This document reviews uterine myomas (fibroids), including their risk factors and pathophysiology. Some key points:
- Uterine myomas are benign muscle tumors that are common in women of reproductive age. Risk factors include age, family history, ethnicity, obesity, diet, pregnancy history, and smoking.
- The tumors are thought to be sensitive to estrogen and progesterone levels, which may explain why they typically grow during reproductive years and shrink after menopause.
- Cells in uterine myomas have a higher density of estrogen receptors compared to normal uterine muscle cells, and they convert estrogen to weaker forms less efficiently. This creates a relatively hyperestrogenic environment conducive to tumor growth.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
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Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
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Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
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Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
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It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
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Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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2. from uterine myoma. The differences between America and Af-
rica may be attributed to differences in life patterns. In the USA,
of the 650,000 hysterectomies performed per year, 27% (175,000)
are due to uterine myoma arenas. Based on the residive incidence
of uterine myoma as much as 15% (4-59%), then as much as 10%
(3-21%) must be performed again [2].
Uterine myoma are often found in women of reproductive age (20-
25%), where the prevalence of uterine myomas increased by more
than 70% by pathological examination of uterine anatomy, proving
that many women suffer from asymptomatic uterine myomas. It is
estimated that the incidence of uterine myoma is about 20% -30%
of all women [3]. Aims of the article is to review uterine myoma,
risk factor and pathophysiology.
3. Discussion
Uterine myoma is a benign tumor in the uterine area or more pre-
cisely the uterine muscle and connective tissue around it. Myomas
have never been found before the occurrence of menarche, where-
as after menopause only about 10% of myomas are still growing.
According to localization, myoma uteri is found in cervical (1-
3%), and corporal. The cervix is less common but when it reaches
a large size it can compress the bladder and cause impaired mictu-
rition and is also technically more difficult to operate [4].
Uterine myomas are usually multiple, separate and spherically or
irregularly lobulated. Although myomas have a pseudocapsule,
they can be clearly distinguished from normal myometrium and
can be enucleated easily from the surrounding tissue. Macroscop-
ically in cross section, the myoma is paler, rounded, slippery and
usually dense and if the myoma that has just been removed is
cleaved, the tumor surface separates and is easily distinguished
from the pseudocapsule. Microscopically, myoma uteri consists
of bundles of smooth muscle and connective tissue, which are ar-
ranged like a whorled like appearance [5].
According to the position of the myoma to the uterine lining, it can
be divided into 3 types:
a. Submucosal Myomas
It grows just below the endometrium and protrudes into the uterine
cavity. Often also growing long and protruding stem through the
cervix into the vagina so that it can be seen inspeculo and is called
Myom Geburt. Myoma in the cervix can protrude into the cervical
canal so that the OUE is crescent shaped [6].
Because it grows under the endometrium and in the endometrium,
the uterine bleeding is the most abundant, so that this submuco-
sal myoma most often causes profuse and irregular uterine bleed-
ing (menometrorrhagia). As a result, a hysterectomy is required
in cases of myoma with profuse bleeding despite its small size.
Myoma submucosa with a stem is often infected (ulcerated) and
torsion (twisted) or becomes necrotic and if this happens then this
condition is a major concern before treating the myoma itself (a
syndrome similar to acute abdomen) [3].
The possibility of sarcoma degeration is also greater in this type
of myoma submucosa. The presence of sub mucosa myoma can be
felt as a "curet bump" (lump curettage time) [6].
b. Intramural / Interstitial Myomas
It grows on the uterine wall between the myometrial fibers. The
size and consistency varies, if large or multiple can cause uterine
enlargement and lumps [4].
c. Subserous / Subperitonal Myoma
It grows under the tunica serosa (grows outside the uterine wall)
so that it protrudes outward on the surface of the uterus, covered
by serosa. This type of myoma can also be stemmed. If the myoma
subserosa with this stem gets extrauterine bleeding from the blood
vessels of the omentum, then the stalk can atrophy and be absorbed
so that it is released so that it becomes "parasitic myoma". Some-
times the veins on the surface rupture and cause intra-abdominal
bleeding. This subserous myoma can also grow between the 2 peri-
toneal layers of the broad ligament into an "intraligamenter myo-
ma" which can compress the ureter and A. iliaca, causing urinary
disorders and pain [1, 7].
