24 h – 100 ppm  Morphine Decrease -- Apnea Thereshold  Local Anasthesia cross Placent by – Simple Diffuion  Scrulfate doesn’t Let Cimetidine to absorb  Cimetidine Decrease Scrulfate Metabolism  More Local Anesthetic in Blood in – Intercostal Block  Delayed Respiratory Depression – Fentanyl  Therapeutic Index Determine – Drug Safety  Potency Determine -- Dose  Benzodiazepine Cause Hypotension in – Hypovolumia > Old age  Highly Selective COX 2 – Celecoxib  Highly Potent COX 2 – Meloxicam  Irreversible COX 1 & COX 2 inhibitor – Aspirin  Reversible COX 1 & COX 2 inhibitor – NSAID  Low dose Aspirin inhibit – TXA2  Cardiotoxic – Bupivacaine  Priaprism by – Trazodon  Gingival Hyperplasia by – Phenytoin  Pulmonary Fibrosis by – Methotrexate  Cardiomegalay by– Adriamycin  Kernicterus by – Sulphonamide  Reversible Oligospermia by– Salfasalazine  Indirect Hyperbilirubinemia by– Methyldopa  Orange urine by – Rifampicin  Gout by– Pyrazinamide  Methmoglobenemia by – Procain  Red Man Syndrome by – Vancomycin  Grey Man Syndrome by – Amidaron  Gray Baby Syndrome by – Chloremphenicol  Allominium hydroxide(No receptor in Body) cause – Constipation  Magnesium Hydroxide cause -- Diarrhea  Low estrogen OCP cause – Hepatic Adenoma  High Estrogen OCP Prolong/Long term use cause – Endometrial CA  Estrogen Containing OCP Increase risk(Common Complication) of – Thromboembolism(DVT)  HRT(Mixed) cause – Breast CA(Robins) > DVT  Digoxin Toxicity increase by – Hypokalemia & Alkalosis  Digoxin Toxicity Cause – Hperkalemia  Thiazide cause – Hypokalemia> Hyperglycemia > Hyperlipidemia> Hyper uricemia >Hyper calcemia  Thrombocytopenia by – Heparin >Quinidine > Thiazide > Chloremphenicol  Diazepam Side effect – Loss of Beat to beat Variability > Neonatal Hypotonia  Thiopental – Action Terminated by Redistribution in Tissue and fat(FA)  Ketamine -- Increase HR and BP(Sympathomimetic) Ketamine  Profound Analgesia  Anasthetic in Asthma  Cause Bronchodilation  Raised ICP( Avoided in Head Injury)  Used in Burn Patient and Haemodynamically Unstable Halothane  Increase Cerebral Blood Flow  Cause Malignant Hyperthermia  Cause Skeletal Muscle Contractions  Dissociates on Light Bupivacain  First Sign of toxicity – Ringing in Ear  Serious Side effect Arrhythmia  Safe Dose 150mg  Rupivacain preferred over it because of Less CNS toxic Neurology  CNS -- Oligodendrocytes  PNS -- Schwann cells  Repairing cells -- Astrocytes  Grey matter -- Protoplasmic astrocytes (overall abundant)  White matter--Fibrous astrocytes (abundant astrocytes )  Adult spinal cord -- Lower border of L1 or upper border of L2  Neonates spinal cord -- Upper border of L3  Endoneurium --- Individual nerve fiber  perineurium ---- Bundle of nerve fibers  Epineurium --- Entire Nerve  Fasciculus Gracilis -- Lower limb Sensations  Fasciculus Cuneatus -- Upper limb Sensations  Loss of light Reflex but intact accommodation reflex -- PRETECTAL NUCLEUS (MIDBRAIN AT THE LEVEL OF SUPERIOR COLLICULUS )  Loss of Accomodation reflex -- Cerebral cortex  Loss of Accomodation -- Cerebral cortex  Loss of Accomodation + 3rd CN Involvment -- Midbrain ( due to Edinger westphal nucleus )  Corneal reflex lost -- Pons  Heating + Sympathetic effect – Post Hypothalmus  Cooling + Parasympathetic – Ant Hypothalmus  Overall temperature