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Phase 1 Exam > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Definition of hypernatremia

A
  • Electrolyte imbalance consisting of a rise in serum sodium conc.
  • More than 145 mmol/L
  • Severe = 150 - 160 mmol/L
  • Represents a water deficit relative to sodium and can result from a number of causes.
  • Mainly occurs in hospitals in ITU.
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2
Q

Aetiology of hypernatremia

A
  • Insufficient fluid intake in elderly, neonates or unconscious patients due to lack of access to water/confusion/coma.
  • Exacerbated by increased fluid loss - diarrhoea/sweating.
  • Associated with diabetes insipidus.
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3
Q

Presentation of hypernatremia

A
  • Non specific: nausea, vomiting, fever and confusion.

- Usually those in hospital or elderly in nursing homes.

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4
Q

Investigations of hypernatremia

A
  • Simultaneous urine and plasma osmolality and serum sodium.
  • If urine osmolality is less than that of blood this is abnormal = Diabetes insipidus.
  • If urine osmolality is more than that of blood this suggests osmotic diuresis or extrarenal water loss (Heat stroke)
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5
Q

Management of hypernatremia

A
  • Underlying cause and replace water (Oral or IV with 5% dextrose).
  • Aim to treat over 48 hrs due to increased fluid intake can lead to cerebral oedema.
  • Severe hypernatremia should also be treated using NaCl 0.9% as there could be a significant drop in sodium.
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6
Q

Complications of hypernatremia

A
  • Treatment related brain oedema/ hyperglycaemia

- Metabolic complications

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7
Q

Definition of hyponatremia

A
  • Low sodium plasma volume
  • Defined when plasma volume is less than 135 mmol/L
  • A disease of water balance - too much total body water in comparison to electrolytes leading to low plasma osmolarity.
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8
Q

Aetiology and risk factors of hyponatremia

A
  • Elderly, hospitalisations, patients taking SSRIs and thiazide like diuretics.
  • Causes depends on the hypovalaemia, normovalaemia and hypervolemia.
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9
Q

Pathophysiology of hyponatremia

A
  • If there is an excess of water in hyponatremia, this could be due to an increase in renal water uptake due to increased levels of vasopressin.
  • If there is excess salt loss along with water, this can be due to diseases such as real conditions and diarrhoea.
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10
Q

Presentation of hyponatremia

A
  • Salt loss: Thirst, nausea and postural dizziness due to hypovolaemia and extra cellular depletion.
  • Water excess: Doesn’t usually present until sodium levels less than 120 mmol/L but can lead to headache, vomiting, nausea and irritability. In severe cases, the patient may present in a common.
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11
Q

Investigations of hyponatremia

A
  • Find the cause.
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12
Q

Management of hyponatremia

A
  • Treat the underlying cause.
  • If salt loss is the reason for the hyponatremia: Replace the extra cellular volume depletion, collaids/crystalloids and also ORT.
  • If water excess: controlled fluid restriction, possible use of vasopressin 2 receptor antagonists and also diuretics.
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13
Q

How are calcium levels controlled within the blood?

A
  • Calcium is controlled by PTH and vitamin D acting on the GI tract, kidney and the bone.
  • Increased levels of PTH, lead to increase calcium in the serum.
  • This is due to increased calcium reabsorption in the kidneys and also the conversion of vitamin D into it’s most active form, which then stimulates the GI tract to absorb calcium and phosphate.
  • In the kidney, 1A - hydroxylase converts calidriol into calcitriol, which also stimulates bone resorption and the release of calcium from the bone. This is also stimulated by the calcium intself. The conversion also increase absorption in the gut.
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14
Q

Definition of hypercalcaemia

A
  • Increased calcium levels in the blood.

- Most commonly seen in elderly women.

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15
Q

Aetiology of hypercalcaemia

A
  • Primary hyperparathyroidism and malignancy.
  • Malignancy can release a peptide like derivative of PTH or directly invade the bone causing the mobilisation of calcium.
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16
Q

What is normal calcium homeostasis?

