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ENDOCRINE > Y2 ENDOCRINE EVERYTHING NON THYROID OR DIABETES > Flashcards

Y2 ENDOCRINE EVERYTHING NON THYROID OR DIABETES Flashcards

1
Q
  • malaise, fatigue.
  • anorexia.
  • weight loss.
  • craving salty food.
  • dizzy spells when in warm places.

Thin patient with postural hypotension. Appears tanned with increased pigmentation in mouth and hand creases.

  • low sodium + high potassium.
A

addison’s

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2
Q

what is the core problem in addison’s disease?

A

adrenal insufficiency:

- reduced steroids therefore low mineralocorticoid activity.

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3
Q

reduced mineralocorticoid activity means?

A

sodium won’t be retained, therefore water is also lost. K+ is retained.
- hyponatraemia and hyperkalaemia.

patient will be clinically dehydrated.

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4
Q

patient’s excess pigmentation in addison’s is due to?

A

excess ACTH production by the pituitary.

ACTH is degraded to MSH.

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5
Q

anterior pituitary is derived from?

A

Rathke’s pouch

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6
Q

anterior pituitary secretes?

A

Trophic and non-trophic hormones:

  • Trophic: TSH, ACTH, FSH, LH.
  • Non-trophic: GH and prolactin.
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7
Q

posterior pituitary secretes?

A

ADH and oxytocin

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8
Q

posterior pituitary contains?

A

non-myelinated axons of neurosecretory neurons

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9
Q

anterior pituitary acidophils?

A

GH (somatotroph) - 50% and prolactin (mammotroph) - 20%.

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10
Q

anterior pituitary basophils?

A

ACTH (corticotrophs) - 20% , TSH (thyrotoph) - 5% and FSH/LH (gonadotroph) - 5%.

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11
Q

what causes hyperfunction of the anterior pituitary?

A

adenoma or carcinoma

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12
Q

what causes hypofunction of the anterior pituitary?

A
  • surgery/radiation.
  • sudden haemorrhage into gland.
  • ischaemic necrosis (sheehan syndrome).
  • tumours extending into sella.
  • inflammatory conditions e.g. sarcoidosis.
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13
Q

what results from hyperfunction of the anterior pituitary?

A

SIADH - the ectopic secretion of ADH by tumours OR due to a primary disorder of the pituitary.

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14
Q

what results from hypofunction of the anterior pituitary?

A

Diabetes insipidus - a lack of ADH secretion that can lead to life-threatening dehydration.

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15
Q

pituitary adenomas account for what percentage of intra-cranial tumours?

A

10%

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16
Q

pituitary adenomas may be sporadic or ass. with?

A

MEN1

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17
Q

large pituitary adenomas may cause?

A
  • visual field defects.
  • pressure atrophy of surrounding tissue.
  • infarction leading to panhypopituitarism.
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18
Q

most common functional pituitary adenoma?

A

prolactinoma

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19
Q

symptoms of prolactinoma?

A
  • infertility, lack of libido, amenorrhoea.
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20
Q

second most common functional pituitary adenoma?

A

GH-secreting

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21
Q

symptoms/signs of a GH-secreting pituitary adenoma?

A
  • gigantism or acromegaly due to the stimulation in growth of bone/ cartilage/ connective tissue.
  • increase in insulin-like growth factors.
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22
Q

signs of an ACTH-secreting pituitary adenoma?

A
  • Cushing’s DISEASE.

- bilateral adrenocortical hyperplasia.

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23
Q

define panhypopituitarism.

A

absent/reduced anterior pituitary hormone production

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24
Q

pituitary hypofunction due to sarcoidosis will show pathological features of?

A

granulomatous inflammation

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25
Q

pituitary hypofunction due to Sheehan’s syndrome will show pathological features of?

A

infarction

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26
Q

craniopharyngioma is derived from?

A

remnants of Rathke’s pouch.

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27
Q

a slow-growing intra-cranial tumour that is often cystic and may calcify.

