Nursing diagnosis for anaemia

Nursing diagnosis for anaemia

1. ENDOCRINE DISORDERS

2. INTRODUCTION The endocrine system consists of a series of endocrine glands and special cells which manufacture hormones and pass them directly in to the blood stream. Hormones are chemical messengers .When released into the blood, exert important regulatory effects on the metabolism and function on the cells of the body

3. The Endocrine Glands Include- 1 pituitary gland -1 thymus gland 1 thyroid gland -2 ovaries 4 parathyroid glands 2-testes 2 adrenal glands I islets of langerhans 1 pineal gland

4. Endocrine system

5. The pituitary gland Anterior lobe TSH : thyroid-stimulating hormone ACTH: adrenocorticotropic hormone FSH: follicle-stimulating hormone LH: luteinizing hormone GH: growth hormone PRL: prolactin MSH: melanocyte-stimulating hormone Posterior lobe ADH: antidiuretic hormone Oxytocin

6. The hypothalamus controls secretion of hormones which in their turn control the secretion of hormones by the thyroid gland, the adrenal cortex and gonads: in this way the brain controls these endocrine glands TRH (thyroid releasing hormone) -----turns on* TSH CRH ( corticotropin releasing hormone) -----turns on ACTH GnRH (gonadotropin releasing hormone) ---turns on FSH and LH PRF (prolactin releasing hormone) -----turns on PRL GHRH (growth hormone releasing hormone) ----turns on GH Inhibiting hormones of hypothalamus PIF (prolactin inhibiting factor) -----turns off PRL GH (growth hormone) inhibiting hormone ---turns off GH

7. So what do the pituitary hormones do? TSH stimulates the thyroid to produce thyroid hormone ACTH stimulates the adrenal cortex to produce corticosteroids: aldosterone and cortisol FSH stimulates follicle growth and ovarian estrogen production; stimulates sperm production and androgen-binding protein LH has a role in ovulation and the growth of the corpus luteum; stimulates androgen secretion by interstitial cells in testes 7

8. The others from the anterior pituitary… Growth Hormone (somatrotropic hormone) stimulates growth of skeletal epiphyseal plates and body to synthesize protein Prolactin stimulates mammary glands in breast to produce milk Melanocyte Stimulating Hormone stimulates melanocytes; may increase mental alertness 8

9. From the posterior pituitary ( neurohypophysis ) ADH (antidiuretic hormone or vasopressin) stimulates the kidneys to reclaim more water from the urine, raises blood pressure Oxytocin prompts contraction of smooth muscle in reproductive tracts, in females initiating labor and ejection of milk from breasts 9

10. Thyroid gland Anterior neck on trachea just inferior to larynx Two lateral lobes and an isthmus Produces two hormones Thyroid hormone : tyrosine based with 3 or 4 iodine molecules T4 (thyroxine) and T3 Calcitonin involved with calcium and phosphorus metabolism 10

11. Some Effects of Thyroid Hormone (Thyroxine) Increases the basal metabolic rate The rate at which the body uses oxygen to transform nutrients (carbohydrates, fats and proteins) into energy Affects many target cells throughout the body; some effects are Protein synthesis Bone growth Neuronal maturation Cell differentiation 11

12. The Effects of Calcitonin Secreted from thyroid parafollicular (C) cells when blood calcium levels are high Calcitonin lowers Ca++ by slowing the calcium-releasing activity of osteoclasts in bone and increasing calcium secretion by the kidney Acts mostly during childhood 12

13. The Parathyroid Glands Most people have four On posterior surface of thyroid gland (sometimes embedded) 13

14. Parathyroid gland Chief cells produce PTH Parathyroid hormone, or parathormone A small protein hormone

15. Function of PTH (parathyroid hormone or “parathormone”) Increases blood Ca++ (calcium) concentration when it gets too low Mechanism of raising blood calcium Stimulates osteoclasts to release more Ca++ from bone Decreases secretion of Ca++ by kidney Activates Vitamin D, which stimulates the uptake of Ca++ from the intestine Unwitting removal during thyroidectomy was lethal Has opposite effect on calcium as calcitonin (which lowers Ca++ levels) 15

16. Adrenal (suprarenal) glands (“suprarenal” means on top of the kidney)

17. Adrenal Gland Adrenal cortex Secretes lipid-based steroid hormones, called “corticosteroids” – “ cortico ” as in “cortex” MINERALOCORTICOIDS Aldosterone is the main one GLUCOCORTICOIDS Cortisol (hydrocortisone) is the main one Adrenal medulla Secretes epinephrine and norepinephrine 17

18. Aldosterone , the main mineralocorticoid Secreted by adrenal cortex in response to a decline in either blood volume or blood pressure (e.g. severe hemorrhage) Is terminal hormone in renin-angiotensin mechanism Prompts distal and collecting tubules in kidney to reabsorb more sodium Water passively follows Blood volume thus increases 18

19. C cortisol , ( glucocorticoid) It is essential for life Helps the body deal with stressful situations within minutes Physical: trauma, surgery, exercise Psychological: anxiety, depression, crowding Physiological: fasting, hypoglycemia, fever, infection Regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions including water balance 19 People with adrenal insufficiency: these stresses can cause hypotension, shock and death: must give glucocorticoids, eg for surgery or if have infection, etc.

20. Cortisol, continued Keeps blood glucose levels high enough to support brain’s activity Forces other body cells to switch to fats and amino acids as energy sources Catabolic: break down protein Redirects circulating lymphocytes to lymphoid and peripheral tissues where pathogens usually are In large quantities, depresses immune and inflammatory response Used therapeutically Responsible for some of its side effects 20

21. Hormonal stimulation of glucocorticoids HPA axis (hypothalamic/pituitary/adrenal axis) With stress, hypothalamus sends CRH to anterior pituitary (adenohypophysis) Pituitary secretes ACTH ACTH goes to adrenal cortex where stimulates glucocorticoid secretion Sympathetic nervous system can also stimulate it Adrenal cortex also secretes DHEA (dehydroepiandrosterone) Converted in peripheral tissues to testosterone and estrogen (also steroid hormones) Unclear function in relation to stress 21

22. The Pineal Gland At the end of a short stalk on the roof of the diencephalon Pinealocytes with dense calcium particles Can be seen on x-ray (because of Ca++) Melatonin helps regulate the circadium rhythm The biological clock of the diurnal (night/day) rhythm Complicated feedback via retina’s visual input 22

23. The Pancreas Exocrine and endocrine cells Acinar cells (forming most of the pancreas) Exocrine function Secrete digestive enzymes Islet cells (of Langerhans ) Endocrine function 23

24. The Pancreas Exocrine and endocrine cells Acinar cells (forming most of the pancreas) Exocrine function Secrete digestive enzymes Islet cells (of Langerhans ) Endocrine function 24

25. pancrease Alpha cells: secrete glucagon raises blood sugar mostly in periphery Beta cells: secrete insulin lowers blood sugar central part (are more abundant) Also rare Delta cells:secrete somatostatin inhibits glucagon

26. 26 The Gonads (testes and ovaries) main source of the steroid sex hormones Testes Interstitial cells secrete androgens Primary androgen is testosterone Maintains secondary sex characteristics Helps promote sperm formation Ovaries Androgens secreted by thecal folliculi Directly converted to estrogens by follicular granulosa cells Granulosa cells also produce progesterone Corpus luteum also secretes estrogen and progesterone

27. 27 Pathology Pituitary Gigantism –too much GH in childhood Acromegaly – too much GH in adulthood Pituitary dwarfs – too little GH in childhood Diabetes insipidus - too much ADH Pancreas Diabetes mellitus – one type of insulin (not enough) Thyroid Hyperthyroidism, commonest is Grave’s disease (autoimmune) Hypothyroidism In childhood leads to cretinism Endemic goiter from insufficient iodine in diet Adult hypothyroidism (myxedema): autoimmune

28. 28 Pathology, continued Adrenal gland Cushing’s syndrome . Usually caused by an ACTH-secreting pituitary tumor Rarely by tumor of adrenal cortex Iatrogenic Addison’s disease Hyposecretion (under secretion) of adrenal cortex Usually involves cortisol and aldosterone : low blood glucose and sodium, severe dehydration, fatigue, loss of appetetie , abdominal pain.

