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Phase 2a - Systems > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

explain the pathophysiology of type 1 diabetes

A

insulin deficiency, due to autoimmune destruction of insulin-secreting pancreatic beta cells

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2
Q

explain the pathophysiology of type 2 diabetes

A

insulin resistance develops - body can no longer produce enough insulin to cope with the high levels of glucose entering the body so the cells become resistant to insulin’s effects.

there is hypersecretion of insulin, by a depleted number of beta cells, so the insulin levels are increased by not enough to control glucose homeostasis.

hyperglycaemia and lipid excess are toxic to beta cells so insulin secretion then drops.

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3
Q

what is the classical triad of symptoms for a presenting type 1 diabetic? what causes each of these

A

polyuria - due to osmotic diuresis from blood glucose exceeding the tubular reabsorption capacity.
thirst - due to fluid and electrolyte loss.
weight loss - fluid depletion and accelerated breakdown of fat and muscle.

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4
Q

give 3 complications a type 1 diabetic may present with

A

staphylococcus skin infections, retinopathy, polyneuropathy, erectile dysfunction, arterial disease e.g. MI.

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5
Q

if you take a random blood glucose as part of general monitoring/while testing for something else, and it comes back at 23mmol/L, what do you need to confirm a diagnosis of diabetes?

A

repeat the blood glucose test at another time.

one result is enough if the patient is symptomatic.

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6
Q

what investigation is used to measures long term glucose control? what are the normal and diagnostic values?

A

HbA1c - glycosylated haemoglobin - glucose is taken up by haemoglobin and remains in blood for 8-12wks - high blood glucose over that period shows up as a raised HbA1c.
diagnostic value is >48mmol/mol.

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7
Q

what is the WHO diagnostic criteria for diabetes mellitus ?

A

hyperglycaemic symptoms - polyuria, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy AND:

fasting plasma glucose >7.0mmol/L OR.
random plasma glucose >11.1 mmol/L.

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8
Q

describe the management of type 1 diabetes, apart from insulin therapy.

A

risk factor management (esp. BP control!).
education, diet and exercise e.g. educate on self-adjusting doses.
frequent self-monitoring of blood glucose and long-term monitoring of HbA1c.

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9
Q

what are the steps of tablet treatment for a type 2 diabetic?

A

1) lifestyle changes and metformin
2) add DPP-1 inhibitor (gliptin)/sulfonyurea/glitazone.
3) add any of the above not used
4) start insulin therapy alongside other medications.

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10
Q

how does metformin work?

A

reduces rate of gluconeogenesis, reducing hepatic glucose output.
increases insulin sensitivity.
decreases absorption of glucose in GI tract.
NO weight gain or hypos, but can cause lactic acidosis.

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11
Q

how does sulfonylurea work?

A

binds to channels on beta cells to increase fusion of insulin granulae with cell membrane.

INCREASES INSULIN SECRETION.
can cause hypoglycaemia and weight gain.

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12
Q

how do glitazones work?

A

interact with PPAR-gamma, which regulates lipid metabolism and insulin action - fatty tissue is redistributed and lower free fatty acid levels - promotes glucose consumption by muscles.

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13
Q

what are the differences in onset between type 1 and type 2 diabetes?

A

type 1 - adolescent onset usual.
type 2 - onset usually >40yrs.
type 1 is linked to HLA D3 and D4, type 2 has no HLA association.

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14
Q

what are the differences in how type 1 and type 2 diabetes present?

A

type 1 will present with polydipsia, polyuria, weight loss, ketonuria etc.
type 2 presents asymptomatically (picked up on blood test), or with complications e.g. MI.

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15
Q

what lifestyle factors is type 2 diabetes associated with?

A

obesity, lack of exercise, calorie and alcohol excess.

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16
Q

list some possible causes of DM

A

drugs - steroids, anti-HIV drugs, antipsychotics, thiazides.
pancreatic - pancreatitis, surgery, trauma, pancreatic destruction (haemachromatosis, CF), pancreatic cancer.
Cushing’s disease.
Acromegaly.
Phaeochromocytoma.
Hyperthyroidism.
Pregnancy (gestational diabetes).

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17
Q

give 3 risk factors for type 2 DM

A 
overweight/obese.
central adiposity.
Asian background.
Age >40yrs.
FHx.
gestational diabetes.
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18
Q

give 3 general measures that should be undertaken in diabetes mellitus

A

inform DVLA.
foot care.
exercise.
diet - low in sat fats and sugar, high in starchy carbs.
avoid binge-drinking - delayed hypo.
educate on managing hypo - sugary drinks, dextrose tablets.

