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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

EACDIT of Carcinoid Syndrome

A

E: Rare.

A: Neuroendocrine tumour; secretes serotonin, histamine and bradykinin. Slow-growing. Commonly metastasizes to liver. Must be present in liver for symptoms.

C: Diarrhoea, SOB (bronchoconstriction due to serotonin), Flushing (Histamine/Bradykinin) & Pruritus. Pellagra (reduced tryptophan; niacin). Tricuspid regurg & pulmonary stenosis (serotonin causes fibrosis).

DDx: Serotonin Syndrome

Ix: Oscreotide Scan, Urinary 5-Hydorxyindoleacetic acid (5-HIAA) & Niacin. Plasma Chromogranin Ay (statin)

Tx: Somatostatin analogues (inhibitory); Ocreotide, Chemo & Lifestyle: reduce stress and alcohol. Surgical resection. Cyproheptadine for diarrhoea.

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2
Q

Pellagra features

A

Niacin (B3) defiency

The 3 D’s

Diarrhoea

Dermatitis

Dementia

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3
Q

(Multiple Endocrine Neoplasia) MEN I EACDIT

A

E: Autosomal Dominant mutation in MEN1 gene (tumour suppressor) on Chromosome 11.

A: affects the Pituitary (adenoma), Parathyroid (95%) & Pancreas (3 P’s). Most common is parathyroid - hyperparathyroidism (increased calcium), early age (25yrs) and affects multiple glands.

C: Headaches/Bitemporal hemianopia/Diplopia (pituitary adenoma). Hypercalcaemia (bones, stones, groans, psychic moans), Peptic Ulcers (gastrinoma aka Zollinger-Ellison), Insulinoma (hypoglycaemia), Glucagonoma (hyperglycaemia). Adenomas (prolactinoma): Galactorrhea/Gynaecomastia. Acromegaly/Gigantism.

Dx: Clinical findings.

Ix: Genetic testing.

Tx: Parathyroidectomy. Pituitary - surgical if ACTH or dopamine agonist (ropinirole) if prolactinoma.

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4
Q

(Multiple Endocrine Neoplasia) MEN IIa EACDIT

A

E: Autosomal Dominant mutation in RET gene (proto oncogene) on chromosome 10.

A: affects the Parathyroid, Medullary (C-cells secrete calcitonin) Thyroid & Phaeochormocytoma (epinephrine/norepinephrine)

C: Anxiety, sweating, HT. Hoarseness, coughing and dysphagia (Thyroid).

Dx: Clinical findings.

Ix: Genetic testing

Tx: Surgery; thyroidectomy

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5
Q

(Multiple Endocrine Neoplasia) MEN IIb EACDIT

A

E: Autosomal Dominant mutation in RET gene (proto oncogene) on chromosome 10.

A: affects the Mucosa (skin and mouth), Marfan, Medullary Thyroid & Phaeochromocytoma (4 M’s). Multiple neuromas (nerve tissue).

C: Hoarseness, coughing and dysphagia (Thyroid).

Dx: Clinical.

Ix: Genetic testing. Urinary metanephrines.

Tx: Surgery; thyroidectomy.

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6
Q

Cushing’s Syndrome

A

A: Excessive cortisol.

Exogenous (more common): long-term steroid use

Endogenous (less common): Pituitary adenoma (Cushing’s disease); secretes ACTH or Ectopic (small cell lung Ca)

Ix: Overnight Dexamethasone suppression test.

Low dose (1mg) suppression: indicates exogenous cause (steroids)

High dose (8mg) suppression: indicates endogenous (pituitary; if cortisol suppressed also). Cortisol unaffected; adrenal adenoma.

No suppression: indicates paraneoplastic (ectopic) secretion (i.e. small cell lung Ca or carcinoid; less common)

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7
Q

Primary Hyperaldosteronism (Conn’s Syndrome)

A

Aetiology: Increased aldosterone (mineralocorticoid; increased Na reabsorption & increased K/H secretion).

Causes: Bilateral idiopathic adrenal hyperplasia (70%; commonest cause). Adrenal adenoma (unilateral). Familial hyperaldosteronism. Adrenal carcinoma (rare).

Signs: HT, Hypokalaemia, alkalosis

Symptoms: Muscle weakness

Ix: Aldosterone:Renin ratio; High:Low (due to high BP). High-res CT; adrenal venous sampling to distinguish between bilateral/unilateral if CT is negative.

