The thyroid gland is situated just below the larynx, with its right and left lateral lobes lying on either side of the trachea, connected together by the isthmus. It plays a major role in the metabolism, growth and development of the human body, regulating body functions by constantly releasing a steady amount of thyroid hormones into the bloodstream. It receives a rich blood supply of about 80 to 120ml per minute.
Retrieved from http://www.aboutcancer.com/thyroid_anatomy.htm on 27th April 2022
Thyroid Gland Histology
The thyroid gland is composed of spherical sacs called thyroid follicles which are covered by a wall made up of Follicular Cells and Parafollicular Cellsa.k.a. C Cells.
Follicular Cells produce thyroxine (T4) and triiodothyronine (T3). Whilst T4 is usually produced in greater quantities than T3, T3 is up to 4 times more potent than T4. Additionally, about a third of T3 is converted to T4 within peripheral tissues, especially within the lungs and the liver.
Parafollicular Cells produce calcitonin (CT).
Retrieved from https://slideplayer.com/slide/13219076/ on 27th April 2022
Thyroid Hormone Formation, Storage & Release
The thyroid gland is the only endocrine gland that stores its hormonal products in large quantities, eventually releasing them steadily over time. Thyroid hormone formation, storage and release occurs through the following process:
Iodide Trapping – iodide ions are actively transported from the blood to the follicular cells
Thyroglobulin Synthesis – during iodide ion trapping, follicular cells synthesise the glycoprotein Thyroglobulin (TGB) which is released into the thyroid follicle lumen by exocytosis, resulting in colloid accumulation within the lumen and Tyrosine (amino acids) iodination in TGB
Iodide Oxidation – iodide ions bind to TGB following oxidation; simultaneously, iodine is formed by the action of peroxidase
Tyrosine Iodination – formed iodine reacts with tyrosine in the colloid; one iodine atom binding forms monoiodotyrosine (T1); a second iodine atom binding produces diiodotyrosine (T2)
T1 and T2 Coupling – T1 and T2 join and form thyroid hormones
Colloid Pinocytosis & Digestion – colloid droplets re-enter the follicular cells though pinocytosis, and then merge with lysosomes in the follicular cells; lysozyme breaks down TGB, and then produce T3 and T4 molecules
Thyroid Hormone Secretion – lipid-soluble T3 and T4 diffuse through the plasma membrane into the interstitial fluid, and then into the blood; T4 is secreted in larger quantities than T3, yet T3 is much more potent than T4
Transport into Blood – Thyroxine-Binding Globulin (TBG) which is a transport protein found within the blood plasma combine with both T3 and T4 and are carried around in the body within the blood; when T4 enters a cell, most of it is converted to T3 following removal of one iodine
NOTE: Iodine supplements may be given to pregnant women and for compensation of hypothyroidism.
Retrieved from https://www.pinterest.com/pin/395261304797063744/ on 27th April 2022
Thyroid Hormone Regulation
Thyroid hormone secretion is stimulated by various factors…
Retrieved from https://quizlet.com/502370009/phys_block-8_-endo-5-6-flash-cards/ on 27th April 2022
Calcitonin (CT)
Calcitonin, which is produced by the parafollicular cells of the thyroid gland, is involved in the homeostasis of blood calcium level:
Calcitonin inhibits bone breakdown and promotes bone calcium absorption
Calcitonin is used in the treatment of post-menopausal osteoporosis along with calcium and vitamin dietary intake
Calcitonin secretion is controlled via a negative feedback system
Retrieved from https://healthjade.net/calcitonin/ on 27th April 2022
NOTE: Diarrhoea is a possible sign of increased thyroid hormone.Similarly, constipation is a possible sign of underactive thyroid.
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Whilst diabetes preventative care can help avoid the development of type 2 diabetes mellitus, adequate diabetes nursing management can help avoid or reduce the occurrence of serious diabetes complications, such as short-term complications which include hypoglycaemia, diabetic ketoacidosis, hyperosmolar non-ketotic coma, as well as long-term complications which include microvascular and macrovascular complications, and neuropathy.
Short-Term Diabetes Complications
Hypoglycaemia
Hypoglycaemia can be defined as a glucose concentration of 3.9mmol/l or below.