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19
Q

describe the common insulin options used to treat diabetes mellitus

A

1) ultra-fast acting (Novorapid) injection at start of meal.
2) isophane insulin - peak at 4-12h.
3) pre-mixed insulins with ultra-fast components.
4) long-acting recombinant human insulin analogues (insulin glargine/detemir) - used at bedtime, no peak so avoids nocturnal hypos.

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20
Q

give examples of possible injection sites for insulin. why is it important they are rotated regularly?

A

outer thigh, abdomen, arm.

rotating reduces risk of infection and lipohypertrophy (lipohypertrophy).

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21
Q

give 3 possible complications of diabetes mellitus

A 
infection/lipohypertrophy at injection sites.
MI, stroke.
nephropathy - microalbuminuria.
retinopathy.
cataracts.
diabetic foot.
neuropathy.
hypoglycaemia - due to insulin spikes, skipped meals, incorrect dose adjustment for exercise etc.
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22
Q

describe the symptoms of hypoglycaemia

A

autonomic - sweating, anxiety, hunger, tremor, palpitations, dizziness.
neuroglycopenic - confusion, drowsiness, visual trouble, seizures, coma

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23
Q

how would you treat hypoglycaemia?

A

oral sugar and long-acting starch (e.g. toast).

IV glucose if can’t swallow.

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24
Q

what is a hypoglycaemic coma? how would you treat it?

A

rapid onset of hypoglycaemia preceded by aggression, sweating, high pulse, seizures - leading to loss of consciousness.
treat with IV glucose - should recover promptly.
sugary drinks and a meal once conscious.

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25
Q

give 3 symptoms of diabetic ketoacidosis

A

lethargy, nausea, vomiting, anorexia, abdo pain, polyuria, polydipsia, weight loss, breathlessnesss

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26
Q

give 3 signs of diabetic ketoacidosis

A

dehydration, reduced consciousness, ketotic breath (pear drops), Kussmaul breathing (deep and laboured).

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27
Q

what causes diabetic ketoacidosis?

A

there’s an excess glucose, but due to lack of insulin this can’t be taken up by cells to be metabolised - body pushed into starvation-like state.
ketoacidosis is the only alternative metabolic pathway.
results in severe acidosis.

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28
Q

does diabetic ketoacidosis generally occur in type 1 or type 2 diabetics?

A

type 1 - rare in type 2.

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29
Q

give 3 possible triggers of DKA

A

infection e.g. UTI.

surgery, MI, pancreatitis, chemo, antipsychotics, wrong insulin dose/non-compliance

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30
Q

what would you find on investigation of a patient presenting with DKA?

A

acidaemia - blood pH less than 7.3

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31
Q

give 3 possible complications of DKA

A

cerebral oedema, aspiration pneumonia, hypokalaemia, hypomagnesaemia, hypophosphataemia, thromboembolism

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32
Q

how would you treat DKA?

A

rehydration - fluids.

IV insulin infusion ± potassium replacement.

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33
Q

is hyperglycaemic hyperosmolar non-ketotic (HONK) state/coma more likely to affect a type 1 or type 2 diabetic?

A

type 2

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34
Q

how would a hyperosmolar hyperglycaemic state present?

A

longer history (1wk) with marked dehydration and raised glucose.
stupor/coma.
impairment of consciousness is directly related to degree of hyperosmolality.

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35
Q

how would you manage a HONK patient?

A

rehydrate slowly with IV saline.
replace potassium when urine flowing.
if blood glucose not falling with rehydration, use insulin.

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36
Q

what are patients with HONK at particular risk of?

A

occlusive events - focal CNS signs, chorea, DIC, leg ischaemia, DVT.

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37
Q

how might diabetic neuropathy present? how would you manage it?

A

stocking and glove distribution of loss of sensation, absent ankle jerks, deformities. may develop ulcers and ischaemia if there’s accompanying peripheral vascular disease.

special foot care and diabetic shoes needed.
control pain with:
paracetamol => amitriptyline => gabapentin => baclofen

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38
Q

explain the disease process underlying Graves’ disease

A

autoimmune - serum IgG antibodies bind to TSH receptors causing thyroid growth and overstimulation of thyroid hormone

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39
Q

name 3 triggers for the development of Graves’ disease

A

stress, infections, childbirth, other autoimmune diseases

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40
Q

if you measures TSH and T3/T4 in Graves’ disease, what would you expect to see?

