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Phase 2a Sheffield Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is hyperthyroidism?

A
  • Hyperthyroidism is a common endocrine condition caused by an overactive thyroid gland causing an excess of thyroid hormone.
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2
Q

What is thyrotoxicosis?

A
  • Thyrotoxicosis is an excess of thyroid hormone, having an overactive thyroid gland is not essential → can consume too much thyroid hormone.
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3
Q

What is the difference between primary and secondary hyperthyroidism?

A
  • Primary hyperthyroidism: involves an excessive production of T3/T4 by the thyroid gland due to pathology affecting the thyroid gland itself.
  • Secondary hyperthyroidism: occurs due to excessive stimulation of the thyroid gland by TSH, secondary to pituitary or hypothalamic pathology, or from an ectopic source such as a TSH-secreting tumour.
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4
Q

What are the risk factors for hyperthyroidism?

A
  • 20-40 years old.
  • Gender → Female > Male.
  • Family history
  • Auto-immune disease → Vitiligo, T1DM, Addison’s disease.
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5
Q

What are the key presentations of hyperthyroidism?

A
  • THYROIDISM nmemonic.
    • T - Thyroidism Tremor
    • H - Heart rate increase
    • Y - Yawning
    • R - Restless
    • O - Oligomenorrhoea
    • I - Irritability
    • D - Diarrhoea
    • I - Intolerance to heat
    • S - Sweating
    • M - Muscle wasting (weight loss)
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6
Q

What are the signs of hyperthyroidism?

A
  • Postural tremor
  • Palmar erythema
  • Hyperreflexia
  • Sinus tachycardia / arrhythmia
  • Goitre
  • Lid lag and retraction
  • Signs specific to Grave’s disease
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7
Q

What are the symptoms of hyperthyroidism?

A
  • Weight loss
  • Anxiety
  • Fatigue
  • Reduced libido
  • Heat intolerance
  • Palpitations
  • Menstrual irregularity
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8
Q

What are the investigations for hyperthyroidism?

A
  • Thyroid function test (TFTs)
  • Anti-TSH receptor antibody test

*If there is serological confirmation no need for imaging
- Thyroid ultrasound
- Glucose levels
- ECG

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9
Q

What would the change be for TSH and T4 in Primary hyperthyroidism?

A
  • Decreased TSH
  • Increased T4
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10
Q

What would the change be for TSH and T4 in subclinical hyperthyroidism?

A
  • Decreased TSH
  • Normal T4
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11
Q

What would the change be for TSH and T4 in secondary hyperthyroidism?

A
  • Increased TSH
  • increased T4
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12
Q

What is the primary management for hyperthyroidism?

A
  • Beta blocker e.g. propranolol for symptomatic relief
  • Anti-thyroid in mild disease e.g. Carbimazole
  • Radioiodine treatment:first line treatment in more than mild Graves’ or toxic multinodular goitre (contraindicated in pregnancy)
    • Often require long-term levothyroxine after radioiodine therapy
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13
Q

What are other management strategies for hyperthyroidism?

A
  • Second line antithyroid medication if Carbimazole not used =Propylthiouracil, but this is associated with hepatotoxicity. In pregnancy, propylthiouracil is used in the first trimester and this is switched to carbimazole thereafter as per NICE
  • Surgery - total or hemithyroidectomy
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14
Q

What are the complications of hyperthyroidism?

A
  • HF, AF
  • Osteoporosis, proximal myopathy
  • Thyrotoxic crisis, thyroid storm
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15
Q

What is Graves disease?

A
  • The most common cause of hyperthyroidism (66% of cases).
  • An autoimmune induced excess production of thyroid hormone.
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16
Q

What are the risk factors for Graves disease?

A
  • Gender - Female > Male.
  • Age - 40-60 years old.
  • Autoimmune disease history.
  • High iodine intake.
  • Stress.
  • Radiation.
  • Tobacco use.
  • Family history.
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17
Q

What are the signs of graves disease?

A
  • Postural tremor
  • Palmar erythema
  • Hyperreflexia
  • Sinus tachycardia / arrhythmia
  • Goitre
  • Lid lag and retraction
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18
Q

What are the symptoms of graves disease?

A
  • Weight loss
  • Anxiety
  • Fatigue
  • Reduced libido
  • Heat intolerance
  • Palpitations
  • Menstrual irregularity
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19
Q

What are the clinical manifestations that are specific to Graves disease?

A
  • Thyroid acropachy - clubbing, swollen fingers and periosteal bone formation
  • Thyroid bruit - continuous sound heard over thyroid mass
  • Pretibial myxoedema - raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin
  • Eye signs
    • Exophthalmos - protruding eye
    • Ophthalmoplegia - paralysis or weakness of eye muscles
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20
Q

What are the investigations for Graves disease?

A
  • Thyroid function test’s
    • Raised T3
    • Raised T4
    • Reduced TSH
  • Other investigations related to hyperthyroidism
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21
Q

What is a thyroid storm?

A
  • Known as Thyroid storm or Thyrotoxic crisis, is a life-threatening complication of hyperthyroidism and is most commonly seen in patients with Grave’s disease or Toxic multi-nodular goitre.
  • Often occurs secondary to infections or trauma in patients with known hyperthyroidism.
  • Could also be the first manifestation of a person with undiagnosed hyperthyroidism.
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22
Q

What are the signs of a thyroid storm?

A
  • Hyperpyrexia: often >40ºC.
  • Tachycardia: often > 140 BPM, with or without atrial fibrillation
  • Reduced GCS - consciousness
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23
Q

What are the symptoms of a thyroid storm?

A
  • Nausea and vomiting
  • Diarrhoea
  • Abdominal pain
  • Jaundice
  • Confusion, delirium or coma
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24
Q

What are the investigations for a thyroid storm?

A
  • TFTs: elevated T3 and T4 levels, suppressed TSH levels
  • ECG: tachycardia; may demonstrate atrial fibrillation
  • Blood glucose: perform in all patients with reduced consciousness
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25
Q

What is the management for a thyroid storm?

A
  • Conservative: IV fluids, NG tube insertion (if vomiting), tepid sponging, paracetamol, ITU admission
  • Antithyroid drugs: propylthiouracil is generally preferred, but carbimazole is an alternative
  • Corticosteroid: IV hydrocortisone or methylprednisolone
  • Beta-blocker: propranolol PO, or IV
  • Oral iodine: Lugol’s iodine is offered > 1 hour after propylthiouracil
  • Sedation: if required, use chlorpromazine
  • Plasma exchange or thyroidectomy: in refractory patients
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26
Q

What is hypothyroidism?

A
  • Hypothyroidism is a common endocrine condition caused by a deficiency in thyroid hormone: T3 and T4.
  • Classified as either primary (95%), secondary or congenital.
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27
Q

What is primary hypothyroidism?

A

Primary hypothyroidism is due to pathology affecting the thyroid gland itself, such as an autoimmune disorder (e.g. Hashimoto’s thyroiditis) or iodine deficiency.

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28
Q

What is secondary hypothyroidism?