A

craniopharyngioma

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28
Q

most craniopharyngiomas are?

A

suprasellar.

some arise within the sella.

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29
Q

craniopharyngiomas have a bimodal incidence of?

A
  • 5-15 years

- 60s-70s.

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30
Q

symptoms of craniopharyngioma?

A

headaches, visual disturbances.

  • growth retardation in children.
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31
Q

management of cranipharyngioma?

A
  • excellent prognosis esp. if <5cm.

- radiation.

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32
Q

what may occur following radiotherapy for craniopharyngioma?

A

SCC- rarely

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33
Q

diabetes insipidus may be due to central (pituitary) causes or?

A

nephrogenic i.e. renal resistance to ADH.

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34
Q

SIADH is what type of syndrome?

A

paraneoplastic

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35
Q

how much does an adrenal gland weigh?

A

approx. 4-5 grams

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36
Q

where can the adrenal glands be found?

A

superior and medial to the upper pole of the kidneys?

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37
Q

what are the adrenal glands composed of?

A

outer cortex and central medulla

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38
Q

what causes hyperfunction of the adrenal cortex?

A

hyperplasia, adenoma, carcinoma.

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39
Q

what causes hypofunction of the adrenal cortex?

A
  • acute: waterhouse-friederichson.

- chronic: addison’s disease

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40
Q

congenital causes of adrenocortical hyperplasia?

A
  • autosomal recessive disorders.

- reduced cortisol stimulating ACTH release - cortical hyperplasia (10-15x normal weight).

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41
Q

acquired causes of adrenocortical hyperplasia?

A
  • endogenous ACTH production (cushing’s disease) or ectopic ACTH (paraneoplastic syndrome e.g. SCLC).
  • bilateral adrenal enlargement.
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42
Q

adrenocortical tumours most commonly affect?

A

male adults.

  • can affect younger: Li-fraumeni syndrome.
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43
Q

adrenocortical carcinomas with necrosis may cause?

A

fever

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44
Q

Well circumscribed, encapsulated lesion that is small (2-3cm) with a yellow-brown surface. Cells resemble adrenocrotical cells. Can be functional, most likely not.

A

adrenocortical adenoma

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45
Q

Rare tumour likely to be functional and may closely resemble an adenoma. Locally invades the retroperitoneum and kidney. May haematogenously metastasise to liver/lung/bone. May spread to peritoneum, pleura and regional lymph nodes.

A

adrenocortical carcinoma

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46
Q

prognosis of an adrenocortical carcinoma?

A

5 year: 20-35% survival.

2 years: 50% mortality.

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47
Q

what is the only definite criteria for malignant adrenocortical tumours?

A

metastasis

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48
Q

features suggestive of adrenocortical carcinoma?

A
  • large size (>50g, often >20cm).
  • haemorrhage and necrosis
  • frequent mitoses/atypical mitoses
  • lack of clear cells
  • capsular or vascular invasion.
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49
Q

Primary hyperaldosteronism otherwise known as?

A

Conn’s syndrome

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50
Q

Usually ass. with diffuse/nodular hyperaplasia of bilateral adrenal glands.
OR
Due to adrenocortical adenoma (rarely carcinoma).

A

Conn’s syndrome/ primary hyperaldosteronism.

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51
Q

hypercortisolism otherwise known as?

A

cushing’s syndrome/disease.

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52
Q

exogenous causes of cushing’s syndrome?

A

steroid therapy.

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53
Q

endogenous causes of cushing’s syndrome/disease?

A

ACTH dependent:
- ACTH-secreting pituitary adenoma = cushing’s disease. Most common.
- Ectopic ACTH e.g. small cell lung cancer.
causes adrenal hyperplasia.

ACTH-independent:
- Adrenal adenoma or carcinoma.

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54
Q

what causes acute primary adrenocortical insufficiency?

A
  • rapid steroid withdrawal.
  • adrenal crisis
  • massive adrenal haemorrhage
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55
Q

what causes massive adrenal haemorrhage?