A

suppressed TSH, high T3/T4.

also TSH receptor antibodies.

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41
Q

give 2 symptoms and 2 signs of thyroid eye disease

A

symptoms - eye discomfort, grittiness, increased tear production, photophobia, diplopia, decreased acuity.
signs - exophthalmos, proptosis (bulging), conjunctival oedema, lid lag, lid retraction, papilloedema, ophthalmoplegia, loss of colour vision

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42
Q

give 4 clinical features of hyperthyroidism

A 
weight loss
diarrhoea
heat intolerance
increased appetite
palpitations
tachycardia
irritability
tremor
hyper-reflexia
lid lag
oedema
sweating

eye disease in Graves’

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43
Q

list 3 causes of hyperthyroidism, not including Graves disease

A

toxic multinodular goitre, toxic adenoma, amiodarone, post partum thyroiditis, iodine excess (e.g. contaminated food, contrast media).

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44
Q

describe the production and general action of thyroid hormones

A

stimulated by TSH produced by pituitary gland.
thyroid gland secretes mostly thyroxine (T4) + some of the active triiodothyronin (T3).

most T3 is produced by peripheral conversion of T4.

gland requires iodine to produce the hormones.
act on nearly every cell, controlling metabolism - increase BMR.

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45
Q

what would you see on blood tests in hyperthyroidism?

A

TSH low - suppressed.
raised T4 and T3.
thyroid autoantibodies seen in Graves’.

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46
Q

how would you treat hyperthyroidism?

A 
beta blockers (propranolol) for rapid symptom control.
anti-thyroid drugs - carbimazole.

radioiodine ablation, thyroidectomy.

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47
Q

what does a thyroidectomy risk?

A

hoarseness due to damage to recurrent laryngeal nerve.

hypoparathyroidism.

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48
Q

name 2 possible complications of hyperthyroidism

A

heart failure, angina, AF, osteoporosis, ophthalmopathy, gynaecomastia

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49
Q

what is thyroid acropachy? give 2 features

A

a dermopathy associated with Graves’ disease.

CLUBBING, painful digit swelling

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50
Q

give 4 symptoms of hypothyroidism

A 
weight gain 
decreased appetite 
lethargy
low mood
cold intolerance
constipation
hoarse voice
decreased memory/cognition
cramps and weakness
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51
Q

give 4 signs of hypothyroidism

A 
BRADYCARDIC:
Bradycardia.
Reflexes relax slowly.
Ataxia
Dry thin hair/skin
Yawning/drowsy/coma
Cold hands ± low temp.
Ascites ± non-pitting oedema ± pericardial effusion.
Round puffy face/double chin/obese.
Defeated demeanour
Immobile
CCF (congestive cardiac failure)
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52
Q

give 3 causes of hypothyroidism

A

Hashimoto’s thyroiditis, iodine deficiency, post-thyroidectomy/radioiodine treatment,
primary atrophic hypothyroidism, antithyroid drugs.

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53
Q

what would you find on investigation of a patient with hypothyroidism?

A

high TSH, low T3/free T4.

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54
Q

how would you treat hypothyroidism?

A

levothyroxine (T4) - given for life, monitor TSH levels, increase dose when pregnant

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55
Q

what is Hashimoto’s thyroiditis?

A 
a primary, autoimmune thyroiditis.
cause hypothyroidism (or euthyroidism), with goitre that is due to lymphocytic and plasma cell infiltration.
more common in women aged 60-70yrs.
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56
Q

give 3 diseases associated with hypothyroidism

A

autoimmune hypothyroidisms are associated with other autoimmune disease - type 1 DM, Addison’s, pernicious anaemia.

Turner’s and Down’s syndromes.
CF, primary biliary cirrhosis, ovarian hyperstimulation, pregnancy problems (eclampsia, anaemia, prematurity, low birthweight etc).

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57
Q

what tumour marker would you look for to confirm a diagnosis of thyroid carcinoma?

A

thyroglobulin

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58
Q

where are the common metastases sites for papillary and follicular carcinomas?

A

lungs and bones

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59
Q

how would you manage a thyroid carcinoma?

A

total thyroidectomy and lymph node clearance ± radioiodine ablation

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60
Q

what are the different types of thyroid cancer?

A

papillary, follicular, medullary.

