Livedr.org

FMGE Important Topics (Taken from some forum)

http://rapidshare.com/files/149532940/FMGE_Important_Topics_A-Z.rar.html

All the Question papers from 2002 to March,2008, the latest MCI Syllabus(2008) & AIIMS Syllabus.

http://rapidshare.com/files/114056484/Latest_question_papers_syllabus.rar

Congratulations to all the AFMGians who made it through the MCI SEP 2008.

Write down pertaining to your preps so that it might prove beneficial to the future MCI aspirants.

PP’s PREPARATION

Well,
My prep goes this way…..
First be acclimatized by my history: - I have been studying all the standard books and have finished them atleast 2 times (except - Panniker Micro) ha ha …..
My specific prep for the MCI cum USMLE started from 5th year….
FIRST THING WE DID - Make a study group (My study group has 100 % result) Astonishing ain’t it ???
Well, My study group rocked from the day we made it and it has proved to be very very effective.

FIFTH YEAR: - We finished HARRISON in medicine - ONLY THE IMPORTANT SECTIONS I.E. GIT, COLLAGEN, KIDNEY, HEART, ENDOCRINE . This was not the first time we were reading HARI ! It was actually we had done it in 4th year during our classes and this was the time for revision, group discussion and also for doing the undone things.

We did LOVE and BAILEY - Started from KIDNEYS, then GIT, then ARTERIES VEINS and the THORAX and ENDOCRINE. Same schedule, discussion plus MCQs.

We did CHAUDHARY - Physiology - Actually this is the subject that is discriminated the most in the med schools of the Russian federation and it was high time to understand that in order to get the concepts straight into the Cortex was the EXTENSIVE KNOWLEDGE of Physio….. As we were doin this for the first time, we selected simple book like chaudhary so that we can get the complete insight of the subject.

(P.S. - The above mentioned schedule was run in hand with the routine classes and also we did the routine work too along with this, you can imagine the amount of fun and enjoyment we had to sacrifice for this)

SIXTH YEAR -
We started the new year by ripping the pages of GHAI (Pedia)
Finished all the sections especially those considered important - the only thing we did not do is the GIT and CARDIO and KIDNEY section (because it is already covered in the HARRI) Pedia specific things can be learnt from the MCQ books.

Next thing we did was PHARMA the TERRIBLE -
We got hold of KDT for pharma - Me and my friends had already done pharma from KDT in 3rd year but revision was the main thing for this subject to make it palatable…. Lolz…..
It was a mission of 5 weeks and we accomplished in 5 weeks + 3 Days. All KDT and MCQs from GOBIND RAI book of MCQ s with explanations, actually the new drugs in that book are quite nice.

JANUARY WAS THE AFMG COACHING IN RUSSIA - Completed the following from the notes
OBS GYNAE - The most read subject and we were doing this like 4th or 5th time
MICROBIO - Had read panniker in 3rd yr, but VIKAS SIR’s Notes made it damn easy.
PHARMA - The pharma wizard Dr. Vikas Dhikav made impact straight to the CORTEX. Actually my planning was a double advantage one, as we did pharma second time from KDT a fortnight earlier, reading DHIKAV’s notes was a cake walk and was quite easy to refine the concepts.
FORENSIC - just a matter of hours after the notes.

NOW WAS A 15 day TIME BREAK FROM THE GROUP DISCUSSION where we were going to do DERMATOLOGY by self reading.
My colleagues did it from HARRI’s skin section. I preferred CMDT 2008. and then we solved MCQs from ACROSS explanation. Too concise but worth donating time.

BACK CAME THE GROUP DISCUSSION -
Started GANONG PHYSIOLOGY - I have no words to describe this wonderfully written book. Really, GUYTON is nuts (I have done CNS and CVS from GUYTON earlier) but the clinical correlation and the sweet text was nice. I recommend this book A MUST for all MCI plus MLE aspirants. (About 20 questions that I found in 2008 MCI were concepts tested from this GANONG)
Also we watched KAPLAN PHYSIOLOGY LECTURES From DVDs. To get an extra edge over the concepts.
PLUS SIDE BY SIDE my colleagues did subjects like RADIO, ORTHO and ENT but I was busy in the political matters of the college and the preparation for the CONVOCATION CEREMONY and so missed the last 2 months of studies (was not distressful, I knew I would cover that later).

