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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Name the 3 endocrine hormones that are released by the pancreas. (3)

A

Insulin, glucagon and somatostatin.

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2
Q

What cells of the pancreas release digestive enzymes e.g. amylase? (1)

A

Acinar cells

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3
Q

Name 3 hormones release by anterior pituitary. (3)

A 
TSH
LH
FSH
ACTH
GH
Prolactin
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4
Q

Name 2 hormones that are released from posterior pituitary. (2)
Where are they synthesised? (1)

A

Posterior pituitary acts as storage for Vasopressin (ADH) and Oxytocin, which are synthesised in hypothalamus and travel down pituitary stalk to posterior pituitary.

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5
Q

Name 2 effects of oxytocin. (2)

A

Milk ejection

Uterine myometrial contractions

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6
Q

Describe negative feedback loop using an example. (3)

A

Thyroid example:
Hypothalamus releases TRH
TRH stimulates anterior pituitary to release TSH
TSH stimulates thyroid gland to release T4 and T3 (most of which comes from peripheral conversion)
High levels of T3 and T4 lower levels of TRH and TSH by acting negatively on the pituitary and hypothalamus.

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7
Q

How can you classify the symptoms produced by a pituitary adenoma? (2)

A

Those from local effects of tumour e.g. bitemporal hemianopia, headaches
Those from over/under production of hormones e.g. GH and acromegaly

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8
Q

What are the 3 main conditions that cause overproduction of hormones from pituitary adenoma? (3)

A

Acromegaly/gigantism: GH
Cushing’s disease: ACTH
Hyperprolactinaemia: Prolactin

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9
Q

Give 3 local effects of a pituitary tumour? (3)

A

Bitemporal hemianopia (optic chiasm)
CN III, IV and VI lesions (cavernous sinus)
Headache
Hydrocephalus (ventricles)
Obesity, altered appetite and thirst, precocious puberty (hypothalamus)

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10
Q

Which imaging is best for locating a pituitary adenoma? (1)

A

MRI head

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11
Q

Describe the normal release of GH. What other hormones is it’s release affected by? (3)

A

Pulsatile release

Stimulated by GHRH and inhibited by somatostatin.

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12
Q

What substance is measured in investigation of suspected acromegaly? (1)
Why? (2)

A

Insulin-like growth factor 1 (IGF-1)
because GH release is pulsatile (and also released acutely during stress) and its activity is exerted indirectly through IGF-1 (it is synthesised by many tissues to induce metabolic changes and so it’s numbers are a lot more stable.

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13
Q

Name hormones released during stress. (3)

A

Adrenaline
Cortisol
GH
Prolactin

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14
Q

Why does GH cause gigantism in children and not acromegaly? (1)

A

Gigantism occurs if excess GH is before the fusion of the epiphyses of the long bones.

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15
Q

Are males or females affected more by acromegaly? (1)

What age group? (1)

A

Both equally.

Also most common in middle age.

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16
Q

How does the glucose tolerance test help in the diagnosis of acromegaly? (2)

A

75g of oral glucose and measure GH 2 hours later.
[Glucose causes release of insulin and somatostatin; somatostatin is inhibitory hormone for GH release]
If 2 hours later GH is not suppressed then test is positive for acromegaly.

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17
Q

Name 4 signs you may see on examination of a patient with acromegaly. (4)

A

Prognathism, Interdental separation, Large tongue, Spade-like hands and feet, Tight rings.
Prominent supra-orbital ridge, Hirsuitism, Thick greasy skin, Carpel tunnel, Visual field loss, Galactorrhoea, Hypertension, Oedema, HF, Arthropathy, Proximal myopathy, DM.
Signs of hypopituitarism.

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18
Q

Name 4 symptoms that suggest acromegaly? (4)

A

Local effects of tumour: Headaches, Visual deterioration,
Effects of GH: Change in appearance, Larger hands and feet, Weight gain, Pain/tingling in hands, Joint pains, Muscle weakness
Other hormones: Amenorrhoea, Galactorrhoea, Impotence, Goitre. Symptoms of Hypopituitarism

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19
Q

Bob is a 68 year old man and you suspect he has acromegaly.

What investigations would you like to perform? (3)

A

Bed: ECG
Bloods: Serum prolactin, Serum IGF-1
Imaging: MRI head
Special: Visual fields plotted by perimetry, Glucose tolerance test.

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20
Q

What is the cause of galactorrhoea in a patient with acromegaly? (2)

A

Pituitary adenoma can compress the pituitary stalk.
Prolactin secretion suppressed by dopamine, if stalk is compress then dopamine is not able to suppress prolactin production.

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21
Q

What is the management of acromegaly? (3)

A

Surgical first: Trans-sphenoidal surgical resection
Medical if surgery not successful: Somatostatin analogues e.g. ocreotide and dopamine agonists (eg bromocriptine and cabergoline).
Radiotherapy can also be used in combo with medical treatment as results are slow.
Manage complications: HTN, DM and hypopituitarism.

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22
Q

How are acromegaly and DM linked? (1)

A

Excess GH can cause peripheral resistance to insulin causing development of T2DM.

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23
Q

Name 2 complications of trans-sphenoidal resection of a pituitary adenoma. (2)

A

Hypopituitarism, Diabetes insipidus, Infection, CSF rhinorrhoea.

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24
Q

What order are hormones depleted in multiple hypopituitarism? (4)
What is different about prolactin? (1)

A

First: GH and LH/FSH
Later: ACTH and TSH
Rarely: Oxytocin and ADH

Prolactin levels increase relatively early as compression of pituitary stalk causes loss of inhibition by dopamine of prolactin.

