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Semester 4: Nutrition and Metabolism > PBL Topic 4 Case 9 > Flashcards

PBL Topic 4 Case 9 Flashcards

1
Q

Identify three hormones secreted by the thyroid

A
  • Thyroxine (T3)
  • Triiodothyronine (T4)
  • Calcitonin
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2
Q

Thyroid secretion is controlled by which hormone? Which gland secretes this homrone?

A
  • Thyroid-stimulating hormone

- Secreted by anterior pituitary gland

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3
Q

What is contained within the thyroid follicles?

A
  • Colloid
  • Which consists of thyroglobulin
  • Which contains the thyroid hormone within its molecule
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4
Q

Outline the process of iodide trapping

A
  • Active pumping of iodine through basal membrane by Na/I transporter
  • Transport through apical membrane by pendrin (I/Cl transporter)
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5
Q

Outline the process of oxidation of iodide ions

A
  • Conversion of iodide to iodine
  • Catalysed by thyroid peroxidase in apical membrane
  • And its accompanying hydrogen peroxide
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6
Q

Outline the organification of iodine

A
  • Iodine binds with tyrosine

- Catalysed by iodinase enzyme

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7
Q

Outline the iodisation of tyrosine

A
  • Tyrosine is iodised to monoiodotyrosine
  • And then to diiodotyrosine
  • MIT + DIT = T3
  • DIT + DIT = T4
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8
Q

Outline the process by which T3 and T4 are cleaved from thyroglobulin

A
  • Apical surface sends out pseudopods
  • Which close around portions of colloid
  • Which form pinocytic vesicles that enter the apex of the thyroid cell
  • Lysosomes fuse with vesicles
  • Proteases digest thyroglobulin to release T3 and T4
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9
Q

What happens to the iodinated tyrosine following digestion of thyroglobulin?

A
  • Iodine is cleaved by deiodinase enzyme

- Which recycles iodine available again for formation of additional thyroid hormone

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10
Q

What happens to the majority of T3 and T4 as it enters the blood?

A
  • Combines with thyroxine-binding globulin

- Delivered to tissues where they bind with intracellular proteins

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11
Q

Outline the cellular action of thyroid hormone

A
  • Retinoid X receptor forms a heterodimer with thyroid hormone receptors
  • Which enhances binding of thyroid hormone at the thyroid response element in the DNA of the target cell nucleus
  • Activation of these receptors causes transcription followed by RNA translation
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12
Q

What is the effect of thyroid hormone on mitochondria?

A
  • Increases number of mitochondria

- Which increases the formation of ATP

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13
Q

What is the effect of thyroid hormone on active transport?

A
  • Increases activity in Na+-K+-ATPase
  • Which increases transport of sodium and potassium through membranes
  • Which increases body’s metabolic rate
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14
Q

What is the effect of thyroid hormone on growth?

A
  • Growth and development of brain

- Growth and development of bones

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15
Q

What are the effects of thyroid hormone on carbohydrate metabolism?

A
  • Increased rate of absorption from GI tract
  • Increased insulin secretion
  • Rapid uptake of glucose by the cells
  • Enhanced glycolysis
  • Enhanced gluconeogenesis
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16
Q

What are the effects of thyroid hormone on fat metabolism?

A
  • Lipids are mobilised rapidly
  • Which decreases the fat stores of the body
  • Which increases the free fatty acid concentration in the plasma
  • And greatly accelerates the oxidation of free fatty acids by the cells
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17
Q

What are the effects of thyroid hormone on fat cholesterol, phospholipids and triglycerides?

A
  • Decreased concentrations of cholesterol, phospholipids and triglycerides
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18
Q

How does thyroid hormone decrease plasma cholesterol concentration?

A
  • Increased numbers of LDL receptors on liver cells
  • With increased LDL removal from plasma
  • Liver cells convert LDL to cholesterol
  • Which are secreted in bile and lost in faeces
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19
Q

Why does thyroid hormone cause vasodilation and increased cardiac output?

