Author: Claire

Claire Galea is the Owner and Director of Mariposa Holistic Care, through which she provides holistic care services tailored to her clients' personal needs. She is also in her final year following a Degree in Nursing at the Faculty of Health Sciences, University of Malta. Claire is keen about public education on health-related subjects as well as holistic patient-centered care. She is also passionate about spreading positivity and awareness on various subjects through her blog Student Nurse Life.

Female Reproductive System

The female reproductive system consists of the following organs:

ovaries – produce secondary oocytes and hormones (progesterone, oestrogens, relaxin, and inhibin)
fallopian tubes – the sites where fertilisation normally occurs; additionally assist in transporting a secondary oocyte to the uterus
uterus – cavity in which a fertilised ovum implants, and develops into a fetus for pregnancy and labour
vagina – the site which receives the penis during sexual intercourse, and which acts as a passageway during childbirth
external organs / vulva / pudendum

The Ovaries

The ovaries are a pair of irregularly scarred surfaced pale white glands measuring between 2.5 to 3.5cm long, 2cm wide, and 1.25cm thick. They produce gametes, which are secondary oocytes that develop into mature ova following fertilisation, and the hormones oestrogen, progesterone, inhibin, and relaxin.

The ovaries are held in place by 3 types of ligaments, namely the broad ligament of the uterus, which is part of the parietal peritoneum that attaches to the ovaries by the mesovarium; the ovarian ligament, which anchors the ovaries to the uterus; and the suspensory ligament, which attaches the ovaries to the pelvic walls.

Each ovary consists of:

GERMINAL EPITHELIUM – a layer of simple epithelium which covers the ovary’s surface and is continuous with the mesothelium that covers the mesovarium. The germinal epithelium does not give rise to ova.

TUNICA ALBUGINEA – a whitish capsule of dense irregular connective tissue found right beneath the germinal epithelium.

OVARIAN CORTEX – consists of ovarian follicles which are surrounded by dense irregular connective tissue containing scattered smooth muscle cells. The ovarian cortex can be found right beneath the tunica albuginea.

OVARIAN MEDULLA – consists of loose connective tissue which contains blood vessels, lymphatic vessels, and nerves.

OVARIAN FOLLICLES – consist of oocytes in various developing phases and surrounding cells which provide nourishment to the oocytes and secrete oestrogens throughout the follicle’s growing phase; single-layered surrounding cells are referred to as follicular cells, while multiple-layered surrounding cells are referred to as granulosa cells.

GRAAFIAN FOLLICLE – large follicle full of fluid in a close-to-being-ruptured state.

CORPUS LUTEUM – contains the remnants of the mature follicle, following ovulation; the corpus luteum produces progesterone, oestrogens, relaxin, and inhibin, before turning into fibrous scar tissue referred to as the corpus albicans.

Retrieved from https://slideplayer.com/slide/8162919/ on 15th April 2022

The Fallopian Tubes

The fallopian tubes are two hollow fibromuscular cylinders lined by epithelium which extend outwards and backwards around 10cm from the uterine cornu to the ovaries. Each fallopian tube is divided into the following parts:

interstitial (approx. 0.7mm x 2.5cm)
isthmus (approx. 1mm x 2.5cm)
ampulla (approx. 6mm x 5cm)
infundibulum (approx. 10mm wide)

The fallopian tubes are made up of 3 layers:

INTERNAL MUCOSA – contains ciliated columnar epithelial cells that help move the fertilised ovum along the tube.

MUSCULARIS – is the middle layer. It is composed of an inner circular ring of smooth muscle and an outer thin region of longitudinal smooth muscle; peristaltic contractions of the muscularis along with the ciliary action of the mucosal cells assist the oocyte or fertilised ovum to move towards the uterus.

SEROSA – the outer layer of the fallopian tubes.

The Uterus

The uterus is a pear-shaped hollow organ that projects anteriorly and superiorly over the urinary bladder, measuring about 7.5cm x 5cm at the fundus, and 2.5cm from front to back. The uterine wall thickness measures around 1 to 2cm.

The uterus features the following anatomical subdivisions:

fundus – dome-shaped portion superior to the fallopian tubes
body – tapering entral portion
cervix – inferior narrow portion which opens into the vagina; projects inferiorly and posteriorly, and enters the vaginal wall at almost a right angle
isthmus – constricted region measuring around 1cm long found between the body and the cervix

The uterine cavity is the uterine body’s inferior. The cervical canal is the interior of the narrow cervix. The cervical canal opens into the uterine cavity at the internal os into the vagina at the external os.

The uterus is made up of 3 layers:

PERIMETRIUM – the outer layer of the uterus becomes the broad ligament laterally, covers the urinary bladder and forms the vesicouterine pouch anteriorly, and covers the rectum and forms the rectouterine pouch a.k.a. pouch of Douglas posteriorly.

MYOMETRIUM – the middle layer of the uterus is thickest and circular in the fundus area and the thinnest and longitudinal in the cervix area; the myometrium responds to oxytocin released by the pituitary during labour and childbirth through contraction coordination which help in expelling the fetus from the uterus.

ENDOMETRIUM – the inner layer of the uterus is highly vascular. It is divided into two layers: the stratum functionalis lines the uterine cavity and sloughs off during menstruation, and the stratum basalis, which is a permanent layer, gives rise to a new stratum functionalis following each menstruation.

Retrieved from https://socratic.org/questions/what-are-the-two-layers-of-the-endometrium on 15th April 2022

Cervical Mucus

Cervical mucus is a secretion produced by the secretory cells of the cervix’s mucosa. It consists of water, glycoprotein, lipids, enzymes, and inorganic salts. Females in their fertile years secrete between 20-60ml of cervical mucus daily, which is more hospitable to sperm at or close to ovulation, when it is less viscous and increasingly alkaline with a pH of 8.5. Viscous mucus forms the cervical plug which stops sperm penetration.

The Vagina

The vagina is a long tubular fibromuscular canal measuring approximately 10cm long which extends from the exterior of the body to the cervix. It acts as a receptacle for the penis during sexual intercourse, an outlet for menstruation, and a passageway during childbirth.

The vaginal mucosa, which is continuous with the uterine mucosa, contains large glycogen stores that, upon decomposing, produce organic acids, which lead to a resulting acidic environment which retards microbial growth.

The Vulva

The vulva a.k.a. pudendum, is the female’s external genitalia. It consists of the following:

mons pubis
labia majora
labia minora
clitoris

Retrieved from https://www.cancer.org/cancer/vulvar-cancer/about/what-is-vulvar-cancer.html on 15th April 2022

Mammary Glands

The mammary glands, which lie over the pectoralis major and the serratus anterior, are modified sweat glands which produce milk.

Functions of the breast in relation to lactation include:

milk synthesis
milk secretion
milk ejection

NIPPLE – pigmented projection.

LACTIFEROUS DUCTS – closely spaced duct openings which allow milk ejection.

AREOLA – circular rough-looking pigmented area surrounding the nipple which contains modified sebaceous glands.

SUSPENSORY LIGAMENTS OF THE BREAST A.K.A. COOPER’S LIGAMENTS – strands of connective tissue found between the skin and the deep fascia that provides support for the breast.

MILK – following production, milk passes from the milk-secreting alveoli into secondary tubules, and then into mammary ducts. Mammary ducts close to the nipple expand and form lactiferous sinuses, where milk is stored, and is eventually drained into the lactiferous ducts, which drain into the exterior.

Retrieved from https://www.brainkart.com/article/Mammary-Glands—Anatomy-and-Physiology_18849/ on 16th April 2022

Hormones Related to the Female Reproductive System

Follicle-Stimulating Hormone (FSH)

in females initiates the development of an ova every month, and stimulates cells within the ovaries to secrete oestrogens
in males stimulates the testes to produce sperm
secretion depends on the hypothalamic regulating factor gonadotropin releasing factor (GnRF), which is released in response to oestrogens in females, and to testosterone in males through a negative feedback system

Luteinizing Hormone (LH)

along with oestrogens, in females it stimulates the release of an ovum within the ovary, prepares the uterus for the implantation of the fertilised ovum, stimulates the formation of the corpus luteum in the ovary to secrete progesterone, and prepares the mammary glands for milk secretion
in males it stimulates the interstitial endocrinocytes in the testes to develop and secrete testosterone
secretion is controlled by GnRF, which works through a negative feedback system

Prolactin (PRL)

requires priming of the mammary glands through oestrogens, progesterone, corticosteroids, growth hormone, thyroxine, and insulin
initiates and maintains milk secretion by the mammary glands (amount of milk is determined by oxytocin)
has an inhibitory and an excitatory negative control system
level rises during pregnancy, falls right after delivery, and rises again during breastfeeding, which is why in the 1st two days following birth, mothers do not produce milk but colostrum

NOTE: women on oral contraceptives may experience lack of milk production due to their hormonal effect.

Pituitary Gland Posterior Lobe

The posterior lobe of the pituitary gland a.k.a. neurohypophysis, does not synthesise hormones. It releases hormones to the circulation via the posterior hypophyseal veins to be distributed to target cells in other tissues. The cell bodies of the neurosecretory cells produce Oxytocin (OT) and Antidiuretic Hormone (ADH) / Vasopressin.

Oxytocin (OT)

is released in high amounts just before birth
stimulates contraction of smooth muscle cells in the pregnant uterus
stimulates the contractile cells around the mammary gland ducts
affects milk ejection
works through a positive feedback cycle which is broken following birthing
is inhibited by progesterone, but can work in conjunction to oestrogens

The Female Reproductive Cycle

The female reproductive cycle a.k.a. menstrual cycle demonstrates regular cyclic changes seeming as periodic preparations for fertilisation and pregnancy, which, if unsuccessful, results in menstruation where the uterine mucosa (stratum functionalis portion of the endometrium) is shed.

The ovarian cycle features a series of events related to the maturation of an ovum which usually occurs on a monthly basis.