Retrieved from https://www.facebook.com/photo/?fbid=272975211310190&set=a.111544340786612 on 16th April 2022
An individual with hypoglycaemia can be asymptomatic, usually due to adaptation of the brain to chronic hypoglycaemia, which presents with symptoms even at normal blood sugar levels. This can be avoided if the individual experiences a few weeks of good glycaemic control.
An individual with hypoglycaemia may also present with mild symptoms which can be self-managed, severe symptoms requiring medical assistance, and even coma.
Retrieved from https://www.researchgate.net/publication/51746090_Hypoglycemia_Revisited_in_the_Acute_Care_Setting/figures?lo=1&utm_source=google&utm_medium=organic on 16th April 2022
Hypoglycaemia Causes
insulin or sulphonylurea overdose (deliberate or accidental) – insulin can cause hypoglycaemia; metformin does not
inaccurate injection administration
renal and liver impairment cause pharmacokinetic change, possibly leading to a hypoglycaemic episode; individuals with renal and liver impairment should be monitored closely
delayed or forgotten meal, or insufficient carbohydrate intake
alcohol intake – food needs to be taken with alcohol, otherwise hypogycaemia can be triggered
exercise – can trigger a hypoglycaemic episode following exercise or even several hours after
hot weather or saunas – insulin is absorbed quicker in warmer temperatures, thus, saunas and hot weather should be avoided
honeymoon period (following diagnosis is usually a period a.k.a. honeymoon period in which remaining beta cells may pump out enough insulin to control blood glucose, thus may require less insulin)
Nursing Management of Hypoglycaemia
If the patient presents with mild hypoglycaemia:
give 15-20g of glucose such as a sugary drink – water with 2 teaspoons of sugar
repeat after 10 minutes
check if patient is still hypoglycaemic through HGT testing
if stable give a snack eg. brown bread sandwich to prevent recurrence
NOTE: sugar helps stabilise the patient for that moment; a snack helps maintain glucose level higher for a longer period of time.
If the patient is uncooperative:
Administer GlucoGel (formerly known as Hypostop – raises sugar levels quickly and provides a fast-acting energy boost in the form of Dextrose Gel – 40% dextrose).
NOTE: following a hypoglycaemic episode, ALWAYS ESTABLISH CAUSE eg. problem with insulin administration.
If the patient is unconscious:
adjust patient into the recovery position
administer glucagon by intramuscular or subcutaneous injection OR 50cc of 50% dextrose intravenously.
Preventative Measures
The older person is at increased risk of suffering from fall injuries, heart attacks and strokes during hypoglycaemic episodes. Thus, teach older adults at risk of hypoglycaemia:
to carry an ID bracelet at all times
to check their blood glucose levels prior to risky activities
to know and identify early signs of an impending hypoglycaemic episode
Diabetic Ketoacidosis
Diabetic Ketoacidosis is the most acute state of Type 1 Diabetes. Diabetic Ketoacidosis onset may be both gradual or sudden, and is characterised by the following findings:
hyperglycaemia (15.0mmol/l and over)
ketonuria (if cells are not supplied with enough glucose, the body burns fat for energy whilst producing ketones which can show up in the blood and urine, evident in a urine dipstick test)
pH of 7.3 or less (normal blood pH level is 7.35 to 7.45)
Common causes for DKA include:
infection – most common cause of DKA eg. gastroenteritis, flu, small infection etc.
insulin cessation – common in adolescents; patients need to be reminded that diabetes is a condition for life, thus needs to be controlled with ongoing treatment
anuria (not passing urine) – a minimum of 30ml/hr of urine should be passed
not eating – increases risk of DKA
Retrieved from https://slideplayer.com/slide/6428754/ on 17th April 2022
Retrieved from https://eliteayurveda.com/blog/3-main-symptoms-or-3ps-of-diabetes/ on 25th June 2022
Kussmaul Breathing
Kussmaul Breathing is a sign of DKA. It is characterised by sweet-smelling breath which is rapid and deep. It manifests as a compensatory mechanism due to build-up of carbon dioxide and lack of oxygen.