A
  • Increased calcium leads to increased calcitonin acting on the thyroid gland, this causes decrease of calcium reabsorption in the kidneys and GI tract as well as decrease in phosphate reabsorption. It also reduces calcium resorption and release of calcium from the bone.
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17
Q

Presentation of hypercalcaemia

A
  • Mild = asymptomatic
  • Severe = General malaise, depression, bone and abdo pain.
  • Most severe = dehydration, confusion or cardiac arrest.
  • Can also present with polyuria/nocturia due to calcium deposits in the kidney.
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18
Q

Investigations of hypercalcaemia

A
  • Fasting serum calcium and phosphate samples.
  • If serum phosphate is low = primary hyperparathyroidism. Normal/high = Other cause.
  • Serum PTH = Normal/high = Primary hyperparathyroidism.
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19
Q

Management of hypercalcaemia

A
  • Important to treat cause and decrease the calcium levels.

- If severe, the patient needs to be rehydrated, use bisphosphonates as well as prevent reoccurrence.

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20
Q

Definition of hypocalcaemia

A
  • Calcium levels too low.
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21
Q

Aetiology of hypocalcaemia

A
  • Increase in serum phosphate, reduced PTH function (thyroidectomy), vitamin D deficiency (UV light, malabsorption, antiepileptic drugs).
  • CKD
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22
Q

How are calcium levels low/decreased?

A
  • Decrease in PTH, leads to decrease calcium reabsorption, increase in renal phosphate, decrease in bone resorption and formation of active vitamin D - leading to calcium levels low.
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23
Q

Presentations of hypocalcaemia

A
  • Increase in nerve/muscle excitability.
  • Leading to numbness around the mouth and in the extremities followed by cramps.
  • Chvaskeks (Tap over the facial nerve in the area of the parotid gland, would lead to ipsilateral facial nerve twitching) or Trousseuas sign for neuromuscular excitability.
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24
Q

Management of hypocalcaemia

A
  • Acute = calcium gluconate.

- Peristent = vitamin D deficiency = ergocalciferol

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25
Q

How does PTH usually work?

A
  • Normally PTH is released in response to low calcium levels.
  • It is released from the parathyroid glands and is controlled by negative feedback.
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26
Q

Aetiology of primary hyperparathyroidism

A
  • Solitary adenoma

- Parathyroid tumours.

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27
Q

Pathophysiology of primary hyperparathyroidism

A
  • Inappropriate increase in PTH.
  • PTH increases causing an increase in bone resorbtion and also decrease in bone absorption of calcium. It also causes increase renal and GI reabsorption of the calcium.
  • Because calidriol can be converted into calcitriol in rapid amounts due to the PTH allowing 1 alpha hydroxylase to do this, this means that there is an increase in GI absorption of calcium but a decrease in phosphate reabsorption.
  • Because the levels of calcium are so high this means that negative feedback loop doesn’t remain as tight and therefore PTH levels are allowed to remain high.
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28
Q

Investigations of primary hyperparathyroidism

A
  • Calcium and PTH levels would be high while phosphate levels would be low.
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29
Q

Management of primary hyperparathyroidism

A
  • Rehydrate the patient, give bisphosphonates to protect againt osteoporotic degeneration and prevent reoccurance (through avoiding diet high in calcium and vitamin D and also avoiding medications such as thiazide like diuretics).
  • Possible parathyroidectomy or excision of the adenoma could be required - this would be done to avoid fractures or ulcers. But under certain criteria, including if the patient had both high serum and urine calcium levels, osteoporosis, bone disease, renal calculi or renal function and also if they were under 50.
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30
Q

Presentation of hyperparathyroidism

A
  • Can be asymptomatic.

- Could present with depression, general malaise, abdo pain, bone pain, renal stones or osteoporosis/osteopenia.