A
  • newborn
  • anti-coagulants
  • disseminated intravascular coagulation
  • septicaemia: waterhouse friderichsen.
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56
Q

what causes chronic primary adrenocortical insufficiency?

A
  • addison’s
  • autoimmune adrenalitis
  • infection (tb, histoplasma fungal, HIV, kaposi’s).
  • metastatic malignancy (lung, breast).

rarely: amyloid, sarcoidosis, haemochromatosis.

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57
Q

when do symptoms of chronic primary adrenocortical insufficiency present?

A

once >90% of the gland is destroyed.

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58
Q

addison’s symptoms?

A
  • vague: weakness, fatigue, anorexia, nausea, vomiting, weight loss, diarrhoea.
  • pigmentation.
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59
Q

addison’s signs?

A

hyperkalaemia, hyponatraemia, volume depletion and hypotension.

hypoglycaemia.

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60
Q

what may cause addison’s crisis?

A

stress, infection, trauma, surgery.

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61
Q

how does addison’s crisis present?

A

vomiting, abdominal pain, hypotension, shock and then death.

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62
Q

neuroendocrine (chromaffin) cells secrete?

A

catecholamines

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63
Q

adrenal medulla innervated by?

A

pre-synaptic fibres from sympathetic NS

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64
Q

tumours of the adrenal medulla?

A
  • phaeochromocytoma

- neuroblastoma

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65
Q

neuroblastoma usually diagnosed at what age?

A

18 months.

40% are diagnosed in infancy.

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66
Q

neuroblastoma typically arise in the?

A

adrenal medulla.

the rest usually found along the sympathetic chain.

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67
Q

what predicts poor outcome in neuroblastoma?

A

amplification of N-myc and telomerase expression

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68
Q

a neoplasm derived from chromaffin cells of the adrenal medulla that secretes catecholamines.

A

phaeochromocytoma

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69
Q

neuroblastoma are composed of primitive appearing cells, but can show maturation and differentiation towards?

A

ganglion cells

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70
Q

a rare cause of secondary hypertension.

A

phaeochromocytoma

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71
Q

what causes hypertension in phaeochromocytoma?

A

stress, exercise, posture, tumour palpation.

  • if arising in the bladder it can be ass. with micturition.
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72
Q

complications of hypertension in phaeochromocytoma?

A

cardiac failure, infarction, arrhythmia, CVA.

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73
Q

how is phaeochromocytoma detected?

A

urinary catecholamines and metabolites

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74
Q

10% rules of phaeochromocytoma?

A
  • 10% extra-adrenal
  • 10% bilateral
  • 10% malignant
  • 10% NOT ass. with hypertension
  • 25% are familial.
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75
Q

extra-adrenal phaeochromocytoma are known as?

A

paragangliomas

76
Q

extra-adrenal phaeochromocytoma are found on the?

A

carotid body, organs of zuckerkandl.

77
Q

which type of phaeochromocytoma are more likely to be malignant?

A

extra-adrenal i.e. paragangliomas.

78
Q

familial cases of phaeochromocytoma more likely to present?

A

in younger patients, bilaterally.

79
Q

what germline mutation increases risk of malignant phaeochromocytoma?

A

B-subunit of succinate dehydrogenase

80
Q

K2Cr2O7 will cause a phaeochromocytoma to?

A

turn dark brown due to oxidation of catecholamines in the tumour cells.

81
Q

phaeochromocytoma have a propensity to metastasis to where?

A

skeleton.

  • also regional lymph nodes, liver and lung.
82
Q

phaeochromocytoma is a feature of?

A

MEN2A and MEN2B

83
Q

MEN2A is ass. with which tumours?

A
  • phaeochromocytoma, medullary thyroid carcinoma, parathyroid hyperplasia.
84
Q

MEN2B is ass. with which tumours?

A
  • phaeochromocytoma, medullary thyroid carcinoma, neuromas, ganglioneuromas, marfanoid habitus.
85
Q

zonaglumerulosa produces?

