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Category Archives: Chronic conditions

CKD and Anaemia

Chronic kidney disease is frequently connected with anaemia; eGFR is used to indicate the degree of kidney function, and determine which of five stages the patient falls into. Anaemia is associated with decreased renal function as the production of erythropoietin (EPO) declines in accordance with low Hb levels. Patient may present with symptoms of tachycardia, fatigue, reduced cognitive function or left ventricular hypertrophy.

Combined with CKD, anaemia can exacerbate other conditions such as diabetes and cardiovascular disease. Human EPO may be prescribed, although it can have the side effect of exacerbating hypertension.

As in all other cases, the cause for the anaemia should be sought in order that the most appropriate treatment can be commenced. The cause may be renal, or it may be caused by iron, folate or b12 eficiency, hypothyroidism, hyperparathyroidism, bone marrow infiltration, chronic inflammation or infection, chronic haemorrhage, aluminium toxicity, pure red cell aplasia, haemolysis or malignancy.

Low Hb can indicate anaemia, it is therefore important to check FBC routinely to review WCC and platelet count to rule out infection and find haematological causes of anaemia. Low white cell and platelet counts can indicate involvement of the bone marrow, whereas if WCC and platelet count is high, this could be associated with inflammation or infection. Acceptable platelet range is 150-400 x 109/l

Parathyroid hormone (PTH) controls calcium levels, ensuring that vitamin D and calcium are absorbed, preventing bone damage. PTH should be measured in all CKD patients with an eGFR <60ml/min/1.73m2. PTH of less than 100pg/ml can show bone disease.  It is important to measure PTH as way of identifying bone condition, as hyperparathyroidsim is associated with bone marrow fibrosis. Hyperparathyroidism can also reduce the response to ESA therapy. However, there is no need to measure TSH at this time.

Serum ferritin should be maintained at 200-500micrograms/l. Haemodialysis patients should be prescribed iron supplements to achieve and maintain this level.

Efficacy of ESA therapy can be reduced by inadequate dialysis. Adequacy of dialysis can be measured by urea reduction ratio before and after dialysis, and for haemodialysis patients levels should be above 65%.

Reticulocytosis can be caused by haemolysis, acute or chronic blood loss. A FOB test maybe required to check for GI bleeding. Anaemia can also be caused by GI tract cancer, so colonoscopy can be performed to exclude cancer.

A positive haemolysis test may indicate anaemia caused by a na infection, or reaction to a drug/infusion, or an autoimmune disorder such as SLE. Bilirubin is raised in patients with a higher level of haemoglobin.

C-reactive protein levels should also be checked as CRP is a marker for inflammation. Ferritin levels can be affected by inflammation, and so determining if there has been inflammation (with the CRP) can aid diagnosis. CRP will help to show whether the anaemia is caused by inflammation or infection. If CRP is normal, the ferritin level can be trusted.

Generally there are two causes for iron deficiency, if it is not due to haemorrhage, it may be due to haemolysis.

Serum creatinine is affected by GFR as well as age, gender, weight, diet, medication, race, and also some laboratory methods. This is a poor test to determine renal function in the elderly. Drugs that affect GFR include ACE inhibitors in patients with renal vascular disease, as will diuretics. It is therefore good practice to check GFR before initiating treatment with these drugs, as well as two weeks after beginning treatment, checking regularly after this as routine. If there is big decrease in GFR, other causes must be ruled out, if ACEI is causing the reduction in GFR, it may need to be discontinued. ACEIs can also affect haemoglobin levels even if previously stable.

ESA treatment should only be considered if Hb levels are not increased with ferritin

 
 

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Osteoarthritis

Osteoarthritis generally effects the hands, feet, knees, hips, shoulders and lumbar/cervical spine. OA is a non-inflammatory degenerative condition affecting the synovial joints resulting in the loss of hyaline cartilage around load-bearing points, degeneration of collagen and agrecan, and altering the configuration of the underlying bone. Generally OA presents as pain in the joints and a reduced range of movement and/or stiffness. OA may occur spontaneously, or it may occur secondary to an underlying condition, or as a result of surgery, injury or repetitive strain; being overweight can also increase the risk of osteoarthritis occurring.

Pain associated with OA is generally a dull, throbbing, localised pain; stiffness after a period of inactivity generally lasts for around 15 minutes. Muscle wastage can sometimes accompany OA as activity is reduced. This may be accompanied by crepitus, joint-line or periarticular tenderness when palpated, or pain on moving the joint. Deformity may be visible if there is bony swelling. Osteoarthritis of the spine is often referred to as spondylosis and is not normally associated with neurological complications.

Diagnosis of OA is generally through x-ray, history and examination, however other diagnoses may need to be ruled out first.