SPARED SOME TIME FOR BIOCHEMISTRY - Did KAPLAN lectures totally…. Excellent, I think no one in the world can teach biochemistry the way KAPLAN ppl do…. A MUST SEE TO MASTER BIOCHEMISTRY.

And then came GOS EXAM, CONVOCATION, became doctors and back we came to INDIA and then DELHI where we sharpened the concepts and knowledge from coaching classes.

CONCLUSION - To get the MCI cracked in the first shot the preparation should be like us. (Atleast I think that way) don’t know what others think. If you have not done uptill now and wanna do it, WORK HARD, miracles do happen if you work…..
COACHING is not COMPULSORY but NECESSARY to ORIENT yourselves especially you are blank. It ALWAYS GIVES CONFIDENCE and INSPIRATION plus the ATMOSPHERE Of COMPETITIVENESS which you cannot get home. But mind one thing - It is not a guarantee to pass the exam 100 percent, but it surely INCREASES YOUR CHANCES if you are NUTS. There are some ppl who do not need coaching yet they join inorder to be with friends and continue with group discussion…. (ha ha …. Those whom I refer have got my point)
P.S. - Anatomy, Radiology, Opthalmo- AFMG notes, Pathology - GOLJAN AUDIO (USMLE STUFF)
Had done ROBBINS in 3rd year, overviewed and revised with GOLJAN PATHO LECTURES.

BACK CAME THE GROUP DISCUSSION -
Started GANONG PHYSIOLOGY - I have no words to describe this wonderfully written book. Really, GUYTON is nuts (I have done CNS and CVS from GUYTON earlier) but the clinical correlation and the sweet text was nice. I recommend this book A MUST for all MCI plus MLE aspirants. (About 20 questions that I found in 2008 MCI were concepts tested from this GANONG)
Also we watched KAPLAN PHYSIOLOGY LECTURES From DVDs. To get an extra edge over the concepts.
PLUS SIDE BY SIDE my colleagues did subjects like RADIO, ORTHO and ENT but I was busy in the political matters of the college and the preparation for the CONVOCATION CEREMONY and so missed the last 2 months of studies (was not distressful, I knew I would cover that later).

SPARED SOME TIME FOR BIOCHEMISTRY - Did KAPLAN lectures totally…. Excellent, I think no one in the world can teach biochemistry the way KAPLAN ppl do…. A MUST SEE TO MASTER BIOCHEMISTRY.

And then came GOS EXAM, CONVOCATION, became doctors and back we came to INDIA and then DELHI where we sharpened the concepts and knowledge from coaching classes.

CONCLUSION - To get the MCI cracked in the first shot the preparation should be like us. (Atleast I think that way) don’t know what others think. If you have not done uptill now and wanna do it, WORK HARD, miracles do happen if you work…..
COACHING is not COMPULSORY but NECESSARY to ORIENT yourselves especially you are blank. It ALWAYS GIVES CONFIDENCE and INSPIRATION plus the ATMOSPHERE Of COMPETITIVENESS which you cannot get home. But mind one thing - It is not a guarantee to pass the exam 100 percent, but it surely INCREASES YOUR CHANCES if you are NUTS. There are some ppl who do not need coaching yet they join inorder to be with friends and continue with group discussion…. (ha ha …. Those whom I refer have got my point)
P.S. - Anatomy, Radiology, Opthalmo- AFMG notes, Pathology - GOLJAN AUDIO (USMLE STUFF)
Had done ROBBINS in 3rd year, overviewed and revised with GOLJAN PATHO LECTURES.

1.Aortic stenosis characteristics SAD:
Syncope
Angina
Dyspnoea

2.MI: basic management BOOMAR:
Bed rest
Oxygen
Opiate
Monitor
Anticoagulate
Reduce clot size

3.ECG: left vs. right bundle block “WiLLiaM MaRRoW”:
W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W in V3-V6 is Right bundle block.
• Note: consider bundle branch blocks when QRS complex is wide.