A

mineralocorticoids e.g. aldosterone

86
Q

zona fasciculata produces?

A

glucocorticoids e.g. cortisol

87
Q

zona reticularis produces?

A

sex steroids and glucocorticoids.

88
Q

MEN1 is ass. with which tumours?

A
  • pituitary adenoma, parathyroid hyperplasia, pancreatic tumours.
89
Q

manifestations of Carney Complex?

A
  • thyroid carcinoma.
  • acromegaly.
  • spotty pigmented sking.
  • myxoma
90
Q

tests for Carney complex?

A

Liddle’s test: paradoxical positive response of urinary glucocorticosteroids to dexamethasone.

91
Q

PPNAD (primary pigmented nodular adrenocortical disease) causes adrenal glands to produce excess cortisol leading to?

A

Cushing’s syndrome

92
Q

Carney complex due to which mutation?

A

PRKAR1A

93
Q
  • Cafe-au-lait skin (“coast of maine”).
  • polyostotic fibrous dysplasia.
  • precocious puberty.
  • thyroid nodules.
A

mccune-albright syndrome.

  • pituitary: excess GH
  • adrenal: cushing’s
94
Q

mccune albright syndrome due to which mutation?

A

GNAS1

95
Q
  • axillary freckling.
  • cafe-au-lait patches
  • optic gliomas
  • scoliosis
  • possible learning difficulties.
  • rare phaeochromocytoma
A

NF1 - neurofibromatosis type 1

96
Q

most common cause of primary adrenal insufficiency?

A

addison’s disease

97
Q

pathogenesis of addison’s?

A

autoimmune destruction of adrenal cortex >90% destroyed before symptoms

98
Q

what other autoimmune diseases are ass. with addison’s?

A
  • T1DM, autoimmune thyroid disease, pernicious anaemia.
99
Q

clinical features of addison’s?

A
  • anorexia, weight loss, fatigue, dizziness, hypotension.
  • abdo pain, vomiting, diarrhoea.
  • skin pigmentation.
100
Q

hyponatraemia, hyperkalaemia and hypoglycaemia are suggestive of ?

A

adrenal insufficiency

101
Q

managing adrenal insufficiency?

A
  • hydrocortisone to replace cortisol (IV if unwell): usually 15-30m/day in divided doses.
  • fludrocortisone (aldosterone) needs careful monitoring of BP and K+.
102
Q

what causes secondary adrenal insufficiency?

A
  • exogenous steroid use.

- pituitary/hypothalamic disease or tumours.

103
Q

how do you differentiate between primary and secondary adrenal insufficiency?

A
  • addison’s will have pigmentation.

- secondary lacks CRH and ACTH and will therefore be pale.

104
Q

management of secondary adrenal insufficiency?

A

hydrocortisone only.

105
Q

pale skin, normal aldosterone production but lack of CRH and ACTH.

A

secondary adrenal insufficiency

106
Q

excess cortisol secretion?

A

cushing’s

107
Q

cushing’s more common in?

A

women aged 20-40

108
Q

clinical features of excess cortisol?

A

easy bruising, facial plethora, striae, proximal myopathy.

  • buffalo hump, moon face, increased abdominal fat.
109
Q

what is primary aldosteronism?

A

aldosterone production independent of its normal regulators (angiotensin II/potassium).

110
Q

significant hypertension, alkalosis and hypokalaemia - esp. if young suggests?

A

primary aldosteronism

111
Q

what are the subtypes of primary aldosteronism?

A
  • adrenal adenoma i.e. conn’s syndrome.
  • bilateral adrenal hyperplasia.
  • genetic mutations and unilateral hyperplasia are rare.
112
Q

surgical management of primary aldosteronism?

A

ONLY FOR ADRENAL ADENOMA.
- unilateral laparoscopic adrenalectomy ONLY if adrenal adenoma (+ excess had been confirmed in adrenal vein sampling).

cures hypokalaemia and hypertension.

