Erythrocytes contain antigens called agglutinogens or isoantigens which are genetically determined. At least, 300 blood group systems may be detected on red blood cells’ surface. However, the focus is on 2 major classifications of blood groups, namely the ABO Blood Grouping System and the Rhesus System.
ABO Blood Grouping System
there are 2 types of agglutinogens: Agglutinogen A and Agglutinogen B
individuals with red blood cells containing Agglutinogen Ahave a Blood Type A
individuals with red blood cells containing Agglutinogen Bhave a Blood Type B
individuals with red blood cells containing both Agglutinogen A and B have Blood Type AB
individuals with red blood cells containing NO Agglutinogen A and NO Agglutinogen B have Blood Type O
The BLOOD PLASMA contains antibodies called agglutinins or isoantibodies.
Agglutinin A attacks Agglutinogen A
Agglutinin B attacks Agglutinogen B
Rhesus (Rh) System
the Rh system is based on the presence (or lack of) of agglutinogens which can be found on the surfaces of erythrocytes
individuals with red blood cells containing Rh agglutinogensare said to be Rh+
individuals with red blood cells containing NO Rh agglutinogens are said to be Rh-
Blood Transfusions
Blood transfusions are commonly indicated for circulatory shock, anaemia (lack of healthy red blood cells leading to inadequate oxygen distribution to the body’s tissues), haemophilia (bleeding disorder, usually inherited, with an improper blood clotting mechanism), and haemolytic disease of the newborn (a disease in which there is fast destruction of red blood cells).
Red Cell Concentrates – indicated for anaemia and acute blood loss: help increase oxygen carrying capacity through raising haemoglobin concentration in the patient. Can be stored in a temperature of 4 +/-2°C for 42 days (or for 28 days if irradiated). If unused or left for more than 30 minutes in the transport box, Red Cell Concentrates should be returned to the Blood Bank to minimise the risk of bacterial growth.
CMV (CytoMegaloVirus) Negative Blood: indicated for intrauterine transfusions, neonate transfusion (28 days post EDD) and pregnant women transfusion.
Irradiated Blood: indicated for intrauterine transfusion, BM/ stem cell transplantation, Hodgkin’s disease, etc.
For more details on the administration of blood and blood components click here.
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The internal environment of the human organism is made up of blood within the blood vessels, interstitial fluid surrounding the body cells, and lymph inside the lymph vessels.
The blood can also act as a transportation means for disease-causing organisms. For this reason, the lymphatic system helps in picking up wastes from the interstitial fluid, cleansing them of bacteria, and returning them bacteria-free into the blood.
Physical Characteristics of the Blood
Blood Functions
1. Transportation
Blood helps in the transportation of:
Oxygen (from the lungs to the body’s cells)
Carbon Dioxide (from the cells to the lungs)
Nutrients (from the digestive organs to the cells)
Waste Products (from the cells to the kidneys, lungs, and sweat glands)
Hormones (from the endocrine glands to the cells)
Enzymes (to various cells)
2. Regulation
Blood helps in the regulation of:
pH (through buffers)
Body Temperature (through heat-absorbing and coolant properties of its water content)
Water within the Cells (mainly through dissolved sodium ions)
3. Protection
Blood helps in protecting the body against:
Blood Loss (through the blood clotting mechanism)
Toxins and Foreign Microbes (through special combat-unit cells such as white blood cells)
Blood Composition
Blood is made up of 2 portions:
1. Formed Elements
make up 45% of the total blood volume
include Red Blood Cells, White Blood Cells (Granular – neutrophils, eosinophils & basinophils; and Agranular – lymphocytes & monocytes), and Platelets.
2. Plasma
makes up 55% of the total blood volume
water (91.5% of total plasma)
proteins (7% of total plasma)
other solutes (1.5% of total plasma)
Haematopoiesis – Blood Cell Formation
Haematopoiesis a.k.a. blood cell formation takes place within the Red Bone Marrow (myeloid tissue in the humerus, femur, sternum, ribs, vertebrae & pelvis) and Lymphoid Tissue (in the spleen, tonsils & lymph nodes).
Red Blood Cells, Leucocytes & Platelets are produced within the Bone Marrow.
Agranular Leucocytes (lymphocytes & monocytes) are produced by the Bone Marrow and the Lymphoid Tissue.