regulation -- Ant Hypothalmus(Preoptic Nucleus)  FOLIA-- Cerebellum Fold  HYPERACUSIS -- Geniculate ganglion ( medial wall of middle Ear )  Broca aphasia -- motor aphasia + Non-fluent + area 44 and 45 + inferior frontal gyrus  Wernicke aphasia -- sensory aphasia + fluent + area 22+ superior temporal gyrus  Global aphasia -- Both Wernicke and broca aphasia + arcuate fasciculus  Anomic aphasia -- mild fluent aphasia + failure of word retrieveal + angular gyrus  Lesion in DCML(Post White Column)-- SENSORYY ATAXIA> ASTEROGNOSIA  Loss of Proprioception lesion in – Posterior Column(DCML)  Loss of Proprioception mechanism is – Lateral Inhibition(Guyton)  Reduced motivation and depression -- FRONTAL LOBE  Characteristic of cerebellum lesion -- Dysdiadochokinesia >Dysarthria  Resting Tremor-- Substansia Nigra  Intentional tremors – Cerebellum  IJV after Coming out of Jugular foramen relation –ICA  IJV With in jugular foramen relation – Accessory Nerve  Neostriatum -- Caudate + Putamen  Corpus Striatum – Caudate + Lentiform  Lentiform -- Putamen + Globus Pallidus  Olfactory Cortex location – Posterior inferior Temporal Lobe +Uncus  Olfactory Area location – Anterior Perforating Substance  Fastest fibers -- A alpha  Fast pain fibers -- A delta  Slow pain fibers -- C fibers  Preganglionic fibers -- Beta fibers(True Autonomic)  Postganglionic fibers -- C fibers(Autonomic)  Pain From finger tip by – A delta  Proprioception from finger tip – B fiber  Type A>B>C affected by -- Pressure  Type B>A>C affected by-- Hypoxia  Type C >B>A affected by-- Anesthesia  Itching -- Slow C fibers  Itching Track – Anterior Spinothalmic Track  Sleep Centre -- Preoptic nucleus  Circadian Rhythm -- Suprachiasmatic nucleus  Chorea (jerky+ quick movements ) -- caudate nucleus  Athetosis ( slow + writhing ) -- Globus pallidus  Hemi-ballismus -- Sub-thalamic nuleus lesion  Fusiform gyrus (TEMPORAL LOBE ) – Face Recognization (unable to recognize face called propognosia )  Cingulate gyrus (LIMBIC SYSTEM) -- EMOTIONS  Sexual centre -- NUCLEUS ACUMBENS  Hippocampus -- Short term memory + recollection in long term memory ( long term memory formed by new Protein synthesis )  Large receptive field -- Pain And temp  Structure close to crus cerebri -- Substantia nigra  Medial leminiscus formed by decussation of --INTERNAL ARCUATE FIBERS  In UMN lesion fibers decussate at the level of -- PYRAMID  Cerebellum connected to Midbrain by -- Superior cerebellar peduncle  Bleeding from mastoid antrum -- Sigmoid sinus  Climbing Purkinje fibers originate from -- Inferior olivary nucleus  Sub-dural hematoma -- Emissary veins >superior cerebral veins + common in Alcoholics and shaken babies + crescent shaped  Extradural Hematoma -- Middle meningela artey ( branch of maxillary artery ) + LUCID INTERVAL (unconsciousness ) + bioconvex shaped  Subarachnoid hemorrhage -- Rupture of saccular aneurysm + worst headache of life + increase risk for hydrocephalus  Spinal nerves -- Mixed nerves ( both sensory and motor fibers ) + formed in intervertebral Foramina + exit intervertebral Foramina  Spinal ganglia -- Pseudounipolar neurons  Skeletal muscle – Multipolar  Olfactory – Bipolar   Dorsal column -- fine touch + pressure + vibrations + proprioception  Meissner corpuscles -Light Touch and Low