here r some topics based on previous mcqs....

1.BODY COMPOSITION:-
in an average young adult male,
18% of body weight is protein & related substances,
7% is mineral
15%is fat..
remaining 60% is water
2/3rd is intracellular & 1/3rd is extracellular...
among 1/3rd extracellular:-1/4th is in vascular system..
& 3/4th as interstitial fluid.

ionic composition:-
ECF ICF
sodium ion:- 142mEq/L 10mEq/L
Potassium ion:- 4mEq/L 140mEq/L
calcium ion:- 2.4mEq/L 0.0001mEq/L
Mg ion :- 1.2mEq/L 58mEq/L
chloride ion:- 103mEq/L 4mEq/L
bicarbonate ion:- 28""/L 10mEq/L
phosphates:- 4mEq/L 75mEq/L
sulphates:- 1mEq/L 2mEq/L
Glucose 90mg/dl 0-20mg/dl
amino acids:- 30mg/dl 200mg/dl

Erlanger & gasser's classification of nerve fibers:-

fibre type:-A,B & C.
*** Fibre A & B are myelinated while C is unmyelinated.
**Fibre A is subdivided into:-
1.alpha
2.beta
3.gamma
4.delta
based on diameter & conduction velocity..
**** A alpha maximum diameter & maximum conduction velocity.

cholinergic receptors distribution:-

Cholinergic receptors can be divided into two types, muscarinic and nicotinic, based on
the pharmacological action of various agonists and antagonists.

1. Nicotinic :-found in N-M junction

Autonomic ganglia
& CNS.
2.Muscarinic:-
M1:-Cortex,Hippocampus
M2:-heart
M3:-Exocrine glands,GI tract
M4:-Neostriatum
M5:-substantia nigra.

***In smooth muscles M2,M3,& M4 type muscarinic receptors are found.

Sensory receptors for pain:-

When sensory nerve fibers are exposed to extremes, they signal pain. Pain receptors are
also called nociceptors.

Two types of sensory nerve fibers transmit signals that the brain interprets as pain.

* Aδ ("A-delta") fibers
o These are thinly-myelinated.
o They transmit signals rapidly that are associated with acute pain. This is "good pain"
because it warns you to do something to take care of the problems, e.g., a hot saucepan.
* C fibers
o These are unmyelinated and thus conduct impulses slowly.
Their activation is associated with diffuse, dull, chronic pain. This is "bad pain" because
it cannot be alleviated simply by removing the stimulus. It is pain generated by such
things as damaged tissue or pain that remains after the stimulus that caused acute pain
has been removed

retina:-some facts..
**** Cones are more in centre & decreases towards periphery cones respond to bright
light & role in color vision.
Fovea centralis:-only cones (max. visual acuity)
macula lutea:- cones > rods (photopic vision)
blind spot:-no rods no cones.
in periphery:-rods> cones (scotopic vision)
Thinnest part of retina:-fovea centralis.

The human cerebral cortex is 2-4 mm (0.08-0.16 inches) thick and plays a central role in
many complex brain functions including memory, attention, perceptual awareness,
"thinking", language and consciousness.
The surface of the cerebral cortex is folded in large mammals where more than two
thirds of the cortical surface is buried in the grooves, called "sulci". The
phylogenetically more ancient part of the cerebral cortex, the hippocampus, is
differentiated in five layers of neurons, while the more recent neo-cortex is
differentiated in six basic layers.

sections:
Occipital lobe - processes vision;
Temporal lobe - processes hearing, speech, language development
Parietal Lobe - processes sensory stimuli
Prefrontal lobe - allows us to plan and rehearse future actions; connected to the limbic
area to help regulate emotions
Frontal lobe - area where critical thinking and problem solving occur
Limbic system - controls emotions and long-term memory
Cerebellum - controls automatic movements and balance

ESR:-erythrocytes sedimentation rate:-some facts:-

Erythrocyte sedimentation rate (ESR) is a nonspecific screening test for various

diseases. It is a simple and inexpensive test that measures the distance that red blood
cells have fallen after one hour in a vertical column of anti coagulated blood under the
influence of gravity.
The amount of fibrinogen (a blood protein) in the blood directly correlates with the
ESR.. The use of the ESR as a screening test in asymptomatic persons is limited by its
low sensitivity and specificity as it is affected by many variables.
Women tend to have higher ESR values, as do the elderly. Obese people too tend to
have raised ESR for some unknown reason though this is not thought to have any
clinical significance.

Any condition that increases fibrinogen levels (e.g., pregnancy, diabetes mellitus, end-
stage renal failure, heart disease, collagen vascular diseases, malignancy, and chronic
infection) may elevate the ESR. In anaemia the ESR rises as the speed of the upward
flow of plasma is altered so that red blood cell aggregates fall faster. Macrocytic (larger)
red cells with a smaller surface-to-volume ratio also settle more rapidly.