Tx: Adrenal adenoma (surgery). Bilateral adrenocortical hyperplasia (spirinolactone; aldosterone antagonist)

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8
Q

Secondary Hyperaldosteronism

A

Aetiology: Increased renin. Renal BP is lower vs. systemic BP. Causes: RAS (atherosclerosis), Renal Artery obstruction, HF.

Clinical Features: HT (tx-resistant), hypokalaemia, alkalosis, muscle weakness.

Ix: Aldosterone:Renin ratio: High:High. Doppler US (RAS). BP. U&Es (hypokalaemia). Alkalosis.

Imaging: CT/MRI (adrenal tumour). Doppler/CT Angio/MRA (RAS, Obstruction).

Tx: Aldosterone antagonists (eplerenone/spironolactone). Surgery (adenoma). Percutaneous renal artery angioplasty (RAS).

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9
Q

Prolactin and galactorrhoea

A

Aetiology: Prolactin is secreted by the Ant. Pituitary. Dopamine inhibits prolactin relaease.

Causes: P’s

  • Pregnancy
  • Prolactinoma
  • Physiological - stress, exercise, sleep
  • Polycystic ovarian syndrome (PCOS)
  • Primary hypothyroidism (TRH)
  • Phenothiazines (chlorpromazine), metoclopramide, domperidone, haloperidol

Clinical Features:

Men; impotence, low libido, galactorrhoea.

Women; amenorrhoea, galactorrhoea.

Tx: Dopamine antagonists (bromocriptine)

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10
Q

Thyroid Cancers

A

Types (by prevalence):

Papillary (3 P’s: Prognosis good, Psamomma bodies (pale empty nuclei), Prevalent): Young females.

Follicular: Solitary nodule.

Medullary: Parafollicular C-cells; secrete calcitonin (low PTH); part of MEN-II. Endocrine features of Skin flushing (Serotonin) & Diarrhoea (VIP).

Anaplastic: Non-responsive to Tx. Elderly females. Aggressive.

Clinical Features: Solitary painless nodule. Firm and non-mobile. Hoarseness. Dysphagia. Non-functional (no signs of thyroidism).

Ixs: US of thyroid gland. FNA.

Treatment (papillary/follicular): Total thyroidectomy + radioiodine (I-131). Yearly thyroglobin levels (disease recurrence).

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11
Q

Primary Adrenal Insufficiency (Addison’s)

A

E:

A: Autoimmune destruction of adrenal cortex (developed countries). Reduced cortisol and aldosterone (destruction of adrenal cortex).

Primary causes

  • TB (developing countries; spreads to adernal cortex)
  • Metastases (e.g. bronchial carcinoma)
  • Meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
  • HIV
  • Antiphospholipid syndrome

Secondary causes

  • pituitary disorders (e.g. tumours, irradiation, infiltration)
  • Exogenous glucocorticoid therapy

C:

  • lethargy, weakness, anorexia, N&V, wt loss, ‘salt-craving’
  • Hyperpigmentation (primary; notably palmar creases), vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
  • Hyponatraemia and hyperkalaemia
  • Addisonian Crisis: collapse, shock, pyrexia

Ix: ACTH stimulation (Synacthen). Primary: High serum ACTH. Secondary: Low ACTH.

  • Renin levels are typically high (stimulates aldosterone release) and aldosterone levels low in Addison’s disease.
  • In secondary adrenal insufficiency, the renin-angiotensin system can function normally.
  • Serum DHEA-S — typically low in Addison’s disease.
  • Thyroid function tests.
  • Autoantibody levels — adrenal cortex autoantibodies or antibodies against 21-hydroxylase are present in more than 80% of people with recent-onset autoimmune adrenalitis.

Tx: Hydrocortisone (glucocorticoid) & Fludrocortisone (mineralocorticoid). DHEA. Double hydrocortisone dose during illness, injury or surgery.

ADDISONIAN CRISIS: IM Hydrocortisone. Features may include hypotension, hypovolaemic shock, delirium, reduced consciousness, acute abdominal pain, vomiting, headache, low-grade fever, and muscle weakness.