A

Secondary hypothyroidism is usually due to pathology affecting thepituitary gland (e.g. pituitary apoplexy) or a tumour compressing the pituitary gland. It may also be caused byhypothalamicdisorders and certain drugs

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29
Q

What is congenital hypothyroidism?

A

Congenital hypothyroidism occurs due to an absent or poorly developed thyroid gland (dysgenesis), or one that has properly developed but cannot produce thyroid hormone (dyshormonogenesis).

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30
Q

What are the risk factors for hypothyroidism?

A
  • Gender → Female > Male
  • Age → 30-50 years old
  • Family history
  • History of auto-immune disorders
  • Genetic → Turner syndrome or Down syndrome
  • Chest or Neck irradiation
  • Thyroidectomy or Radioiodine
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31
Q

What are the signs of hypothyroidism?

A
  • Dermatological: hair loss, loss of lateral aspect of the eyebrows (Queen Anne’s sign), dry and cold skin, coarse hair
  • Bradycardia
  • Goitre
  • Decreased deep tendon reflexes
  • Carpal tunnel syndrome
  • Hoarse voice
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32
Q

What are the symptoms of hypothyroidism?

A
  • Myxoedema - seen in autoimmune hypothyroidism
  • Fluid retention - oedema, pleural effusions, ascites
  • Weight gain
  • Cold intolerance
  • Lethargy
  • Dry skin
  • Constipation
  • Menorrhagia: followed later by oligomenorrhoea and amenorrhoea
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33
Q

What are the investigations for hypothyroidism?

A
  • Thyroid function test’s
  • Anti-TPO antibody test
  • Serum glucose and Hb1Ac
  • FBC and serum B12
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34
Q

What would the change be for TSH and T4 in primary hypothyroidism?

A
  • Increased TSH
  • Decreased T4
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35
Q

What would the change be for TSH and T4 in subclinical hypothyroidism?

A
  • Increased TSH
  • Normal T4
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36
Q

What would the change be for TSH and T4 in secondary hypothyroidism?

A
  • Decreased or normal TSH
  • Decreased T4
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37
Q

What is the management for hypothyroidism?

A
  • Levothyroxine (T4) - review every 3 months
  • Dose will need to be higher in pregnant women
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38
Q

What are the complications of hypothyroidism?

A
  • Ischaemic heart disease
  • Carpal tunnel syndrome, Peripheral neuropathy, Proximal myopathy
  • Myxoedema coma
  • Thyroid lymphoma
  • Side effects of medication
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39
Q

In what conditions would you see anti-TSH receptor?

A
  • Graves’ disease - 90-100%
  • Hashimoto thyroiditis - 0-5%
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40
Q

In what conditions would you see anti-TPO receptor?

A
  • Grave’s disease - 70-80%
  • Hashimoto’s thyroiditis - 90-95%
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41
Q

In what conditions would you see anti-thyroglobulin?

A
  • Graves’ disease - 20-40%
  • Hasimoto’s thyroiditis - 30-50%
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42
Q

What is Hashimoto thyroiditis?

A
  • A hypothyroid condition caused by anti-thyroid antibodies.
  • Most common cause of hypothyroidism in the western world.
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43
Q

What are the risk factors for Hashimoto thyroiditis?

A
  • Gender → Female > Male.
  • Age
  • Associated with auto-immune disease e.g. T1DM
  • Genetic disorders → Turner and Down syndrome.
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44
Q

What is subacute granulomatous thyroiditis?

A
  • Sub-acute → Between acute and chronic disease, typically develops after a viral infection of the upper respiratory system.
  • A granulomatous disease → aggregation of immune cells (macrophages) forming nodules on the thyroid gland.
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45
Q

What is post-partum thyroiditis?

A

Inflammation of the thyroid gland that women experience after giving birth.

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46
Q

What is a pituitary adenoma?

A
  • Tumours of the pituitary gland
  • They can be either non-functional (causing compressive symptoms) or functional (prolactinoma, acromegaly, Cushing’s disease etc)
  • Can either be microadenoma or macroadenoma
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47
Q

What are the risk factors for a pituitary adenoma?

A
  • MEN-1 gene
  • Carney complex
  • Familial isolated pituitary adenomas - rare
  • Age → peak incidence at 30-60 years old
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48
Q

What are the differential diagnosis for pituitary adenoma?

A
  • Rathke’s cleft cyst
  • Craniopharyngioma
  • Meningioma
  • Hypophysitis
  • Infection
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49
Q

What are the complications of a pituitary adenoma?

A
  • Hyperpituitarism
  • Hypopituitarism - may be due to compressive effects or iatrogenic
  • Conditions related to hypopituitarism e.g. hypothyroidism
  • Surgery related complications - such as mortality, meningitis, cerebrospinal fluid rhinorrhoea
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50
Q

What is a prolactinoma?

A

A benign tumour of the pituitary gland which secretes prolactin.

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51
Q

What are the risk factors for a prolactinoma?

A
  • Gender → Females > Males
  • MEN-1 → causes tumours in hormone producing glands.
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52
Q

What are the signs of a prolactinoma?

A
  • Infertility in both males and females.
  • Bones fractures.
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53
Q

What are the symptoms of a prolactinoma?

A
  • Micro-prolactinomas → often no symptoms.
  • Bi-temporal hemianopia.
  • Headaches.
  • Decreased libido.
  • Galactorrhoea - milky nipple discharge (women).
  • Amenorrhea - missed menses (women).
  • Vaginal dryness (women).
  • Brittle bones (women).
  • Gynecomastia (males)
  • Erectile dysfunction (males).
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54
Q

What are the investigations for a prolactinoma?

A
  • Prolactin test → Raised prolactin.
  • Thyrotropin releasing hormone can also be raised.
  • MRI → can visualise the prolactinoma and classify it on size.
  • PET-CT or CT can also be used to do this.
  • DNA testing → MEN-1 mutation.
  • First and second degree relatives of those with a known family history may be screened annually.
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55
Q

What is the management for a prolactinoma?

A
  • Dopamine agonist such as bromocriptine or cabergoline which will inhibit prolactin release from the prolactinoma.
  • Surgery → those who have failed medical therapy or have macro-prolactinomas.
  • Radiation therapy may be given to patients whom have had surgical treatment; however, prolactin levels are still raised.
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56
Q

What are the complications of prolactinoma?

A
  • Infertility
  • Osteoporosis
  • Pregnancy complications
  • Vision loss
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57
Q

What is acromegaly?

A

Acromegaly is a condition caused by an excess of growth hormone (GH) most commonly related to a pituitary adenoma.

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58
Q

What is gigantism?

A

Gigantism refers to excess GH production before fusion of the epiphyses of the long bones.

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59
Q

What are the risk factors for either acromegaly or gigantism?

A
  • MEN-1: pituitary adenomas, primary hyperparathyroidism, and pancreatic neuroendocrine tumours; MEN-1 is present in 6% of cases.
  • McCune-Albright syndrome
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60
Q

What are the signs for acromegaly/gigantism?

