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Endocrinology Flashcards

1
Q

What is the immediate management for a diabetic patient in ketoacidosis?

A

Isotonic insulin, saline and potassium

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2
Q

A patients blood results show low TSH levels and high T4/T3 levels. What is the most likely diagnosis?

A

Hyperthyroidism

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3
Q

What is the most likely diagnosis when TSH-receptor antibodies are present (in hyperthyroidism)?

A

Grave’s disease diagnosis

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4
Q

SGLT-2 inhibitors are liked for type 2 diabetic patients because…

A

They are weight-neutral/Weight-losing. Compared with the older T2D medications

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5
Q

What is the HBA1C target for type 2 diabetes patients?

A

48 mmol/mol.

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6
Q

After dietary and lifestyle which medication is first line for type 2 diabetes?

A

Metformin

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7
Q

A patient has low TSh and high T4 with normal T3. What is the most likely diagnosis

A

Primary hyperthyroidism

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8
Q

Which visual field defect is most associated with pituitary ademonas? And how does this occur?

A

Bitemporal Hemianopia. Through a lesion of the optic chiasm.

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9
Q

What are the 3 features of polycystic ovary syndrome which need to be present to make a diagnosis (must have 2 or more) ?

A

Oligomenorrhea/amenorrhea
Signs of hyperandrogenism (acne, excess hair)
US - polycystic ovaries (12 or more follicles in 1 ovary)

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10
Q

What are main symptoms of hypothyroidism?

A

Menorrhagia, Low mood, weight gain, tiredness, joint and muscle pain, sensitive to cold temperatures, dry skin and hair

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11
Q

How is diabetes insipidus characterised? (what occurs to cause this? )

A

Reduced ADH secretion or insensitivity to ADH

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12
Q

What are the symptoms of diabetes insipidus?

A

Increased urination (polyuria, polydipsia and nocturia), chronic dehydration, Hypovolaemia (low BP) and Hypernatraemia

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13
Q

What is the most likely cause of low TSH, T4 and T3 levels?

A

Euthyroid sick syndrome

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14
Q

At what days during a woman’s cycle is she most fertile?

28 day cycle

A

9-16 days.

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15
Q

What is the first step in diabetic ketoacidotic treatment?

A

Fluid resuscitation

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16
Q

What is Addison’s disease? (Causes?)

A

Primary Hypoadrenalism. Usually at 30-50 years old and more common in women. 90% are due to autoimmune disorders with the remainder being most likely due to TB

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17
Q

What are the symptoms of Addison’s disease?

A

o Fatigue and Myalgia
o Hyponatraemia
o Hypovolemia and Hypotension – mineralocorticoid deficiency
o Nausea and vomiting
o Weight loss and Anorexia
o Dizziness and Fainting
o Low self-esteem and Depression and Irritable
o Abdominal pain and change in bowel habits
o Muscle and joint pain
o Pigmentation (dull brown) – increased ACTH/CRH

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18
Q

What bedside investigations would be done for suspected Addison’s?

A

U&E’s - hyponatremia, hyperkalemia and possible hypercalcaemia
Glucose - may have hypoglycaemia

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19
Q

For suspected Addison’s disease what specific tests would be done? (suppression or stimulation) ?

A

ACTH Stimulation test (synacthen)
0900 ACTH levels
Adrenal antibodies

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20
Q

What is the immediate treatment for suspected hypoadrenalism (Addison’s) ?

A

Treat hyponatremia (slowly to avoid demyelination). Give hydrocortisone and saline until patient stabilises.

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21
Q

What is the long term treatment of Addison’s?

A

Glucocorticoid and mineralocorticoid replacement

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22
Q

What are the symptoms of hyperthyroidism?

A 
Heat intolerance
Fine straight hair 
bulging eyes 
Weight loss 
Facial flushing 
enlarged thyroid 
Tachycardia 
hyperthyroidism 
Muscle wasting 
menstrual changes (amenorrhea) 
Tremors 
Diarrhoea 
Clubbing
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23
Q

What are the 3 stages of pathophysiology of diabetes type 1?
(immune mediated reaction)

A
  1. β-cell antigens are taken up by the dendritic cells where in lymph nodes they are shown to CD4 cells.
    - CD4 cells escape thymus and present this to immune cells including B cells = auto-antibodies
    ! there is a loss of negative regulatory mechanism !
  2. Immune cells then move back to the β-cells and cause their destruction - particularly CD8 and macrophages (increase CD8)
  3. development of symptoms due to the threshold destruction of β-cells
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24
Q

Which form of diabetes is due to a absolute deficiency of insulin?