29. 29 Exophthalmos of Grave’s disease Enlarged thyroid (goiter) from iodine deficiency

30. 30 Before and after onset of Cushing’s disease After Before

31. Pituitary conditions include Gigantism –too much GH in childhood Acromegaly – too much GH in adulthood Pituitary dwarfs – too little GH in childhood Diabetes insipidus - too much ADH Hypopituitarism Hyper prolactinaemia hypopituitarism

32. HYPERPITURISM This is a condition in which there is over secretion of hormones of the pituitary gland. This presents with various conditions and syndromes in other hormones This may include; Acromegaly due to excess GH Cushing’s syndrome due excess ACTH Secondary hyperthyroidism due to excess TSH Precocious puberty due to excess FSH and LH

33. Conti… The clinical features and management are discussed under each condition or syndrome later in the text

34. GIGANTISM This is a condition in which there is hypersecretion of growth hormone in childhood . Before closure of epiphyses of long bones i.e. before ossification of bones is complete. Occurs mainly in childhood and adolescents. Usually caused by tumors especially adenomas of the pituitary gland. Diagnosis is made when the blood growth hormone level is high

35. pathophysiology There is excessive production of growth hormone leading to delayed epiphyseal closure with extended growth period. There is tremendous increase in size of bones that lead to formation of giants whose height is 8 feet or more These giants tend to have short lifespan, die early life They develop signs of increased intracranial pressure from the tumor and are also subjected to infection

36. pathophysiology There is excessive production of growth hormone leading to protein synthesis in many tissues ,increase the breakdown of fatty acids in adipose tissue ,increase in glucose level and delayed epiphyseal closure with extended growth period. There is tremendous increase in size of bones that lead to formation of giants whose height is 8 feet or more These giants tend to have short lifespan, die in early life They develop signs of increased intracranial pressure from the tumor and are also subjected to infection

37. diagnosis Exams and tests CT scan or MRI scan of the head showing pituitary tumor High prolactin levels Damage of pituitary may lead to low levels of other hormones e.g. Cortisol, estradiol(girls),testorone (boys) ,thyroid hormone

38. Medical management Medications to reduce growth hormone release ,block the effects of growth hormone or prevent growth in stature e .g Dopamine agonist like bromocriptine mesylate, carbagoline( dostinex ) They reduce growth hormone release GH antagonist ,pegvisomant (somavet) –blocks effect of GH Sex hormones therapy e.g. estrogen and testosterone may inhibit growth of long bones Somatostatin analogs e.g. octreotide ,somatuline which reduce GH release

39. management Prepare and assist in investigations e.g. blood for GH , scan of the skull. Administer drugs as prescribed e.g. dopamine antagonists e.g. Bromocryptine inhibit the release of GH Closely monitor vital signs Reassure the patient and relatives Surgical management involves resection or removal of pituitary gland and is indicated if; There is no improvement in medical treatment Intracranial pressure is causing blindness

40. Conti… Prepare the patient for theatre Provide post- operative care to include ; When receiving the patient from theatre , check pulse respiratory, level of consciousness and bleeding from the operated site. Put the patient in bed and observe ¼ hourly till fully awake Maintain IV fluids and keep accurate input output charts If BP is low, give the patient hydrocortisone IV Observe the limbs and pupils for movement Observe for any fits and report to the doctor Provide care of pressure areas Encourage early ambulation Start the patient on oral feeding once able to swallow

41. Conti… Give medication as prescribed Remove alternate sutures and all by 7 th day If the patient is in a radiotherapy, observe for side effects Provide adequate diet , fluids and rest Provide health education to include compliance with treatment since it is for lifetime. other treatment include radiation of the pituitary gland-less recommended due to side effects e.g. obesity, emotional impairment, and learning disabilities

42. complications Delayed puberty Difficulty functioning in every day due to large size and un usual features Diminished vision or blindness Embarassment,isolation,difficulties with relationship and other social problem Hypothyroidism Severe chronic headache Sleep apnea

43. ACROMEGALLY This is a condition in which there is overproduction of growth hormone which starts in adulthood after complete ossification of the bone (30-40 years). It may be due to growth hormone secreting tumors in the pituitary gland or over secretion of growth hormone releasing factor from the hypothalamus. There is marked overgrowth of soft tissue and bone.

44. Predisposing factors/ causes Growth hormone secreting tumors of pituitary gland Over secretion of growth hormone release factor (GHRF)

45. pathophysiology existence of a secreting pituitary tumor causes over secretion of GH arising after bones have ossified causing widening or enlargement of bones, over growth of many tissues e.g. face, hands, feet, and enlargement of viscera but there is no increase in height of bones. Signs and symptoms Enlargement of lower jaw (pragmatism) causing teeth gapping. Progressive enlargement of feet and hands and become spade-like paresthesia

46. Conti… Hypertrophied tongue Joint and back pains Face enlarges with thick lips, nose ears and supraorbital ridges causing prominent forehead Bow legs due to thickening of muscles Osteoporosis and degenerative, arthritis, headache , nausea and vomiting due to increase in ICP caused by the tumor Visual disturbances due to pituitary tumor involving the optic nerve leading to blindness. Lowered libido importence in men and amenorrhea in women

47. Conti… Hoarseness of voice due to thickening of vocal cords Raised BP Muscle weakness Reduced carbohydrate tolerance leading to diabetes Thick course skin Enlarged liver, heart ,glands

48. investigations Visual field test Assessment of other pituitary hormones- prolactin, adrenal, thyroid and gonadal hormones. MRI scan of pituitary and hypothalamus cardiac assessment-ECG

49. management Admit the patient and ensure comfort Take the vital signs of the patient and monitor closely Reassure the patient and relatives to allay anxiety Prepare and assist in investigations e.g. pain skull, x-ray CT scan of the skull. Give medication as prescribed e.g. dopamine antagonists e.g. L-dopa, bromocriptine 5-30mg; somatostatin to suppress GH Radioactive seeds may be planted in pituitary fossa to destroy the tumor

50. Conti… Surgical management involving resection or selective removal of pituitary gland tumor. It is indicated if ; There is no improvement on medical treatment There is involvement of optic nerve leading to blindness Provide the general preoperative care to the patient After the operation, the preoperative care is like for gigantism Provide health education to the family for continued care Discharge the patient home through MOPC or SOPC for follow up

51. complications Cardiac failure Diabetes mellitus Blindness o steoporosis and pathological fractures Hoarseness of voice Degenerative arthritis Impotence in men Amenorrhea in women

52. prognosis Patients often have DM but often die of cardiac failure. The disease causes changes in body growth which are irreversible even if the disease is arrested

53. DWARFISM This is a condition that result from decreased secretion of growth hormone in childhood causing short stature. Predisposing factors Metabolic factors Disease of bones Inability of hypothalamus to produce GH Congenital heart disease Genetic and familial factors

54. HYPOPITUITARISM This is a condition in which there is decreased secretion of pituitary gland hormones which are atrophic, i.e. they target other cells. It therefore results in failure of thyroid, adrenal, gonads gland to produce hormones. This will therefore present with features of diminished functions of these glands It is rare but affects females more than males.

