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Endocrine Flashcards

1
Q

What are the 6 hormones produced by the anterior pituitary

A
  • FLATPIG
  • FSH
  • LH
  • Adrenocorticotrophic hormone
  • TSH
  • Prolactin
  • Ignore
  • GH
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2
Q

What controls FSH and LH secretion and what are their function

A
  • GnRH

- Stimulate menstrual cycle and oestrogen in women, testosterone and sperm production in women

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3
Q

What controls ACTH secretion and what is its function

A
  • Corticotropin releasing hormone (CRH)

- Stimulate cortisol and androgen release from adrenal glands

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4
Q

What controls TSH secretion and what is its function

A
  • Thyrotropin releasing hormone

- Stimulates thyroid to produce TH (T4/T3)

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5
Q

What controls prolactin secretion and what is its function

A
  • Dopamine inhibits secretion

- Stimulates breast growth and lactation

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6
Q

What controls GH secretion and what is its function

A
  • GHRH and somatostatin (decreases)

- Increases protein synthesis and growth

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7
Q

What is the function of cortisol (4)

A
  • Increases carbohydrate and protein metabolism
  • Increases fat deposition
  • Part of bodies response to stress
  • Anti-inflammatory (hence suppresses immune system)
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8
Q

What is the function of Thyroid hormone (4)

A
  • Increases metabolism (fat/carb.)
  • Increases protein synthesis
  • Increases HR/CO
  • Increases resp. rate
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9
Q

What are the two hormones secreted by the posterior pituitary

A
  • ADH

- Oxytocin

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10
Q

What is the epidemiology of hyperthyroidism (2)

A
  • 2-5% of women get it in lifetime

- Most common 20-40

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11
Q

What can cause hyperthyroidism (5)

A
  • Graves disease
  • Toxic multinodular goitre
  • Adenoma
  • De Quervains thyroiditis
  • Drug induced
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12
Q

Describe the pathophysiology of Graves disease

A
  • TSH receptor stimulating antibodies bind to TSH receptor on thyroid
  • This stimulates TH production
  • Also leads to hyperplasia and hence goitre
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13
Q

How might hyperthyroidism present (7)

A
  • Weight loss and increased appetite
  • Warm and sweaty
  • Oligomenorrhea
  • Tremor
  • Palpitations
  • Goitre
  • Children
    • Excessive height and learning difficulties
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14
Q

How do you diagnose hyperthyroidism (2)

A
  • Thyroid function tests
    • TSH low due to negative feedback
    • T3/4 raised
  • TSHR antibodies in Graves
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15
Q

How do you treat hyperthyroidism (4)

A
  • B blockers to control symptoms (propanolol)
  • Anti-thyroid drugs
    • Propylthiouracil (stops T3 - T4 conversion)
    • Carbimazole (Lowers T3/T4 production)
  • Radioactive iodine
  • Surgery (thyroidectomy)
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16
Q

What is the epidemiology of hypothyroidism (3)

A
  • More common in females
  • Autoimmune/atrophic is most common cause
  • Increases with age
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17
Q

What are the causes of primary hypothyroidism (5)

A
  • Autoimmune/atrophic
  • Iatrogenic
  • Hashimotos thyroiditis (autoimmune + goitre)
  • Iodine defficiency
  • Drug induced
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18
Q

How might hypothyroidism present (5)

A
  • Weight gain/decreased appetite
  • Cold
  • Low mood/tired
  • Goitre
  • Myalgia/weakness
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19
Q

What are the signs of hypothyroidism

A
  • BRADYCARDIC
  • Bradycardia
  • Reflexes relax slowly
  • Ascites
  • Dry
  • Yawning/drowsy
  • Cold hands
  • Ataxia
  • Round puffy face
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20
Q

How do you diagnose hypothyroidism (2)

A
  • Thyroid function tests
    • High TSH (unless secondary)
    • Low T3/T4
  • Thyroid antibodies
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21
Q

How do you treat hypothyroidism

A
  • Levothyroxine (T4 replacement)
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22
Q

What is the epidemiology of thyroid carcinoma (3)

A
  • Rare
  • More common in females
  • Minimally active hormonally
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23
Q

What are the types of thyroid carcinoma (3)

A
  • Papillary (70%)
    • Well differentiated, good prognosis
  • Follicular (20%)
    • Well differentiated, good prognosis
  • Anaplastic (5%)
    • Poorly differentiated, poor prognosis
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24
Q

How might thyroid carcinoma present (2)

