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Medicine Phase 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Define Diabetes Mellitus

A

A group of chronic disorders characterised by the body’s impaired ability to produce/respond to insulin resulting in abnormal glucose metabolism

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2
Q

Types of diabetes

A
  • Type 1
  • Type 2
  • Gestational (oft improves after birth )
  • Maturity Onset Diabetes of the Young (autosomal dominant)
  • Neonatal
  • Steroid induced
  • Wolfram’s syndrome and Alstrom syndrome
  • Type 3 (including cystic fibrosis)
  • Latent Autoimmune Diabetes in Adults
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3
Q

RFx for T1DM

A
  • Northern European
  • Family Hx/Personal Hx of Diabetes/other AI conditions
  • Genetic predisposition: HLA-DR3/DR4 or DQ8
  • Environmental factors
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4
Q

Pathophys T1DM

A
  • GLUT4 is insulin dependant
  • Is unable to bind to cell membrane if low insulin
  • Glucose unable to enter cells leading to starvation state and gluconeogenesis
  • hyperglycaemia as glucose builds up in blood
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5
Q

Typical presentation T1DM

A
  • Polyuria (osmotic diuresis as kidneys are unable to reabsorb excess glucose)
  • Polydipsia (thirst centre in hypothalamus stimulated)
  • Weight loss (from excessive lipolysis, proteolysis and fluid depletion)
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6
Q

T1DM diagnosis

A

If symptomatic:
- only 1 raised plasma glucose reading is needed

  • Fasting >= 7mmol/L
  • Random glucose >= 11.1 mmol/L

If asymp:
- 2 positive readings needed

Can also do oral glucose test and measure fasting and 2 hours post-prandial glucose levels

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7
Q

Normal blood sugar range

A
  • Fasting: 4.0 - 5.4 mmol/L
  • 2 hours post-prandial: up to 7.8
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8
Q

Definition of diabetic ketoacidosis

A

Medical emergency characterised by:

  • Hyperglycaemia (>11.1)
  • Ketosis i.e ketones > 3 mmol/L (norm < 0.6)
  • Acidosis i.e pH < 7.3 (norm 7.35-7.45)
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9
Q

RFx for DKA

A
  • untreated T1DM
  • Infection/Illness
  • Myocardial Infarction (also more likely to happen if ketotic)
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10
Q

Presentation of DKA

A

Diabetes:
- Polydipsia/polyuria/nocturia -> Dehydration -> hypotension

Ketosis:
- Fruity breath

Acidosis:
- N+V
- Abdo pain
- Kussmaul breathing

Drowsy/Confused

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11
Q

DKA pathophys

A
  • 0 insulin -> decreased uptake into cells + uncontrolled hepatic gluconeogenesis
  • hyperglycaemia -> osmotic diuresis -> DEHYDRATION
  • Peripheral lipolysis -> raised free fatty acids -> converted to KETONES in mitochondria -> METABOLIC ACIDOSIS
  • Low intracellular potassium (insulin drives potassium into cells)
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12
Q

Investigations for DKA

A

Clinical diagnosis +

  • Blood glucose
  • ABG
  • U+E (raised due to dehydration)
  • Urine dipstick (glycosuria + ketonuria)
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13
Q

DKA Tx

A
  • ABCDE if unconscious
  • Slow FLUID REPLACEMENT (IV 0.9% NaCl)
  • Insulin + Glucose
  • Monitor Potassium
  • Treat any underlying infections/triggers
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14
Q

Complication of DKA Tx

A

Cerebral oedema
- from OSMOTIC SHIFT due to sudden decreased osmolality

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15
Q

RFx for T2DM

A

Non-modifiable:

  • Older age
  • Black, Chinese, south Asian ethnicity
  • FHx
  • MALE

Modifiable:

  • Obesity
  • Sedentary lifestyles
  • High carb diet
  • HYPERTENSION
  • Smoking
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16
Q

T2DM Sx

A
  • Polyuria
  • Polydipsia
  • Polyphagia (significant weight loss uncommon initially)
  • Glycosuria
  • Acanthosis nigricans
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17
Q

