Diabetic Foot

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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.

diabetic foot conditions assessment
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:

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

However…

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

“When people with diabetic foot ulcers heal, just like with cancer, they are not really healed. Our patients are in remission. We tend to think about wounds when they are open but why don’t we think about them when they are closed?

We should be aiming for having people at home in diabetic foot remission monitoring themselves”

Armstrong, Boulton and Bus, 2017.
Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S1067251607600015 on 2nd July 2022

Diabetic Foot Lesions Risk Factors

Retrieved from https://www.wjgnet.com/1948-9358/figures/v6/i1/37.htm on 2nd July 2022
Retrieved from https://www.researchgate.net/publication/242514797_DIABETIC_FOOT_DISORDERS/figures?lo=1 on 2nd July 2022

Routine Diabetic Foot Screening

1. COLLECT MEDICAL HISTORY

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

2. INSPECT & ASSESS FOOT

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

3. ASCERTAIN PATIENT UNDERSTANDING & EDUCATION

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

Peripheral Arterial Disease

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

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

Assessing Dorsalis Pedis & Posterior Tibial Pedal Pulses

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

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

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

Diabetic Neuropathy

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

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

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

  • temperature changes
  • pressure
  • pain
  • vibration

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

The Motor Neuropathic Diabetic Foot

Neuropathic foot features include:

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

Complications include:

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

Neuropathic Ulcer

Charcot Foot

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

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)
diabetic foot conditions assessment
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
diabetic foot conditions assessment
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:

  • ulcers
  • callus
  • gangrene
  • deformity
  • infection
  • inflammation
  • charcot foot
  • limb ischaemia
  • neuropathy

Wound Assessment and Description

Retrieved from https://slideplayer.com/slide/12696492/ on 27th March 2022
Retrieved from https://www.researchgate.net/publication/311988179_Triangle_of_Wound_Assessment_Made_Easy_Revisited/figures on 27th March 2022

Assessing Sensation with a tuning fork

Assessing for Neuropathy using 10g Monofilament

Assessing for Vascular Problems

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

Calculating Ankle-brachial index

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

Osteomyelitis

Foot Ulcer Treatment – Key Elements

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

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

Offloading

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

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

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

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

References

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


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Diabetes Prevention and Management

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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:

  1. individuals are first assessed for the risk of prediabetes through an adequate risk assessment tool such as the German Diabetes Risk Score
  2. if high risk result is achieved, the individual should be tested for prediabetes or Type 2 Diabetes
  3. individuals found with prediabetes should have their blood glucose monitored every year
diabetes prevention and management
Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK535456/figure/article-18425.image.f1/ on 21st March 2022
diabetes prevention and management
Retrieved from https://dryatendrayadav.com/2018/10/17/measure-waist-measure-risk/ on 21st March 2022
diabetes prevention and management
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/m2 AND/OR who have 60 years or more AND/OR women with past GDM (gestational diabetes mellitus) can be prescribed Metformin.

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

Diabetes Management

Nutrition

Eating a healthy balanced diet promotes:

  • weight control
  • blood glucose level stabilisation
  • serum lipid level decrease

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

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

Exercise

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

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

Caution should be taken:

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

Pharmacological Therapy

Type 1 Diabetes Management

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

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

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

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

Patient on insulin should be instructed to:

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

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

diabetes prevention and management
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.

DPP-4i (Dipeptidyl peptidase 4 inhibitor)

alogliptin, linagliptin, saxagliptin, sitagliptin, viltagliptin

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

Glitazones

pioglitazone

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

but…

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

Sulphonylureas

glicazide, glimepiride, gliplizide, tolbutamide

  • stimulates secretion of pancreatic insulin

but…

increases the risk for hypoglycaemia and weight gain.

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

canagliflozin, dapagliflozin, empagliflozin, ertugliflozin

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

but…

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

GLP-1 mimetic

dulaglutide, exenatide, liraglutide, lixisennatide, semaglutide

Administered via weekly subcutaneous injection.