CVS II

4.Pericarditis: causes CARDIAC RIND:
Collagen vascular disease
Aortic aneurysm
Radiation
Drugs (such as hydralazine)
Infections
Acute renal failure
Cardiac infarction
Rheumatic fever
Injury
Neoplasms
Dressler’s syndrome

5.Murmurs: systolic types SAPS:
Systolic
Aortic
Pulmonic
Stenosis
• Systolic murmurs include aortic and pulmonary stenosis.
• Similarly, it’s common sense that if it is aortic and pulmonary stenosis it could also be mitral and tricusp regurgitation.

6.MI: signs and symptoms PULSE:
Persistent chest pains
Upset stomach
Lightheadedness
Shortness of breath
Excessive sweating

7.Heart compensatory mechanisms that ’save’ organ blood flow during shock “Heart SAVER”:
Symphatoadrenal system
Atrial natriuretic factor
Vasopressin
Endogenous digitalis-like factor
Renin-angiotensin-aldosterone system
• In all 5, system is activated/factor is released

8.Murmurs: right vs. left loudness “RILE”:
Right sided heart murmurs are louder on Inspiration.
Left sided heart murmurs are loudest on Expiration.
• If get confused about which is which, remember LIRE=liar which will be inherently false.

9.ST elevation causes in ECG, ELEVATION:
Electrolytes
LBBB
Early repolarization
Ventricular hypertrophy
Aneurysm
Treatment (eg pericardiocentesis)
Injury (AMI, contusion)
Osborne waves (hypothermia)
Non-occlusive vasospasm

10.Beck’s triad (cardiac tamponade) 3 D’s:
Distant heart sounds
Distended jugular veins
Decreased arterial pressure

11MI: therapeutic treatment ROAMBAL:
Reassure
Oxygen
Aspirin
Morphine (diamorphine)
Beta blocker
Arthroplasty
Lignocaine

12.CHF: causes of exacerbation FAILURE:
Forgot medication
Arrhythmia/ Anaemia
Ischemia/ Infarction/ Infection
Lifestyle: taken too much salt
Upregulation of CO: pregnancy, hyperthyroidism
Renal failure
Embolism: pulmonary

13.Murmurs: systolic vs. diastolic PASS: Pulmonic & Aortic Stenosis=Systolic.
PAID: Pulmonic & Aortic Insufficiency=Diastolic.

14.Murmurs: systolic vs. diastolic Systolic murmurs: MR AS: “MR. ASner”.
Diastolic murmurs: MS AR: “MS. ARden”.
• The famous people with those surnames are Mr. Ed Asner and Ms. Jane Arden.

15.Mitral stenosis (MS) vs. regurgitation (MR): epidemiology MS is a female title (Ms.) and it is female predominant
MR is a male title (Mr.) and it is male predominant.

16.Pericarditis: EKG “PericarditiS”:
PR depression in precordial leads.
ST elevation.

17.Jugular venous pressure (JVP) elevation: causes HOLT: Grab Harold Holt around the neck and throw him in the ocean:
Heart failure
Obstruction of venea cava
Lymphatic enlargement - supraclavicular
Intra-Thoracic pressure increase

18.Depressed ST-segment: causes DEPRESSED ST:
Drooping valve (MVP)
Enlargement of LV with strain
Potassium loss (hypokalemia)
Reciprocal ST- depression (in I/W AMI)
Embolism in lungs (pulmonary embolism)
Subendocardial ischemia
Subendocardial infarct
Encephalon haemorrhage (intracranial haemorrhage)
Dilated cardiomyopathy
Shock
Toxicity of digitalis, quinidine

19.Murmurs: innocent murmur features 8 S’s:
Soft
Systolic
Short
Sounds (S1 & S2) normal
Symptomless
Special tests normal (X-ray, EKG)
Standing/ Sitting (vary with position)
Sternal depression

20.Murmur attributes “IL PQRST” (person has ill PQRST heart waves):
Intensity
Location
Pitch
Quality
Radiation
Shape
Timing

21.Murmurs: locations and descriptions “MRS A$$”:
MRS: Mitral Regurgitation–Systolic
A$$: Aortic Stenosis–Systolic
• The other two murmurs, Mitral stenosis and Aortic regurgitation, are obviously diastolic.