Red Blood Cells a.k.a. Erythrocytes
do not contain a nucleus
cannot reproduce
cannot carry on extensive metabolic activities
plasma membrane is selectively permeable
plasma membrane encloses cytoplasm and haemoglobin
have a biconcave shape which promotes increased surface area for diffusion purposes
contain a lot of haemoglobin molecules which increase their capacity for oxygen transportation
allow transportation of a small amount of carbon dioxide along with haemoglobin
Normal Haemoglobin Values
Infants
14-20gm/dl
Adult Females
12-15gm/dl
Adult Males
14-16.5gm/dl
Erythropoiesis – Erythrocyte Production
erythropoiesis and erythrocyte destruction usually proceed at the same pace
if the balance between erythropoiesis and erythrocyte destruction is disrupted, a homeostatic mechanism is initiated to promote erythrocyte production
in oxygen deficiency, particular kidney cells release the enzyme Renal Erythropoietic Factor which converts plasma protein into the hormone erythropoietin, which, when reaching the red bone marrow, stimulates haemocytoblasts to develop into red cells
NOTE: Blast is a short name for an immature WBC, such as a lymphoblast or myeloblast. In normal circumstances, less than 5% of the cells in healthy bone marrow at any one time are blasts. Within the bone marrow, normal blasts develop into mature, functioning blood cells and are then released into the bloodstream.
Haemoglobin in Erythrocytes
erythrocyte life span is around 120 days long
the plasma membrane of depleted cells are removed from the circulation by macrophages in the spleen, liver, and bone marrow
haemoglobin is broken down into Haemosiderin (iron-containing pigment which is stored or used in the bone marrow for the production of new haemoglobin for new RBCs), Bilirubin (pigment secreted by the liver into bile) and Globin (protein metabolised in the liver).
White Blood Cells a.k.a. Leucocytes
there is a much lesser amount of WBCs than RBCs in the human body: 700 RBCs per 1 WBC
leucocytes contain nuclei
leucocytes do NOT contain haemoglobin
leucocytes have surface proteins called Human Leucocyte Associated Antigens (HLA) which are unique to each and every person
There are 2 types of WBCs:
GRANULAR LEUCOCYTES:
NEUTROPHILS (POLYMORPHS) – make up the biggest amount of total leucocytes; involved in phagocytosis of bacterial pathogens and the release of antimicrobial chemicals
EOSINOPHILS – involved in phagocytosis of antigen-antibody complexes, allergens and inflammatory chemicals, and the release of enzymes which help weaken or destroy parasites
BASOPHILS – involved in the secretion of histamine which promotes blood flow to a particular tissue, and the secretion of heparin which promotes mobility of other WBCs by clotting prevention
develop from red bone marrow
have granules in the cytoplasm
have a lobed nuclei
AGRANULAR LEUCOCYTES:
MONOCYTES – turn into macrophages; phagocytise pathogens, dead neutrophils, and dead cells debris; and present antigens that activate other cells within the immune system
LYMPHOCYTES – assist with immune memory, secrete antibodies, present antigens for the activation of other cells within the immune system, and help in destroying cancer cells, virus-infected cells, and foreign cells
develop from lymphoid and myeloid tissue
do not have granules in the cytoplasm
Differential Blood Count
Type of White Blood Cell
Normal Differential Count
High WBC Count Implication
Neutrophils
60% – 70%
damage caused by invading bacteria
Eosinophils
2% – 4%
allergic reaction
Basophils
0.5% – 1%
allergic reaction
Lymphocytes
20% – 25%
antigen-antibody reaction
Monocytes
3% – 8%
chronic infection
Life Span of Leucocytes
leucocytes can live from just a few days to a few months, depending on what type of leucocytes they are
during infection, white blood cells become very active, usually living for only a few hours
Platelets
platelets contain no nucleus
platelets have a life span of between 5 to 9 days
platelets help prevent fluid loss through a chain of reaction leading in blood clotting
stem cell development from haemocytoblast to platelets takes place in the red bone marrow
Plasma
Plasma is made up of:
WATER – 90% of total amount of water in plasma is derived from the GI tract; 10% is derived from cellular respiration; water absorbs heat and acts as a solvent and suspending medium for the blood’s solid components
SOLUTES – makes up 8.5% of the total plasma volume
PROTEINS – ALBUMINS (55% of plasma proteins) are produced by the liver; provide viscosity in the blood which helps maintain blood pressure; exert osmotic pressure to help in maintaining water balance between the blood and the tissues; help regulate blood volume; GLOBULINS (38% of plasma proteins) a.k.a. antibodies; FIBRINOGEN (7% of plasma proteins) is produced by the liver; it helps in the blood clotting process
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The phrase thyroid disease refers to medical conditions which affect the way the thyroid gland works. The thyroid gland typically produces an amount of hormones which help the body to function well. Too much thyroid hormone production is referred to as hyperthyroidism, whilst too little thyroid hormone production is referred to as hypothyroidism.
