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MEDICINE NEW > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

A patient has a large goitre with possibly some nodules, how should it be investigated?

A

TFTs
Ultrasound (cystic or solid? Aka typically benign or malignant)
Fine needle aspiration

Consider a radioiodine isotope scan to determine cause of hyperthyroidism- absent isotope uptake suggests inflammation or destroyed tissue

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2
Q

Which diseases put patients at risk of thyroid disease?

A 
Hyperlipidaemia
Diabetes mellitus
Those on amiodarone (arrhythmia) or lithium (bipolar)
Down's or Turner's
Addison's
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3
Q

Signs of thyrotoxicosis not specific to Graves:

A 
Underdressed for temperature
Warm moist skin
Fine tremor
Palmar erythema
Thin hair
Lid lag- eyelids lag behind the eye's descent
Lid retraction
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4
Q

3 Signs of Grave’s disease specifically:

A

1 Eye: opthalmaplegia, proptosis (exopthalmus is Grave’s is cause)
2 Pretibial myxoedema
3 Thyroid acropachy- clubbing, painful fingers and toes (Extreme manifestation)

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5
Q

Cause of Grave’s disease:

A

Circulating IgG autoantibodies that activate G-protein coupled thyrotropin) receptors

= smooth thyroid enlargement and increased hormone production

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6
Q

Causes of thyrotoxicosis:

A

Graves’ (2/3rds)
Toxic multinodular goitre (related to gene mutations, nodules secrete hormones)
Toxic adenoma (solitary nodule producing T4/3, rest of gland is supressed)
Ectopic thyroid tissue- metastatic follicular cancer
Exogenous- iodine excess, levothyroxine
Subacute De Quervain’s Thyroditis- postviral self limiting

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7
Q

How can you try to differentiate between Graves and multinodular goitre or toxic adenoma on palpation of the gland?

A

Graves- smooth diffuse enlargement
Toxic adenoma or multinodular goitre- more palpable nodules

Other nodular:
Carcinoma

Other diffuse enlargement:
Hashimoto’s, subacute De Quervain’s

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8
Q

Drug treatment of thyrotoxicosis:

A
  1. Propranolol
  2. Carbimazole (agranulocytosis SE) ± levothyroxine
    Inhibits the thyroid peroxidase enzyme iodinating the hormones
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9
Q

Risk of thyroidectomy? (Things to look for if someone has a thyroid placed scar)

A

Recurrent laryngeal nerve damage- hoarse voice

Hypoparathyroidism- tingling, burning sensation, muscle cramps

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10
Q

In which diseases might anti-thyroid peroxidase antibodies be present?

A

Graves disease

Or Hashimoto’s (chronic autoimmune hypothyroidism)

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11
Q

Signs of Graves eye disease:

A

I- Exopthalmus- appearance of protruding eye
Proptosis- eyes protrude beyond the orbit
Conjunctival oedema
Corneal ulceration
F- Papilloedema
A- Loss of colour plates
CNIII- opthalmaplegia from muscle swelling and fibrosis restricting movement

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12
Q

How is Graves eye disease treated?

A

Caused by lymphocyte infiltration and periorbital swelling:

Mild- symptomatic (artificial tears, sunglasses, avoid dust, elevate head at night, prisms on glasses for diplopia)

Severe- with opthalmaplegia or gross oedema:
IV methylprednisolone
Surgical decompression

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13
Q

What are the symptoms of hypothyroidism:

BRADYCARDIC

A 
Bradycardia
Reflexes relaxing slowly
Ataxia (cerebellar)
Dry skin/hair
Yawning/drowsy
Cold hands + low T
Ascites ± non-pitting oedema ± pleural/pericardial effusion
Round puffy face
Defeated demeanor
Immobile
CCF

Neuropathy, myopathy

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14
Q

Causes of primary hypothyroidism:

A

Autoimmune- atrophic or Hashimoto’s (lymphocytic)
Iodine deficiency
Iatrogenic- thyroidectomy, radioiodine therapy, amiodarone, lithium
Subacute De Quervain’s- postviral (temporary)

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15
Q

What does POEMS syndrome stand for:

A 
Polyneuropathy
Organomegaly
Endocrinopathy
M-protein band (plasmacytoma)
Skin tethering/pigmentation
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16
Q

How can amiodarone cause thyrotoxicosis and why may thyroid problems persist once stopped?

A

Has a cytotoxic effect on thyroid follicular cells, may cause a thyroiditis causing thyroid release

Amiodarone has a half life of 80 days

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17
Q

What effect does excess cortisol have?

A

In excess, it acts like aldosterone
Salt retention at the expense of H+ and K+
= hypokalaemic hypertensive alkalosis

Ie in Cushing’s, adrenal hyperplasia, ectopic ACTH

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18
Q

Patient has the signs of Grave’s disease but is euthyroid, what could the cause be?

A

Could still be Graves, before thyroid disease has occurred yet
There are TSH-receptors in the eye

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19
Q

Rx for grave’s

A

Carbimazole
Propylthiouracil

SE: agranulocytosis- rash, fever, sore throat

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20
Q

Features of MEN1?

