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2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is diabetes mellitus?

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency or insulin resistance or both.

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2
Q

What is T1DM?

A

An autoimmune disorder where the islet of Langerhans cells in the pancreas are destroyed by the immune system. This causes a deficiency of insulin which results in raised glucose levels.

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3
Q

What is T2DM?

A

Caused by a relative deficiency of insulin due to an excess of adipose tissue, resulting in raised blood glucose.

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4
Q

How does diabetes present?

A 
Polyuria
Polydipsia
Weight loss
Fatigue
DKA Sx
Complications Sx
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5
Q

How can you check blood glucose?

A
  • finger prick
  • one off glucose
  • HbA1c
  • glucose tolerance test
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6
Q

What is the diagnostic criteria for diabetes?

A

> fasting plasma glucose >/7.0mmol/L
random plasma glucose >/11.1mmol/L
HbA1c >/48mmol/L (6.5%)

Symptomatic pt needs 1 abnormal value
Asymptomatic pt needs 2 abnormal values

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7
Q

How is T1DM managed?

A

Insulin
If BMI>25 add metformin
Monitor HbA1c levels

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8
Q

SE of insulin?

A

Hypoglycaemia
Weight gain
Lipodystrophy

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9
Q

How is T2DM managed?

A 
Dietary changes
Metformin
Sulfonylurea
Gliptin
Piolitazone
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10
Q

What is DKA?

A

Diabetic ketoacidosis: metabolic emergency

- uncontrolled catabolism associated with insulin deficiency

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11
Q

What can cause DKA?

A

5 I’s:

  1. infection
  2. intoxication
  3. infarction
  4. inappropriate withdrawal of insulin
  5. intercurrent illness
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12
Q

How does DKA present?

A 
Pear drop breath
Kussmaul's breathing
Profound dehydration 
Abdo pain
Drowiness, vomiting
Sunken eyes, decreased tissue turgor, dry tongue
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13
Q

How is DKA diagnosed?

A

Blood glucose >11.1mmol/L
Raised plasma ketones >3mmol/L
Acidaemia (blood pH <7.3)
Metabolic acidosis with bicarbonate <15mmol/L
Urine stick test: heavy glycosuria + ketonuria
High urea + creatitine

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14
Q

How is DKA treated?

A

0.9% saline
Restore electrolyte + fluid loss
Insulin + gluocse

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15
Q

What are some complications of DKA management?

A

Hypotension
Coma
Cerebral oedema
Hypothermia

Later: pneumonia, DVT

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16
Q

Definition of hypoglycaemia

A

Plasma glucose <3mmol/L

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17
Q

Causes of hypoglycaemia?

A

Diabetics: insulin/sulphonylurea treatment
Non-diabetics:
- Exogenous drugs
- Liver failure
- Addison’s disease
- Islets cell turnover + immune hypoglycaemia
- Non-pancreatic neoplasm

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18
Q

How does hypoglycaemia present?

A

Autonomic:
- sweating, anxiety, hunger, tremor, palpitations, dizziness

Neuroglycopenic:
- confusion, drowsiness, seizures, coma

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19
Q

How is hypoglycaemia diagnosed?

A

Fingerprick blood test during attack

Bloods: glucose, insulin levels etc

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20
Q

How is hypoglycaemia treated?

A

Oral sugar + long-acting starch (e.g. toast)

> IM glucagon, IV glucose

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21
Q

What is hyperosmolar hyperglycaemic state?

A

Life-threatening emergency characterised by marker hyperglycaemia, hyperosmolality and mild/no ketones
> metabolic emergency characteristic of uncontrolled T2DM

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22
Q

How does hyperosmolar hyperglycaemic state present?

A 
Severe dehydration
Decreased LOC
Hyperglcyaemia
Hyperosomolality
No ketones in blood or urine 
Stupor or coma
Bicarbonate normal
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23
Q

How is hyperosmolar hyperglycaemic state diagnosed?

A

Blood glucose >11mmol/L
Heavy glycosuria
Very high plasma osmolality
Total body K+ is low

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24
Q

How is hyperosmolar hyperglycaemic state treated?

A

Lower rate of infusion of insulin
0.9% saline fluid
LMWH (SC Enoxaparin)
Restore electrolyte loss

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25
Q

What is MODY?

A

Maturity-onset diabetes of the young

  • diagnosed <25yrs old
  • autosomal dominant
  • absence of islet autoantibodies
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26
Q

What is hyperthyroidism and what causes it?

