Module 10: Disorders of Endocrine Function PDF

NURT2304 Alterations in Health and Wellness Module 10 Disorders of Endocrine Function Lecturer: Dr. Zuhair Rushdi Mustafa PhD Adult Nursing Disorders of the posterior pituitary Diabetes insipidus This condition is caused by hyposecretion of anti-diuretic...

NURT2304 Alterations in Health and Wellness Module 10 Disorders of Endocrine Function Lecturer: Dr. Zuhair Rushdi Mustafa PhD Adult Nursing Disorders of the posterior pituitary Diabetes insipidus This condition is caused by hyposecretion of anti-diuretic hormone (ADH). ADH acts on increasing water reabsorption from the filtrate. It therefore reduces the volume of urine excreted. Deficiency of ADH prevents the kidney from reabsorbing water, leading to the production of large volumes of dilute urine. Management Treatments for diabetes insipidus aim to reduce the amount of urine that the body produces, a manufactured hormone called Desmopressin is used. This medication replaces the missing ADH and lowers the amount of urine the body makes.  Diabetes mellitus diabetes is a group of disorders characterised by raised blood levels of glucose in the blood. There are two main types of diabetes – type 1 (insulin-dependent diabetes (IDDM) and type 2 diabetes (Non-insulin-dependent diabetes mellitus (NIDDM)); however, the signs and symptoms of the two types are similar: high blood glucose levels (hyperglycemia) Glycosuria (glucose in the urine) ketonuria (ketones in the urine) frequency in passing urine (Polyuria) including waking at night (Nocturia). Excessive thirst (polydipsia) increased appetite (usually type 1 only) weight loss (usually type 1 only) fatigue abdominal pain. Types of diabetes mellitus The WHO (2019) classification of diabetes mellitus lists 5 main types: I. type 1 diabetes II. type 2 diabetes III. Gestational diabetes (hyperglycaemia first detected during pregnancy). IV. diabetes of other specific types V. hybrid forms of diabetes (diabetes with combined features of type 1 and type 2 diabetes. Type 1 diabetes Type 1 diabetes develops most commonly in childhood or early adulthood, and so is sometimes referred to as juvenile- onset diabetes. Globally, type 1 diabetes mellitus (T1DM) accounts for 5% to 10% of DM cases. Type 1 diabetes is normally caused by autoimmune destruction of the beta cells of the pancreas and is therefore associated with a severe reduction in, or complete loss of, insulin production. Girls and boys are equally affected, and white populations have higher rates than non-white populations. Genetic There is no single ‘diabetes’ gene: multiple genes are involved. In identical twins, if one is type 1 diabetic, the risk to the other is only 30% to 50%, and the risk to a child if the mother has T1DM is less than 4%. Pathophysiology The beta cells within islets of Langerhans of the pancreas produce Insulin. Insulin acts like a key, opening body cells so that glucose can enter the cell to provide a source of energy. T1DM is characterised by destruction of the β-cells of the pancreatic islets and leads to an absolute deficiency of insulin. In up to 90% of affected people it is an autoimmune disorder.  Autoreactive T-cells directed against β-cells also contribute to their destruction. It is also thought that some cases develop after a triggering event, such as a viral infection, which initiates the autoimmune response. Histological examination of the pancreas shows infiltration with a range of inflammatory and immune cells, including macrophages, T cells, and B cells. Other Autoantibodies in Type 1 Diabetes include:Islet cell antibodies (ICA), antibodies to glutamic acid decarboxylase (GAD-65), insulin autoantibodies (IAA), and IA-2A. Signs and symptoms 1.weight loss 2. Fatigue 3. a raging thirst 4. Polyuria 5. in children failure to thrive. 6. There may also be a history of urinary tract infections because the high glucose content of the urine favours microbial growth. 7. ketoacidosis is high. Prognosis and management Because the pancreatic islets are usually completely destroyed, the patient produces no insulin of their own and requires lifelong insulin treatment. T1DM reduces the expected lifespan by 13 years. However, how well patients do in the long term is strongly influenced by how well controlled their blood glucose levels are. Good glycaemic control delays the onset of complications and can reduce their severity when they do develop.  