A
  • Hard, enlarged, irregular thyroid

- May be hoarseness of voice and dysphagia due to pressing on local structures

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25
Q

How do you diagnose thyroid carcinoma (3)

A
  • Needle aspiration biopsy
  • Ultrasound
  • TFTs
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26
Q

How do you treat thyroid carcinoma (3)

A
  • Radioactive iodine
  • Levothyroxine to supress TSH (stimulates growth)
  • Thyroidectomy
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27
Q

What are the causes of cushings syndrome (4)

A
  • Iatrogenic - oral steroids (most common)
  • Cushings disease
    • ACTH secreting pituitary adenoma
  • Ectopic ACTH secreting adenoma
  • Adrenal adenoma
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28
Q

How might cushings syndrome present (8)

A
  • Central obesity
  • Round, ruddy face
  • Mood change
  • Muscle wasting/weakness
  • Infection
  • Thick skin, easily bruises
  • Acne
  • Raised B.P
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29
Q

How do you diagnose cushings syndrome (4)

A
  • Random cortisol test (raised)
  • Dexamethasone suppression test
    • In normal causes dec. cortisol, in cushings cortisol
      still high
  • Serum ACTH (raised = ectopic/cushings disease, normal = adrenal adenoma)
  • Cortictrophic releasing hormone test
    • If it causes further increase in cortisol then cushings
      disease
    • If not then ectopic adenoma
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30
Q

How do you treat cushings syndrome (4)

A
  • Iatrogenic - stop steroids
  • Cushings disease
    • Remove pituitary adenoma
    • Adrenalectomy
  • Adrenal adenoma
    • Adrenalectomy
  • Ectopic - removal
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31
Q

What is gigantism

A
  • Acromegaly in children
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32
Q

What is the epidemiology of acromegaly (3)

A
  • Rare
  • Most commonly caused by benign GH secreting pituitary tumour
  • Usually presents in middle age
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33
Q

How might acromegaly present (6)

A
  • Headache (very common)
  • Large hands and feet
  • Visual deterioration
  • Excess sweating
  • Increased weight
  • Arthralgia and backache
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34
Q

What are the signs of acromegaly (5)

A
  • Wide nose
  • Pertruding jaw
  • Deep voice
  • Large tongue
  • Carpal tunnel syndrome
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35
Q

How do you diagnose acromegaly (2)

A
  • Serum GH (not diagnostic as pulsatile)

- Insulin like growth factor 1 (IGF-1) raised (diagnostic)

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36
Q

How do you treat acromegaly (3)

A
  • Remove pituitary tumour
  • Somatostatin analogues
  • GH receptor agonists
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37
Q

What is the epidemiology of hyperprolactinaemia (2)

A
  • More common in females

- Most common pituitary hormonal disturbance

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38
Q

What are the causes of hyperprolactinaemia (4)

A
  • Prolactinoma
  • Pituitary stalk damage
  • Drugs (most common cause)
  • Pregnancy/breast feeding
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39
Q

How might hyperprolactinaemia present (4)

A
  • Amenorrhea
  • Galactorrhoea
  • E.D/facial hair loss in males
  • Infertility
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40
Q

How do you diagnose hyperprolactinaemia

A
  • Serum prolactin raised
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41
Q

How do you treat hyperprolactinaemia

A
  • Dopamine agonists (cabergoline)
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42
Q

What is Conns syndrome

A
  • Primary excess production of aldosterone independent of RA system, leading to increased Na and water retention and increased K secretion
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43
Q

What are the causes of Conns syndrome (2)

A
  • Adrenal adenoma

- Adrenal hyperplasia

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44
Q

How might Conns syndrome present (2)

A
  • Hypertension

- Hypokalaemia (cramp/spams, paraesthesiae)

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45
Q

How do you diagnose Conns syndrome

A
  • Serum renin (low) : aldosterone (high)
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46
Q

How do you treat Conns syndrome (2)

A
  • Laproscopic adrenalectomy

- Spiralactone (aldosterone agonist)

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47
Q

What is addisons disease

A
  • Destruction of the entire adrenal cortex leading to lack of cortisol, aldosterone and androgens
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48
Q

What is the epidemiology of addisons disease (2)

A
  • More common in females

- Very rare

49
Q

What are the causes of addisons disease (3)

A
  • Autoimmune adrenitis (most common)
  • Long term steroids (atrophy due to low ACTH)
  • TB
50
Q

How might addisons disease present (8)

A
  • Low mood, lethargy, depression
  • Tanned
  • Weight loss/anorexia
  • Hypotension
  • Amenorrhea/ E.D
  • Dehydration
  • Nausea, vomiting and abdo. pain
  • Loss of body hair
51
Q