A
  • Bitemporal hemianopia: due to compression of optic chiasm by pituitary tumour
  • Facial features:
    • Prominent jaw and supra-orbital ridge
    • Coarse facial appearance
    • Prognathism: protrusion of the lower jaw
    • Splaying of teeth
    • Macroglossia: large tongue
  • Spade like hands
  • Sweaty palms and oily skin
  • Hypertension
  • Organomegaly
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61
Q

What are the symptoms for acromegaly/gigantism?

A
  • Visual disturbance
  • Headaches
  • Obstructive sleep apnoea
  • Rings and shoes are tight
  • Polyuria and polydipsia due to T2DM
  • Tingling in hands: carpal tunnel syndrome
  • Hyperprolactinaemia (20%)
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62
Q

What are the investigations for acromegaly/gigantism?

A
  • GH levels - note. not diagnostic of acromegaly as levels will vary throughout the day, as well as episodic bursts throughout growth.
  • Serum IGF-1 - elevated
  • Oral glucose tolerance test
  • Pituitary MRI
  • Visual perimetry
  • Pituitary hormone screen
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63
Q

What are the differential diagnoses for acromegaly/gigantism?

A

Acromegaloidism or pseudo-acromegaly

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64
Q

What is the primary management for acromegaly/gigantism?

A

Surgery:trans-sphenoidal resection of the pituitary. Surgery isfirst-lineas acromegaly can have significant systemic complications

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65
Q

What is the second line management for acromegaly/gigantism?

A
  • Medical:for patients unsuitable for surgeryor if there are persistent symptoms after surgery
  • Mild - Dopamine agonist e.g. cabergoline is FIRST-LINE, bromocriptine is an alternative.
  • Moderate - Somatostatin analogues e.g. octreotide
  • Severe - GH antagonist pegvisomant - usually avoided due to cost.
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66
Q

What is the third line management for acromegaly/gigantism?

A

Radiotherapy:reserved for patients who have failed medical and surgical treatment, or in elderly patients unsuitable for surgery

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67
Q

What are the complications of acromegaly/gigantism?

A
  • Cardiomyopathy, HF, hypertension
  • Sleep apnoea
  • Carpal tunnel syndrome, proximal myopathy
  • T2DM, panhypopituitarism
  • CRC
  • Organ dysfunction
  • Arthritis
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68
Q

What are the differences between acromegaly and gigantism?

A
  • Acromegaly is over secretion of growth hormone AFTER fusion of growth plates, gigantism is over secretion of growth hormone BEFORE fusion of growth plates.
  • Acromegaly has onset in adulthood, gigantism had onset in childhood.
  • Acromegaly facial features - large lips, tongue and protruding jaw.
  • Gigantism facial features - prominent forehead and jaw.
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69
Q

What is diabetes insipidus?

A
  • Diabetes insipidus (DI) is a metabolic disorder characterised by an absolute or relative inability to concentrate urine, resulting in the production of large quantities of dilute urine.
  • It is due to the patient’s inability to make ADH or respond to ADH. This leads to polydipsia, polyuria, and hypotonic urine.
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70
Q

What is cranial diabetes insipidus?

A

No ADH produced or secreted.

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71
Q

What nephrogenic diabetes insipidus?

A

Pathology affecting the kidney.

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72
Q

What are the risk factors for diabetes insipidus?

A
  • Pituitary surgery.
  • Craniopharyngioma
  • Brain injury
  • Congenital pituitary abnormalities
  • Medication e.g. lithium
  • Autoimmune disease - some cases linked to antibodies against ADH secreting cells
  • Family history
  • CNS infections
  • Pregnancy
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73
Q

What are the signs of diabetes insipidus?

A
  • Postural hypotension
  • Hypernatremia
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74
Q

What are the symptoms of diabetes insipidus?

A
  • Polyuria
  • Polydipsia
  • Dehydration
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75
Q

What are the differential diagnoses for diabetes insipidus?

A
  • Primary polydipsia
  • Diabetes mellitus
  • Hypercalcaemia
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76
Q

What are the investigations for diabetes insipidus?

A
  • Water deprivation test (desmopressin suppression test) - GOLD STANDARD
  • U&E
  • Serum glucose
  • Urine osmolarity
  • Serum osmolarity
  • MRI for cranial DI
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77
Q

What is the management for cranial DI?

A
  • Correct underlying cause
  • Mild cases can be managed conservatively e.g. low sodium diet
  • Synthetic ADH analogue - oral desmopressin
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78
Q

What is the management for nephrogenic DI?

A
  • Treat the cause - most likely renal disease
  • Thiazide diuretic e.g. Bendroflumethiazide
  • NSAIDS e.g. ibuprofen
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79
Q

What is SIADH?

A
  • The syndrome of inappropriate anti-diuretic hormone (SIADH) results from excess ADH secretion.
  • ADH excess, as the name suggests, results in reduced diuresis - water excretion and urinary output are reduced. This leads to an increase in total body water and hyponatraemia.
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80
Q

What are the risk factors for SIADH?

A
  • Age >50
  • Pulmonary conditions
  • Malignancy
  • Medicine associated SIADH induction
  • CNS disorder
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81
Q

What are the clinical manifestations of SIADH?

A
  • Mild(130-135 mmol/L):
    • Nausea, vomiting, headache, lethargy, anorexia
  • Moderate(125-129 mmol/L):
    • Weakness, muscle aches, confusion, ataxia, asterixis
  • Severe (< 125 mmol/L):
    • Reduced consciousness, seizures, myoclonus, respiratory arrest
  • NOTE - A large proportion of cases will be asymptomatic → clinical features developing during chronic disease.
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82
Q

What are the investigations for SIADH?

A
  • There is no single test that conclusively diagnoses SIADH. Instead, diagnosis relies upon suggestive biochemistry results and the clinical context.
  • Renal function
  • Serum osmolarity
  • Urine osmolarity
  • Urine sodium
  • Patient will be euvolemic
  • U&Es
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83
Q

What is the acute management for SIADH?

A

Acute hyponatraemia (<48 hours) must be treated urgently due to the risk of cerebral oedemaand herniation

  • Hypertonic (3%) salineis preferred - slow infusion to avoid complications
  • Furosemide (diuretic) -in patients who have fluid overload. Causes an increase in water, Na+, Ka+ and Cl- excretion. (Note: KCl should be replaced)
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84
Q

What is the chronic management for SIADH?

A
  • Correction should not occur too quickly and aim for amaximum increase in 10 mmol/L per day
  • Mild to moderate asymptomatic cases: fluid restriction to increase Na+ concentration
  • Severe or symptomatic cases: guidelines differ but demeclocycline or tolvaptan may be considered
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85
Q

What are the complications of SIADH?

A
  • Cerebral oedema
  • Central pontine myelinolysis
  • ‘locked in syndrome’
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86
Q

What is primary adrenal insufficiency?

A
  • Addison’s disease (primary adrenal insufficiency) is caused by destruction or dysfunction of the adrenal cortex.
  • Results in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and gonadocorticoid (androgens) deficiency
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87
Q

What are the risk factors for Addison’s disease?

A
  • Gender → Female > Male
  • Autoimmune conditions
  • Autoimmune polyendocrinopathy syndrome
  • Adrenal haemorrhage
  • Warfarin which may predispose to adrenal haemorrhage
  • TB
  • HIV
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88
Q

What are the signs of Addison’s disease?