4. Risk Factors of Uterine Myomas
4. 1. Age of the Patient
Most women are diagnosed with uterine myoma in their 40s; but
it is not certain whether uterine myomas occur due to increased
formation or increased enlargement secondary to hormonal chang-
es at this time of age. Based on the autopsy, Novak found 27%
of women aged 25 years had a myoma nest. Myomas have never
been reported before menarche and after menopause only 10% of
myomas are still growing [8].
4. 2. Endogenous Hormones (Endogenous Hormonal)
Very few uterine myomas were found in specimens taken from the
results of hysterectomy for women who had menopause, it was
explained that the endogenous estrogen hormone in menopausal
women was low or low. Early menarche (age under 10 years) was
found to increase the risk (RR 1.24) and past menarche (age after
16 years) decreased the risk (RR 0.68) for suffering from uterine
myoma [8].
4. 3. Family History
Women with first-degree lineages with uterine myoma sufferers
have a 2.5 times increased risk of suffering from uterine myoma
compared with women without lineage with uterine myoma. Myo-
ma sufferers who have a family history of uterine myoma sufferers
have 2 times the power of expression of VEGF-α (a myoma-relat-
ed growth factor) compared to myoma patients who do not have a
family history of uterine myoma sufferers [9].
4. 4. Ethnicity
From a study conducted involving self-reports by patients regard-
Volume 4 Issue 3 -2021 Review Article
clinicsofoncology.com 2
3. ing uterine myoma, medical records, and sonographic examina-
tions showed that African-American ethnic groups have a 2.9
times likelihood of suffering from uterine myoma compared to
women with caucasian ethnicity, and this risk is not related to risk
factors. another. It was also found that African-American women
suffer from uterine myomas at a younger age and have myomas
that are many and larger and show clinical symptoms. However, it
is not clear whether these differences are due to genetic problems
or differences in circulating estrogen levels, estrogen metabolism,
diet, or the role of environmental factors. However, a recent study
demonstrated that the Val / Val genotype for an essential enzyme
for estrogen metabolism, catechol-O-methyltransferase (COMT)
was present in 47% of African-American women versus only 19%
of white women. Women with this genotype are more prone to
suffer uterine myoma. This explains why the high prevalence of
uterine myoma among African-American women is higher [8].
4.5. Weight Loss
One prospective study was conducted and found that the possible
risk of developing uterine myoma was as high as 21% for every
10kg increase in body weight and with an increase in body mass
index. The same findings were also reported for women with 30%
excess body fat. This occurs because obesity causes increased con-
version of adrenal androgens to estrone and decreased sex-binding
globulin. The result causes an increase in estrogen biologically
which could explain why there is an increase in the prevalence of
uterine myoma and its growth [7].
Several studies have found an association between obesity and an
increased incidence of uterine myoma. A study at Harvard con-
ducted by Dr. Lynn Marshall found that women who have a Body
Mass Index (BMI) above normal are 30.23% more likely to suffer
from uterine myoma. Ros et al, (1986) found that the risk of uter-
ine myoma increases by 21% for every 10 kg of weight gain and
this is in line with the increase in BMI [1, 7, 8].
4.6. Diet
There are studies that link the increase in the occurrence of uter-
ine myoma with consumption of such as beef or red meat or ham
which can increase the incidence of uterine myoma and green veg-
etables can reduce it. This study is very difficult to interpret be-
cause this study does not calculate the caloric value and fat intake
but for information only and it is also not certain whether vitamins,
fiber or phytoestrogens are associated with uterine myoma [7, 8].
