Excessive jocularity can cause water, milk, or soda to come out the nose.
Food and drink should be going down the
esophagus and into the stomach. Air should be going down the trachea, then into the branching bronchial tubes, and
ending into the lungs.But those two tubes, the trachea and the esophagus, are quite close to each other. So the drink can go
down the trachea and bronchial tubes, which is the wrong pipe, and then be expelled out the nose. Instead of being
swallowed, the fluid goes up the nasal passages and out through the nostrils.
Hyperventilation refers to over breathing, in which ventilation exceeds the metabolic demand,
and its related physiological consequences. Excessive breathing can cause dizziness, lightheadedness, weakness, shortness of breath, a sense of unsteadiness, muscle spasms in the
hands and feet, and a tingling feeling around the mouth and fingertips. All of these symptoms
are the result of abnormally low levels of carbon dioxide in the blood caused by over breathing.
The term hyperventilation syndrome (HVS) is sometimes used to describe the effects of
hyperventilation observed in an emergency department setting. Many acute (sudden onset)
cases of hyperventilation arise from panic, anxiety, and other emotional conditions.
Hyperventilation, particularly chronic hyperventilation (that persists over time), can also be due
to a range of medical conditions.
s we all know spermatogenesis and oogenesis are two processes that are initiated in the human
gonads to produce gametes.
Let us highlight some facts about these two series of events: facts about the number of cells
produced per each germ stem cell, the number of chromosomes in each cell and the number of
chromatids per each chromosome.
- Each human Spermatogonium ( germ stem cell) gives rise to many Spermatogonia by mitosis.
So the number of chromosomes in each Spermatogonium cell is conserved at 46 chromosomes.
- Each Spermatogonium will then grow and develop into a Spermatocyte I which will duplicate its
DNA so that each of its 46 chromosomes will have two chromatids per each chromosome at the
end of the growth stage.
- Each Spermatocyte I will divide by Meiosis I ( reductional meiosis) to give rise to two haploid
Spermatocyte II each having 23 chromosomes and each chromosome is made up of two
chromatids.
- Each Spermatocyte II will then divide by Meiosis II ( equational meiosis) to give rise to two
Spermatids. Each spermatid will have 23 chromosomes but the number of chromatids per
chromosome is ONE.
- Since the Spermatid only changes in shape and does not divide to produce a Sperm, the
number of chromosomes and chromatids will stay the same as in the spermatid. The Sperm will
have 23 chromosomes ( one chromatid per each chromosome).
- Each Oogonium will give rise to many oogonia.
- One Oogonium will grow into One Oocyte I.
- One Oocyte I will divide into One Oocyte II and One Polar body ( 1st polar body).
- One Oocyte II will divide into One Ootid ( quickly changes into Ovum) and one polar body (the
second polar body).The first polar body will also divide into 2 polar bodies that will stay near the
Ootid that will later change into the ovum.
- At last, each Oocyte I will have given rise to only One functional Ovum and 3 polar bodies.
Whereas, each spermatocyte I will give rise to four functional Spermatozoa!
Note that after fertilization, the female pronucleus ( that of the ovum) and the male pronucleus (
coming from the sperm) will fuse and mix their chromosomes.
During this process, DNA replication takes place so that the Zygote cell will have after the
fusion 46 chromosomes , each chromosome made up of two chromatids and this way it can
enter mitosis quickly and efficiently!
Gigantism refers to abnormally high linear growth due to excessive action of insulinlike growth
factor I (IGF-I) while the epiphyseal growth plates are open during childhood. Acromegaly is the
same disorder of IGF-I excess but occurs after the growth plate cartilage fuses in adulthood.
In acromegaly, a severe disease that is often diagnosed late, morbidity and mortality rates are
high, particularly as a result of associated cardiovascular, cerebrovascular, and respiratory
disorders and malignancies.[1]
Signs and symptoms
Gigantism
The presentation of patients with gigantism is usually dramatic, unlike the insidious onset of
acromegaly in adults. Manifestations include the following:
Tall stature
Mild to moderate obesity (common)
Macrocephaly (may precede linear growth)
Headaches
Visual changes
Hypopituitarism
Soft tissue hypertrophy
Exaggerated growth of the hands and feet, with thick fingers and toes
Coarse facial features
Frontal bossing
Prognathism
Hyperhidrosis
Osteoarthritis (a late feature of IGF-I excess)
Peripheral neuropathies (eg, carpel tunnel syndrome)
Cardiovascular disease
Benign tumors
Endocrinopathies
Acromegaly
Signs and symptoms of acromegaly include the following:
Doughy-feeling skin over the face and extremities
Thick and hard nails
Deepening of creases on the forehead and nasolabial folds
Noticeably large pores
Thick and edematous eyelids
Enlargement of the lower lip and nose (the nose takes on a triangular configuration)
Wide spacing of the teeth and prognathism
Cutis verticis gyrata (ie, furrows resembling gyri of the scalp)[2]
Small sessile and pedunculated fibromas (ie, skin tags)
Hypertrichosis
Oily skin (acne is not common)
Hyperpigmentation (40% of patients)
Acanthosis nigricans (a small percentage of patients)
Excessive eccrine and apocrine sweating
Breast tissue becoming atrophic; galactorrhea
High blood pressure
Mitral valvular regurgitation
Mild hirsutism (in women)
How do you treat acromegaly and gigantism?