Hyperthyroidism usually causes tachycardia, weight loss, and nervousness. On the other hand, hypothyroidism may cause lethargy, weight gain, and cold intolerance.
Thyroid Disease Risk Factors
family history of thyroid disease
medical conditions eg. type 1 diabetes and rheumatoid arthritis)
shortness of breath – patient has high metabolism, muscle wasting, leading to exhaustion and fatigue, all of which can cause shortness of breath
weight loss – imbalanced nutrition due to high metabolic rate (adequate food intake needs to be ensured)
muscle weakness – in case of inadequate food intake, if no carbs or glucose are available to be broken down, the body turns to protein breakdown, leading to muscle wasting
Hypothyroidism Causes
Thyroiditis
Hashimoto’s Thyroiditis
Post-Partum Thyroiditis (usually temporary)
Iodine Deficiency
Non-Functioning Thyroid Gland
Symptoms
cold sensitivity
memory problems
voice hoarseness
hair dryness and coarseness
fatigue
weight gain
frequent and heavy periods
Thyroid Disease Diagnostic Tests
TFTs (TSH, T4 and T3 levels) – to check the amount of thyroid stimulating hormone (TSH) and circulating thyroid hormones in serum, so thyroid gland’s thyroid hormone production and regulation ability is assessed
CBC – to check amount of red blood cells in the blood (to rule out anaemia)
Renal Profile – to determine the kidneys’ health by evaluating parameters such as proteins, electrolytes, and minerals
Subclinical Thyroid Dysfunction
Subclinical Thyroid Dysfunction is a biochemical diagnosis in which TSH levels are outside the reference range, and circulating T4 and T3 are within the reference range.
Subclinical Thyroid Dysfunction is most commonly detected incidentally. However, in certain cases, individuals may exhibit symptoms of hypothyroidism or hyperthyroidism. Studies related to long-term consequences of subclinical thyroid dysfunction indicate increased cardiovascular morbidity and mortality, increased risk of osteoporosis, and possible links to dementia.
Thyroid Disease Patient Education – Based On NICE Guidelines (2019)
Ensure that information is presented to facilitate shared decision making…
Explain to people with thyroid disease who need treatment, and their family or carers…that:
– Thyroid disease usually responds well to treatment.
– The goal of treatment is to alleviate symptoms and align thyroid function tests within or close to the reference range.
– People may feel well even when their thyroid function tests are outside the reference range.
– Even when there are no symptoms, treatment may be advised to reduce the risk of long-term complications.
– Even when thyroid function tests are within the reference range, changes to treatment may improve symptoms for some people.
– Symptoms may lag behind treatment changes for several weeks to months.
– Day-to-day changes in unexplained symptoms are unlikely to be due to underlying thyroid disease because the body has a large reservoir of thyroxine.
Provide people with thyroid disease, and their family or carers…with written and verbal information on:
– their underlying condition, including the role and function of the thyroid gland and what the thyroid function tests mean
– risks of over-and under-treatment
-their medicines
-need for and frequency of monitoring
– when to seek advice from a healthcare professional
– how thyroid disease and medicines may affect pregnancy and fertility
Provide people with hypothyroidism, and their family…with written and verbal information on:
– possible drug interactions of thyroid hormone replacements, including interactions with over-the-counter medicines
– how and when to take levothyroxine
NICE Guidelines, 2019
Patients with thyroid disease need to have a clear understanding on the disease, treatment goals, and connection between thyroid function tests and symptoms. Medication (Levothyroxine) is frequently taken incorrectly, possibly leading to suboptimal treatment.
Patient information and support on thyroid disease help patients make informed decisions on the management of their condition.
A complete drug history of the patient helps determine if Levothyroxine may interfere with other medications currently being taken, in which case, the patient may be recommended to take Levothyroxine earlier or half hour before food and other medications.