22.Betablockers: cardioselective betablockers “Betablockers Acting Exclusively At Myocardium”
• Cardioselective betablockers are:
Betaxolol
Acebutelol
Esmolol
Atenolol
Metoprolol

23.Apex beat: abnormalities found on palpation, causes of impalpable HILT:
Heaving
Impalpable
Laterally displaced
Thrusting/ Tapping
• If it is impalpable, causes are COPD:
COPD
Obesity
Pleural, Pericardial effusion
Dextrocardia

24.MI: treatment of acute MI COAG:
Cyclomorph
Oxygen
Aspirin
Glycerol trinitrate

25.Coronary artery bypass graft: indications DUST:
Depressed ventricular function
Unstable angina
Stenosis of the left main stem
Triple vessel disease

26.Peripheral vascular insufficiency: inspection criteria SICVD:
Symmetry of leg musculature
Integrity of skin
Color of toenails
Varicose veins
Distribution of hair

27.Heart murmurs “hARD ASS MRS. MSD”:
hARD: Aortic Regurg = Diastolic
ASS: Aortic Stenosis = Systolic
MRS: Mitral Regurg = Systolic
MSD: Mitral Stenosis = Diastolic

28.Mitral regurgitation When you hear holosystolic murmurs, think “MR-THEM ARE holosystolic murmurs”.

29.Sino-atrial node: innervation Sympathetic acts on Sodium channels (SS).
Parasympathetic acts on Potassium channels (PS).

30.Supraventricular tachycardia: treatment ABCDE:
Adenosine
Beta-blocker
Calcium channel antagonist
Digoxin
Excitation (vagal stimulation)

31.Ventricular tachycardia: treatment LAMB:
Lidocaine
Amiodarone
Mexiltene/ Magnesium
Beta-blocker

32.Pulseless electrical activity: causes PATCH MED:
Pulmonary embolus
Acidosis
Tension pneumothorax
Cardiac tamponade
Hypokalemia/ Hyperkalemia/ Hypoxia/ Hypothermia/ Hypovolemia
Myocardial infarction
Electrolyte derangements
Drugs

33.Sinus bradycardia: aetiology “SINUS BRADICARDIA” (sinus bradycardia):
Sleep
Infections (myocarditis)
Neap thyroid (hypothyroid)
Unconsciousness (vasovagal syncope)
Subnormal temperatures (hypothermia)
Biliary obstruction
Raised CO2 (hypercapnia)
Acidosis
Deficient blood sugar (hypoglycemia)
Imbalance of electrolytes
Cushing’s reflex (raised ICP)
Aging
Rx (drugs, such as high-dose atropine)
Deep Anaesthesia
Ischemic heart disease
Athletes

35.Rheumatic fever: Jones criteria • Major criteria: CANCER:
Carditis
Arthritis
Nodules
Chorea
Erythema
Rheumatic anamnesis
• Minor criteria: CAFE PAL:
CRP increased
Arthralgia
Fever
Elevated ESR
Prolonged PR interval
Anamnesis of rheumatism
Leucocytosis

36.JVP: wave form ASK ME:
Atrial contraction
Systole (ventricular contraction)
Klosure (closure) of tricusps, so atrial filling
Maximal atrial filling
Emptying of atrium

37.Coronary artery bypass graft: indications DUST:
Depressed ventricular function
Unstable angina
Stenosis of the left main stem
Triple vessel disease

38. Exercise ramp ECG: contraindications RAMP:
Recent MI
Aortic stenosis
MI in the last 7 days
Pulmonary hypertension

39.ECG: T wave inversion causes INVERT:
Ischemia
Normality [esp. young, black]
Ventricular hypertrophy
Ectopic foci [eg calcified plaques]
RBBB, LBBB
Treatments [digoxin]

40.Rheumatic fever: Jones major criteria JONES:
Joints (migrating polyarthritis)
Obvious, the heart (carditis, pancarditis, pericarditis, endocarditis or valvulits)
Nodes (subcutaneous nodules)
Erythema marginatum
Sydenham’s chorea