Frequency Vibration—Upto 40Hz &At fingertips  Paccinian corpuscle – High frequency Vibrations(40-400Hz) and Deep Touch  Rapidly Adapting -- Pacinian > Meissner  Ruffini nerve endings – Deep static pressure  Meckle nerve endings -- Position + Deep Static touch + Secrete Serotonin  Fine movements of hand -- Controlled by CEREBELLUM and Carried by Corticospinal tracts  Centre for direct autonomic reflexes -- Hypothalamus  MCA (upper limbs + Aphsia ) Supplies – Insula and Opercula  ACA ( lower limbs + aphasia ) Supplies – Secondary Somasthetic Area  TABES DORSALIS -- ATONIC BLADDER  Proximal muscle Flexion -- Rubrospinal tracts  Proximal muscle Extension -- Vestibulospinal tracts  Inhibitory output in CNS -- Purkinje cells  Ptosis + Mieosis-- Horner syndrome  Ptosis+Mydriasis -- 3rd Nerve palsy  Ptosissis + normal pupil -- Myesthenia gravis  Site of fusion of binocular vision -- Visual cortex  Day vision+ color Vision -- Cones  Night vision + increased sensitivity to low light -- Rods  Anterior layer of retina contains -- Retinal pigment epithelium CSF  CSF Density is 1.0005.  CSF Specific Gravity is 1.005.  CSF PH is 7.33.  CSF is isotonic with serum.  CSF has Equal sodium as compared to plasma.  CSF has High magnesium and chloride as compared to plasma.  CSF has More Creatinine as compared to plasma.  Rest every thing is Low in CSF as compared to plasma (Protien more Low than glucose)  CSF is produced by – Ependymal cells   CSF Provides nutrition to – CNS  Arachnoid granulations are seen by naked eye  Indicator for CSF Leak -- Beta 2 Transferin  CSF Has Cushion like effect  Maximum determinant of CSF composition is Ependymal cells  CSF Pressure – 10-20 cm H2O or 60-150mm H2O or 6-15mmhg  CSF production – 20ml/h  CSF production – 450 -500 ml /day  CSF in Ventricle – 150ml  Lateral ventricle to 3rd via Interventricular Foramina of Monro  3rd to 4th via cerebral aqueduct ( blockage can cause hydrocephalus )  4th to Subarachnoid space via Foramen Magendie and Foramen Luschka  CSF made by choroid plexus (Ependymal cells ) in 4th and lateral ventricle  CSF absorbed by arachnoid granulations and then drains into Dural venous sinus Lamina  Lamina 1-6 – Dorsal(Posterior) Horn  Lamina8-9 -- Ventral(Anterior) Horn  Lamina 7 &10 – Intermediate Horn  Lamina 1 – High Threshold mechanoreceptor, Noxious stimulus & A delta pain  Lamina 2 – C fiber Pain & Substantia gelatinosa  Lamina 3-4 -- Low Threshold mechanoreceptor  Lamina 6 – Deepest Layer, Joint skin Signal  Lamina 7 – Largest Area, Dorsal Nucleus of Clarke  Lamina 10 – Central Canal Medulla Upper Medulla -Vestibular cochlear -Inferior olivary -Spinal trigeminal Middle Medulla -Nucleus ambiguas -Hypoglosal Nucleus -Dorsal motor Nucleus Vagus -Spinal Trigeminal Lower Medulla -Hypoglosal Nucleus -Dorsal Motor Nucleus Vagus -Spinal Trigeminal Anatomy  Most Common Bone injured in Body – Clavicle  Most Common Long Bone Fracture in Body – Clavicle  Most Common Long Bone Fracture in Lower Limb – Tibia  Most Common Carpal Bone Fracture – Scaphoid(Radial Artery)  Most Common Dislocated Carpal Bone – Lunate(Median Nerve- Carpal Tunnel)  Fracture of Hook of Hamate – Ulnar Nerve Damage (Cubital Tunnel)  Anatomical Snuff box Pain – Radial Artery  Fracture of Surgical Neck of Humerus – Axillary Nerve Damage  