Review of other drug intake should be made so if needed, changes may be made to drug prescription. Example: Iodine may cause toxicity problems with the thyroid gland and may lead to hypothyroidism. Example: Lithium use blocks thyroid hormone production.
The patient needs to be made aware that any side effects experienced may be due to thyroid disease, and that, if kept under control, such side effects may be reduced. Constipation, which is one of the side effects of hypothyroidism, may subside following regular use of Levothyroxine. However, if it persists, increasing high fibre intake and more fluids should help further. Movicol may also be prescribed to help with constipation (if other methods fail to help).
Regular exercise needs to be encouraged, starting slowly, and increasing gradually. This is because patients with thyroid disease such as hypothyroidism tend to gain weight. If necessary, patient may be referred to a dietitian.
Medication compliance is very important with regards to Levothyroxine. The patient needs to be educated about the condition – that it is a lifelong condition which needs to be controlled by medication. It is a chronic disease. Thus, Levothyroxine should not be stopped, even if patient feels well.
Patient should be encouraged to attend all follow-ups so as to ensure that the right dose has been prescribed. It may take a couple of follow-ups until the right dose is achieved. The patient should be instructed that in case of palpitations, chest pain, and tachycardia, contact should be made with clinician so as to ensure she is not going into hyperthyroidism instead.
References
Cleveland Clinic (2020). Thyroid Disease: Causes, Symptoms, Risk Factors, Testing & Treatment. Retrieved from https://my.clevelandclinic.org/health/diseases/8541-thyroid-disease on 5th May 2022
NICE Guidelines (2019). Thyroid Disease: assessment and management. Retrieved from https://www.nice.org.uk/guidance/ng145 on 5th May 2022
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The thyroid gland 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. At times however, an individual may require a thyroidectomy, which is the surgical removal of all or part of the thyroid gland. This may happen due to thyroid-related conditions such as Goitre and Carcinomas.
Hypothyroidism vs Hyperthyroidism
In hypothyroidism, the thyroid gland is underactive, hence it doesn’t produce enough thyroid hormone. On the other hand, in hyperthyroidism, the thyroid gland is overactive, hence it produces too much thyroid hormone.
Thyroidectomy Indications
Goitre
A goitre a.k.a. goiter refers to swelling of the thyroid gland which causes a lump located at the front of the neck which moves up and down with swallowing. Nodules are lumps located within the thyroid gland.
Solitary Nodular Goitre (single swelling) – most commonly benign, solitary nodular goitres are often left untreated. If upon examination cancer is not excluded, surgery is usually recommended. An overactive nodule a.k.a. hot nodule can be treated by pharmacological medication, radioactive iodine treatment, or surgery.
Multi-Nodular Goitre (multiple swellings) – common multiple swellings which usually do not require surgery unless breathing and/or swallowing become compromised, or in case of rapidly growing nodules, or the individual prefers to undergo surgery for aesthetic purposes (unsightly goitre).
Carcinoma
Thyroid cancer is a rare type of cancer affecting the thyroid gland. Types of thyroid cancers include:
papillary carcinoma – the most common type, affecting mostly females under 40; papillary carcinomas appear as irregular solid or cystic masses or nodules
follicular carcinoma – affecting mostly middle-aged females, these malignant epithelial tumors account for about 15% of malignant thyroid tumors
rare carcinomas – include thyroid teratomas, lymphomas, and squamous cell carcinomas.