41.Myocardial infarctions: treatment INFARCTIONS:
IV access
Narcotic analgesics (eg morphine, pethidine)
Facilities for defibrillation (DF)
Aspirin/ Anticoagulant (heparin)
Rest
Converting enzyme inhibitor
Thrombolysis
IV beta blocker
Oxygen 60%
Nitrates
Stool Softeners

42.Atrial fibrillation: causes PIRATES:
Pulmonary: PE, COPD
Iatrogenic
Rheumatic heart: mirtral regurgitation
Atherosclerotic: MI, CAD
Thyroid: hyperthyroid
Endocarditis
Sick sinus syndrome

43.Atrial fibrillation: management ABCD:
Anti-coagulate
Beta-block to control rate
Cardiovert
Digoxin

44.Anti-arrythmics: for AV nodes “Do Block AV”:
Digoxin
B-blockers
Adenosine
Verapamil

45.Murmurs: systolic MR PV TRAPS:
Mitral
Regurgitation and
Prolaspe
VSD
Tricupsid
Regurgitation
Aortic and
Pulmonary
Stenosis

46.Apex beat: differential for impalpable apex beat DOPES:
Dextrocardia
Obesity
Pericarditis or pericardial tamponade
Emphysema
Sinus inversus/ Student incompetence

BIOCHEM I

Galactosaemia: enzyme deficiency
GALIPUT: Galactose 1 Phosphate Uridyl Transferase.
• There is an assay called the Galiput test for this.

Citric acid cycle compounds
“Our City Is Kept Safe And Sound From Malice”:
Oxaloacetate Citrate Isocitrate alpha-Ketoglutarate Succinyl-CoA Succinate Fumarate Malate

Folate deficiency: causes A FOLIC DROP:
Alcoholism
Folic acid antagonists
Oral contraceptives
Low dietary intake
Infection with Giardia
Celiac sprue
Dilatin
Relative folate deficiency
Old
Pregnant

Mitochondrial DNA (mt DNA) properties
“mt DNA”.
mt stands for: Maternal Transfer Mutates Tremendously (high mutation rate)

Vitamins: which are fat soluble
“The FAT cat is in the ADEK (attic)”:
Fat soluble vitamins are A,D,E,K.

Enzyme kinetics: competitive vs. non-competitive inhibition
With Kompetitive inhibition: Km increases; no change in Vmax. With Non-kompetitive inhibition: No change in Km; Vmax decreases.

Glycogen storage: names of types I through VI
“Viagra Pills Cause A Major Hardon”:
Von Gierke’s
Pompe’s
Cori’s
Anderson’s
McArdle’s
Her’s

Sickle cell disease pathophysiology
SICKle cell disease is due to a Substitution of the SICKsth amino acid of the B chain.

Glucagon function
“Mr. Gluca has Gone to the cAMP to bring out some Glucose”:
• Glucagon elevates glucose by cAMP mechanism.

Van den Bergh reaction (Jaundice test)
“Indirect reacting bilirubin = Unconjugated bilirubin”:
Both start with vowels, so they go together:
Indirect & Unconjugated.

Hemoglobin binding curve: causes of shift to right
“CADET, face right!”:
CO2
Acid
2,3-DPG (aka 2,3 BPG)
Exercise
Temperature

BIOCHEM II

DNA bond strength (nucleotides)
“Crazy Glue”:
Strongest bonds are between Cytosine and Guanine, strong like Crazy Glue (3 H-bonds), whereas the A=T only have 2 H-bonds. • This is relevant to DNA replication, as the weaker A=T will be the site where RNA primer makes the initial break.

Dicarboxylic acids (alpha, omega) C2 through C10: common names
“Oh My, Such Good Apple Pie, Sweet As Sugar!”:
Oxalic Malonic Succinic Glutaric Adipic Pimelic Suberic Azelaic Sebacic

Infantile Beriberi symptoms
Restlessness Sleeplessness Breathlessness Soundlessness (aphonia) Eatlessness (anorexia) Great heartedness (dilated heart)
• Alternatively: Get 5 of ‘em with BERI: Breathless/ Big hearted, Eatless, Restless, Insomnia.