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61
Q

give one physiological and one pathological cause of goitre

A

physiological - puberty, pregnancy.

pathological - iodine deficiency, high dose of carbimazole/propylthiouracil

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62
Q

if goitre became painful, what could be the cause?

A

bleeding, thyroiditis, malignancy

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63
Q

give 2 indications for surgery in goitre

A

malignancy, pressure symptoms, toxic nodule, cosmetic reasons

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64
Q

what does the adrenal cortex produce, and what do they do?

A

steroids.
Salt - Sugar - Sex (it gets sweeter as you go deeper)
mineralocorticoids (e.g. aldosterone) - control sodium and potassium balance.
glucocorticoids (e.g. cortisol) - affect carbohydrate, lipid and protein metabolism.
androgens - sex hormones.

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65
Q

how is the adrenal cortex stimulated to produce cortisol/androgens?

A

corticotrophin-releasing factor (CRF) from hypothalamus stimulates ACTH secretion from pituitary - stimulates cortisol and androgen production.

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66
Q

what is Cushing’s syndrome?

A

clinical state produced by chronic glucocorticoid excess + loss of normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and loss of circadian rhythm of cortisol secretion

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67
Q

what is the main cause of Cushing’s syndrome?

A

oral steroids

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68
Q

what are the two classes of causes of Cushing’s syndrome?

A

increased circulating ACTH from a pituitary/ectopic tumour with glucocorticoid excess - ACTH dependent.
primary excess of cortisol secretion by an adrenal tumour or nodular hyperplasia with ACTH suppression - ACTH independent.

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69
Q

give 3 symptoms of Cushing’s syndrome

A 
weight gain
stretch marks
red puffy, round face
tanned skin - Cushing's disease
muscle weakness
depression
tiredness
70
Q

give 3 signs of Cushing’s syndrome

A 
central obesity, moon face and buffalo hump.
skin and muscle atrophy.
bruising.
purple abdominal striae (stretch marks).
osteoporosis
hypertension.
pigementation, in ACTH dependent causes.
71
Q

what is the specific test used for Cushing’s syndrome and what would you expect the results to be?

A

48h low dose dexamethsone test - this would normally suppress cortisol, but in Cushing’s you see normal/low ACTH and high cortisol.

72
Q

what is Cushing’s disease?

A

bilateral adrenal hyperplasia due to ACTH-secreting pituitary adenoma

73
Q

give 2 ACTH-dependent causes of Cushing’s syndrome

A

Cushing’s disease, ectopic ACTH production

74
Q

give 2 ACTH-independent causes of Cushing’s syndrome

A

adrenal adenoma/cancer, adrenal nodular hyperplasia, iatrogenic - STEROIDS.

75
Q

why would you not test for Cushing’s by taking random plasma cortisols?

A

can be misleading - variation due to illness, time of day, and stress (e.g. venepuncture!)

76
Q

how would you manage a patient with Cushing’s syndrome?

A

stop steroids if possible.
surgical removal of any tumour ± radiotherapy.

metyrapone, ketoconazole and fluconazole decrease cortisol secretion when pre-op/awaiting affects of radiotherapy.

77
Q

what is the main cause of acromegaly?

A

pituitary adenoma - secretes excess GH

78
Q

give 4 symptoms of acromegaly

A 
persistent numbness and tingling in hands and feet
headache
amenorrhoea
sweating
arthralgia
increase in weight
low libido, backache
"my rings and shoes don't fit anymore"
79
Q

give 4 signs of acromegaly

A 
growth of hands, feet and jaw
coarsening face, wide nose
macroglossia
darkened skin
obstructive sleep apnoea
goitre
carpal tunnel syndrome
puffy lips
laryngeal dyspnoea
80
Q

what cardiac disease can acromegaly cause?

A

hypertrophic cardiomyopathy

81
Q

what would you find on blood tests in acromegaly?

A

raised IGF-1, GH and prolactin - secreted by adenoma

82
Q

what specific test would you do to confirm a diagnosis of acromegaly? what else can be helpful when trying to diagnose acromegaly?

A

oral glucose tolerance test - diagnostic if GH is not suppressed by the glucose.

old photos of the patient.

83
Q

what is the 1st line treatment of acromegaly?

if that is CI, what would you try?

A

transphenoidal surgery.

if CI - somatostatin analogues (GH is inhibited by somatostatin) - lanreotide, ocreotide.
GH antagonist - pegvisomant.