Fracture of medial epicondyle – Ulnar Nerve Damage  Fracture of Shaft of Humerus – Radia Nerve Damage  Wrist Drop – Radial Nerve Damage  Anterior Dislocation of Shoulder joint – Axillary Nerve Damage & Post Circumflex artery Damage  Quadrangular Space injury -- Axillary Nerve Damage & Post Circumflex artery Damage  Small Muscle of Hand affected lesion in – C8-T1 > Ulnar+Median > T1 > Ulnar  Ulnar nerve damage at Elbow – Loss of Sensations in medial 1/3rd palmar and dorsal aspect + Hypothenar wasting  Ulnar nerve damage at Wrist – Claw Hand  Median nerve damage at Elbow – Hand of Benedict  Median nerve damage at Wrist –Carpal tunnel Syndrome ( Thenar sensation lost > wasting )  In median nerve damage – Opposition and abduction is not possible  Abduction of Arm upto 15 Degree – Supraspinatus(Suprascapular Nerve)  Abduction of Arm upto 90 Degree – Deltoid (Axillary Nerve)  Abduction of Arm Above 90 – Trapezius(Spinal Accessory Nerve) & Serratous Anterior (Long Thoracic Nerve)  Scratching of Back – Lattismus Dorsi(Dorsal Thoracic Nerve)  Chief Supinator of Hand -- Bicep Brachi  Total Claw Hand – Lumbricals Paralysed  Tendon Courses through Shoulder Joint – Long Head Bicep  Head of Humerus Supplied by – Arcuate > Anterior Circumfex artery  Neck of Humerus Supplied by – Posterior Circumflex artery  Most commonly dislocated bone in the lower limb is -- Patella  Most common neuropathy in the lower limb is -- Compression of common peroneal nerve against neck of fibula  Longest muscle in the body is -- Sartorius  Thickest nerve in the body is -- Sciatic nerve  Largest bone of the body is -- Femur  Largest & most complicated Joint in the body is -- Knee joint  Largest sesamoid bone in body is -- Patella  Strongest ligament in the body is -- iliofemoral ligament  Strongest tendon in the body is -- Tendocalcaneus  Largest synovial cavity in the body is synovial cavity of the -- Knee joint  Most commonly nerve used in the body for grafting is -- Sural nerve  Most commonly used vein in body for grafting is -- Great saphenous vein  Most commonly used muscle in the body for grafting is -- Plantaris & Palmaris longus  Locking muscle for knee is -- Quadriceps Femoris  Unlocking muscle for knee is -- Popliteus  ACL injured – Anterior Dislocation of Tibia  PCL injured – Posterior Dislocation of Tibia  ACL injured – Posterior Dislocation of Femur  PCL injured – Anterior Dislocation of Femur  Ankle Sprain(Inversion) Ligament Injured – Lateral ligament >Anterior Talofibular  Excessive Eversion ligament Injured – Tibial Collateral(Medial)  Saphenous nerve accompany Great saphenous vein  Sural nerve accompany small saphenous vein  Deep peroneal nerve accompany anterior tibial artery  Head of Femur Supplied by in Adults – Retinacular >Medial Circumflex artery  Head of Femur Supplied by in Child – Obturator artery  Neck of Femur Supplied by – Medial &Lateral Circumflex artery  Foot Drop – Common peroneal nerve Injured  Left or right dominant supply of heart is determined by -- Posterior interventricular(Descending) artery.  