Oestrogen

Oestrogen assists in the development and maintenance of the endometrial lining of the uterus, secondary sex characteristics, and breasts
Oestrogen helps keep fluid and electrolyte balance
Oestrogen increases protein anabolism (process in which amino acids are transformed into proteins) and is synergistic with the Growth Hormone a.k.a. Somatotropin
Oestrogen helps in keeping a low blood cholesterol level

NOTE: Moderate levels of oestrogens in the blood inhibit GnRF (Gonadotropin-Releasing Hormone) release by the hypothalamus. This causes the inhibition of FSH (Follicle Stimulating Hormone) secretion by the anterior pituitary gland.

pROGESTERONE

Progesterone works in conjunction with Oestrogen in preparing the endometrium for implantation of a fertilised ovum, and in preparation of the mammary glands for milk secretion

NOTE: High levels of progesterone inhibit GnRF (Gonadotropin-Releasing Hormone) and LH (Luteinizing Hormone).

Inhibin

Inhibin inhibits the secretion of FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone). This happens so as to inhibit multiple ovum maturation following the release of a mature ovum following ovulation.

Relaxin

Relaxin helps relax the uterus through the inhibition of myometrium contractions
Relaxin is produced by the placenta during pregnancy to help increase relaxation of the uterine smooth muscle
Relaxin increases the flexibility of the pubic symphysis near the end of pregnancy, and may also help in the cervix dilation process in preparation for childbirth

The Menstrual Cycle

Retrieved from https://sofreshnsogreen.com/wellness/cycle-syncing-guide/ on 16th April 2022

The menstrual cycle can be divided into 3 phases:

THE MENSTRUAL PHASE – the periodic discharge of 25ml to 65ml of blood, tissue fluid, mucus and epithelial cells, caused by a sudden reduction in oestrogens and progesterone. This phase usually lasts for around 5 days.

During this phase, 20 to 25 primary follicles start to produce small amounts of oestrogens.
By the end of menstruation, around 20 of these primary follicles develop into secondary follicles, while surrounding cells increase in number, differentiate, and secrete follicular fluid.
The follicular fluid forces an immature ovum to the edge of the secondary follicle and fills the follicular cavity, whilst secondary follicles produce oestrogens, leading to an elevation of oestrogen levels in the blood.
Ovarian follicle development results from GnRF secretion by the hypothalamus, which then stimulates high FSH production by the anterior pituitary.

THE PREOVULATORY PHASE – the second phase of the menstrual cycle which covers the phase between menstruation and ovulation.

FSH and LH stimulate ovarian follicles to increase oestrogen production, which stimulates the rebuilding of the endometrium, which by the end of this phase doubles to up to 6mm.
With the thickening of the endometrium, short straight endometrial glands develop, and arterioles coil and lengthen whilst penetrating the functionalis.
LH is secreted in increasing quantities as this phase starts to near its end.
A secondary follicle matures into a vesicular ovarian a.k.a. graafian follicle, ready for ovulation. At this time, just before ovulation occurs, the vesicular ovarian starts producing small amounts of progesterone.

OVULATION – the immature ovum in the vesicular ovarian follicle is released into the pelvic cavity around the middle of the menstrual cycle.

Immediately prior to ovulation, high levels of oestrogen inhibit GnRF production by the hypothalamus, which in turn inhibits FSH secretion by the anterior pituitary via a negative feedback effect.
At the same time, high levels of oestrogen work through a positive feedback effect, causing the anterior pituitary to release a high amount of LH which triggers ovulation.
Following ovulation, the vesicular ovarian follicle collapses, the follicular cells enlarge, change, and form the corpus luteum.

THE POSTOVULATORY PHASE – represents the time between ovulation and onset of upcoming menses. This phase is consistent in duration.

Following ovulation, LH secretion stimulates the development of the corpus luteum.
The corpus luteum secretes increasing quantities of oestrogens and progesterone.
FSH secretion increases gradually whilst LH secretion decreases.
During this phase, progesterone becomes the most dominant ovarian hormone.

SEQUELAE

If fertilisation and implantation do not occur, the increasing progesterone and oestrogen levels secreted by the corpus luteum inhibit GnRF and LH secretion.
The corpus luteum degenerates, which causes decreased secretion of progesterone and oestrogens.
The corpus luteum becomes the corpus albicans, whilst the decrease in progesterone and oestrogens trigger another menstrual cycle to begin, along with increased output of GnRF by the hypothalamus and a new output of FSH.

Retrieved from https://quizlet.com/au/232342424/hormonal-control-of-menstrual-cycle-diagram/ on 16th April 2022

Conditions & Operations Related to the Female Reproductive System

Hysterectomy

Hysterectomy is the most common gynaecological operation, commonly indicated in endometriosis, pelvic inflammatory disease, recurrent ovarian cysts, excessive uterine bleeding, and cancer of the cervix, uterus, or ovaries.

There are 3 types of hysterectomies:

Total Hysterectomy – removal of the uterine body and cervix
Partial Hysterectomy – removal of uterine body only (cervix is left in situ)
Radical Hysterectomy – removal of uterine body, cervix, fallopian tubes (and possibly the ovaries), the vagina’s superior portion, the pelvic lymph nodes, and supporting structures

Retrieved from https://www.gleneagles.com.sg/specialties/medical-specialties/women-gynaecology/hysterectomy on 15th April 2022

Cystocoele

Cystocoele is a herniation of the bladder wall into the vaginal cavity.

Rectocoele

Rectocoele is a herniation of the rectum into the vaginal wall.

Retrieved from https://fascrs.org/patients/diseases-and-conditions/a-z/rectocele-expanded-information on 14th April 2022

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Male Reproductive System

The male reproductive system consists of the following organs:

testes
ducts system (ductus deferens, ejaculatory ducts, urethra)
accessory sex glands (seminal vesicles, prostate gland, bulbourethral gland)
supporting structures (scrotum, penis)

The function of the testes is to produce sperm and secrete hormones, while the ducts system is responsible for the transportation and storage of sperm, assistance in sperm maturation, as well as conveyance of the sperm to the exterior.

male reproductive system — Retrieved from https://www.slideserve.com/coy/chapter-28-the-reproductive-systems on 5th April 2022

The Scrotum

The scrotum acts as a supporting structure for the testes, consisting of loose skin and superficial fascia that hangs from the root of the penis. The left testis is suspended lower than the right testis. The spermatic cord passes up the scrotum’s back, through the inguinal ring, and into the pelvic cavity.

The external structure of the scrotum consists of rich sensory innervation, sebaceous glands, darker pigmentation, and sparse hair.

Within the internal structure of the scrotum is the scrotal septum (made up of the superficial fascia and the dartos muscle), which divides the scrotum into 2 sacs.

The testes are kept cooler by the following 3 structures:

cremaster muscle of the spermatic cord – relaxes when warm, contracts when cool, thus raising or lowering the scrotum and testes
dartos muscle in the scrotal wall – contracts and tautens the scrotum when cool
pampiniform plexus of blood vessels in the spermatic cord – acts as countercurrent heat exchanger, cooling blood on its way to the testis

The Testes

The testes are paired oval glands measuring around 5cm long with a diameter of 2.5cm. Each testis weighs between 10-15g. During foetal development, the testes originate near the kidneys, from where they start descending through the inguinal canals towards and into the scrotum by the end of the 7th month of pregnancy.

The testis has a fibrous capsule known as Tunica Albuginea. Within the fibrous septa are up to 300 compartments known as lobules, each of which contains up to 3 sperm-producing seminiferous tubules. Between these tubules are clusters of interstitial cells which secrete testosterone.

Retrieved from https://radiopaedia.org/cases/testis-cross-section?lang=us on 5th April 2022

The Seminiferous Tubules

The seminiferous tubules contain the following two types of cells:

spermatogenic cells – produce sperm
sertoli cells – support spermatogenesis

Sertoli Cells

Sertoli cells, a.k.a. sustentacular cells, support and protect spermatogenic cells through their development.

Retrieved from https://www.nagwa.com/en/videos/104129276305/ on 5th April 2022

Leydig Cells

Leydig cells a.k.a. interstitial endocrinocytes, are found in clusters within the spaces between adjacent seminiferous tubules. They secrete testosterone.

Retrieved from https://histology.siu.edu/erg/RE028b.htm on 7th April 2022

The Ducts

Sperm cells pass through a number of ducts to exit the body. Once they leave the testes, sperm cells pass through the epididymis, ductus deferens, ejaculatory duct, and urethra.

EFFERENT DUCTULES – carry sperm from the posterior side of the testis to the epididymis thanks to ciliated cell clusters which assist the sperm through.

EPIDIDYMIS – whilst travelling through the epididymis, sperm cells mature, and are then stored in the epididymis’s tail, where they remain fertile for 40 to 60 days.

DUCTUS DEFERENS – sperm cells travel from the epididymis’s tail before uniting with the seminal vesicle duct.

EJACULATORY DUCT – allows the sperm cells through the prostate gland before emptying into the urethra.

SEMINIFEROUS TUBULES – open up into a collection of very short ducts known as straight tubules, which lead into the rete testis.

EFFERENT DUCTS – sperm moves into a series of coiled ducts within the epididymis.

DUCTUS EPIDIDYMIS – efferent ducts empty into a single tube a.k.a. ductus epididymis.

Retrieved from https://quizlet.com/213934544/chapter-27-male-reproductive-system-flash-cards/ on 7th April 2022

Accessory Sex Glands within the Male Reproductive System

Seminal Vesicles

Seminal Vesicles are a pair of glands associated with the ductus deferens, posterior to the urinary bladder base and anterior to the rectum. Seminal vesicles secrete an alkaline yellowish secretion, which helps in neutralising the acidic environment of the male urethra and the female reproductive tract. It totals about 60% of semen, containing Fructose (used for sperm ATP production), Prostaglandins (provide sperm motility and viability), and Clotting Proteins (promote semen coagulation following ejaculation).

Prostate Gland

The prostate gland is a single gland situated immediately inferior to the bladder, surrounding the urethra and the ejaculatory duct. It secretes a thin, milky, slightly acidic secretion totaling around 30% of semen, containing Citric Acid (used for sperm ATP production via Krebs’ cycle), Proteolytic Enzymes (promote breakdown of clotting proteins from the seminal vesicles), and Acid Phosphatase.