T2DM investigations

A

Gold:
- HbA1c > 48 mmol/mol
- >42 - 72 = pre-diabetes

Blood glucose
Oral glucose tolerance test

Only 1 +ve needed if symp; 2 if asymp

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18
Q

T2DM Tx

A
  • Life style mods
    • weight loss
    • diet
    • stop smoking
    • exercise
    • control blood pressure + cholesterol
  • Metformin if HbA1c >48
  • Sulfonylurea, thiazolidinedione, GLP-1 analogue, DPP-4 inhib, SGLT-2 inhib
  • Potentially insulin in late stage
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19
Q

T2DM complications

A

Macrovascular:

  • Atherosclerosis (hyperglycaemia induces oxidative stress) -> CVD

Microvascular:

  • Nephropathy
  • Retinopathy
  • Peripheral neuropathy
  • Autonomic neuropathy

+ decreased immunity due to hyperglycaemia

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20
Q

Pathophys of Hyperosmolar Hyperglycaemic state

A
  • Decreased insulin -> hyperglycaemia + gluconeogenesis
  • BUT Sufficient insulin to stop ketogenesis
  • Volume depletion -> raised osmolarity + hyperviscosity
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21
Q

Presentation of HHS

A

General:

  • Fatigue/lethargy
  • N+V

Neuro:

  • Raised ICP
    • Papilloedema, headaches, altered consiousness
  • weakness

Haem:
- Hyperviscosity (risk of MI, stroke, DVT/thrombosis)

Cardio:
- Dehydration -> Hypotension -> Tachycardia

NO significant acidosis

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22
Q

HHS Diagnosis

A
  • Serum glucose > 30 mmol/L
  • Hypotension
  • Hyperosmolarity (>32 mosmol/kg)
  • NO significant acidosis (> 7.3) or ketosis
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23
Q

HHS Tx

A
  • FLUID REPLACEMENT
  • VTE prophyl (LMWH)
  • Insulin if persisting w/ treatment (risk of hypoglycaemia/kalaemia so oft give w/ glucose/dextrose + monitor potassium)
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24
Q

Define Hypoglycaemia

A

Serum glucose < 4.0 mmol/L

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25
Q

Normal physiological response to hypoglycaemia

A
  • Alpha islet cells stimulated -> glucagon + inhibits insulin production -> hepatic gluconeogenesis/lysis
  • Increased production of adrenaline, growth hormone and CORTISOL -> gluconeogenesis
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26
Q

Non-diabetic causes of hypoglycaemia

A

ExPLAIN:

  • Exogenous medication (alcohol, aspirin overdose, IGF-1 which inhibits hepatic gluconeogenesis)
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Insluinoma/Islet cell tumours
  • Non-pancreatic neoplasm (fibrosarcoma)
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27
Q

Presentation of hypoglycaemia

A

Blood glucose <3.3 = AUTONOMIC:

  • Sweating
  • Shaking
  • Hunger
  • Anxiety
  • Nausea

Blood glucose <2.8 = NEUROGLYCOPENIC:

  • Weakness
  • Vision changes
  • Confusion
  • Dizziness

Severe + uncommon:
- Convulsion
- Coma

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28
Q

Wipple’s triad

A
  • signs and symptoms of hypoglycaemia
  • low blood glucose
  • resolution of symptoms with correction of blood sugar
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29
Q

Investigation of hypoglycaemia in non-diabetic

A

Gold = 48 - 72 hour FAST with serial blood glucose

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30
Q

Hypoglycaemia Tx

A

Community:

  • ORAL GLUCOSE 10-20g
  • May have ‘hypokit’ -> IM/SC glucagon

Hospital:

  • Quick acting carbs/oral glucose
  • Unconscious/unable to swallow:
    • SC/IM glucagon
    • OR IV 20% glucose solution
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31
Q

Define hypothyroidism

A

Syndrome of thyroid hormone deficiency leading to generalised slowing of metabolic processes

32
Q

Causes of primary hypothyroidism

A
  • Hashimoto’s thyroiditis
  • de Quervain’s thyroiditis
  • Radiotherapy
  • Drugs:
    • Lithium
    • Amiodarone
    • Antithyroid drugs e.g. carbimazole
  • Dietary iodine deficiency
33
Q