A 
Overproduction of the thyroid hormone
Causes:
- Grave's disease
- Toxic multi nodular goitre
- De Quervain's thyroiditis
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27
Q

What is grave’s disease?

A

Autoimmune induced excess production of thyroid hormone.

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28
Q

Clinical presentation of hyperthyroidism?

A

Tremor, anxiety, palpitations, weight loss, diarrhoea, increased appetite, double vision, SOB, sweating, heat intolerance, Palma erythema, irritatibility

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29
Q

Clinical presentation of Grave’s disease?

How is it treated?

A 
Grave's opthalmology:
Exopthalmos
Proptosis
Diplopia
Ophthalmoplegia

Grave’s dermopathy:

  • pretibial myxoedema
  • thyroid acropachy

Tx:

  • IV methylprednisolone
  • surgical decompression
  • eyelid surgery
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30
Q

How is hyperthyroidism diagnosed?

A

Bloods to test thyroid function

  • low TSH
  • high T4
  • high T3

USS thyroid

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31
Q

How is hyperthyroidism treated?

A

Oral carbimazole
Radioactive iodine
Total thyroidectomy
Beta-blockers

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32
Q

What is de quervain’s thyroiditis?

A

Transient hyperthyroidism sometimes results from acute inflammation of the thyroid gland, probably due to viral infection.
- tender goitre
- hyperthyroidism
- raised ESR
- globally reduced uptake on tectretium thyroid scan
Treat with aspirin.

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33
Q

What is the triad for grave’s treatment?

A
  1. propanolol
  2. propylthiouracil
  3. prednisolone
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34
Q

What drugs can induce hyperthyroidism?

A

Amiodarone
Iodine
Lithium

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35
Q

What are some complications of total thyroidectomy?

A 
Tracheal compression (from post-op bleeding)
Laryngeal nerve palsy (hoarse voice)
Transient hypocalcaemia (removal of parathyroid gland)
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36
Q

What is a complication of hyperthyroidism?

A

Thyroid storm/crisis

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37
Q

What is hypothyroidism?

A

Under-activity of the thyroid gland, underproduction of the thyroid hormone.

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38
Q

What can cause hypothyroidism?

A

Primary

  • Hashimoto’s thyroiditis
  • iodine deficiency
  • post-thyroidectomy
  • post-partum
  • drugs: carbimazole, lithium, amiodarone, interferon

Secondary
- hypopituitarism

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39
Q

What is the clinical presentation of hypothyroidism?

A

Bradycardia, constipation, cold intolerant, weight gain, menorrhagia, tired, weak, myxoede,a, ascites, dry thin hair and skin, ataxia

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40
Q

Investigations for hypothyroidism?

A

Primary: high TSH, low T4 + T3
Secondary: low TSH, low T4

Thyroid antibodies (e.g. TPO-Ab)
High serum aspartate transferase
High serum creatinine kinase

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41
Q

How is hypothyroidism treated?

A

Oral levothyroxine (T4)

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42
Q

Complications of hypothyroidism?

A

Myxoedema

  • may present with confusion and coma
  • medical emergency

Tx: give IV/oral T3 and glucose infusion

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43
Q

What are the different types of thyroid carcinoma?

A 
Papillary (70%)
Follicular (20%)
Anaplastic
Lymphoma
Medullary cell
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44
Q

How do thyroid carcinomas present?

A

Thyroid nodules
Cervical lymphadenopathy
Dysphagia
Hoarse voice

O/E:
- thyroid gland: increase in size, hard + irregular

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45
Q

How do you diagnose thyroid carcinomas?

A

> Fine needle aspiration cytology biopsy

> Blood tests

  • thyroglobulin
  • TFTs

> US of thyroid

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46
Q

How are thyroid carcinomas treated?

A

Radioactive iodine
Levothyroxine
Thyroidectomy
External radiotherapy

47
Q

What are the 3 presentation features of an anterior pituitary tumour?

A
  1. pressure on local structures
    - optic chasm: bitemporal hemianopia
  2. pressure on normal pituitary
    - hypopituitarism
  3. functioning tumour
    - hyperpituitarism
48
Q

What is Cushing’s syndrome?

A

Chronic excessive and inappropriate elevated levels of circulating cortisol whatever the cause.

49
Q

What is Cushing’s disease?

A

Excess glucocorticoids resulting from inappropriate ACTH secretion from the pituitary due to tumour.