113
Q

medical management of primary aldosteronism?

A

FOR BILATERAL ADRENAL HYPERPLASIA.

- mineralocorticoid receptor antagonists e.g. spironolactone or eplerenone.

114
Q

without cortisol and aldosterone replacement in adrenal insufficiency, what will happen?

A

death

115
Q

bilateral adrenal hyperplasia is treated?

A

medically e.g. spironalactone or eplenerone.

116
Q

adrenal adenoma is treated?

A

surgically

117
Q

what is the commonest enzyme defect ass. with congenital adrenal hyperplasia?

A

21a-hydroxylase deficiency.

118
Q

congenital adrenal hyperplasia is inherited by?

A

autosomal recessive inheritance

119
Q

classical variant of 21a-hydroxylase deficiency?

A

salt-wasting and simple virilising

120
Q

non-classical variant of 21a-hydroxylase deficiency?

A

hyperandrogenaemia

121
Q

how does classical congenital adrenal hyperplasia present in males?

A
  • adrenal insufficiency around 2-3 weeks after birth.
  • poor weight gain.
  • biochemical abnormalities similar to addison’s: (hyperkalaemia, hyponatraemia, volume depletion and hypotension and hypoglycaemia).
122
Q

how does classical congenital adrenal hyperplasia present in females?

A

genital ambiguity

123
Q

how does non-classical congenital adrenal hyperplasia present?

A
  • hirsutism
  • acne
  • oligomenorrhoea
  • precocious puberty
  • infertility or sub-fertility
124
Q

paediatric management of congenital adrenal hyperplasia?

A
  • glucocorticoid replacement.
  • mineralocorticoid replacement in some.
  • surgical correction.
  • achieve maximal growth potential.
125
Q

adult management of congenital adrenal hyperplasia?

A
  • control androgen excess.
  • restore fertility
  • avoid steroid over-replacement
126
Q

labile hypertension, postural hypotension, paroxysmal sweating, headache, pallor and tachycardia suggest?

A

phaeochromocytoma

127
Q

complications of phaeochromocytoma?

A
  • LV failure
  • myocardial necrosis
  • stroke
  • shock
  • paralytic ileus of bowel
128
Q

biochemical abnormalities of phaeochromocytoma?

A
  • hyperglycaemia (adrenaline secreting tumours).
  • hypokalaemia
  • raised Hb
  • mild hypercalcemia
  • lactic acidosis in the absence of shock
129
Q

how do you manage phaeochromocytoma medically?

A

full α and β blockade - α before β!!!

  • α: phenoxybenzamine.
  • β: propranolol/ atenolol/ metoprolol.
  • fluid +/or blood replacement.
  • careful anaesthetic assessment.
  • chemotherapy if malignant.

long term follow up, genetic testing + family tracing and investigation.

130
Q

how do you manage phaeochromocytoma surgically?

A

laparoscopically:

  • total excision when possible.
  • tumour de-bulking where full removal not possible.
131
Q

when might phaeochromocytoma levels of catecholamine be low?

A
  • if malignant or extra-adrenal as they are less efficient at catecholamine synthesis.
  • catecholamine excretion is episodic.
132
Q

endocrine causes of hypertension?

A
  • cushing’s syndrome
  • conn’s syndrome
  • phaeochromocytoma
133
Q
  • dehydration, confusion and polyuria (excessive thirst).

bones, groans, stones and psychic moans.
i.e. osteopenia/fractures, abdominal pain (pancreatitis, ulcers), renal stones, depression.

A

hypercalcaemia

134
Q

chronic hypercalcaemia leads to?

A
  • myopathy.
  • osteopenia.
  • fractures.
  • depression.
  • hypertension.
  • abdominal pain (pancretitis, ulcers, renal stones
135
Q

Low/normal albumin +

  • high/normal PTH
  • low/normal phosphate
  • increased urine Ca2+ suggests?
A

primary or tertiary hyperparathyroidism

136
Q

Low/normal albumin +

  • high/normal PTH
  • low/normal phosphate
  • reduced urine Ca2+ suggests?
A

familial hypocalciuric hypercalcaemia (FHH)

137
Q

Low/normal albumin +
- suppressed PTH
- high phosphate
suggests?