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31
Q

Complications of hyperparathyroidism

A
  • Hypoparathyroidism, recurrent laryngeal nerve damage and symptomatic drop in calcium.
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32
Q

Definition of hypoparathyroidism

A
  • Decrease in the reduction in the amount of PTH or decrease in the activity of the PTH.
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33
Q

Pathophysiology of hypoparathyroidism

A
  • Decreased PTH, leads to decreased bone resorption and increased bone reabsorption. Leads to decrease reabsorption within the kidneys but increase in phosphate. Decrease in the amount of calidriol into calcitriol leading to decreased reabsorption in the GI tract of calcium.
  • All together decrease in calcium.
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34
Q

Defintion of primary hypoparathyroidism

A
  • Decrease in the production of PTH due to the gland itself.
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35
Q

Aetiology of primary hypoparathyroidism

A
  • Autoimmune diseases, Di George syndrome
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36
Q

Investigations of primary hypoparathyroidism

A
  • Decrease in CA, but increase in phosphate levels.
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37
Q

Management of primary hypoparathyroidism

A
  • Treat as hypocalcaemia.

- Use calcium gluconate and calcitriol.

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38
Q

Aetiology of secondary hypoparathyroidism

A
  • Radiography, surgery (Parathyroidectomy or thyroidectomy) and hypomagnesium.
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39
Q

Defintion of pseudohypoparathyroidism

A
  • Failure of target cells to respond to PTH due to resistance due to genetics.
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40
Q

Presentation of pseudohypoparathyroidism

A
  • Short stature, round founds, short metacarpals, calcified basal ganglia and low IQ.
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41
Q

Investigations of pseudohypoparathyroidism

A
  • Serum calcium is low but PTH is high.
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42
Q

Management of pseudohypoparathyroidism

A
  • Same as primary hypoparathyroidism.
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43
Q

Definition of pseudopseudohypoparathyroidism

A
  • Genetic but due to normal calcium levels.
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44
Q

Definition of hyperthyroidism

A
  • Increased activity of the thyroid gland.

- Usually seen in women between the ages of 20 and 40.

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45
Q

Aetiology of hyperthyroidism

A
  • Graves disease
  • Toxic adenoma
  • Toxic multinodular goitre
  • Viral
  • Post partum
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46
Q

Presentation of hyperthyroidism

A
  • Weight loss, heat intolerance and irritability.
  • Tremor, hyperkinesis, AF/Tachycardia, warm vasodilator peripheries and goitre.
  • In terms of Graves, all of them above plus sweating as well as wide pulse, cardiac murmur, velvety skin.
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47
Q

Investigations of hyperthyroidism

A
  • Increased T3/T4 levels and suppressed TSH levels.
  • Increased TSH antibodies level if Graves disease is the aetiology.
  • Can do thyroid ultrasound to identify different causes.
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48
Q

Management of hyperthyroidism

A
  • Antithyroid drugs - Carbimazole - prevents the biosynthesis of thyroid stimulating hormone - but takes around 10 to 20 days to become therapeutic and therefore patients would require beta blockers for immediate symptom control.
  • Radioactive iodine - Uptake and accumulation in the thyroid gland and begin local irradiation.
  • Surgery - Thyroidectomy
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49
Q

Complications of hyperthyroidism

A
  • Usually seen in older patients, including arrthymias, bone mineral loss, high output cardiac failure and thyroid storm.
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50
Q

How does T3/T4 normally get produced?

A
  • The pituitary gland is stimulated to produced TSH, which cases the thyroid gland to produce T3/T4.
  • Small amount of T3 is released from the thyroid gland, but most in the circulation is created by T4 being converted to T3 in the peripheral tissues.
  • T3 and T4 circulate in the body bound to binding proteins, most commonly thyroxine binding globulin, with drugs and illnessess affecting the concentrations of these proteins.
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51
Q

Definition of hypothyroidism

A
  • Under activity of the thyroid gland, meaning reduced production of T3 and T4.
  • Usually seen in women and incidence increases with age.
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52
Q

Aetiology of hypothyroidism

A
  • Primary due to failure of the gland.