A
  • Increased cellular metabolism causes rapid utilisation of oxygen
  • Increasing metabolic end product release from tissues
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20
Q

Why does thyroid hormone cause increased heart rate?

A
  • Direct effect of TH on excitability of the heart
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21
Q

What is the effect of thyroid hormone on the respiratory system?

A
  • Increase in rate and depth of respiration

- Due to increased rate of metabolism (increased utilisation of oxygen and formation of CO2

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22
Q

What are the effects of thyroid hormone on the GI system?

A
  • Increased appetite and food intake
  • Increased secretion of digestive juices
  • Increased motility of GI tract
  • Hyperthyroid: Diarrhoea
  • Hypothyroid: Constipation
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23
Q

What are the effects of thyroid hormone on the CNS?

A
  • Increases rapidity of cerebration

- Hyperthyroid: Nervous and psychoneurotic tendencies (anxiety, worry paranoia)

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24
Q

What are the effects of thyroid hormone on muscles?

A
  • Initially muscles react with vigor

- Though excessive TH causes weakened muscles due to protein catabolism

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25
Q

What are the effects of thyroid hormone on sexual function

A
  • Men: lack of TH causes loss of libido, excess libido causes impotence
  • Women: lack of TH causes loss of libido, menorrhagia
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26
Q

Identify 6 effects of TSH on the thyroid gland

A
  • Increased proteolysis of thyroglobulin
  • Increased activity of iodide pump
  • Increased iodination of tyrosine
  • Increase number of thyroid cells
  • Increased secretory activity
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27
Q

Outline the cellular action of TSH

A
  • TSH binds with TSH receptors on basal membrane of thyroid cells
  • Which activates adenylyl cyclase
  • With increased formation of cAMP
  • cAMP activates phosphatidyl inositol 3-kinase
  • With an increase in secretion of thyroid hormones
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28
Q

Outline the control of TSH secretion

A
  • TSH is controlled by TRH
  • Which is secreted by median eminence of hypothalamus
  • Which binds to TRH receptors on anterior pituitary cells
  • Which activates the phospholipase C second messenger system
  • Which leads to TSH release
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29
Q

Identify factors that reduce TSH secretion

A
  • Increased thyroid hormone causes negative feedback of TSH secretion
  • Somatostatin reduces basal TSH release
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30
Q

Which cells of the thyroid gland secrete calcitonin?

A
  • Parafollicular cells
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31
Q

What is the primary stimulus for calcitonin secretion?

A
  • An increase in plasma calcium ion concentration
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32
Q

How does calcitonin decrease plasma calcium concentration?

A
  • Decrease activity and formation of osteoclasts
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33
Q

Identify thyroid function tests

A
  • TSH

- Plus free T4 or free T3

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34
Q

What are the problems in the interpretation of thyroid function tests in serious acute or chronic illness?

A
  • Reduced concentration and affinity of binding proteins

- Decreased peripheral conversion of T4 to T3

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35
Q

What are the problems in the interpretation of thyroid function tests in pregnancy and with oral contraceptives?

A
  • Greatly increased TBG levels so high T4.

- TSH is suppressed in the first trimester

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36
Q

What are the problems in the interpretation of thyroid function tests in patients taking amiodarone?

A
  • Amiodarone decreases T4 to T3 conversion

- Amiodarone may induce both hyper-and hypothyroidism

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37
Q

What is the most likely diagnosis?

  • TSH undetectable
  • T4 raised
  • T3 raised
A
  • Primary thyrotoxicosis
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38
Q

What is the most likely diagnosis?

  • TSH undetectable
  • T4 normal
  • T3 raised
A
  • Primary T3 toxicosis
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39
Q

What is the most likely diagnosis?

  • TSH undetectable
  • T4 raised
  • T3 low, normal or raised
A
  • Sick euthyroidism
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40
Q

What is the most likely diagnosis?

  • TSH undetectable
  • T4 low
  • T3 low
A
  • Secondary hypothyroidism
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41
Q

What is the most likely diagnosis?

  • TSH elevated
  • T4 low
  • T3 low
A
  • Primary hypothyroidism
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42
Q

What is the most likely diagnosis?