50
Q

Where is cortisol released from?

A

Zona fasiculata of the adrenal cortex

51
Q

What are the functions of cortisol?

A
  • sodium retention
  • increased renal potassium loss
  • increased carbohydrate + protein catabolism
  • increased deposition of fat + glycogen
52
Q

Causes of high cortisol?

A

ACTH-dependent causes

  • Cushing’s disease
  • Ectopic ACTH production
  • ACTH treatment

ACTH-independent causes

  • adrenal adenoma
  • iatrogenic
53
Q

Clinical presentation of Cushing’s disease?

A 
Obese: buffalo hump
Moon face + plethoric complex
Osteoporosis
Hyperglycaeimia
Mood changes
Irregular period + ED
Muscle atrophy
Thin skin
Purple stirae on abdo, breasts + thighs
54
Q

How is Cushing’s disease diagnosed?

A

> Random plasma cortisol - if this is high continue with:

  1. Overnight dexamethasone suppression test
  2. Urine free cortisol over 24hrs
  3. 48hr dexamethasone suppression test

If above tests are positive:
> plasma ACTH
Undetectable: adrenal tumour likely
Detectable: do high dose dex suppression test or CRH test
- if cortisol responds to CRH: Cushing’s disease likely
- if cortisol does not respond to CRH: find ectopic source of ACTH

55
Q

How can you find ectopic source of ACTH?

A
  • IV contrast CT of chest, abdo, pelvis
  • MRI of neck, thorax + abdo
  • CXR lungs for SCLC
56
Q

How do you treat cushings?

A 
Trans-sphenoidal removal of pituitary adenoma
Bilateral adrenalectomy
Stop steroids
Drugs that inhibit cortisone synthesis
- metyrapone, ketoconazole, fluconazole
57
Q

What is acromegaly?

A

Excess GH in adults

- 5% assoc with MEN1

58
Q

What are some symptoms of acromegaly?

A 
Insidious onset, many years between Sx + Dx
Headaches
Increased size of hands + feet
Excessive sweating
Visual deterioration
Snoring
Wonky bite
Increased weight
Decreased libido
Amenorrhoea
Arthralgia + back ache
Acroparaesthesia
59
Q

What are some signs of acromegaly?

A 
Skin darkening
Coarsening face with wide nose
Prognathism
Big supraorbital ridge
Interdental separation
Rings become tight
Fatigue 
Deep voice
Carpel tunnel syndrome (50%)
Large tongue
60
Q

What are some co-morbidities/complications of acromegaly?

A 
Impaired glucose tolerance
Diabetes mellitus
Sleep apnoea
HTN, ventricular hypertrophy, cardiomyopathy, arrhythmias, stroke
Colon cancer
Arthritis
61
Q

How is acromegaly diagnosed?

A 
> High glucose, calcium + phosphate
> IGF-1 screening test
> Plasma GH levels
- exclude it if GH <0.4ng/ml + normal IGF-1
- if delectable ---> do GTT
> Visual field examination
> MRI of pituitary fossa
62
Q

What causes an increase in GH?

A

GH secretion is pulsatile. Increases in:

- stress, sleep, puberty + pregnancy

63
Q

How do you treat acromegaly?

A
  1. Trans-sphenoidal surgery (remove tumour)
  2. IM octreotide (inhibit GH release)
  3. SC pegvisomant (suppresses IGF-1)
  4. Oral cabergoline/bromocriptine
  5. Radiotherapy
64
Q

What is a prolactinoma?

A

Lactotroph cell tumour of the pituitary

65
Q

What is the effect of prolactinoma?

A
  • menstrual irregularity/amennorhea
  • infertility
  • galactorhhoea
  • low libido
  • low testosterone in men
  • headache
  • visual field defect
  • CSF leak
66
Q

What is the visual field defect seen in prolactinoma?

A

Bitemporal hemianopia

67
Q

What can cause prolactinoma?

A 
Pituitary adenoma
Anti-dopaminergic drugs
Stress
Drugs
Pressure on pituitary stalk
68
Q

How do you diagnose a prolactinoma?

How is it treated?

A

Serum prolactin

Tx: Dopamine agonists

  • cabergoline
  • bromocriptine
  • quinagolide
69
Q

What does the anterior pituitary produce?

A 
FSH
LH
ACTH
TSH
Prolactin
GH
70
Q

What does the posterior pituitary produce?