How do you diagnose addisons disease

A
  • Bloods

- ACTH stimulation test (in addisons no/poor response of cortisol secretion to ACTH)

52
Q

How do you treat addisons disease (2)

A
  • Acute
    • IV hydrocortisone, fluids, glucose
  • Oral prednisolone and fludrocortisone
    • Advise patient on when to increase dose
53
Q

What is diabetes insipidus

A
  • Passage of large volumes of dilute urine due to impaired water retention by the kidneys (related to ADH)
54
Q

What are the two causes of diabetes insipidus

A
  • Cranial
    • Decreased ADH secretion by posterior pituitary
  • Nephrogenic
    • Decreased response of kidneys to ADH
55
Q

How might diabetes insipidus present (4)

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Hypernatraemia (weakness, confusion, lethargy)
56
Q

How do you diagnose diabetes insipidus (3)

A
  • Measure urine volume
  • Water deprivation test
  • Urine dipstick to check for glycosuria (DM)
57
Q

How do you treat diabetes insipidus (2)

A
  • Cranial
    • Desmopressin (ADH analogue)
  • Nephrogenic
    • Treat cause
    • Thiazide diuretic
58
Q

What is syndrome of inappropriate ADH secretion

A
  • Continued secretion of ADH despite low plasma osmolality leading to hypervolaemia and hyponatraemia
59
Q

How might syndrome of inappropriate ADH secretion present (4)

A
  • Malaise/nausea
  • Confusion
  • Weakness and aches
  • Anorexia
60
Q

How do you diagnose syndrome of inappropriate ADH secretion

A
  • Bloods
    • Low Na
    • Low osmolality
61
Q

How do you treat syndrome of inappropriate ADH secretion (4)

A
  • Loop diuretics (furosemide)
  • Treat underlying cause
  • Restrict fluid intake
  • Hypertonic saline (high salt)
62
Q

What is the function of parathyroid hormone (PTH) (4)

A
  • Increases bone resorption
  • Increases Ca absorption in intestines
  • Increases Calcitriol production
  • Increases Ca retention and Phosphate excretion
63
Q

What is the function of Calcitriol (4)

A
  • Inhibits PTH release (negative feedback)
  • Increases bone resorption
  • Increases Ca and phosphate absorption
  • Increases Ca and phosphate retention
64
Q

Describe the epidemiology of hypercalcaemia (2)

A
  • Most seen in old women

- Mostly caused by hyperparathyroidism and malignancy

65
Q

What are the causes of hypercalcaemia (3)

A
  • Primary hyperparathyroidism (Adenoma/hyperplasia)

- Malignancy secreting PTH like substance

66
Q

How might hypercalcaemia present (4)

A
  • Bones (pain, fracture, osteoporosis)
  • Stones (renal and gall)
  • Groans (abdominal pain, malaise, nausea, polyuria and polydipsia - dehydration)
  • Psychiatric moans (depression, anxiety, confusion)
67
Q

How do you diagnose hypercalcaemia

A
  • Bloods
  • Primary (inc. Ca, PTH, dec. phosphate)
  • Malignancy (inc. Ca, phosphate, dec. PTH)
68
Q

How do you treat hypercalcaemia (4)

A
  • Acute (iv. saline/fluids, biphosphonates)
  • Hyperparathyroidism
  • Adenoma - Surgical resection
  • Hyperplasia - PTectomy
  • Calcimimetic - increases PT sensitivity to Ca
69
Q

What is the epidemiology of hypocalcaemia (2)

A
  • All ages + sexes

- Common in hospital, correlates with severity of illness

70
Q

What are the causes of hypocalcaemia (4)

A
  • CKD (dec. Calcitriol production) - most common
  • Hypoparathyroidism
  • Pseudohypoparathyroidism (dec. sensitivity of PTH recptors)
  • Vitamin D deficiency
71
Q

How might hypocalcaemia present (5)

A
  • SPASM
  • Spasm
  • Paraesthesiae
  • Anxious
  • Seizure/convulsions
  • Muscle tone increased
72
Q

How do you diagnose hypocalcaemia (2)

A
  • Clinical history and Low Ca

- PTH low in hypoparathyroidism, raised in other causes

73
Q

How do you treat hypocalcaemia (3)

A
  • Acute - IV calcium gluconate
  • Hypoparathyroidism - Calcitriol and Ca supplements
  • Vitamin D deficiency - Oral adcal (vit. D and Ca)
74
Q

What are the important values for hyperkalaemia (2)