Bulbourethral a.k.a. cowper glands

Bulbourethral Glands a.k.a. Cowper’s Glands, are pea-sized glands located posterior to the prostate. They produce a clear, slippery fluid during sexual arousal, which helps lubricate the penis’s head in preparation for intercourse. It also neutralises the acidity of residual urine found in the urethra, since this acidity would be harmful to the sperm.

The Penis

The penis provides a passageway for sperm ejaculation and urine excretion through the urethra. It consists of the Root (attached portion), the Body (2 corpora cavernosa, and 1 corpus spongiosum), and the Glans penis.

Hormones related to the Male Reproductive System

ANDROGENS – masculinising steroid sex hormones eg. testosterone (normally secreted in both sexes)

OESTROGENS – feminising steroid sex hormones (normally secreted in both sexes)

PITUITARY GONADOTROPHINS – FSH (follicle-stimulating hormone) helps in maintaining spermatogenic epithelium and sertoli cells within the male, and LH (luteinizing hormone) stimulates testosterone production from the Leydig Cells within the testes.

Testosterone

Testosterone, which is the primary hormone in the testes:

promotes male development
is responsible for an inhibitory feedback response on the pituitary’s secretion of LH
develops and maintains male secondary sex characteristics eg. body hair growth, larynx enlargement and voice deepening, increased stature, etc.
exerts a protein anabolic, growth-promoting effect
maintains gametogenesis, along with FSH

Testicular Function Control

FSH:

maintains gametogenic function, along with androgens
is tropic to the Sertoli cells
stimulates secretion of androgen-binding protein and inhibin (inhibin feeds back to inhibit FSH secretion)

LH:

stimulates testosterone secretion (testosterone feeds back to inhibit LH secretion)
is tropic to the Leydig cells

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Infection Control Measures in Immunosuppressed Patients

Infection complications are most often predictable and possibly preventable through adequate infection control measures. In immunosuppressed patients this is of high importance, especially since the greater the impairment, the higher the risk of infection. Recognising patients with increased risk, identifying and correcting risk factors in advance, and reducing sources of infection are important aspects related to prevention of infection.

Immunosuppressed Patients

Immunosuppressed patients typically are those patients who have:

extensive burns
organ transplants
particular genetic disorders eg. immunoglobulin A deficiency
HIV infections
leukaemias (cancer of white blood cells)
lymphomas (cancer of the lymphatic system)
high-dose chemotherapy
haematological malignancies (cancers originating in blood-forming tissue eg. bone marrow, or in immune system cells)
neutropenia (lack of neutrophils)

Neutropenia

Neutropenia is characterised by lack of neutrophils – white blood cells that help fight infections, especially those caused by bacteria. Normal range for neutrophils is 2.5-7.5 x 10⁹/L. The lower the neutrophil count, the steeper the fall or the longer the duration of neutropenia, the higher the risk of infection.

immunosuppressed patients — Retrieved from https://www.haematologica.org/article/view/7075 on 2nd April 2022

Protective Precautions vs Protective Isolation

COMMENSAL MICRO-ORGANISMS – can be found on body surfaces which are covered by epithelial cells and exposed to the external environment (GI tract, respiration tract, vagina, skin, etc).

COMMENSAL BACTERIA – although co-evolved with their hosts, in specific circumstances can overcome protective responses in the host, causing pathologic effects.

NOSOCOMIAL INFECTIONS – eg. healthcare associated infections & MRSA.

OPPORTUNISTIC INFECTIONS – infections affecting solely the immunosuppressed patient eg. Kaposi’s sarcoma.

Infection-causing micro-organisms in immunosuppressed patients may be acquired through:

the presence of the individual’s normal flora
hospital staff hands
hospital equipment
food

Protective isolation components include:

physical separation from the main population through the use of a single room
restriction on movement, visitors and diet
antimicrobial prophylaxis and selective decontamination of the digestive system
care for the maintenance of skin and mucous membrane integrity
application of hand hygiene to prevent exogenous acquisition of micro-organisms

NOTE: Signs & symptoms of infection are most commonly absent in immunosuppressed patients.

Transferring an immunosuppressed patient in Protective Isolation may not be enough to prevent subsequent development of infection.

Infection Control Measures

Infection control measures help prevent infection in immunosuppressed patients. Standard precautions should be applied when caring for neutropenic patients as well as severely immunosuppressed patients.

Component	Recommendations
Hand hygiene	after contact with body fluids (including contaminated items), after glove removal, and between one patient and another
Gloves	use when touching body fluids (including contaminated items), when touching mucous membranes, and non-intact skin
Gown	use during procedures and patient care which require contact with clothing and exposed skin with anticipated exposure to body fluid
Face protection (eg. masks, goggles, visors)	use during procedures and patient care which are likely to generate splashes of body fluids, including aerosol-generating procedures with suspected or proven infections that transmit by respiratory aerosols (in which case wear an N95 or higher respirator along with gloves, gown, face and eye protection)
Soiled equipment	handle using preventative measures to avoid transferring micro-organisms to other individuals and to the environment; perform hand hygiene and wear gloves when handling visibly contaminated items
Environmental control	support/advocate for routine care, cleaning and disinfection of surroundings, especially surroundings close to patient-care areas

Standard Precautions

Textiles and laundry	handle using preventative measures to avoid transferring micro-organisms to other individuals and to the environment
Sharps	avoid recapping, bending, breaking or manipulating used needles; if recapping is needed, use one-hand scoop technique; use safety features if available; use appropriate sharps disposal containers
Patient resuscitation	use mouthpiece, resuscitation bag, or other ventilation devices to prevent oral contact and contact with oral secretions
Patient placement	use single-patient room if patient is at increased risk of transmission, contamination, lacking hygiene maintenance, or if patient is at increased risk of becoming infected or developing adverse outcomes following infection
Hygiene etiquiette	teach symptomatic patients to cover mouth and nose when sneezing and coughing, correct use and disposal of tissues, wearing of surgical mask if tolerated, or maintaining spatial separation (if possible more than 3 feet)

Patient Placement

SINGLE ROOM – promotes reinforcement of infection control measures; should be prioritised for isolating individuals with communicable diseases or epidemiologically important organisms, to avoid exposing immunosuppressed patients to such organisms. A patient placed in a single room should:

have an isolation notice displayed on the door
have an ensuite bathroom
have its door closed at all times
have limited staff entering the room
be provided with psychological support and reassurance whilst in isolation
not have staff with infections to provide patient care
not have staff to provide patient care whilst providing care to infectious patients in the same duty shift

SINGLE ROOM + HIGH EFFICIENCY PARTICULATE AIR (HEPA) FILTERS – promote reduction of risk to healthcare associated infections due to airborne fungi such as Aspergillus Genus (especially where construction-related work is in progress).

Patient Hygiene

FATIGUE – Immunosuppressed patients are often fatigued. Thus, patient hygiene must be assessed on a daily basis, and assistance must be provided where necessary.

PERINEAL CARE – Immunosuppressed patients frequently suffer from irritation or infection in the perineal area – an area which would be heavily colonised with bacteria. Thus, particular attention to this area is a must to maintain patient hygiene. Note that the use of soap may irritate the mucous membranes, leading to irritation exacerbation.

STAFF ILLNESS – immunosuppressed patients should not be nursed by staff with known or suspected infections or communicable diseases eg. oral-facial herpes simplex and upper respiratory tract infections; contact between such individuals should be reported to the infection control team and to the patient’s medical consultant.

Hand Hygiene

Environment and Equipment

Removal of dust from surfaces may help prevent infection (routine use of chemical disinfectant has not yet been proven to reduce infection) – surfaces need to be damp-dusted daily with single use cleaning cloths and neutral detergent; mop head needs to be laundered daily
Isolation rooms require cleaning with the use of gloves and aprons, followed by hand hygiene prior to leaving the room
Vacated rooms must be cleaned thoroughly before they are reoccupied
Medical equipment should be decontaminated after each use
Single-use items must be discarded and not re-used
Toys of immunosuppressed children should be decontaminated
Flowers and plants have not been directly linked to infection in immunosuppressed patients, however, are usually not permitted since they may act as a reservoir for Gram Negative bacteria or fungal spores like Aspergillus

Personal protective equipment

Use of face masks is not known to prevent infection in immunosuppressed patients, but can help protect healthcare staff from body fluid splashing
Routine use of non-sterile gloves and aprons/gowns may help in preventing acquisition of micro-organisms
PPEs must be minimally used to prevent contact with body fluids or contaminated items, and when in contact with non-intact skin and mucous membranes
Must be removed and discarded of as clinical waste after use, followed by application of hand hygiene
Sterile gloves are only required in certain aseptic or invasive procedures, or when in contact with sterile sites

Nutrition

Immunosuppressed patients have an increased risk of acquiring food-borne illnesses and harmful micro-organisms, and so, should be advised to avoid high-risk foods such as shellfish, pate’, soft cheeses and foods that are made with raw eggs
Neutropenic individuals have an increased risk of acquiring infection from Gram-Negative bacteria which is commonly found in sink plugholes and overflow outlets

Immunosuppressed Patient Visitors

Visitors should:

report to a staff member prior to entering the patient’s room so precautions can be explained, and infections that may pose danger for the patient may be identified
not visit if they have any transmissible infection
not bring any pets, and plants or flowers (fresh or dried)

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Metabolic Syndrome and Obesity

Obesity is a disease which involves excessive body fat that increases the risk of additional diseases and health issues, such as cardiovascular disease, diabetes, hypertension, and cancer. Metabolic syndrome is closely linked to obesity and inactivity, as well as insulin resistance.

Retrieved from https://twitter.com/gainalliance/status/854273300389916672?lang=bn on 28th March 2022

Obesity

Obesity is “a chronic relapsing progressive disease progress” (Bray et al., 2017). It is determined by the following factors:

Energy Balance
Obesogenic Environment
Nature VS Nurture

eNERGY BALANCE

Energy In (dietary intake) VS Energy Out (physical activity)

Obesogenic Environment

An environment that promotes weight gain and is not conducive to weight loss.