Retrieved from https://www.aafp.org/afp/2013/0301/p337.html on 17th April 2022
Retrieved from https://nurseyourownway.com/2016/03/21/sickly-sweet-understanding-diabetic-ketoacidosis/ on 17th April 2022
Diabetes Nursing Management of DKA
An individual with DKA needs:
treatment for hyperglycaemia – patient needs to be kept nil-by-mouth along with administration of a continuous low dosage of insulin by IV pump. NOTE: monitor blood glucose levels and ensure it isn’t lowered at a rate faster than 5mmol/hr to avoid cerebral oedema.
treatment for dehydration, electrolyte imbalance, and acidosis – patient needs administration of IV fluids with electrolytes (eg. Hartmann’s – a clear solution of sodium chloride, potassium chloride, calcium chloride dihydrate and sodium lactate 60% in water) to help with dehydration and electrolyte imbalance, and insulin, which usually also corrects acidosis without the need for sodium bicarbonate administration. NOTE: monitor serum potassium levels and ECG tracings to ensure correct potassium level is achieved, and monitor for signs of fluid overdose. NOTE: if not NBM, patient should be encouraged to drink high-carb drinks eg. broth, soup, juices etc.
treatment for precipitating factors – DKA is commonly induced by infection, thus, antibiotic therapy should begin following C&S specimen, wound drainage, or blood results are obtained.
NOTE: If patient is sick with flu/cold etc., blood glucose needs to be monitored, insulin needs to be administered still. Within the body, carbs start to be broken down in an attempt to avoid going into DKA. Monitoring carb intake to avoid going into hyperglycaemia is recommended.
Additionally, monitor frequently the patient’s:
vital signs: blood pressure, pulse, temperature, and respirations
level of consciousness
intake and output
urine
blood glucose
ketone bodies
GFR renal profile – to check kidney function and serum electrolytes
HbA1c – to monitor glucose for the past 3 months
CBC – to check volume of white blood cells (low white blood cell count may be a sign of infection which could have been the reason behind the patient going into DKA
ABGs, serum K levels, urea, and RBGs – to check the partial pressure of CO2 and to see if the patient is going into respiratory acidosis; tests also give an indication of electrolyte status (eg. potassium is lost in DKA due to polyuria, and kidney function may become impaired, causing electrolyte imbalance)
ECG (due to risk of cardiac arrest from hypokalaemia)
and ensure that the patient:
receives mouth care due to NBM and dehydration
for dehydration encourage patient to drink water unless NBM, in which case, IV fluids should be administered – monitor fluid intake and output!
is cared for in case of pain (assess for need of analgesics), abdominal pain, nausea (administer antiemetics) and vomiting (provide vomiting bags just in case)
is kept safe (attention: side rails, frequent turnings, call bell at arms’ length, and skin care)
airway patency is maintained (if unconscious)
always provide reassurance (helps reduce patient anxiety)
DKA Possible Treatment Complications:
hypokalaemia
hypotension
dehydration
impaired renal function
cardiac arrest
HAIs – ensure proper infection control principles are maintained so as to avoid patient getting an infection (may already be infected since infection is one of the problems leading to DKA)
When DKA is resolved:
insulin is administered subcutaneously (insulin IV should be continued for 1hr following SC insulin injection)
food is provided 30 minutes following insulin administration
monitor for DKA recurrence
teach patient ways to prevent recurrence
Hyperosmolar Non-Ketotic Coma
Hyperosmolar non-ketotic coma usually happens in individuals who have not been diagnosed with diabetes, usually type 2 diabetes, and is more common in individuals over 60 years of age. Characteristics are usually less severe, and most commonly develop over a long period of time.
Characteristics of hyperosmolar non-ketotic coma include:
hyperglycaemia
dehydration
no ketoacidosis
Nursing Management of Hyperosmolar Non-Ketotic Coma
Patients with Hyperosmolar Non-Ketotic Coma need to be treated in the same way as in Diabetic Ketoacidosis EXCEPT:
if serum Na (Sodium) is MORE THAN 155mmol/l use 0.45% NaCl instead of 0.9% NaCl
patient may require insulin infusion at a lower rate
patient should be administered an anticoagulant due to an increased risk for thromboembolism
patient should have central venous pressure catheter
NOTE: following resolution, patient may require insulin subcutaneously for a few weeks before transitioning to new treatment regimen consisting of diet, exercise, and hypoglycaemic agents.