A
  • Hyperpigmentation (caused by increased levels of ACTH) - especially in palmar creases and buccal mucosa
  • Vitiligo - due to loss of androgens
  • Loss of pubic hair in women
  • Hypotension and postural drop
  • Associated autoimmune conditions
  • Tachycardia
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89
Q

What are the symptoms of Addison’s disease?

A
  • Lethargy and generalised weakness
  • Loss of libido
  • Nausea and vomiting
  • Cachexia - weight loss and muscle wasting
  • Dehydration
  • Salt-cravings
  • Collapse and shock (Addisonian crisis)
90
Q

What are the investigations for Addison’s disease?

A
  • GOLD STANDARD - ACTH stimulation test (Synacthen test)
  • FIRST LINE - 8-9 am cortisol levels
  • 8am ACTH - inappropriately high
  • Adrenal antibodies
  • U&Es
  • Aldosterone: Renin ratio
  • Adrenal CT
  • ⅓ of people with undiagnosed Addison’s may have the following characteristic electrolyte disturbances: hyponatraemia, hyperkalaemia, hypoglycaemia and metabolic acidosis.
91
Q

What are the differential diagnoses for Addison’s disease?

A
  • Haemochromatosis due to hyperpigmentation
  • Hyperthyroidism due to weight loss and tachycardia
  • Anorexia nervosa due to weight loss
92
Q

What is the management for Addison’s disease?

A
  • Cortisol replacement - Oral hydrocortisone
  • Aldosterone replacement - Oral fludrocortisone
  • Androgen replacement - mainly in women
93
Q

What is the patient education regarding their management for Addison’s disease?

A
  • Patients should be advised regarding medication compliance and not missing doses
  • Advise patients to wear a MedicAlert bracelet or carry steroid cards in case of an Addisonian crisis
  • Advise patients todoubletheir glucocorticoid dose (hydrocortisone) if they develop an intercurrent illness
  • When travelling, patients should take extra medication plus an emergency hydrocortisone injection kit
94
Q

What are the complications of Addison’s disease?

A
  • Secondary Cushing’s due to excess hormone replacement
  • Osteopenia and osteoporosis
  • Secondary hypertension
  • Addisonian crisis - drop in glucocorticoid levels usually due to non-compliance with medication
95
Q

What is Addisonian crisis?

A

Addisonian crisis, also known as an adrenal crisis, is a state of acute insufficiency of adrenocortical hormones. It most often occurs on a background of established Addison’s disease due to precipitating factors such as poor medication compliance, infection, trauma, surgery, and myocardial infarction.

96
Q

What are the signs of an Addisonian crisis?

A
  • Hypotension
  • Hypovolemic shock
  • Reduced GCS - consciousness
  • Confusion
  • Pyrexia - increased temperature
97
Q

What are the symptoms of an Addisonian crisis?

A
  • Nausea and vomiting
  • Abdo pain
  • Trigger e.g. infection or MI
98
Q

What are the investigations for an Addisonian crisis?

A
  • 12-lead ECG
  • VBG
  • U&Es
  • FBC
  • CRP and ESR
  • TFTs
99
Q

What is the management for an Addisonian crisis?

A
  • IV fluids
  • Corticosteroids - IV hydrocortisone
  • Treat the underlying cause
100
Q

What is hyperaldosteronism?

A

Define as excess levels of aldosterone. The causes of this can either be primary (independent of RAAS) or secondary (dependent on RAAS)

101
Q

What is Conn syndrome?

A

Conn syndrome refers to primary hyperaldosteronism.

102
Q

What is primary hyperaldosteronism?

A

Primary hyperaldosteronism - Describes adrenal dysfunction causingraised aldosteronelevels withdecreased reninlevels due to negative feedback from sodium retention.

103
Q

What are the causes of primary hyperaldosteronism?

A
  • Adrenal hyperplasia
  • Adrenal adenoma
  • Adrenal carcinoma
  • Familial hyperaldosteronism
104
Q

What is secondary hyperaldosteronism?

A

Secondary hyperaldosteronism - Describes inappropriate activation of the RAAS, therefore patients haveraised aldosterone and raised reninlevels.

105
Q

What are the causes of secondary hyperaldosteronism?

A
  • Renal artery stenosis
  • Heart Failure: arterial hypovolemia due to reduced oncotic pressure causes reduced renal perfusion
106
Q

What are the risk factors for hyperaldosteronism?

A
  • Age → common in middle aged adults.
  • Family history of early onset hypertension.
  • Family history of primary hyperaldosteronism.
107
Q

What are the signs of hyperaldosteronism?

A
  • Refractory hypertension
  • Hypokalaemia - increased K+ secretion by the kidneys.
  • Metabolic alkalosis - increased H+ secretion by the kidneys.
108
Q

What are the symptoms of hyperaldosteronism?

A
  • Lethargy
  • Mood disturbance
  • Paresthesia and muscle cramps
  • Polyuria and nocturia
109
Q

What are the investigations for hyperaldosteronism?

A
  • Aldosterone: renin ratio
  • CT imagine should be performed if there is a raised ratio
  • Serum U&Es
  • ABG
  • High resolution CT of the abdomen
  • Adrenal venous sampling
  • Diagnostic method is increased plasma aldosterone which isn’t suppressed with 0.9% saline infusion or fludrocortisone administration
110
Q

What are the differential diagnoses for hyperaldosteronism?

A
  • Other forms of hypertension
    • Essential hypertension
    • Secondary hypertension
    • Liddle syndrome
111
Q

What is the management for hyperaldosteronism?

A
  • Laparoscopic adrenalectomy
  • Aldosterone antagonist - Oral spironolactone
  • ENaC inhibitor:Amiloride, a potassium-sparing diuretic, may be used if aldosterone antagonists are not tolerated.
  • In secondary hyperaldosteronism- percutaneous renal artery angioplasty
112
Q

What are the complications of hyperaldosteronism?

A
  • Secondary to long-standing hypertension:
    • Ischaemic heart disease
    • Stroke
    • Hypertensive nephropathy
    • Chronic kidney disease
  • Iatrogenic - hyperkalaemia
113
Q

What is Cushing syndrome?

A

Cushing’s syndrome is the clinical manifestation of pathological hypercortisolism from any cause.

114
Q

What are the risk factors for Cushing’s syndrome?

A
  • Gender → Female > Male
  • Age → Commonly affects people aged 20-50.
  • Long term steroid use.
  • Pituitary adenoma.
  • Small cell lung cancer.
  • Neuroendocrine tumour.
115
Q

What are the signs of Cushing’s syndrome?

A
  • Hypertension
  • Moon face
  • Buffalo hump
  • Central adiposity
  • Violaceous striae
  • Muscle wasting and proximal myopathy
  • Ecchymoses and fragile skin
  • Acne
116
Q

What are the symptoms of Cushing’s syndrome?