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25
Q

Name 3 causes of hypopituitarism. (3)

A 
Vasc: pituitary apoplexy
Infect: Encephalitis, syphilis
Trauma: Surgery, skull fractures**
AI: Pituitary antibodies
Metabolic: Anorexia
Infiltration: Sarcoidosis, Haemochromatosis
Neoplasm: Primary pituitary** or hypothalamic, lymphoma
Others: Chemo and Radiation
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26
Q

Thinking logically, name some clinical features associated with total multiple hypopituitarism. (4)

A

Loss of GH: short stature in children
Loss of FSH/LH: loss of libido, amenorrhoea, erectile dysfunction.
Hyperprolactinaemia: galactorrhoea, hypogonadism
Hypothyroid and adrenal failure: tiredness, slowness of thought, mild hypotension.
Long standing hypopituitarism may give sign of alabaster skin: pale and hairless.

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27
Q

What part of history can suggest that multiple hypopituitarism is unlikely? (1)

A

Normal gonadal function eg ovulation, menstruation and functional erections suggest FSH/Lh are ok and as these are the first to be affected (along side GH) then multiple hypopituitarism is unlikely.

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28
Q

Sheila is a 16 year old girl who has been diagnosed with multiple hypopituitarism.
What is the management? (4)

A 
Steroid replacement
Thyroxine replacement
Oestrogen and androgens for symptomatic control, (oestrogens (and progesterone to stop endometrial ca) for women and androgens for men)
FSH and LH is fertility desired.
GH replacement under specialist control.
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29
Q

Which thyroid hormone is produced most copiously? (1)
Which thyroid hormone is the most potent? (1)
What is 99% of T4 and T3 bound to when circulating in the blood? (1)

A

T4
T3
Thyroid binding globulin

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30
Q

Why should TFT’s not be taken while the patient is suffering from an acute illness? (1)

A

Sick Euthyroid Syndrome

Acute illness eg pneumonia can cause changes in TBG, and low total and free T3 and T4 with normal TSH.

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31
Q

Name 3 causes of hypothyroidism. (3)

A

Autoimmune thyroiditis *
Iatrogenic eg thyroidectomy, radiotherapy, radioactive iodine treatment, carbimazole, lithium, and amiodarone.
Iodine deficiency
Congenital

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32
Q

What is the term for a patient with the following results:
TSH slightly raised
T3 and T4 normal (1)

A

Subclinical hypothyroidism

Recheck yearly to look for development of overt hypothyroidism.

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33
Q

What is the name of the acute medical emergency caused by hypothyroidism? (1)
Name 3 clinical features. (3)

A

Myxoedema coma

Hypothermia, HF, Hypoventilation, Hypoglycaemia, Hyponatraemia.
Previous history of thyroid disease, or history of hypothyroid symptoms.

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34
Q

What is the management of myxoedema coma? (3)

A

T3 oral or IV
Oxygen
Gradual rewarming for hypothermia
Hydrocortisone IV (in case it is manifestation of hypopituitarism)
Glucose infusion to prevent hypoglycaemia.

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35
Q

Name 3 main disorders responsible for hyperthyroidism. (3)

A

Graves, Toxic multinodular goitre, toxic adenoma. *

Rarer: de Quervains, amiodarone, metastatic differentiated thyroid carcinoma, TSH-secreting tumour eg pituitary

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36
Q

What immunoglobulin is to blame in Grave’s disease? (1)

A

IgG stimulating TSH receptor on thyroid gland.

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37
Q

Name 2 other autoimmune diseases associated with Graves disease? (2)

A

Myasthenia gravis

Pernicious anaemia.

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38
Q

What is de Quervain’s thyroiditis? (2)

How is it treated? (1)

A

Transient hyperthyroidism caused by acute inflammation from a viral infection. It is accompanied by fever, malaise and neck pain.
Aspirin

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39
Q

Describe pre-tibial myxoedema. (2)

A

Raised, purple-red symmetrical skin lesions over anterior-lateral shins occurring in Grave’s disease.

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40
Q

What thyroid eye signs would you expect to see in Grave’s disease? (3)

A 
Exopthalmos (proptosis)
Lid retraction
Lid lag
Conjunctival oedema
Periorbital oedema
Opthalmoplegia
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41
Q

What is thyroid acropachy? (1)

A

Occurring in Grave’s disease. Causes periosteal new bone formation, clubbing and swelling of the fingers.

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42
Q

Name 3 investigation that may help with the diagnosis of Grave’s disease. (3)

A

TFTs (TSH, T3 and T4)
Anti TPO or Thyroglobulin antibodies
Thyroid ultrasound

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43
Q

Describe the medical treatment of hyperthyroidism and Grave’s disease. (2)

A

First line: Carbimazole- blocks the synthesis of thyroid hormones and also has immunosuppressive properties.
But takes 10-20 days to take effect so Propranolol is used or symptomatic treatment during this time (most symptoms are from activation of sympathetic activation).
If carbimazole is not tolerated, propylthiouracil can be used.

Another option is radioactive iodine-131. It is contraindicated in pregnancy and breastfeeding, and results in thyroid tissue destruction. A second dose can be used if hyperthyroidism persists.

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44
Q

Give 3 complications of a subtotal thyroidectomy. (3)

A

blleding, infection, hypocalcaemia, hypothyroidism, hypoparathyroidism, recurrent laryngeal nerve palsy, recurrent hyperthyroidism.

