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2A > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Where are glucagon and insulin produced?

A

In the islets of langerhans at the pancreas. Alpha cella = glucagon, beta cells = insulin

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2
Q

What does glucagon do?

A

Stimulates glycogenolysis and gluconeogenesis to increase blood glucose.

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3
Q

What does insulin do?

A

Stimulates glucose uptake via GLUT 4 and suppresses lipolysis to reduce blood glucose.

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4
Q

What are the limits for diabetes diagnosis?

A

Symptoms & random plasma glucose (OGTT) >11mmol/l
Symptoms & fasting plasma glucose >7mmol/l
HbA1c greater than or equal to 48mmol/mol

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5
Q

What are the levels of hypoglycaemia?

A

Level 1 = glucose <3.9mmol/l
Level 2 = glucose <3.0mmol/l
Mild = self-treated, Severe = requires help to treat

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6
Q

What are the autonomic symptoms of hypoglycaemia and when do they occur?

A

Trembling, palpatations, sweating, anxiety and hunger. These occur when glucose levels drop below 3.5mmol/l, the body will release adrenaline to get stored glucose into the blood stream more rapidly.

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7
Q

What are the neuroglycpenic symptoms of hypoglycaemia and when do they occur?

A

Difficulty concentrating, confusion, weakness, drowsiness, dizziness, vision changes, difficulty speaking. These occur once glucose levels drops below 3.2mmol/l.

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8
Q

What are the two main types of insulin?

A

Basal insulin = keeps glucose at a constant level when not eating.
Prandial insulin = acts rapidly to reduce glucose levels after eating

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9
Q

S&S of T1DM?

A

unquenchable thirst, polyuria, weight loss and fatigue, hunger, pruitis valvae and blantitis, blurred vision

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10
Q

What is T1DM?

A

Autoimmune destruction of the beta cells in the pancreas leading to no insulin being produced by the body.

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11
Q

What is DKA?

A

Diabetic Ketoacidosis = hyperglycaemia with raised plasma ketones and metabolic acidosis. Lack of insulin in the body means that cells must get energy from other sources, fat breakdown begins (insulin prevents this normally) to produce glycerol and free fatty acids. FFAs are oxidised in the liver to form ketone bodies.

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12
Q

S&S of DKA?

A

Hyperventilation, polyuria (leads to dehydration and hypotension), tachycardia, hyperkalaemia, nausea, weight loss, weakness, drowsiness, confusion and coma

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13
Q

Management of DKA?

A

Rehydration, insulin treatment, replace electrolytes (particularly potassium - levels are already low and fluid further decrease concentration, if not corrected = cardiac arrest), treat underlying cause.

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14
Q

Name 3 complications of DKA?

A

Over-rehydration = cerebral oedema in children, respiratory distress syndrome in adults.
Extreme dehydration = thromboembolism
Comatosed patients = aspiration pneumonia

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15
Q

Risk factors for T2DM?

A

Obesity, hypertension, >40 (if white) or >25 (if Afro-carribean, black african or south asian), sedentary life style, polycystic ovary syndrome

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16
Q

S&S of T2DM?

A

Polyuria (leading to dry mouth, headaches and polydypsia), hunger, weight loss/fatigue, blurred vision. DKA will NOT occur.

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17
Q

What is T2DM?

A

Impaired insulin secretion and insulin resistance leading to hyperglycaemia

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18
Q

How is T2DM treated?

A

Initially with weight loss, exercise and blood pressure control (these can reverse the diabetes). Initial medical treatment is metformin (or sulphonylurea) but if the disease progresses insulin must be given.

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19
Q

What is MODY?

A

Maturity Onset Diabetes of the Young. It is autosomal dominant and non-insulin dependant disease (insulin production is disturbed by genetic mutations)

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20
Q

What are the 3 types of MODY?