AcetylCoA and acetacetylCoA: amino acids forming them
“A Lighter Lease” (A LyTr LeIs):
A=AcetylCoA or Acetoacetyl CoA
Ly=Lysine
Tr=Tryptophan
Le=Leucine
Is=Isoleucine

Fasting state: branched-chain amino acids used by skeletal muscles
“Muscles LIVe fast”:
Leucine
Isoleucine
Valine

Glycolysis steps
“Goodness Gracious, Father Franklin Did Go By Picking Pumpkins (to) Prepare Pies”:
Glucose
Glucose-6-P
Fructose-6-P
Fructose-1,6-diP
Dihydroxyacetone-P
Glyceraldehyde-P
1,3-Biphosphoglycerate
3-Phosphoglycerate
2-Phosphoglycerate (to)
Phosphoenolpyruvate [PEP] Pyruvate • ‘Did’, ‘By’ and ‘Pies’ tell you the first part of those three: di-, bi-, and py-.
• ‘PrEPare’ tells location of PEP in the process.

Fabry’s disease
FABRY’S:
Foam cells found in glomeruli and tubules/ Febrile episodes
Alpha galactosidase A deficiency/ Angiokeratomas
Burning pain in extremities/ BUN increased in serum/ Boys
Renal failure
YX genotype (male, X linked recessive)
Sphingolipidoses

B vitamin names
“The Rhythm Nearly Proved Contagious”:
• In increasing order: Thiamine (B1) Riboflavin (B2) Niacin (B3) Pyridoxine (B6) Cobalamin (B12)

BIOCHEM III

Citric acid cycle compounds
“Can I Ask Sharon Stone For My Orgasm?”:
Citrate Isocitrate Alpha-Ketoglutarate Succinyl CoA Succinate Fumerate Maleate Oxaloacetate

Golgi complex: functions
“Golgi Distributes A SPAM”:
Distributes proteins and lipids from ER
Add mannose onto specific lysosome proteins
Sulfation of sugars and slected tyrosine
Proteoglycan assembly
Add O-oligosugars to serine and threnonine
Modify N-ologosugars on asparagine

Pyruvate: products of complete oxidation
“4 Naked Fun 3 Coeds + 1 Guy”:
• Complete oxidation of pyruvate yields:
4 NADH FADH2 3 CO2 1 GTP

Catabolism steps of branched chain amino acids
“Truck hit the Ox to Death”:
Transamination
Oxidative decarboxylation
Dehydrogenation

Niacin deficiency: signs and symptoms
The famous 4 D’s:
Diarrhoea Dermatitis Dementia Death (if untreated)

Creatine phosphate: amino acid precursors
“Nice GAMs!”: Glycine Arginine Methionine
• Gam is slang for a person’s leg, especiallay an attractive female’s leg: “Nice gams = nice legs!”
• Creatine phosphate is a muscle energy store, and spontaneously converts to creatinine which is excreted in the urine in direct proportion to muscle mass: clinically useful, such as in MS Dx.

Enzymes: classification
“Over The HILL”:
Oxidoreductases
Transferases
Hydrolases
Isomerases
Ligases
Lyases
• Enzymes get reaction over the hill.

Insulin: function
INsulIN stimulates 2 things to go IN 2 cells: Potassium and Glucose.

Collagen concisely covered
COLLAGEN:
C-terminal propeptide (procollagen)/ Covalent Cross links/ C vitamin/ Connective tissue/ Cartilage/ Chondroblasts/ Copper Cofactor (Covalent Cross linking)
Outside the cell is where collagen normally functions/ Osteoblasts/ Osteogenesis imperfecta
Lysyl hydroxylase/ Lysyl oxidase (oxidatively deaminates lysyl and hydroxylysyl residues to form collagen cross links, last biosynthesis step)
Long triple helical fibers/ Ligaments
Alpha chains/ Attached by H bonds form triple helix/ Ascorbate for hydroxylation of lysyl and prolyl residues of pro-Alpha chains (postranslational modification)
Gly in every third position/ Glycosylation of hydroxyl group of hydroxylysine with Glucose and Galactose; GOlgi allows procollagen to GO outside of cell
Extracellular matrix/ Eye (cornea, sclera)/ Ehlers-Danlos Syndrome
N-terminal propeptide (procollagen)/ Nonhelical terminal extensions
• Note: Procollagen LEAVEs the cell to be cLEAVEd by procollagen peptidases

BIOCHEM IV

Malate-aspartate shuttle
“MAD commute”:
Malate in. Alpha-ketoglutarate and D (Aspartate) out.