Osteoarthritis is managed through controlling pain, reducing stiffness, and where possible improving or at least maintaining joint mobility. Aids to consider are orthotics, splints or braces depending on the site of the arthritis. Walking aids may also be considered, although this has an impact on body image, and therefore needs to be thoroughly considered. Exercise is important in the management of osteoarthritis and can help to improve or maintain joint mobility, boost fitness and therefore health, and strengthen supporting muscles, as well as enabling weight loss where required. Exercise needs to be carefully considered and tailored to the patient to avoid injury and complications. Heat/cool therapy may be effective in relieving pain and discomfort.

Mild osteoarthritic pain is generally treated first line with paracetamol, with or without codeine. If appropriate for the patient, this can then be augmented with oral NSAIDs. If NSAIDs are taken frequently, a proton pump inhibitory is also advisable. Corticosteroid injections may be useful for short-term pain relief.

 
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Posted by on March 14, 2012 in Chronic conditions

 

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Risk Factors for CHD

  • Age
  • Gender
  • Ethnicity
  • Family history
  • Past medical history of CVA or MI
  • High total cholesterol or LDL
  • Low HDL levels
  • Hypertension
  • Sedentary lifestyle
  • Obesity
  • Diabetes mellitus
  • Excessive alcohol consumption
 

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Coeliac Disease

This is an autoimmune condition triggered by the consumption of gluten found in wheat, barley, rye and occasionally oats. Frequently there is confusion of a patient’s symptoms, sometimes leading to a diagnosis of IBS or wheat intolerance. Untreated celiac disease can lead to increased risk of osteoporosis and small bowel cancer.

Symptoms of celiac disease include:

  • Nausea
  • Bloating
  • Flatulence
  • Constipation
  • Diarrhoea
  • Weight loss
  • Fatigue
  • Joint or bone pain
  • Mouth ulcers
  • Dematitis herpetiformis (a skin condition associated with coeliac disease)

Coeliac disease is diagnosed first of all with a blood test for immunoglobulin A or tissue transglutaminase amtonpdoes (tTGA). If this proves inconclusive. Endomysial antibodies may also be tested for, and later with an endoscopy and biopsy of the duodenum.

Gluten-free food including pasta, flour, biscuits, crackers and even breads and pizza bases are available on prescription.

 
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Posted by on March 13, 2012 in Chronic conditions

 

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Signs and symptoms of ankylosing spondylitis

  • Morning stiffness
  • Pain in sacroiliac joints, buttocks and chest
  • Fever
  • Weight loss
  • Excessive kyphosis of thoracic spine
  • Reduced spinal flexion

Taken from Independent Nurse 21/11/2011 p29

 
 

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Conditions causing lower back pain

  • Injury
  • Strain
  • Fibromyalgia
  • Osteoarthritis
  • Spinal stenosis
  • Opsteomyelitis
  • Osteoporosis
  • Malignancy
  • Prolapsed intervertebral disc

Taken from Independent Nurse 21/11/2011 p30

 
 

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Leg Ulcers

In venous leg ulcers, the incompetency of venous valves means there may be backflow in the veins of the lower leg which results in venous hypertension. This can cause fluid to accumulate in the tissues, developing oedema.

Brown haemosiderin staining is caused by the breakdown of red blood cells which become trapped in the skin. Induration occurs from fibrosis of the subcutaneous layer which may result in a classic ‘champagne leg’. Other venous symptoms are varicose eczema, oedema, ankle flare (distended veins in medial ankle area) pain (with relief on elevating the limb), varicose veins, ulcers in gaiter or malleolus regions.

Risk factors of venous ulceration are: DVT, varicose veins, swollen oedematous legs, multiple pregnancies, lower leg fracture, thrombophlebitis, previous leg ulceration, previous vascular or orthopaedic surgery.

Arterial signs include: reduced or absent pedal pulses, history of intermittent claudication, reduced ABPI, deep punched out ulcers on toes, heels or foot, necrosis or gangrene, loss of hair to the limb, shiny, pale hairless skin on shin, dusky coloured foot, cool to touch, thickened toe nails, pain in feet and blanching when elevated, delayed capillary refill.

Risk factors for arterial ulcers include ischaemic heart disease, smoking, hypertension, diabetes mellitus, TIA/CVA, MI or angina, rheumatoid arthritis or previous arterial surgery.

Compression bandaging used in treatment of venous leg ulcers is designed to aid venous return. Laplace’s law is that the pressure applied to the limb is determined by the width of the bandage, the degree of overlap and degree and technique of stretch applied (usually both 50%) but this is dependent on the ankle being smaller than the calf. Shortstretch bandaging is different in that it is applied at 100% stretch.

  • 80% of leg ulcers are venous
  • Venous ulcers are caused by chronic venous insufficiency; pooling in the leg leads to venous congestion, leading to fluid being forced out of the vessel and into the surrounding tissues as oedema.
  • Erythrocytes leaking through into the tissue can stain the leg, a symptom of chronic venous disease.
  • Oedema can also be caused or exacerbated by renal or cardiac conditions, and therefore their involvement needs to be ascertained as part of care planning.
 