A

Type 1

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25
Q

Name symptoms of hyperglycaemia?

A 
extreme Fatigue 
Polyuria 
Polydipsia 
Increased thirst/dehydration 
Weight loss and wasting 
Abdominal aching 
Leg cramps 
Blurred vision 
Drowsiness
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26
Q

At what level is a HbA1c indicative of diabetes?

A

Over 48 mmol/mol (6.5%)

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27
Q

At which fasting plasma glucose is diabetes indicative?

A

7 mmol/L or above

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28
Q

At which random plasma glucose is diabetes indicative?

A

11 mmol/L or above

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29
Q

What is the first line treatment for a patient diagnosed with T2 diabetes with a HbA1c below 75 mmol/mol?

A 
Lifestyle changes (exercise and dietary) 
Metformin
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30
Q

Which T2 diabetes medication is best for weight loss?

A

SGLT2 inhibitor such as empagliflozin

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31
Q

What is a possible S/E or complication of increasing the glucose in a patient’s urine?

A

Fournier’s gangrene (Necrotising fasciitis of genitals)

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32
Q

Lixisenatide and Exenatide are examples of which group of T2 diabetes meds? And what is their mode of action and S/E’s ?

A

GLP1 agonists
Increase insulin secretion and decrease glucagon secretion as well as slowing gastric motility.

Not to be used in ketoacidosis or GI disease

S/E = back pain, diarrhoea, infection risk, N+V, Drowsy and dizziness

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33
Q

What is type 2 diabetes a combination of (pathology)?

A

Insulin resistance and reducing insulin secretion

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34
Q

What are the 4 main risk factors for T2 Diabetes?

A

Age (over 40), obesity, Family history, ethnicity

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35
Q

A patient presents with signs of acanthosis nigrican, skin tags, central obesity and hirsutism. What is this showing and what is therefore the most likely diagnosis?

A

Shows insulin resistance indicative of T2 diabetes

36
Q

What is metformins mode of action (general)?

A

Decreases gluconeogenesis and increases the utilisation of peripheral glucose

37
Q

What is the mode of action of sulfonylureas? and name a sulfonyluria?

A

Augment insulin secretion. (only works if there is remaining function of the β-cells).

Gliclazide
Glibenclamide

38
Q

What medication has this mode of action:

Reduces peripheral insulin resistance therefore reduces blood glucose concentration

A

Glitazones - Pioglitazone

39
Q

Alogliptin and Sitagliptin are examples of what T2 diabetes medication? And what is the mode of action?

A

Gliptins (DPP-4 inhibitor)

Increase insulin secretion and reduces glucagon secretion

40
Q

A patient is admitted with persistent UTIs as well as a history of increasing lethargy, polyuria/polydipsia and weight loss. What investigation would you want and what would be indicative of the expected diagnosis?

A

HbA1c >48 mmol/mol (6.5%)
or fasting glucose of >7 mmol/L or random glucose of >11.1 mmol/L

If so would indicate type 2 diabetes for which you would refer to diabetes team and recommend lifestyle changes as well as metformin to begin treatment with (unless HbA1c was very high)

41
Q

What are the chronic microvascular complications of diabetes?

A

Retinopathy
Nephropathy
Neuropathy
Circulatory problems –> leads to macrovascular

42
Q

What are the chronic macrovascular complications of diabetes?

A

Peripheral vascular disease
Ischaemia heart disease
cerebrovascular disease

43
Q

How does neuropathy occur in diabetes?

A

Axonal loss, focal demyelination and nerve regeneration attempts. As well as thickening of the vasa nervorum BM occludes the artery (small arteries supplying the peripheral nerves) –> occlusion. Therefore leading to reduced supply of the nerves and slower conduction.

44
Q

What can neuropathy (loss of sensation to the limbs) and PVD lead to?