Long-Term Diabetes Complications
Microvascular Complications
Microvascular complications of diabetes are long-term complications which affect small blood vessels. Complications typically include:
retinopathy – retina disease (most common cause of blindness in young people)
nephropathy – kidney function deterioration (affects 45% of diabetic patients, 25% of which develop end-stage renal disease)
peripheral neuropathy – impaired sensation in the peripheries (feet and hands)
autonomic neuropathy – bowel and bladder disorders
MACROVASCULAR COMPLICATIONS
Macrovascular complications of Type 2 Diabetes are primarily diseases of the coronary arteries, peripheral arteries, and cerebrovasculature. Cardiovascular disease is the primary cause of death in diabetic patients. Early macrovascular disease is associated with atherosclerosis.
Preventative Measures for Microvascular and Macrovascular Complications
in patients with stable glycaemic control assess glycaemic status through A1C or other glycaemic measurements at least every 6 months
in patients with unstable glycaemic control and/or who have had recent treatment change assess glycaemic status through A1C at least every 3 months
promote lipid management through the Mediterranean Diet or DASH, reduction of saturated fat and trans fat intake, increase in healthy fats intake, viscous fiber, plant sterols intake (found in vegetable oils, nuts and seeds), and increased physical activity to prevent atherosclerosis development
promote optimum glycaemic control in patients with triglyceride levels of >150mg/dL (1.7mmol/L) and low HDL Cholesterol amounting to <40mg/dL (1.0mmol/L) in men and <50mg/dL (1.3mmol/L) in women
screen for renal disease at least yearly through urinary-albumin-to-creatinine ratio and estimated glomerular filtration rate (EGFR) in individuals with 5 years or more of type 1 diabetes, and in all individuals with type 2 diabetes (monitor every 6 months patients with >300mg/g creatinine and EGFR 30-60mL/min/1.73m2)
refer to ophthalmologist for eye complication screening patients with type 1 diabetes within 5 years of diabetes diagnosis, and patients with type 2 diabetes upon diabetes diagnosis
provide general preventative diabetic foot self-care education to all patients with diabetes, and refer to registered podiatrist for annual foot evaluation to identify risk factors for ulcer formation and amputations
Statin Therapy
Retrieved from https://www.uchealth.org/ on 23rd April 2022
CVD Risk Assessment Tool for Healthcare Professionals
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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
Retrieved from https://www.slideserve.com/csilla/anatomy-and-physiology-the-female-reproductive-system on 9th April 2022
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.
Retrieved from https://quizlet.com/180196971/female-reproductive-system-flash-cards/ on 15th April 2022
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)
Retrieved from https://www.britannica.com/science/uterus on 15th April 2022
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.
Retrieved from https://courses.lumenlearning.com/boundless-ap/chapter/the-female-reproductive-system/ on 15th April 2022
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:
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
Retrieved from http://www.pharmacy180.com/article/pituitary-gland-3595/ on 5th March 2022
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
Retrieved from https://basicmedicalkey.com/uterine-drugs/ on 16th April 2022
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 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
Retrieved from https://www.easynotecards.com/notecard_set/85750 on 16th April 2022
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.
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.
Retrieved from https://www.chicagourogynecologist.com/center-services/pelvic-organ-prolapse/cystocoele/ on 14th April 2022
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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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.
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
Retrieved from https://en.wikipedia.org/wiki/Scrotal_septum on 5th April 2022
Retrieved from https://www.rrnursingschool.biz/unity-companies/scrotum.html on 5th April 2022
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
Retrieved from https://microbenotes.com/spermatogenesis/ on 5th April 2022
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
Retrieved from https://www.flexiprep.com/NIOS-Notes/Secondary/Science/NIOS-Class-10-Science-Chapter-24-Reproduction-Part-2.html on 7th April 2022
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.
Retrieved from https://www.uptodate.com/contents/image?imageKey=EM%2F76391&topicKey=PEDS%2F6587&source=see_link on 7th April 2022
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.