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45
Q

What is a thyroid crisis? (2)

Name 2 symptoms. (2)

A

aka thyroid storm.
Rare, life threatening condition in which there is rapid deterioration of thyrotoxicosis.
Hyperpyrexia, tachycardia, extreme restlessness and eventually, delirium, coma and death.

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46
Q

What is the role of potassium iodide in hyperthyroidism? (2)

A

Acutely blocks the release of thyroid hormone from the gland.
used in treatment of thyroid crisis and in preparation for subtotal thyroidectomy.

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47
Q

Name 3 drugs used in the management of thyroid crisis. (3)

A

Carbimazole
Propranolol
Potassium iodide
Hydrocortisone (blocks peripheral conversion of T4 to T3)

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48
Q

Describe lid lag. (1)

A

Delay in movement of the upper eye lid as the eye moves downwards.

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49
Q

Describe lid retraction. (1)

A

As patient looks forwards, the white of the sclera is visible above the cornea.

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50
Q

Why do lid lag and lid retraction occur? (1)

A

Increased catecholamine sensitivity of the levator palpabrae superioris.

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51
Q

Why do the opthalmic Grave’s signs of proptosis and opthalmoplegia occur? (2)

A

T lymphocytes react with antigens shared by the thyroid and orbit (same embryological origin) and cause retro-orbital inflammation. Extra-occular muscles become swilled and oedematous causing proptosis and opthalmoplegia.
More severe in smokers.

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52
Q

When in the course of Grave’s disease do eye signs occur? (1)

A

Any time, before or after onset of hyperthyroidism.

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53
Q

Gertrude is a 46 year old woman who has presented with a swelling in her central neck.
After examination you believe she has a goitre.
How will you investigate this? (3)

A

Bed: ECG if AF
Bloods: TFTs, Anti-TPO antibodies
Imaging: Thyroid USS, CXR for large goitres.
Special: FNA if nodules.

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54
Q

Name the 5 types of thyroid carcinoma. (5)
Which is the most common? (1)
Which is the most aggressive? (1)

A

Papillary, Follicular, Anaplastic, Lymphoma, Medullary cell.
Papillary (70%)
Anaplastic

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55
Q

Which 2 types of thyroid cancer are most likely to metastasise more than locally? (2)

A

Anaplastic and Medullary cell.

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56
Q

What is the management for follicular and papillary thyroid carcinomas? (2)

A

Total thyroidectomy and neck dissection for local spread.

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57
Q

Where is cortisol produced from? (1)

A

Cortex of the adrenal gland

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58
Q

What is produced from the medulla of the adrenal gland? (1)

A

Catecholamines

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59
Q

What is produced from the cortex of the adrenal gland? (2)

A

Cortisol, Aldosterone and Androgens

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60
Q

Why are one-off serum cortisol measurements not useful for diagnosis? (1)

A

Cortisol levels fluctuate, they are affected by circadian rhythm and stress and so a one-off level is not a reliable indicator of long term levels.

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61
Q

Name 4 effects of cortisol. (4)

A 
Protein catabolism
Increased fat and glycogen deposition
Sodium retention
Renal potassium loss
Decreased host response to infection
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62
Q

What is Addisons’ disease? (1)

A

Autoimmune destruction of the entire adrenal gland. (Primary hypoadrenalism)

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63
Q

Name 3 causes of primary hypoadrenalism. (3)

A 
Autoimmune (Addison's)
Adrenal gland TB
Surgical removal
Malignant infiltration
Haemorrhage from meningococcal septicaemia

NB: Sudden cessation of long term corticosteroid therapy is an example of secondary, think about negative feedback mechanism

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64
Q

Name 4 symptoms/signs that may be present in insidious onset on Addison’s disease. (4)

A

Non-specific: weight loss, anorexia, lethargy, depression
Postural hypotension
Hyperpigmentation of buccal mucosa, skin creases, recent scars or pressure points due to excess ACTH
Vitiligo or loss of body hair due to dependence on androgens

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65
Q

How may an Addinsonian crisis present? (3)

A

Vomiting, hypoglycaemia, abdominal pain, profound weakness and hypovolaemic shock.

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66
Q

What are the 3 aims of investigations in suspected hypoadrenalism? (3)

A

Demonstrate low cortisol
Determine specific cause
Determine if dependant or independent of ACTH i.e. primary or secondary/tertiary

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67
Q

What investigations will be helpful in the diagnosis of hypoadrenalism? (4)

A

Serum cortisol and serum ACTH level to determine primary or secondary/tertiary cause.
Short synACTHen test: failure of exogenous ACTH to increase cortisol levels. (no differentiation between 1’ and 2’)
Long synACTHen test: diagnose 2’ hypoadrenalism or suppression by steroids.
Adrenal antibodies: Addison’s
U+E’s, Ca and glucose: hyponatraemia, hyperkalaemia, raised urea, hypoglycaemia, hypercalcaemia.
CXR and AXR: evidence of TB with calcified adrenals

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68
Q

Describe the short synacthen test. (2)

A

Measure plasma cortisol
Give exogenous ACTH (tetracosactide) IM/IV
Measure cortisol after 30 mins
Adrenal insufficiency is excluded if cortisol levels increase.

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69
Q

Describe the long synacthen test. (2)

A

Measure plasma cortisol
Give exogenous ACTH (tetracosactide 1mg IM)
Measure cortisol at 4, 8 and 24 hours.
Interpret: normal adrenals will rise to 1000nmol/L by 4 hours. In Addison’s the cortisol response is impaired throughout whereas in secondary causes the response is delayed but normal.