A

bone pathology

138
Q
  • hypercalcaemia
  • raised albumin
  • raised urea
    suggests?
A

dehydration

139
Q 
Low/normal albumin +
- suppressed PTH
- high phosphate 
\+ low alk. phosphatase (ALP)
suggests?
A
  • myeloma.
  • vit. D excess
  • mild alkali syndrome (thyrotoxicosis, sarcoidosis, raised HCO3)
140
Q 
Low/normal albumin +
- suppressed PTH
- high phosphate 
\+ high alk. phosphatase (ALP)
suggests?
A
  • bone mets
  • sarcoidosis
  • thyrotoxicosis
141
Q

what causes hypercalcaemia?

A
  • primary or tertiary hyperthyroidism
  • malignancy
  • drugs: Vit. D and thiazides.
  • granulomatous disease e.g. sarcoid, TB.
  • FHH
  • bedridden, thyrotoxicosis, pagets.
142
Q

hypocalciuric hypercalcaemia is inherited by?

A

autosomal dominant inheritance

143
Q

urine calcium excretion in hypocalciuric hypercalcaemia is?

A

low

  • elevated serum calcium
  • PTH may be elevated
144
Q

A progressive systemic disease of the skeleton.

  • low bone mass
  • microarchitectural deterioration of bone tissue
  • increase in bone fragility and risk of fracture
A

osteoporosis

145
Q

common fracture sites in osteoporosis

A
  • NOF
  • vertebral body
  • distal radius
  • humeral neck
146
Q

How many hip fracture patients die within a year of the fracture?

A

=20%

147
Q

How many hip fracture patients lose the ability to live independently?

A

=50%

148
Q

how much of the adult skeleton is remodelled each year?

A

=10%

149
Q

In women, what causes accelerated bone loss?

A

menopause

  • even higher risk of fragility fracture if early menopause
150
Q

Therapeutic intervention for osteoporosis should be targeted at?

A

those at high risk of low impact fracture

151
Q

Modifiable risk factors for osteoporosis fragility fractures?

A
  • bone mineral density
  • alcohol and smoking
  • weight
  • physical inactivity
  • medications
152
Q

what tool is used to assess fracture risk?

A
  • Qfracture
  • WHO fracture risk calculator
  • FRAX
153
Q

what important information does Qfracture not assess?

A

bone mineral density

154
Q

FRAX underestimates?

A

risk of vertebral fracture

155
Q

When should you assess for fracture risk?

A
  • anyone over 50 with risk factors.

- anyone under 50 with very strong clinical risk factors e.g. early menopause, glucocorticoid use.

156
Q

when should you refer someone for DEXA?

A

anyone with a 10 year risk for any osteoporosis fracture of at least 10%

157
Q

what is the most common method of measuring BMD?

A

DEXA scan

158
Q

normal bone mineral density?

A

within 1 SD of the young adult reference mean

159
Q

osteopenia bone mineral density?

A

more than 1 SD but less than 2.5SD below the young adult reference mean

160
Q

osteoporosis bone mineral density?

A

greater than or equal to 2.5SD below the young adult mean

161
Q

severe osteoporosis bone mineral density?

A

greater than or equal to 2.5SD below the young adult mean with a fragility fracture

162
Q

lifestyle advice for management of osteoporosis?

A
  • high intensity strength training
  • low impact weight bearing exercise
  • avoidance of excess alcohol
  • avoid smoking
  • prevent falls
163
Q

RNI of calcium in the management of osteoporosis?

A

700mg/day (2-3 portions from dairy)

164
Q

RNI of calcium in the management of osteoporosis for postmenopausal women?