4.7. Pregnancy and Parity
Increased parity reduces the incidence of uterine myoma. Uterine
myomas exhibit the same characteristics as normal myometrium
in pregnancy including increased extracellular matrix production
and increased expression of receptors for peptides and steroid hor-
mones. The postpartum myometrium returns to original weight,
blood flow and size by apoptosis and differentiation. This remod-
eling process may be responsible for the reduction in the size of
the uterine myoma. Another theory also says that the blood vessels
in the uterus return to their original state or size in postpartum and
this causes the uterine myoma to lack blood supply and lack of nu-
trients to continue to enlarge. Pregnancy at mid-reproductive age
(25-29 years) was also found to provide protection against myoma
enlargement [7, 8].
4.8. Smoking Habits
Smoking can reduce the incidence of uterine myoma. Many fac-
tors can reduce the bioavailability of the hormone estrogen in tis-
sues, such as: decreased conversion of androgens to estrone by
inhibition of the aromatase enzyme by nicotine [7, 8].
5. Patophysiology of Uterine Myomas
Each uterine myoma is derived from a single myocyte progenitor
cell. Thus, various tumors of the uterus indicate their respective
cytogenic origins. Some of the defects involve chromosomes 6,
7, 12, and 14 and some correlate with the rate and direction of
tumor growth. Some of the specific genetic mutations, including
the MED12 and HMGA2 genes, which are less common are the
COLAA5-A6 or the FH gene, causing most uterine myomas. Of
the genes, the FH (Fumarate Hydratase) gene is a rare gene murasi
but can lead to Hereditary Leimyomatasis and Renal Cell Can-
cer (HLRCC) syndrome. This is characterized by skin and uterine
leiomyoma and renal cell cancer [8, 9].
Based on its origin, myoma uteri is a tumor that is sensitive to es-
trogen and progesterone, so as a result, myoma uteri grows during
the reproductive period. In the postmenopausal period, uterine my-
oma generally shrinks and new tumor growth rarely occurs. The
above sex steroids may have an effect either stimulating or inhib-
iting transcription or cell growth factor production. Myoma uteri
itself creates a hyperestrogenic environment, which is needed for
its growth and maintenance. Compared with normal myometrial
cells, cells from myoma uteri have a higher density of estrogen
receptors, which makes more bonds from estradiol. Then these tu-
mors also convert less estradiol to weaker estrone. The third mech-
anism is the large amount of cytochrome P450 in uterine myoma
compared to normal myocyte cells, this specific enzyme catalyzes
the conversion of androgens to estrogens [10].
Some conditions also provide continuous estrogen exposure which
triggers the formation of uterine myoma. For example, in a high
BMI condition because obese women produce more estrogen due
to the conversion of androgens to estrogen in adipose tissue by
aromatase. Women with Polycystic Ovarian Syndrome (PCOS)
also have a greater risk of developing uterine myoma. Of the many
factors, estrogen and progesterone hormonal therapy in premeno-
pausal women does not have much of an effect that induces the
formation of uterine myoma. Smoking alters estrogen metabolism
and decreases physiologically active serum estrogens. This ex-
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clinicsofoncology.com 3
4. plains why women who smoke have a lower risk of developing
uterine myoma [8, 11].
Apart from estrogen, uterine myoma also carries more progester-
one receptors than the surrounding myometrium. Progesterone is
considered to have an important role in mitogen in the growth of
uterine myoma and maintain progesterone receptors. Thus, cell
proliferation, accumulation of extracellular matrices, cellular hy-
pertrophy all lead to the growth of uterine myoma directly con-
trolled by progesterone and in some role by estrogen. This rela-
tionship is evidenced by the provision of anti-progestins, atrophy
occurs in most uterine myomas [9, 11].
6. Conclusion
Some conditions also provide continuous estrogen exposure which
triggers the formation of uterine myoma. This risk factor including
age, family history, ethnic, bad habit, diet, weight loss and preg-
nancy.
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