ESR in healthy adults:-

Age<50
Men:- 0-15mm/hr
women:-0-20mm/hr

Age>50
Men:-0-20mm/hr
Women:-0-30mm/hr

*******The ESR remains an important diagnostic criterion only for polymyalgia

rhuematica and temporal arteritis.

# The ESR is an inexpensive, simple test of chronic inflammatory activity.

# Indications for the ESR have decreased as the sophistication of laboratory testing has
increased.
# The ESR rises with age, but this increase may simply reflect a higher disease
prevalence in the elderly.
# The use of the ESR as a screening test in asymptomatic persons is limited by its low
sensitivity and
specificity.
# When there is a moderate suspicion of disease, the ESR may have some value as a
"sickness index."
# An extremely elevated ESR (>100 mm/hr) will usually have an apparent cause--most
commonly infection, malignancy or temporal arteritis.
# A mild to moderately elevated ESR without obvious etiology should prompt repeat
testing after several months rather than an expensive search for occult disease.

*** Stages of iron deficiency & their detectable lab. abnormalities:-

Stage1:-Depleted iron stores:- Low ferritin & absent B.M iron.

Stage2:-Latent iron deficiency:-Low transferrin saturation,Low serum iron,

raised serum transferrin,normal Hb.

Stage3:-Low Hb.

message:-don't forget to read table for normal values & haematological values in
deficiency.

Vit.B12 metabolism:-Vitamin B12 is synthesized only by microorganisms, and in our

diets it is supplied nearly exclusively by animal foods. Meat contains adenosyl-, and
hydroxycobalamin; dairy products contain methyl-, and hydroxycobalamin. These
protein-bound forms of Vit B12 are digested by gastric acid and pepsin so that the Vit
B12 is released into gastric juice where it becomes bound to a salivary B12 binding
protein (haptocorrin) rather than to gastric intrinsic factor (IF). Secretion of IF from
parietal cells is stimulated by the same agents that stimulate acid secretion, but drugs
such as omeprazole which inhibit the H+/K+ pump do not block IF secretion.
Haptocorrin and IF are not digested by acid-pepsin, but pancreatic proteases can digest
haptocorrin, but not IF. Therefore, in the duodenojejunal lumen, Vit B12 is transferred
from haptocorrin to IF. The Vit B12-IF complex binds to a specific receptor in the brush
border of ileal absorptive cells. The Vit B12-IF complex enters the ileal absorptive cells
by endocytosis and Vit B12 is transferred to transcobalamin which exits through the
basolateral membrane into portal venous blood.

Hepatocytes secrete Vit B12 into bile and biliary B12 can be reabsorbed by ileal
mucosa. This enterohepatic circulation of Vit B12 helps to maintain normal body stores
of the vitamin. Patients who have had an ileal resection may become B12-deficient in 2-
3 years. Subjects ingesting a Vit B12-deficient diet may require 10-20 years to manifest
B12-deficiency because they are able to conserve biliary Vit B12.

Vit B12 is a cofactor for two enzymatic reactions which maintain the supply of
methionine and tetrahydrofolate, and which promote the synthesis of succinyl co-
enzyme A. Vit B12 deficiency leads to macrocytic anemia, and to neuropsychiatric
abnormalities.

Absorption of Vit B12 can be assessed by a Schilling test.

****major site 4 vit.B12 absorption is ileum & that of folic acid is jejunum.

ZOLLINGER-ELLISON SYNDROME:-
The cardinal features include:

* pancreatic non-beta islet cell tumor

* severe and recalcitrant upper gastrointestinal ulcerative disease (90-95% of the patients)

* excessive gastric acid secretion

* diarrhea in about 40% of the cases .
Seventy-five percent of the patients have ulcers localized in the first portion of the
duodenum or in the stomach. The ulcer symptoms are fulminant, progressive and
persistent and respond poorly to medical and surgical peptic ulcers treatment. Prompt
recurrence of ulcer after usual peptic surgery is characteristic of gastrinoma.

The diagnosis of Zollinger-Ellison syndrome is made on the demonstration of high serum

gastrin levels. Fasting gastrin levels in normals and in patients with ordinary duodenal
ulcer average approximately 60 pg/ml. Patients with gastrinoma almost always have
levels greater than 150 pg/ml and not uncommonly greater than 1,000 pg/ml.

V/Qratio:- In respiratory physiology, the ventilation/perfusion ratio (or V/Q ratio) is a

measurement used to the efficiency and adequacy of the matching of two variables:

* "V" - ventilation - the air which reaches the lungs

* "Q" - perfusion - the blood which reaches the lungs
A normal value is approximately 0.8.