Great Cardiac vein accompany -- Left ant. Descending Artery  Middle Cardiac vein accompany -- Post. Interventricular artery  Small Cardiac vein accompany – Marginal artery  Ant. Cardiac vein drains directly into -- RT. Atrium  Left lobe – 5cm  Right Lobe – 2.5cm  Pain of angina from heart is carried by -- Sympathetic nerves  Pain of pericarditis is carried by -- Phrenic nerve  Fibrous Pericardium and Parietal layer of Serous Pericardium is supplied by Phrenic nerve  Mediastinal Pleura Supplied by – Phrenic Nerve  Visceral layer of serous pericardium is called Epicardium  Right border of Heart formed by -- Right Atrium  Right border of Heart formed on Xray by – SVC >>SVC+Right Atrium  Base of heart is formed by -- Left atrium  Left border of Heart formed by -- Left Ventricle(Apex Beat)  Anterior(Sternocostal) Surface formed by – Right Ventricle  Inferior(Diaphragmatic) Surface formed by – Left Ventricle  Epicardium supplied by – Coronary Artery  Pericardium supplied by – Pericardiophrenic artery  Anterior 2/3rd IV Septum supplied by – LAD(LCA)  Posterior 1/3rd IV Septum supplied by – PDA(RCA)  Left Circumflex supply – Left and Right Ventricle  Xiphisternum Vertebrae level – T9  IVC begin at – L5  True Ribs – 1-7  False Ribs – 8-10  Floating Ribs –11-12  Upper Esophagous -- Inferior Thyroid artery  Middle Eophagous – Descending thoracic aorta  Lower Esophagous – Left Gastric  Azygous vein anterior to Right root of lung  Aorta posterior to Left root lung  Phrenic nerve anterior to Root of lung  Vagus Nerve posterior to Root of Lung  IVC Blocked Above Azygous vein dilation in – Azygous vein > Left Gastric Vein  IVC Blocked Upto Azygous vein dilation in – Right Ascending Lumber vein & Right Subcostal Vein  IVC Blocked Below Azygous vein dilation in – Ascending Lumber vein  Muscle of Quite Inspiration – Diaphram and External Intercostal  Muscle of Forced Inspiration – SCM & Serratous Anterior  Quite Expiration – Passive and by Elastic Recoil of Lung  Muscle of Forced Expiration -- Internal Intercostal  Accessory Muscle of Expiration – External Oblique  T8 - Caval Opening -- Inferior Vena Cava and Right Phrenic Nerve , Extent of IVC = T8 to L5  T10 -- Umbilicus , Esophageal Hiatus (Esophagus , Esophageal vessels , and Vagus nerves)  T12 – Aortic Opening (Aorta , Azygous , and Thoracic Duct)  T3 to T6 – Oblique Fissure of Lung  T4-5 – Bifurcation of Trachea ,,Dermatome Nipple ,, Extent of Trachea = C6 to T4  C3 – Hyoid in erect position  C2 - C3(C2>C3) – Tracheostomy Level Adults  C3 - C4(C3>C4) – Tracheostomy Level Children  C6 – Cricoid Level ( Esophagus and Trachea Starts )  C2-3—Supraclavicular  C3-4 – Infraclavicular  Foramen Ovale -- Acessory Meningeal artery pass  Foramen Spinosum -- Middle Meningeal artery pass  Superior Orbital Fissure -- V1(Opthalmic nerve) pass  Foramen Rotandum-- V2(Maxillary Nerve) Pass  Foramen Ovale -- V3(Mandibular Nerve) pass  Jugular Foramen – CN 9,10,11(Accessory part) & Sigmoid Sinus  Hypoglossal Canal – CN 12  Foramen Magnum – Brainstem & Spinal Part of CN11  Esophagous Passed through -- Left Crus of Diapharam(Big Snell)  Medial Arcuate ligament formed by -- Psoas Muscle  Median Arcuate ligament formed by – Right & Left Crura  T12 – Celiac Trunk  L2 – Renal Artery  L1 – Superior mesenteric artery  L3 – Inferior Mesenteric Artery  L4 – Bifurcation of Descending Aorta  L5 --Start of IVC  Transpyloric Plane – Pylorus of Stomach , Fundus of Gallbladder, Hilum of Kidney, First part of Duodenum , Origin of SMA , Tip of 9th Costal Cartilage , Lower end of Spinal Cord  Right Kidney anteriorly Related to—Liver  Right Kidney Hilum Anteriorly Related to – 2nd Part Duodenum  Posterior to Right Kidney – 12th Rib &Diaphram  Anterior to Left Kidney – Stomach & Pancreas  Posterior to Left Kidney – 10th -11th Ribs & Diaphram  2nd Part of duodenum Attached posteriorly to – Transverse Mesocolon  Right Accessory Hepatic Artery Branch of – SMA  Superior Epigastric Artery Branch of – Internal Thoracic Artery  Inferior Epigastric Artery Branch of – External iliac Artery  Superficial Epigastric Artery Branch of – Femoral Artery  Superior Rectal Branch of – Inferior Mesenteric artery  Middle Rectal Branch of – Internal iliac artery  Inferior Rectal Artery Branch of – Internal Pudendal Artery  Bulbourethral Gland -- Deep Pouch  Greater Vestibular Gland – Superficial pouch  Difficulty in Standing from Sitting – Gluteus Maximux Damage(Inferior Gluteal Nerve)  Shuffling Gate – Gluteus medius + minimus(Superior Gluteal Nerve)  Right Pelvis Sink – Left Gluteus medius +minimus Damage  Injection Given in Superior Lateral Compartment to avoid Damage to – Sciatic Nerve(Bailey)  Mediolateral Episiotomy Damage to – Bulbospongiosus > Superficial Tranverse Perineal Mucle  Mediolateral Episiotomy Structure at Risk – Levator Ani  Median Episiotomy Damage to – External Anal Sphinter  During Episiotomy Perineal Body Damage then Muscle Injured – Levator ani  Major Support of Uterus -- Cardinal(Tranverse Cervical) Ligament   Dynamic Support – Pelvic Diaphram Ureter  During Hystrectomy Ureter Damag at A>B>C A-Cardinal Ligament(Uterine Vessel) B-Behind Broad Ligament C-At Pelvic Brim(Ovarian artey)  Ureter Damage at Pelvic Brim – While crossing Common iliac Vessel  While removing Ovary damage to – Internal iliac Artery  Anterior to Ureter – Gonadal Vessel  Posterior to Ureter – iliac Vessel  Common Site of Lodging of ureteric stones overall/Adults – Vesico ureteric Junction  Common Site of Lodging of ureteric stones in Child – Pelvico ureteric Junction  Ureter Narrows at -- Vesico ureteric Junction > Where it enters Bladder Uterus Prolapse 1st Degree – Decent of Cervix within Vagina 2nd Degree –Decent of Cervix to Introitus 3rd Degree –Decent of Cervix Outside Introitus 4th Degree(Procidentia) -- Whole Uterus outside Introitus In 1st and 2nd Degree – Uterosacral Ligament Damage 3rd Degree – Uterosacral > Cardinal Ligament Damage 4th Degree – Cardinal Ligament Damage Random  Important Test For Transplant – HLA typing  Best Blood Cell for HLA Sampling– WBC  Best Site for HLA Sampling –Bucal Mucosa  Best Tissue for HLA Sampling – Bone marrow  Hyper acute Rejection – Pre formed antibodies(Type 2 Hypersensitivity)  Acute Rejection -- CD8 Cells(Type 4 Hypersensitivity)  Chronic Rejection -- CD4 Cells(Type 2+4 Hypersensitivity)  Dense Granules and IgE receptor – Basophil  Granules and IgE receptor – Mast cell  Granule and Histaminase enzyme – Eosinophil  Most Common complication of DM –Dry Gangrene  Most Common complication of Diabetic Foot – Wet Gangrene  Most Common Complication of 3rd Degree Burn over all – Contracture  Most Common Complication of 3rd Degree Burn in Black – Keloid  Most common Complication of Burn – Scar  Endarteritis Obliterans Associated with – Syphilitic aneurysm  Neonatal Recurrent