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Stages of Migraine

  • Pre-headache: changes in mood, energy levels, appetite and behaviour. Aches and pains can sometimes happen hours before a migraine
  • Aura: flashes of light or blind spots, difficulty focusing, seeing things as if through a broken mirror. This phase can last between 15 minutes and one hour.
  • Headache: pulsating or throbbing pain on one side of the head. Sometimes there can also be nausea and vomiting, sensitivity to bright light and loud sounds, and a strong desire to lie in a dark room. This can last up to 72 hours.
  • Resolution: gradual fade away. Being sick can sometimes bring the migraine to an abrupt end. Sleep often relieves symptoms.
  • Recovery: can include exhaustion and weakness.

Taken from Independent Nurse 5/9/2011 p36

 
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Posted by on March 13, 2012 in Chronic conditions

 

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Triggers for Migraines

  • Routine changes
  • Stress
  • Sleep
  • Caffeine
  • Hormone changes (women)
  • Environment
  • Computer screens
  • Particular foods
  • Lack of food
  • Additives
  • Alcohol
  • Cheese
  • Dehydration
  • Drugs
  • Exercise
  • Oral contraceptives
  • Grinding teeth

Taken from Independent Nurse  5/9/2011 p37

 
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Posted by on March 13, 2012 in Chronic conditions

 

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Thyroid

Thyroid hormones affect basal metabolic rate, regulate long bone growth, affect protein synthesis, and promote neuronal maturation.

The thyroid gland also develops the nervous system, increases metabolism of carbohydrates, affects heart beat by increasing the number of beta-adrenergic receptors, whilst also affecting the force of the heart’s contractions by affecting the proportions of cardiac proteins, thyroid also stimulates consumption of oxygen by metabolically active tissues including the brain, pituitary, spleen, lymph nodes, and increases metabolic rate.

The thyroid gland weighs approximately 20g and is therefore one of the largest endocrine glands. It is larger in females than males.

The gland itself is a butterfly shaped gland with the two lobes joined in the lower centre by the ‘isthmus’ a band of thyroid tissues. It is situated beneath the laynx and extends from vertebra C5 to T1. it is contained within the perithyroid sheath, the ligament of Berry attaches it to the cricoid cartilage.

The thyroid gland contains spherical follicles which contain walls consisting of a layer of cuboidal epithelial cells. The lumen of each follical contains thyroglobulin, a protein – thyroid hormones bind to this.

Blood supply is by the bilateral carotid arteries, the supercriothyroid artery and subclavian system. Venous drainage occurs through the superior, middle and inferior thyroid veins.

The gland has both sympathetic and parasympathetic autonomic nerves. The exterior laryngeal nerve is a branch of the vagus nerve which supplies the cricothyroid muscle. Damage to this nerve affects speech.

The parathyroid glands are situated on either side of the thyroid gland. Parathyroid hormone and vitamin D regulates concentrations of calcium and phosphorus. The thyroid gland produces triodothyronine (T3) and thyroxine (T4) which have a role during development and metabolic homeostasis in adults.

T4 is only produced in the thyroid gland. 80% of T3, however, is prodced when T4 is concerted to T3 in the peripheral tissues. Only 20% of T3 comes from the thyroid gland itself. Synthesis of thyroid hormone depends on adequate intake of dietary iodine.

Thyroid hormone sysnthesis is also dependent on TSH which is produced in the anterior lobe of the pituitary gland. Thyroid hormones attach to thyroglobulin in the thyroid follicles.

TRH (thyrotropin releasing hormone) is generated in the hypothalamus and with TSH increases the secretion of T3 and T4 in the thyroid gland. When TRH increases, so does the secretion of TSH. As T3 and T4 increase, the secretion of TSH an TRH decreases.

TSH is an accuate test as levels of TSH are dramatically affected by changes in T3 and T4. if TSH is found to be abnormal, circulating thyroid hormone levels must be checked to consider hyper or hypo thryoidism.

Thyrotoxicosis is caused by abnormally high levels of circulating T3 and T4, and is generally caused by hyperthyroidism. This is often treated by radioactive iodine to slow the hormonal production, or anti-thyroid drugs to prevent synthesis of thyroid hormones. If this is ineffective partial or total removal of the thyroid gland may then be reconsidered.

Graves disease is charactised by thyrotoxicosins, infiltrative opthalmopathy and infiltrative dermopathy. It is more common in women than men and most prevalent in people between 20-40 years. Generally the thyroid gland is enlarged in such cases. Graves disease is indicated with raised serum T3 and T4 and decreased TSH.

Hyperthyroidism often manifests as tachycardia, weight loss, thyroid hypertrophy, tremors, muscle weakness, lower extremity oedema.

Goitres are generally caused by dietary iodine deficiency (found in eggs, fish, seaweed and cheddar cheese). It leads to a rise in TSH.

 
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Posted by on March 13, 2012 in Chronic conditions

 

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