Because the lung is centered vertically around the heart, part of the lung is superior to
the heart, and part is inferior. This has a major impact on the V/Q ratio:

* apex of lung - higher

* base of lung - lower

The V/Q ratio can be measured with a ventilation/perfusion scan.

An area with no ventilation (and thus a V/Q of zero) is termed a shunt.

cyanosis:-

Cyanosis is the characteristic blue color of the skin observed when the amount of
unoxygenated hemoglobin in the blood exceeds 5 grams per 100 milliters of blood (out
of anywhere from 10 to 15 grams of hemoglobin per 100 milliliters). Cyanosis may be
harmless - as in acrocyanosis of newborn babies - but is usually a bad sign.

Cyanosis may be caused by lung problems when not enough oxygen is getting into the
bloodstream, or by circulatory problems. Circulatory problems include abnormal mixing
of unoxygenated blood with oxygen carrying blood. Cyanosis is usually noted first
around the lips and mouth, and perhaps in the nailbeds.

Erythropoietin:-

*. Primary hormone regulator of RBC production

**. Erythropoietin sources
1. Fetus: Monocyte and Macrophage system in liver
2. Postnatal: Peritubular cells in kidney

Any condition that causes a reduction in tissue oxygenation will stimulate the kidney
cells to produce the hormone. These conditions include anaemia, chronic lung diseases
and chronic heart failure. Erythropoietin then exerts its effect on bone marrow cells to
cause an increase in number and rate of development and maturation of erythrocytes.
When tissue oxygenation reverts back to normal, the stimulus for erythropoietin
production is removed and thus its secretion is ceased.
***GIT glandular cells:-
The stomach
The wall of the stomach is lined with millions of gastric glands, which together secrete
400–800 ml of gastric juice at each meal. Several kinds of cells are found in the gastric
glands

* parietal cells
* chief cells
* mucus-secreting cells
* hormone-secreting (endocrine) cells

Parietal cells:-
Parietal cells secrete

* hydrochloric acid
* intrinsic factor.

Chief Cells:-

The chief cells synthesize and secrete pepsinogen, the precursor to the proteolytic
enzyme pepsin.

Hormones of the Gut:-

Over two dozen hormones have been identified in various parts of the gastrointestinal
system.

* All of them are peptides.

* Many of them are also found in other tissues, especially the brain.
* Many act in a paracrine manner as well as being carried in the blood as true hormones.

* Their importance to health is uncertain as no known deficiency disorders have been

found for any of them.

* gastrin
* somatostatin
* secretin
* cholecystokinin (CCK)
* ghrelin
* neuropeptide Y (NPY)
* peptide YY3-36 (PYY3-36)

**G-cells :-pylorus/antrum:-secretes Gastrin.

**Brunner's gland:-duodenum:-mucus.
**paneth cells:- small intestine:-antimicrobial peptides that sterilized the contents of
intestine.
**Enterochromaffin cells:-mucosa of small intestine:-Serotonin.
Basal ganglia:-

Basal Ganglia:

* Location: The basal ganglia is surrounds the thalamus, is enclosed by the cerebral
cortex and cerebral white matter.
* Function: The basal ganglia forms the major part of the extrapyramidal motor system.

Neurotransmitters

The different types of neuron of the basal ganglia biosynthesize a different

neurotransmitter. The most widely produced is the inhibitory transmitter GABA which
is biosynthesized in the Purkinje neurons .
Dopamine is biosynthesized in the dopaminergic neurons, primarily in the substantia
nigra. Disruption in the biosynthesis or transmission of dopamine can lead to serious
motor and cognitive deficits, such as occurs in Parkinson's disease.

**acetylcholine is an excitatory neurotransmitter in the basal ganglia ,whereas

dopamine is inhibitory.
**GABA:-the most prevalent neurotransmitter in CNS(20%)

*** Specialized excitatory and conductive system of the heart

***specialized cardiac cells that have few myofibrils and contract only weakly

sinus node (sinoatrial or S-A node)

internodal pathways

A-V node

A-V bundle (Bundle of His)

left and right bundle branches

Purkinje fibers

*** Initiation of the action potential by pacemaker cells

SA node contains pacemaker cells

automatic electrical rhythmicity

membrane potential between discharges: 55-60mV

slow leak of Na+ at "rest" is essential for rhythmicity

action potential of pacemaker cells triggered by opening of the calcium-sodium

channels

normal rate of firing: 70/min

The rate of firing is subjected to control by ANS

parasympathetic nervous system

sympathetic nervous system

***Conduction speeds in cardiac tissue:-

SA node:-0.05 m/s
Atrial pathway:-1m/s
AV node:-0.02-0.05 m/s(slowest)
Bundle of his:- 1 m/s
Purkinje system:- 4m/s (fastest)
Ventricular muscles:-1m/s.