  • TSH elevated
  • T4 normal
  • T3 normal
A
  • Subclinical hypothyroidism
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43
Q

What is thyrotoxicosis?

A
  • Increased metabolic rate

- Due to effect of excess T3/T4 on tissues

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44
Q

What is the commonest cause of thyrotoxicosis?

A
  • Hyperthyroidism
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45
Q

Identify the three main pathological causes of hyperthyroidism

A
  • Grave’s Disease
  • Functioning adenoma
  • Toxic nodular goitre
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46
Q

What is struma ovarii?

A
  • Teratoma
  • Ovary comprising thyroid tissue
  • With ectopic secretion of thyroid hormones
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47
Q

Outline the epidemiology of hyperthyroidism

A
  • Affects up to 5% of women
  • More common in women 5:1
  • Most common between 20-40
  • Most caused by intrinsic thyroid disease (pituitary cause is rare)
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48
Q

Outline the pathology of Grave’s thyroiditis?

A
  • IgG autoantibody called long-acting thyroid stimulator (LATS)
  • Binds to thyroid epithelial cells
  • And mimics the action of TSH
  • Stimulating function and growth of thyroid follicular epithelium
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49
Q

Identify the three clinical features of Grave’s thyroiditis

A
  • Exophthalmos
  • Pretibial myxoedema
  • Thyroid acropachy
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50
Q

What is exophthalmos?

A
  • Anterior bulging of eyes

- Results from infiltration of orbital tissues by adipocytes and mucopolysaccharides

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51
Q

What is pretibial myxoedema

A
  • Accumulation of mucopolysaccharides in dermis of skin
  • Skin appears puffy
  • Outer third of eyebrow is lost
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52
Q

What is thyroid acropachy?

A
  • Clubbing
  • Swollen fingers
  • Periosteal knee bone formation
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53
Q

Outline the genetic component of Grave’s thyroiditis

A
  • HLA-B8, DR3 and DR2
  • E.coli and other gram negatives have TSH binding sites
  • Which initiates infection mimicry in genetically susceptible patients
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54
Q

What is de Quervain’s thyroiditis? What are the features and treatment

A
  • Transient hyperthyroidism from an acute inflammatory process
  • With fever, malaise, neck pain, raised ESR
  • Proceeded by hypothyroidism
  • Treatment is with aspirin
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55
Q

What is Type 1 Amiodarone-Induced Thyrotoxicosis?

A
  • Associated with pre-existing Graves or multi nodular goitre
  • Hyperthyroidism is triggered by high iodine content of amiodarone
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56
Q

What is Type 2 Amiodarone-Induced Thyrotoxicosis?

A
  • Not due to previous thyroid disease
  • Direct effect of drug on thyroid follicular cells
  • Leading to destructive thyroiditis
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57
Q

What is the effect of amiodarone on iodine?

A
  • Inhibits the deiodination of T4 to T3
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58
Q

What are the 6 most common symptoms of hyperthyroidism?

A
  • Weight loss
  • Increase appetite
  • Heat intolerance
  • Palpitations
  • Tremor
  • Irritability
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59
Q

What are the eye signs in hyperthyroidism?

A
  • Lid lag

- Stare

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60
Q

What is the presentation of hyperthyroidism in the elderly?

A
  • Atrial fibrillation, tachycardia, heart failure

- ‘Apathetic thyrotoxicosis’ where clinical picture is more like hypothyroidism

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61
Q

What is the presentation of hyperthyroidism in children?

A
  • Excessive height or excessive growth rate

- Behavioural problems such as hyperactivity

62
Q

What are the investigations in hyperthyroidism?

A
  • Suppressed TSH
  • Raised T4 or T3
  • Thyroid peroxidase and thyroglobulin antibodies are present in Grave’s disease
63
Q

Outline the mechanism of action of radioiodine?

A
  • Emits beta radiation

- Which has a cytotoxic action on thyroid follicular cells

64
Q

Why is surveillance important with radioiodine therapy?