Secondary vs tertiary hypothyroidism

A
  • Secondary = pituitary failure (low TSH)
  • Tertiary = hypothalamic failure (low TRH)
    • basically non-existant
34
Q

Which genetic conditions are associated with a higher risk of developing hypothyroidism

A
  • Down’s
  • Turner’s (only in females - due to reduced/missing X chromosome)
  • Coeliac’s
  • Type 1 DM
35
Q

Presentation of hypothyroidism

A
  • Wight gain
  • Cold intolerance
  • Lethargy
  • Dry coarse scalp
  • CONSTIPATION
  • MENHORHAGIA
  • general myxoedema - waxy, non-pitting -> looks doughy

Hashimoto’s is also associated with losing the lateral aspect of eyebrow

36
Q

Investigations for hypothyroidism

A
  • 1st line = Thyroid function tests
    -> esp look at TSH and T4 levels
  • Thyroid peroxidase antibodies
    • elevated in Hasimoto’s
  • Fasting blood glucose
    • T1DM is a differential for non-specific fatigue + weight gain AND it’s often associated with autoimmune thyroid conditions
37
Q

Tx for hypothyroidism

A

Levothyroxine

38
Q

Pathophys of Hashimoto’s thyroiditis + conditions that are often associated with it

A
  • Anti-TPO and Anti-thyroglobulin Ab are formed/elevated
  • These attack the thyroid tissue causing progressive fibrosis
    • Damage is primarily caused/mediated in an immune response by CYTOTOXIC T CELLS
  • Can cause transient thyrotoxicosis in acute phase as thyroid tries to compensate

Oft associated with:

  • T1DM
  • Addison’s
  • Pernicious anaemia
39
Q

Hyperthyroidism vs thyrotoxicosis

A
  • Hyperthyroidism = increased synthesis of T3 and T4 in the thyroid gland
  • Thyrotoxicosis = Increased T3 and T4 in circulation (clinical syndrome)
40
Q

Causes of hyperthyroidism

A
  • GRAVE’S = most common
  • Toxic multinodular goitre
  • Toxic adenoma
  • De Quervain’s thyroiditis
  • Drug induced
    • Iodine excess
    • LITHIUM
    • AMIODARONE
    • radiocontrast agents

Less common:
- Congenital (neonatal) hyperthyroidism
- Non autoimmune hereditary hyperthyroidism
- Subacute thyroiditis
- Silent thyroiditis
- Postpartum thyroiditis
- Hyperemesis gravidarum
- Molar pregnancy (hCG)
- Thyrotoxicosis factitia
- Metastatic differentiated thyroid - Ca
- Struma ovarii
- Pituitary resistance to thyroid hormone
- Pituitary adenoma (TSHoma)

41
Q

What processes does the thyroid play an important role in

A

Metabolism, growth and development

42
Q

Presentation of hyperthyroidism

A
  • Weight loss,
  • heat intolerance,
  • palpitations/tachycardia
  • increased sweating,
  • anxiety,
  • tremor
  • diarrhoea,
  • oligomenorrhea
  • lid lag + stare
43
Q

Investigations for hyperthyroidism

A
  • 1ST LINE: Thyroid function tests(TFTs)- Primarily look at TSH ad T4 levels
  • TSH-RECEPTOR ANTIBODIES
    • elevated in GRAVE’S
  • Isotope scan, MRI, CT, Ultrasound
44
Q

Tx for hyperthyroidism

A
  • PROPANOLOL to initially control symps like tremor
  • Anti-thyroid meds
    • 1st line = CARBIMAZOLE (blocks TPO + reduces hormone levels)
    • risk of congenital malformation so CI in preg
    • Agranulocytosis also common SE (lowered immunity)
    • Alt = PROPYLTHIOURACIL
  • Radioiodine treatment (can exacerbate any exophthalmos)
  • Thyroidectomy