Milk Ejection Reflex:-

The milk ejection reflex is a neuroendocrine reflex. The reflex has an afferent pathway
(conducted from the teats to the brain via neurons) and an efferent pathway (conducted
from the pituitary to the mammary gland via blood-borne hormones).

Afferent Pathway:

The greatest amount of innervation in the mammary gland is in the teats, where there are
pressure sensitive receptors in the dermis. Mechanical stimulation of the teats activates
pressure sensitive receptors in the dermis where the pressure is transformed into nerve
impulses that travel via the spinothalamic nerve tract to the brain. These nerves synapse
in the paraventricular nucleus and in the supraoptic nucleus in the hypothalamus. When
the cell bodies of the oxytocin-containing neurons are stimulated by these impulses
originating in the teat, an action potential moves down the oxytocin-containing neurons
from the cell body in the hypothalamus down the axon to the neuron ending in the
posterior pituitary. This causes release of oxytocin and neurophysin into the blood. The
efferent pathway starts at this point.

Efferent Pathway:

The efferent pathway begins with the release of oxytocin into the blood. The oxytocin
then travels to the mammary gland via the blood, binds to oxytocin receptors on the
myoepithelial cells, causing the myoepithelial cells to contract, and resulting in
increased intra-lumenal (intramammary) pressure and ejection of milk from the alveolar
lumen.

Oxytocin receptors are associated with the myoepithelial cells, not the smooth muscle of
the mammary gland.

**There is no parasympathetic innervation in the mammary gland.

Hormonal influences:-

From the third month of pregnancy (the second and third trimesters), a woman's body
produces hormones that stimulate the growth of the milk duct system in the breasts:

* Progesterone — influences the growth in size of alveoli and lobes. Progesterone and
estrogen levels drop after birth. This triggers the onset of copious milk production.
* Estrogen — stimulates the milk duct system to grow and become specific. Estrogen
levels drop at delivery and remain low for the first several months of breastfeeding. It is
recommended that breastfeeding mothers avoid estrogen-based birth control methods, as
a spike in estrogen levels may reduce a mother's milk supply.
* Follicle stimulating hormone (FSH)
* Luteinizing hormone (LH)
* Prolactin — contributes to the increased growth of the alveoli during pregnancy.
* Oxytocin — contracts the smooth muscle of the uterus during and after birth, and
during orgasm. After birth, oxytocin contracts the smooth muscle layer of band-like
cells surrounding the alveoli to squeeze the newly-produced milk into the duct system.
Oxytocin is necessary for the milk ejection reflex, or let-down to occur.
* Human placental lactogen (HPL) — From the second month of pregnancy, the
placenta releases large amounts of HPL. This hormone appears to be instrumental in
breast, nipple, and areola growth before birth.

By the fifth or sixth month of pregnancy, the breasts are ready to produce milk. It is also
possible to induce lactation.

****Suckling reflex (which is a neonatal reflex) sets the stimulus for both
milk ejection & maintenance of galactopoiesis.

RBC's :-

Howell-Jolly bodies: associated with megaloblastic anemia, hemolytic anemia, post-

splenectomy state

b. Pappenheimer bodies: associated with iron loading anemias, post-splenectomy state,

some hemolytic anemias
a. Basophilic stippling:

· coarse stipples are associated with lead poisoning, megaloblastic anemia, other severe
anemias

· fine stipples are a marker of reticulocytosis (polychromasia)

d. Heinz bodies: associated with hereditary hemoglobinopathies and hemolytic anemias

due to G-6-PD or drug induce hemolysis

e. Siderocytes: associated with post-splenectomy state, iron loading anemias, some

hemolytic anemias

f. Ringed sideroblasts: associated with iron loading anemias, lead poisoning,

thalassemias, megaloblastic anemia, leukemia, ethanolism, sideroblastic anemias.

***Maurer's dots:-falciparum malaria.

***Schuffner's dots:-P.vivax.
***James dots:-P.ovale.
***Zeimann's dots:-P.malariae.

DIFFUSION:-
There are three main types of diffusion: simple, channel, and facilitated diffusion.

1.Simple diffusion is when a small,

non-polar molecule passes through a lipid bilayer.
It is classified as a means of passive transport.

In simple diffusion, a hydrophobic molecule

can move into the hydrophobic region of
the membrane without getting rejected.

Simple diffusion does not involve a proteIin.

***Hydrophilic molecules cannot participate in simple diffusion because they

would move into the hydrophobic region of the membrane and be rejected.

***Saturation does not occur with simple diffusion or with channel diffusion.
The bigger the gradient, the greater the transport of materials.

2.Channel diffusion is another type of passive transport.

Channel diffusion involves channel proteins where

material moves through an open, aqueous pore.
Channel diffusion can be regulated.
Ions and charged particles can
pass through the open pore.