Infection Deficiency of – IgG  Child Recurrent Infection Deficiency – IgA  Neonatal Infection Diagnosed by -- IgM  Mother Affected with Rubella and Baby got Symptoms Diagnosed by – IgM  Mother Affected with Rubella and Baby Symptoms less to See immunoglobulin – IgG2  Rubella in pregnancy complication overall – Deafness > Cataract  Rubella in pregnancy complication With in 7 weeks – Cataract  Rubella in pregnancy complication After 7 weeks – Deafness  After Transplant most Common malignancy – Skin  After Transplant Common malignancy in 1 or 5 Year – Lymphoproliferative  After Transplant Common malignancy after 10-15 Years – Skin  Most Common Manifestation of autoimmune disease – Hematological  SLE involve most commonly – Joints(90%) And Skin(85%)  SLE Involve most common organ then – Skin  Potent Antioxidants – Glutathione > Vit E > C> A  Radicals – OH >H2O2 >Superoxide  Uninucleate – Most Cells  Binucleate – Liver Cells  Multinucleate – Skeletal Muscle  Cannot Regenerate – Lens> Skeletal Muscle > Neuron > Cardiac  Cannot Reproduce -- RBC  Most Common remnant of Allantois – Urachal Cyst  Patent Lumen of Allantois – Urachal Fistula  Complete Failure of Urachus to obliterate – Urachal Sinus(Urine Disharge)  Stratified Cuboidal – Sweat Gland Lining Duct  Stratified Columnar –Salivary Gland Lining Duct  Vertebral Bodies Limited by –Anterior an posterior Longitudinal Ligament  Vertebral Bodies kept in position by –Anterior an posterior Longitudinal Ligament  Vertebrae joined to Adjacent Lamina – Ligament Flavum  Hyperextension of neck Ligament Injured – Anterior Longitudinal Ligament  Hyper flexion of neck Ligament Injured – Ligament Nuche  Drowning – Pulmonary edema  Near Drowning – Metabolic acidosis  Emboli First first go to – IVC  Emboli first loadge in – Pulmonary artery  In response to Haemorrhage – Decrease venous Capacitance  After Compensation of Haemorrhage – Decrease Heart Rate  Least Circulate in Blood – Pleuri potent Stem cell > Basophil (Clinical Hematology Book)  Corneal Opacity – Chloroquine  Retina Deposit – Thioridazine  Lens Deposit – Chlorpromazine  Post Infleunza Most Common Organism – Strep Pneumonae  Post Infleunza Brown Rusty Sputum – Strep Pneumonae  Post Infleunza Yellow thick Sputum – Staph Aureus  Post Infleunza Current jelly Sputum – Klebsiella Pneumonae  After Meal – Glycolysis occur(FA)  Between Meal – Glycogenolysis > Gluconeogenesis(FA)  Just Lateral to Xiphisternum Structure damage – IVC  Just Lateral and Below to Xiphisternum Structure damage – IVC  Needle passed in 6th ICS on Right damage to – Right atrium  Cut end of Vagus nerve Stimulated – Decrease HR  Vagus nerve proximal end cut and Central Part Stimulated – Apnea occur  Patient Naked heat loss by -- Radiation  Patient Naked and lying on Surface(Table) heat loss by –Conduction  Patient Naked and Temp Mention heat loss by – Radiation+Conduction  Patient Naked and Humidity mention heat loss by—Convection  Remodeling of tissue by – Metalloproteinase >Collagenase > Elastase  Asthma Involve – Medium sized bronchioles  Infarction Involve – Small sized Bronchi  Line of Zahn seen in -Coraline Thrombus -Pre mortem Thrombus -Arterial Thrombus  Chicken Fat Appearance seen in – Post Mortem Thrombus  Post traumatic epilepsy – With in 2 Year (Current Medicine