55. causes Atrophy of anterior lobe of pituitary gland Tumors from the brain pressing on pituitary glands Infections of the brain e.g. meningitis, syphilis, TB etc. Vascular incision of pituitary gland Radiotherapy Congenital lesions of the hypothalamus Idiopathic Congenital Growth hormone deficiency

56. Clinical features Depends on the region of lesion presenting differently Deficiency of gonadotrophins will lead to: Decreased libido Impotence Extreme weight loss Failure to establish lactation in females Reduced menstrual flow ( oligomenorrhoea) Atrophy of genital organs with sparse pubic hair Hair loss Reduced metabolic rate Amenorrhea hypoglycemia

57. Conti… Deficiency of adrenal hormone will lead to; Patient can not withstand stress Reduced electrolyte Na+, K+ and Ca+ Reduced secretion of thyroid stimulating hormone Bradycardia Slurred speech Dry brittle hair Reduced body metabolic rate Weakness and apathy Extreme weight loss and due to hypothyroidism

58. diagnosis Thyroid function test Adrenal function test Gonadotrophin levels in blood

59. management Give the patient the lacking hormone Start the patient on cortisol therapy e.g. hydrocortisone 50mg and adjust according to patient needs. Observe the patient for weight gain whether he is lethargic Give ADH (vasopressin) to regulate water loss in renal tubules Thyroxine given 0.1 – 0.15mg od to replace thyroid hormones. Never give thyroxine to patient with adrenal insufficiency until they are protected by cortisone , (Addison crisis) Deficiency of sex hormone can be given testosterone oral or injectable at the dose of 250-500mg.

60. Conti… You can also put implants discharging the hormones but the body should be monitored on its concentration. Women are given hormonal drugs e.g. Ethyl-estradiol 20-30ug od*3/52. Give progesterone preparations at the dose of 5mg daily If there is tumor, the patient is treated with radiotherapy or the tumor is removed surgically. Do reversed barrier nursing to these patients Observe the patients closely for side effects of these drugs

61. HYPERPROLACTINAEMIA This is a condition in which there is excessive secretion of prolactin commonly associated with pituitary adenomas. Clinical features Amenorrhea Infertility Galactorrhea Loss of libido and fertility in men

62. causes Pituitary adenomas Destructive lesions of the hypothalamus Pressure on the pituitary stalk interfering with transport of dopamine to the anterior pituitary. Treatment with drugs that alter endogenous dopamine turnover or with dopamine receptor antagonist e.g. methyldopa ,metoclopramide, reserpine. Pregnancy leads to physiological hyperprolactinaemia

63. Management This can be controlled by administering dopamine agonists e.g. Bromocryptine, L-dopa.

64. DIABETES INSPIDUS This is a disorder in which the posterior lobe of pituitary gland produces insufficient or no ADH. There is excessive amount of dilute urine with low specific gravity. Types of diabetes insipidus Cranial diabetes insipidus- there is disorder in the hypothalamus leading into inadequate production of ADH. Nephrogenic diabetes insipidus- the ADH is produced but the renal tubules are not responsive to it.

65. causes Cranial diabetes insipidus Pituitary tumor Chronic infection e.g. meningitis Surgery (hypophysectomy) Genetic defects Cranial defects Cranial phariangioma Idiopathic factors

66. Causes Nephrogenic diabetes insipidus Genetic defects Metabolic disorders e.g. hypokalemia Drug therapy e.g.. A thium salts Poisoning with heavy metals e.g. mercury and lead

67. Clinical features Cranial diabetes insipidus Nephrogenic diabetes insipidus Polyuria polydipsia Dilute urine low specific gravity Loss of body weight Constipation dehydration anorexia Fatigue and anxiety Low blood

68. management Carry out investigation to identify cause and correct it. e.g. ultrasound, MRI, CT scan Give drugs to increase water reabsorption at the renal tubules e.g. desmopressin 10-100ug bd In severe cases, give desmopressin at intervals of 36-40 hours usually evening to ensure maximum reabsorption. Other drugs include desmopressin renal spray short acting Chloral opromide (diabenese) PO125-250mg daily to enhance renal responsiveness to ADH

69. Conti… Observe for signs of hypoglycemia since treatment is given when there is hyperglycemia. If there is tumor, prepare and take the patient for surgery Encourage the patient by giving health education.

70. SYNDROME OF INNAPROPRIATE ADH SECRETION This is a syndrome in which there is excessive secretion of ADH. It leads to water retention with resultant hyponatremia and hypoosmolarity. Causes Ectopic secretion of ADH by oat cell carcinoma of the lungs Meningitis Subarachnoid hemorrhage following head injury Pneumonia Patients on mechanical ventilation

71. management Bed rest Position to promote good venous return 2 hourly turn to prevent bed sores Restrict fluids intakes Anti seizure Assist with ambulating and provision of hygiene

72. THE THYROID GLAND THE THYROID GLAND

73. HYPERTHYROIDISM This refers to excess exposure of the body to amount of thyroid hormones. Causes Graves disease Multinodular goiter Solitary active nodule (toxic adenoma) Sub acute thyroiditis/ post partum thyroiditis Excess stimulation of thyroid gland by TSH Hydatiform mole choriocarcinoma –HCG from the placenta stimulates thyroid gland. Metastasis/ cancer of thyroid tissue

74. GRAVES DISEASE This is diffuse enlargement of thyroid gland mainly due to TSH receptor antibody. There is overproduction of thyroid hormone due to production of antibodies which will act as TSH binding with thyroid gland and make the gland enlarged with increase of T3 and T4 production.

75. Clinical features Diffuse goiter GIT – anorexia, vomiting, diarrhea, stearrtorrhoea Cardiac - palpitations, tachycardia, angina, cardiac failure. Respiratory – dyspnea on exertion, exacerbation of asthma Skin - purititis, alopecia , pretibial myoedema . Eyes - diplopia, retraction of eyelids, excessive lacrimation, exophthalmos. Neuromuscular - emotional irritability, psychosis, aggitiation muscle weakness, increase tender reflex

76. Conti… Reproductive - impotence, libido, spontaneous abortion, oligo- menorrhea, amenorrhea, infertility. Heat intolerance Osteoporosis Weight loss

77. GOITRE This is a condition in which there is enlargement of the thyroid gland. It is more common in women than in men. There are 3 main types namely; non- toxic goiter (simple) Toxic goiter Malignant goiter Causes Deficiency of iodine in the diet Lack of TSH in pituitary gland Over production of T4 caused by toxic /malignant goitre

78. Predisposing factors Hereditary factors Tumors of thyroid gland Goitrogens .(substances that disrupt production of thyroid hormones by interfering with iodine uptake triggering release of TSH ) e.g cassava , soya beans salicylates, sulfonamides Emotional stress Trauma of thyroid gland

79. SIMPLE /NON-TOXIC GOITRE In this type of goiter, the thyroid gland enlarges without symptoms of thyroid dysfunction. Causes Deficiency of iodine in the diet Inability of the thyroid gland to use iodine Increased demand for iodine e.g. during pregnancy , stress Goitrogens e.g. carrots, sulfonamides, salicylates

80. Signs and symptoms Painless swelling on the neck that moves up and down when swallowing. Dysphagia Dyspnea and stridor Cough Hoarseness of voice Engorged neck veins anxiety

81. Treatment and management In most cases, this type needs little treatment since the goitre subsides on its own Give foods rich in iodine to correct iodine deficiency Add iodine to table salt If due to goitregen foods, exclude them from diet If due to drugs, avoid them if possible Do thyroidectomy if the gland is grossly enlarged

82. MALIGNANT GOITRE This may develop from toxic goiter Signs and symptoms Enlarged thyroid gland Dyspnea Dysphagia Stridor Firm and hard painful gland

83. treatment Surgical removal of the whole gland (thyroidectomy) Radioactive iodine treatment may follow surgery

84. TOXIC GOITRE This type of goitre is common in young women. There are two forms of toxic goitre Toxic multinodular goitre Diffuse/Exophthalmic goitre TOXIC MULTINODULAR GOITRE This type of goiter is usually accompanied by tumor formation which may be single tumor or multiple tumors which are likely to become malignant goitre Occurs in people who have a previous history of longstanding non-toxic goitre. The patient usually has pronounced cardiovascular symptoms

85. Conti… b) DIFFUSE/ EXOPHTHALMIC GOITRE This is an autoimmune or genetic components of the disease or related to severe emotional stress.