3.Facilitated diffusion is a type of passive transport that is dependent on single transport

protein carriers.
These protein carriers operate on a bind, flip, release mechanism.
Facilitated diffusion is non-diffusional because the molecule moves along with the
carrier.

****Saturation occurs in facilitated diffusion because not enough

carriers may be available to handle all the free solute molecules.
The rate of movement may reach a maximum.

OXYHEMOGLOBIN DISSOCIATION CURVE:-some facts.......

Factors that Affect the Standard Dissociation Curve

The effectiveness of hemoglobin-oxygen binding can be affected by several factors. The

factors can be viewed as having the effect of shifting or reshaping the oxyhemoglobin
curve ("the standard curve") of a typical, healthy person. The standard curve is shifted to
the right by an increase in temperature, 2,3-DPG, or PCO2, or a decrease in pH. The
curve is shifted to the left by the opposite of these conditions. A rightward shift, by
definition, causes a decrease in the affinity of hemoglobin for oxygen. This makes it
harder for the hemoglobin to bind to oxygen (requiring a higher partial pressure to
achieve the same oxygen saturation), but it makes it easier for the hemoglobin to release
bound oxygen. Conversely, a leftward shift increases the affinity, making the oxygen
easier for the hemoglobin to pick up but harder to release.

We list several of the factors here and indicate how the curve is affected:

* Variation of the hydrogen ion concentration. This changes the blood's pH. A decrease
in pH shifts the standard curve to the right, while an increase shifts it to the left. This is
known as the Bohr effect.
* Effects of carbon dioxide. Carbon dioxide affects the curve in two ways: first, it
influences intracellular pH (the Bohr effect), and second, CO2 accumulation causes
carbamino compounds to be generated through chemical interactions. Low levels of
carbamino compounds have the effect of shifting the curve to the right, while higher
levels cause a leftward shift.
* Effects of 2,3-DPG. 2,3-diphosphoglycerate, or 2,3-DPG, is an organophosphate, which
are created in erythrocytes during glycolysis. The production of 2,3-DPG is likely an
important adaptive mechanism, because the production increases for several conditions in
the presence of diminished peripheral tissue O2 availability, such as hypoxemia, chronic
lung disease, anemia, and congestive heart failure, among others. High levels of 2,3-DPG
shift the curve to the right, while low levels of 2,3-DPG cause a leftward shift, seen in
states such as septic shock and hypophosphatemia.
* Temperature. Temperature does not have so dramatic effect as the previous factors, but
hyperthermia causes a rightward shift, while hypothermia causes a leftward shift.
* Carbon Monoxide. Hemoglobin binds with carbon monoxide 240 times more readily
than with oxygen, and therefore the presence of carbon monoxide can interfere with the
hemoglobin's acquisition of oxygen. In addition to lowering the potential for hemoglobin
to bind to oxygen, carbon monoxide also has the effect of shifting the curve to the left.
With an increased level of carbon monoxide, a person can suffer from severe hypoxemia
while maintaining a normal PO2.
* Effects of Methemoglobinemia (a form of abnormal hemoglobin). Methemoglobinemia
causes a leftward shift in the curve.
* Fetal Hemoglobin. Fetal hemoglobin (HbF) is structurally different from normal
hemoglobin (Hb). The fetal dissociation curve is shifted to the left relative to the curve
for the normal adult. Typically, fetal arterial oxygen pressures are low, and hence the
leftward shift enhances the placental uptake of oxygen.

*****Classification of Hormones by Chemical Structure

Polypeptides:-GnRH,TRH,CRH,GHRH,Somatostatin,Oxytocin.

Modified amino acid:-melatonin.

Protein:-Relaxin, Inhibin,Prolactin,ACTH,TSH,GH,FSH,LH.

Sex steroid:-Estradiol,Progeterone,Testosterone.

Fatty acid:-PGF.

OXYGEN CONSUMPTION BY DIFFERENT ORGANS OF THE BODY:-

the oxygen consumption (ml O2/min per 100g) :-

1.brain :- 3.
2.kidney:- 5.
3.skin:-0.2.
4.resting muscles:-1.
5.contracting muscles:-50.
6.arrested heart:-2.
7.resting heart:-8.
8.after heavy exercise consumption of oxygen by heart:-70.
**** blood flow:-Liver>Kidney>Ske.Muscle>brain.

resistance to blood flow:-

Determinants of Resistance to Flow (Poiseuille’s Equation)

There are three primary factors that determine the resistance to blood flow within a single
vessel: vessel diameter (or radius), vessel length, and viscosity of the blood.
Of these three factors, the most important quantitatively and physiologically is vessel
diameter. The reason for this is that vessel diameter changes because of contraction and
relaxation of the vascular smooth muscle in the wall of the blood vessel.