NB: need to render euthyroid before radioiodine/surgery

45
Q

Risk factors for Grave’s Hyperthyroidism

A
  • Smoking
  • Stress
  • Drugs:
    • High iodine intake
    • Alemtuzumab (MS drug)
  • FEMALE SEX - it mostly affects young or middle aged women
    - 2% of women will get Graves’ disease or autoimmune hypothyroidism (5-10 times the frequency in men)
  • Family history (25% concordance in monozygotic twins)
  • HLA-DR3 and other immunoregulatory genes contribute
    • Myasthenia gravis is also associated with Graves’ disease
46
Q

Pathophys of Grave’s disease

A

TSH receptor antibodies (thyroid stimulating antibodies) stimulate the TSH receptor causing more free t4 to be produced

TSH-R antibodies may cross the placenta can result in neonatal Graves’ disease. (could also result in stillbirth, miscarriage or preterm birth)

Opthalopthy caused by swelling in extraoccular muscles (probs from autoantigen similar to/reacting with thyroid autoantigen)

47
Q

Sx of Grave’s disease

A
  • EXOPHTHALMOS (bulging eyeball) and ophthalmoplegia (weakness of eye muscles)
  • PRETIBIAL MYXOEDEMA
    • orange peel appearance on anterior aspect of the lower legs, spreading to the dorsum of the feet, or a non-localised, non-pitting edema of the skin in the same areas
  • THYROID ACROPACHY
    • triad of digits clubbing, soft tissues swelling of hands/feet, and periosteal new bone formation
  • DIFFUSE GOITRE
  • typical Sx of hyperthyroidism
48
Q

First line Tx for patients with moderate-severe/sight threatening orbitopathy

A

IV CORTICOSTEROIDS

49
Q

Define De Quervain’s thyroiditis

A

Subacute granulomatous thyroiditis is a self-limited inflammation of the thyroid gland. It results in the rapid swelling of the thyroid gland resulting in pain and discomfort

(often thought occur after viral infection)

50
Q

Pathophys of De Quervain’s thyroiditis

A

There are typically 4 phases:

  • Phase 1- lasts 3-6 weeks: hyperthyroidism (initial presentation), painful goitre, Raised ESR
  • Phase 2- Lasts 1-3 weeks: Euthyroid (normal function)
  • Phase 3- weeks to months: Hypothyroidism
  • Phase 4- Thyroid structure and function goes back to normal
51
Q

Main Sx of De Quervain’s thyroiditis

A
  • NECK PAIN + ENLARGED THYROID
  • Fever
  • Palpitations
52
Q

investigation of De quervain’s

A
  • 1ST LINE: Total T4, T3 resin uptake, free thyroxine index- ALL ELEVATED,
  • CRP = elevated
53
Q

Tx of De Quervain’s

A

Hyperthyroid phase
- NSAIDs and corticosteroids may be used for pain.

Hypothyroid phase
- Normally no treatment given but if severe hypothyroidism occurs give small dose of levothyroxine

54
Q

Complications of De Quervain’s

A

Thyroid storm,
Long term hypothyroidism

55
Q

Define goitre

A

Palpable & visible thyroid enlargement

56
Q

Diff types of goitres

A
  • Toxic vs non-toxic
  • Diffuse (spread evenly)
  • Multinodular
  • Solitary nodule
  • Dominant nodule
  • Benign vs malig
57
Q

4 main thyroid malignancies + where they commonly spread to

A
  • Papillary (70%)
    • local followed by pulmonary and skeletal
    • younger peak of incidence than follicular
      -overall good prognosis
  • Follicular (10-20%)
    • pulmonary and skeletal
    • 3x more common in women
    • good prognosis if caught early but still poorer than papillary
  • Anaplastic (1-5%)
    • local, liver, lung, skeletal spread
    • 25% familial associated with MEN type 2
    • prognosis is highly dependant on age and stage
  • Medullary (<3%)
    • Local, skin, brain spread (maybe co-existing differentiated thyroid cancer)
    • mean age of onset 65, highly aggressive
    • poor prognosis, median survival 3-6 months
58
Q