84
Q

what are the metabolic actions of GH?

A

stimulates IGF-1 to be produced and secreted by the liver.
increases collagen and protein synthesis, opposing the action of insulin (same as glucagon).
promotes retention of calcium and nitrogen.
mainly secreted nocturnally.

85
Q

explain the pathophysiology underlying Conn’s syndrome

A

excess aldosterone production causing sodium retention, potassium loss and less renin release - causes hypertension.

86
Q

explain the renin-angiotensin-aldosterone system

A

renin is secreted by the kidneys in response to hypoperfusion of the kidneys, which then cleaves angiotensinogen into angiotensin I, which is an inactive form.
angiotensinogen is made in the liver, and circulates in the plasma.
angiotensin I is converted by ACE (produced in lungs) into angiotensin II in the lung and vascular endothelium.
angiotensin II causes vasoconstriction and stimulates the zona glomerulosa to increase its production of aldosterone - raises blood pressure and sodium retention - increasing blood volume.

87
Q

what is Conn’s syndrome?

A

a cause of hyperaldosteronism - there’s an aldosterone-producing adrenal adenoma

88
Q

what are the 2 main causes of primary hyperaldosteronism?

A

Conn’s disease (adrenal adenoma) and bilateral adrenocortical hyperplasia.

89
Q

hyperaldosteronism/Conn’s is normally asymptomatic and picked up on a routine test, what test is this?

A

testing BP - hypertension.

90
Q

before you begin to investigate hyperaldosteronism/Conn’s, what medications should you stop?

A

ACEi, beta-blockers, spironolactone, ARBs

91
Q

what are the sodium and potassium levels seen in patients with hyperaldosteronism/Conn’s, and how does this present?

A

high serum sodium, low serum potassium.

features - headaches, polyuria (compensatory), muscle weakness, tetany, nocturia.

92
Q

how would you treat primary hyperaldosteronism?

A

Conn’s (adrenal adenoma) - surgery ± post-op spironolactone.

benign adrenal hyperplasia - spironolactone.

93
Q

what causes secondary hyperaldosteronism?

A

excess renin stimulation of zona glomerulosa due to decreased renal perfusion - accelerated hypertension, renal artery stenosis

94
Q

Addison’s disease is describe as adrenal insufficiency - which part of the adrenal gland is destroyed and therefore what hormones are affected?

A

the adrenal cortex - decreased production of mineralocorticoids (aldosterone), sex steroids and glucocorticoids (cortisol).

95
Q

how might a patient present in an Addisonian crisis?

A

severe hypotension and dehydration, abdominal pain and vomiting, skin pigmentation (increased ACTH).

96
Q

list some causes of Addison’s disease

A

autoimmunity - 80% of UK cases.
TB, adrenal metastases (lung, breast, kidneys), lymphoma, opportunistic infection in HIV (CMV, M avium).
adrenal haemorrhage, congenital.

97
Q

how might Addison’s disease present?

A

mild, non-specific symptoms:
lean, tanned, tired and tearful ± weakness, anorexia, dizzy, faints, flu-like illness.
depression, psychosis, low self-esteem.
GI - nausea/vomiting, abdo pain, diarrhoea/constipation.

98
Q

what is Addison’s disease commonly misdiagnosed as?

A

viral infection or anorexia nervosa

99
Q

what specific investigation would you perform to confirm a diagnosis of Addison’s disease?

A

short ACTH stimulation test - measure cortisol, give IV/IM synthetic ACTH and measure cortisol again - its positive if the cortisol decreases - Addison’s is excluded if cortisol after is >550nmol/L

100
Q

what happens to serum sodium and potassium levels in Addison’s disease?

A

sodium is decreased and potassium is increased - due to decreased mineralocorticoid

101
Q

how would you test for autoimmune Addison’s disease?

A

21-hydroxylase adrenal autoantibodies will be +ve

102
Q

what is the treatment for an acute flare-up of Addison’s, and in the long-term?

A

acute - IM hydrocortisone and IV saline.

chronic - hydrocortisone and fludrocortisone - px should carry a steroid card/bracelet.

103
Q

what causes secondary adrenal insufficiency?

A

long-term steroid therapy suppressing the pituitary-adrenal axis - becomes apparent when steroids are withdrawn.

104
Q

what is diabetes insipidus?

A

passage of large volumes (>3L/day) of dilute urine due to impaired water resorption by kidney

105
Q

what is the difference between cranial and nephrogenic DI?