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70
Q

What is the long term management for Addison’s disease? (2)

A

Twice daily hydrocortisone (20mg OM and 10mg ON)
Once daily fludrocortisone
Medic alert bracelet
Emergency amp of hydrocortisone at home.

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71
Q

When would a person with Addison’s disease require increase in the dose of steroids? (2)

A

During illness
Following trauma
For surgery

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72
Q

What preventative medications should be started with long term steroid therapy? (2)

A

PPI
Bisphosphonate
Calcium and D3

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73
Q

What single test will help identify between primary and secondary causes of hypoadrenalism? (1)

A

Long synacthen test

74
Q

Why is there no skin hyperpigmentation in secondary causes of hypoadrenalism? (1)

A

No excess ACTH to activate melanocytes.

75
Q

Name 2 causes of secondary hypoadrenalism? (2)

A 
Sudden cessation of long term corticosteroid therapy
Pituitary lesion (may also have other symptoms of hypopituitarism)
76
Q

What is the treatment for secondary causes of hypoadrenalism? (1)

A

Hydrocortisone, fludrocortisone not needed.

77
Q

What is the difference between Cushing’s disease and Cushing’s syndrome? (2)
What is pseudo- Cushing’s? (1)

A

Cushing’s disease: Excess production of ACTH from pituitary micro adenoma
Cushing’s syndrome: Abnormalities resulting from chronic excess of glucocorticoids.

Alcohol excess mimicking Cushing’s syndrome.

78
Q

Describe some of the signs/symptoms you would expect to see in a patient with Cushing’s syndrome. (5)

A 
Central obesity
Buffalo hump
Plethoric complexion with a moon face
Thin skin
Bruising
Hypertension
Striae
proximal myopathy
Proximal muscle wasting
Depression 
NB theres loads more
79
Q

How is hyperpigmentation a symptom of both Addison’s and Cushing’s? (1)

A

Symptom of excess ACTH.

80
Q

Name 5 adverse effects of long term corticosteroids. (5)

A

Adrenal suppression
CV: HTN
GI: Peptic ulceration, acute pancreatitis
Renal: polyuria
CNS: depression, euphoria, psychosis, insomnia
Endo: weight gain, DM, impaired growth in children
Bone and Muscle: osteoporosis, proximal myopathy and wasting, aseptic necrosis of the hip, pathological fractures
Skin: thinning, easy bruising
Eyes: cataracts
Infection: Septicaemia, TB reactivation, oral candida

81
Q

How is Cushing’s Syndrome diagnosed? (2)

Name 4 investigations. (4)

A

CONFIRM RAISED CORTISOL
1- 24 hour urinary free cortisol: raised
2- 48 hour low dose dexamethasone suppression test: dex 0.5mg given orally 6 hourly for 48 hours and plasma cortisol measured. Suppressed if normal, raised if Cushing’s.
ESTABLISH CAUSE
3- Adrenal CT/MRI: adrenal adenoma
4- Pituitary MRI: pituitary adenoma
5- Plasma ACTH levels: low in adrenal gland disease, high in pituitary disease or ectopic production.
6- High dose dex suppression test: 2mg 6 hourly for 48 hours. Failure of suppression suggests ectopic ACTH or adrenal tumour
7- CRH test

82
Q

How is Cushing’s syndrome managed? (2)

A

Surgical removal of cause e.g. adrenal tumour, pituitary tumour, ectopic ACTH producing tumour.
Metyrapone is a drug which inhibits cortisol synthesis may be used when surgery is not amenable.

83
Q

What is it that controls the secretion of vasopressin from the posterior pituitary? (1)

A

Plasma osmolality
when less than 280mOsm/kg ADh secretion is suppressed
when over 295mOsm/kg ADH secretion is at maximum

84
Q

What is the hormonal action of ADH? (1)

A

Collecting tubule of the kidney to cause water resorption.

Large concentrations also cause vasoconstriction.

85
Q

What are the two classifications of diabetes insipidus? (2)

What is the difference between the 2? (1)

A

Central (cranial): impaired ADH secretion

Nephrogenic: resistance to its actions

86
Q

What are the classic symptoms associated with diabetes insipidus? (2)

A

Polyuria (dilute urine in excess of 3L in 24 hours)
Compensatory polydipsia
Nocturia

87
Q

What differentials would you consider in a patient with polydipsia? (3)

A 
Primary polydipsia (psychiatric)
Diabetes mellitus
Diabetes insipidus
Hypercalcaemia
Hypokalaemia
CKD
Diuretics
Alcohol
88
Q

Name 2 central and 2 nephrogenic causes of diabetes insipidus. (4)

A

CDI: HYPOTHALAMUS- neurosurgery, trauma, 1’/2’ tumours, sarcoidosis and idiopathic.
NDI: hypokalaemia, hypercalcaemia, renal tubular acidosis, sickle cell disease, familial (ADH receptor mutation), drugs: lithium and glibenclamide.

89
Q

Name 3 investigations to help with diagnosis in a patient with polydipsia. (3)

A

Confirm polyuria by measuring urine volume.
DM: serum glucose
U+E’s and Ca: other causes

DI: Plasma osmolality (high), urine osmolality (low)
Water deprivation test

90
Q

Describe the water deprivation test. (4)

When would test be abandoned? (1)

A

Serum + Urine osmolality, urine volume and body weight are measured hourly while fasting (food and fluid) for up to 8 hours.
a) Normal: normal serum osmolality and concentrated urine
b) Suggestive of DI: Raised serum osmolality and dilute urine
If b- give desmopressin and monitor urine osmolality while allowing free fluids.
a) no change = NDI
b) urine osmolality increased by >50% = CDI

Abandon if body weight drops by >3% (dehydration)

91
Q

What is the management of CDI and NDI? (3)

A

NDI: usually responds to treating cause
CDI: treat underlying condition rarely helps. Give desmopressin orally, nasally or IM.
NB in mild cases thiazides or carbamazepine can sensitise the renal tubules to endogenous ADH.