A
  • Hypothyroidism will eventually occur

- Which is easily managed by replacement therapy with T4

65
Q

Identify a contra-indication to radioiodine therapy

A
  • Children

- Pregnant patients

66
Q

Identify three thioureylenes

A
  • Carbimazole
  • Methimazole (active metabolite of carbimazole)
  • Propylthiouracil
67
Q

Outline the mechanism of action of thioureylenes

A
  • Competitively inhibits the oxidation of iodide by thyroid peroxidase
  • Which inhibits iodination of tyrosine residues in thyroglobulin
68
Q

Which chemical group is essential for the antithyroid activity of thioureylenes?

A
  • Thiocarbamide (S-C-N)
69
Q

Why does propylthiouracil act more rapidly than other drugs in its class?

A
  • It has an additional effect

- To inhibit the peripheral conversion of T4 to T3

70
Q

Both methimazole and propylthiouracil cross the placenta, why is this effect less pronounced with propylthiouracil?

A
  • Propylthiouracil is more strongly bound to plasma protein
71
Q

What are the most dangerous unwanted effects of thioureylenes?

A
  • Neutropenia

- Agranulocytosis

72
Q

What are the most common unwanted effects of thioureylenes?

A
  • Rashes
73
Q

Why is propranolol indicated in hyperthyroidism?

A
  • Beta adrenoreceptor antagonist

- That reduces tachycardia, dysrhythmias, tremor and agitation

74
Q

What is the role of guanethidine in the treatment of hyperthyroidism?

A
  • Noradrenergic blocking agent
  • Used to improve exophthalmos
  • By relaxing the sympathetically innervated smooth muscle
  • That causes eyelid retraction
75
Q

What is the role of glucocorticoids in the treatment of hyperthyroidism?

A

-Mitigate severe exophthalmia in Grave’s disease

76
Q

What is the surgical procedure used in the treatment of hyperthyroidism and what are the risks associated with it?

A
  • Thyroidectomy
  • Bleeding causing tracheal compression and asphyxia
  • Laryngeal nerve plasy
  • Transient hypocalcaemia
77
Q

What is thyroid crisis?

A
  • Rare, life-threatening complication
  • Signs of fever, agitation, confusion, tachycardia, AF, cardiac failure
  • Precipitated by infection in unrecognised thyrotoxicosis
78
Q

How is thyroid crisis treated?

A
  • Rehydrate
  • Broad spectrum antibiotic
  • Propranolol
  • Sodium ipodate
79
Q

What is the mechanism of action of sodium ipodate?

A
  • Restores serum T3

- Which inhibits release of thyroid hormone

80
Q

Outline the pathophysiology of thyroid eye disease

A
  • TSH receptor is degraded by APC
  • Activation of T-cells, and B-cells
  • Which activates cytokines which induces differentiation of B cells into plasma cells
  • Which secrete anti-TSH receptor antibodies
81
Q

Outline 5 clinical features of thyroid eye disease

A
  • Soreness
  • Watering
  • Proptosis
  • Lid retraction
  • Peri-orbital oedema and inflammation
82
Q

Outline the treatment of thyroid eye disease

A
  • Methylcellulose or hypromellose aid lubrication and improve comfort
  • Steroids reduce inflammation
  • Surgical decompression may be required
  • Corrective eye muscle surgery if diplopia occurs
83
Q

What is a goitre?

A
  • Enlargement of the thyroid without hyperthyroidism
  • Cause by lack of T3 or T4
  • TSH rises and causes hyperplasia of thyroid epithelium
84
Q

Identify 3 causes of goitre

A
  • Iodine deficiency
  • Rare inherited enzyme defects
  • Drugs that induce hypothyroidism
85
Q

Identify and describe two types of goitre

A
  • Parenchymatous goitre: hyperplasia of thyroid epithelium, fibrosis results in multinodular goitre
  • Colloid goitre: Colloid forms cysts, with haemorrhage, fibrosis and calcification
86
Q

Identify 3 indications for surgical intervention of a goitre

A
  • Possibility of malignancy
  • Pressure symptoms on trachea or oesophagus
  • Causes considerable anxiety
87
Q

What is hypothyroidism?