A
  • Bloating and weight gain
  • Mood change
  • Tiredness
  • Easy bruising
  • Increase susceptibility to infection
  • Menstrual irregularity
  • Reduced libido
117
Q

What are the investigations for Cushing’s syndrome?

A
  • GOLD STANDARD - 24-hour urinary free cortisol
  • GOLD STANDARD - Overnight dexamethasone suppression test
  • Late night salivary cortisol
  • 9am ACTH
118
Q

What are the differential diagnoses for Cushing’s syndrome?

A
  • Obesity
  • Metabolic syndrome
119
Q

What is the management for Cushing’s syndrome with an ACTD-dependent cause?

A
  • This is Cushing’s disease
  • FIRST LINE - Trans-sphenoidal resection of the pituitary
  • Glucocorticoid antagonist or radiotherapy if surgery fails.
120
Q

What is the management for Cushing’s syndrome with an ACTH-independent cause?

A
  • Iatrogenic:review the need for medication and try weaning if possible
  • Adrenal tumour:tumour resection or adrenalectomy
121
Q

What are the complications of Cushing’s syndrome?

A
  • Osteoporosis
  • Increased susceptibility to infection
  • Diabetes mellitus
  • Hypertension
122
Q

What is hyperparathyroidism?

A

Refers to a condition where there is an overproduction of parathyroid hormone.

123
Q

What is primary hyperparathyroidism?

A
  • Caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands (independent of calcium levels). This leads to hypercalcaemia.
  • Most often caused by a single parathyroid adenoma.
  • Rarely caused by hyperplasia or parathyroid carcinoma.
124
Q

What is secondary hyperparathyroidism?

A
  • Insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones. This causes hypocalcaemia. This is usually due to kidney issues as the kidney can’t filter out the phosphate or make active vitamin D.
  • The parathyroid glands reacts to the low serum calcium by excreting more parathyroid hormone. Over time the total number of cells in the parathyroid glands increase as they respond to the increased need to produce parathyroid hormone. The glands become more bulky.
  • The serum calcium level will be low or normal but the parathyroid hormone will be high.
125
Q

What is tertiary hyperparathyroidism?

A
  • This happen when secondary hyperparathyroidism continues for a long period of time. It leads to hyperplasia of the glands. The baseline level of parathyroid hormone increases dramatically.
  • Then when the cause of the secondary hyperparathyroidism is treated the parathyroid hormone level remains inappropriately high. This high level of parathyroid hormone in the absence of the previous pathology leads to high absorption of calcium in the intestines, kidneys and bones and causes hypercalcaemia.
126
Q

What are the clinical manifestations of hyperparathyroidism?

A
  • ‘Stones, thrones, bones, groans, and psychiatric overtones’
  • Stones:kidney stones or gallstones
  • Thrones: refers to the toilet,polyuriathat results from impaired sodium and water reabsorption.
  • Bones:bone pain
  • Groans: refers to symptoms ofconstipation, nausea and vomiting
  • Psychiatric overtones:depressed mood, fatigue, psychosis and confusion
127
Q

What are the investigations for hyperparathyroidism?

A
  • Bloods:
  • High levels of parathyroid hormone
  • Testing for blood levels of calcium
  • Phosphate
  • Vitamin D to confirm the type of hyperparathyroidism.
  • 24-hour urinary calcium
  • ALP
128
Q

What changes would you expect from PTH, Calcium, Phosphate and Vitamin D in primary hyperparathyroidism?

A
  • Increased PTH
  • Increased calcium
  • Decreased phosphate
  • Normal vitamin D
129
Q

What changes would you expect from PTH, Calcium, Phosphate and Vitamin D in secondary hyperparathyroidism?

A
  • Increased PTH
  • Decreased calcium
  • Increased phosphate
  • Decreased vitamin D
130
Q

What changes would you expect from PTH, Calcium, Phosphate and Vitamin D in tertiary hyperparathyroidism?

A
  • Increased PTH
  • Increased calcium
  • Normal phosphate
  • Decreased vitamin D
131
Q

What changes would you expect from PTH, Calcium, Phosphate and Vitamin D in hypoparathyroidism?

A
  • Decreased PTH
  • Decreased calcium
  • Increased phosphate
  • Normal vitamin D
132
Q

What changes would you expect from PTH, Calcium, Phosphate and Vitamin D in pseudo-hypoparathyroidism?

A
  • Increased PTH
  • Decreased calcium
  • Normal phosphate
  • Normal vitamin D
133
Q

What is the management for primary hyperparathyroidism?

A
  • If mild,increase fluid intake, avoid thiazides and high Ca2+ intake
  • Surgical removal of the tumour
  • Calcimimetics:drugs that imitate the action of calcium by attaching to the calcium-sensing receptors on parathyroid cells
134
Q

What is the management for secondary hyperparathyroidism?

A
  • Correcting the vitamin D deficiency
  • Phosphate binders
  • Renal transplant to treat renal failure
  • Sometimes parathyroidectomy
135
Q

What is the management for tertiary hyperparathyroidism?

A

Surgical removal of parathyroid tissue.

136
Q

What is hypoparathyroidism?

A

Hypoparathyroidism refers to a condition where there is a underproduction of parathyroid hormone.

137
Q

What are the three causes of primary hypoparathyroidism?

A
  • Autoimmune polyendocrine syndrome type 1
  • DiGeorge syndrome
  • Autosomal-dominant hypoparathyroidism
138
Q

What are the causes of secondary hypoparathyroidism?

A
  • Removal of parathyroid gland during surgery
  • Hypomagnesium:magnesium is needed for PTH secretion
139
Q

What are the signs of hypoparathyroidism?

A
  • Chvostek’s sign → tapping on a individual’s cheek → twitch of the facial muscles.
  • Trousseau’s sign → Carpopedal spasm which involves flexion of the wrist, thumb, and MCP joints
  • Arrhythmias
140
Q

What are the symptoms of hypoparathyroidism?

A
  • Tetany
  • Paraesthesia
  • Seizures
141
Q

What are the investigations for hypoparathyroidism?

A
  • Bloods:low PTH, low calcium, low vitamin D, high phosphate.
  • Electrocardiogram:may show prolonged QT, prolonged ST segment, and arrhythmias e.g. torsade de pointes and atrial fibrillation.
142
Q

What is the differential diagnosis for hypoparathyroidism?

A
  • Pseudohypoparathyroidism type 1A (Albright hereditary osteodystrophy)
    • The kidneys and bones don’t respond to parathyroid hormone because of a defect in their parathyroid hormone receptor.
    • Presents with: short metacarpals, round face, short stature, calcified basal ganglia. Low calcium, high phosphate.
143
Q

What is the management for hypoparathyroidism?

A
  • Calcium and vitamin D supplements
  • Recombinant human parathyroid hormone
144
Q

What is thyroid cancer? and what are the four types?

A
  • Cancers of the thyroid gland: Papillary, Follicular, Anapaestic and Medullary account for 98%.
  • The most common endocrinological malignancy.
145
Q

What are the clinical manifestations of thyroid cancer?

A
  • Palpable thyroid nodule in most cases
  • Thyroid gland may increase in size, become hard and may be irregular in shape
  • Tracheal deviation
  • Neck enlargement
  • Dysphagia
  • Hoarseness of voice
  • Dyspnoea
146
Q

What are the investigations for thyroid cancer?

