posted by my friend Dhruv

Hello Guys,

This is a place to share your self made notes for NBDE part 1 or Part 2. I am using my friend Dhruv's notes in here. Much more to come and see things. I am sure there is a lot more in our bags than you can digest..
So be ready with your antacid pills ('')



Random Notes...TRANSPORT
Random Notes....
TRANSPORT:

DIFFUSION:
[O2] transport across Alveolar epithelium!

FACILIATED DIFFUSION:
[GLUCOSE] reabsorption through KIDNEY!!!

OSMOSIS:
[H2O] transport across INTESTINAL epithelium/ Collecting DUCT
Mostly 2* to [Na+] transport!

1* active transport : ATPase pump activity!!!
[Na+-K+] ATPase PUMP activity::::: 02 K+ Influx --03 Na+ Efflux
As in during “REPOLARIZATION”!!!
[Ca++]- ATPase PUMP activity
[Glucose/GALACTOSE]-ATP ase PUMP activity in SMALL INTESTINE
[AminoAcid]-ATPase PUMP activity in SMALL INTESTINE
HCl secretion by STOMACH ::::: [H+--K+]ATPase PUMP ===Also Known as PROTON PUMP!!

2* active transport: electrochemi. potential diff. created by pumping ions out of the cell is used!
Counter-Transport = ANTIPORT ----- Exchanger pathway OF [Na+ --Ca++]!!!
- 03 Na+ influx [Goes from HIGH to LOW concentration-Gradient]
- 01 Ca++ Efflux [Goes from LOWER to HIGH concentration-Gradient]
- NOTE: ‘EXCHANGER’ mechanism is MORE=70 times efficient than Ca++-ATPase PUMP!

CO-Transport ==== Same Directed Pathways!
SOLUTE species goes in direction of concentration-gradient!
Other Molecule is OPPOSITE to concentration Gradient!
NOTE: Integral cell membranous TRANSPORT proteins are REQUIRED!
E.g. GLUT=SGLT!!!
1) GLUT-1: Neurons, RBC, Blood-Brain BARRIER!
2) GLUT-2: Liver, Pancreas
3) GLUT-3: Neurons
4) GLUT-4: Skeletal Muscle, Adipose Tissue
5) GLUT-5: Small Intestine, Testis ------- for FRUCTOSE
Exception: as Here GLUCOSE is 1* active transport!

FILTRATION: =======All 2* to BLOOD PRESSURE!!!
CVS circulation ----> ISF
Bowman’s Capsule

PINOCYTOSIS:====== (-PINO-)====== Drinking Of Cell!
Proximal Tubule----> Kidney tubular cells

EMINOCYTOSIS===== [K+] entry related!

Random Notes 3.....
Random Notes 3
A patient has been on a self-imposed "starvation diet" for four months, and has lost 60 pounds while consuming only water and vitamin pills. If extensive blood studies were performed, which of the following would be expected to be elevated?

A. Acetoacetic acid
B. Alanine
C. Bicarbonate
D. Chylomicrons
E. Glucose

Ans.) A

STARVATION ------> HIGHER Glucose requirement!
Body maintains BLOOD GLUCOSE level to the max. possible
level by activating Glucagon/E/NE!!!
###### INCREASED
? Glycogenlysis
? Gluconeogenesis
? B-oxidation
? KETOLYSIS
? Proteolysis (Alanine Utilization INCREASES!!!)
###### RESULT:
? INCREASED ----- (AcetoAcetic Acid + B-OH-Butatrate) in blood!
? DECREASED----- Alanine / HCO3- / Chylomicrons!!!
? NORMAL/Subnormal -----Glucose

[NOTE: HCO3- decreases due to its buffering action with [H+] released from (–ve) charged Ketones!!! …………………… Due to (-Ve)KETONE binding with the (K+)]

###### Interpretation: STARVATION!!!
? Ketoacidosis
? HypoKalemia
? Hypertension
? Hyperpolarized muscle cells!

Random Notes 2.....Epithelium
Random Notes 2....
EPITHELIUM:

? Bowman’s Capsule:
# Bowman capsule: 02-layered-epithelium!
1) visceral inner layer = specialized cells ===== podocytes == Filtrating Epithelium!
2) parietal outer layer= single layer= flat cells= simple squamous epithelium!

? MACULA DENSA:
# Cells lining THE “DISTAL CONVULATED TUBULE”!!!
1) MACULA DENSA= *Highly Sensitive to the [IONIC] content & [H2O] volume of the fluid in DCT!
- WITHOUT ‘Aldosterone’ ---> [K+] & [H+] Secretion!
- WITH ‘Aldosterone’---> [Na+] Reabsorption!!!
- Macula Densa functions to STIMULATE “Juxtra-Glomerular” cells to release “RENIN” & in turn helps to STIMULATE “Renin-Angiotensin-ALDOSTERONE” AXIS!!!