A
  • Inadequate levels of T3 and T4
  • Metabolic rate is lowered
  • Mucopolysaccharides accumulate in dermal connective tissue
  • To produce myxoedema face
88
Q

What is the commonest cause of acquired hypothyroidism?

A
  • Hashimoto’s thyroiditis
89
Q

Outline the pathophysiology of Hashimoto’s thyroiditis

A
  • Autoantibodies for thyroid peroxidase and thyroglobulin
  • Formed from plasma cells infiltrating thyroid due to loss of Ts cells
  • Colloid content reduced and increased mitochondria (oncocytes)
90
Q

Identify 3 other causes of primary hypothyroidism

A
  • Postpartum thyroiditis (due to modification in immune system during pregnancy)
  • Dietary iodine deficiency (endemic goitre)
  • Dysmorphogenesis (defective synthesis of thyroid hormones)
91
Q

What is Prendred’s syndrome?

A
  • Defect in the transporter pendrin
  • Due to deletion mutation in chromosome 7
  • Reduced movement of iodide ions through through apical membrane
  • Causes sensorineural hearing loss
92
Q

What are the most common features of hypothyroidism

A
  • Weight gain
  • Cold intolerance
  • Bradycardia
  • Constipation
  • Dry hair and thick skin
  • Deep voice
93
Q

Outline the clinical picture of hypothyroidism in children

A
  • Slow growth velocity
  • Poor school performance
  • Arrest of pubertal development
94
Q

What results from thyroid function tests would indicate hypothyroidism

A
  • High TSH

- Low free T4

95
Q

Outline other abnormalities from blood tests in primary hypothyroidism

A
  • Anaemia
  • Increased AST
  • Increased creatine kinase
  • Hypercholesterolaemia
  • Hyponatraemia
  • Bradycardia, ST segment, T wave abnormalities
96
Q

What is secondary hypothyroidism?

A
  • Failure of TSH secretion
  • With hypothalamic or anterior pituitary disease
  • Characterised by low TSH, low T4
97
Q

What is the treatment for hypothyroidism? How and when are they given?

A
  • Levothyroxine, given orally, first line

- Liothyronine given intravenously, reserved for myxoedema coma

98
Q

What are the adverse effects of levothyroxine and liothryonine?

A
  • In severe overdose:
  • Angina pectoris
  • Cardiac dysrhythmias
  • Cardiac failure
99
Q

What is myxoedema coma?

A
  • Severe hypothyroidism occurring in the elderly
  • Presents with confusion or coma
  • High mortality (50%)
100
Q

What is the treatment for myxoedema coma?

A
  • T3 orally or IV
  • Oxygen
  • Monitoring of cardiac output
  • Hydrocortisone IV
  • Glucose infusion
101
Q

What is myxoedema madness?

A
  • Demented or psychotic symptoms with striking delusions
  • Occurring rarely in severe hypothyroidism
  • May occur shortly after T4 replacement
102
Q

What do TFTs show subclinical thyrotoxicosis?

A
  • TSH undetectable
  • Serum T3 and T4 in upper end of normal range
  • Often present with multinodular goitres
103
Q

How is subclinical thyrotoxicosis managed?

A
  • Annual review and treatment with radioactive iodine
104
Q

What do TFTs show subclinical hypothyroidism?

A
  • Raised TSH

- T3 and T4 in lower end of reference range

105
Q

When and how is subclinical hypothyroidism managed?