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

but…

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

Monitoring

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

Average Glucose Estimation for HbA1c Values…

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

Glycaemic Targets…

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

Reference

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


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Diabetes Mellitus

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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

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

Signs & Symptoms

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

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

Diabetes Type 1 VS Diabetes Type 2

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

Type 1 Diabetes

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

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

Type 2 Diabetes

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

gestational diabetes

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

LADA – Latent Autoimmune Diabetes in Adults

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

Ketosis-Prone Type 2 Diabetes

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

Other Types of Diabetes

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

Criteria for Asymptomatic Prediabetes and Diabetes Mellitus Testing

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

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

NOTES:

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

Diabetes Mellitus Diagnosis

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

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

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


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

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

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

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

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


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

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

Prediabetes

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

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

Prediabetes is determined by the following test results:

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

Diabetes Mellitus Nursing Care Management

Additional Notes…

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

Reference

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


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The Endocrine System – The Adrenal Glands

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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.

adrenal glands
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:

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

The OUTER ADRENAL CORTEX is made up of 3 parts:

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

  1. Aldosterone acts on the kidneys’ tubule cells, causing them to increase sodium reabsorption
  2. Sodium ions are removed from the urine and returned to the blood
  3. 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

RAAS system
Retrieved from https://www.pinterest.com/pin/557813103821299549/ on 13th March 2022

Aldosterone Control #2 – Potassium Ion Concentration

  1. Increased potassium concentration in extracellular fluid causes the adrenal cortex to secrete aldosterone
  2. Aldosterone secretion causes excess potassium to be eliminated by the kidneys
  3. 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:

  1. stress and low blood glucocorticoid level stimulate the hypothalamus to secrete CRF (corticotropin releasing factor)
  2. CRF secretion causes ACTH to be released from the anterior lobe of the pituitary
  3. ACTH is carried to the adrenal cortex, where it stimulates glucocorticoid secretion
adrenal glands
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
  • increases respiration rate
  • dilates respiratory passageways
  • decreases digestion rate
  • increases muscular contraction efficiency
  • increases blood sugar level
  • stimulates cellular metabolism

However, both epinephrine and norepinephrine:

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

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The Endocrine System – Pancreas Anatomy and Physiology

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

pancreas anatomy and physiology
Retrieved from https://en.wikipedia.org/wiki/Pancreas on 7th March 2022

Pancreas Blood Supply

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

pancreas anatomy and physiology
Retrieved from https://epos.myesr.org/posterimage/esr/ecr2014/120564/mediagallery/539242?deliveroriginal=1 on 7th March 2022

Pancreas Nerve Supply

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

pancreas anatomy and physiology
Retrieved from https://clinicalgate.com/thorax-2/ on 7th March 2022

The Endocrine Portion

The Islets of Langerhans contain 4 types of cells:

  1. Alpha Cells – make up 15% of the pancreatic islet cells; secrete Glucagon
  2. Beta Cells – make up 80% of the pancreatic islet cells; secrete Insulin
  3. Delta Cells – make up 5% of the pancreatic islet cells; secrete Somatostatin
  4. F Cells – secrete Pancreatic Polypeptide
Retrieved from https://slideplayer.com/slide/7426531/ on 7th March 2022
  • Glucagon INCREASES blood glucose level
  • Insulin DECREASES blood glucose level
  • Somatostatin INHIBITS insulin and glucagon, acting as a regulator
  • Pancreatic Polypeptide INHIBITS somatostatin secretion, gallbladder contraction, and digestive enzyme secretion (Pancreatic Polypeptide is secreted near the end of the digestive system)

Glucagon

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

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

lysis = breaking down of glycogen

neo = new

genesis = production

Secretion of glucagon is STIMULATED by:

  • decreased blood glucose level
  • protein-based foods
  • exercise

Secretion of glucagon is INHIBITED by:

  • somatostatin
  • insulin

Insulin

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

Insulin decreases blood sugar level through the following process:

  1. increases glucose transportation from the blood into the cells
  2. increases glucose conversion into glycogen (glycogenesis)
  3. decreases glycogenolysis and gluconeogenesis
  4. stimulates glucose conversion to fatty acids
  5. stimulates protein synthesis

Secretion of insulin is STIMULATED by:

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

Secretion of insulin is INHIBITED by:

  • somatostatin (GIF – growth hormone inhibiting factor)

Insulin production is also AFFECTED by:

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

Insulin vs Glucagon

Somatostatin

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

Somatostatin secretion is INHIBITED by pancreatic polypeptide.