86. pathophysiology The thyroid gland overactive resulting in excess amount of thyroid hormone released to the tissues and this accelerates metabolic activity in the body. There is more oxygen and energy use leading to high heart output Signs and symptoms Enlarged thyroid gland Excessive appetite Alert and irritable Nervousness

87. Conti… Anxiety and restlessness Diarrhea and vomiting Hoarseness of voice Rapid irregular pulse Protruding of eye balls (exophthalmos) Diastolic pressure but systolic remains normal Body weakness Fluctuating emotional moods Weight loss Fine tremors of the fingers Heat intolerance

88. Conti… Breathlessness Moist skin Excessive sweating Dysphagia Palpitations with dyspnea Raised basal metabolic rate (BMR) Atrial fibrillation

89. diagnosis From clinical features Raised blood thyroxine levels Raised BMR

90. management Admit and nurse the patient in a quiet room to ensure rest Sedate the patient with phenobarbital 30mg tds and restrict visitors into the room. Take vital signs 4 hourly and report any abnormality. In case of tachycardia, administer digoxin. Prepare and assist in investigations e.g. CXR , blood for circulating T4, blood for BMR, biopsy if malignancy is suspected.

91. Conti…. Administer drugs as prescribed Non-toxic goiter give thyroxine 50-150mg od*6/12 Toxic –carbimazole 150 mg 24/52 then reduce the dose late to maintain … state -propranolol – 60-40mg in 3 divided doses daily Lactating mothers are not given ant- thyroid drugs while pregnant women are given with caution it affects intra uterine growth of the foetus Encourage intake of a lot of sugar and oral fluids Provide comfort by changing linen at right timedue to excessive sweating Give diet rich in proteins, vitamins, minerals and calories to compensate energy being used by the increased metabolism.

92. Conti… For patients contraindicated for surgery and medical treatment is not suitable, give radioactive iodine treatment Maintain good personal hygiene by giving daily bath to prevent infection. If the condition improves, discharge the patient through MOPC Prepare the patient for surgery Indications for thyrodectomy. Increase in size of the gland Substantial malignancy Increase pressure symptoms Thyrotoxicosis patients not responding to medical treatment Operation done may be partial or total thyroidectomy

93. pre –op management of thyrodectomy Before surgery, patients need a period of treatment to return their thyroid hormones to normal to prevent risk of thyroid storm and hemorrhage after surgery. Carbimazole is given for several weeks and stopped 10 days before surgery Administer the following pre-operatively Glucose iodine 0.3-0.9ml p.o tab*10 14/7 Propranolol 120-160mg od Valium 5mg note to quieten patient and ensure sleep Digoxin 0.25mg if there are trial fibrillations

94. Conti… Carry out investigations to include X-Ray of trachea and thoracic inlet, blood for serum thyroxine, blood for GXM post operative care after thyrodectomy. Checking respiratory pulse, level of consciousness , bleeding from the operation site Nurse the patient with the head deviated and supported with pillows neck slightly flexed to avoid strain on suture line. if there is blood transfusion, observe ¼ hourly. Maintain IV fluids running well Nurse that patient in sitting up position

95. Cont` thyrodectomy Take care of drainage tubes and observe for any blockage , internal bleeding and formation of hematoma indicated by(cyanosis) tachycardia, dyspnea, restlessness). If any noted, inform the doctor for insertion of endotracheal tube (ETT) or tracheostomy Report any changes in voice hoarseness , inability to speak because they may be due laryngeal nerve injury, or vocal voice paralysis. Patient should minimize talking. Check for tremors, numbness, tingling sensation in extremities which may be due to removal of parathyroid gland leading to tertiary tetany

96. Conti… Watch for repeated clearing of the throat or for complaint of smothering or difficulty swallowing, which may be early signs of hemorrhage Remove drainage tubes 2 nd post operative day Remove alternate stitches on 3 rd day and the rest on 4 th ad 5 th day

97. Conti… If observation e.g. pulse rate are normal, no heart problem, and would has healed well, discharge the patient through SOPC Patients who have undergone total thyroidectomy are put on thyroid drugs for life so encourage on drug compliance at home. Complications of thyroidectomy Hemorrhage Laryngeal paralysis Voice coarseness Myxedema Thyroid storm or crisis

98. Conti… Teary due to removal of thyroid gland Infection Keloids

99. Complications of goiter (toxic) Susceptible to infections Metastasis to other parts of the body Malignancy Congestive cardiac failure (CCF) Protruding eye balls (exophthalmos)

100. GRAVES DISEASE This is diffuse enlargement of thyroid gland mainly due to TSH receptor antibody. There is overproduction of thyroid hormone due to production of antibodies which will act as TSH binding with thyroid gland and make the gland enlarged with increase of T3 and T4.

101. Clinical features Diffuse goiter GIT – anorexia, vomiting, diarrhea, stearrtorrhoea Cardiac- palpitations, tachycardia, angina, cardiac failure. Respiratory – dyspnea on exertion, exacerbation of asthma Skin- purititis, alopecia , pretibial myoedema . Eyes- diplopia, retraction of eyelids, excessive lacrimation, exophthalmos. Neuromuscular- emotional irritability, psychosis, aggitiation muscle weakness, increase tender reflex

102. Conti… Reproductive- impotence, libido, spontaneous abortion, oligo- menorrhea, amenorrhea, infertility. Heat intolerance Osteoporosis Weight loss Mangement Similar to that of goitre in addition to: Give antithyroid drugs eg carbimazole,methimazole,propylthiouracil to make patient euthyroid

103. Management of graves disease Sub total thyrodectomy can be done Withdraw antithyroid drugs 10-14 days before surgery and put patient on potassium iodide 170mg daily to make the gland less vascular and firm for operation Radio active iodide used to destroy cells in the thyroid gland Dress any wounds with corticosteroids In case there is excessive lacrimation use tinted glasses

104. THYROIDSTORM It is a life threatening complication of hyperthyroidism that results from a sudden increase in thyroid hormone levels in blood following thyroidectomy. It occurs after surgery in patients who were poorly prepared. Signs and symptoms High temperature (fever) Increased metabolic rate Vomiting Low BP Confusion Atrial fibrillation Profuse sweating

105. Conti… Rapid pulse Anxiety Dehydration Tachycardia Patient may collapse and die

106. management Administer oxygen by mask Give antipyretics to lower the body temperature Start the patient on IV fluids to correct dehydration Give hydrocortisone and narcotic drugs Give sodium iodopodate to prevent release of thyroid hormone from the gland After 2/52 withdraw sodium iodopodate and continue with carbimazole

107. HYPOTHYROIDISM This is a condition in which there is low or depressed levels of thyroid hormone. It presents as cretinism in children and myxedema in adults. Causes Spontaneous atrophy Following treatment with radio iodide Congenital hypothyroidism Sub acute thyroiditis Drug- induced e.g. lithium Dyshormonogenesis due to lack of enzyme necessary for form action of hormones Following surgery

108. Conti… Clinical features Constipation Anemia Bradycardia Depression Tendon reflexes decrease Weight gain Angina Hypertension Cardiac failure Decreased libido

109. Conti… Dry skin Impotence Infertility Amenorrhea Alopecia Non pitting oedema (myxedema)

110. Conti… investigations Measure T4 and levels (T4 and T5H). T3 not measured Management Do hormonal replacement of T4 ( thyroxine tabs 150mg od for life Complications Myxedema coma

111. CRETINISM This is a condition in which there is lack of thyroid activity from childhood resulting into lack of physical growth and mental development. Clinical features May present with congenital absence of thyroid gland Retarded physical growth and mental development Disproportionally short limbs Large protruding tongue Coarse dry skin Poor abdominal muscle tone Umbilical hernia Early RX can lead to complete cure

112. MYXOEDEMA This is a condition resulting from insufficient thyroid activities in adults due to the loss or destruction of thyroid gland tissues It is a complication of hypothyroidism. Causes Surgical removal of thyroid gland in thyrotoxic and malignant goitre Primary atrophy of thyroid gland ( autoimmune process) Radioactive iodine in therapy of exophthalmic goitre Severe and prolonged iodine deficiency Chronic thyroiditis Anti thyroid drugs and those containing iodine, e.g. lithium carbonate Failure of primary pituitary glands to secrete TSH Hypothermic effect of production of TSHRF

113. Conti… Pathophysiology Deficiency in thyroid hormone leads to decrease in basal metabolic rate. Fat mobilization from the tissues is impaired and cholesterol level is high. Vasodilation of peripheral vessels occurs and this lowers cardiac output leading to cardiomegaly. Metabolism of carbohydrates, fat and proteins are affected.