A

Diabetic foot! - ulceration
- patient injure their foot or there is repeated damage. Due to reduced blood supply to the area (peripheral vascular disease) there is limited healing of this especially in feet and hands (just that hands are seen more).
- Therefore this does not heal and tends to get infected which requires amputation
This is also in fact due to them not recognising that it has been injured as they can’t feel the pain it may cause.

45
Q

What is charcot’s foot?

A

Common in diabetic patients. Bones become weak and there is dislocation at the joints. If not caught (possibly not due to neuropathy) these changes become permanent and the foot is left deformed. This makes pressure sores more likely for the patient.

46
Q

A 21 year old female comes into ED, PMH of type 1 diabetes with severe vomiting. In the history they have been going to the toilet more and drinking more recently. They say they have a new diagnosis of diabetes and have been struggling to manage it. O/E they have abdominal pain as well as dry mucous membranes. And the obvious vomiting.
What investigations would you want to carry out to confirm your diagnosis? And what is your provisional diagnosis?

What would be the treatment/management?

A

ABCDE
O2 sats - 92% (low due to metabolic acidosis and respiratory compensation) –> hyperventilating.
GCS - may be confused or delirious

Bloods: 
FBC, U+E's, CRP and formal glucose 
Blood culture - Infection could be cause of DKA 
Ketones - high 
Glucose - very high 
pH (VBG) - acidic

Diagnosis of diabetic ketoacidosis

Fix through ABCDE
- put on oxygen if sats low
- Give fluids (if hypotensive then 500ml bolus) - 0.9% saline
- Think about potassium (if hypo then treat)
- Give fixed rate intravenous insulin infusion (based off weight)
Until VBG pH is above 7.3 or ketones are below 0.6 mmol/L

47
Q

A 65yr old female comes in you have their blood results but are yet to see them yet for their possible thyroid problem. The results are High TSH and Low T4. Based on the diagnosis what would you expect to see (the patient), what would be the most likely cause and what would be the most likely treatment?

A

Primary Hypothyroidism.
- Weight gain, cold intolerance, low mood, dry skin, loss of hair and 1/3rd eyebrow, lethargy and fatigue.
Most likely to be autoimmune cause - hashimoto’s
Treatment is levothyroxine (T4 supplement) which is given and matched to the TSH level - slowly titrated up. Takes 7 days due to long half life so takes a while to get right.

48
Q

A30 yr old female is coming in complaining of weight loss, sweating all the time, palpitations and a tremor alongside general fatigue. What is your first thought? Based on that what is the plan (investigations, likely diagnosis and treatment)?

A

Sounds like hyperthyroidism
Want to test T4/3 and TSH. Expect to get back Low levels of TSH and high levels of T4/3.
- Likely to be Grave’s disease based on age of patient
Treatment would be anti-thyroid medications such as carbimazole - titrate till euthyroid and then adjust

49
Q

In what other chronic condition is secondary hyperparathyroidism present? - what levels would confirm secondary HPT

A

Chronic kidney disease.

High PTH and Low calcium

50
Q

In what age group is primary hyperparathyroidism prevalent? What would the PTH and calcium levels be?

A

Post menopausal women.

PTH low and Calcium High

51
Q

What is the common presentation of primary hyperparathyroidism? and what are other signs and symptoms that can occur?

A

70-80% are asymptomatic - found by chance
Osteoporosis/osteopenia
Renal calculi
HYpercalcaemia - muscle weakness, hypertension, anorexia, polydipsia, polyuria, dehydration, haematuria, depress, confusion, dementia.

52
Q

In tertiary parathyroidism what would the PTH and calcium levels be and what is the most likely cause?

A

PTH and Calcium high.
Most likely due to long term secondary HPT which has now been resolved however the glands have had hyperplasia and now have a loss of response to calcium so secrete PTH regardless of the calcium levels.

53
Q

What genetic condition is linked to hypoparathyroidism as well as heart problems, cleft palate and immune deficiency?

A

DiGeorge’s syndrome.

54
Q

A patient has untreated hypothyroidism what do you expect their TSH and T4 levels would be (high/low) ?

A

TSH High

T4 Low

55
Q

What antibodies are found in the majority of graves disease patients?

A

TSH receptor antibodies

56
Q

What is the treatment of neurogenic diabetes insipidus?

A

synthetic ADH - desmopressin

57
Q

What is the treatment of nephrogenic diabetes insipidus?