- Autoimmune (Goitre or atrophy), iatrogenic (surgery or hyperthyroidism), post partum, iodine deficiency or congenital.

53
Q

Presentation of hypothyroidism

A
  • Weight gain/difficulty losing weight, cold intolerance, fatigue, dry skin, amenorrhoea and bradycardia.
54
Q

Investigations of hypothyroidism

A
  • TFTs showing increased TSH levels and decreased T3/T4 levels.
55
Q

Management of hypothyroidism

A
  • Levothyroxine - titre up until normal levels of TSH then monitor a first 6 wks then every 3 months to allow consistent levels of TSH.
56
Q

Complications of hypothyroidism

A
  • Myxoedema coma/madness
57
Q

Definition of Hashimoto’s Thyroiditis

A
  • Autoimmune thyroid condition that leads to a diffuse enlargement of the thyroid gland, resulting in increased secretion of thyroid antibodies - T3/T4.
  • Common, mostly seen in middle aged females.
58
Q

Risk Factors of Hashimoto’s Thyroiditis

A
  • Post partum, female
59
Q

Pathophysiology of Hashimoto’s Thyroiditis

A
  • Activated CD4+ T helper cells recruit CD8+ cytotoxic T cells destroy the epithelial thyroid cells.
  • Autoimmune antithyroid antibodies released by activated B cells.
60
Q

Presentation of Hashimoto’s Thyroiditis

A
  • Weight loss, nervousness, extreme fatigue, palpitations, small non tender goitre, bloating.
61
Q

Management and Investigations of Hashimoto’s Thyroiditis

A
  • The same as hyperthyroidism.
62
Q

Definition of Addison’s disease

A
  • Primary adrenal insufficiency.
  • Results in destruction to the adrenal gland and cortex leading to decreased production of cortisol, aldosterone, dehyerepiandersterone.
  • Most commonly seen in women (Middle age and young age).
63
Q

Aetiology of Addison’s disease

A
  • Autoimmune destruction of the gland due to organ specific antibodies.
  • In the developing world, disseminated TB
64
Q

Pathophysiology of Addison’s disease

A
  • Marked reduction in glucocorticoids and mineralocorticoids due to gland destruction.
  • Symptoms don’t present until around 90% destruction.
65
Q

Presentation of Addison’s disease

A
  • Non specific symptoms
  • Including fatigue, depression, anorexia, weight loss, nausea/vomiting, hyperpigmentation, postural hypertension, hair loss (in women).
66
Q

Investigations of Addison’s disease

A
  • Short ACTH stimulation test (Shows a failure to produce increased levels of cortisol).
  • Increase in ACTH but decrease in cortisol = primary
  • Decrease in ACTH and decrease in cortisol = secondary.
  • Adrenal autoantibodies = autoimmune.
67
Q

Management of Addison’s disease

A
  • Corticosterioids - hydrocortistone and fludrocortisone.
68
Q

Definition of syndrome of inappropriate ADH secretion

A
  • Continued excretion of ADH despite normal plasma hypotonicity and normal/expanded plasma volume.
  • Characterised by hypotonic hyponatraemia, concentrated urine and euvolemic state.
69
Q

Aetiology of syndrome of inappropriate ADH secretion

A
  • Examples include TB, pneumonia, meningitis, encephalitis, drugs such as opioids.
  • Risk factors include over 50’s, respiratory illness, care home residents and post op.
70
Q

Presentation of syndrome of inappropriate ADH secretion

A
  • Presents as hyponatraemia
  • Mild = irritability, nausea, postural hypertension, headache.
  • Severe = coma, fits, cardiac arrest.
71
Q

Investigations of syndrome of inappropriate ADH secretion

A
  • About distinguishing the difference between SIADS an dilutional hyponatraemia.
  • In SIADHS - low sodium, low osmolarity in urine and serum, continued excretion of Na, no hypocalcaemia, hypotension and hypovoleamiaa and no renal, adrenal and thyroid issues.
72
Q

Management of syndrome of inappropriate ADH secretion

A
  • Treat cause if mild.