A

cranial is due to reduced ADH secretion from posterior pituitary.
nephrogenic is due to impaired response of the kidney to ADH.

106
Q

give 3 causes of cranial DI

A

idiopathic, congenital, tumour (craniopharyngioma, metastases, pituitary tumour), trauma, hypophysectomy, autoimmune hypophysitis, infiltration (histiocytosis, sarcoidosis), haemorrhage, infection (meningoencephalitis).

107
Q

give 3 causes of nephrogenic DI

A 
inherited.
metabolic - low potassium, high calcium.
drugs - lithium, demeclocycline.
chronic renal disease.
post-obstructive uropathy.
108
Q

give 3 symptoms of diabetes insipidus

A

polyuria, nocturia, polydipsia, hypernatraemia

109
Q

give 3 signs of diabetes insipidus

A

dehydration, enlarged and palpable bladder, no weight loss

110
Q

what specific test can you do to confirm a diagnosis of diabetes insipidus, and what result would you expect?

A

fluid deprivation test - failure of urine concentration despite fluid restriction.

can give desmopressin - cranial DI will show an increase in urine osmolality.

111
Q

how would you treat cranial diabetes insipidus?

A

desmopressin - synthetic ADH analogue.

MRI head to find cause.

112
Q

why would treatment for cranial DI not work for nephrogenic and what would you use instead?

A

nephrogenic DI is a defect in channels rendering the kidneys insensitive to vasopressin - so desmopressin will have no effect.

treat cause.
if persists - bendroflumethiazide, and NSAIDs to lower the urine volume and plasma sodium.

113
Q

explain the effect of vasopressin on the body

A

vasopressin is synthesised in the hypothalamus and migrates to the posterior pituitary where it is released into the circulation.
stimulates V2 receptors in kidney, making the collecting ducts more permeable to water via aquaporin 2 channels - decreasing diuresis and promoting water retention.

114
Q

what types of malignancy can cause the syndrome of inappropriate ADH secretion?

A

small cell lung cancer, pancreas, prostate, thymus, lymphoma

115
Q

list some causes of the syndrome of inappropriate ADH secretion

A

malignancies.
neuro - stroke, SAH, Guillain-Barre, SLE, vasculitis, meningoencephalitis.
resp - TB, pneumonia, abscess.
endocrine - hypothyroidism.
drugs - opiates, psychotropics, SSRIs, cytotoxics.

116
Q

what is the main metabolic abnormality in the syndrome of inappropriate ADH secretion?

A

hyponatraemia

117
Q

despite water retention, what is NOT a feature of the syndrome of inappropriate ADH secretion?

A

oedema

118
Q

describe the urine of a patient with the syndrome of inappropriate ADH secretion

A

concentrated urine with hyponatraemia and a low plasma osmolality

119
Q

what clinical features might you see in the syndrome of inappropriate ADH secretion?

A

hyponatraemia features - anorexia, nausea and malaise.

then headache, irritability, confusion, weakness, decreased GCS and seizures.

120
Q

how would you treat the syndrome of inappropriate ADH secretion?

A

restrict fluid intake + treat cause.

give salt ± a loop diuretic if severe.

121
Q

describe the usual function of parathyroid hormone

A

secreted in response to low ionised calcium levels (-ve feedback).
acts by increasing osteoclastic activity - releases calcium/phosphate from bones.
increases calcium reabsorption in kidney.
decreases phosphate reabsorption in kidney.
increases active 1,25-dihydroxy-vitamin D3 production.

overall effect = increases calcium, decreases phosphate.

122
Q

name a primary, secondary and tertiary cause of hyperparathyroidism

A

primary - solitary parathyroid adenoma, malignancy (lung small cell, breast, renal), hyperplasia of parathyroid gland.
secondary - compensatory hypertrophy of gland in response to low calcium from renal failure.
tertiary - long term hyperparathyroidism.

123
Q

in hypercalcaemia, you can classify the clinical features as bones, stones, psychic moans and abdo groans- give an example of each of these

A

bones - pain, cysts, tumours.
psychic moans - depression, psychosis.
stones - renal colic, polyuria, nocturia, haematuria, hypertension.
abdo groans - abdo pain, nausea, vomiting, constipation, anorexia.

124
Q

what metabolic state usually accompanies hyperparathyroidism?

A

hypercalcaemia

125
Q

what biochemical tests and what imaging tests would you perform in assessing hyperparathyroidism?