A
  • Fine needle biopsy
  • TFTs
  • Ultrasound of the neck
  • Laryngoscopy
  • Radioiodine scan
147
Q

What are the differential diagnosis for thyroid cancer?

A
  • Goitre
  • Benign thyroid nodule
148
Q

What are the complications of thyroid cancer?

A
  • Airway obstruction
  • Surgery related - hypoparathyroidism, recurrent laryngeal nerve damage, bleeding
  • TSH suppression - AF, bone mineral loss
  • Radioiodine related - secondary tumours, dryness of mouth
149
Q

What is the management for thyroid cancer?

A
  • Lobectomy (or total thyroidectomy with lymph node removal).
  • If possible a total thyroidectomy is done (anaplastic thyroid cancer)
  • TSH suppression with thyroid hormone replacement (not for Medullary)
  • Chemotherapy and radiation (anaplastic thyroid cancer)
150
Q

What is pheochromocytoma?

A

Pheochromocytoma is a rare tumour (usually benign) arising from chromaffin cells in the adrenal medulla resulting in the overproduction of catecholamines.

151
Q

What are the risk factors for pheochromocytoma?

A
  • MEN 2A gene
  • MEN 2B gene
  • von-Hippel-Lindau syndrome
  • Neurofibromatosis 1
152
Q

What are the signs of pheochromocytoma?

A
  • Hypertension
  • Tachycardia
  • Paroxysmal atrial fibrillation
  • Hypertensive retinopathy
153
Q

What are the symptoms of pheochromocytoma?

A
  • Episodic headaches
  • Palpitations
  • Anxiety
  • Sweating
154
Q

What are the investigations for pheochromocytoma?

A
  • 24 hour urinary metanephrine collection and chromogranin A
  • Plasma-free metanephrines
  • CT abdomen and pelvis
155
Q

What is the management for pheochromocytoma?

A
  • Peri-operative -initial alpha blockade (e.g. phenoxybenzamine)followed bybeta-blockade (e.g. propranolol)
  • Surgical:definitive management with laparoscopic adrenalectomy
  • Patients not suitable for surgery should be treated with long term anti-hypertensives.
156
Q

What are the complications of pheochromocytoma?

A
  • Hypertensive crisis.
  • Metastatic spread
157
Q

What is a carcinoid tumour?

A

Carcinoid tumour refers to a tumour of the neuroendocrine cells, resulting in excessive release of certain hormones.

158
Q

What are the clinical manifestations of a carcinoid tumour?

A
  • Diarrhoea
  • Shortness of breath
  • Flushing
  • Itching
  • Hepatic metastases: may cause RUQ pain
  • Symptoms are worsened by alcohol and stress: stimulate the neuroendocrine cells.
159
Q

What are the investigations for a carcinoid tumour?

A
  • 24 hr urine 5-hydroxyindoleacetic acid - increased
  • Chest X-ray/ chest or pelvis MRI/ CT - location
  • Plasma chromogranin A
  • Ostreoscan
  • ECG and brain natriuretic peptide
160
Q

What is the management for a carcinoid tumour?

A
  • Decreasing emotional stress and alcohol consumption
  • Somatostatin analogues: e.g. octreotide, inhibit hormone release
  • Surgical resection
  • Debulking embolisation or radiofrequency ablation of hepatic metastases
161
Q

What is DMT1?

A

Type 1 Diabetes Mellitus (T1DM) is a metabolic disorder characterised by hyperglycaemia due to an absolute deficiency of insulin due to an autoimmune destruction of beta cells in the islet of Langerhans in the pancreas.

162
Q

What are the risk factors for DMT1?

A
  • Northern European - Especially Finnish.
  • Family history → HLA-DR3-DQ2 or HLA-DR4-DQ8.
  • Autoimmune thyroid
  • Coeliac disease
  • Addisions disease
  • Pernicious disease
163
Q

What are the key presentations of DMT1?

A

Patients are generally leaner than patients with T2DM.

164
Q

What are the signs of DMT1?

A
  • BMI typically < 25 kg/m2
  • Glycosuria
  • Ketonuria
  • Failure to thrive in children: dropping off height and weight centiles
  • Glove and stocking sensory loss
  • Reduced visual acuity
  • Diabetic retinopathy
  • Diabetic foot disease:
    • Reduced peripheral pulses
    • Calluses
    • Ulceration
    • Charcot join
165
Q

What are the symptoms of DMT1?

A
  • Polydipsia
  • Polyuria
  • Nocturia
  • Weight loss
  • Lethargy
  • Recurrent infections - e.g. patients may complain of balanitis or pruritic vulvae due to repeat candida infections
  • Evidence of complications: Blurred vision or paraesthesia
166
Q

What is the NICE diagnostic criteria for DMT1?

A
  • NICE guidelines stipulate a diagnosis should be made taking into accountclinical featuresand evidence of hyperglycaemia, e.g.random glucose ≥ 11.1 mmol/L. Additionally, NICE state that type 1 diabetics will usually have one of the following:
    • Ketosis
    • Rapid weight loss
    • Age of onset < 50 years
    • BMI < 25 kg/m2
    • Personal and/or family history of autoimmune disease
167
Q

What are the primary investigations for DMT1?

A
  • Random blood glucose:taken at any time of day and ≥11mmol/L is diagnostic
  • Fasting blood glucose:≥7.0 mmol/L
    • For both tests one abnormal value is DIAGNOSTIC in symptomatic individuals
    • Two abnormal values are required in asymptomatic individuals
  • For borderline cases
    • Oral glucose tolerance test:>11mmol/L two hours after a 75g oral glucose load. 7.8-11mmol/L suggests pre-diabetes.
    • HbA1C:measures amount of glycated haemoglobin. ≥48 mmol/mol suggests hyperglycaemia over the preceding 3 months
168
Q

What are the differential diagnoses for DMT1?

A
  • Monogenic diabetes
  • Neonatal diabetes
  • Latent autoimmune diabetes in adults
  • DMT2
169
Q

What are the lifestyle management approaches to DMT1?

A
  • Educate patient on disease and risk
  • Maintain lean weight, stop smoking and take care of feet (to reduce gangrene
    risk)
  • Patients should be educated regarding carbohydrate counting. This is a technique which allows the insulin dose to be matched to intake
  • NICE recommend that dietary advice should be tailored to the patient’s personal needs and culture
170
Q

What is the insulin management in DMT1?

A
  • Basal-bolus regimen: the FIRST LINE regimen of choice, whereby a long-acting insulin is given regularly (basal) and supplemented with a rapid-acting insulin before each meal (bolus)
    • Basal:Levemir (Detemir) is the first line basal insulin given twice-daily. Lantus (Glargine) once-daily is an alternative
    • Bolus:Humalog (Lispro) or Novorapid (Aspart) are examples
171
Q

Aside from basal-bolus regimen what are the other insulin management strategies for DMT1?