Thyroidectomy Types
Hemi-Thyroidectomy – removal of half of the thyroid gland
Lobectomy – removal of either the right or the left thyroid gland lobe, commonly done in the case of solitary goitre
Total Thyroidectomy – removal of the whole thyroid gland, commonly done in cases of malignant thyroid tumors
Subtotal Thyroidectomy – removal of almost whole thyroid gland, commonly done in multi-nodular goitre (some thyroid tissue surrounding one parathyroid gland is preserved)
Near-Total Thyroidectomy – removal of almost whole thyroid gland, commonly done in multi-nodular goitre (some thyroid tissue surrounding one parathyroid gland is preserved)
Isthmusectomy – removal of the thyroid isthmus
Thyroidectomy Perioperative Nursing Care
Thyroidectomy Preoperative Care
BLOOD INVESTIGATIONS:
CBC
Urea, Electrolytes, & Creatinine
T3, T4, & TSH (Thyroid Stimulating Hormone)
SCANS:
Thyroid Gland ultrasound scan
Radio-Iodine Thyroid Scan
Neck X-ray
Chest X-ray
OTHER INVESTIGATIONS:
FNAC (Fine Needle Apiration Cytology) of thyroid nodule, if palpable
Indirect Laryngoscopy for pre-operative assessment of vocal cords functioning
CARE:
patient reassurance through answering of any questions in relation to surgery so as to help reduce patient anxiety and fear; this also helps in acquiring informed consent
patient education regarding neck support in preparation for post-operative self-care
administration of anti-thyroid medication eg. Methimazole to promote a euthyroid (normal thyroid function) state
preparation of Potassium Iodide (Iodine) which helps to decrease thyroid gland vascularity, thus reducing risk for haemorrhage
avoid prophylactic antibiotic administration in such a clean elective surgery unless indicated
Thyroidectomy Postoperative Care
PATIENT CARE ON DAY OF SURGERY:
monitor patient’s vital signs and document accordingly
keep patient NBM (nil-by-mouth)
administer between 2.5l-3l of supplemental IV fluid
administer analgesics as prescribed to reduce severe post-operative pain
in case of excessive blood loss during surgery, blood transfusion may be required
PATIENT CARE FROM DAY 2:
encourage initial sips of clear fluid; move on to free fluids, to a soft diet, and finally to a normal diet once each phase is tolerated
maintain vital signs monitoring – temperature rise following 3rd day of surgery indicates infection
monitor surgical site for signs of infection; change initial dressing after 48-72hrs following surgery (unless it’s soaked beforehand, in which case should be changed earlier); use dry dressings every alternate day if suture line is clean and dry; removal of sutures is recommended for the 5th day post-op to avoid scarring as much as possible
monitor daily output from Redivac Drain – remove drain after 48 hours OR when drainage is reduced to a few milliliters in a 24hr period
keep on administering prescribed analgesics, monitoring their effectiveness and taking necessary measures in case of inefficacy
Redivac Drain
Thyroidectomy Complications
haemorrhage – assess surgical wound area for drainage, monitor blood pressure and pulse to notice possible hypovolaemic shock earlier on; risk of haemorrhage is at its peak in the first 24 hours post-op
respiratory distress – assess respiratory rate, rhythm, depth, and strength; prepare suction equipment, oxygen, and tracheostomy set at hand since possible haemorrhage and oedema may result in tracheal compression
wound infection
voice hoarseness and aphonia (total vocal cord paralysis due to nerve damage which causes sounds to come out as just whispers) – assess speaking tone and ability; hoarseness, which eventually subsides, happens due to oedema or endotracheal tube used during surgery
hypocalcemic tetany (low calcium levels in the blood caused by accidental parathyroid glands removal in total thyroidectomy) – this complication may occur in up to 7 days post-op; signs and symptoms include tingling of toes, fingers, and lips; prepare calcium gluconate or calcium chloride in case it’s needed for IV use
Further Related Information
Graves’ Disease
Graves’ disease is an immune system disorder that causes overproduction of thyroid hormones a.k.a. hyperthyroidism. Signs and symptoms of Graves’ disease can be wide ranging.
Hashimoto’s Disease
Hashimoto’s Thyroiditis a.k.a. Hashimoto’s Disease is an autoimmune disease that causes the body to produce antibodies which attack thyroid cells, leading to the under-production of the thyroid hormone. Symptoms of Hashimoto’s Disease may include goitre, lethargy, weight gain, and muscle weakness.
Thyroid Storm
Thyroid storm a.k.a. thyrotoxic crisis is an acute, life-threatening, hypermetabolic state caused by excessive release of thyroid hormones in individuals with thyrotoxicosis. Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed paediatric patients, especially neonates.
Myxedema Coma
Myxedema coma, which is considered to be a medical emergency with a high mortality rate, is defined as severe hypothyroidism that causes decreased mental status, hypothermia, and other organs to slow down their functions.
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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.
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).
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.
Thyroid Hormone Regulation
Thyroid hormone secretion is stimulated by various factors…
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
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.
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.
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
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.
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
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
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.
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.
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
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.
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 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
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.
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
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.
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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.
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.
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.
Leydig Cells
Leydig cells a.k.a. interstitial endocrinocytes, are found in clusters within the spaces between adjacent seminiferous tubules. They secrete testosterone.
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.
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 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.
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.
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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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.
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
Obesity Health Risks
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
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
Weight Loss Benefits & Guidelines
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.
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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