114. Conti… Signs and symptoms Anemia Constipation Chronic headache Hypersomnia Decreased libido Wrinkled scalp Deep hoarse voice Swelling of the face puffy eyelids and thick nostrils Dull and sluggish mentally

115. Conti… Slurred speech Bradycardia Slow movement Cardiomegaly Slow relaxation of tendon reflexes Increased sensitivity to cold Amenorrhea or menorrhagia Weight gain with low appetite Muscle pain Dry coarse thickened skin

116. Conti… Non-pitting oedema Dry coarse hair that tends to fall Irritability Low temperature Loss of memory (confusion) Numbness and tingling of arms and legs

117. Conti… Investigations Protein bound iodine is low Blood analysis- low thyroxine level, high cholesterol, low BMR LCG- enlarged heart with bradycardia

118. Conti… Management Give thyroid hormones e.g. sodium levothyroxine 0.05mg p.o then increase gradually to reach maintenance dose of 0.2-0.3mg daily after 2 weeks Give triiodothyronine (Cytomol) 0.05mg p.o then increase gradually to 0.2mg Observe for side effects of drugs such as tachycardia, dyspnea, sweating, skin rash, palpitations, dizziness, weight loss , pericardial pain, diarrhea Nurse the patient in a warm room and add him live because he has poor tolerance to cold.

119. Conti… Take vital signs and report any abnormality e.g. low temperature Patient to massage the skin with lotion or cream that will prevent it from being dry and course Give diet low in cholesterol To prevent constipation, give diet rich in roughage and have adequate fluid intake. Give antibiotics to treat any infection. Advise the patient to avoid factors that make the condition worse e.g. cold, stress, trauma, infection Give health education to the patient about the condition. Discharge home through MOPC

120. Conti… Complications Hypothermia Anemia Myxedema coma Arteriosclerosis cardiomegaly

121. MYXEDEMA COMA This is a medical emergency due to profound hypothyroidism. It is precipitated by hypothermia, stress, coma or infection. Management Ensure the patient is warm Give the patient thyroxine 2hourly and IV hydrocortisone 100mg Clear IV fluids and maintain fluid balance charts closely monitor vital signs and report any abnormality. Prognosis 50% of patients die while the others take drugs the rest of their life

122. Differences between hyperthyroidism and hypothyroidism hyperthyroidism hypothyroidism 1.Increased basal metabolic rate 1.Decreased basal metabolic rate 2.anxiety, restlessness, excitability 2.Depression, mental slowness 3.tachycardia, palpitations 3. Bradycardia 4.diarrhea 4. constipation 5. Weight loss , good appetite 5. Weight gain , anorexia 6.Hair loss 6. Dry skin with brittle hair 7. Warm sweaty skin, intolerance to heat 7. Dry cold skin prone to hypothermic 8.Oxphthalmos in graves disease 8. Dropping eyelids 9.Treated by ant thyroid drugs e.g. propylthiouracil, B- blockers or thyroidectomy 9. Treated by thyroid hormone replacement 10.Causes are grave disease, thyroid neoplasm 10. Caused by thyroiditis, surgical destruction, iodine deficiency , cretinism or reduced TSH/TRH 11.Goitre occurs 11. Myxedema occurs

123. Parathyroid gland. Functions of calcium in the body include; Stability of nervous excitability Regulation of permeability of cell membranes thus control intracellular metabolism Helps in the formation of bones and teeth It is a factor of clotting in blood

124. HYPERPARATHYROIDISM T his refers to a condition in which there is excessive production of parathyroid hormone. This leads to increase in calcium level in blood by; Increasing osteoclastic activity (bone resorption) thus increase Ca+ Increasing absorption of calcium in renal tubules Increasing absorption of calcium in small intestines Excess of this hormone leads to hypercalcemia

125. types Primary parathyroidism- occurs when there is parathyroid adenoma or tumor leading to excess production of PTH Secondary hyperparathyroidism – occurs due to excessive stimulation of parathyroid glands when there is low Ca+ levels in the blood. Tertiary hyperthyroidism- occurs due to 2o hyperparathyroidism which causes parathyroid gland to increase in size Malignancies Thiazide diuretics

126. Signs and symptoms Presents with signs of hypercalcemia Polyuria Polydipsia Anorexia Constipation Dyspepsia general Fatigue Bone pain and tenderness Calcification of soft tissue Renal calculi Drowsiness Peptic ulceration

127. Conti… Fractures Muscle weakness Hypertension Investigations Urinary levels of Ca2+ Plasma level of Ca2+ Parathyroid levels in blood Phosphate levels in blood

128. Causes Obstruction of blood supply to parathyroid gland during thyroid surgery Pseudo hypoparathyroidism; the parathyroid gland secretes normal levels of PTH but still there is hypocalcemia due to defect in receptor mechanism. Ionizing radiation e.g. iodine in Rx of hyperthyroidism Development auto antibodies to PTH gland Idiopathic Congenital abnormality of the gland

129. management For primary hyperparathyroidism , do surgery to remove all parathyroid tissue. If the tumor can be located, it is only removed For secondary hyperparathyroidism, the patients are dehydrated so require rehydration Administer Bisphosphonates drugs e.g. palmidronate, chodronate and sodium etidronate . They will bind to free Ca 2+ and also inhibit osteoclastic activity. Administer IV fluids together with Lasix to cause forced diuresis which will remove Ca2+ from the blood

130. Conti… In severe cases do hemodialysis Glucocorticoids such as prednisone are given to reduce serum Ca2+ levels.

131. HYPOPARATHYROIDISM This is a condition in which there is deficiency of parathyroid hormone leading to absorption of Ca2+ in the small intestines reduced absorption of Ca2+ in the renal tubules and decreased bone resorption . These leads to hypocalcemia.

132. Signs and symptoms Hyperparathyroidism presents with symptoms of hypocalcemia Tetany (muscle spasms Gradual epilepsy Psychiatric disturbances Brittle nails Bone weakness Paresthesia Development of cataracts

133. investigations Serum PTH will be decreased Serum Ca2+ will be decreased Trousseau's signs – if you tie BP cuff on the upper arm and inflate it above systolic BP, 3 minutes later there will be carpal spasms. Chrostek’s sign- when you press the facial nerve as it emerges on the face, just in the front of the ears there will be facial spasms.

134. Management In acute phase when the patient presents with tetany i.e. generated muscle spasm, give calcium gluconate 20mls IV followed by calcium gluconate 1m If the patient has no tetany, treat hypocalcemia by giving drugs which will increase levels of vitamin D e.g. alfacalcidol, calcitriol, to promote Ca2+ absorption in the small intestines. Protect the patient from injury during convulsions.

135. TETANY This is a condition characterized by high neuromuscular excitation and a great irritability due to reduced serum Ca2+ levels (hypocalcaemia). There are very strong painful spasms of skeletal causing characteristic bending inwards of the hands, fore arm and feet. In children it may present as laryngeal spasms and convulsions.