A

HNF1A mutation = MODY 3 (requires sulphonylurea)
HNF4A mutation = MODY 1 (requires suphonylurea)
GCK mutation = MODY 2 (the set point for insulin release is higher - can be modified with lifestyle changes)

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21
Q

Give an acute and a chronic cause of inflammatory diabetes?

A

Acute = transient hyperglycaemia e.g. due to pancreatic shock in acute alcohol poisoning
Chronic = chronic pancreatitis in alcoholics
Hereditary haemochromotosis can also lead to diabetes.

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22
Q

S&S of hyperosmolar hyperglycaemic state?

A

Hyperglycaemia, hyperosmolality, severe dehydration, decreased conscioussness, stupor/coma. NO KETONE BODY PRODUCTION.

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23
Q

Treatment for hyperosmolar hyperglycaemic state?

A

Insulin (small dose as these patients are EXTREMELY sensitive to insulin), fluid replacement, LMW heparin e.g. enoxaparin, restore electrolytle levels (especially K+).

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24
Q

Name a macrovascular complication of DM?

A

Atherosclerosis. This will lead to increased risk of MI/PVD/stroke.

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25
Q

Name the microvascular complications of DM?

A

Diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, diabetic foot ulceration.

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26
Q

S&S of diabetic neuropathy?

A

Allodynia, paraesthesia, burning pain (worse at night), postural hypotension, glove and stocking sensory loss.. These patietns are at risk of diabetic foot ulceration.

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27
Q

Why does diabetes increase infection risk?

A

Poorly controlled DM impaires the function of polymorphonuclear leucocytes = increased infections such as UTIs and skin infections

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28
Q

What is lipohypertrophy?

A

Lumps of fat which accumulate at areas where insulin is frequently injected - avoid by altering injection sites daily

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29
Q

What are the two types of diabetes insipidus? Name a cause of each?

A 
Cranial = lack of vasopressin - e.g. neurosarcoidosis
Nephrogenic = resistance to vasopressin - e.g. reduction in medullary concentration due to chronic renal imapirment
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30
Q

S&S of Diabetes Insipidus?

A

Polyuria (>3L/day), polydypsia, dry skin, colourless urine, constipation, NO GLUCOSURIA

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31
Q

How can you tell between CDI/NDI and how do you treat?

A

Water deprivation test - when desmopressin is given if urine concentration increases = CDI, if it does not increase = NDI.
Treat CDI with desmopressin, NDI is hard to treat so avoid precipitating drugs and ensure patient has water access

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32
Q

What are the different types of hyponatraemia?

A 
Hypovolaemic = low circulating volume (e.g. after severe diarrhoea)
Euvolaemic = normal circulating volume
Hypervolaemic = high circulating volume (e.g. after heart failure, liver cirrhosis and inaprropriate IV giving)
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33
Q

S&S of hyponatraemia?

A

Headaches, nausea, irritability/confusion and unstable gait.
In acute/severe patients there may also be convulsions, respiratory arrest and coma - chronic is often mild or asymptomatic.
Acute <48hrs, chronic >48hrs

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34
Q

What are the serum sodium concentrations for the severity of hyonatraemia?

A 
Mild = 130-135nmol/l
Moderate = 125-129nmol/l
Severe = <125nmol/l
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35
Q

Where is vasopressin made?

A

Paraventricular and supraoptic nerves in the hypothalamus. Stimulated by osmoreceptors (and in emergency baroreceptors in the brain)

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36
Q

What are the 3 types of vasopressin and what do they stimulate?

A 
V1a = vasculature to cause vasoconstriction
V1b = pituitary gland to cause ACTH release
V2 = renal collecting ducts to stimulate water reabsorption
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37
Q

What is SIADH? and what causes it?

A

Syndrome of Inappropriate ADH secretion, caused by CNS disorders e.g. meningoencephalitis, prescription drugs e.g. opiodis , ADH secreting tumours e.g. SC lung cancer and lung diseases e.g. TB

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38
Q

S&S of SIADH?