Nature vs Nurture

Genes affect the metabolic rate, fuel use, brain chemistry, and body shape. Over-eating is learned earlier on in childhood eg. encouraging child to eat whatever is on the plate. Environmental factors add to weight gain influences. Social status affects weight status eg. poverty may lead to unhealthy food choices.

Nutrition Assessment of Obesity

Obesity is characterised by excessive body fat: women with >35% body fat and men with >25% body fat. Excessive body fat puts the individual at increased risk for health problems. Body fat is calculated by measuring skin folds using calipers.

BMI calculation = weight (kg) / height (m²). BMI should ideally be between 18.5 and 24.9kg/m²

Retrieved from https://bjcardio.co.uk/2014/11/obesity-module-1-management-in-primary-care/4/ on 28th March 2022

Retrieved from https://www.researchgate.net/publication/346569912_Obesity_Weight_Loss_and_Cardiovascular_Risk/figures?lo=1&utm_source=google&utm_medium=organic on 28th March 2022

Obesity Health Risks

(Adapted from Bray GA. Gray DS, Obesity, part 1: Pathogenesis. West J Med 149:429, 1988; and Lew EA, Garfinkle L; Variations in mortality by weight among 750,000 men and women. J Clin Epidemiol 32:563, 1979.) Retrieved from https://slideplayer.com/slide/5330508/ on 28th March 2022

Android vs Gynoid Body Fat Distribution

ANDROID

obesity centered in the upper-body area – apple shape
abdominal fat is released into the liver
associated with cardiovascular disease, hypertension and type 2 diabetes
related hormone at play – testosterone

GYNOID

obesity centered in the lower-body area – pear shape
not as risky as android
related hormones at play – estrogen and progesterone

Retrieved from http://www.myhealthywaist.org/index.php?id=56&tx_nurebook_pi1[page]=9&cHash=644d9e5b11 on 28th March 2022

Health Problems Associated with Obesity

cardiovascular disease
hypertension
type 2 diabetes
pulmonary disease
cancer of the breast,colon, pancreas and gallbladder
sleep apnea
gallstones
bone/joint disorders
infertility
difficult delivery following pregnancy
increased surgical risk
reduced agility
poor quality of life
early death

Retrieved from https://slidetodoc.com/obesity-pathophysiology-risk-assessment-and-prevalence-obesity-excessive/ on 29th March 2022

In women, the incidence of coronary heart disease increased with increasing body mass index levels for both age groups. Among women older than 50 years, the heaviest group experienced 292 incidents of coronary heart disease compared with 223 in the BMI group < 25. In women younger than 50 years of age, the group of 30+ BMI experienced 179 incidents compared with only 76 in the < 25 BMI category. BMI Levels. Adapted from Hubert HB et al. Circulation 1983;67: Metropolitan Relative Weight of 110 is a BMI of approximately 25. Retrieved from https://slideplayer.com/slide/5330508/ on 29th March 2022

Obesity as an independent risk factor for cardiovascular disease was reexamined by Helen Hubert in the 5,209 men and women of the original Framingham cohort. Observations of disease occurrence over the 26 years indicate that obesity was an independent predictor of CVD, particularly among the younger members of the cohort and in women more than men. This study also showed that weight gain after the young adult years conveyed an increased risk of CVD in both sexes that could not be attributed to the initial weight or the levels of the risk factors that may have resulted from the weight gain. This slide shows the increasing incidence of coronary heart disease with increasing body mass index levels for both age groups of men. However, the gradient of risk was steeper among the younger men and women (< 50 years) . Among men younger than 50 years, the heaviest group experienced twice the risk of coronary disease compared with the leanest group. BMI Levels. Retrieved from https://slideplayer.com/slide/12116399/ on 29th March 2022

Weight Loss Benefits & Guidelines

Metabolic Syndrome and Obesity — Retrieved from https://community.jennycraig.com/healthy-habits-blog/live-life/10-ways-losing-5-10-of-your-body-weight-may-benefit-your-health/ on 29th March 2022

Adult Weight Loss…

total energy intake should be less than energy expenditure
consider diets with 600kcal/day deficit
consider low-fat diets alongside expert support and follow-ups for sustainable weight loss
keep in mind that low-calorie diets may not provide all nutritional requirements
include behaviour change strategies using a biopsychosocial approach and history in relation to past diet experiences as well as comorbidities

Metabolic Syndrome

Metabolic syndrome is a worldwide growing epidemic, affecting about 1 of every 4 or 5 adults in every country. Its incidence increases with age.

The term Metabolic Syndrome refers to a group of risk factors which increase the risk for cardiovascular disease, diabetes, stroke, and other health-related problems.

Metabolic Syndrome Risk Factors

hyperglycaemia
hypertension
abdominal obesity a.k.a. android obesity
low HDL cholesterol level
high triglyceride level (including individuals on treatment for high triglyceride level)

WHO Recommendations

Insulin Resistance

While a third of all individuals with Metabolic Syndrome have normal insulin sensitivity, the two are still associated with each other. Insulin resistance features high plasma insulin concentration which fails to suppress plasma glucose as normally happens. Contributing factors include unresponsiveness to insulin at a cellular level due to receptor-based mechanisms.

Hypertension

Insulin resistance and hyperinsulinaemia may cause hypertension due to an increase in catecholamine activity, as happens with increased insulin concentration through insulin-mediated renal tubular reabsorption of sodium. Weight loss helps in improving both hypertension and hyperinsulinaemia.

Dyslipidaemia

High trygliceride and low HDL cholesterol levels are key factors for metabolic syndrome, both commonly leading to cardiovascular disease. The term dyslipidemia refers to an increase in plasma cholesterol, triglycerides, both, or low HDL cholesterol level which leads to atherosclerosis development.

Preventing or Reversing Metabolic Syndrome

weight loss through healthy eating
regular exercise
smoking cessation
alcohol cessation
pharmacological interventions

Reference

Bray, G.A., Kim, K.K., & Wilding, J.P.H. (2017). Obesity: a chronic relapsing progressive disease process. A position statement of the World Obesity Federation. Obesity Reviews, 18: 715-723.

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Diabetic Foot

The diabetic foot is prone to complications, as clearly indicated by the high number of hospital admissions amongst individuals with diabetes due to foot problems. What may seem like a ‘simple’ foot ulcer can easily lead to an amputation. Sadly, a leg is amputated every 30 seconds, with up to 70% of all leg amputations happening to individuals with diabetes. Yet up to 85% of amputations can be avoided with preventative measures and adequate care.

Retrieved from https://www.diabetesfeetaustralia.org/welcome-world-diabetes-day/ on 2nd July 2022

Retrieved from https://www.diabetesfeetaustralia.org/diabetic-foot-disease-is-a-top-10-cause-of-global-disability/ on 2nd July 2022

Diabetic Foot Ulcers – Treat as an Aggressive Cancer!

Diabetic foot complications, including amputations, can be avoided by:

applying a preventative approach through cost-effective strategies
identifying high risk individuals and providing them with related health literacy eg. to check their feet daily, dry them thoroughly, and wear appropriate footwear
knowing when a diabetic foot ulcer has become a complicated lesion: ischaemia and infection
knowing which and when to apply a proper off-loading device
providing continuity in treatment and management between hospital and the community, along with organisation and communication between both settings

However…

5% of individuals with new ulcers die within 12 months following their first physician visit regarding a foot ulcer
42.2% of individuals with foot ulcers die within 5 years
70% of diabetic foot ulcers recur over the following 3 years

“When people with diabetic foot ulcers heal, just like with cancer, they are not really healed. Our patients are in remission. We tend to think about wounds when they are open but why don’t we think about them when they are closed?
We should be aiming for having people at home in diabetic foot remission monitoring themselves”
Armstrong, Boulton and Bus, 2017.

Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S1067251607600015 on 2nd July 2022

Diabetic Foot Lesions Risk Factors

Retrieved from https://www.wjgnet.com/1948-9358/figures/v6/i1/37.htm on 2nd July 2022

Retrieved from https://www.researchgate.net/publication/242514797_DIABETIC_FOOT_DISORDERS/figures?lo=1 on 2nd July 2022

Routine Diabetic Foot Screening

1. COLLECT MEDICAL HISTORY

ask regarding any previous foot ulcers or lower extremity amputations
assess regarding poor access to healthcare and financial constraints
ask if patient is experiencing foot issues eg. foot pain (walking or resting), numbness, claudication (pain whilst walking or using arms – may be a symptom of peripheral artery disease)
ask if patient is experiencing dyspnoea
ask if patient has end stage renal disease

2. INSPECT & ASSESS FOOT

assess skin colour, temperature, and for callus or oedema presence
assess for lesions such as pre-ulcerative signs, active ulcers, fissures, cracks and blisters
check for bone and joint deformities eg. claw or hammer toes, abnormal large bony prominences, or limited joint mobility
check if patient is using ill-fitting or inadequate footwear
inspect patient feet for poor feet hygiene eg. improperly cut toenails, unwashed feet, superficial fungal infections, or unclean socks
notice any patient physical limitations that may hinder proper foot care eg. obesity, visual impairment, etc.
question patient on foot care health literacy – see what patient education is required for better self-care

3. ASCERTAIN PATIENT UNDERSTANDING & EDUCATION

explain the screening process and the rationale behind it
provide reassurance in case of anxiety
provide patient education, counseling and support whilst screening the patient’s feet
following screening, provide results to the patient, including any risks for foot problems, both in verbal and written form, along with contact details in case of any future questions

Peripheral Arterial Disease

Peripheral arterial disease is the main cause of delayed healing in the diabetic foot, associated with neuropathy in about 80% of all cases:

macroangiopathy – similar to atherosclerosis, but is distributed in the distal segments of the lower extremities i.e. the calf and foot arteries
arterial calcification – ‘hardening of the arteries’ – calcium forms hard crystals in the blood vessel walls
microangiopathy – thickening of the capillary basement membrane which compromises gaseous exchange

Assessing Dorsalis Pedis & Posterior Tibial Pedal Pulses

absence of both pedal pulses on one foot strongly suggests pedal vascular disease
if no pulse can be located, refer patient to a vascular specialist or a relevant health professional for further assessment

NOTE: further examinations which need to be performed by a trained healthcare professional include the Ankle Brachial Pressure Index (ABPI), Systolic Toe Blood Pressure (STBP), and the Toe Brachial Pressure Index (TBPI)

Retrieved from https://journals.rcni.com/nursing-standard/leg-ulceration-part-2-patient-assessment-ns2004.09.19.2.45.c3699 on 2nd July 2022

Diabetic Neuropathy

Up to 70% of individuals with diabetes have mild to severe forms of nervous system damage. This includes:

impaired sensation or pain in extremities
slow food digestion in the stomach
carpal tunnel syndrome
other nerve issues

With diabetic peripheral neuropathy, one may not be able to feel:

temperature changes
pressure
pain
vibration

NOTE: individual with peripheral neuropathy may also experience painful sensory neuropathy which includes burning and tingling sensations a.k.a. paresthesia.