Because gigantism occurs during childhood, parents should be alert for any signs of abnormal
vertical growth. If you suspect your child is abnormally tall for his age, speak to his pediatrician
for a proper diagnosis. Most cases of gigantism are caused by a tumor on the pituitary gland
making surgery the treatment of choice. If surgery is not an option or fails to solve the problem,
medications to reduce the amount of growth hormone can be prescribed.
Much like gigantism, acromegaly is often the result of a tumor on the pituitary gland. So surgery
and medication treatments are also considered for people with acromegaly. One medication,
Octreotide, has been proven to suppress growth hormones in some patients with acromegaly.
However, this drug is expensive and can cause gastrointestinal side effects like gall stones.
Rh Disease (Erythroblastosis Fetalis)
When a mother who is pregnant with a baby whose blood type is incompatible with the baby's,
antibodies in the mother's blood may cross the placenta and attack the baby's red blood cells.
This causes anemia in the baby. If it is severe enough, it can cause the baby to die before birth.
Symptoms
Causes and Risk Factors
This most commonly happens when a woman with Rh-negative blood becomes pregnant by a
man with Rh-positive blood and conceives a baby with Rh-positive blood.
Red blood cells from the baby can leak across the placenta into the woman's bloodstream during
pregnancy or delivery. This causes the mother's body to make antibodies against the Rh factor.
If the mother becomes pregnant again with an Rh-positive baby, it is possible for her antibodies
to cross the placenta and attack the baby's red blood cells.
After birth, an affected newborn may develop kernicterus. This happens when bile pigments are
deposited in the cells of the brain and spinal cord and nerve cells are degenerated.
Incompatibilities between ABO blood types can also cause this condition. These are less common
than those of the Rh factor and tend to be less severe.
Diagnosis
During a pregnant woman's first prenatal doctor's visit, she should be screened for blood and Rh
type. If she has Rh-negative blood, the father's blood and Rh type should be tested.
If the father has Rh-positive blood and tests of the mother's blood indicate that she hasn't
become sensitive to Rh-positive blood, she should be tested again at 18 to 20 weeks of
pregnancy and at 26 to 27 weeks of pregnancy.
Depending on the test results, she may need amniocentesis and other tests to measure the
levels of bilirubin (a bile pigment) in the amniotic fluid every two weeks starting at 28 weeks of
pregnancy. The amniotic fluid surrounds the baby as it grows inside the mother during
pregnancy.
Women who are already sensitive to the Rh factor should have amniocentesis at 26 to 30 weeks
of pregnancy, depending on how great their apparent sensitivity is.
Treatments
If monitoring shows that the bilirubin levels in the amniotic fluid are normal, no treatment may
be needed as the pregnancy proceeds to delivery.
If the levels are high, showing a threat to the fetus, it may be given transfusions inside the uterus
every 10 days to two weeks until it has reached the 32nd to 34th weeks of pregnancy. Then a
delivery should be done. These procedures must be done at a medical center that can care for
high-risk pregnancies.
The baby should be delivered with as little trauma as possible. The placenta should not be
removed manually to avoid squeezing cells from the baby's blood into the mother's blood
stream. A newborn born with Rh disease should be seen immediately by a pediatrician who can
do an exchange transfusion at once if necessary.
Prevention
Steps can be taken to assure that antibodies aren't made in the first place. This can be done by
giving the mother a shot of anti-Rh antibodies within 72 hours of the delivery of the baby. This
causes any of the baby's red blood cells that may have crossed into the mother's blood to be
destroyed before sensitizing the mother's immune system.
This has to be done with each pregnancy -- normal or ectopic -- whether it ends in a delivery or
an abortion.
If there is much blood loss during delivery, additional injections may be needed. Between 1 and
2% of the time this treatment fails. This is apparently because the mother has already become
sensitized during pregnancy rather than at delivery.
The treatment can be done preventatively to mothers with Rh-negative blood and no apparent
sensitization at about 28 weeks of pregnancy. Any antibodies circulating in the mother's blood
are gradually destroyed and the mother remains unsensitized. The treatment should also be
given after any bleeding or after amniocentesis or chorionic villus sampling.