Pancreatic Polypeptide

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

Secretion of pacreatic polypeptide is STIMULATED by:

  • protein-containing meals
  • fasting
  • exercise
  • hypoglycaemia

Secretion of pancreatic polypeptide is INHIBITED by:

  • somatostatin
  • hyperglycaemia

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The Endocrine System – Hypothalamus & Pituitary Gland

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

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

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

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

The Hypothalamus

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

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

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

Hypothalamus-Released Hormones

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

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

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

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

The Pituitary Gland

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

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

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

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

The Endocrine System - Hypothalamus & Pituitary Gland
Retrieved from https://www.nature.com/articles/nrdp201692 on 5th March 2022

The 5 Types of Glandular Cells

  1. Somatotroph Cells – produce GH (growth hormone) which is responsible for general body growth
  2. Lactotroph Cells – synthesise PRL (prolactin) which promotes milk production by the mammary glands
  3. Corticolipothroph Cells – synthesise ACTH (adrenocorticotropic hormone) which stimulates hormone secretion, and MSH (melanocyte-stimulating hormone) which is responsible for skin pigmentation
  4. Thyrothroph Cells – produce TSH (thyroid-stimulating hormone), which controls the thyroid gland
  5. Gonadotroph Cells – produce FSH (follicle-stimulating hormone), which stimulates egg and sperm production in the ovaries and testes, and LH (luteinizing hormone), which stimulates other sexual and reproductive activities.
The Endocrine System - Hypothalamus & Pituitary Gland
Retrieved from http://www.pharmacy180.com/article/pituitary-gland-3595/ on 5th March 2022

Growth Hormone (GH)

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

Growth Hormone Secretion Stimuli and Inhibition

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

Prolactin (PRL)

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

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

Melanocyte-Stimulating Hormone (MSH)

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

Thyroid-stimulating factor (TSH)

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

Adrenocorticotropic Hormone (ACTH)

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

Follicle-Stimulating Hormone (FSH)

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

Luteinizing Hormone (LH)

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

Pituitary Gland Posterior Lobe

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

Antidiuretic hormone (ADH)

  • affects urine volume; it causes the kidneys to excrete water from fresh urine and return it to the bloodstream, reducing urine volume
  • absence causes an increase in urine output
  • raises blood pressure by constricting arterioles
  • secretion varies based on the body’s needs
  • causes a decrease in sweat
Retrieved from https://slideplayer.com/slide/10623655/ on 6th March 2022

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The Lymphatic System – Playing a Vital Part In The Immune System

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The lymphatic system, which comprises of lymph, lymphatic vessels, and lymphatic tissue, has an important role within the body. It:

  • drains excess fluid and protein from the interstitial tissue back into the blood
  • transports fat from the GI tract to the blood
  • produces and circulates lymphocytes that help in keeping the body protected

Lymph

Lymph is the same as the interstitial fluid. Fluid that bathes the cells is referred to as interstitial fluid, while when it flows through the lymphatic vessels, it is called lymph.

Lymphatic Vessels

The lymphatic vessels are microscopic vessels in between the cells spaces known as lymph capillaries. They are slightly larger than blood capillaries and more permeable. Whilst we can find lymphatic capillaries throughout the whole body, they are not found in the avascular tissue, CNS, splenic pulp and bone marrow.