The Motor Neuropathic Diabetic Foot

Neuropathic foot features include:

predominant neuropathy
adequate circulation
palpable pulses
warm, dry, and often painless

Complications include:

muscle weakness
muscle twitching
muscle paralysis
neuropathic ulcer commonly found at the sole of the foot
charcot foot
neuropathic oedema

Neuropathic Ulcer

Charcot Foot

Charcot foot is a condition that causes bones in the foot to weaken, leading to fractures and shape changing. This typically occurs in individuals with neuropathy.

Neuropathic Oedema

The Neuro-Ischaemic Diabetic Foot

Neuro-Ischaemic foot features include:

neuropathy
absent foot pulses
feels cool to touch
thin, shiny, hairless skin
subcutaneous tissue atrophy
increased pain at rest (may be absent due to neuropathy)

The Ischaemic Diabetic Foot

Ischaemic foot features include:

peripheral vascular disease
absent signs of peripheral neuropathy
cold, shiny, hairless skin
rare in diabetic patients

Diabetic Foot Assessment

To perform a diabetic foot assessment, shoes, socks, and any would dressings from both feet should be removed. This should be followed by a thorough examination for evidence of the following risk factors:

ulcers
callus
gangrene
deformity
infection
inflammation
charcot foot
limb ischaemia
neuropathy

Wound Assessment and Description

Retrieved from https://slideplayer.com/slide/12696492/ on 27th March 2022

Retrieved from https://www.researchgate.net/publication/311988179_Triangle_of_Wound_Assessment_Made_Easy_Revisited/figures on 27th March 2022

Assessing Sensation with a tuning fork

Assessing for Neuropathy using 10g Monofilament

Assessing for Vascular Problems

Is lower limb blood supply adequate for normal function and tissue viability?
Can you identify any arterial or venous vascular problems which may compromise the current state of the tissues?
Are there any vascular abnormalities that may affect the patient’s healing or treatment options?
What can you do to avoid possible complications?
Does the patient have a vascular condition that requires further investigations by a specialist?

Calculating Ankle-brachial index

Retrieved from https://www.researchgate.net/publication/233765986_Anklebrachial_index_to_everyone/figures?lo=1 on 27th March 2022

Osteomyelitis

Foot Ulcer Treatment – Key Elements

providing local wound care
providing pressure relief for ulcer protection
providing infection treatment
restoring skin perfusion
preventing recurrence
treating or controlling other comorbidities eg. diabetes
providing related health literacy to patients and their relatives

Provide the patient with oral and written information in detail, including information about diabetes control, foot emergencies, and contact person details.

Offloading

Offloading promotes reduction, redistribution, or removal of detrimental forces applied to the foot. Offloading alleviates pressure at areas of high vertical and shear stress.

Foot plantar pressure is the pressure field which acts between the foot and the support surface during everyday activities. The main aim of offloading devices is to redistribute plantar pressures evenly, which helps avoid areas of high pressure that prevent or delay healing.

A, Total contact cast; B, Charcot Restraint Orthotic Walker boot; C, prefabricated walker; D, DH walker; E, IPOS shoe; F, OrthoWedge; G, postoperative shoe; H, healing sandal; I, reverse IPOS; J, L’nard splint; K, patella tendonbearing brace; L, MABAL shoe. 1, Dorsal digit; 2, plantar digit; 3, plantar metatarsal; 4, medial metatarsal; 5, lateral metatarsal; 6, heel.

Retrieved from https://www.researchgate.net/publication/269766812_The_Management_of_Diabetic_Foot_Ulcers_Through_Optimal_Off-Loading_Building_Consensus_Guidelines_and_Practical_Recommendations_to_Improve_Outcomes/figures?lo=1 on 3rd July 2022

References

Armstrong, D., Boulton, A., & Bus, S. (2017). Diabetic Foot Ulcers and Their Recurrence. The New England Journal of Medicine, 376(24), 2367-2375. Retrieved from http://81.143.226.227/Medicine/Papers/2017_06_15%20NEJM%20Diabetic%20Foot%20Ulcers%20and%20Their%20Recurrence.pdf on 2nd July 2022.

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Diabetes Prevention and Management

Type 2 Diabetes prevention aims to prevent or delay the onset of diabetes, or to prevent complications arising from Type 2 Diabetes. For diabetes prevention it is recommended that:

individuals are first assessed for the risk of prediabetes through an adequate risk assessment tool such as the German Diabetes Risk Score
if high risk result is achieved, the individual should be tested for prediabetes or Type 2 Diabetes
individuals found with prediabetes should have their blood glucose monitored every year

diabetes prevention and management — Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK535456/figure/article-18425.image.f1/ on 21st March 2022

Diabetes Prevention and Delay

Lifestyle Changes

Type 2 Diabetes can be prevented or delayed by:

intensive lifestyle behaviour change programmes (include a calorie-reduced diet coupled with exercise – also promote reduction of risk factors such as hypertension, hyperlipidaemia, and inflammation)
achievement and maintenance of 7% loss of body weight
physical activity such as brisk walking for at least 150 minutes per week

Pharmacological Therapy

Prevention of Type 2 Diabetes can also be assisted with pharmacological therapy, where individuals with a BMI of 35kg/m² AND/OR who have 60 years or more AND/OR women with past GDM (gestational diabetes mellitus) can be prescribed Metformin.

NOTE: long term use of Metformin has been associated with vitamin B12 deficiency, therefore, vitamin B12 levels should be monitored on a regular basis especially in individuals with peripheral neuropathy and/or anaemia.

Diabetes Management

Nutrition

Eating a healthy balanced diet promotes:

weight control
blood glucose level stabilisation
serum lipid level decrease

A patient with diabetes should be encouraged reduce sugar intake to a minimum, to reduce carb intake, and to distribute caloric intake throughout the day in smaller meals with snacks in between. This helps to reduce the chance of experiencing a hypoglycaemic episode. Carbs which are high in fibre are a better choice.

Retrieved from https://www.hsph.harvard.edu/nutritionsource/healthy-eating-plate-vs-usda-myplate/ on 22nd March 2022

Exercise

A 30-minute walk per day promotes better Diabetes management. Exercise:

lowers blood glucose level
promotes weight loss
reduces blood lipids
decreases the blood pressure
promotes better circulation

Caution should be taken:

when the individual is using insulin since hypoglycaemia can occur during exercise OR up to several hours after exercise; patient should be encouraged to check blood glucose before and after exercising
if the individual’s urine contains ketones and blood glucose is over 14mmol/l
if the individual has other complications such as cardiovascular disease, neuropathy and retinopathy
patient should be encouraged to keep a blood glucose diary, listing down blood glucose values as well as when it was taken (before/after meal/exercise) so as to evaluate results and see if any changes in individualised care plan are necessary

Pharmacological Therapy

Type 1 Diabetes Management

An individual’s daily amount of needed insulin is calculated on the person’s weight: 0.4 to 1.0 units per kg per day. About 50% of the total amount of insulin needed per day is given as basal, while the other half is given in relation to food intake a.k.a. prandial.

Rapid acting insulin helps in reducing the risk of hypoglycaemia. Patient education is recommended with regards to bolus insulin dose adjustment prior to meals, based on carbohydrate intake, blood glucose, and exercise.

Lantus is long-acting, usually with no peak. It is taken ideally at bedtime or else early in the morning.

Actrapid is a short-acting insulin which works rapidly. It peaks in 2-3 hours with a duration of 5-8 hours. Actrapid is usually recommended to be administered 30 minutes before eating.

Patient on insulin should be instructed to:

always check blood glucose after washing hands with soap and water and not use alcohol rub; to use the lancet at the side of the finger and to wipe and discard first drop of blood before testing with the 2nd drop
check blood glucose 30 minutes before eating or 2 hours after eating
taught how the prescribed medications work
told when to administer insulin to self
told to rotate injection site every time
told to carry glucose or sugar in case a hypoglycaemic episode is experienced
told to store opened insulin vials in a dark cupboard away from sunlight and to discard after 30 days
told to store unopened insulin vials in the fridge
told to discard insulin if change in colour occurs, even if still unexpired, as that could be a sign that it has been denatured

NOTE: during puberty, pregnancy, and illness, higher doses of insulin need to be administered.

Retrieved from https://www.researchgate.net/publication/332836996_Therapies_for_Type_1_Diabetes_Current_Scenario_and_Future_Perspectives/figures?lo=1&utm_source=google&utm_medium=organic on 14th June 2022

Blood glucose control depends on the technique used for insulin administration…

short needle (4mm pen needle)
correct dose
rotate site
alcohol should not be used to clean site prior to injecting insulin
dose should be injected subcutaneously (pinch tissue and inject at a 90 degree angle)

Retrieved from https://www.manula.com/manuals/sirma-medical-systems/diabetes-m-user-guide/mobile/en/topic/injection-sites on 24th March 2022

Insulin Pen

Continuous Subcutaneous Insulin Infusion

Type 2 Diabetes Management

Initially, a newly diagnosed diabetes type 2 patient is started on a 3 month trial of diet and exercise. Following this 3 month period, if the patient’s HbA1c still increases to 48mmol/mol (6.5%), pharmacological treatment is initiated.