92
Q

What is SIADH? (2)

A

Syndrome of inappropriate ADH secretion - continued ADH secretion despite plasma hypotonicity and normal or expanded plasma volume.

93
Q

Name 3 causes of SIADH. (3)

A

Brain: meningitis, cerebral abscess, head injury, tumour
Cancer: many, small cell lung cancer most common
Lung: pneumonia, TB, lung abscess
Metabolic: Porphyria, alcohol withdrawal
Drugs: opiates, carbamazepine.

94
Q

What are the clinical features of SIADH? (3)

A

Nausea, irritability and headache if mild hypervolaemic hyponatraemia.
Seizures and coma if severe hyponatraemia.

95
Q

What are the criteria for diagnosis of SIADH? (3)

A

Low drum sodium
Low plasma osmolality with “inappropriate” urine osmolality
Continued urinary sodium excretion
Absence of hypokalaemia, hypotension and hypovolaemia
Normal renal, adrenal and thyroid function.

96
Q

What is the treatment of SIADH? (3)

A

Water restriction (500-1000ml/24 hours)
Demeclocycline 600-1200mg daily (inhibits ADH action on kidney i.e. causes nephrogenic diabetes insipidus)
Tolvaptan is specific vasopressin antagonist, used for treatment of hyponatraemia secondary to SIADH.

97
Q

Name 3 actions of PTH. (3)

A

Stimulates calcium reabsorption from the kidney
Activates Vitamin D in the kidney
Releases calcium from bone
Increases intestinal calcium from GI (1,24-dihydroxyvitamin D strictly)

98
Q

What is corrected calcium levels? (2)

A

About 40% of calcium is free, the rest is bound to albumin. Routine tests only measure total calcium, so corrected calcium takes albumin into consideration.

99
Q

Name 4 causes of hypercalcaemia. (4)

A

Excess PTH: Primary hyperparathyroidism, tertiary hyperparathyroidism
Malignancy: multiple myeloma, bone mets, PTH-related secretion
Excess action of vit D: self-administration, lymphoma, granulomatous disease (sarcoid or TB)
Drugs: thiazides, vit d analogues, lithium
Others: (mild hypercalcaemia) thyrotoxicosis and Addison’s

100
Q

What is the difference between primary, secondary or tertiary hyperparathyroidism? (3)

A

Primary: single parathyroid adenoma (may be associated with MEN)
Secondary: physiological compensatory hypertrophy of glands in response to prolonged hypocalcaemia eg CKD, calcium is low or low-normal.
Tertiary is development of apparently autonomous hyperplasia after long standing secondary hyperparathyroidism, most often in renal disease. Plasma calcium and PTH are both raised.

101
Q

Give 5 features of hypercalcaemia. (5)

A

Mild: asymptomatic
Mod: malaise, depression, bone pain, abdo pain, nausea, constipation. Polyuria and nocturia from calcium deposition in the tubules. Renal calculi and CKD may develop.
Sev: dehydration, confusion, clouding of consciousness, risk of cardiac arrest.

102
Q

Tina has come into clinic following a raised serum corrected calcium. She is normally fit and well, but had been suffering with constipation, nausea and malaise.
What is the most likely cause of her hypercalcaemia? (1)

A

Usually fit ad well: primary hyperparathyroidism is most likely.
If linked to malignancy, it is rarely the presenting feature and malignancy is already apparent.

103
Q

How are phosphate levels affected in primary, secondary and tertiary hyperparathyroidism? (3)

A

1’: low (also low in some cases of malignancy

Normal or high in other causes

104
Q

Fifi has renal stones, nocturia, bone pain, malaise and depression.
You are considering hypercalcaemia. What investigations will you perform? (4)

A

Fasting serum calcium and phosphate, serum PTH
If PTH is low… look for other causes… protein electrophoresis (myeloma), TSH (hyperthyroidism), short synacthen test (Addison’s), hydrocortisone suppression test (vitamin D mediated, sarcoidosis)

105
Q

Severe hypercalcaemia has a risk of cardiac arrest and so is an emergency. How will you treat this? (4)

A

Rehydrate with IV saline.
Bisphosphonate: after rehydration give pamidronate
Measure: U+Es and Calcium
Prednisolone: may help in myeloma, sarcoidosis or bit D excess but otherwise no help.
Prevent recurrence: treat cause or if palliative consider bisphosphonates long-term.

106
Q

What is the treatment for primary hyperparathyroidism? (1)

What is the treatment for tertiary hyperparathyroidism? (1)

A

Surgical removal of adenoma

Surgical removal of all 4 hyperplasia glands.

107
Q

How does CKD cause hypocalcaemia? (2)

A

Inadequate production of 1,25-dihydroxyvitamin D and renal phosphate retention, causing micro precipitation of calcium phosphate in the tissues.