A

Hyponatraemia - this causes most of teh symptoms (e.g. confusion, headaches, nausea, coma etc.), cramps, depression, dark low volume urine

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39
Q

How do you treat chronic SIADH?

A

Veptans (V2 antagonists) and sodium saline (increase sodium slowly to prevent death of neural tissue)

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40
Q

What is De Quervain’s Thyroiditis? How do you treat?

A

Hyperthyroidism due to the acute inflammation of the thyroid gland - treat with aspirin

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41
Q

S&S of Grave’s disease?

A

Periorbital oedema, proptosis of the eyes, diploplia, peritibial myexedema, acropachy, goitre, heat sensitivity, weight loss

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42
Q

What antibodies cause Grave’s disease?

A

TSH-R aka thyroid stimulating antibodies (TSAb)

43
Q

What drugs can be given to treat Grave’s?

A

Carbimazole plus levothyroxine (a thinoamide) or PTU

44
Q

What is toxic multinodular goitre?

A

This is when the thyroid becomes enlarged due to nodules that secrete TSH

45
Q

Causes of hyperthyroidism?

A

Grave’s disease, toxic multinodular goitre, toxic adenoma, iodine/lithium, amioderone (can also cause hypothyroidism)

46
Q

S&S of hyerthyroidism?

A

Anxiety, hair loss, bulging eyes, enlarged thyroid, heat intolerance, weight loss, tachycardia, diarrhoea, menstrual disturbances

47
Q

How do you treat hyperthyroidism?

A

Carbimazole/Methimazole plus levothyroxine, PTU, radioiodine therapy or surgery. Beta blockers e.g. propanolol are also good as tehy allow rapid symptom control

48
Q

What are the issues with hyperthyroidism in pregnancy?

A

Can cause low birth weight, pre-eclampsia, pre-term delivery as well as increasing the risk of stillbirth/miscarriage

49
Q

How do you treat hyperthyroidism in pregnancy?

A

PTU in first trimester and carbimazole/surgery after that

50
Q

What are the types of amioderone induced thyrotoxicosis?

A

Type 1 = autoimmune but induced by amioderone

Type 2 = destructive and requires steroids to treat

51
Q

What antibodies are usually found in auoimmune hypothyroidisms?

A

Thyroglobulin and TPO

52
Q

What casues hypothyroidism?

A

Thyroidectomy, carbimazole, radioactive iodine treatment, lithium, amioderone, iodine deficinecy (cuases goitre). Pituitary disease = secondary cause, hypothalamic dysfunction = tertiary casue

53
Q

S&S of hypothyroidism

A

Slow cerebration, hair loss/dry skin, hoarse voice, fatigue, weight gain, cold intolerane, bradycardia, muscle cramps, constipation, menstrual disturbances

54
Q

Treatment for hypothyroidism?

A

Levothyroxine (synthetic T4)

55
Q

How can you tell between Hashimoto’s Thyroiditis and Atrophic Thyroiditis?

A 
Hashimoto's = goitre
Atrophic = NO GOITRE, atrophy and fibrosis
56
Q

What are the issues with hypothyroidism in pregnancy?

A

It can cause gestational hypertension, placental abruption, low birth weight, preterm delivery, neonatal goitre and neonatal respiratory distress

57
Q

What is post-partrum thyroiditis?

A

Occurs after pregnancy and can lead to hyper or hypo thyroidism - it is normally self limiting but can lead to permenant disease.

58
Q

What is thyroid crisis/storm?

A

A complication of uncontrolled hyperthyroidism leading to hyperpyrexia, tachycardia, extreme restlessness, delirium and even death - THIS IS A MEDICAL EMERGENCY

59
Q

How do you treat thyroid storm?

A

Large doses of oral carbimazole, potassium iodide and propanolol and IV hydrocortisone

60
Q

What is myxodema coma?