? Juxta-Glomerular Cells =
# Cells lining the AFFERENT arterioles:
? CONSTRICTION of Afferent-Arterioles’!
? Stimulates ‘RENIN’ synthesis!
> Angiotensinogen --RENIN----> Angiotensin 1 ---ACE(Lung)----->Angiotensin 2
> Angiotensin 2 -------------------> Constriction of efferent arterioles!!!
> Angiotensin 2 -------------------> Adrenal Cortex Stimulation to Secrete Aldosterone

? MASSANGIAL cells:
# Located in close proximity with arterioles!!!
? INTRAGLOMERULAR massangial cells:
-------> FILTRATION (along with outer parietal layer of FENESTRATED simple squamous
Epithelium & INNER visceral layer of PODOCYTES)
STRUCTURAL SUPPORT
PHAGOCYTOSIS ( of BASAL LAMINA COMPONENTS & Immunoglobulins )
? EXTRAGLOMERULAR massangial cells:
-------> Erythropoitin Synthesis!!!

Random Notes 4
Random Notes 4
The medical record of a patient indicates a systolic murmur due to increase in afterload, producing a pressure gradient between the ventricle and aorta during ejection. Which of the following best describes the condition?

A. Aortic insufficiency
B. Aortic stenosis
C. Mitral insufficiency
D. Mitral stenosis

ANS) B


? Venous Return ---> Preload ----> End Diastolic Volume
So, INCREASED/DECREASED preload(END diastolic Volume) -----------> DIASTOLIC MURMUR!


? Systolic Pressure ->Afterload --> CARDIAC output
So, INCREASED/DECREASED Afterload (cardiac output) ------------------> SYSTOLIC MURMUR!!!


a) AORTIC INSUFFICIENCY:
? INCREASED end-diastolic-volume!
? INCREASED Pre-load!
? DIASTOLIC MURMUR

b) AORTIC STENOSIS:
? INCREASED Systolic pressure ( INCREASED contractibility of LEFT VENTRICLE)
? INCREASED after-load!
? SYSTOLIC MURMUR!

c) MITRAL INSUFFICIENCY:
? Reduced SYSTOLIC ejection (Due to BACK-FLOW from Ventricle to ATRIUM)
? REDUCED AFTER-LOAD
? SYSTOLIC Murmur!!!

d) MITRAL STENOSIS:
? REDUCED END-DIASTOLIC-VOLUME
? REDUCED PRE-LOAD
? DIASTOLIC MURMUR!!!!

Random Notes 5
Random Notes 5
At 25 weeks of pregnancy, an unidentified infection greatly compromises the viability of a developing fetus. The level of which of the following hormones in the mother's blood is most likely to be affected?

A. Estriol
B. Free thyroxine
C. Human chorionic gonadotropin
D. Human chorionic somatomammotropin
E. Progesterone

ANS) A
ESTORGEN release in mother is Dependent on active fetus, as ACTIVE FETUS’ ADRENAL CORTEX & Liver releases DHEA, which in turn stimulates ESTORGEN release from Mother placenta!!!
MOTHER placenta desulfates ‘DHEA’!
DHEA aromatize “Estorgen” to “Estriol”!!!!!

So, HERE ‘Estriol’ will be compromised,
NOW “TBG” proteins’ concentration is DIRECTLY proportional to “ESTORGEN” in serum!!!
So, “TBG” will be reduced & so, TOTAL SERUM thyroxine, too!!!!
But, “FREE THYROXINE” remains INTACT due to FEED-back-Regulation!!!

Random Notes 6
Random Notes 6
COLLAGEN SYNTHESIS:

##############Rough Endoplasmic Reticulum (RER)#############

1) Three peptide chains in ribosomes::::
? PREproCollagen: ------------------------------- Synthesis in ‘RIBOSOME’ !!!
# registration peptides at one end
# signal peptide at another end
2) PREproCollagen---> sent into ---> lumen of the RER
? ‘Signal Peptides’ cleaved inside the RER
? Procollagen: after cleavage of signal peptide inside the lumen of RER, now it’s known as PROCOLLAGEN---------- in “Rough Endoplasmic Reticulum”
? Hydroxylation of lysine and proline--------- in “Rough Endoplasmic Reticulum”!!

########### GOLGI APPARATUS ###################

? PROCOLLAGEN & Hydroxyproline/Hydroxylysine -- Golgi Apparatus!!!
? Glycosylation of specific hydroxyproline/lysine--------- in “GOLGI apparatus”!!!
? “Triple helix” structure --------------------------------------- in RER
# HYDROXYPROLINE/HL ? essential for Stabilization of Triple Helix!!
? Procollagen/TRIPLE helix is shipped to the--------------- golgi apparatus,
[where it is packaged and secreted by exocytosis]
# FINAL Packaging --------- in Golgi Apparatus
# Secreted by Exocytosis --- from Golgi APP.