A

high calcium and PTH, low phosphate, high calcium excretion (24h urinary calcium).
DEXA scan to show any skeletal involvement, abdo XR for renal stones

126
Q

what classical sign is seen on imaging a patient with hyperparathyroidism?

A

pepper pot skull

127
Q

how would you treat hyperparathyroidism?

A

partial/total parathyroidectomy, IV saline, IV bisphosphonates (alendronate).
cinacalcet - increases sensitivity of parathyroid cells to calcium.
avoid thiazide diuretics, low calcium/vit D diet.

128
Q

explain how high parathyroid levels can lead to high calcium levels

A

PTH causes increased release of calcium from bone matrix, increased calcium reabsorption by kidney, increased phosphate excretion, increased renal production of calcitriol (leads to increased intestinal absorption of calcium)

129
Q

what would biochemical tests show in a patient with hypoparathyroidism?

A

low calcium, low/normal phosphate

130
Q

how would you treat hypoparathyroidism?

A

treat the hypocalcaemia - calcium supplements and calcitriol.

131
Q

give 2 possible causes of secondary hypoparathyroidism

A

radiation, surgery, hypomagnesaemia

132
Q

from what malignancies do you most commonly get hypercalcaemia?

A

squamous cell lung, breast, bone mets, myeloma, GI cancer

133
Q

how does hypercalcaemia of malignancy occur in myeloma?

A

stimulation of osteoclasts by IL-1 and TNF promotes calcium loss from bones

134
Q

how would you treat hypercalcaemia of malignancy, other than normal malignancy management?

A

rehydration

bisphosphonates - pamidronate, inhibit osteoclast activity.

135
Q

give 3 symptoms of hypercalcaemia of malignancy

A

lethargy, anorexia, nausea, polydipsia, polyuria, constipation, dehydration, confusion, weakness

136
Q

what are the clinical features of hypocalcaemia?

A

SPASMODIC:
Spasms.
Perioral paraesthesiae.
Anxious, irritable, irrational.
Seizures.
Muscle tone increased in smooth muscle - colic, wheeze, dysphagia.
Orientation impaired (time, place and person) and confusion.
Dermatitis.
Impetigo herpetiformis.
Chvostek’s sign, choreasthetosis, cataract, cardiomyopathy.

137
Q

what is Chvostek’s sign and what does it indicate?

A

when facial nerve is tapped at the angle of the jaw, facial muscles on the same side of the face contract - indicates nerve hyperexcitability due to hypocalcaemia.

138
Q

give 2 causes of hypocalcaemia with high phosphate

A

CKD, hypoparathyroidism, acute rhabdomyolysis, vitamin D deficiency, hypomagnesaemia

139
Q

give 2 causes of hypocalcaemia with normal/low phosphate

A

osteomalacia, acute pancreatitis, over-hydration, respiratory alkalosis

140
Q

what would you see on the ECG of a patient with hypocalcaemia?

A

prolonged QT interval.

141
Q

how would you treat hypocalcaemia?

A

calcium supplements + alfacalcidol (derivative of vitamin D).

142
Q

what makes hyperkalaemia a medical emergency?

A

causes cardiac hyperexcitability, leading to ventricular fibrillation and cardiac arrest.

143
Q

give 3 possible causes of hyperkalaemia

A

Addison’s disease, renal impairment, potassium-sparing diuretics, metabolic acidosis, burns, ACEi, rhabdomyolysis (crush injury)

144
Q

give 3 changes you would see on an ECG of a patient with hyperkalaemia

A

tall tented T waves, reduced P waves, widened QRS complexes

145
Q

give 2 possible clinical features of hyperkalaemia

A

fast irregular pulse, chest pain, weakness, palpitations, light-headedness, ECG changes

146
Q

explain what ‘artefactual’ hyperkalaemia is

A

if patient is well, but shows hyperkalaemia the test should be repeated - may have been an artefactual result due to:
contamination with potassium EDTA anticoagulant in FBC bottles; thrombocythaemia; delayed analysis (potassium leads out of RBCs).

147
Q

how would you manage a patient with severe hyperkalaemia?

A

acutely - insulin - drives potassium into cells, give with glucose to avoid hypos.
long term - polystyrene sulphonate resin - binds to potassium in gut and stops absorption, give with laxatives.

148
Q

give a chronic and an acute cause of hypokalaemia

A

acute - IV fluid without potassium, vomiting/diarrhoea.

chronic - diuretics, Conn’s.