A

Vasopressin (ADH)

Oxytocin

71
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism - excess production of aldosterone, independent of RAAS. Resulting in increased sodium and water retention and decreased renin release.

72
Q

What causes Conn’s syndrome?

A

2/3rds: adrenal adenoma that secretes aldosterone

1/3rd: bilateral adrenocortical hyperplasia

73
Q

How does Conn’s syndrome present?

A
  • hypertension

- hypokalaemia (weakness, cramps, polyuria)

74
Q

How is Conn’s syndrome diagnose?

A

Plasma aldosterone:renin ration
- aldosterone is much higher

Fludrocortisone or 0.9% saline infusion unable to suppress plasma aldosterone.

ECG: hypokalaemia
CT/MRI adrenals to differentiate adenomas from hyperplasia

75
Q

What is seen on a hypokalaemic ECG?

A

Flat T-waves
ST depression
Long QT

76
Q

How is Conn’s syndrome treated?

A 
Laparoscopic adrenalectomy
Aldosterone antagonist (e.g. oral spironolactone)
77
Q

What is Addison’s disease?

A

Primary hypoadrenalism - destruction of the entire adrenal cortex resulting in mineralocorticoid, glucocorticoid and sex steroid deficiency.

78
Q

What causes Addison’s?

A 
Autoimmune (80%)
- destruction of adrenal cortex by organ-specific Ab
TB
Long term steroid use
Adrenal haemorrhage
79
Q

How does Addison’s present?

A 
Tanned bronze skin
Lethargy, depression, low mood and self esteem
Anorexia + weight loss
Postural hypotension
Impotence/amenorrhoea
Vitilgo
N+V
New scars + palmar creases
Diarrhoea, constipation + abdo pain
Dehydration
80
Q

How is Addison’s diagnosed?

A 
Unexplained abdo pain/vomiting
Bloods
- hyponatraemia + hyperkalaemia
- hypoglycaemia
- hypoaldosternoism
- low cortisol

Short ACTH stimulation test
- measure plasma cortisol before and 30mins after IM Tetracosactide

Adrenal antibodies
- 21-hydroxylase antibody

9am ACTH levels
- inappropriately high

AXR/CXR

81
Q

How is Addison’s treated?

A

Seriously ill:

  • IV hydrocortisone
  • IV 0.9% saline 1L
  • Glucose infusion (if hypoglycaemic)

Replace steroids daily 3x a day (mimic circadian rhythm)

  • oral hydrocortisone/prednisolone
  • oral fludrocortisone
82
Q

What is secondary hypoadrenalism?

A

Issue with pituitary, not adrenal glands. Reduction of release of ACTH = low glucocorticoid (cortisol.)
Mineralcorticoid production remains normal.
Tx: oral hydrocortisone

83
Q

What is diabetes insidious?

A

Passage of large volumes of dilute urine due to impaired water reabsorption in the kidney, either because of:

  • reduced ADH secretion (cranial DI)
  • impaired response of kidney to ADH (nephrogenic DI)
84
Q

How does DI present?

A 
Polyuria
Polydipsia
No glycosuria
Hypernatreaemia (lethargy, thirst, weakness, irritability)
Dehydration

Ix: water deprivation test

85
Q

How do you treat cranial DI?

How do you treat nephrogenic DI?

A

MRI head + ant pituitary
Oral desmopressin

Oral bendroflumethiazide
Ibuprofen

86
Q

What is SIADH?

A

Continuous secretion of ADH despite the plasma being very dilute leading to retention of water and excess blood volume, thus hyponatraemia.

87
Q

Clinical presentation of SIADH?

A
  • anorexia, nausea, malaise, weakness, aches, confusion, drowsiness, fits
88
Q

What is seen biochemically in blood/urine in SIADH?

A

BLOOD

  • low sodium
  • low osmolarity

URINE

  • high sodium
  • high osmolality
89
Q

How is SIADH treated?

A 
Restrict fluid intake
Hypertonic saline
Oral demeclocyline daily
Oral tolvaptan
Oral furosemide
90
Q

What are the actions of PTH?

A
  1. increase osteoclastic resorption of bone
  2. increase intestinal absoption of calcium
  3. activation of 1,25-dihydroxyvitD in kidney
  4. increase renal tubular reabsorption of calcium
  5. increase excretion of phosphate
91
Q

What is calcitrol?

What are its roles?

A

Active form of vitamin D
Roles:
- increase calcium + phosphate absorption in gut
- inhibit PTH release
- enhanced bone turnover by increased no. of osteoclasts
- increased calcium + phosphate reabsorption in kidneys

92
Q

Clinical presentation of hypercalcaemia?