- If patient is symptomatic then think about water retention (vasodilators), vasopression V2 antagonists.

73
Q

Definition of hyperaldosteronism

A
  • Increased secretion of aldosterone - more than the body requires.
  • Normal production is regulated by the renin angiotensin II system.
74
Q

Aetiology of hyperaldosteronism

A
  • Adrenal adenoma secreting aldosterone or bilateral adrenal hyperplasia.
  • Risk Factors include family history and family history of early onset hypertension/stroke.
75
Q

Pathophysiology of hyperaldosteronism

A
  • Excess secretion of aldosterone, independant to the renin angiotensin II system.
  • Leads to increased Na and Water retention and decreased renin release.
  • Urinary loss of K+ and H+ and also exchange of Na at the distal nephron, possibly leading to hyperkalaemia.
76
Q

Presentation of hyperaldosteronism

A
  • Hypertension, usually patients between 20 to 70.

- Can be asymptomatic, or muscle pain, lethargy and mood changes.

77
Q

Investigations of hyperaldosteronism

A
  • Plasma aldosterone: renin ratio. Increase in aldosterone despite saline or fludrocortisone.
  • CT/MRI to distinguish aetiology.
78
Q

Management of hyperaldosteronism

A
  • Surgical resection = adenoma.

- Hypertension treatment with spironlactone = hyperplasia.

79
Q

Definition of Cushing’s Syndrome

A
  • Clinical manifestations of pathological hypercortisolism.

- Pathological hypercortisolism is an increase in free circulating glucocorticoids that persistent and inappropriate.

80
Q

Aetiology of Cushing’s Syndrome

A
  • Synthetic steroid use or ACTH use in conditions such as asthma.
  • Pituitary tumour.
81
Q

Pathophysiology of Cushing’s Syndrome

A
  • Increased release of ACTH (Adrenocorticotropin hormone) that leads to an increase in cortisol.
82
Q

Risk Factors of Cushing’s Syndrome

A
  • Diabetes, dyslipidaemia, metabolic bone disease and hypertension.
83
Q

Presentation of Cushing’s Syndrome

A
  • Weight gain - central obesity, moon face and buffalo hump neck.
  • Proximal muscle weakness.
  • Thin skin with easy bruising.
84
Q

Investigations of Cushing’s Syndrome

A
  • Confirmed raised cortisol: use dexamethasone to suppress the cortisol levels, late night salivary levels, urine cortisol levels, and 1mg every night suppression test.
  • Establish the aetiology: MRI/CT and morning ACTH.
85
Q

Differentials of Cushing’s Syndrome

A
  • Obesity/ metabolic syndrome.
86
Q

Management of Cushing’s Syndrome

A
  • Pituitary tumour surgical removal.
  • Use of medication inhibit cortisol production.
  • External beam irradiation (Slow/ contraindicated)
  • Iatrogenic - reduced levels of steroids.
87
Q

How does Growth hormone work?

A
  • Released by the pituitary gland, controlled by growth hormone releasing hormone stimulating release and somatotroponin inhibits release.
  • Grelin also stimulates the release of growth hormone.
  • Excessive GH leads to gigantasism in children and acromegaly in adults.
88
Q

Definition of acromegaly

A
  • Chronic progressive multisystemic condition that has increased mortality and high morbidity.
  • Excessive secretion of GH.
  • Female and males at the same risk and increased with increasing age.
89
Q

Aetiology of acromegaly

A
  • Pituitary somatroph adenoma.