***Vessel resistance (R) is directly proportional to the length (L) of the vessel and the
viscosity (h) of the blood, and inversely proportional to the radius to the fourth power
(r4).

Skeletal muscle fibers:-

***TWO types:-

Type I

Type I muscle fibers (slow-oxidative fibers) use primarily cellular respiration and, as a
result, have relatively high endurance.

To support their high-oxidative metabolism, these muscle fibers typically have lots of
mitochondria and myoglobin, and thus appear red.
***Diameter:-narrow.

Type II

Type II muscle fibers use primarily anaerobic metabolism and have relatively low
endurance. These muscle fibers are typically used during tasks requiring short bursts of
strength, such as sprints or weightlifting. Type II muscle fibers cannot sustain
contractions for significant lengths of time.

There are two sub-classes of type II muscle fibers, type IIa (Fast-Oxidative) and IIb
(Fast-Glycolytic).

* Type IIa (fast-oxidative) fibers actually also appear red, due to their high content of
myoglobin and mitochondria.
***Diameter :-medium.

* Type IIb (fast-glycolytic) are the fastest twitch and most powerful, twitching in
upwards of 120 times per second.
****Diameter:-wide.

GASTRIC ACID SECRETION:-

Regulation of secretion

Gastric acid production is regulated by both the autonomic nervous system and several
hormones. The parasympathetic nervous system, via the vagus nerve, and the hormone
gastrin stimulate the parietal cell to produce gastric acid, both directly acting on parietal
cells and indirectly, through the stimulation of the secretion of the hormone histamine
from enterochromaffine-like cells (EPC). Vasoactive intestinal peptide, cholecystokinin,
and secretin all inhibit production.

The production of gastric acid in the stomach is tightly regulated by positive regulators
and negative feedback mechanisms. Four types of cells are involved in this process:
parietal cells, G cells, D cells and enterochromaffine-like cells. Besides this, the endings
of the vagus nerve (X) and the intramural nervous plecus in the digestive tract influence
the secretion significantly.

Nerve endings in the stomach secrete two stimulatory neurotransmitters: acetylcholine

and gastrin-releasing peptide. Their action is both direct on parietal cells and mediated
through the secretion of gastrin from G cells and histamine from enterochromaffine-like
cells. Gastrin acts on parietal cells directly and indirectly too, by stimulating the release
of histamine.

The release of histamine is the most important positive regulation mechanism of the
secretion of gastric acid in the stomach. Its release is stimulated by gastrin and
acetylcholine and inhibited by somatostatin.

***glucagon inhibits gastric acid production.

Renal water handling:-

Maintenance of normal body volume and osmolality (280-295 mOsm/kg water) depends
upon a balance between oral intake and renal excretion.

proximal tubule - Under normal conditions, the proximal tubule reabsorbs 60-70% of the
filtered fluid in an isosmotic fashion, i.e., salt and water are reabsorbed in the same
concentrations as that found in tubule fluid and plasma. Hence, the proximal tubule does
not directly contribute to the formation of dilute or concentrated urine. The proximal
tubule can respond to changes in plasma volume by decreasing salt and water
reabsorption if plasma volume rises or by increasing salt and water reabsorption if plasma
volume falls.

2. Loop of Henle - The thick ascending limb of Henle's loop reabsorbs sodium and
chloride from tubule fluid. This segment is impermeable to water, hence dilute urine is
generated (down to 100 mOsm/kg water). The reabsorbed salt can be carried into the
renal medulla where it accumulates and helps raise medullary tonicity up to about 1200
mOsm/kg H2O (you may need to review the physiology notes since time does not allow a
detailed review of this system). Ultimately, it is the thick ascending limb of Henle's loop
that is responsible for urinary dilution and for providing the hypertonic medullary
interstitium that permits generation of concentrated urine.

3. Distal tubule and collecting duct - In the absence of antidiuretic hormone (ADH, also
referred to as vasopressin or arginine vasopressin), the distal tubule and collecting duct
are impermeable to water and sodium continues to be reabsorbed. The result is that the
urine osmolality falls even further and during a maximal water diuresis an osmolality of
about 50 mOsm/kg water can be achieved. In the presence of ADH, the collecting ducts
are permeable to water. ADH increases cyclic AMP levels which results in insertion of
water channels (aquaporin-2) into the collecting duct plasma membrane. Water can now
move from the more dilute urine into the hypertonic medullary interstitium, thereby
concentrating the urine up to a maximum of about 1200 mOsm/kg water or about 4 times
as concentrated as normal plasma.

surfactant:-***Produced by type 2 alveolar epithelial cells.