A

Stones (renal colic, biliary stones)
Bones (pains, fractures)
Moans (abdo pain, nausea, constipation)
Psychic groans (depression, anxiety, insomnia)

93
Q

Difference between primary and secondary hyperparathyroidism?

A

Primary: usually caused by adenoma

  • high PTH, high calcium
  • low phosphate
Secondary: physiological compensatory hypertrophy of all parathyroids causes excess PTH due to low calcium
e.g. CKD, vit D deficiency
Sx: osteomalacia, joint pain
- high PTH, low calcium
- high phosphate
94
Q

What is tertiary hyperparathyroidism?

A

Occurs many years after secondary, causing glands to act autonomously having undergone hyperplastic or adenomatous change
= XS PTh secretion that is unlimited by feedback control
e.g. chronic renal failure
- high PTH, high Ca
- high phosphate

95
Q

How do you treat acute severe hypercalcaemia?

A

Medical emergency

  • IV 0.9% saline fluids
  • IV pamidronate
  • glucocorticoid steroids
96
Q

Causes of hypocalcaemia?

A

CKD
Severe vit D deficiency
Reduced PTH function
Drugs (e.g. bisphosphonates)

97
Q

How does hypocalcaemia present?

A 
Parathesia
Cramps
Tetany
Increased excitability of muscles + nerves
Chvostek + Trousseau's sign
Diarrhoea
Impetigo herpetiformis
Dermatitis
Confusion
Papilloedma

Prolonged QT on ECG

98
Q

What is Chvostek’s sign?

A

Tapping over the facial nerve in region of parotid gland causes twitching of the ipsilateral facial muscles.

99
Q

What is Trousseau’s sign?

A

Carpopedal spasm induced by inflation of sphygmomanometer cuff to a level above systolic BP

100
Q

How do you treat acute hypocalcemia?

A

eg. tetany

IV calcium gluconate

101
Q

What is definition of hyperkalaemia?

A

Serum K+ > 5.5mmol/L

> 6.5mmol/L = medical emergency

102
Q

Causes of hyperkalaemia?

A 
Drugs
Renal failure
Endocrine (e.g. Addison's)
Artefact (pseudo high K+)
DKA
103
Q

Clinical presentation of hyperkalaemia?

A

Asymptomatic until high enough to cause cardiac arrest

- fast, irregular pulse, chest pain, weakness, light headed, fatigue, Kussmaul’s respiration

104
Q

What is seen on ECG in hyperkalaemia?

A

Tall tented T-waves
Small P waves
Wide QRS complez

105
Q

How is hyperkalaemia treated?

A

URGENT

  • IV 10ml 10% calcium gluconate
  • IV actrapid
  • IV/neb salbutamol

NON-URGENT

  • underlyng cause
  • dietary restriction
106
Q

Definition of hypokalaemia?

A

Serum K+ <3.5mmol/L

<2.5mmol/L = urgent

107
Q

Causes of hypokalaemia?

A

Increased renal excretion (e.g. diuretics)
Reduced dietary intake
Redistribution to cells (e.g. salbutamol)
GI losses (e.g. vomiting, diarrhoea)

108
Q

Clinical presentation of hypokalaemia?

A

Muscle weakness, cramps, hypotonia, hyporefelxia, tetany, palpitations, light headed, constipation

109
Q

What is seen on ECG in hypokalaemia?

A

Small of inverted T waves
Prominent U waves
Long PR interval
Depressed ST segments

110
Q

How is hypokalaemia treated?

A

Oral K+ supplements if mild

IV K+ if severe

111
Q

What is a carcinoid tumour?

A

Tumours that originate from the enterochromaffin cells and are capable of production serotonin.

112
Q

What are the effects of serotonin?

A 
Bowel function
Mood
Clotting
Nausea
Bone density
Vasoconstriction
Increased force of contraction and heart rate
113
Q

What is carcinoid crisis?

A

When a tumour outgrows its blood supply or is handled too much during surgery (mediators flow out.)

  • vasodilation
  • hypotension
  • tachycardia
  • bronchoconstriction
  • hyperglycaemia

Tx: octereotide

114
Q

How do you diagnose carcinoid tumour?

A

US liver
CXR chest/pelvis
MRI/CT

Urine: high conc of 5-hydroxyindoleacetic acid

2a (7 decks)

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