Vitamins: which are fat soluble
KADE: Vitamin K Vitamin A Vitamin D Vitamin E

Phenylketonuria: which enzyme is deficient
PHenylketonuria is caused by a deficiency of: Phenylalanine Hydroxylase

GENETICS

Down syndrome features: complete
“My CHILD HAS PROBLEM!”:
Congenital heart disease/ Cataracts
Hypotonia/ Hypothyroidism
Incure 5th finger/ Increased gap between 1st and 2nd toe
Leukemia risk x2/ Lung problem
Duodenal atresia/ Delayed development
Hirshsprung’s disease/ Hearing loss
Alzheimer’s disease/ Alantoaxial instability
Squint/ Short neck
Protruding tongue/ Palm crease
Round face/ Rolling eye (nystagmus)
Occiput flat/ Oblique eye fissure
Brushfield spot/ Brachycephaly
Low nasal bridge/ Language problem
Epicanthic fold/ Ear folded
Mental retardation/ Myoclonus

Blots: function of Southern vs. Northern vs. Western
“SN0W DR0P”:
• Match up the 1st word letter with 2nd word letter:
Southern=DNA
Northern=RNA
Western=Protein
• The 0’s in snow drop are zeros, since there is no Eastern blot.

Down syndrome Pathology DOWN:
Decreased alpha-fetoprotein and unconjugated estriol (maternal)
One extra chromosome twenty-one
Women of advanced age
Nondisjunction during maternal meiosis

Pyrimidines nucleotides
“CUT the PY” (cut the pie):
Cytosine Uracil Thiamine are the PYrimidines

DiGeorge/ Velocardiofacial syndrome: features CATCH 22: Cardiac abnormalities
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia
22q11 deletion

Marfan syndrome features MARFAN:
Mitral valve prolapse
Aortic Aneurysm
Retinal detachment
Fibrillin
Arachnodactyly
Negative Nitroprusside test (differentiates from homocystinuria)

Cell cycle stages
“Go Sally Go! Make Children!”:
G1 phase (Growth phase 1)
S phase (DNA Synthesis)
G2 phase (Growth phase 2)
M phase (Mitosis)
C phase (Cytokinesis)

Cri-du-chat syndrome:
chromosomal deletion causing it is 5p(-)
What’s another name for a cat that’s five letters long and starts with a P? (Answer: AIPGE ).
Why is the cat crying? Missing its P.

APKD: genetics
ADult Polycystic Kidney Disease is Autosomal Dominant
• Also, “Polycystic kidney” has 16 letters and is due to a defect on chromosome 16.

Tay Sach’s features SACHS:
Spot in macula
Ashkenazic Jews
CNS degeneration
Hex A deficiency
Storage disease
• Extra details with TAY:
Testing recommended
Autosomal recessive/ Amaurosis
Young death (<4 yrs)

Chromosome 15 diseases
Chromosome 15 has its own MAP:
Marfan syndrome
Angelman syndrome
Prader-Willi syndrome

Bartter syndrome: inheritance
BARtter syndrome is autosomal recessive (AR).

Nucleotides: double vs. triple bonded basepairs
“TU bonds” (two bonds):
T-A and U-A have Two bonds. G-C therefore has the three bonds.

Imprinting diseases: Prader-Willi and Angelman
“Pray to an Angel”:
Prader-Willi and Angelman are the 2 classic imprinting diseases. • Which disease results, depends on whether 15q deletion is maternal or paternal. Keep them straight by: Paternal is Prader-Willi.