A
  • In patients with non-specific symptoms or positive autoantibodies
  • Thyroxine
106
Q

Outline the anatomy of the parathyroid glands

A
  • Four glands
  • Located behind the thyroid gland, one behind each of the upper and each of the lower poles of the thyroid
  • Contains mainly chief cells and a small to moderate number of oxyphil cells
107
Q

Outline the synthesis of parathyroid hormone

A
  • Ribosomes synthesise preprohormone
  • Which is cleaved to prohormone and then parathyroid hormone
  • By the endoplasmic reticulum
  • Packaged into secretory granules in the cytoplasm
108
Q

Outline the effects of an increase in [PTH] on the serum [Ca2+] and [PO42-]

A
  • Calcium: Increase

- Phosphate: Decrease

109
Q

Identify the two main effects of PTH that increase serum calcium concentration

A
  • Increased resorption from bone

- Decreased excretion from urine

110
Q

Outline the effect of PTH on bones

A
  • PTH binds to PTH-1 receptor on osteoblasts
  • Which increases osteoblast expression of RANKL
  • Which binds to RANK on osteoclast precursors
  • Differentiation of osteoclast precursors to mature osteoclasts
111
Q

Outline the effect of PTH on the kidneys

A
  • Reduced PCT reabsorption of PO42-

- Increased DCT reabsorption of Ca2+

112
Q

Outline the effect of PTH on intestines

A
  • PTH greatly enhances both calcium and phosphate absorption from the intestines
  • By increasing the formation in the kidneys of 1,25-dihydroxycholecalciferol from vitamin D
113
Q

What is the difference between the three types of hyperparathyroidism?

A
  • Types 1 and 3 are pathological and involve hyperplasia

- Type 2 is physiological and occurs in CKD or Vitamin D deficiency

114
Q

Identify 7 clinical features of hyperparathyroidism

A
  • Renal stones
  • Thirst and polyuria
  • Muscle weakness
  • Tiredness
  • Anorexia and constipation
  • Peptic ulceration
  • Osteitis fibrosa
  • Brown tumour
115
Q

Identify three findings from investigations suggesting hyperparathyroidism

A
  • Raised PTH levels
  • Raised serum calcium
  • Lower plasma phosphate
  • Mild metabolic acidosis
116
Q

What is the main cause of hyperparathyroidism?

A
  • Secretory adenoma of parathyroid gland
117
Q

Outline the treatment for hyperparathyroidism

A
  • Operative inspection of all four parathyroid glands
  • Followed by removal of any suspected adenoma
  • Which is then submitted for intraoperative diagnosis
118
Q

Outline five clinical features of hypoparathyroidism

A
  • Tetany
  • Convulsions
  • Paresthesia
  • Psychiatric disturbances
  • Cataracts
  • Brittle nails
119
Q

Identify three causes of hypoparathyroidism

A
  • Removal or damage to parathyroid glands during thyroidectomy
  • Autoantibodies
  • Congenital deficiency (DiGeorge syndrome)
120
Q

Outline the clinical features of DiGeorge syndrome

A
  • Intellectual impairment
  • Cataracts
  • Calcified basal ganglia
121
Q

Outline the pathology of pseudohypoparathyroidism

A
  • Resistance to PTH

- Due to mutation of GNAS1 which is coupled to PTH receptor

122
Q

Outline the clinical features of pseudohypoparathyroidism

A
  • Short stature
  • Short metacarpals
  • Intellectual impairment
123
Q

What is pseudo-pseudohypoparathyroidism

A
  • Describes the phenotypical defects of pseudohypoparathyroidism
  • But with no abnormalities in calcium metabolism
124
Q

What is Cushing’s syndrome?

A
  • Increased circulating glucocorticoids (cortisol)

- Usually following administration of synthetic steroids or ACTH

125
Q

Identify the two groups of causes of Cushing’s syndrome

A
  • Increased ACTH from pituitary (Cushing’s disease) or ectopic release from an ACTH releasing tumour
  • Excess of endogenous cortisol secretion by an adrenal tumour or hyperplasia
126
Q

What are the clinical features of Cushing’s syndrome?

A
  • Pigmentation with ACTH-dependent causes
  • Cushingoid appearance caused by excess alcohol consumption
  • Impaired glucose tolerance or diabetes in ectopic ACTH syndrome
  • Hypokalaemia due to mineralocorticoid activity in ectopic ACTH secretion
  • Hypertension
127
Q

How is Cushing’s syndrome diagnosed?

