Prof. Henri - Transport across cell membrane

Kindly see this URL for my nest class on haemoglobin
https://www.facebook.com/pages/Prof-Henri-Mgmcri/348212735334855

Prof. Henri - Mgmcri Transport across cell membrane

As she passed her coach and friends at the 15-mile mark
of the Boston Marathon, the 28-year-old runner smiled
and waved cheerily. She looked good as she passed
Heartbreak Hill, about 6 miles from the finish. Two
miles later, she stopped to drink a cup of fluid. Another
runner remembers her saying she felt dizzy and disoriented.
She began to falter and told a friend running next
to her that she felt rubber-legged, and then tumbled to
the pavement.
When she reached the hospital, she was unresponsive
with stable vital signs. After endotracheal intubation, a
blood serum sodium value was found to be very low at
113 mmol/L. Computed tomography of the brain and
chest radiography showed diffuse cerebral and pulmonary
edema. She was given intravenous isotonic saline
(150 mmol/L) but never regained consciousness. Diffuse
cerebral edema was found at postmortem examination. A
few days later, the newspapers reported she died from a
condition called hyponatremic encephalopathy.
Hyponatremia, defined by a blood sodium concentration
less than 135 mmol/L, may lead to hypotonic encephalopathy
with fatal cerebral edema. Of 488 runners in the
2002 Boston Marathon providing a usable blood sample at
the finish line, 13% were hyponatremic and 0.6% had critical
hyponatremia (120 mmol/L or less). The study concluded
that hyponatremia occurs in a substantial fraction
of nonelite marathon runners and can be severe. It is usually
caused by drinking excessive amounts of fluid that exceed
the kidney’s capacity to excrete water during exercise.
Considerable weight gain during the race, a long racing
time, and body mass index extremes were associated with
hyponatremia, whereas female s*x, composition of fluids
ingested, and use of nonsteroidal anti-inflammatory
drugs were not. Mild cases can be managed by restricting
fluids until the onset of urination. Manifestations of hyponatremic
encephalopathy indicate the need for emergent
treatment with hypertonic solutions such as 3% saline
(513 mmol/L).
Na+ and Cl− account for most of the osmotic strength
of the serum. If Na+ levels are low, the serum will be hypotonic
and water will move into all the cells of the body
causing them to swell (edema). This can have serious effects
in the brain because it is in the closed space of the
cranium and the swollen tissue will restrict blood flow
and therefore oxygen supply. Swelling may cause herniation
of the brain through the tentorium and foramen
magnum, compressing the brainstem and causing respiratory
arrest. Blood sodium level is influenced by salt
and water intake, sweating, and urinary secretion and is
regulated by the endocrine system. The recommendation for
marathon runners is to drink only when thirsty.

Lipid and protein contribute to the functional entity of the cell membrane. Lipid for the passage of lipid soluble substances - oxygen, carbon-dioxide and hormones derived from fat (cholesterol)-glucocorticoid, estrogen and progesterone and testosterone. Here passage occurs by diffusion, simple diffusion; the difussate being taken up by the cell/by the circulation and hence the diffusate flows from higher to lower concentration.
Fat insoluble substances like water, sodium, glucose and potasium use proteins of the cell membrane as carriers/channels. Water channels are known as aquaporins and are found in the epithelial cells of the intestines for water absorption and for water reabsorption in the cells linning the nephrons of the kidneys.
The carrier proteins have active sites which when occupied by solute molecules makes the carrier change shape and internalize/externalize the solute molecule with regards to the cell.
In the nerve cells sodium influx into the neurons brings about impulse generation. The sodium that has come in intracellularly has to be pumped out from 7mEq/L in the intracellular compartment to 140mEq/L in the extracellular fluid compartment. This is achieved by the sodium-potasium ATPase pump; it breaks ATPand utilizes the energy. Just by virtue of the fact that energy is utilized it is called active transport.
When sodium and glucose are absorbed/reabsorbed from the linning cells of the intestines and nephrons respectively, active pumping of sodium is done from these cells to the intercellular fluid. So sodium and glucose first entering these cells by co-transport and glucose and sodium leave these cells to enter the blood via intercellular fluid by glucose transporter protein and sodium pump respectively. This is process is called secondary active transport.