Retrieved from https://www.austincc.edu/apreview/PhysText/Reproductive.html on 7th April 2022
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 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
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.
Retrieved from https://www.haematologica.org/article/view/7075 on 2nd April 2022
Retrieved from https://www.aafp.org/afp/2015/1201/p1004.html 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.
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.
Retrieved from https://studylib.net/doc/18818582/protective-precautions on 2nd April 2022
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
Retrieved from http://www.ivicourse.com/wp-content/uploads/2017/01/Hand_Hygiene_Policy.pdf on 2nd April 2022
Retrieved from https://www.hha.org.au/hand-hygiene/5-moments-for-hand-hygiene on 2nd April 2022
Retrieved from https://www.slideserve.com/trina/are-your-hands-clean on 2nd April 2022
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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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 https://edu.glogster.com/glog/android-and-gynoid-body-types/2b8qtfg5144 on 28th March 2022
Retrieved from http://www.myhealthywaist.org/index.php?id=56&tx_nurebook_pi1[page]=9&cHash=644d9e5b11 on 28th March 2022
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
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
Retrieved from https://www.nice.org.uk/guidance/cg189/chapter/1-recommendations on 29th March 2022
Metabolic Syndrome
Retrieved from https://pucketteintegrativehealthcare.com/what-is-syndrome-x/ on 1st April 2022
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)
Retrieved from https://www.researchgate.net/publication/297600439_A_clinical_perspective_of_obesity_metabolic_syndrome_and_cardiovascular_disease/figures?lo=1 on 1st April 2022
WHO Recommendations
Retrieved from https://adamvirgile.com/2021/01/19/world-health-organization-2020-guidelines-n-physical-activity-and-sedentary-behaviour/ on 1st April 2022
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.
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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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.medicostuff.com/category/medicine/diabetes-mellitus/ on 26th March 2022
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
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.
Retrieved from https://peninsulapod.com/charcot-foot/ on 26th March 2022
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)
Left: Neuropathic foot with prominent metatarsal heads and pressure points over the plantar forefoot. Right: Neuroischaemic foot showing pitting oedema secondary to cardiac failure, and hallux valgus and erythema from pressure from tight shoe on medial aspect of first metatarsophalangeal joint – Retrieved from https://europepmc.org/article/med/16484268 on 26th March 2022
The Ischaemic Diabetic Foot
Ischaemic foot features include:
peripheral vascular disease
absent signs of peripheral neuropathy
cold, shiny, hairless skin
rare in diabetic patients
Retrieved from https://en.wikipedia.org/wiki/Ischemia on 26th March 2022
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:
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.
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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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
Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK535456/figure/article-18425.image.f1/ on 21st March 2022
Retrieved from https://dryatendrayadav.com/2018/10/17/measure-waist-measure-risk/ on 21st March 2022
Retrieved from https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/simple-cutoff-for-waisttoheight-ratio-05-can-act-as-an-indicator-for-cardiometabolic-risk-recent-data-from-adults-in-the-health-survey-for-england/5D882EE63FA4B3C530B48D6232BDB355 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/m2AND/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:
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://agamatrix.com/blog/different-types-of-insulin/ on 24th March 2022
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.
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.
commonly causes nausea (which tends to decrease by time); rarely causes acute pancreatitis.
Monitoring
Monitor A1c and other glycaemic factors at leasttwice 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 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
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 includesfasting plasma glucose of 5.1-6.9mmol/L OR1 hour post-load plasma glucose of at least 10.0mmol/L OR2 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:
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
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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.
Retrieved from https://www.jaypeedigital.com/book/9789350903025/chapter/ch16 on 12th March 2022
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
Retrieved from https://www.majordifferences.com/2014/04/difference-between-adrenal-cortex-and.html on 12th March 2022
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
Retrieved from https://www.pinterest.com/pin/557813103821299549/ on 13th March 2022
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
Retrieved from https://quizlet.com/279451837/chapter-9-vocabulary-flash-cards/ on 13th March 2022
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
mimic the sympathetic nervous system – they are sympathomimetic
help in stress resistance
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