Lymph capillaries connect through larger lymph vessels known as lymphatics, which converge into two main channels, namely the thoracic duct and the right lymphatic duct. Lymphatics have thinner walls and valves (more valves than veins). Lymph nodes can be found at various intervals.

lymphatic system
Retrieved from https://www.lymphedemablog.com/2012/02/15/comparison-of-blood-and-lymph-vessels/ on 29th May 2022

Drainage of the Lymphatic System

The left side of the head, neck, chest, upper left extremities and the entire body below the ribs all drain into the thoracic duct.

The upper right side of the body drains into the right lymphatic duct.

lymphatic system
Retrieved from https://www.amboss.com/us/knowledge/male-reproductive-organs on 29th May 2022

Lymphatic Tissue

Lymphatic tissue is rich in lymphocytes and accessory cells such as macrophages and reticular cells. It is scattered in the linings of the GI tract, the respiratory tract, the urinary tract, the reproductive tract, and in the stroma a.k.a. core of multiple organs. Lymphatic tissue can also be found surrounded by a capsule within the lymphatic organs a.k.a. lymph nodes, spleen, and the thymus gland.

Lymph nodes

Lymph nodes are oval structures measuring between 1-25mm in length, commonly found in groups, located along the lymph vessels’ pathway.

Afferent Lymphatic Vessels => Sinuses => Efferent Lymphatic Vessels

  1. Lymph passes through the nodes and is filtered from foreign substances by the reticular fibres within the node
  2. Macrophages destroy foreign substances through phagocytosis
  3. T Cells destroy foreign substances through the release of various products
  4. B Cells produce antibodies to destroy them
lymphatic system
Retrieved from https://pubs.rsna.org/doi/abs/10.1148/rg.2021210053?journalCode=radiographics on 29th May 2022

Lymphatic ORgans: Tonsils

Tonsils are a pair of soft tissue masses located at the pharynx. Their location helps protect against the invasion of foreign substances through the production of lymphocytes and antibodies.

Retrieved from https://www.aboutkidshealth.ca/Article?contentid=1918&language=English on 29th May 2022

Lymphatic Organs: Spleen

The spleen is an oval shaped organ measuring around 12cm in length which is made up of lymphatic tissue. It is located in the upper left side of the abdomen, next to the stomach and behind the left ribs. Functions of the spleen include:

  • B Lymphocyte Production – eventually develop into antibody-producing plasma cells
  • Phagocytosis – of bacteria and damaged or worn-out red blood cells and platelets
  • Blood Storage and Release – in cases such as haemorrhage

NOTE: the spleen does not filter lymph.

Retrieved from https://www.researchgate.net/publication/309457531_A_Brief_Survey_of_Spleen_Segmentation_in_MRI_and_CT_Images/figures?lo=1&utm_source=google&utm_medium=organic on 29th May 2022

Lymphatic Organs – Thymus Gland

The thymus gland is found in the superior mediastinum, between the lungs and behind the sternum. It reaches it’s maximum size during puberty, after which it starts to break down. The main function of the thymus gland is to produce T Lymphocytes.

Retrieved from https://www.thoracic.theclinics.com/article/S1547-4127(10)00194-5/fulltext on 29th May 2022

Body Defences

The human body aims to maintain haemostasis by counteracting pathogens or related toxins in the environment.

Resistance = the body’s ability to keep off disease

Susceptibility = the body’s inability to resist disease

Body defences can be divided in two groups: Non-Specific Defence and Specific Defence a.k.a. Immunity

lymphatic system
Retrieved from https://ib.bioninja.com.au/standard-level/topic-6-human-physiology/63-defence-against-infectio/lines-of-defense.html on 30th May 2022

Non-Specific Defences

The non-specific defence mechanism provides an immediate response to protect the body from foreign substances. Components of the non-specific defence mechanisms include:

  • SKIN & MUCOUS MEMBRANESMECHANICAL FACTORS include the epidermis‘ anatomy i.e. made up of closely packed cells, continuous layering and the presence of keratin; mucous membranes that secrete mucus to prevent cavities from drying up whilst trapping microbes at the same time (eg. in nose through hairs and in the upper respiratory tract through cilia); lacrimal apparatus; saliva which helps prevent microbe colonisation; epiglottis which helps prevent microbes from entering the lower respiratory tract; CHEMICAL FACTORS include sebum which forms a protective film over the skin’s surface and inhibits bacterial growth; perspiration which flushes microbes from the skin; gastric juice produced by the stomach glands which is highly acidic due to being made of hydrochloric acid, enzymes and mucus, all of which help preserve the stomach’s sterility whilst destroying bacteria and most bacterial toxins; lyzozyme (found in perspiration, tears, saliva, nasal secretions and tissue fluids) which is an enzyme that can break down cell walls of various bacteria;
  • ANTI-MICROBIAL SUBSTANCESINTERFERON (IFN) (alpha, beta & gamma) which are produced by lymphocytes and other leucocytes and fibroblasts; COMPLEMENT – a group of 11 proteins found in normal blood serum which complements immune and allergic reactions involving antibodies – once activated, destroys microbes; PROPERDIN – a protein found in the serum which together with COMPLEMENT causes the destruction of several types of bacteria, enhances phagocytosis, and triggers inflammatory responses;
  • PHAGOCYTOSIS– the ingestion and destruction of microbes or other foreign particulate matter by phagocytes through the Adherence process and the Ingestion process;
  • INFLAMMATORY PROCESS – when cells are damaged by microbes, inflammation is triggered, characterised by redness, pain, heat, swelling, and loss of function; during inflammation, vasodilation increases permeability of blood vessels, neutrophils migrate to the injured area within one hour, nutrients are released to help support defensive cells and increased metabolic reactions of the affected cells, fibrin formation, and pus formation;
  • FEVER – inhibits microbial growth and speeds up body reactions which help the body to heal

HIGH FEVER => HIGH BODY TEMPERATURE => INCREASED RATE WITH WHICH THE BODY WORKS TO FIGHT OFF INFECTION, BACTERIA OR VIRUSES.

Specific Defences a.k.a. immunity

Immunity involves the production of a specificy cell type or molecule a.k.a. antibody that can destroy a particular antigen.

An antigen is a chemical substance which causes the body to produce specific antibodies which can react with the antigen. Antigens have immunogenicity (can stimulate the formation of specific antibodies) and reactivity (can react specifically with the produced antibodies). Antigens with both immunogenicity and reactivity are called complete antigens eg. proteins, nucleoproteins, lipoproteins, glycoproteins, and some polysaccharides. Non-microbial antigens include pollen, egg white, incompatible blood cells, and transplanted tissues and organs.

An antibody is a protein produced by the body in response to antigen presence. An antibody can combine with the antigen.

Antibodies belong to a group of proteins called globulins, hence the name immunoglobulins.

lymphatic system
Retrieved from https://www.toppr.com/ask/content/concept/antibodies-intermediate-266269/ on 30th May 2022

Cellular immunity & Humoral Immunity

The body can defend itself against bacteria, toxins, viruses and foreign tissues thanks to 2 components:

  1. CELLULAR IMMUNITY A.K.A. CELL-MEDIATED IMMUNITY – includes the formation of specially sentisised lymphocytes which can attach to the foreign agent and destroy it; T cells are responsible for cellular immunity
  2. HUMORAL IMMUNITY A.K.A. ANTIBODY-MEDIATED IMMUNITY – includes the formation of circulating antibodies able to attack an invading agent; B cells are specialised plasma cells which produce antibodies and provide humoral immunity
lymphatic system
Retrieved from https://ib.bioninja.com.au/higher-level/topic-11-animal-physiology/111-antibody-production-and/immune-pathways.html on 30th May 2022
Retrieved from https://www.pinterest.com/pin/729442470871870835/ on 30th May 2022

The Immune Response

The immune response of the body, be it cellular or humoral, is more intense after a second or subsequent exposure to an antigen than after initial exposure, as illustrated below…

Retrieved from https://www.elevise.co.uk/gab3q5.html on 3th May 2022

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