136. Predisposing factors Hyperparathyroidism Inadequate dietary calcium intake Chronic renal failure with excessive secretion of Ca2+ Removal or injury of parathyroid gland Lack of vitamin D necessary for absorption of Ca2+ in the gut Alkalosis- e.g. metabolic due to vomiting , ingestion of excess alkalis or respiratory alkalosis due to hyperventilation alter calcium. Lack of Na+ absorption like malabsorption syndrome Idiopathic autoimmune response by antibodies against PTH

137. Pathophysiology Deficiency of PTH causes a fall in serum Ca2+ with a great irritability of nerves which is manifested by spasms and twitching of muscles. Signs and symptoms Dysphagia Nausea and vomiting Photophobia due to cataracts Stiffness of hands and feet Numbness and tingling sensation in extremities or around the lips ( paresthesia) Trousseau's sign – when blood supply in the arms if secluded for 3 minutes, there will be carpal pedal spasm which may cause inward bending of arms and feet

138. Conti… Chrostek’s sign- quick touch of facial nerve near the ear produces twitching of facial muscles. Anxiety and irritability Convulsions Bronchospasms with dyspnea Laryngeal spasms leading to stridor and cyanosis Patchy alopecia and loss of eyebrows Nails become brittle and break easily Rickets and osteomalicia Cardiac arrhythmias

139. Conti… Psychosis due to deposition of calcium basal ganglia depression and delirium Coarse dry skin with brown pigment Anxiety and irritability Diagnosis Clinical features Low serum calcium Raised serum potassium Positive chrostek’s sign Low PTH levels

140. management Admit and nurse the patient in a warm room quiet with dim light and with limited movement to minimize neuromuscular excitation and photophobia. Prepare and assist in investigations e.g. blood for Ca2+, BP level X ray to rule out rickets and osteomalicia, administer medication as prescribed e.g. IV calcium gluconate , vitamin D e.g. calciferol 1-5mg daily, parenteral parathormone is given in acute hypoparathyroidism Give sedative e.g. valium to control convulsions / spasm If the patient develops respiratory distress , do tracheostomy or give mechanical ventilation in addition to bronchodilators

141. Conti… Give diet high in calcium and low potassium Closely observe the patient’s vital signs and for convulsions ¼ hourly and report any abnormality. Reassure the patient and relatives to allay anxiety Give health education once the patient stabilizes and discharge him home. Take medication as prescribed and complete the dose How to recognize the side effects of drugs Importance of taking diet with high calcium and low potassium

142. THE PANCREASE

143. DIABETES MELLITUS This is a metabolic disorder affecting glucohydrate metabolism characterized by chronic elevation of glucose concentration in the blood (hyperglycemia) due to inability of the body to produce or utilize insulin hormone.

144. Classification Type 1; Insulin Dependent Diabetes Mellitus (IDDM) It occurs as a result of absence or deficiency in insulin production by beta cells of islets of Langerhans. Usually occurs in the non-obese young adults (less than 40 years) and is associated with ketoacidosis. The patients are insulinogenic and acquire insulin to sustain life. Their urine has sugar and acetone. Type 2 Non-insulin Dependent Diabetes Mellitus (NIDDM) The beta cells produce insulin but there is resistance to action of insulin which may be due to;

145. Conti… Abnormality in insulin receptors Abnormal insulin molecule Excess antagonists of insulin in circulation The age of onset is usually 50 years and occurs mostly in obese people. These patients do not need insulin except when there is hyperglycemia like in the following cases; Ineffective oral hyperglycemia drugs ( persisted polyuria and hyperglycemia)

146. Conti… Ketonuria During distress e.g. when there is infection Other infections e.g. renal failure Type 3 secondary diabetes mellitus Develops as a complication of; Acute and chronic pancreatitis Some drugs e.g. corticosteroids, phenytoin, thiazide diuretics Secondary to other hormonal disturbances involving hypersecretion e.g. GH Pregnancy (gestational diabetes mellitus)

147. Causes of diabetes mellitus Genetic predisposing – insufficient or complete lack of insulin. Infection e.g. chronic pancreatitis, mumps rubella Presence of antibodies that interfere with insulin action i.e. autoimmune reaction that may be triggered by EBV, CMV Trauma in the pancreas Reduced tissue sensitivity to insulin action e.g. in Cushing’s syndrome Conditions that lead to excess production of hormones that antagonize e.g. GH (acromegaly), cortisol ( Cushing’s syndrome) phacochromocytoma.

148. Conti… Drugs e.g. corticosteroids, thiazide diuretics, phenytoin Exposure to cow’s milk at early age. The milk has BSA (Bovine Serum Albumin) structure that is similar to that of B cells that antibodies form against BSA may also destroy B -cells

149. Predisposing factors Obesity – cause impaired ability in tissues to utilize glucose Stress- adrenaline and cortisol produced in stress antagonize insulin Lack of exercises (become obese) Vitamin C deficiency Strain of pregnancy ( insulin demand is increased) Pancreatic diseases e.g. pancreatitis, ca pancreas or pancreatectomy

150. pathophysiology Pancreatic secretion of insulin is stimulated by increase in blood sugar and inhibited by low blood sugar level. Insulin increases utilization of glucose by body cells. It ; Increase glycogenesis in muscles and liver Moves glucose from blood to cellular compartment where it is converted to glycogen and stored (glycogenesis) or used for energy production. When insulin is insufficient, there is impaired glucose metabolism leading to change in homeostasis (hyperglycemia) i.e. increased blood sugar.

151. Conti… Blood sugar rises leading to increase in osmotic pressure of body fluids and when renal threshold is reached, glucose is excreted in urine,(glycosuria) carrying large amount of H2O / polyuria Cells fail to metabolize and there is gluconeogenesis from amino acids and body proteins causing wasting and weight loss. As the body metabolizes fats and proteins to provide energy, there is production of ketones and increased demand for proteins. Due to reduced glucose metabolism, the amount of oxaloacetic acid is reduced and this leads to accumulation of acetyl coenzyme A excess of which is converted to ketones which are acidic leading to ketoacidosis. There is hyperventilation and acidification of urine.

152. Signs and symptoms Polyuria Polydipsia Polyphagia Glycosuria Hyper glycaemia Tachycardia Dyspnea Ace tonic breath Recurrent infections e.g. boils

153. Conti… Pruritis (itching of vulva and glans penis) Oral or vaginal thrush Low blood pressure Temporary blurred vision Weight gain or weight loss Muscle wastage Nocturia Irritability and coma (mental changes) Paranesthesia( tingling sensation in fingers and feet) Lassitude and loss of energy

154. diagnosis Clinical features Investigations Urinalysis- (sugar in urine, acetone, and ketones in severe cases Blood plasma glucose test if fasting glucose is more or equal to 8mmol/L in more than one occasion. Random blood sugar is raised RBS more or equal 11mmol/L Blood far U/E – urea is high while K+ ,Na+ and Cl+ are low Oral glucose tolerance test (OGTT) patient takes unrestricted carbohydrate diet for 3/7 then fast the night before test. In the morning you do BS and if > 7mmol/L , the patient is diabetic. Give oral glucose 75mg e.g. sprite 300mls then monitor blood glucose ½ hourly from 2 hours. If after 2 hours BS>11mmol/L, the patient is diabetic and if less than 7-11mmol/L he has impaired glucose tolerance

155. Differences between type 1 and 2 diabetes mellitus. Sudden onset with weight loss polydipsia, polyphagia polyuria Onset is gradual and symptoms are slight or absent Occurs in age less than 30 years Occurs in the age of 40 years and above There is weight loss and thin looking There is weight gain and the patient is usually obese Urine has sugar and acetone Urine has sugar only, no ketones If poorly managed they are likely to go to coma Not likely go to coma Treatment is by insulin and diet Treatment is by restricted diet and oral hyperglycemia agents mainly

156. management Medical treatment of diabetes mellitus depends on the type Type 1 – treated with high calories diet and insulin Type 2 – treated with restricted calories diet and hyperglycemia drug Insulin is given sub cut IV or IM but not orally because stomach acids destroys its potency. There are several types of insulin namely; Soluble insulin (short acting) it is the only group give IV tads and acts between 6-8 hours. It should be given 30-40 minutes before meals. Other routes may be subcutenous , IM. There are three types namely, regular, neutral and acid insulin