A

1000mg/day (3-4 portions)

165
Q

non-dairy sources of calcium?

A
  • fortified bread and cereals
  • fish with bones
  • nuts, green vegetables and beans
166
Q

drug management of osteoporosis?

A
  • calcium and Vit. D supplements
  • bisphosphonates
  • denosumab
  • teriparatide
  • HRT
  • SERMS
  • testosterone
167
Q

what do you give to reduce risk of non-vertebral fractures in those at risk of deficiency due to insufficent diet or limited sunlight exposure?

A

calcium and vitamin D

168
Q

what should be advised for patients taking calcium and bisphosphonates?

A

calcium supplements should not be taken within 2 hours of oral bisphosphonates

169
Q

Abnormal osteoclast activity followed by increased osteoblast activity. Result is abnormally structured bone with reduced strength and increased risk of fracture.

A

Paget’s disease of bone

may be at a single site - monostotic
or multiple sites - polyostotic

170
Q

which bones are predominantly affected in Paget’s disease?

A
  • long bones
  • pelvis
  • lumbar spine
  • skull predominantly
171
Q
  • bone pain
  • bone deformity (varus)
  • deafness
  • compression neuropathy
    rarely ass. with osteosarcoma as a complication.
A

paget’s disease

172
Q

management of Paget’s disease?

A
  • analgesia

- bisphosphonates if pain doesn’t respond to analgesia

173
Q

why does deafness occur in Paget’s?

A

compression of the CN VIII (vestibulocochlear) in the bony meatus

174
Q

Rare genetic disorders typically affecting bone secondary to type I collagen mutations. Mostly inherited by autosomal dominance.

A

osteogenesis imperfecta

175
Q

May be ass. with blue sclera and dentinogenesis imperfecta.

Type II form is neonatal lethal.

A

osteogenesis imperfecta

176
Q

management of osteogenesis imperfecta?

A

no cure.

  • fix fractures as they occur.
  • correct deformities (surgery).
  • bisphosphonates.
177
Q

if suspicion of non-accidental injury, what other disease should also be considered in the differential?

A

osteogenesis imperfecta

178
Q

rickets is a result of Vit. D deficiency which causes?

A

non-ossification of the soft osteoid resulting in bone deformity, pain and growth abnormality with widened growth plates and irregular, flared metaphyses.

179
Q

Osteomalacia (rickets but in adults) is due to vitamin deficiency causing?

A

non-ossification of the soft osteoid resulting in bone deformity, pain and tendency to partial fractures with poor corticomedullary differentiation.

180
Q
  • initial lytic phase - well defined lucency.

- later sclerotic phase - enlarged bone, increased density and coarse trabecular pattern.

A

paget’s disease

181
Q

what causes hypocalcaemia?

A
  • hypoparathyroidism
  • Vit. D deficiency
  • chronical renal failure
  • pancreatities, hyperventilation, osteoblastic bone metastases, rhabdomyolysis.
182
Q

long term consequences of Vit. D deficiency?

A
  • demineralisation/fractures.
  • osteomalacia/rickets.
  • malignancy (esp. colon)
  • heart disease, diabetes.
183
Q

management of chronic vit. D deficiency?

A
  • vit. D3 tablets: calcitriol or alfacalcidol.
    or combined calcium + Vit D.
    e.g. adcal D3
184
Q

management of vit. D -resistant rickets due to X-linked hypophosphataemia?

A
  • phosphate
  • Vit. D supplements
  • +/- surgery
185
Q

What causes primary adrenocortical insufficiency in Addison’s disease?

A

Destruction or dysfunction of the entire adrenal cortex.

186
Q

Describe the biochemical findings of Addison’s disease.

A
  • Hyponatraemia.
  • Hyperkalaemia.
  • Mild non-anion gap metabolic acidosis.
187
Q

Loss of the adrenal gland in Addison’s disease results in reduced function of which corticosteroids?

A
  • Glucocorticoids.

- Mineralocorticoids.

ENDOCRINE (12 decks)

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