Care must be taken to ensure that the insulin administered. If the dose of insulin administered is not matched by sufficient intake of food, the patient will eventually become comatose and may die. Conscious patients may be given a sugary snack or drink and some form of carbohydrates; the patient will then require monitoring of their blood glucose until the crisis has passed. Unconscious patients require immediate medical assistance and the administration of an intramuscular injection of glucagon and potentially intravenous glucose. Type 2 diabetes mellitus (T2DM) T2DM accounts for up to 95% of all cases of DM. Type 2 diabetes is normally characterised by the development of resistance to the effects of insulin in the tissues, and a reduction in the ability of the beta cells to increase the production of insulin in response to this increased insulin resistance in the body. The resulting high blood levels of glucose lead to damage of the beta cells, thus further reducing the production of insulin. Risk Factors of T2DM 1. increasing age. T2DM is traditionally thought to be a disease of people over the age of 40, but because the numbers of overweight and obese children and young people are increasing in most societies, it is increasingly common in these age groups as well. 2. Smoking 3. Obesity 4. a family history 5. a sedentary lifestyle 6. a diet high in processed foods, red meat, fat, and carbohydrates. 7. Body fat distribution. People who carry a higher proportion of their body fat around their abdominal organs are at higher risk, even when their body weight falls in the normal range. Pathophysiology T2DM is a complex condition, in which pancreatic β-cells begin to fail, leading eventually to reduced insulin secretion. β-cell failure is thought to be due essentially to overwork – the result of prolonged and excessive insulin production because of prolonged and sustained exposure to excessive blood glucose concentrations. In association with consistently high insulin levels, body cells lose their capacity to respond normally to insulin ( insulin resistance ). Insulin resistance is much more common in obese people than in those of normal weight. As the pre-diabetic state progresses, and β-cell function deteriorates, insulin levels begin to fall. As this happens, blood glucose levels begin to rise, symptoms appear and frank diabetes becomes apparent. Some β-cell function may be retained in many people, who therefore continue to produce some insulin, in contrast to those with T1DM, whose pancreatic islets are completely destroyed and who produce no insulin at all. Signs and symptoms Of all people with T2DM, 60% have no symptoms at the time of diagnosis, but others present with the classic symptoms of: 1. Polydipsia (excessive thirst) 2. Polyuria 3. Polyphagia (hunger). 4. weight loss 5. Fatigue 6. Others may present with indications of diabetes-induced end-organ damage, such as paraesthesias, deterioration in vision or renal impairment. 7. Diabetic retinopathy generally appears more quickly post- diagnosis in T2DM than type 1 because it is likely the T2DM patient has had a long pre-diabetic period with undetected hyperglycaemia.  Management and Prognosis In some patients, weight reduction, increased exercise and reduced food intake can resolve the raised blood sugar levels. However, once the beta cell damage has occurred, the need for medications is increased. Current drug therapies for type 2 diabetes (oral hypoglycaemics) target several aspects of the disease, including reducing glucose production by the liver, enhancing insulin output from the pancreas or increasing the sensitivity of the muscle, fat and liver cells to the effects of insulin and thus reducing insulin resistance. If these measures fail, the next step has been to start insulin therapy. Hyperglycaemia of pregnancy Pregnancy induces a state of insulin resistance, leading to a tendency to hyperglycaemia and sometimes precipitating frank diabetes. Diabetes that occurs in pregnancy in a previously