**major constituent:-Di-palmitoyl-phosphatidyl-choline.
**surfactant reduces the alveolar surface tension &
-prevents alveolar collapse.
-prevents pulmonary edema.
**Respiratory distress syndrome/Hyaline membrane disease is produced due to
deficiency of surfactant.
*Thyroid hormone increases activity of Type-2 pneumocytes.
*Glucocorticoids enhance maturation of surfactant.
*Insulin inhibits activity of Type -2 pneumocytes.

***surfactant deficiency may also occur with:-

-. occlusion of main bronchus.
- occlusion of pulmonary artery.
-long term inhalation of 100% oxygen.
-cigarette smokers.
Respiratory failure:-

Respiratory failure is a medical term for inadequate gas exchange by the respiratory
system. Respiratory failure can be indicated by observing a drop in blood oxygen level
(hypoxemia) and/or a rise in arterial carbon dioxide (hypercapnia) which can be written
as (PaO2 < 60 mmHg, PaCO2 > 45 mmHg).
Classification into type I or type II relates to the absence or presence of hypercapnia
respectively.

Type 1

* Type 1 respiratory failure is defined as hypoxia without hypercapnia, indeed the CO2
level may be normal or low.
It is typically caused by a ventilation/perfusion mismatch; the air flowing in and out of
the lungs is not matched with the flow of blood to the lungs.

Type 2

* Type 2 respiratory failure is defined as hypoxia with hypercapnia. It is due to

inadequate air flow in the alveoli of the lungs that causes a build up of carbon dioxide
that has been generated by the body.

Stages of sleep:-

NREM:-Stage1:-first & lightest stage of sleep.

:- predominantly (theta) waves are seen.
Stage2:-characterized by two typical EEG-changes:-
- Sleep spindles & K-complexes.
Stage 3:- (Delta) waves first appear.
Stage 4:-predominantly (delta)-activity in EEG.
-Disorders of stage 4:-
* sleep walking (somnambulism)
* sleep terror (pavor nocturnus)
* sleep enuresis (bed wetting)
* Bruxism (tooth grinding)
* sleep talking (somniloquy)

REM:- Is a light phase of sleep, but arousal is difficult.

beta-like activity on EEG.
dreaming is seen.
Also present are muscular atony,penile erection,autonomic hyperactivity.
Nightmares occur.
Ascending & descending spinal tracts:-

Ascending (Sensory)
*Fasciculus gracilis - Carries muscle and joint sensations for proprioception . It increases
in size as it ascends and picks up more fibers from the upper segments of the body. It
terminates in the nucleus gracilis in the medulla in the brain.

*Fasciculus cuneatus - Also carries muscle and joint sensations for proprioception .
Increases in size as it ascends. Like the fasciculus gracilis, it is derived from thoracic and
cervical regions. It terminates in the medulla in the cuneate and accessory cuneate nuclei.

*Lateral Spinothalamic Fasciculus - Transmits sensations of pain and temperature . It

originates in the cells of the dorsal horn of the gray matter. The fibers cross to the
opposite side of the cord through the anterior commissure and ascend to the ventral
posterior lateral nucleus of the thalamus.

*Ventral Spinothalamic Fasciculus - Transmits sensations of touch . It originates in the

cells of the posterior horn, and the fibers cross to the opposite side in the anterior
commissure. The fibers end in the thalamus.

*Dorsal Spinocerebellar Fasciculus - Conducts impulses from the leg and trunk muscles
for unconscious proprioception . It runs from the spinal cord through the inferior
cerebellar peduncle and terminates in the cerebellum.

Ventral Spinocerebellar Fasciculus - Specific functions are unknown. It originates at the

level of the third lumbar spinal nerves and terminates in the cerebellum.

Spinotectal Fasciculus - Probably concerned with visual reflexes. It arises from cells in
the dorsal horn, crosses to the opposite side, and ascends to the superior colliculi (tectum)
of the midbrain.

Spinoolivary Fasciculus - Exact function unknown. The fibers run from the spinal cord to
the inferior olivary nucleus of the medulla.

Descending:-
*Lateral Corticospinal Fasciculus - Concerned with voluntary movement . The fibers
originate in the large pyramidal cells of the precentral gyrus of the cerebral hemispheres
and extend through the entire spinal cord. They cross to the opposite side of the cord at
the pyramidal decussation . Most of them terminate in the dorsal horn cells.

*Ventral Corticospinal Fasciculus - Concerned with voluntary movement . The fibers

arise in the pyramidal cells of the motor area of the cortex and descend to the spinal cord.
This is a small tract.
Rubrospinal Fasciculus - Transmits impulses relating to the cerebellar reflexes. It
originates in the red nucleus of the midbrain on the opposite side. The fibers descend as
far as the sacral region.