108
Q

Name 4 causes of hypocalcaemia. (4)

A

Increased phosphate: CKD*
Reduced PTH: Post-thyroidectomy, autoimmune, severe hypomagnesaemia, pseudohypoparathyroidism
Vit D deficiency: No sunlight, malabsorption, anti epileptic drugs
Drugs: calcitonin, bisphosphonates
Other: acute pancreatitis

109
Q

Name 2 clinical features of hypocalcaemia. (2)

A

Increased excitability of muscles and nerves: numbness around mouth and in extremities, followed by cramps and tetany.
Tetany is carpopedal spasm, convulsions and death.

110
Q

What are the two clinical tests that can demonstrate neuromuscular excitability in tetany? (2)

A

Chvostek’s: tapping over facial nerve around parotid gland causes twitching of ipsilateral facial muscles.
Trousseau’s sign: carpopedal spasm caused by sphygmomanometer inflation.

111
Q

What ECG change might you see in severe hypocalcaemia? (1)

A

Prolonged QT interval

112
Q

Louise has had blood tests which show hypocalcaemia. What investigations do you want to perform? (3)

A

Look for CKD: U+E, Cr.
Serum PTH
25-hydroxyvitamin D levels
Serum magnesium

113
Q

What is the acute and chronic management of hypocalcaemia? (3)

A

Acute: 10% calcium gluconate with ECG monitoring
Chronic:
Vit D def- give cholecalciferol (D3)
Alfacalcidol for CKD or hypoparathyroidism.

114
Q

Name 3 hypertensive patients who should be screened for secondary causes of hypertension. (3)

A

Young (<35 years old)
Malignant hypertension
Resistant hypertension (3 + drugs)
Abnormal baseline screening test

115
Q

Describe the renin-angiotensin system. (5)

A

Angiotensinogen is a circulating peptide of hepatic origin.
Renin is secreted by the kidneys in response to decreased renal perfusion pressure or flow.
Renin converts angiotensinogen into angiotensin I which is inactive.
ACE is present in lungs and vascular endothelium converts AT1 to AT2.
AT2 is powerful vasoconstrictor, and stimulates adrenal zona glomerulosa to increase aldosterone production.

116
Q

Name 2 actions of angiotensin II. (2)

A 
Powerful vasoconstrictor (within seconds)
Stimulates aldosterone production from zona glomerulosa.
117
Q

What is the function of aldosterone? (2)

A 
Sodium retention (and potassium loss) over hours-days.
Causing increase in blood pressure and suppresses renin production.
118
Q

What is Conn’s syndrome? (2)

A

Rare condition of primary hyperaldosteronism, where adrenal adenoma causes high aldosterone levels to exist independent of RAAS.

119
Q

What are the two causes of primary hyperaldosteronism? (2)

A

Conn’s (adrenal adenoma)

Bilateral adrenal hyperplasia

120
Q

How does primary hyperaldosteronism cause hypertension? (2)

A

Aldosterone causes exchange transport of Na and K in the collecting duct of the renal tubule.
Excess production causes excess Na to be absorbed and water follows causing hypervolaemia and so hypertension. (also causes hypokalaemia)

121
Q

What investigations may help to diagnose primary hyperaldosteronism? (2)

A 
BP
U+Es (hypokalaemia)
Plasma aldosterone:renin ratio
Saline or fludrocortisone to test for suppression of aldosterone
CT or MRI of adrenals.
122
Q

What is the management of primary hyperaldosteronism? (2)

A

Bilateral adrenal hyperplasia: spironolactone

Conn’s: surgical removal of tumour.

123
Q

What is a phaeochromocytoma? (2)

A

Rare cause of hypertension where a tumour of the sympathetic nervous system produces catecholamines. (90% are within the adrenal gland).
Can be associated with multiple endocrine neoplasia.

124
Q

What clinical features may suggest a phaeochromocytoma? (2)

A

Headaches, HTN, tachycardia, sweating, palpitations, anxiety, weight loss, pallor, hyperglycaemia.

125
Q

What would be your initial investigations for diagnosis of phaeochromocytoma? (2)

A

24 hour urine collection for catecholamines and metanephrines. (normal on 3 occasions virtually exclude diagnosis)
Raised levels of plasma catecholamines confirm diagnosis
CT/MRI to locate tumour.

126
Q

What is the management of phaeochromocytoma? (2)

A

Surgical excision of tumour under alpha and beta blockade; phenoxybenzamine and propranolol.

127
Q

What are multiple endocrine neoplasia syndromes? (2)

A

Autosomal dominant inherited syndrome of synchronous or metachronous occurrence of tumours of a number of endocrine glands.

128
Q

What is the genetic difference between MEN type 1 and MEN type 2? (1)

A

Type 1: mutation of tumour suppressor gene on chromosome 11.

Type 2: abnormality of proto-oncogene on chromosome 10.

129
Q

Liam has been diagnosed with MEN type 1.
How is this condition inherited? (1)
How can his family be screened? (1)

A 
Autosomal dominant
Serum calcium (95% have hyperparathyroidism and hypercalcaemia)
130
Q

Name 3 tumours seen in MEN type 1. (3)

A

Functional adenomas:
parathyroid: hypercalcaemia
pituitary: acromegaly, Cushing’s disease, prolactinoma
enteropancreatic tumours: insulinoma, glucagonoma, gastrinoma, VIPoma.

Also adrenal cortex adenomas (non-functional) , cutaneous tumours and foregut carcinoids.

131
Q

Name the 3 tumours seen in MEN syndrome type 2. (3)

A 
Medullary thyroid carcinoma
Adrenal medulla (phaeochromocytoma)
Parathyroid hyperplasia (hypercalcaemia)
132
Q

Name 2 drugs that can cause diabetes. (2)

A

Thiazides and glucocorticosteroids.