A
  • Elevated plasma cortisol
  • Elevated urinary excretion of 17-hydroxysteroids
  • Measurements of plasma ACTH
128
Q

What are the effects of untreated Cushing’s?

A
  • Hypertension
  • Myocardial infarction
  • Infection
  • Heart failure
129
Q

Identify a drug used in the treatment of Cushing’s syndrome

A
  • Metyrapone
  • An 11-beta hydroxylase blocker
  • Which is involved in the formation of cortisol from cholesterol
130
Q

Identify an antifungal agent that is synergistic with metyrapone and how it works

A
  • Ketoconazole

- Inhibits steroidogenesis

131
Q

Identify the treatment of pituitary-dependent hyperadrenalism

A
  • Trans-sphenoidal removal of tumour
  • External pituitary radiation
  • Medical therapy to reduce ACTH (e.g. bromocriptine)
  • Bilateral adrenalectomy
132
Q

Name an adrenolytic therapy that inhibits growth of adrenal tumours

A
  • Mitotane
133
Q

What is hyperaldosteronism?

A
  • Autonomous secretion of excess aldosterone
134
Q

Identify two causes of hyperaldosteronism

A
  • Adenoma of the zona glomerulosa (Conn’s syndrome)

- But can also be caused by hyperplasia of the zona glomerulosa

135
Q

Outline the pathology of hyperaldosteronism

A
  • Sodium and water retention leads to hypertension

- Potassium loss leads to muscular weakness and cardiac arrhythmias, tetany and paraesthesia

136
Q

What is secondary hyperaldosteronism

A
  • Reduced renal perfusion (e.g. fall in blood pressure)
  • Stimulates aldosterone secretion
  • Commonest type of hyperaldosteronism
137
Q

What investigations are used in the diagnosis of hyperaldosteronism?

A
  • Plasma aldosterone:renin ratio (elevated aldosterone and suppressed renin)
  • Hypokalaemia and urinary potassium loss
138
Q

Outline the treatment of hyperaldosteronism

A
  • Adenoma: Laparoscopic surgical removal

- Hyperplasia: Aldosterone antagonists e.g. spironolactone

139
Q

Identify 3 adverse effects of spironolactone and an alternative drug

A
  • Gynaecomastia
  • Rashes
  • Nausea
  • Eplerenone
140
Q

Identify the two factors that must be balanced to maintain a stable body weight over time

A
  • Energy intake

- Energy expenditure

141
Q

How is BMI calculated?

A
  • Weight (KG) / Height (M2)
142
Q

A BMI between which values indicates overweight?

A
  • 25 and 29.9 kg/m2
143
Q

A BMI over which value indicated obesity?

A
  • 30 kg/m2
144
Q

Identify a disadvantage of BMI measures?

A
  • Not a direct estimate of adiposity

- Does not take into account high BMI due to a large muscle mass.

145
Q

Obesity is defines as [X%] or greater total body fat in men and [Y%] in females

A
  • [X] = 25%

- [Y] = 35%

146
Q

What causes obesity

A
  • Greater energy Intake than energy expenditure
147
Q

For each [X] number calories of excess energy that enter the body, approximately 1 gram of fat is stored.

A
  • [X] = 9.3 calories
148
Q

How is weight lost?

A
  • Energy intake must be less than energy expenditure.
149
Q

What is meant by expert patient?

A
  • People living with a long-term health condition
  • Who are able to take more control over their health
  • By understanding and managing their conditions
  • Leading to an improved quality of life
150
Q

Identify an advantage and disadvatnage of self-manageemtn

A
  • Increases confidence and reduces anxiety

- Benefits for some disease (COPD) but not others (arthritis)

151
Q

What is meant by Shared Care?

A
  • Enabling all patients to manage aspects of their own care that they choose to
  • With added nursing support to bridge any shortfalls.
152
Q

Outline the epidemiology of anxiety

A
  • Highest in young women (2:1)
  • Associated with alcohol use and smoking
  • Associated with stress and sleep disorders
  • Antidepressants are most commonly used pharmacological treatment

Semester 4: Nutrition and Metabolism (17 decks)

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