non-diabetic woman is called gestational diabetes. Worldwide affects about 14% of pregnancies. Risk factors include: 1. maternal overweight/obesity 2. having had gestational diabetes in a previous pregnancy 3. a family history of diabetes. Pathophysiology The reasons why some women develop gestational diabetes are not clear. Consequences of hyperglycaemia of pregnancy This condition affects both mother and baby. It increases the risk of pre-eclampsia and premature birth, and of the development of T2DM and cardiovascular disease in later life in the mother. The baby is likely to be of above-average birth weight and is more likely to need delivery by caesarean section. There is evidence that gestational DM increases the risk of stillbirth and of the child becoming obese and/or developing T2DM in later life. Diabetes of other specific types 1. Pancreatitis 2. pancreatic cancer 3. cystic fibrosis damage pancreatic tissues, including the β-cells. 4. Some hormones (e.g., thyroxine and cortisol) antagonise (opposing its effects) the actions of insulin and lead to diabetes. Hyperthyroidism and Cushing syndrome are therefore associated with DM. 5. Drugs that mimic the actions of adrenaline (β-adrenergic agonists and α-adrenergic agonists) also antagonise the action of insulin and lead to diabetes. 6. Infections can lead to β-cell-destruction; rubella and mumps, for example, are associated with DM. Complications of diabetes mellitus A. Microvascular complications of diabetes mellitus I. Diabetic retinopathy: Damage to the retina of the eyes. This is a leading cause of blindness worldwide. II. Diabetic neuropathy: This causes paraesthesias (including tingling, pricking, aching, and hypersensitivity to touch) and numbness, increasing the risk that injury, often to the feet, may go unnoticed. Pain in diabetic neuropathy is caused by direct damage to nervous tissue thus does not respond to conventional analgesics.  An autonomic nerve damage causes erectile dysfunction, diarrhoea or constipation, arrhythmias, poor regulation of blood pressure, urinary retention, and sweating. III. Diabetic nephropathy. The glomerular capillaries are progressively destroyed, leading ultimately to renal failure. Diabetic nephropathy is the commonest cause of chronic renal failure in the Western world and develops in about 40% of diabetic people. B. Macrovascular complications of diabetes mellitus This form of vascular injury is more common in type 2 DM than type 1. I. Diabetic foot This is very common in diabetes and accounts for nearly half of all diabetes-related hospital admissions. Because of poor circulation, increased incidence of infection, and poor sensation, diabetic people are predisposed to developing foot ulcers, which heal poorly and frequently lead to gangrenous changes, necrosis, and the necessity of amputation. II. Diabetic ketoacidosis (DKA) This is associated mainly with type 1 DM. In the absence of insulin, cells cannot take up glucose source of energy. The main alternative fuel source to glucose is the triacylglycerols, the body’s stored fats. The body cells convert triacylglycerols to acetyl-CoA, which the liver then converts to ketone bodies-acetoacetate. Acetoacetate is then converted to acetone. This is called ketogenesis, and the ketone bodies can be used by body cells, including the brain, for energy. Rising levels of ketones in the blood can spill into the urine (ketonuria) and cause metabolic acidosis (ketoacidosis). They are excreted in the breath, giving it a distinctive odour of acetone. DKA is a medical emergency. Untreated, DKA can lead to loss of consciousness and, eventually, death. It requires immediate treatment with insulin to restore glucose supply to body cells, and fluid and electrolyte replacement.  III. Diabetic people are at elevated risk of cataract. IV. uterine and pancreatic malignancies, is increased. V. Infections are more common in diabetes than in the general population. Hyperthyroidism Excessive production of thyroid hormone (free thyroxine (T4) and free triiodothyronine (T3) is commonly due to Graves’ disease, an autoimmune disorder where autoimmune antibodies mimic the effect of pituitary thyroid stimulating hormone (TSH), thus stimulating the excessive release of thyroid hormone. Other causes include thyroid cancer, thyroid nodules (usually non-cancerous), viral thyroiditis, postpartum thyroiditis and iodine-containing drugs. signs and symptoms Because thyroid hormones accelerate the metabolism of virtually all body cells, the signs and symptoms associated with hyperthyroidism are wide-ranging. 