Peptic ulcers: treatment
Peptic ulcers occur in the stomach gastric ulcers and the duodenum (the first part of the
small intestine) duodenal ulcers. They result from an imbalance between the amount of acid in
your stomach and its protective lining.
In the past it was believed that ulcers were caused by stress, poor eating habits, too much rich,
fatty food or spicy food, alcohol or caffeine. However, it is now known that most peptic ulcers are
caused by the Helicobacter pylori bacterium (also known as H. pylori). This is particularly true of
duodenal ulcers.
The cause of most other peptic ulcers is the regular use of medicines such as aspirin and other
non-steroidal anti-inflammatory drugs (NSAIDS), which are often used to treat the symptoms of
arthritis.
Treatment for peptic ulcers depends on the cause of the ulcer and can include any or all of the
following:
antibiotics to eradicate the H. pylori bacteria;
medicines to reduce the amount of acid in your stomach and promote healing of the ulcer; and
stopping or changing any medicines that may have caused the ulcer.
Eradication of H. pylori
The majority of duodenal ulcers and a large percentage of gastric ulcers are caused by the
bacterium H. pylori. Most people with ulcers will be tested to see if they are infected with H.
pylori.
The medicines used to treat ulcers associated with H. pylori infection include:
a medicine that suppresses the production of stomach acid (usually a proton pump inhibitor),
which helps the ulcer to heal and relieves peptic ulcer pain; plus
antibiotics to eradicate the H. pylori bacteria.
Unfortunately, no single antibiotic is effective against H. pylori, so combination therapy is given
to reduce the risk of the bacteria becoming resistant to treatment.
Triple therapy
The first-choice treatment for eradicating H. pylori is called triple therapy, and includes a proton
pump inhibitor (omeprazole or esomeprazole) plus 2 antibiotics clarithromycin and
amoxycillin. These medicines need to be taken twice daily for 7 days.
There are other combinations of medicines that can be used if you are allergic to penicillin or if
first-line therapy is not effective in eradicating H. pylori. Your doctor will advise you which
combination will be most likely to work for you. Convenient combination packs containing all
the medicines for the treatment are available.
This treatment has revolutionised the treatment of peptic ulcers worldwide. Depending on the
medicines used, it can have a success rate of 85 to 90 per cent in eradicating H. Pylori and
treating peptic ulcers. Eradicating H. pylori also significantly reduces the chance of relapse.
It is vital that you follow the treatment exactly according to your doctors instructions the
success rate is much lower if the tablets are not taken as directed. Common side effects include
taste disturbance, nausea and loose stools, although side effects are usually mild.
Some people (for example, those with complicated ulcers or ulcers associated with both H.pylori
infection and use of NSAIDs) may need ongoing treatment with a proton pump inhibitor for a
period of time after completing the antibiotic course. Histamine H2-receptor antagonists (a
different type of medicine that reduces stomach acid secretion) can be used but are less
effective than proton pump inhibitors.
NSAID-induced ulcers
About 30 per cent of all gastric ulcers may be caused by the long-term use of painkillers known
as non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen. Some NSAIDs
are more likely to cause ulcers than others.
In addition, among people who use NSAIDs, some are at higher risk of developing peptic ulcers
than others. NSAID users who are infected with H.pylori have a greatly increased risk of
developing a peptic ulcer. Other risk factors include older age, a history of peptic ulcer disease
and being a smoker.
The risk of developing an ulcer while taking an NSAID can be reduced by minimising the use of
NSAIDs, treating H. pylori infection (if present) and, in some cases, taking a proton pump
inhibitor.
Treatment for NSAID-induced ulcers
Treatment for NSAID-induced ulcers involves stopping the NSAID (if possible) and taking a
medicine to suppress acid secretion and promote healing. Proton pump inhibitors are usually
used, as they are more effective than H2-receptor antagonists.
Your doctor will also recommend testing for H. pylori infection and eradication treatment if
necessary.
Antacids
Antacids neutralise the stomachs acid and so usually give temporary relief from ulcer pain.
There are many varieties available without a prescription. Ask your pharmacist for advice about
which one would be best for you.
If you are being treated for H. pylori infection, you should check with your doctor before taking
an antacid, because some of the antibiotics used in eradication therapy for H. pylori dont work
as well when combined with an antacid.
Lifestyle changes
Your doctor may also give you dietary guidelines to follow, such as reducing or eliminating
alcohol, as it can worsen ulcers and prevent healing. Its a good idea to avoid any foods that tend
to aggravate your symptoms.
If you are a smoker, your doctor will also recommend you stop smoking as it has been shown
that smokers have a higher incidence of ulcer complications and that it takes longer to heal their
ulcers than non-smokers.