A

A complication of uncontrolled hypothyroidism leading to hypoventilation, hypothermia, hypoglycaemia, hyponatraemia, confusion and coma - THIS IS A MEDICAL EMERGENCY

61
Q

How do you treat myxodema coma?

A

IV T3, IV glucose infusion, gradual warming

62
Q

What causes hypoparathyroidism?

A

DiGeorge syndrome, haemochromatosis or Wilson’s disease, surgical/radiation/autoimmune damage to the parathyroid gland

63
Q

S&S of hypoparathyroidism?

A

Symptoms mainly due to HYPOCALCAEMIA. Depression, dry skin/brittle nails/hair loss, cataracts, muscle spasms in hands/feet, paraesthesia, seizures, hoarse voice,

64
Q

What is Chvostek’s sign?

A

Twitching of the facial muscles in response to tapping over the area of the facial nerve - indicates hypoparathyroidism

65
Q

What is Trousseau’s sign?

A

Carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure - indicates hypoparathyroidism

66
Q

Treatment of Hypoparathyroidism?

A

Calcium and vitamin D supplements

67
Q

What causes hyperparathyroidism?

A 
Primary = hyperplasia of the parathyroid gland, malignancy or benign adenoma
Secondary = low vitamin D/kidney failure
Tertiary = chronic kidney disease
68
Q

S&S of hyperparathyroidism?

A

Symptoms are mainly due to HYPERCALCAEMIA.
Polyuria, polydypsia, constipation, kidney stones, acute pancreatitis, confusion, coma and osteoporosis (due to PTH increase)

69
Q

Treatment of Hyperparathyroidism?

A 
Primary = surgery
Secondary = vitamin D supplements
Tertiary = Cinacalcet
70
Q

What is Addison’s disease and what causes it?

A

Primary adrenal deficiency, the adrenal gland is not working.
This may be caused by autoimmune adrenalitis, autoimmune polyglandular syndrome type 1, congenital adrenal hyperplasia and TB infection

71
Q

What are the types of adrenal insuficiency and what causes them?

A 
Primary = adrenal gland not working due to autoimmune conditions, TB infection etc.
Secondary = hypopituitarism (causes low ACTH) due to radiotherapy and pituitary macroadenoma
Tertiary = suppression of the HPA axis due to steroid use
72
Q

S&S of adrenal insufficiency?

A

Weight loss, fatigue, hyperpigmentation, hypotension, hyponatraemia, muscle weakness and poor recovery from illness

73
Q

Treatment of adrenal insufficiency?

A

Hydrocortisone to replace cortisol (and fludrocortiosone to replace aldosterone in primary)

74
Q

Why do you get hyperkalaemia in primary adrenal insufficiency only?

A

Aldosterone is released from the adrenal gland so in Addisons it will not be released. Normally aldosterone causes potasssium excretion.
Other forms of adrenal insufficiency are not a result of a direct adrenal gland issue so aldosterone can still be released

75
Q

What is adrenal crisis?

A

A complication of peristant adrenal insufficiency characterised by hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia and cardiovascular collapse/seizure - may present with shock.

76
Q

What is Conn’s syndrome and what causes it?

A

This is characterised by too much aldosterone, it is caused by a unilateral adenoma of the renal tissues or by bilateral adrenal hyperplasia

77
Q

S&S of Conn’s syndrome?

A

Hypernatraemia, hypertension, hypokalaemia, muscle cramps/weekness, pins & needles

78
Q

Treatment of Conn’s syndrome?

A 
Unilateral = surgery to remove the affected gland
Bilateral = give spironolactone (an aldosterone antagonist)
79
Q

What is Cushing’s syndrome and what causes it?

A

This is an excess of cortisol caused by tumour of the pituitary gland, ACTH secreting tumours e.g. in the lungs or tumour of the adrenals themselves

80
Q

S&S of Cushing’s syndrome?