157. Conti.. Intermediate acting insulin- acts between 7-12 hours thus it is given bd. Examples are semi Lente and isophane. Long acting insulin- they act between 24-30 hours so they can be given od. Examples are ultra Lente protamine zinc insulin. Mixtard- this is a combination of short acting insulin (35%) and intermediate acting insulin (70%) T hese insulin come in different strength of 40,80 and 100 units. The side effects of insulin includes Peripheral edema due to salt retention

158. Conti… Hyperglycemia/ insulin coma Weight gain Hypokalemia Allergy hypersensitivity Atrophy of muscles due to repeated injections For type II diabetes mellitus oral hyperglycemic agents used include; Chrlorpropamide ( long acting so given od) Tolbutamide and tolazomide (short acting ) Glipizide Met formin ( used in obese patient to reduce weight Acarbose Triglitazone (increase peripheral action of insulin

159. Conti… Diet Patients with normal weight are given normal diet Obese patients are given diet with les calories i.e. carbohydrates 50% fats 30-35% proteins 10-15% Put the patient on low salt diet Can take alcohol in moderation for it induces hypoglycemia N/B good of diabetes can be achieved by insulin , oral hypoglycemia agents and diet

160. Nursing management Admit the patient in the ward and give bed rest Start the patient on IV fluids to which NaHCO3 is added to alkalinize blood and prevent acidosis. Administer drugs to the patient as prescribed i.e. insulin or oral hypoglycemia agents Prepare and assist in carrying out the investigations Take urine 6 hourly for urinalysis and record accurately Closely observe the vital signs TPR, BP, to detect any determination and onset of complications. Given antibiotics e.g. X –pen prophylactically to prevent infections.

161. Conti.. Observation for side effects of insulin or hypoglycemic drugs give the patient the appropriate diabetic diet with adequate nutrition quantity of sugar, fats and proteins. Ensure the patient is served with meals to prevent hyperglycemia following insulin administration. For type 1 meals should be regular and some amount at the same time every day to avoid hyperglycemia. If there are any wounds, dress using aseptic technique because the patient have less resistance to infection. Treat any concurrent infection promptly.

162. Give health education to the patient to include; Should take the drugs at the right time and right dose Should have supplies at all times Patient on insulin, teach them on injection technique, site i.e. thigh, abdomen , deltoid muscles. Strengths of insulin and to keep away from heat and light. Sterilize injection apparatus after use and disposal Never substitute one type of insulin for the other How to recognize signs and symptoms of hypoglycemia and hyperglycemic coma and should have sips of glucose to take whenever they note signs of hyperglycemia

163. Conti… never take insulin and miss meals (prevents hypoglycemia) Teach them collection of urine for testing Carry diabetic cards with them and encourage them to join the diabetic associations for support. To come for a follow-up in diabetic (MOPC ) clinic.

164. complications Hyperglycemia Hypoglycemic coma Diabetic Keto - acidosis (DKA) Atherosclerosis leading to M.I Hypertension Dehydration Infertility in women Large babies leading to difficulty in delivery Nephropathy

165. Conti… Peripheral neuropathy Retinopathy Cataracts Gangrene of feet and toes Sexual impotence in men Infection e.g. UTI . Vulvitis, carbuncle

166. HYP O GLYCAEMIC COMA This is a condition in which there is low blood sugar level leading to loss of consciousness (coma) causes Overdose of insulin or oral hypoglycemia agents Increased amount of exercises Nutritional imbalances e.g. when a patient misses a meal or is vomiting.

167. Signs and symptoms Weakness and anxiety Feeling of hunger Sweating a lot Lethargy Pale, cool, charming skin

168. Conti…. Blood sugar is very low Dilated pupils Double vision Headache Slow pulse rate Palpitation Confusion and coma Tremors of fingers confusion and coma

169. Conti… Rapid respiration Normal blood pressure

170. management Admit the patient in the ward and provide bed rest the inform the doctor If a patient can swallow, give a sweetened drink to raise blood glucose If unconscious give IV dextrose immediately. Test urine and check for BS Closely observe the patients vital signs and the level of unconsciousness. Stabilize the conduction and then give health education before discharging the patient home.

171. HYPERGLYCAEMIA/ DIABETIC COMA This is a condition that occurs as a result of low or lack of insulin. Common in IDDN patients. Lack of insulin production leads to hyperglycemia, glycosuria and progressive metabolic acid. Signs and symptoms Severe thirst and polyuria Abdominal pain Deep sighing breath due to acidosis Raised weak pause Low blood pressure

172. Conti… Smell of acetone in breath Loss of consciousness leading to coma Ketones +++ Constipation Muscle cramps Dry red tongue Weakness and drowsiness High levels of BS Warm and dry skin Glucosuria +++

173. management Aims –reduces the elevated blood sugar - correction of fluid and electrolyte imbalance - clear ketonic bodies from the blood and urine This is a medical emergency thus admit the patient Take vital signs and note any abnormality If the patient is unconscious, nurse in semi-prone position to ensure patient airway. Give the IV fluids to correct the fluid- electrolyte imbalance as follows -1litre of normal saline in the first 30min -1litre of normal saline in the next 1 hour

174. Conti… 1litre of normal saline in the next 2 hours 1litre of normal saline in the next 4 hours and then 500mls hourly or as clinical status indicate then change to 5% dexitose alternating with normal saline when BS is 12-12.5mmol/L. continue IV fluids till ketonuria has disappeared. Start the patient as insulin therapy as follows; -give insulin 10units IV + 10units IM stat then change to 6-10 IM every hour until BS is 14mmol/L the 8-16 units submit 4-10 hourly. When the patient is eating, give 8 units submit Tds Start replacement of k immediately after first dose of insulin i.e. give 1litre with10mls of 15% k Once patient starts oral … give KCL orally till K is corrected

175. Conti… Administer antibiotics since infection is a precipitation factor Give anticoagulant e.g. heparin 2500 units submit bd to prevent BVT For the first few hours, do plasma potassium and 1 hourly BS to monitor progress. Monitor urinary output, (no urine 3 hours catheterize the patient and leave it in situ. Test every specimen of urine Pass NG tuber for suction to prevent aspirations Monitor the patient’s condition to determine response or lack of response to therapy. When ketoacidosis is corrected, start oral intake

176. Conti… Provide general nursing care to cater for physical and psychological needs. Give health education to patient and relatives before discharging home.

177. Differences between hyperglycemic coma and hypoglycemic coma Hyperglycemic coma hypoglycemic coma There is insufficient or no insulin or dietary indiscretion There is excessive insulin and too little food 2. Onset is slow from hours to days Onset is sudden in minutes 3. Skin is flashed dry and hot skin is pale, moist and cool 4. Patient is drowsy Patient is excited 5. Breath has smell of acetone Breath is normal 6. Respiration shows air hunger and deep sigh Respiration is normal to rapid 7.Pulse is raised and weak Pulse is normal or slow 8.BP is low BP is normal 9. There is no sweating There is sweating ++

178. Conti… 10. Patient is dehydrated No dehydration 11. Coma follows drowsy state Coma is sudden preceded by convulsion 12. Urine has large amount of sugar Urine has no sugar 13. Blood sugar level is very high Blood sugar is very low 14.Dextrose therapy not needed Dextrose therapy necessary 15. There is rapid response to treatment There is slow response to treatment

179. Conti… Diabetic foot care Wear well fitting shoes Avoid wearing open shoes Dry feet well especially between toes Avoid busking in open fires Avoid walking bare footed Avoid dipping foot in hot water until it is felt by somebody else.

180. Rationale They have decreased sensation and reduced blood supply to the periphery therefore they do not sense any injury. Diabetic foot starts with small scratch which the patient does not sense and may not care for because they have not seen it. The scratch will not heal spontaneously because of reduced peripheral blood supply that accompanies diabetes. The scratch will enlarge and go deep.