FIRST LINE TREATMENT

If HbA1c = 48mmol/mol (6.5%):

Start on metformin (standard-release) morning + evening dose
Gradually increase dose (gradually = due to GI side effects)
In case of side effects switch to modified release metformin (evening dose)
If metformin tolerability is confirmed in cases where patient has CHF or CVD, Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) can be introduced
If metformin is contraindicated, SGLT-2i can be considered as a stand-alone medication

FIRST INTENSIFICATION

If HbA1c = 58mmol/mol (7.5%):

metformin and a DPP-4i (Dipeptidyl peptidase 4 inhibitor) OR
metformin and pioglitazone OR
metformin and a SU (Sulfonylurea) OR
metformin and a SGLT-2i (Sodium-glucose cotransporter 2 inhibitors)

PLUS consider introducing Insulin.

NOTE: aim for HbA1c 53mmol/mol (7%)

SECOND INTENSIFICATION

If HbA1c = 58mmol/mol (7.5%):

Triple Therapy is recommended…

insulin-based treatment OR
metformin + DPP-4i + SU OR
metformin + pioglitazone + SU OR
metformin + pioglitazone OR SU + SGLT-2i

NOTE: aim for HbA1c 53mmol/mol (7%)

If triple therapy is ineffective, not tolerated, or contraindicated, combine metformin + SU + GLP-1 mimetic.

(ideal for adults with type 2 diabetes with BMI 35kg/m² or more AND adults with same BMI experiencing significant occupational implications on insulin)

Metformin

inhibits gluconeogenesis
increases uptake of glucose by body tissues
may prevent weight gain

To avoid GI disturbances, dose should be increased gradually.

DPP-4i (Dipeptidyl peptidase 4 inhibitor)

alogliptin, linagliptin, saxagliptin, sitagliptin, viltagliptin

effects of hormones released from the intestine based on food intake are prolonged
pancreatic insulin secretion is increased
no known side effects

Glitazones

pioglitazone

improves insulin sensitivity
improves beta cell function
does not cause GI upset
no added risk of hypoglycaemia
dose once daily

but…

action onset happens at 6 weeks or more; pioglitazone is also associated with an increased risk of heart failure, bone fracture, and bladder cancer.

Sulphonylureas

glicazide, glimepiride, gliplizide, tolbutamide

stimulates secretion of pancreatic insulin

but…

increases the risk for hypoglycaemia and weight gain.

SGLT-2i (Sodium-glucose cotransporter 2 inhibitors)

canagliflozin, dapagliflozin, empagliflozin, ertugliflozin

prevents reabsorption of glucose into the blood by the kidneys
causes glucose excretion through urine
promotes weight loss
dose once daily

but…

is contraindicated for patients with renal dysfunction; increases the risk of severe genital infections and UTIs; increases risk of DKA when taken and shortly after stopping them.

GLP-1 mimetic

dulaglutide, exenatide, liraglutide, lixisennatide, semaglutide

Administered via weekly subcutaneous injection.

inhibits glucagon secretion
stimulates insulin secretion
slows gastric emptying
increases beta cell mass
promotes weight loss

but…

commonly causes nausea (which tends to decrease by time); rarely causes acute pancreatitis.

Monitoring

Monitor A1c and other glycaemic factors at least twice a year in patients responding to treatment (with stable glycaemic control)
Monitor A1c and other glycaemic factors at least 4 times a year in patients who have had recent change in therapy and who are not meeting glycaemic goals

Average Glucose Estimation for HbA1c Values…

Retrieved from https://ptsdiagnostics.com/a1cnow-systems-overview/ on 26th March 2022

Glycaemic Targets…

Retrieved from https://www.researchgate.net/publication/338390896_Insulin_Therapy_in_Adults_with_Type_1_Diabetes_Mellitus_a_Narrative_Review/figures?lo=1 on 26th March 2022

Reference

NICE (2022). Type 2 diabetes in adults: management. Retrieved from https://www.nice.org.uk/guidance/ng28 on 26th March 2022

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Diabetes Mellitus

Diabetes Mellitus is a metabolic disorder in which the body does not produce enough insulin, or does not respond normally to insulin, leading to hyperglycaemia – abnormally high blood sugar level a.k.a. glucose. Causes include defects in insulin secretion, insulin action, and abnormal carbohydrate, fat, and protein metabolism.

Diabetes Mellitus Pathophysiology

Food is ingested
The pancreas produces LESS insulin than required
High level of glucose is retained in the blood
Breakdown of proteins and body fats lead to production of ketones, resulting in weightloss
Excess glucose is excreted in urine, causing increased urine output and excessive thirst due to osmotic diuresis
In case of very low insulin availability, accumulation of ketones result in ketoacidosis

Signs & Symptoms

polyuria – excessive urination
polydipsia – excessive thirst
polyphagia a.k.a. hyperphagia – excessive hunger due to cells being in a state of starvation
weightloss
fatigue
blurred vision
tingling and/or numbness in extremities – usually if diagnosed at a later stage, after peripheral nerve damage has already occurred
slow-healing wounds
recurrent infections – both women and men experiencing frequent infections should be tested for diabetes

NOTE: if uncontrolled, patient appears to be drowsy and may become unconscious; severe signs of diabetes include drowsiness and coma.

Diabetes Type 1 VS Diabetes Type 2

diabetes mellitus type 1 vs diabetes mellitus type 2 — Retrieved from https://www.homage.sg/health/type-1-type-2-diabetes/ on 16th March 2022

Type 1 Diabetes

In Type 1 Diabetes there are very low levels of C-peptide in the blood or urine, which at times go undetected. Insulin becomes a requirement for survival. In the worst case scenario, the diabetic person may develop diabetic ketoacidosis (DKA) – a serious complication of diabetes that can be life-threatening. In DKA, the body undergoes an auto-immune process where it destroys beta cells, leading to lack of insulin production, making it impossible for blood sugar to enter the cells to be converted into energy. A person in DKA requires immediate acute care.

Type 1 Diabetes is not related to lifestyle factors, but to genetic predisposition and environmental factors.

Type 2 Diabetes

In Type 2 Diabetes, DKA can occur in stressful situations, although quite rare (since insulin is still produced even if in small amounts). Insulin is required as a controlling measure. Risks for Type 2 Diabetes include increasing age, obesity, unhealthy lifestyle, familial predisposition, and past gestational diabetes. This type of diabetes may remain undiagnosed for a long time.

gestational diabetes

Gestational Diabetes Mellitus (GDM) is diagnosed during pregnancy in the 2nd or 3rd trimester. Diagnosis criteria includes fasting plasma glucose of 5.1-6.9mmol/L OR 1 hour post-load plasma glucose of at least 10.0mmol/L OR 2 hour post-load plasma glucose of 8.5-11.0mmol/L.

LADA – Latent Autoimmune Diabetes in Adults

LADA a.k.a. slowly evolving immune-mediated diabetes is a hybrid form of diabetes which does not require insulin upon diagnosis, but which eventually does move on to needing insulin at a much faster rate than a person with Type 2 Diabetes. A person with LADA is usually over 35 years of age on diagnosis, testing positive for GAD auto-antibodies (antibodies to glutamic acid decarboxylase).

Ketosis-Prone Type 2 Diabetes

In this type of hybrid diabetes which typically affects young African-Americans, the person presents with severe insulin deficiency and ketosis.

Other Types of Diabetes

MONOGENIC DIABETES includes Neonatal Diabetes, and MODY (Maturity Onset Diabetes of the Young)
EXOCRINE PANCREATIC INSUFFICIENCY (EPI) include pancreatitis and cancer
DRUG-INDUCED DIABETES such as glucocorticoids
INFECTIONS such as cytomegalovirus
MONOGENIC DEFECTS OF INSULIN ACTION
ENDOCRINE DISORDERS such as Cushing’s Syndrome
GENETIC SYNDROMES such as Down’s Syndrome and Huntington’s Chorea
UNCLASSIFIED DIABETES

Criteria for Asymptomatic Prediabetes and Diabetes Mellitus Testing

Prediabetes is not considered as a clinical condition. Testing for prediabetes and diabetes in asymptomatic overweight or obese individuals is recommended for those with at least one of the following risk factors:

diabetic first-degree relative
ethnicity
history of cardiovascular disease
sedentary lifestyle
hypertension (including individuals on anti-hypertensives)
low HDL Cholesterol level and/or high triglyceride level
women with PCOS
conditions related to insulin-resistance
HIV

NOTES:

Individuals diagnosed with prediabetes should be re-tested for diabetes on a yearly basis
Women who have had Gestational Diabetes Mellitus should be re-tested for diabetes every 3 years
From the age of 35, every individual should start undergoing diabetes testing. Following a normal result, testing should be repeated after 3 years unless the person is considered to be high risk

Diabetes Mellitus Diagnosis

FASTING PLASMA GLUCOSE (FPG) – blood testing following an 8 hour fasting period (a test result of 7.0mmol/L / 126mg/dl or more indicates diabetes).

Patient should have the appointment scheduled early in the morning. Hypoglycaemics should NOT be administered whilst fasting. Patients on Lantus need to take their dose in the evening, without the bonus dose in the morning; they should then check their blood glucose before they leave in the morning to ensure they are not hypoglycaemic – if they are, they need to take something and reschedule their FPG test.

About 7ml of venous blood is drawn into a red or grey top tube. Patient should eat after FBG test.

ORAL GLUCOSE TOLERANCE TEST (OGTT) – blood testing following 75g oral glucose intake 2 hours before (a test result of 11.1mmol/l / 200mg/dl or more indicate diabetes).

Encourage patient to take full 75g dose since it is difficult to ingest. Smoking affects results so tell your patient to avoid smoking.