Textbook)  Amoeba Produce Lesion in – Caecum(Davidson)  Cavernous Sinus Infection – Superior ophthalmic vein(KLM)  Cavernous Sinus Thrombosis – Superior ophthalmic vein(KLM)  Cushing Syndrome Differ from Obesity by – Proximal Myopathy  Longest Incubation Period – Latent HIV > Hep B > IM > HIV  Pure Serous – Parotid  More Mucinous +Few Serous – Sublingual  More Serous + Few Mucinous – Submandibular  True Conjugate –Sacral Promontry to upper pubic Symphysis(11cm)  Obstetric Conjugate –Sacral Promontry to middle or posterior pubic Symphysis(12cm)  Diagonal Conjugate–Sacral Promontry to Lower pubic Symphysis(10.5cm)  Antigen Presenting cells in Skin – Langerhan  Spleen Filteration function – Red Pulp (FA)  Spleen Immunological Function – White Pulp  High Karyo pyknotic Index – Increase Estrogen activity >Cervical Dysplasia  Cell Membrane Bond – Hydrophobic+ Hydrogen > Hydrophobic +Covalent  Integral Protien by – Hydrophobic  Peripheral Protien by – Electrostatic Interactions  Coccygeal Segment – L1  Coccygeal Ligament – S2 –Cocyx 1  Mural Thrombi Arise From – Left Ventricle >> Left Atrium  Dialyzing Fluid has more Glucose and HCO3 as compared to plasma  Tear Has High Sodium in its composition  Tear Compare to plasma Has Equal Sodium  Tear Compare to plasma has Low Glucose and Urea  Tear Compare to plasma has More K,Cl,Ca & Amino acids  Foreign Body in Supine – Apical(Superior) Segment of Right Lower Lobe  Foreign Body in Sitting/Standing(Upright) -- Posterior basal Segment of Right Lower Lobe  Foreign Body in Right Lateral – Posterior Segment of Right Upper Lobe  Foreign Body in Left Lateral – Inferior Lingular of Left Upper Lobe  Carboxy Hb Half life at Room Air(21%) – 4-5 H  Carboxy Hb Half life at 100% O2 – 90min  Carboxy Hb Half life at Hyperbaric O2 – Less than 30 min  Zero Order Kinetic Drugs – Phenytoin , Ethanol &Aspirin  Zero Order Kinetic – Half Life Increase with increase Dose  First Order Kinetic – Half Life Constant with Increase Dose  Uncoupling Oxidative Phosphorylation – NE >Thyroxin >Epinephrine  Anti Tumor Cell –NK Cells  Anti Cancer Nature Mechanism – Apoptosis  Drug Woarsen Angina – Vasopressin > Theophyllin  Glucose Transport in Placenta(Facilitated) and Kidney(2ndry Active-Biport)  Typhoid Reside in Payer patches(1-4weeks) & Gall Bladder(>4 weeks)  Lymphoid Tissue and Simple Cuboidal Epithelium – Payer patches  Lymphoid Tissue and Simple Squmous Epithelium – Palatine Tonsil  Ovary – Simple Cuboidal  GIT –Simple Columnar  Conjunctiva—Stratified Columnar  Central Venous Pressure Increased in(Ganong) -Decrease HR -Increase Blood Volume -Straining   Bicep Jerk – C6  Tricep Jerk – C7  Knee Jerk – L3  Knee Cap – L4  Ankle Jerk – S1 BioStat Case Control Study -Disease vs Non Disease -Related to ODD Ratio Cohort Study -Group with Risk Factors and Group without Risk Factors -Related to Relative Risk -Cause to Effect -Forward Study Cross Sectional Study -Disease and Risk Factors Sensitivity (True Positive) -Detect Disease and Rule out Disease(FA) Specificity(True Negative) -Detect Non Disease and Rule in Disease(FA) Attrition Bias – Related to Follow up and Prognosis Berkson Bias – Related to Different Exposure Normal Distribution(Gaussian) Curve – Mean=Median=Mode Positive Skew – Mean >Median >Mode Negative Skew – Mean