############# Outside the cell ##################

1) “Registration peptides” are cleaved
2) Triple Helix(Procollagen) -----> “Tropocollagen” [ procollagen peptidase.]
3) Multiple tropocollagen ---------->“collagen fibrils” [Lysyl Oxidase , Cu++ ]
4) multiple collagen fibrils -------> collagen fibers
5) Collagen is attached to cell membranes ---> fibronectin and integrin.

Random Notes 6
Random Notes 7
least effective emulsifying agent

A. lecithin
B. bile salt
C. cholic acid
D. cholesterol
E. deoxycholic acid
ANS.) D

Note: Water-solubility depends on Surface-tension!
# Lesser the SURFACE TENSION -------------------------------> HIGHER water-solubility!!! # “LIPIDS” [CHOLESTEROL esters / TAG / Neutral lipids] ----> HYDROPHOBIC & Higher Surface-Tension!!!

# BILE ACIDS = Amphipathic nature
? CHOLIC ACID ---------------- Hydrophobic = Unconjugated = Remains in LIVER & Reabsorbed BACK!!!

? Chenodeoxycholic acid------ Hydrophobic = Unconjugated = --Same as abov
? Deoxycholic Acid------------- Hydrophilic== Conjugated == NOT Reabsorbed!!!
? Lithocholic Acid--------------- Hydrophilic== Conjugated == NOT Reabsorbed!!!



All ingradients of BILE in LIVER:
? CHOLESTEROL: esters --- Hydrophobic ---- HIGHEST surface Tension---NOT an emulsifier!!!
? Cholesterol Degradation -------> CHOLIC ACID + CHENO[deoxy]Cholic Acid

? BILE ACIDS:
? Bile Acid --> CHOLIC ACID + CHENO[deoxy]Cholic Acid
[ 1* synthesized in LIVER = 1* BILE ACIDS]
? Common Bile Duct opens through Ampulla of VATER in the 2nd part of small intestine: Where, in the ileum ; they are converted in to
---->Deoxycholic Acid+ Lithocholic Acid!!! [BY: Bacterial Degradation]
[2* synthesized by BACTERIA = 2* BILE ACIDS]

From here, BOTH 1* & 2* are REABSORBED back to ENTERO-HEPATIC
CIRCULATION & goes back to LIVER!!!

? 2* bile acids, though can be CONJUGATED with GLYCINE & TAURINE in the LIVER to be water-soluble!!!!!

? BILE SALTS:
? SALTS of Bile ACIDS (=CHOLATE!!!) --- Na Cholate!!!
? DeoxyCholic/Lithocholic Acid (Cholyl-Co-A) + Glycine/Taurine + Na Cholate(=Bile Salts
[CONJUGATION of 2* bile acids with AAs]

Random Notes 8.... Cytochrome!!!
Random Notes 8.... Cytochrome!!!
101) Pyrole ---> Porphyrobillinogen ----> Porphyrin + Fe ----> Heme ----> Cytochrome
Porphyrin+ Mg ---> Chlorophyl

# INNER MITOCHONDRIAL MEMBRANE:
? Complex-1 NADH Dehydrogenase [H+] into Cytoplasm , [e-]transfer
? Comlex-2 Succinyl Dehydrogenase [e-]transfer

Co-enzyme-Q [Ubiquinone = Derived from Intermediate products of cholesterol]

? Complex-3: Cytochrome B,C1 [H+] into Cytoplasm, [e-]transfer

Cytochrome C

? Complex-4 : Cytochrome A,A3 [H+] into Cytoplasm, [e-]transfer
O2 from mitochondria is utilized for: [H+]+[e-]+O2 in cytoplasm ? Metabolic [H2O]

? Complex-5::: ATP synthase: [H+] in cytoplasm ---> [H+] in Mitochondria
ATP synthesis
FAD--------> FADH2 : 02 P/O
NAD-------> NADH2: 03 P/O

# UNCOUPLERS: Aspirin/ 2-DNP=Dinitrophenol /COLD=Shivering ---> 00 P/O -->HEAT!!!
# CYANIDE: acts on Cytochrome-C

# Cytochrome B, B5 -------------> Ribosomes ( Important for PROTEIN Synthesis)
SER ---> DESATURATION of Fatty Acids after synthesis!
RER---->PROTEIN synthesis!!!
# Cytochrome P450 -------------> LIVER = Glucoronide Conjugation/ Drug Detoxification!!!
PRESENT in PEROXISOME!!!!!
# Cytochrome B6, F -----------> Plastoquinol / Prostacyanin Reductase