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12
Q

Addisonian Crisis

A

Causes

  • Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  • Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  • Steroid withdrawal

Management

  • Hydrocortisone 100 mg IM or IV
  • 1L NaCl infused over 30-60 mins or with dextrose if hypoglycaemic
  • Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
  • Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
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13
Q

Interpret the Thyroid results:

TSH 14.3 (05.-5.5)

Free T4 14 (9-18)

A

Poor Compliance with Thyroxine

TSH High

T4 Low

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14
Q

Interpret the Thyroid results:

TSH 3.4 (0.5-5.5)

Free T4 21.3 (9-18)

A

Thyrotoxicosis (e.g. Graves’ disease)

TSH Low

T4 High*

*In T3 thyrotoxicosis the free T4 will be normal

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15
Q

Interpret the Thyroid results:

TSH 7.2 (0.5-5.5)

Free T4 4.3 (9-18)

A

Primary hypothyroidism

TSH High

T4 Low

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16
Q

Interpret the Thyroid results:

TSH 0.2 (0.5-5.5)

Free T4 3.7 (9-18)

A

Secondary hypothyroidism

TSH Low

T4 Low

Replacement steroid therapy is required prior to thyroxine

17
Q

Interpret the Thyroid results:

TSH 0.1 (0.5-5.5)

Free T4 3.9 (9-18)

A

Sick euthyroid syndrome

TSH Low

T4 Low

Common in hospital inpatients
T3 is particularly low in these patients

18
Q

Interpret the Thyroid results:

TSH 7.6 (0.5-5.5)

Free T4 11.3 (9-18)

A

Subclinical hypothyroidism

TSH High

T4 Normal

19
Q

Interpret the Thyroid results:

TSH 0.2 (0.5-5.5)

Free T4 12.9 (9-18)

A

Steroid therapy

TSH Low

T4 Normal

20
Q

Thyroidism Causes

A

Hypothyroidism

Hyperthyroidism

21
Q

Grave’s Disease

A

E: 30-40yrs. F:M (8:1). FHx. Smoking.

A: Autoimmune. 80% genetic. IgG Abs to TSH Rs; cause chronic stimulation.

C: Heat intolerance, wt loss, sweating, palpitations, tachycardia, anxiety, tremor. Eye disease: exophthalmos. Pretibial myxoedema: waxy discolouration of shins.

Ix: TFTs: TSH low, T3/4 High. Specific test: TSH R. Abs (TRAbs). Technetium scan of thyroid gland: considered if TRAbs are negative.

Tx:

ß-blockers (Symptom-control)

  • For rapid control of hyperthyroidism symptoms, including palpitations, tachycardia, anxiety, and heat intolerance. E.g. propranolol.

Radioactive iodine:

  • 1st line definitive treatment, unless antithyroid drugs are likely to achieve remission or it is unsuitable. It may be unsuitable due to pregnancy, attempts to conceive within the next 4-6 months, presence of active eye disease, or concerns about compression or malignancy.
  • Patients often become hypothyroid, thus may require replacement therapy.

Antithyroid drugs

  • Offer a 12-18 month course as first-line definitive treatment if it is likely to achieve remission, or if radioactive iodine and surgery are unsuitable.
  • Remission is the continuation of euthyroid status after withdrawal of antithyroid drugs and occurs in around 50% of Graves’ patients. Remission is more likely in mild and uncomplicated Graves’ disease.
  • Examples include carbimazole (first-line) and propylthiouracil.

Surgery

  • Total thyroidectomy offered as first-line definitive treatment if concerns about compression or malignancy, or radioactive iodine and antithyroid drugs unsuitable.
  • Consider if antithyroid drugs have been tried but hyperthyroidism persisted or relapsed.
  • Risks: recurrent laryngeal nerve damage, hypoparathyroidism.
  • Patients become hypothyroid, thus require replacement therapy.
22
Q

When to avoid radioactive Iodine

A

Important exceptions to using radioactive iodine first-line include:

  • Pregnancy
  • Attempts to conceive within the next 4-6 months
  • Presence of active eye disease
  • Concerns about compression or malignancy.
  • In these cases, it must be considered whether surgery or antithyroid drug therapy is the most appropriate option.
23
Q

Hypothyroidism

A

E: 5-10x more common in females.

A: Hashimoto’s thyroiditis (developed). Iodine deficiency (developing). Iatrogenic (surgery, medications - lithium, amiodarone).

Secondary causes (rare): Hypopituitarism (TSH impaired); tumours, infection, vascular (sheehan’s) and radiation.

C: Weight gain, fatigue, Cold intolerance (sensitive to cold), fatigue, ammenorrhoea, constipation, fluid retention. Deep tendon reflexes. Hoarse voice. Dry, coarse scalp hair, loss of lateral aspect of eyebrows

Ixs: TSH, TFTs: Primary Hypothyroidism:TSH High & TFTs Low(no negative feedback).Secondary Hypothyroidism:TSH & TFTs Low.