- Genetics

90
Q

Presentation of acromegaly

A
  • Can be grouped into metabolic effects and compression of the tumour.
  • Symptoms include coarsening of the facial features, soft tissues and skin changes.
  • Carpal tunnel syndrome, joint pain and dysfunction.
91
Q

Investigations of acromegaly

A
  • If there is no detectable levels of GH then acromegaly is ruled out.
  • Increase IGF -1 is seen.
  • Glucose tolerance test is diagnostic - no suppression less than 1 = acromegaly.
  • MRI
92
Q

Management of acromegaly

A
  • Reduce the levels of IGF -1.
  • Surgical resection.
  • Medication ( Somatroponin analogues and growth hormone receptor anatgonist to suppress the levels of GH).
  • External beam radiotherapy.
93
Q

Complications of acromegaly

A
  • Increased mortality due to CVD/Cancer.

- Vascular complications including high BP and LVH.

94
Q

Definition of growth hormone deficiency

A
  • Low GH

- Can be alone or in combination with other anterior/posterior pituitary.

95
Q

Aetiology of growth hormone deficiency

A
  • Congenital and acquired (tumour or cystic)
96
Q

Risk factors of growth hormone deficiency

A
  • Family history, other hormone deficiencies, CNS tumours or radiotherapy.
97
Q

Pathophysiology of growth hormone deficiency

A
  • Hypothalmus released GHRH stimulates the pituitary to release GH and is inhibited by somatostatin.
  • GH then binds to receptors and signal a cascade causing IGF - 1.
  • Low IGF = hypothyroidism and malnutrition.
  • So with GH deficiency, then this can lead to poor growth and puberty delays.
98
Q

Presentation of growth hormone deficiency

A
  • Short stature, poor growth velocity, short height for age, absent/delayed puberty.
  • CNS presentations and some facial characteristics.
  • Lean body mass.
99
Q

Management of growth hormone deficiency

A
  • Recombinant growth hormone (Somatropin) and treat underlying cause.
100
Q

Complications of growth hormone deficiency

A
  • Osteoporosis, short final height and central hypothyroidism.
101
Q

Definition of diabetes insipidus

A
  • Metabolic disorder where the patient is unable to concentrate urine at the kidneys leading to the production of large amounts of diluted urine.
102
Q

Aetiology of diabetes insipidus

A
  • Cranial - pituitary tumours, trauma or neurosurgery.
103
Q

Presentation of diabetes insipidus

A
  • Polyuria and polysdipsia
  • Signs of hypernatraemia
  • Signs of volume depletion.
104
Q

Pathophysiology of diabetes indispidus

A
  • Impaired vasopressin secretion or renal resistance.
105
Q

Investigations of diabetes insipidus

A
  • Urine volume measured over a period of time.
  • Increase in serum sodium levels and osmolality.
  • Decrease in volume osmolality.
  • Water deprivation test = more than 50% osmolality increase.
  • Desmopressin test leads to reduce urine output and increased osmolality.
106
Q

Management of diabetes insipidus

A
  • Treat cause
  • Desmopressin
  • Mild cases = thiazide diuretics and low sodium diet.
107
Q

Definition of hypoglycaemia

A
  • Low plasma glucose levels leading to impaired brain function - neuroglycopenia.
  • Less than 3mmol/l
  • Mild/severe
  • One of the most common endocrine emergencies.
108
Q

Aetiology of hypoglycaemia

A
  • Middle aged, women, increase alcohol consumption and post bariatric surgery.
109
Q

Presentation of hypoglycaemia

A
  • Key symptoms usually excess sweating, anxiety, hunger and tremour.
  • Could also include dizziness, confusion, palpitations, drowsiness and coma.
110
Q

What is fasting hypoglycaemia?

A
  • Usually caused by insulin or sulfylurea in diabetics, due to missed meals, accidental or non accidental overdose.
111
Q

What is post prandial hypoglycaemia?