1. cardiovascular effects including hypertension, tachycardia, palpitations (atrial fibrillation is common in the elderly). The increased workload and oxygen consumption of the heart can cause heart failure in untreated hyperthyroid disease. 2. Increased metabolic rate leads to heat intolerance 3. Goitre (swelling of the thyroid gland). 4. nervousness, restlessness, fatigue, insomnia 5. shortness of breath 6. weight loss despite an increased appetite, frequency of passing stools (diarrhea), nausea, vomiting. 7. muscle weakness, tremors 8. warm, moist flushed skin 9. fine hair 10. staring gaze, exophthalmia 11. Thyroid function test reveals T3 and T4 levels rise above normal, while TSH from the anterior pituitary decrease in the blood test. Normal Thyroid function test Hyperthyroidism Complications of hyperthyroidism The long-term effects of hyperthyroidism can include cardiovascular disease and osteoporosis. Consequences of hyperthyroidism of pregnancy 2. In pregnancy, hyperthyroidism has been linked with higher rates of miscarriage, premature labour, eclampsia and low birth weight of the baby. Management: 1. Surgery (thyroidectomy) to remove part or all of the thyroid gland (rarely used except for surgical removal of thyroid tumours, a large goiter that causes symptoms, thyroid nodules that cause symptoms, Graves’ disease). 2. Radioactive iodine to destroy thyroid tissue. Radioactive iodine usually causes hypothyroidism, which then in turn must be treated with thyroid hormone replacement therapy. Radioactive iodine is contraindicated in pregnancy. 3. Antithyroid drugs: these are hormone inhibitor reduce thyroid hormone production but do not damage the gland. Example: methimazole (brand name: Tapazole), and Carbimazole. 4. beta-blockers such as atenolol to relief tachycardia, palpitations, tremors and nervousness can be achieved with. Hashimoto thyroiditis This autoimmune disorder tends to appear in middle age. It is commoner in women than men. There is a strong familial tendency. Signs and symptoms Falling levels of thyroid hormone stimulate the anterior pituitary to produce TSH to restore them, and Hashimoto thyroiditis is usually characterised by low levels of T 3 and T 4 , despite elevated levels of TSH. Management and prognosis The treatment of choice is lifelong thyroxine replacement therapy. Hypothyroidism Worldwide, the commonest cause of hypothyroidism is iodine deficiency. In populations for which iodine deficiency is not a problem (e.g., because of good diet, iodine-supplemented water, and/or foodstuffs), the commonest cause of hypothyroidism is Hashimoto disease. Other causes of hypothyroidism include: failure of the thyroid to develop during fetal life (congenital agenesis), treatment for hyperthyroidism (especially anti-thyroid drugs and radioactive iodine therapy), thyroid destruction by radiation therapy of cancer of the neck, thyroid infections, and and certain drugs, such as amiodarone and lithium. Sings and Symptoms 1. confusion, lethargy, memory loss, depression 2.bradycardia, cardiomegaly, pericardial effusions 3. constipation, weight gain 4. muscle cramps, myalgia (generalised muscle aches), stiffness 5. dry cool skin 6. brittle nails 7. coarse hair, hair loss 8. oedema of hands and eyelids 9. cold intolerance 10. Thyroid function test reveals T3 and T4 decrease while TSH from the anterior pituitary increase in the blood test. Falling levels of thyroid hormone stimulate the anterior pituitary to produce TSH to restore them. Consequences of hypothyroidism of pregnancy 1. In pregnancy, hypothyroidism has been linked to recurrent miscarriages and preterm labour; it is also suspected that untreated maternal hypothyroidism is linked to reduced IQ in the child. Management and prognosis The treatment of choice of hypothyroidism is lifelong thyroxine hormone (tablet) replacement therapy.