۞Gayathri

Hi Dr. Sumer..
I highly appreciate your effort to throw somelight in our matters…
i got few ques…

1-having completed DMRD…hw difficult is to complete DNB final?..its atleast a shorter and cheaper way to be DNB radio(equivalent to MD radio)…atleast for those..who r not single rankers and cant either afford 1 cr.

2-Can you list subjects…which u think..can be left…for MCI..i mean..or which can be given THE LAST PREFERENCe?.depending upon..hw tough they are and hw much weightage they constitue..eg..somebdy told me..anatomy is not worth reading initially as it hardly constitues 8-9 ques ..but comparitively demands more attention..dunno..hw true is tht…wht do u say abt this?(especially for MCI exam)
Thanks..dr. sumer

MCI Screening

Dr. Sumer..
having seen Sep`08 MCI paper…Wats ur personal view abt the paper-setters..?
Were the ques really of tougher quality…or it was mere preparedlessness which brought <10% result?
Few guys compared the Ques to be of AIIMS level..
I have studied quite many ques from AIIMS paper…they are just made of different quality..unlike many state PG exams..they are really smart and at times tough..
However..screening test like DNB …donot constitue such twisting ques…as its a qualifying exam and not a competitive exam..
Similary..does MCI too contain basic ques..as ideallly a qualifying exams shud contain?
==
Bottom line, i wanted to touch was…do we need to follow each subject rigorously, trying to beat AIIMS questions..or basic knowledge of ALL the subjects first should be grasped..than deepening into any particular subject?

Thanks a tonne..for replying:
Regards.

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Hello Dr Sumer!
I FINISHED MY FINAL MBBS &DOING MY INTERNSHIP NOW
PLS GUIDE REGARDING APPG MED ENTRANCE…..1.which series of mcq is best? 2.what sub &which topics 2 b conc more??

MCI screening

There r 2 institutes, so far i know, giving training to foreign student doctors for appearing FMGE. Delhi Institute for Advanced Medical Studies (DIAMS) and AFMG

Here r the links to their sites, DIAMS- http://diamsonline.org.in/index.php
AFMG- http://www.afmg.co.in/

Advertsiement from DAMS-Another coaching centre

Advertisement from Apex &AFMG

SIR,
I have passed out my final prof n now started my internship………… i have started to study mudit khanna 1 mcq…….. but i have a few doubts could you plz help me out?
1.My question is that after i had read the mcq n explanations of 1 year of a particular subject do i need to go to the main texbook or reference books to read bout the concerned topics in detail?……… could u please enlighten me on this topic………
2.Are postal coaching courses of ne use….. if yes how shud i go bout it?
3.Wat are the topics that shud be read from harrison in detail?
4.Shud i prepare notes for quick revision?
5.wat is the most effective way of memorising things so that i can recall them easily later?
Sir i hope u will surely answer my questions at the earlist…… i wud be highly obliged.
Thank you sir.

Sumer

Internship Study method

PG in germany is in german Language. To be eligible for it,you have to spend 2 years learning the german language, because you have to pass german language at the level of higher secondr schools in germany. The german language courses & their examination is held in India at MAX MULLER Bhavun Mumbai.

For non-EU is a very hard duty to achieve a chance for PG in any discipline however there are no.of vacancy created all day in germany.
For PG you must have.:-
-three years post diplom Experience,
-a good knowledge of German
-Recommendation from health ministry of your own country for higher education
-Stipend or sponsership from any organization or any body to accomodate here.
Some more demands from bureaucrate may be…?

In short cut for non EU doctors it is difficult to adapt here.Other than xaminations,bureucratie here is peak complexed.
For the residency,Germans,EU then non EU doctors resp.are prefered.However sometimes doctors from third world are selected by Chief doctors,but they would not take any guarantee for work permit and residential permit in Germany which is quite tough and complex.

It depends upon states,u have to pay or not?Possiblity to get admission is also depends upon University and seats available.The major problem is financial support.If u possess any stipend then easier to accomodate otherwise officially students are
allowed just for 90days(full time)per year or 180days(half time) to work.Using these benifits one can earn some money during vacation,though employers prefer employee for long term at least six months in full term,i.e.troublesome in Market to find a high payment Job.Parellel to study ,involvement im Job deteriotes your actual target.