A
  • Usually seen in type 2 diabetics or post bariatric surgery.
  • Episodic types can be control by eating regular high carb meals and restricting insulin.
112
Q

Definition of puberty delays

A
  • Defined as lack of pubertal signs in girls over the age of 13 and boys over the age of 14.
  • More common in boys.
113
Q

Aetiology of puberty delays

A
  • Most patients have a temporary delay to puberty associated with inhibition of the hypothalamopituitary axis.
  • Gondatrophin deficiency can be due to surgery, tumours or genetics.
  • Congenital/chromsomal disorders.
114
Q

What is Turners?

A
  • 45X, most common in females.
  • Cardiovascular abnormalities, webbed neck, widely spaced nipples and gonadal dysgenesis.
  • Survillence, somatropin and CVD protection.
115
Q

What is Klinefelters?

A
  • 47XXY, associated with osteoporosis, males
116
Q

What is Kallaman’s?

A
  • Males
117
Q

Risk factors of puberty delays

A
  • Family history, congenital pituitary structural abnormalities, genes and chromosomal disorders.
118
Q

Presentation of puberty delays

A
  • Testes less than 3ml in males.
  • Lack of breast development and periods in girls.
  • Lack of pubic and axillary hair, acne and odour in all.
119
Q

Investigations of puberty delays

A
  • X ray of non dominant wrist to look for delayed bone age through epispheal plates.
  • LHR stimulation test and gonadotrophin stimulation test.
120
Q

Management of puberty delays

A
  • Treat cause, use of GnRH agonists and somatropin.
121
Q

Definition of diabetes

A
  • Metabolic disorder that is characterised by chronic hyperglycaemia due to lack of insulin.
  • Type 1: usually present earlier in life and in the Western world, onset usually over days and weeks.
  • Type 2: usually presents later in life and due to affluent lifestyle.
122
Q

Aetiology of diabetes

A
  • Type 1: genetic predisposition, caused by the autoimmune destruction of pancreatic B cells.
  • Type 2: obesity (around 30% loss of B cells).
123
Q

Pathophysiology of diabetes

A
  • Type 1: autoimmune destruction of pancreatic B cells leading to no insulin production, causing absolute insulin deficiency.
  • Type 2: Gradual resistance to insulin, or lack of production by B cells or a combination.
124
Q

Presentation of diabetes

A
  • Type 1: polyuria, polydipsia, lethargy, weight loss, diabetic ketoacidosis.
  • Type 2: sometimes asymptomatic, candidal infection, skin infection, UTI, lethargy and blurred vision.
125
Q

Management of diabetes

A
  • Type 1: insulin regime and a diet high in carbs.
  • Type 2: lifestyle changes, metformin (Works by decreasing hepatic glucose production, which decreases intestinal glucose absorption, to allow improved sensitivity to insulin, increasing peripheral glucose uptake and utilisation), after add combination of other agents such as sulfylureas, meglitinde and then insulin.
126
Q

Investigations of diabetes

A
  • Serum glucose - Fasted = more than or equal to 7 mmol/L or random = more than 11.1 mmol/L
  • Oral glucose tolerance test = more than or equal to 11.1 mmol/L
  • HbA1c more than 48 mmol/mol
127
Q

Complications of diabetes

A
  • Neuropathic pain, autonomic neuropathy, sensory loss and consequences, peripheral vascular disease, retinopathy and nephropathy.
128
Q

What medical emergencies are there in diabetes?

A
  • Diabetic ketoacidosis: due to insulin deficiency, usually seen in undiagnosed type 1 diabetes, those with interruptions to their management or with stress from intercurrent medical conditions. Presents with profound dehydration, vomiting, sunken eyes, low BP, Kussmaul’s resp and breath that smells like ketones. Treatment would be through insulin therapy (Important never to stop) and fluid over 24 hrs.
  • Hyperosmolar hyperglycaemic state - usually seen in type 2 diabetics, presents in coma, investigations would indicated hyperglycaemia, hyperosmolairity and mild/no ketosis. Difference would be high glucose and osmolarity.

Phase 1 Exam (25 decks)

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