A
  • Mixed insulin regimen:a mixture of a short or rapid-actingandintermediate-acting insulin. It is given twice daily and used in those who cannot tolerate multiple injections as part of a basal-bolus regimen
  • Continuous insulin infusion:indicated if the patient has disabling hypoglycaemia or persistently hyperglycaemic (HbA1c>69mmol/mol) on multiple injection insulin therapy
172
Q

What are the complications of insulin therapy in DMT1?

A
  • Hypoglycaemia - most common (also caused by SULFONYLUREA - antidiabetic drug)
  • Injection site - lipo-hypertrophy
  • Insulin resistance - mild and associated with obesity
  • Weight gain - insulin makes people feel hungry
173
Q

What are the macrovascular complications of DMT1?

A
  • Cardiovascular
    • Ischemic heart disease
    • HF
    • Peripheral vascular disease
  • Stroke
174
Q

What are the microvascular complications of DMT1?

A
  • Neuropathy
  • Diabetic nephropathy and CKD
  • Retinopathy
175
Q

What is DMT2?

A

T2DM is characterised by acquired insulin resistance and less severe insulin deficiency.

176
Q

What are the risk factors for DMT2?

A
  • Family history → genetics. 75% risk if both parents have T2DM.
  • Increasing age.
  • Gender → Male > Female.
  • Ethnicity → Middle Eastern, South-east Asian and Western pacific.
  • Obesity and poor exercise → can be a trigger in genetically susceptible individuals.
  • Hypertension.
  • Dyslipidaemia.
  • Gestational diabetes.
  • Polycystic ovary syndrome.
  • Drugs → Corticosteroids, Thiazide diuretics.
177
Q

What are the key presentations for DMT2?

A

Generally overweight in comparison to DMT1 patients.

178
Q

What are the signs of DMT2?

A
  • Acanthosis nigricans - characterised by blackish pigmentation at the nape of the neck and in the axillae
  • Glove and stocking sensory loss
  • Reduced visual acuity
  • Diabetic retinopathy
  • Diabetic foot disease
    • Reduced peripheral pulses
    • Calluses
    • Ulceration
    • Charcot joint
179
Q

What are the symptoms of DMT2?

A
  • Weight loss
  • Polyuria
  • Polydipsia
  • Lethargy
  • Recurrent infections
  • Evidence of complications e.g. blurred vision or paraesthesia
180
Q

What are the investigations for DMT2?

A
  • Random blood glucose:taken at any time of day and ≥11mmol/L is diagnostic
  • Fasting blood glucose:≥7.0 mmol/L
    • For both tests one abnormal value is DIAGNOSTIC in symptomatic individuals
    • Two abnormal values are required in asymptomatic individuals
  • For borderline cases
    • Oral glucose tolerance test:>11mmol/L two hours after a 75g oral glucose load. 7.8-11mmol/L suggests pre-diabetes.
    • HbA1C:measures amount of glycated haemoglobin. ≥48 mmol/mol suggests hyperglycaemia over the preceding 3 months
181
Q

What is the diagnostic criteria for DMT2?

A

Diagnosing T2DMrequires an elevated plasma glucose sample and/or HbA1c on one occasion if symptomatic or two occasions if asymptomatic.

182
Q

What are the differential diagnoses for DMT2?

A
  • Pre-diabetes
  • T1DM
  • LADA - can be mistaken due to late onset
  • Monogenic diabetes - MODY
  • Ketosis-prone diabetes - idiopathic diabetes. Unprovoked ketosis or ketoacidosis. Some patients may have type 2 presentation.
  • Gestational diabetes
183
Q

What is the target HbA1c for DMT2 and what is the management?

A

Target HbA1c with lifestyle management is48 mmol/mol(6.5%). Metformin should be commenced if HbA1crises above this.

  • High fibre, low glycaemic index sources of carbohydrates
  • Include low-fat dairy products and oily fish
  • Control intake of trans and saturated fats, and limit sucrose-containing foods
  • Discourage the use of foods marketed specifically for people with diabetes
  • Aim for an initial weight loss of 5-10%
184
Q

What is the pharmacological therapy for DMT2 with the corresponding Hb1Ac level?

A
  • FIRST LINE agent and target HbA1c with metformin is 48 mmol/mol(6.5%). If level rises above this, the dose should be increased
  • Dual therapy (with a second anti-diabetic drug) should be commenced if HbA1Crises above 58 mmol/mol(7.5%) despite maximal dose (1g BD)
  • If not tolerated, monotherapy with an alternative anti-diabetic should be used and then further anti-diabetic agents added in as the HbA1c rises above 58mmol/mol (7.5%)
  • If triple therapy fails, metformin with a sulfonylurea and GLP-1 or insulin based therapy.
185
Q

What is the management for complications of DMT2?

A
  • Ramipril for BP control
  • Statins for hyperlipidaemia control
  • Orlistat - to promote weight loss in paients’s who are obese
186
Q

What are some side-effects of DMT2 treatment?

A
  • Hypoglycaemia - due to insulin or antidiabetic drugs such as sulfonylurea
  • Injection site - lipohypertrophy
  • Side effects of metformin: anorexia, diarrhoea, nausea, abdominal pain
187
Q

What are some examples of anti-diabetics?

A
  • Metformin
  • Sulfonylureas (contraindicated in pregnancy)
  • Dipeptidyl peptidase-4 inhibitor (DPP-4i)
  • Pioglitazone
  • Sodium–glucose cotransporter 2 inhibitor (SGLT-2i)
188
Q

What are the macrovascular complications of DMT2?

A
  • Cardiovascular
    • Ischemic heart disease
    • HF
    • Peripheral vascular disease
  • Stroke
189
Q

What are the microvascular complications of DMT2?

A
  • Neuropathy
  • Diabetic nephropathy and CKD
  • Retinopathy
190
Q

What is ketoacidosis?

A
  • Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment.
  • It is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes mellitus.
191
Q

What are the risk factors for ketoacidosis?

A
  • Infection
  • Undiagnosed diabetes
  • Inadequate insulin or non-adherence to insulin therapy
  • Myocardial Infarction
  • Physiological stress: e.g. trauma or surgery
  • Other co-morbidities: e.g. hypothyroidism and pancreatitis
  • Drugs that affect carbohydrate metabolism: e.g. corticosteroids, diuretics and salbutamol
192
Q

What are the signs of ketoacidosis?

A
  • Fruity smell of acetone on breath
  • Dehydration
    • Mild: only just detectable
    • Moderate: dry skin and mucus membranes; reduced skin turgor
    • Shock: tachycardia, hypotension (late), drowsiness, reduced urine output
  • Kussmaul respiration: deep, laboured breathing trying to reverse the metabolic acidosis
  • Hypotension
  • Abdominal tenderness
  • Reduced consciousness/ coma
193
Q

What are the symptoms of ketoacidosis?

A
  • Abdominal pain
  • Leg cramps
  • Headache
  • Nausea and vomiting
  • Polyuria
  • Polydipsia
  • Weight loss
  • Inability to tolerate oral fluids
  • Lethargy
  • Confusion
194
Q

What are the investigations of ketoacidosis?