181. ADRENAL GLAND

182. ADDISON’S DISEASE This is a disease characterized by decreased secretion of adrenal cortex hormones (mineralocorticoids and glucocorticoids) but mainly cortical. It can be acute which is unrecognized and potentially fatal or chronic that is simple to treat. Causes Bilateral adrenolectomy ( all adrenal glands removed) Destruction of adrenal cortex by infections e.g. TB, histoplasmosis. Autoimmune disease leading to (ant adrenal cortical cells) Metastatic carcinomas Atrophy of zona glomerulosa and zona recticularis

183. Conti… Sudden withdrawal of adrenocortical hormone therapy. Inadequate secretion of ACTH Pathophysiology Decrease in secretion of these hormone result in decreased vascular sufficiency, circulatory failure , hypoglycemia , decreased aldosterone secretion which impairs Na+ and H2O reabsorption, decreased physiological response to stress. There may be also deficiency of adrenal androgens Adrenal crisis may arise.

184. diagnosis Low level of adrenal cortical hormones in the blood or urine Random cortisol will be decreased Random blood sugar will be decreased Electrolytes- Na+ will be decreased due to lack of aldosterone Clinical features Muscular weakness and fatigue Anorexia leading to weight loss Dark pigment of the skin ( reduced effect of cortisol on melanocytes stimulating hormone) Nausea and vomiting

185. Conti… Abdominal pain Hypotension Hypoglycemia Chronic dehydration Menstrual disturbance Headache Addisonian crisis Low temperature and metabolic rate Hyponatremia and hyperkalemia Sparse hair and loss of hair from some parts

186. management Combat shock by administering hydrocortisone / dextrose alternating with normal saline. Administer antibiotics as prescribed Give IV fluids e.g. Normal saline and when vomiting subsides, give orally Radiotherapy may be done following surgery If adrenolectomy was done, patient should be on cortisone drugs for life. Take daily body weights to assess the progress

187. Conti… Upon discharge, give the patient health education to comply to medication as per prescription To have drugs at all times Should avoid infection and if any should be treated early Advise on signs and symptoms of hyperglycemic and hypoglycemic coma. Importance of coming follow up in the MOPC.

188. ADDISONIAN CRISIS This is a medical emergency marked by very low level of adrenal cortex hormones. Features of addisonian crisis Cyanosis Fever Rapid respiration Severe dehydration Headache Confusion Diarrhea Abdominal pain Circulatory collapse

189. diagnosis Blood for electrolytes :reduced sodium, increased potassium Adrenalcorticol hormone levels Reduced blood glucose levels Increased WBC levels.

190. management The basic management is as highlighted in Addison’s disease plus the following; Patient is put in recumbent position with legs elevated to increase venous return Administer 02 by mask or nasal catheter to correct cyanosis Keep the patient warm Put hydrocortisone and dopamine 250-300mg in 50% dextrose to constrict blood vessels to raise BP Administer noradrenaline or isopropanol in infusion of 5% dextrose to revive the vascular space. Encourage intake of plenty of oral fluids, soup juices to correct fluid ,glucose electrolyte imbalance Give high salt diet and check BP 4 hourly

191. Conti… Administer corticosteroids e.g. prednisolone Encourage and reassure the patient to reduce stress Treat the patient of any other infection appropriately Give health education on how to prevent addisonian’s crisis Monitor vital signs to counter hypotension Complications Pathological fractures Hypoglycemic coma Renal failure Psychotic depression Hypotension

192. CUSHINGS SYNDROME Excess glucocorticoids or excess ACTH due to --Pituitary tumor --Pituitary hyperplasia --adrenal tumor --on going glucocorticoid therapy Excess ACTH stimulates the release of cortisol

193. Signs and sysmptom Amenorrhea Changes in mental status Striae on abdomen ,breast and thighs Skin changes e.g. acne ,infections ,easy bruising Muscle weakness Hirsutism on face ,neck ,chest (women) Impotence, decreased fertility, and sex drive

194. ---Signs and Symptoms moon face Buffalo hump osteoporosis

195. Tests Done Dexamethasone suppression test Increased cortisol in 24 hrs urine CT scan—pituitary, adrenal Blood glucose Increased sodium Decreased potassium

196. Treatment Surgical removal of tumors Radiation RX for pituitary tumors Cortisol replacement during recovery

197. Nursing Diagnosis Disturbed body image related to illness Excess fluid volume due to excess water and sodium reabsorption Risk for infection owing to immunosuppression a nd inadequate primary defence

198. care of the patient undergoing adrenalectomy Adrenalectomy may be unilateral or bilateral to treat adrenal tumours, Cushing's syndrome, or hyperaldosteronism Preoperative MBP and fluid volume are optimizedanagement

199. Cont` Surgery and nursing care are explained to patient. Patient is shown where adrenal glands lie on top of kidneys and where incision may be on abdomen or loin area. BP will be checked frequently before and after surgery and glucocorticoids will be given to cover period of stress (surgery) because at least one adrenal gland will be removed. Patient is prepared as for major abdominal surgery (see page 637).

200. Postoperative Management postoperative care for abdominal surgery includes frequent check of vital signs; assessment for haemorrhage; turning, coughing, and deep breathing; early ambulation; slow progression of diet when bowel sounds return; and control of pain with scheduled opioid administration or patient-controlled analgesia . I.V. hydrocortisone (Solu-Cortef) is given as directed to prevent adrenal crisis

201. Post op Non stressful environment is maintained, rest is promoted, and meticulous care is given to protect the patient from infection and from other complications that could cause adrenal crisis. Serum sodium, potassium, and glucose are monitored for abnormality Sodium and potassium may normalize, or potassium may become elevated (because of transient adrenal insufficiency after surgery). Electrolyte imbalances may persist for 4 to 18 months after surgery. Hypertension may persist for 3 to 6 months after surgery

202. Post op` Hydrocortisone treatment causes glucose to rise and worsens control in patients with diabetes; may require additional treatment Nursing Diagnoses Risk for Injury related to nature of surgery Readiness for Enhanced Knowledge about corticosteroid replacement

203. PHAEOCHROMOCYTOMA This is a benign tumor originating from chromatin cells of adrenal medulla 80-90% extra adrenal chromatin cells. It causes excessive secretion of adrenaline and noradrenaline. It can occur in tissues like ovary, spleen and aorta. Is more common in ages 50-80 years. A few of them become malignant. Pathophysiology There is increased production of catecholamine leading to increase in blood pressure and increased cardiac output. There is glycolysis ( breakdown of glycogen thus there is a lot of glucose in blood ( hyperglycemia)

204. Conti… Clinical features High BP of about 350/210mmhg that complicate to stroke, acute renal failure, cardiac arrhythmias. Anxiety Blurred vision Hyperglycemia Tachycardia Vomiting Flushing Tremors polyuria

205. Conti… Palpitations Perspiration Tinnitus Diarrhea Management Admit the patient for total bed rest Take blood to determine catecholamine levels Take 24 hours urine to determine catecholamine levels Determine the urine level of vanillil mandelic acid (end product catecholamine)

206. Conti… Assess the activity of sympathetic nervous system e.g. is he salivating or not. Nurse the patient in a sitting up position to enhance reduction of BP by gravity. If the BP is very high, nurse the patient in ICU to monitor cardiac function Administer the following drugs Adrenergic blockers to control cardiac function Smooth muscle relaxants In case a tumor has been identified, patient is taken for surgery, so prepare for pre and post operational care.

207. Conti… Postoperatively administer corticosteroids depending on catecholamine levels Give health education to the patient on the disease process before discharge

208. Conti… Cardiac failure Athesclerosis Obesity NURSING DIAGNOSIS Impaired physical mobility Risk for activity intolerance Risk for imbalanced fluid volume

209. HYPERALDOSTERONISM This is a condition in which there is excess aldosterone. It is associated with adrenocortical adenoma. If it is independent of the rennin- angiotensin –aldosterone system it is referred to as C onn’s syndrome . Clinical features Polydipsia Polyuria Tetany due to K+ depletion Hypertension due to high Na+ levels Arrhythmias due to hypokalemia paresthesia

210. Conti… myxedema resulted atrophy of thyroid gland in adult in which the patient becomes sluggish both mentally and physically. Overactive thyroid gland leads to thyrotoxicosis