A
  • K > 5.5mmol/L = hyperkalaemia

- K > 6.5mmol/L = EMERGENCY

75
Q

What can cause hyperkalaemia (3)

A
  • AKI/ renal failure
  • Drugs (NSAIDs, K sparing diuretic, ACE inhibitors)
  • Addisons (dec. aldosterone)
76
Q

How might hyperkalaemia present (5)

A
  • Fast irregular pulse
  • Light headed/ dizzy
  • Palpitations
  • Chest pain
  • Weakness/ fatigue
77
Q

How do you diagnose hyperkalaemia (2)

A
  • U&Es (K > 5.5, > 6.5 = EMERGENCY)

- ECG

78
Q

How do you treat hyperkalaemia (4)

A
  • Acute
  • Calcium gluconate (stabilises cardiac myocytes)
  • Insulin (+glucose) to drive K into cells
  • Nebulised salbutamol to drive K into cells
  • Non-acute
  • Treat cause/ diet restriction
79
Q

What are the important values for hypokalaemia (2)

A
  • K <3.5 = hypokalaemia

- K <2.5 = EMERGENCY

80
Q

What can cause hypokalaemia (4)

A
  • Thaizide and loop diuretics
  • Renal failure
  • Increased aldosterone (Cushings, Conns)
  • GI loss (vomiting/diarrhoea)
81
Q

How might hypokalaemia present (5)

A
  • Weakness/ fatigue
  • Palpitations
  • Cramps
  • Light headed
  • Hypertonia/hypereflexia
82
Q

How would you diagnose hypokalaemia (2)

A
  • U&Es Low K > 3.5, >2.5 = EMERGENCY

- ECG

83
Q

How do you treat hypokalaemia (4)

A
  • Acute
  • IV K (carefully)
  • Non-acute
  • Medication review/treat cause
  • K sparing diuretic (spironolactone)
  • K supplements
84
Q

What is Diabetes mellitus (2)

A
  • A syndrome of hyperglycaemia due to insulin deficiency/resistance or both
  • Results in serious micro/macrovascular complications
85
Q

What is type 1 diabetes

A
  • Disease of insulin deficiency due to autoimmune destruction of Beta cells on the islets of langerhans
86
Q

What is the epidemiology of type 1 diabetes (2)

A
  • Usually presents in younger people

- Patients usually leaner

87
Q

Describe the pathophysiology of type 1 diabetes

A
  • Autoimmune destruction of Beta cells on islets of langerhans
  • Leads to insulin deficiency causing increased liver glucose production and decreased uptake by cells
  • This causes glycosuria which causes polyuria and polydipsia due to increased urine osmolality due to increased glucose in the urine
  • Also decreased uptake of glucose by cells leads to ketogenesis which can lead to muscle wasting and ketoacidosis
88
Q

What is type 2 diabetes

A
  • Hyperglycaemia resulting from a combination of decreased insulin secretion and resistance
89
Q

What is the epidemiology of type 2 diabetes (2)

A
  • Usually presents in older people

- Fatter patients

90
Q

What are the risk factors for type 2 diabetes (4)

A
  • Obesity
  • Lack of exercise
  • Family history
  • Increasing age
91
Q

How might diabetes mellitus present (5)

A
  • Triad of
  • Polyuria
  • Polydipsia
  • Weight loss
  • More rapid onset in type 1
  • Complications may be presenting complaint
  • Neuropathy
  • Retinopathy
  • Erectile dysfunction
  • Skin infection
92
Q

How do you diagnose diabetes mellitus (2)

A
  • In symptomatic 1 in asymptomatic both
  • Random plasma glucose > 11.1 mmol/L
  • Fasting plasma glucose > 7 mmol/L
93
Q

How do you treat type 1 diabetes (5)

A
  • Educate patients on self adjusting dose
  • Finger prick before (short acting)/after (long acting) meals
  • 3 Types of insulin
  • Short acting insulin (4-6 hours) before meal
  • Short acting insulin analogue (4-6 hours) before meal eg. insulin aspart
  • Long acting insulin (12-24+ hours) after meal, mixed with retarding agents eg. isophane insulin
94
Q

How do you treat type 2 diabetes (5)

A
  • Lifestyle change (weight loss/diet/exercise)
  • B.P and cholesterol management
  • 1st line oral metformin (decreases liver glucogenesis and increases cell senstivity to insulin)
  • Add oral gliclazide (promotes insulin secretion)
  • Add insulin eg. isophane insulin
95
Q

What are the risk factors for diabetic ketoacidosis (4)