A
  • Laboratory glucose: > 11.0 mmol/L
  • Venous/Arterial blood gas
  • Ketone testing
  • Urine dip
  • U&Es
  • FBC
  • CRP and ESR
  • LFTs
  • Troponin
  • ECG
195
Q

What are the the differential diagnoses for ketoacidosis?

A
  • Hyperosmolar glycaemic state
  • Lactic acidosis
  • Starvation ketosis
  • Alcoholic ketoacidosis
  • Salicylate poisoning
  • Ethylene glycol / methanol intoxication
  • Uremic acidosis
196
Q

What is the management for ketoacidosis?

A
  • ABCs
  • IV fluids
  • Insulin perfusion
  • Potassium replacement
  • Anticoagulation
197
Q

What are the complications of ketoacidosis?

A
  • Hypokalaemia
  • Hypoglycaemia
  • Cardiovascular - VTE
  • Acute kidney injury
  • Gastric stasis
  • Non-anion gap hyperchloremic acidosis
198
Q

What is hyperosmolar hyperglycaemic state?

A
  • Hyperosmolar hyperglycaemic state (HHS) is characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis, and is a serious complication of diabetes (T2DM).
  • It is often the first presentation of T2DM in up to 20-30% of patients.
199
Q

What are the risk factors for hyperosmolar hyperglycaemic state?

A
  • Infection
  • Myocardial infarction
  • Stroke
  • Poor medication compliance
  • Vomiting
  • High-dose steroids → can increase blood glucose.
200
Q

What are the signs of hyperosmolar hyperglycaemic state?

A
  • Reduced GCS - reduced consciousness/ coma
  • Dehydration - tachycardia and hypotension, dry mucous membranes, reduced skin turgor
  • Could be confused for a stroke - e.g. hemiparesis
  • Seizures
201
Q

What are the symptoms of hyperosmolar hyperglycaemic state?

A
  • Generalised weakness
  • Leg cramps
  • Lethargy
  • Confusion
  • Hallucinations
  • Headache
  • Visual disturbances
  • Polyuria
  • Polydipsia
  • Nausea, vomiting and abdominal pain: possible, but more common in DKA
202
Q

What is hypercalemia?

A

Hypercalcemia refers to a higher than normal calcium levels in the blood, generally over 10.5 mg/dL.

203
Q

What are the clinical manifestations of hypercalcemia?

A
  • Abdominal pain
  • Vomiting
  • Constipation
  • Dehydration
  • Polydipsia
  • Polyuria
  • Absent reflexes
  • Muscle weakness
  • Weight loss
  • Depression
  • Confusion
  • Hallucinations
  • Stupor
  • Hypertension
  • Pyrexia
204
Q

What are the investigations of hypercalcemia/hypocalaemia?

A
  • Bloods: high calcium. Also check parathyroid hormone, vitamin D, albumin, phosphorus, and magnesium levels.
  • 24 hour urinary Ca2+
  • ECG
  • Chest X-ray or isotope bone scan
205
Q

What is the management for hypercalcemia?

A
  • Increase urinary calcium excretion
    • Rehydration
    • Loop diuretics
  • Decrease calcium absorption
    • Glucocorticoids
  • Prevention of bone resorption
    • Bisphosphonates
    • Calcitonin
206
Q

What are the complications of hypercalcemia?

A
  • Kidney stones: due to dehydration combined with hypercalciuria
  • Renal failure
  • Ectopic calcification e.g. cornea
  • Cardiac arrest
207
Q

What is hypocalcaemia?

A

Hypocalcaemia refers to lower than normal calcium levels in the blood, generally less than 8.5 mg/dL.

208
Q

What are the signs of hypocalcaemia?

A
  • SPASMODIC
  • Spasms (Trousseau’s sign)
  • Perioral numbness/ paraesthesia
  • Anxious, irritable, irrational
  • Seizures
  • Muscle tone increases: colic, wheeze and dysphagia
  • Orientation impaired and confusion
  • Dermatitis
  • Impetigo herpetiformis (severe pustular psoriasis occurring in pregnancy)
  • Chvostek’s sign
209
Q

What is the management for hypocalcaemia?

A
  • Calcium supplements e.g. calcium gluconate
  • Vitamin D supplementation e.g. alfacalcidol, if appropriate
  • If alkalosis, correct alkalosis
210
Q

What is hyperkalaemia?

A
  • A serum level >5.5 mmol/L is considered to be hyperkalaemia.
  • A serum level >6.5 mmol/L is considered to be a medical emergency.
211
Q

What are the signs of hyperkalaemia?

A
  • Tachycardia (arrhythmia)
  • Fast irregular pulse
  • ECG differences - tall tented T waves, small P waves, wide QRS
212
Q

What are the symptoms of hyperkalaemia?

A
  • Muscle weakness
  • Light-headedness
  • Muscle cramps
  • Paraesthesia (tingling in skin)
  • Palpitations
  • Chest pain
213
Q

What are the investigations for hyperkalaemia?

A
  • 12-lead ECG
  • U&Es
  • Lithium heparin sample - rule out pseudo-hyperkalaemia
  • VBG
214
Q

What is the management for hyperkalaemia?

A
  • Non-urgent - treat underlying cause
  • Urgent
    • 10ml of 10% IV calcium gluconate or calcium chloride should be givenIMMEDIATELY if ECG changes present.
    • Insulin/dextrose infusion
    • Nebulised salbutamol
215
Q

What is hypokalaemia?

A

Potassium is an essential body cation, which has a normal plasma concentration of 3.5-5.5 mmol/L. Hypokalaemia is defined as a plasma potassium concentration < 3.5 mmol/L.

216
Q

What are the signs of hypokalaemia?

A
  • Arrhythmias
  • Muscle paralysis and rhabdomyolysis (severe)
  • Hypotonia - decreased muscle tone
  • Hypoflexia - muscles less responsive to stimuli
217
Q

What are the symptoms of hypokalaemia?

A
  • Fatigue
  • Generalised weakness
  • Light headedness
  • Muscle cramps and pain
  • Tetany
  • Palpitations
  • Constipation
218
Q

What are the different severities of hypokalaemia?

A

The diagnosis of hypokalaemia is based on a laboratory sample of plasma potassium:

  • Mild:3.0-3.4 mmol/L
  • Moderate:2.5-2.9 mmol/L
  • Severe:< 2.5 mmol/L or symptomatic
219
Q

What is the management for mild/moderate hypokalaemia?

A
  • Treat underlying cause
  • Review medication
  • Potassium replacement - Oral (SANDO-K)
220
Q

What is the management for severe hypokalaemia?

A
  • IV replacement with 40 mmol of KCL in 1 litre of normal saline
  • Do not give K+ if oliguric
  • Never give K+ as a fast stat bolus dose
221
Q

What is hypernatremia?

A
  • Defined as a high sodium plasma level of above 145mmol/L.
  • The concentration depends on both the sodium and water levels in the body.
222
Q

What is hyponatraemia?

A
  • Defined as a high sodium plasma level of below 135 mmol/L.
  • The concentration depends on both the sodium and water levels in the body.

Phase 2a Sheffield Medicine (10 decks)

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