Prior to testing day, patient should consume adequate carbohydrate intake and perform physical activity, and should eat a 30-50g carbohydrate-based meal the evening before the test and fast for 8 hours, drinking water only if necessary. Drugs may be stopped based on physician’s recommendation. Patient’s weight should be measured to determine recommended oral glucose dose.

During test, a fasting blood specimen should be taken prior to administration of oral glucose – 75g carbohydrate load (patient can drink water if needed – no smoking). Blood is drawn after 2 hours. Patient should be monitored for transient reactions such as dizziness, sweating and weakness.

Note any drugs which can impact the result on the laboratory slip and send to the lab. Patient can drink and eat as normal, and if required, insulin or oral hypoglycaemic agents can be administered if prescribed.

HAEMOGLOBIN A1c (HbA1c) – average blood glucose level testing covering the previous two to three months (a test result of 6.5% / 48mmol/mol or more indicates diabetes)

NOTE: If asymptomatic, repeat the same test on a different day. Two test results above the threshold are required for diabetes diagnosis.

Prediabetes

Prediabetes refers to the phase in which the criteria for diabetes is not met, but the glucose levels are higher than normal. It is associated with obesity, high triglyceride level, low HDL cholesterol level, and hypertension.

Whilst prediabetes is not considered to be a clinical condition, it increases the risk for diabetes as well as cardiovascular disease, and so, individuals diagnosed with prediabetes should take preventative measures to avoid progressing to type 2 diabetes.

Prediabetes is determined by the following test results:

FPG 100mg/dl (5.6mmol/l) to 125mg/dl (6.9mmol/l) OR
2hr PG during 75-g OGTT 140mg/dl (7.8mmol/l) to 199mg/dl (11.0mmol/l) OR
HbA1c 5.7-6.4% (39-47mmol/mol)

Diabetes Mellitus Nursing Care Management

Additional Notes…

blood glucose control may be lost when the patient is going through stress, exercise, puberty, fever, etc.
excessive thirst is a possible warning sign for diabetes
sense of smell is not affected in individuals with diabetes
individuals with diabetes can still eat foods high in carbs as long as they make adjustments in their medication doses (as instructed by their clinician)
frequent urination is a possible warning sign for diabetes
individuals with diabetes can still exercise
numbness in the hands and feet is common in individuals with diabetes
being overweight or obese doesn’t increase the risk of getting type 1 diabetes
individuals with diabetes can still enjoy some sweets or ice cream (in moderation)
diabetes is a life threatening condition – over a century ago, having diabetes without insulin treatment being available meant having a terminal illness

Reference

World Health Organization (2019). Classification of diabetes mellitus. Retrieved from https://apps.who.int/iris/rest/bitstreams/1233344/retrieve

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The Endocrine System – The Adrenal Glands

The adrenal glands are small triangular-shaped structures located at the top of both kidneys. Their function is to produce hormones that help in the regulation of the metabolism, immune system, blood pressure, stress response, and more.

The adrenal glands, which are covered by an inner thick layer of connective tissue with an outer thin fibrous capsule, contain two sections:

OUTER ADRENAL CORTEX – makes up the biggest part of the gland
INNER ADRENAL MEDULLA – the core

The OUTER ADRENAL CORTEX is made up of 3 parts:

Zona Glomerulosa – makes up 15% of the total volume (secretes mineralocorticoids)
Zona Fasciculata – makes up the widest part of the total volume (mainly secretes glucocorticoids)
Zona Reticularis – secretes amounts of hormones, mostly gonadocorticoids and androgens

Adrenal Cortex vs Adrenal Medulla

Mineralocorticoids

Mineralocorticoids are responsible for water and electrolyte homeostasis through control of sodium and potassium concentrations. 95% of all mineralocorticoid activity happens through Aldosterone:

Aldosterone acts on the kidneys’ tubule cells, causing them to increase sodium reabsorption
Sodium ions are removed from the urine and returned to the blood
Rapid depletion of sodium from the body is prevented

Aldosterone causes:

potassium excretion
sodium reabsorption
hydrogen ions elimination
sodium, chloride, and bicarbonate ions retention
water retention

NOTE: Aldosterone reduces potassium reabsorption, thus, large potassium amounts are lost in urine excretion.

Electrolyte balance Secondary Effects

Sodium retention and potassium excretion lead to secondary effects:

Sodium reabsorption causes Hydrogen ions to pass into the urine to replace positive sodium ions, making the blood less acidic, thus preventing acidosis.
Sodium ions movement creates a positively charged field in the blood vessels surrounding the kidney tubules. This causes Chloride and Bicarbonate ions to move out from urine, back into the blood.
When ADH (antidiuretic hormone) is present, increased sodium concentration in the blood vessels causes water to move by osmosis from the urine into the blood.

Aldosterone control #1 – the raas system

Aldosterone Control #2 – Potassium Ion Concentration

Increased potassium concentration in extracellular fluid causes the adrenal cortex to secrete aldosterone
Aldosterone secretion causes excess potassium to be eliminated by the kidneys
Decreased potassium concentration in the extracellular fluid causes a decrease in aldosterone production, leading to less potassium excretion by the kidneys

Glucocorticoids

Glucocorticoids promote normal metabolism by:

increasing the rate of protein catabolism
increasing the rate at which amino acids are removed from cells and transported to the liver to undergo protein synthesis
releasing fatty acids from adipose tissue to be converted into glucose
promoting gluconeogenesis

Glucocorticoids promote stress resistance:

gluconeogenesis from amino acids causes a sudden increase in glucose availability, prompting the body to become more alert
blood vessels become more sensitive to chemicals that cause vasoconstriction so as to allow an increase in blood pressure

Glucocorticoids are anti-inflammatory compounds:

cause a reduction in mast cells
stabilise lyosomal membranes, leading to the inhibition of histamine release
decrease blood capillary permeability
depress phagocytosis by monocytes

Glucocorticoids:

Cortisol (hydrocortisone) – most abundant and responsible for about 95% of all glucocorticoid activity
Corticosterone
Cortisone

NOTE: Cortisol Serum blood test indicates adrenal function.

NOTE: Glucocorticoids slow down connective tissue regeneration, which leads to slow wound healing.

NOTE: Steroids are a synthetic form of glucocorticoids.

ACTH (Adrenocorticotropic hormone) Control

Glucocorticoid secretion is controlled through a negative feedback mechanism stimulated by stress and low blood glucocorticoid level:

stress and low blood glucocorticoid level stimulate the hypothalamus to secrete CRF (corticotropin releasing factor)
CRF secretion causes ACTH to be released from the anterior lobe of the pituitary
ACTH is carried to the adrenal cortex, where it stimulates glucocorticoid secretion

Gonadocorticoids

The adrenal cortex is responsible for the secretion of both male and female sex hormones – oestrogens and androgens.

Adrenal Medulla

The adrenal medulla is made up of chromaffin cells (hormone-producing cells) surrounding sinuses containing blood
These chromaffin cells are considered to be postganglionic cells specialised in secretion
Preganglionic fibres pass directly into the chromaffin cells of the gland within the adrenal medulla
Secretion of hormones is controlled by the autonomic nervous system and innervation by preganglionic fibres that allows rapid response to a stimulus by the gland

Epinephrine and Norepinephrine

The adrenal medulla synthesises the following two hormones:

Epinephrine (adrenaline)
Norepinephrine (noradrenaline)

Epinephrine is stronger than norepinephrine. It:

increases the blood pressure by increasing the heart rate and constricting the blood vessels
increases respiration rate
dilates respiratory passageways
decreases digestion rate
increases muscular contraction efficiency
increases blood sugar level
stimulates cellular metabolism

However, both epinephrine and norepinephrine:

mimic the sympathetic nervous system – they are sympathomimetic
help in stress resistance

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The Endocrine System – Pancreas Anatomy and Physiology

The pancreas, which is located in the curve of the duodenum, is a flat organ measuring between 12.5cm-15cm. It is a composite gland – both an exocrine and an endocrine gland: Exocrine acini secrete digestive enzymes into the duodenum, while the Islets of Langerhans help with carbohydrate metabolism.

Pancreas Blood Supply

The Splenic Artery supplies the pancreas with blood, while venous return is completed through small veins within the Splenic Vein.

Pancreas Nerve Supply

The Autonomic Nervous System (ANS) innervates the pancreas. Parasympathetic Vagal Fibres stimulate exocrine secretion, while Sympathetic Vasoconstrictor Impulses travel through nerves derived from spinal cord segments T6-T10 which pass through blood vessels within the pancreas. This reflects why pancreatic pain frequently radiates these nerve pathways.

The Endocrine Portion

The Islets of Langerhans contain 4 types of cells:

Alpha Cells – make up 15% of the pancreatic islet cells; secrete Glucagon
Beta Cells – make up 80% of the pancreatic islet cells; secrete Insulin
Delta Cells – make up 5% of the pancreatic islet cells; secrete Somatostatin
F Cells – secrete Pancreatic Polypeptide

Retrieved from https://slideplayer.com/slide/7426531/ on 7th March 2022

Glucagon INCREASES blood glucose level
Insulin DECREASES blood glucose level
Somatostatin INHIBITS insulin and glucagon, acting as a regulator
Pancreatic Polypeptide INHIBITS somatostatin secretion, gallbladder contraction, and digestive enzyme secretion (Pancreatic Polypeptide is secreted near the end of the digestive system)

Glucagon

The main function of glucagon is that of increasing blood glucose level. This is carried out through the following process:

Glucagon increases glycogen conversion into glucose within the liver (glycogenolysis) AND increases nutrient (amino acids, glycerol and lactic acid) conversion into glucose within the liver (gluconeogenesis)
Liver releases glucose into the blood, causing an increase in blood sugar level
Blood sugar level controls secretion of glucagon through a negative feedback mechanism

lysis = breaking down of glycogen

neo = new

genesis = production

Secretion of glucagon is STIMULATED by:

decreased blood glucose level
protein-based foods
exercise

Secretion of glucagon is INHIBITED by:

somatostatin
insulin

Insulin

Islet beta cells produce insulin, which increases protein build-up within the cells. Insulin regulation is controlled by a negative feedback mechanism based on the blood sugar level.