133
Q

What is a normal capillary glucose reading in a diabetic? (1)
What is the target HbA1c? (1)

A

4-7 mmol/L

48-59 mmol/mol

134
Q

What does HbA1c indicate? (1)

A

Management of diabetes over previous 6 weeks.

135
Q

Name 2 causes of secondary diabetes mellitus. (2)

A

total pancreatectomy, chronic pancreatitis, haemochromotosis, acromegaly, Cushing’s syndrome

136
Q

How would Gordon be diagnosed with DM if he was

a) symptomatic
b) asymptomatic? (2)

A

Fasting blood glucose >7mmol/L
Random blood glucose >11.1 mmol/L
HbA1c >48mmol/mol

On one occasion if symptomatic and on two occasions if asymptomatic.

137
Q

When is HbA1c not suitable for diagnosing diabetes? (4)

A

All children and young people
Patients with symptoms of diabetes for less than 2 months
Patients at high risk who are acutely ill
Patients taking medication that may cause rapid glucose rise e.g. steroids, antipsychotics
Pregnancy
Patients with pancreatic disease

138
Q

Describe the oral glucose tolerance test. (3)

A

Measure fasting blood glucose at 0hr
Give 75g of oral glucose
Measure blood glucose at 2hr

Normal if F: 7 mmol/L and 2hr: >11.1 mmol/L

139
Q

What things is it important to include when counselling a newly diagnosed diabetic? (4)

A

What is DM.
Importance of controlling blood glucose and foot care
Importance of controlling risk factors for IHD
Risks of poor control
Diet changes
Support available

140
Q

Describe the diet advised to diabetics. (4)

A 
Low in sugar but not sugar free.
Switch sugar for sweeteners
Low in fat (<35% total energy)
Protein (15% total energy)
High in starchy carbs (40-60% of total energy)
141
Q

Why are starchy carbohydrates such a big part of a diabetic diet? (2)

A

Slowly absorbed and have less fluctuations in blood glucose levels.
Also important to spread meals throughout the day for this same reason.

142
Q

What ar the 3 main groups of patients presenting with DKA? (3)

A

Previously undiagnosed DM
Acutely unwell (stress caused by infection or surgery)
Stopped insulin due to vomiting or not eating.

143
Q

What is the pathophysiology of DKA? (2)

A

No insulin produced.
Liver is not restricted and continues gluconeogenesis.
High levels of glucose cause osmotic diuresis and dehydration.

Peripheral lipolysis causes free fatty acids which become ketones.

144
Q

What symptoms would you expect when you see a patient with DKA? (3)

A

Dehydration: dry mucous membranes, reduced skin turgor, sunken eyes, hypotension
Acidosis: Kussmaul breathing, abdominal pain, vomiting.
Others: Pear drop breath and decreased GCS.

145
Q

Which is the main ketone to test for in DKA? (1)

A

Beta-hydroxybutyrate, test for in blood ketone testing but not urine testing.

146
Q

What investigations would help with diagnosis of DKA and its causes? (4)

A 
Blood glucose
Blood ketones
Venous blood gases or ABGs
U+Es (potassium)
FBC (WCC)

CXR, blood cultures, urine dipstick, etc for infective cause.

147
Q

What is the cause of the hyperosmolar hyperglycaemic state? (2)

A

Medical emergency of type 2 diabetics.
Background endogenous insulin is enough to stop ketosis but not to restrain gluconeogenesis.
Therefore they present as dehydrated and decreased GCS.

148
Q

Why do those presenting with hyperosmolar hyperglycaemic state require prophylactic s/c heparin? (1)

A

HHS predisposes to arterial thrombosis, stroke and MI.

149
Q

What is lactic acidosis? (1)

A

Rare adverse effect of met forming therapy.
Severe metabolic acidosis but without ketones or hyperglycaemia.
Treatment is with rehydration and bicarbonate.

150
Q

Name 3 causes of hyperprolactinaemia. (3)

A 
Prolactinoma (pituitary adenoma)
Other pituitary or hypothalamic tumours: interference with dopamine inhibition of prolactin
Drugs: metoclopramide, phenothiazines
PCOS
Hypothyroidism (TRH can stimulate PL)
151
Q

Define glactorrhoea. (2)

A

Spontaneous flow of milk unassociated with childbirth or breast feeding. (can occur in men and women)

152
Q

Name 3 symptoms of hyperprolactinaemia. (3)

A 
Glactorrhoea
Amenorrhoea (PL inhibits GnRH)
Decreased libido
Subfertility
Erectile dysfunction
(if tumour cause: headaches, visual field defects)
153
Q

What investigations may help diagnosis of hyperprolactinaemia? (1)

A

Serum prolactin levels (3 measurements)
TFTs (causation)
MRI head (causation)
Visual fields (if tumour)

154
Q

What is the management for prolactinaemia? (4)

A

Treat any underlying cause eg hypothyroidism or drugs
Dopamine agonists eg cabergoline or bromocriptine
Trans-sphenoidal resection is an option but contraversial due to high rate of late recurrence.

155
Q

What is the target for blood pressure in a diabetic patient, with a) no end organ damage and b) evidence of end-organ damage? (2)

A

a) 140/90

b) 130/80

156
Q

Name 5 complications of diabetes mellitus? (5)

A

Macrovascular: atherosclerosis (IHD, stroke, PVD)
Microvascular: retinopathy, nephropathy and neuropathy

157
Q

name 3 ways that diabetes can affect the eyes. (3)

A

Retinopathy
Cataracts
Ocular palsie of CN 3 and 6.