A

Central obesity, moon face and buffalo hump
Hypernatraemia, hypertension and hypokalaemia
Diabetes and muscle waisting
Menstrual disturbances and loss of libido
Thin skin, easy bruising and poor healing
Malaise, depression and psychosis

81
Q

How to test and treat Cushing’s syndrome?

A

Test with low dose dexamethasome suppression test (cortisol should decrease by 50%).
Treat with surgery/radiotherapy if casued by tumour and metyrapone (a glucocorticoid synthesis inhibitor)

82
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

Cushing’s syndrome = excess cortisol

Cushing’s disease = when cushing’s syndrome is caused by a pituitary tumour

83
Q

What casues hyperprolactinaemia?

A

Lactotroph cell tumour of the pituitary
Macro/microprolactinomas which secrete prolactin
Non-functioning pituitary tumour which compresses the pituitary stalk

84
Q

S&S of hyperprolactineamia?

A 
Menstrual disturbances (amenorrhoea/oligomenorrhoea), erectile dysfunction, loss of libido, infertility
Galactorrhoea
85
Q

Treatment of hyperprolactinaemia?

A

Cabergoline/bromocriptine (dopamine agonists), surgery/radiotherapy

86
Q

What causes Acromegaly?

A

An increase in IGF-1 due to the presence of a GH secreting tumour

87
Q

S&S of Acromegaly?

A

Large hands/feet, enlarged tongue, excessive sweating, large prominant facial features, diabetes, hypertension and gigantisism in children

88
Q

Treatment for Acromegaly?

A

Pituitary surgery/raiotherapy, dopamine/somatostatin angonists, pegvisomant (GH receptor antagonist)

89
Q

What can cause hyperkalaemia?

A

Renal failure, metabolic acidosis, potassium sparring diuretics, potassium therapy, uncontrolled Addison’s disease

90
Q

S&S of hyperkalaemia?

A

Fast/irregular pulse, palpitations, chest pain, tall tented T-waves/small P waves/wide QRS, weakness

91
Q

Treatment of hyperkalaemia?

A

Treat underlying cause, polystyrene sulphonate (prevents potassium absorption at the gut)

92
Q

What causes hypokalaemia?

A

Diuretics, D&V, Conn’s/Cushing’s syndrome, metabolic alkalosis, burns

93
Q

S&S of hypokalaemia?

A

Muscle weakness, cramps, hypotonia, light-headedness, constipation, palpitations, small inverted T waves/ST depression/prominent U waves

94
Q

Treatment of hypokalaemia?

A

Give potassium (oral or IV), switch to potassium sparring diuretics

95
Q

What malignancies lead to hypercalcaemia?

A

Lytic bone metastases, myeloma, PTH-like hormones produced by a tumour

96
Q

S&S of hypercalcaemia?

A

Lethargy, nausea, polyuria/polydypsia, anorexia, constipation, confusion, muscle weakness

97
Q

Treatment of hypercalcaemia?

A

Rehydration, bisphosphonates, treat underlying malignancy

98
Q

What causes hypocalcaemia?

A

With increased phosphate: hypoparathyroidism, vitamin D deficiency, CKD
With normal/low phosphate: osteomalacia, overhydration, respiratory alkalosis

99
Q

S&S of hypocalcaemia?

A

Spasms, increased muscle tone, Chvostek’s sign, cataracts, dermititis, irritability, anxiousness, seizures and long QT waves

100
Q

Treatment of hypocalceamia?

A

Oral calcium or IV calcium gluconate (if severe)

101
Q

How do you treat papillary and follicular thyroid cancers?

A

Total thyroidectomy and ablative radioactive iodine. GOOD PROGNOSIS

102
Q

How do you treat anaplastic and lymphoma thyroid cancers?

A

Do not respond to radioactive iodine, give external radiation. THIS IS PALLIATIVE

103
Q

How do you treat medullary thyroid cancer?

A

Thyroidectomy and lymph node removal

104
Q

S&S of thyroid cancer?

A

Dysphagia, hoarse voicem large/hard/irregularly shaped thyroid gland

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