A
  • Stopping insulin therapy
  • Infection
  • Surgery
  • Undiagnosed type 1
96
Q

What is the pathophysiology of diabetic ketoacidosis

A
  • Low insulin leads to low glucose uptake by cells causing increased ketone body formation
  • Also glycosuria leads to increased fluid and electrolyte loss
  • This results in a raised concentration of acidic ketones in the blood
  • Leads to acidosis, attempted respiratory compensation and impaired kidney excretion of H+ and ketones due to dehydration
97
Q

How might diabetic ketoacidosis present (6)

A
  • Severe dehydration - decreased consciousness/ drowsiness
  • Hyperventilation
  • Vomiting
  • Pear drop breath
  • Low body temperature
  • May be severe abdominal pain
98
Q

How do you diagnose diabetic ketoacidosis (2)

A
  • Bloods
  • Acidaemia Ph <7.35
  • Rasied ketones >3 mmol/L
  • Lowered bicarb. <15 mmol/L
  • Hyperglycaemia >11 mmol/L
  • Heavy keto/glycosuria
99
Q

How do you treat diabetic ketoacidosis (4)

A
  • IV. fluids
  • Replace electrolytes
  • Restore acid-base balance
  • Insulin + glucose (to avoid hypoglycaemia)
100
Q

What is a hyperosmolar hyperglycaemic state

A
  • A life-threatening emergency with marked hyperglycaemia and hyperosmolality
101
Q

Describe the pathophysiology hyperosmolar hyperglycaemic state

A
  • Usually caused by infection
  • Insulin deficiency leads to hepatic glucogenesis but insulin levels still high enough to suppress ketogenesis
  • Leads to severe dehydration
102
Q

How might hyperosmolar hyperglycaemic state present (2)

A
  • Severe dehydration

- Decreased consciousness, confusion, drowsiness

103
Q

How would you diagnose hyperosmolar hyperglycaemic state (2)

A
  • Bloods
  • Hyperglycaemia
  • Very high serum osmolality
  • Heavy glycosuria
104
Q

How do you treat hyperosmolar hyperglycaemic state (4)

A
  • Iv fluids
  • Replace electrolyte loss
  • Insulin
  • LMW heparin as predisposed to thrombus due to hyperosmolality
105
Q

What are the main reasons for diabetic complications (4)

A
  • Poor glycaemic control
  • Poor B.P control
  • Long duration of diabetes
  • Pregnancy
106
Q

What is diabetic macrovascular disease (2)

A
  • Diabetes predisposes to atherosclerosis and hence embolus leading to increased chance of stroke/MI/preipheral ischaemia
  • Treat with B.P control and statins
107
Q

What is diabetic retinopathy (2)

A
  • Microaneurysm and haemorrhage leads to progressive retinal damage and hence progressive visual loss
  • Treat with laser surgery (stops progression, cannot reverse)
108
Q

What is diabetic nephropathy (2)

A
  • Basement membrane damage and glomerular damage due to poor glycaemic and B.P control
  • Treat by improving glycaemic control and B.P control
109
Q

What is diabetic neuropathy (2)

A
  • Paraesthesiae, numbness, burning of limbs and erectile dysfunction
  • Treat with paracetamol/opioids (codeine) anticonvulsants
110
Q

What is diabetic foot ulcer (2)

A
  • Trauma unnoticed due to numbness of foot leads to ulceration
  • Treat by patients checking foot, keeping good hygiene and wearing lose shoes
111
Q

What are the causes of hypoglycaemia (7)

A
  • Diabetics - Insulin
  • Non diabetics - Explain
  • Exogenous drugs
  • Pituitary insufficiency
  • Liver failure
  • Addisons
  • Islets tumour
  • Neoplasm
112
Q

How might hypoglycaemia present (5)

A
  • Hunger
  • Anxiety/sweating
  • Dizziness
  • Palpitations
  • Confusion/drowsiness
113
Q

How do you diagnose hypoglycaemia (2)

A
  • Finger prick glucose test (<3 mmol/L)

- Look for cause

114
Q

What is the treatment for hypoglycaemia

A
  • Oral sugar/ iv glucose
115
Q

What ECG changes would you expect to see in hypercalcaemia

A
  • Short QT interval
116
Q

What ECG changes would you expect to see in hypocalcaemia

A
  • Long QT interval
117
Q

What ECG changes would you expect to see in hyperkalaemia

A
  • Tall tented T waves

- Rapid QRS

118
Q

What ECG changes would you expect to see in hypokalaemia

A
  • Small T waves

- U waves

Finals (11 decks)

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