158
Q

What is the most common cause of blindness in people under the age of 65? (1)

A

Diabetic retinopathy

159
Q

What percentage of newly diagnosed diabetics have background retinopathy? (1)

A

30%

160
Q

What are the 2 forms of diabetic retinopathy? (2)

A

Non-proliferative
Proliferative
Maculopathy also

161
Q

What is the pathophysiology behind diabetic retinopathy? (2)

A

Microvascular occlusion results in retinal ischaemia leading to AV shunts and neovascularisation.

162
Q

What are the four stages of diabetic retinopathy and what might be seen on slit-lamp examination? (4)

A

Non-proliferative: at least 1 micro aneurysm
Pre-proliferative: microaneurysms, blot haemorrhages, cotton wool spots, venous beading, hard exudates
Proliferative: neovascularisation, vitreous haemorrhage
Advanced retinopathy: retinal fibrosis

163
Q

What is the treatment for diabetic retinopathy? (1)

A

Laser photocoagulation of the retina.

164
Q

Name 3 ways in which diabetes can affect the kidneys. (3)

A

Glomerular disease
Ischaemic renal lesions (can affect both afferent and efferent arterioles)
Ascending UTI

165
Q

What is the process of diabetic nephropathy? (3)

A

Initially microalbuminuria (undetectable on dipsticks)
Developing to intermittent albuminuria
Developing to persistent proteinuria (5-10 years from ESKD)
Sometimes to frank nephrotic syndrome

166
Q

Name two things that can help delay the disease progression of diabetic nephropathy. (2)

A

Control of blood pressure <130/80

ACEi

167
Q

Symmetrical sensory neuropathy affecting the feet first is the most common type of diabetic neuropathy.
What sensations are lost first? (3)

A

Vibration, deep pain and temperature

Later loss of proprioception causes sensation of walking on cotton wool and patients may lose balance in the dark.

168
Q

What complications can occur as part of diabetic neuropathy? (2)

A

Blistering and ulceration caused by repeated unfelt trauma

Abnormal mechanical stress (usually prevented by pain) can lead to deformed Charcot joints in the ankle and knee.

169
Q

What is the most widespread type of diabetic neuropathy? (1)

Name 3 systems that may be affected. (3)

A

Autonomic neuropathy
CV: resting tachycardia, postural hypotension, peripheral vasodilation)
GI: diarrhoea, gastroparesis with vomiting
Urinary: incomplete emptying followed by atonic painless distended bladder, male erectile dysfunction

170
Q

Why are diabetics more prone to infections? (1)

A

Poorly controlled diabetes impaired the function of polymorphonuclear leucocytes.

171
Q

Name 3 infections more common in diabetic patients. (3)

A 
UTIs
Cellulitis
TB
Candidiasis
Abscesses
172
Q

Why do diabetic patients require insulin during infection even if they are not eating? (1)

A

Infection can cause loss of glycaemic control and is a common cause of ketosis.

173
Q

Why do diabetics need to move their injection sites daily? (1)

A

Prevent lipohypertrophy

174
Q

Doug is a diabetic man who has developed waxy brown discolouration over his shins, which began as erythematous plaques.
What is the diagnosis? (1)

A

Necrobiosis lipoidica diabeticorum

175
Q

How is insulin managed in a diabetic patient undergoing major surgery (i.e. general anaesthetic)? (3)

A

Day before: Normal s/c insulin or oral (but stop metformin)
Day of surgery: omit morning insulin (and orals); glucose/potassium infusion is started at 8am with hourly monitoring
Post-op: maintain infusion until eating and drinking normally, then restart normal insulin with 30 min overlap with infusion.

176
Q

What are the risks of a diabetic mother becoming pregnant? (2)

A

Poorly controlled diabetes is associated with congenital malformations, macrosomia, polyhydramnios, pre-eclampsia and intrauterine death.
Neonatally: neonatal hypoglycaemia and hyaline membrane disease.

177
Q

Why are acutely ill hospital diabetic patients at risk of hyperglycaemia? (2)

Why should metformin be stopped in an acutely unwell patient? (1)

A

Stress hormones such as cortisol, adrenaline or growth hormone counteract insulin.
Additional factors include physical inactivity and change in diet.

Metformin should not be given due to risk of lactic acidosis.

178
Q

What is an insulinoma? (1)

A

Rare pancreatic islet cell tumour that secretes insulin. (may be part of MEN syndrome)

179
Q

Name 4 causes of hypoglycaemia. (4)

A 
Drug: insulin, sulphonylureas, salicyclate overdose
Insulinoma
Addison;s disease
Fulminant liver failure
End stage kidney failure
Excess alcohol
Post gastric surgery
180
Q

What are the symptoms of an insulinoma? (4)

A

Fasting hypoglycaemia
Symptoms caused by neuroglycopenia and activation of the sympathetic nervous system
eg sweating, palpitations, weakness, diplopia leading to confusion, abnormal behaviour, seizures and coma.

181
Q

What is porphyria? (3)

A

Rare group of inherited disorders of haem synthesis.
This causes an overproduction of the intermediate compounds called porphyrins, within the liver or the bone marrow.
Porphyrias can be acute (hepatic) or non-acute (hepatic or erythropoietic).

182
Q

What are the features of acute porphyria? (3)

A

Abdominal pain, constipation, vomiting (mimicking acute abdomen) especially with fever and leucocytosis.
Additional features can include tachycardia, hypertension, neuropsychiatric disorders or urine turing brown or red on standing.

Medicine (14 decks)

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