A

Access to plenty of drinking water and to fix any metabolic problems (e.g. drugs causing it)
If it is severe then high dose desmopressin can also be given.

58
Q

How is the pituitary gland connected to the hypothalamus?

A

Via the pituitary stalk (infundibulum)

59
Q

Which tumour can be responsible for bitemporal hemianopia?

A

Anterior lobe adenomas

60
Q

What is the posterior lobe (neurohypophysis) formed from?

A

Neural tissue

61
Q

WHat is the function of the posterior pituitary gland?

A

Stores and secretes hormones that are produced by the hypothalamus. Oxytocin and ADH in response to the hypothalamus.

62
Q

What is the anterior lobe (adenohypophysis) formed from?

A

Glandular tissue

63
Q

What is the function of the anterior pituitary gland?

A

Manufacture hormones via endocrine cells controlled via the hypothalamic hormones

64
Q

Name the hormones produced by the anterior pituitary gland.

A 
corticotropin 
FSH/LH 
Growth hormone 
Prolactin 
TSH
65
Q

What hormone stimulates the production of corticotropin and what is its function?

A

Corticotropin RH

Works on the adrenal glands to stimulate the production of glucocorticoids (metabolism and stress)

66
Q

What hormones stimulates the production of FSH/LH and what is its function?

A

Gonadotropic RH
FSH = stimulates maturation and production of sex cells
LH = stimulates sex hormones by the gonads

67
Q

What hormones stimulates the production of growth hormone and what is its function?

A

Growth hormone RH/IH (somatostatin)

Induces production of insulin like growth factors that stimulate brody growth and higher metabolic rate

68
Q

What hormones stimulates the production of prolactin and what is its function?

A

Prolactin RH and Prolactin IH (dopamine)

Promotes milk production

69
Q

What hormones stimulates the production of TSH and what is its function?

A

Thyrotropin-RH

stimulates release of thyroid hormones

70
Q

What is produced in the adrenal cortex?

A

Cortisol - stimulated by corticotropin in pituitary gland

Aldosterone

71
Q

What is the function of cortisol and when is it released?

A

Glucocorticoid released in response to stress and low blood-glucose levels.
Promotes gluconeogenesis
suppresses the immune system
aids the metabolism of fat, protein and carbohydrates

72
Q

What is the function of aldosterone and when is it released?

A

Mineralocorticoid
Increases blood volume
Promotes the reabsorption of sodium and water and increases potassium excretion

73
Q

What is produced in the adrenal medulla?

A

Adrenaline and noradrenaline

74
Q

What is the function of adrenaline and NA?

A

Fight/flight - released during periods of stress

increased heart rate, BP and muscle perfusion

75
Q

What controls the release of adrenaline and NA?

A

Hypothalamus

76
Q

What is addisons disease?

A

Primary adrenal insufficiency causing a reduction in cortisol and aldosterone secretion.

77
Q

What is the most common cause for addison’s disease?

A

Autoimmune

78
Q

What is the cause of secondary adrenal insufficiency?

A

Inadequate ACTH stimulating the adrenal glands = reduced cortisol release. Due to loss or damage to the pituitary gland

79
Q

What is the cause of tertiary adrenal insufficiency?

A

Inadequate CRH release by hypothalamus = can be due to long term oral steroid use which suppresses the hypothalamus

80
Q

What are the symptoms and signs of adrenal insufficiency?

A 
Fatigue 
Nausea 
Cramps 
Abdominal pain 
reduced libido 
Bronze hyperpigmentation of skin 
hypotension (postural)
81
Q

How do the levels of ACTH differ between primary and secondary adrenal failure?

A 
Primary = ACTH levels are high - due to lack of negative feedback 
Secondary = ACTH level is low as it is not being released
82
Q

What happens to the sodium and potassium levels in adrenal insufficiency?

A

Hyponatraemia

Hyperkalaemia

83
Q

What is the test of choice to diagnose adrenal insufficiency?

A

Short synacthen test (ACTH stimulation test)

- less than double the baseline is indicative of addison’s

84
Q

What is the treatment for addison’s disease?

A

Hydrocortisone and fludrocortisone (replacements)
Steroid card and emergency ID tag
Told that if they have a acute illness to double their doses.

85
Q

What cells in the adrenal glands produce adrenaline?

A

Chromaffin cells

Medicine (26 decks)

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