RFx for thyroid cancer

A

Head and neck irradation
Female sex

59
Q

Presentation of thyroid cancer

A

Palpable thyroid nodule

+/- signs of mets, hypo/hyperthyroidism etc

60
Q

Investigations for thyroid cancer

A
  • 1st line: Ultrasound neck,
  • fine needle biopsy
  • laryngoscopy
61
Q

Treatment of thyroid cancer

A

Thyroidectomy followed by radioactive iodine ablation and suppression of TSH

62
Q

Complications of thyroidectomy

A
  • Risk of recurrent laryngeal nerve damage
  • Hypoparathyroidism
  • If whole thyroid removed -> hypothyroidism
63
Q

Which test can be used to screen for medullary thyroid cancer recurrence

A

Serum calcitonin

Medullary thyroid cancers often secrete calcitonin and monitoring the serum levels of this hormone is useful in detecting sub clinical recurrence

64
Q

Define thyroid storm

A

Severe thyrotoxicosis characterised by compromised organ function

65
Q

Causes of thyroid storm

A
  • Graves disease,
  • Post thyroidectomy,
  • Infection,
  • Trauma,
  • Abrupt cessation/Lack of adherence with Antithyroid drugs
  • MI,
  • DKA,
  • Pregnancy etc,
  • Exogenous iodine,
66
Q

Presentation of thyroid storm

A
  • Fever,
  • cardiovascular dysfunction,
  • profuse sweating,
  • tachyarrhythmias,
  • nausea and vomiting
67
Q

investigation for thyroid storm

A

Free thyroxine and TSH
- in thyroid storm TSH is completely suppressed with high thyroxine if of a primary cause

68
Q

Treatment for thyroid storm

A

1ST LINE: Antithyroid treatment- Carbimazole (or Propylthiouracil (PTU))

Hydrocortisone administration is also recommended. It treats possible relative adrenal insufficiency while also decreasing T4 to T3 conversion (t3 is active form so less free t3 means less hyperthyroidism symptoms)

Gold Standard: Thyroidectomy

69
Q

What are the 2 types of Cushing’s syndrome

A
  • ACTH independant - ACTH levels normal but cortisol levels high
  • ACTH dependant - ACTH levels high anf cortisol levels high
70
Q

Causes of ACTH independent Cushing’s syndrome

A

Iatrogenic - caused by oral steroids such as glucocorticoid e.g. PREDNISOLONE – MOST COMMON CAUSE

Adrenal adenoma - benign tumour of the adrenal gland that secretes increased levels cortisol

71
Q

causes of ACTH dependant Cushings

A
  • ACTH secreting anterior pituitary adenoma (most common)
  • Ectopic ACTH production - typically small cell lung cancer or carcinoid tumour
72
Q

Presentation of Cushing’s syndrome

A
  • Round moon face
  • Central obesity
  • Abdominal striae
  • Buffalo hump (fat pad on back)
  • PROXIMAL limb muscle wasting
  • Mood change
    • depression, lethargy, irritability, psychosis
  • Amenorrhoea
  • Acne
  • Hirsutism
73
Q

Investigations for Cushing’s

A
  • 1st line = Raised plasma cortisol (unreliable)
  • Gold = Dexamethasone suppression test
  • 24hr urinary free cortisol (accurate but less indicative of underlying cause)

MRI brain for pituitary adenoma
Chest CT for small cell lung cancer
Abdominal CT for adrenal tumours

74
Q

Dexamethasone suppression test

A
  • Low dose 1mg:
    • If low cortisol then cortisol secretion normal
    • if high/normal cortisol -> cushing’s
  • High dose test (8mg):
    • low cortisol -> cushing’s disease (i.e pituitary adenoma)
    • high/normal cortisol
      ** ACTH low -> adrenal cushing’s
      ** ACTH high -> ectopic ACTH
75
Q

Tx of Cushing’s

A

If the cause was iatrogenic - STOP taking steroids!
If adrenal adenoma - adrenalectomy
If pituitary adenoma - trans-sphenoidal surgery to remove
If ectopic ACTH production - surgery to remove neoplasm if it can be located and hasn’t metastesised

If surgical removal of cause if not possible - alternative: remove both adrenal glands and give patient replacement steroid hormones for life

76
Q

Complications of Cushing’s

A
  • DMT2
  • Hypertension
  • CVD
  • Osteoporosis
  • DVT +/- PE
77
Q

Role of cortisol

A

Medicine Phase 2 (13 decks)

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