Insulin decreases blood sugar level through the following process:

increases glucose transportation from the blood into the cells
increases glucose conversion into glycogen (glycogenesis)
decreases glycogenolysis and gluconeogenesis
stimulates glucose conversion to fatty acids
stimulates protein synthesis

Secretion of insulin is STIMULATED by:

increased blood glucose level
acetylcholine (released by parasympathetic vagus nerve fibres)
amino acids (arginine and leucine)
growth hormone (GH) (which causes increase in blood sugar level)
ACTH (adrenocorticotropic hormone) (stimulates glucocorticoids secretion leading to hyperglycaemia, indirectly stimulating insulin release)

Secretion of insulin is INHIBITED by:

somatostatin (GIF – growth hormone inhibiting factor)

Insulin production is also AFFECTED by:

stomach and intestinal gastrin
secretin
cholecystokinin
gastric inhibitory peptide (GIP)

Insulin vs Glucagon

Somatostatin

Somatostatin is secreted by delta cells in the Islets of Langerhans following an increase in blood glucose, fatty acids, and amino acids due to an ingested meal. Somatostatin travels in the blood, slowing down the absorption of nutrients from the GIT, acting as paracrine secretion, diffusing into tissue fluid targeting nearby cells, and inhibiting both insulin and glucagon release from nearby alpha and beta cells.

Somatostatin secretion is INHIBITED by pancreatic polypeptide.

Pancreatic Polypeptide

Pancreatic Polypeptide inhibits secretion of somatostatin, gallbladder contraction, and secretion of pancreatic digestive enzymes.

Secretion of pacreatic polypeptide is STIMULATED by:

protein-containing meals
fasting
exercise
hypoglycaemia

Secretion of pancreatic polypeptide is INHIBITED by:

somatostatin
hyperglycaemia

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The Endocrine System – Hypothalamus & Pituitary Gland

The endocrine system is made up of hormone-producing glands within the body which facilitate communication between cells. Glands that make up the endocrine system include the hypothalamus, pituitary gland, and pineal gland, all of which can be found within the brain; the thyroid and parathyroid glands which can be found in the neck; the thymus which is situated between the lungs; the adrenals, which sit on the kidneys; the pancreas, which is found behind the stomach; and the ovaries (women) or testes (men) which are in the pelvic region.

endocrine system hypothalamus and pituitary gland — Retrieved from https://www.blendspace.com/lessons/tv-3ufAxEQI3pQ/group-3-307-313-331-endocrine-system on 3rd March 2022

Within the endocrine system, an endocrine gland or tissue releases an amount of hormone, which amount is determined by the body’s need for that hormone. Through sensing and signalling systems, hormone-producing cells receive information and regulate hormone release amount and duration. Released hormones are carried by the blood to target cells, which contain receptors that bind the hormone, leading to the desired effect. This effect is then recognised by secretory cells through a feedback signal. Once the required hormonal effect is fully accomplished, the hormones are either removed by the liver or the kidneys, or else degraded by the target cells.

Hormonal secretion is regulated by negative feedback control so homeostasis within the body is maintained.

The Hypothalamus

The hypothalamus, which is located below the thalamus, acts as a link between the nervous system and the endocrine system. It receives inputs from various parts of the brain, and sensory signals from internal organs and the retina. Changes are triggered in the hypothalamic activity due to pain, stress, and other emotional factors. The hypothalamus controls the autonomic nervous system and regulates various bodily factors such as temperature, hunger and thirst, sexual behaviour, and defensive reactions.

The Endocrine System - Hypothalamus & Pituitary Gland — Retrieved from https://kids.frontiersin.org/articles/10.3389/frym.2021.534184 on 3rd March 2022

Within the hypothalamus are clusters of specialised neurons – neurosecretory cells, which synthesise the hypothalamic hormones in their cell body. The hormones are transported inside vesicles by axonal transport.

Hypothalamus-Released Hormones

The hypothalamus is an important endocrine gland that produces hormones which, after being released into the blood, travel in the portal veins to a secondary capillary bed found in the anterior lobe of the pituitary, where their effects are produced. Hormones released in this way include:

Thyrotropin-releasing hormone (TRH) – related to thyroid gland growth and function
Gonadotropin-releasing hormone (GnRH) – related to the reproductive system
Growth hormone-releasing hormone (GHRH) – related to growth
Corticotropin-releasing hormone (CRH) – related to hormone secretion
Somatostatin – related to the growth hormone
Dopamine – acts as a neurotransmitter

Hormones which travel in the neurons to the posterior lobe of the pituitary before being released into circulation include:

Antidiuretic Hormone (ADH) / Vasopressin – promotes regulation of the amount of water within the body
Oxytocin – involved in childbirth and breastfeeding

The Pituitary Gland

The pituitary gland, which measures just about 1.3cm in diameter, is located in the cella turcica of the sphenoid bone. It is attached to the hypothalamus via the infundibulum – a stalklike structure. Pituitary gland hormones regulate body activities. The pituitary gland is divided into two lobes: the anterior lobe and the posterior lobe.

The pituitary gland anterior lobe accounts to around 80% of the pituitary gland. It is involved in growth regulation, metabolism, and reproduction, through its produced hormones. Hormone production happens through stimulation or inhibition by chemical messages originating from the hypothalamus. Thus, hypothalamic hormones act as a link between the nervous system and the endocrine system. They reach the anterior pituitary through the Hypophyseal Portal System.

The pituitary gland posterior lobe is involved in hormone transmission. Hormones originating from neurons within the region of the hypothalamus are secreted directly into peripheral circulation.

The lobes are divided by the pars intermedia – a relatively avascular zone.

The 5 Types of Glandular Cells

Somatotroph Cells – produce GH (growth hormone) which is responsible for general body growth
Lactotroph Cells – synthesise PRL (prolactin) which promotes milk production by the mammary glands
Corticolipothroph Cells – synthesise ACTH (adrenocorticotropic hormone) which stimulates hormone secretion, and MSH (melanocyte-stimulating hormone) which is responsible for skin pigmentation
Thyrothroph Cells – produce TSH (thyroid-stimulating hormone), which controls the thyroid gland
Gonadotroph Cells – produce FSH (follicle-stimulating hormone), which stimulates egg and sperm production in the ovaries and testes, and LH (luteinizing hormone), which stimulates other sexual and reproductive activities.

Growth Hormone (GH)

is released through two regulating factors from the hypothalamus, namely GHRF (growth hormone releasing factor) and GHIF (growth hormone inhibiting factor) or Somatostatin
causes cells to grow and multiply by increasing the rate at which amino acids enter the cells to be built up into proteins
acts on the skeleton and the skeletal muscles firstly by increasing their growth rate, and then maintaining their size when growth is attained
increases the rate of protein synthesis a.k.a. protein anabolism
promotes fat catabolism by causing cells to change from burning carbohydrates to burning fats to produce energy
accelerates rate at which glycogen stored within the liver converts into glucose and releases itself into the blood
converts other factors into growth-promoting substances – somatomedins and insulin-like growth factors (IGF), both of which are similar to insulin yet more potent than insulin

Growth Hormone Secretion Stimuli and Inhibition…

Retrieved from https://basicmedicalkey.com/normal-endocrine-function/ on 5th March 2022

Prolactin (PRL)

requires priming of the mammary glands through oestrogens, progesterone, corticosteroids, growth hormone, thyroxine, and insulin
initiates and maintains milk secretion by the mammary glands (amount of milk is determined by oxytocin)
has an inhibitory and an excitatory negative control system
level rises during pregnancy, falls right after delivery, and rises again during breastfeeding, which is why in the 1st two days following birth, mothers do not produce milk but colostrum

NOTE: women on oral contraceptives may experience lack of milk production due to their hormonal effect.

Melanocyte-Stimulating Hormone (MSH)

increases skin pigmentation through the stimulation of melanin granules dispersion in melanocytes
secretion is stimulated by the melanocyte-stimulating hormone releasing factor (MRF), or inhibited by the melanocyte-stimulating hormone inhibiting factor (MIF)
lack causes the skin to look pallid
excess causes the skin to look dark

Thyroid-stimulating factor (TSH)

stimulates the synthesis and secretion of hormonal production within the thyroid gland
secretion is controlled by the thyrotropin releasing factor (TRF), which is released based on thyroxine blood level, metabolic rate of the body, and other factors through a negative feedback system

Adrenocorticotropic Hormone (ACTH)

controls the production and secretion of some adrenal cortex hormones
is secreted by the hypothalamic regulating factor called corticotropin releasing factor (CRF), which is released depending on stimuli and hormones through a negative feedback system

Follicle-Stimulating Hormone (FSH)

in females initiates the development of an ova every month, and stimulates cells within the ovaries to secrete oestrogens
in males stimulates the testes to produce sperm
secretion depends on the hypothalamic regulating factor gonadotropin releasing factor (GnRF), which is released in response to oestrogens in females, and to testosterone in males through a negative feedback system

Luteinizing Hormone (LH)

along with oestrogens, in females it stimulates the release of an ovum within the ovary, prepares the uterus for the implantation of the fertilised ovum, stimulates the formation of the corpus luteum in the ovary to secrete progesterone, and prepares the mammary glands for milk secretion
in males it stimulates the interstitial endocrinocytes in the testes to develop and secrete testosterone
secretion is controlled by GnRF, which works through a negative feedback system

Pituitary Gland Posterior Lobe

Oxytocin (OT)

is released in high amounts just before birth
stimulates contraction of smooth muscle cells in the pregnant uterus
stimulates the contractile cells around the mammary gland ducts
affects milk ejection
works through a positive feedback cycle which is broken following birthing
is inhibited by progesterone, but can work in conjunction to oestrogens

Antidiuretic hormone (ADH)

affects urine volume; it causes the kidneys to excrete water from fresh urine and return it to the bloodstream, reducing urine volume
absence causes an increase in urine output
raises blood pressure by constricting arterioles
secretion varies based on the body’s needs
causes a decrease in sweat

Retrieved from https://slideplayer.com/slide/10623655/ on 6th March 2022

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