Specific tests: Thyroid peroxidase antibody (TPOAb) & Thyroglobulin antibody (TgAb)

Tx: Oral levothyroxine (synthetic T4). Measured monthly until stable (TSH high indicates low dosage. TSH low indicates high dosage).

24
Q

Subacute Thyroiditis

A

E: 20-30yrs. F:M (4:1)

A:

C: Initial Hyperthyroid followed by prologonged Hypothyroid phase.

  • phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
  • phase 2 (1-3 weeks): euthyroid
  • phase 3 (weeks - months): hypothyroidism
  • phase 4: thyroid structure and function goes back to normal

Ix: Thyroid scintigraphy: globally reduced uptake of iodine-131

Tx:

  • usually self-limiting - most patients do not require treatment
  • thyroid pain may respond to aspirin or other NSAIDs
  • in more severe cases steroids are used, particularly if hypothyroidism develops
25
Q

General Management of T1DM

A

Insulin regime

  • offer multiple daily injection basal–bolus insulin regimens, rather than twice‑daily mixed insulin regimens, as the insulin injection regimen of choice for all adults
  • Twice‑daily insulin detemir (long-acting insulin) is the regime of choice. Once-daily insulin glargine or insulin detemir is an alternative
  • Offer rapid‑acting insulin analogues injected before meals, rather than rapid‑acting soluble human or animal insulins, for mealtime insulin replacement for adults with type 1 diabetes

Metformin

  • NICE recommend considering adding metformin if the BMI >= 25 kg/m²

HbA1c

  • should be monitored every 3-6 months
  • adults should have a target of HbA1c level of 48 mmol/mol (6.5%) or lower.
  • NICE do however recommend taking into account factors such as the person’s daily activities, aspirations, likelihood of complications, comorbidities, occupation and history of hypoglycaemia

Self-monitoring of blood glucose

  • 4x daily, including before each meal and before bed
  • more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding.

Blood glucose targets

  • 5-7 mmol/l on waking and
  • 4-7 mmol/l before meals at other times of the day
26
Q

Diabetes Sick Day Rules

A
  • Increase frequency of blood glucose monitoring to four hourly or more frequently
  • Encourage fluid intake aiming for at least 3 litres in 24hrs
  • If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
  • It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
  • Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
27
Q

Diabetes indication for admission (Warning Signs of DKA)

A
  • Suspicion of underlying illness requiring hospital treatment eg myocardial infarction
  • Inability to keep fluids down - admit if persisting more than a few hours
  • Persistent diarrhoea
  • Significant ketosis in an insulin dependent diabetic despite additional insulin
  • Blood glucose persistently >20mmol/l despite additional insulin
  • Patient unable to manage adjustments to usual diabetes management
  • Lack of support at home e.g. a patient who lives alone and is at risk of becoming unconscious
28
Q

Diabetic Neuropathy Management

A

Diabetes typically leads to sensory loss and not motor loss in peripheral neuropathy. Painful diabetic neuropathy is a common problem in clinical practice.

NICE updated it’s guidance on the management of neuropathic pain in 2013. Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:

  • 1st Line: Amitriptyline, Duloxetine, Gabapentin or Pregabalin
  • if the first-line drug treatment does not work try one of the other 3 drugs
  • Tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
  • Topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
  • Pain management clinics may be useful in patients with resistant problems
29
Q

DKA Features and Management

A

Clinical Features

  • abdominal pain
  • polyuria, polydipsia, dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’ smell)

Management

Fluid replacement

  • most patients with DKA are deplete around 5-8 litres
  • isotonic saline is used initially, even if the patient is severely acidotic

Insulin

  • an IV infusion should be started at 0.1 unit/kg/hour
  • once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started

Correction of electrolyte disturbance

  • Add Potassium (0.9% sodium chloride 1L with potassium chloride)
  • serum potassium is often high on admission despite total body potassium being low
  • this often falls quickly following treatment with insulin resulting in hypokalaemia
  • if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
  • Continue with long-acting insulin
  • Stop short-acting insulin

DKA resolution is defined as:

  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L

Further points

  • both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist
  • if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin
  • the patient should be reviewed by the diabetes specialist nurse prior to discharge
30
Q

DKA treatment complications

A

Complications may occur from DKA itself or the treatment:

  • gastric stasis
  • thromboembolism
  • arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  • acute respiratory distress syndrome
  • acute kidney injury

* children/young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought

Finals (21 decks)

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