149
Q

list 2 clinical features of hypokalaemia

A

muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness, constipation.

150
Q

what ECG changes might be seen in a patient with hypokalaemia?

A

small/inverted T waves.
prominent U waves.
long PR interval.
depressed ST segments.

151
Q

how would you treat hypokalaemia

A

mild - oral potassium supplement.

severe - IV potassium.

152
Q

what are carcinoid tumours and where are they most commonly found?

A

diverse group of tumours of enterochromaffin cell (neural crest) origin, capable of producing 5HT.

appendix, ileum, rectum, elsewhere in GI tract, ovary, testis, bronchi.

153
Q

what is carcinoid syndrome?

A

only occurs if there are liver metastases.
spontaneous red-blue flushing mainly on face and neck (kinis), pulmonary stenosis/tricuspid incompetence (5-HT), hepatomegaly.

tumours secrete serotonin, kinin, histamine, prostaglandins.

154
Q

how would you treat carcinoid syndrome?

A

somatostatin analogues - ocreotide and lanreotide.

resection of primary tumour.

155
Q

somatostatin analogues are used in which pituitary disease and how do they work?

A

acromegaly, they inhibit the release of growth hormone from the anterior pituitary

156
Q

what renal drug can you use to treat Conn’s?

A

spironolactone - it is an aldosterone antagonist, so increases potassium reabsorption.

157
Q

carbimazole is used to treat hyperthyroidism, what is the mechanism of action?

A

stops coupling and iodination of thyroglobulin to TPO (thyroid peroxidase)

158
Q

why do you give nebulised salbutamol, insulin and calcium gluconate to treat hyperkalaemia?

A

calcium gluconate increases the threshold potential and restores normal gradient between that and the resting membrane potential - protects heart, but doesn’t change K+ levels.
insulin forces potassium back into cells - give with glucose.
salbutamol lowers serum potassium levels by promoting movement of potassium back into cells.

159
Q

how do levothyroxine and liothyronine work as treatments for hypothyroidism?

A

levothyroxine is a synthetic T4, so gets converted into T3.

liothyronin is synthetic T3 - quicker onset, used in emergencies.

160
Q

name 2 antithyroid drugs, describe how they work.

A

carbimazole, methimazole.
prevent thyroid peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin - so reduces the production of the thyroid hormones T3 and T4.

161
Q

name 2 calcitonin drugs, and what they treat

A

miacalcin, fortical.

postmenopausal osteoporosis, hypercalcaemia

162
Q

how do calcitonin drugs work?

A

calcitonin is produced in thyroid gland by C cells and increases deposition of calcium and phosphate in bone, lowering circulating levels.
calcitonin drugs inhibit calcium resorption by intestine, inhibit osteoclast activity in bones, stimulate osteoblast activity and inhibit renal reabsorption of calcium.

163
Q

what class of drug is pegvisomant and what is it used to treat?

A

growth hormone receptor antagonist.

acromegaly, if pituitary tumour can’t be controlled with surgery/irradiation

164
Q

how does pegvisomant work?

A

blocks action of GH at the GH receptor to reduce production of insulin-like growth factor-1 (responsible for most of the symptoms of acromegaly).

165
Q

what generally causes a patient to go into hyperosmolar, hyperglycaemic state?

A

very high glucose levels develop due to combination of:
illness e.g. infection (pneumonia!)
dehydration
inability to take normal diabetes meds due to illness (so poor control).

166
Q

how does sitagliptin, a DPP-1 inhibitor, work?

A

inhibits DPP-1, which results in increased insulin secretion in response to meals, and decreased glucagon secretion by alpha cells of pancreas.
brings glucose levels nearer to normal, without any risk of hypos.

167
Q

what are phaeochromocytomas? where are they usually found?

A

rare catecholamine-producing tumours.
arise from sympathetic paraganglia cells - collections of chromaffin cells.
usually found in adrenal medulla.

168
Q

what is the 10% rule of phaeochromocytomas?

A

10% are malignant, 10% are extra-adrenal, 10% are bilateral and 10% familial.

169
Q

what is the main problem caused by phaeochromocytomas?

A

hypertension

170
Q

what is the classic triad of clinical features of phaeochromocytomas?

A

episodic headache, sweating and tachycardia

171
Q

how might a phaeochromocytoma be treated?

A

surgery - alpha blockade pre-op, then beta blockade.

Phase 2a - Systems (18 decks)

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