Reticulospinal Fasciculus - Also concerned with cerebellar reflexes and is part of the
reticular activating system. It originates in the reticular substance of the tegmentum.
Reticulospinal fibers travel with both the tectospinal fasciculus and the rubrospinal
fasciculus.

Tectospinal Fasciculus - Probably concerned with visual refelxes since the cells originate
in the opposite superior colliculus of the midbrain. It terminates in the ventral horn cells.

Olivospinal Fasciculus - Function unknown. It arises in the cells of the inferior olive of
the medulla. It is found only in the cervical region of the spinal cord.

Vestibulospinal Fasciculus - Transmits impulses related to equilibrium and antigravity

reflexes. The fibers originate in the vestibular nuclei of the medulla and can be traced to
the level of the sacral spinal nerves.

Medial Longitudinal Fasciculus - Is the principal connection between the vestibular

complex and the centers in the medulla that coordinate head and eye movements. It
descends to the second or third thoracic segments. It actually contains both ascending and
descending fibers.

Vasopressin:-
*it is a hormone of the pituitary gland,& is synthesized in the cell bodies of the
magnocellular neurons in the supra-optic & paraventricular nuclei of
hypothalamus.
*Bcoz..one of its principal physiologic effects is the retention of water by the kidney, it is
often called the ADH .i.e. increase the conc. of urine & decrease
the osmolality of the plasma.
*It's deficiency cause- Diabetes insipidus i.e. polyuria .
*Secretion is increased by:-Increased effective osmotic pressure of plasma,
Decreased ECF volume, pain,emotion,stress,exercise,nausea vomitting,
standing,drugs like
carbamazepine,clofibrate,chlorpropamide,vincristine,vinblastine,cyclophosphamide,
,angiotensin-2,oxytocin,GA,Narcotics,TAD.
*Secretion is decreased by:-decreased effective osmotic pressure off plasma,increased
ECF volume,alcohol.

Basal ganglia:-
1.it consists of five nuclei:-
*caudate nucleus.
*putamen
*Globus pallidus.
*subthalamic nucleus.
*substantia nigra.

**Striatum:-caudate + putamen.
**Lenticular nucleus:-putamen + globus pallidus.

2. functions:-
Basal ganglia are involved in the planning & programming of the movements
or more broadly in the process by which an abstract thought is converted into
voluntary action.
* help the cortex execute subconcious but learned pattern of movements.
* help plan multiple parallel & sequential patterns of movement that the mind must put
together to accomplish a purposeful task.i.e skilled movements.

3.lesions of basal ganglia:-

a.Hemiballismus.:- due to lesion in subthalamic nu.
b.huntington's disease/chorea:-caudate & putamen.
c.parkinson's disease:-substantia nigra ...cog-wheel rigidity & leadpipe rigidity,
involuntary tremors,akinesia are some of the C/F.
d. athetosis:-globus pallidus.

The nervous system:-fact file:-

*The nervous system is composed of only two principal types of cells:-
1.neurons.
2.supporting cells.
supporting cells aid the functions of neurons & are about five times more abundant than
neurons.In the CNS, supporting cells are collectively called
neuroglia,or simply glial cells.
Unlike neurons,glial cells retain limited mitotic abilities(brain tumors that occur in adults
are usually composed of glial cells).
*Cell body of neuron contains densely staining areas of rough endoplasmic
reticulum known as Nissl bodies.
*There are 6-types of supporting cells:-
1.Schwann cells:-which form myelin sheaths around peripheral axons.
2.oligodendrocytes:-which form myelin sheaths around axons of the CNS.
3.microglia:-phagocytic cells that migrates through the CNS.
4.Astrocytes:-help to regulate external environment of neural cells in CNS.
5.satellite cells:-support neuron cell bodies within the ganglia of the PNS.
*Axons that are smaller than 2 micrometers in diameter are usually unmyelinated.
*The myelin sheaths around axons of the CNS give this tissue a white colour:areas of
CNS that contain a high conc. of axons thus form the white matter.
The gray matter of CNS is composed of high conc. of cell bodies & dendrites,which lack
myelin sheaths.
*Botulinum toxins are neurotoxins released by the bacterium Clostridium
botulinum.These toxins are endopeptidases- enzymes that cleave peptide bonds within a
protein .Because of their specificity & location within axo terminals,these toxins cleave
certain synapsins.
This inhibits the exocytosis of synaptic vesicles & prevents the release of
neurotramnsmitters resulting in the disease botulism.
*Nerve gas exerts its odious efects by inhibiting AChE in skeletal muscles.Since ACh is
not degraded,it can continue to combine with receptor proteins & can continue to
stimulate the postsynaptic cells,leading to spastic paralysis.
Clinically,cholinesterase inhibitors such as neostigmine are used to enhance the effects of
ACh on muscle contraction when neuromuscular transmission is weak, as in the disease
myasthenia gravis.