A

Pituitary tumours
Pancreatic neuroendocrine tumours (VIPoma)
Parathyroid tumours- all 4 glands may be affected

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21
Q

What test can determine whether a patient has high Ca2+ because of a familial kidney condition?

A

Urine calcium should be low if they have benign hypocalciuric hypercalcaemia

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22
Q

Secondary causes of diabetes:

A

Drugs: steroids, thiazides, atypical antipsychotics (olanzepine)

PMH: CF, chronic pancreatitis, haemochromotosis, Cushing’s/phaeochromocytoma, acromegaly

MODY, gestational, DIDMOAD

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23
Q

Patient has random glucose of 10, what would your next line of investigation be?

A

Between 7-11 do a fasting glucose test

If fasting glucose is >7 do an oral glucose tolerance test
+ve if above 11

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24
Q

How long do you fast for before taking a fasting blood glucose?

A

8 hours

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25
Q

How is an oral glucose tolerance test performed?

A

Fast for 8 hours
75mg of glucose
Measure at 2 hours

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26
Q

Complications of diabetes:

A

Macrovascular: Stroke, peripheral arterial disease, MI
Microvascular: Nerve, eyes, kidneys

Acute: hypoglycaemic crisis, DKA

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27
Q

Types of thyroid carcinoma

A

Please Feel My Airway Lightly

Papillary (commonest- orphan annie nuclei on histology)
Follicular (female, favourable prognosis, faraway mets)
Medullary (calcitonin, Men2 associated, Ca low)
Anaplastic (old, poor survival)
Lymphoma (A with Hashitomo’s thyroiditis)

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28
Q

Tumour markers for thyroid cancers

A

Thyroglobin: follicular + papillary

Calcitonin

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29
Q

What are the electrolyte abnormalities classically associated with Cushing’s?

A

Mineralocorticoid effect: low K+, high Na+

Glucocorticoid effect: hyperglycaemia

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30
Q

Causes of Cushing’s that are ACTH-dependent and independent

A

ACTH dependent: Pituitary adenoma (Cushing’s disease) or hyperplasia, ectopic source

ACTH independent: Adrenal hyperplasia, adrenal adenoma, exogenous

Pseudo-Cushing’s: severe depression, alcoholism

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31
Q

Tests for Cortisol if suspected:

A
  1. Best: Urinary 24hr cortisol
    But often: Midnight cortisol
  2. Low dose Dexamethasone test = confirms
    Dexamethasone at midnight, measure in AM
  3. Measure ACTH = dependent or independent
    High- dependent
    Low- adrenal cause (CT or adrenal vein sampling)
  4. High dose Dexamethasone = ?ectopic
    Low Cortisol- Cushing’s disease in pituitary
    High Cortisol- Ectopic ACTH
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32
Q

Rx of Cushing’s:

A

Pituitary adenoma:
Ketoconazole then transphenoidal excision

Adrenal site:
Ketoconazole then adrenalectomy

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33
Q

Which is the more potent suppresser of TSH- T3 or T4?

A

T3

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34
Q

In someone taking levothyroxine, is it more important to measure T3 or T4?

A

T4 as this acts as the thyroid store, each cell converts as much of T4 as it needs into T3

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35
Q

What is Sheehan’s syndrome?

A

Pituitary necrosis after postpartum haemorrhage hypovolaemia

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36
Q

What basal tests can be performed to look for hypopituitarism?

A 
Low:
LH and FSH 
Testosterone, oestradiol
TSH, T4
IGF-1 (measures GH axis)
Cortisol

High from disinhibition:
Prolactin

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37
Q

What dynamic tests of pituitary function can be performed?

A
  1. Short synacthen test: ACTH given and cortisol measured

2. Insulin tolerance test: IV insulin, measure GH and cortisol increase

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38
Q

Which hormones are produced by the anterior and posterior pituitary gland?

A

Anterior: TSH, Prolactin, FSH, LH, ACTH
Posterior: ADH, GH

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39
Q

Features of polycystic ovarian syndrome:

A

Oligomenorrhoea/amenorrhoea
Infertility
Obesity, acne, hirsutism

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40
Q

Causes of gynaecomastia

A

Oestrogens may be increased by:
Tumours- testicular, adrenal, bronchial HCG producing

Failure to convert them
Hypogonadism
Liver cirrhosis
Hyperthyroidism

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41
Q

Causes of erectile dysfunction:

A

Big 3: smoking, alcohol and diabetes

Endocrine: hypogonadism, high prolactin or thyroid, kidney/liver dysfunction

Neurological: prostate or bladder surgery damage, MS, cord lesions, autonomic neuropathy

Penile abnormalities: Peyronie’s, post-priaprism

Drugs: F DDAB (can’t properly F)
digoxin, diuretics, antidepressants, antipsychotics, b blocker, finasteride

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42
Q

Management of erectile dysfunction:

A

LFTs, U+Es, glucose, TFTs, LH, FSH, lipids, testosterone, prolactin

  1. PDE5 inhibitor- sildenafil
    Inhibition prevents break down of cGMP, which activates Ca+ activated K+ channels to hyperpolarise and relax smooth muscle cells (= engorgement)

Vacuum aids
Intracavernosal injections
Inflatable prostheses
Bioengineered tissue engineering

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43
Q

CI to PDE5 inhibitors like sildenafil

A

PC: bleeding from peptic ulcer
PMH: unstable angina, MI in 3 months, stroke
Renal or liver impairment, hypertension, retinal disorders (PDE in the eye affected)

DHx: concurrent nitrates

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44
Q

Causes of primary hypogonadism in males:

A

Chromosomal- XXY (Klinefelter’s)
Post orchitis- mumps, HIV, leprosy
Local trauma- torsion, chemo

Systemic- Renal failure, liver cirrhosis, alcohol excess (toxic to Leydig cells)

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45
Q

Causes of secondary hypogonadism:

A

Low LH and FSH:
Hypopituitarism, Prolactinaemia
Kallman’s syndrome- isolated GnRH deficiency ± colour blind

Systemic- COPD, HIV, DM, Age

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46
Q

Patient with end-stage renal failure, polydactyly and low IQ?
Other features?

A

Laurence Moon syndrome
Autosomal recessive- obesity, hypogenitalism, reduced body hair, azoospermia
Retinitis pigmentosa
Kidney- calyceal clubbing, cysts, diverticula

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47
Q

What affects does high aldosterone have?

A

Sodium and water retention
Leading to reduced renin release from juxtaglomerular cells

Renin release is stimulated by:

  1. Sympathetic action (B1-adrenorecptors)
  2. Low Na+ at DCT
  3. Renal artery hypotension
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48
Q

Patient has a BP of 160/95
U+Es:
K+ 3mmol
Na+ 144mmol

What endocrine cause is there?

A

Primary aldosteronism:
Acts on ENaC to increase Na/K exchange at collecting duct

Stimulates a proton-ATPase increasing proton excretion leading to a metabolic alkalosis

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49
Q

Causes of primary aldosteronism:

A

66% solitary adenoma of adrenals (Conn’s syndrome)
33% adrenocortical hyperplasia

Rarely: adrenal carcinoma
Glucocorticoid-remediable aldosteronism

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50
Q

What is the pathophysiology and Rx of glucocorticoid-remediable aldosteronism?

A

The ACTH regulatory element fuses with the aldosterone synthase gene, bringing aldosterone under control of ACTH + increasing production.

Rx: Dexamethasone normalises biochemistry but perhaps not BP
By suppressing ACTH release

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51
Q

Tests if suspecting primary aldosteronism:

A
  1. U+Es, venous blood gas- hypokalaemic alkalosis
  2. Plasma Renin- normally low due to dilutional effects of salt + water retention
    Plasma aldosterone to renin ratio- high aldosterone vs renin

Drugs may interfere- diuretics, steroids, antihypertensives, laxatives

  1. CT or MRI to localise cause
  2. Adrenal vein sampling- identify adenoma
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52
Q

How are the common causes of aldosteronism (Conn’s, adrenal hyperplasia) managed differently?

A

Conn’s: spironolactone for 4 weeks then laparoscopic adrenalectomy

Hyperplasia: medical management- spironolactone, amiloride, eplerenone

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53
Q

Causes of secondary hyperaldosteronism?

A

High renin and high aldosterone

Reduced renal perfusion (renin release stimulated by low pressure, lack of salt in DCT or sympathetic input) from:
Renal artery stenosis
Accelerated hypertension
Diuretics, CCF, hepatic failure

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54
Q

What is Bartter’s syndrome and what U+Es findings would you expect?

A

Autosomal recessive salt wasting
Sodium chloride leak in the loop of Henle via a defective channel

Sodium loss > aldosteronism > low K+ and alkalosis
PC: polydipsia, polyuria and failure to thrive in childhoos

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55
Q

What is a phaeochromocytoma?

A

Catecholamine-producing tumour
Arising from sympathetic paraganglionic cells (chromaffin cells) in the adrenal medulla

10% rule
10% malignant
10% extra-adrenal (by aortic bifurcation)
10% bilateral
10% inheritable (MEN2a, MEN2b, neurofibromatosis, von Hippel Lindau)

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56
Q

What is the classic triad of phaeochromocytoma?

A
  1. Episodic headache
  2. Sweating
  3. Tachycardia
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57
Q

Tests for phaeochromocytoma?

A

3 x 24 hour urine samples- metadrenalines and normetadrenalines

Localisation: Abdo CT/MRI
or MIBG chromaffin seeking isotope scan

58
Q

Rx of phaeochromocytoma:

A

a-adrenoreceptor blockade- phenoxybenzamine
as unopposed a-stimulation will cause vasoconstriction (b adrenorecptors dilate vessels to skeletal muscle)

b-blockers if tachycardic

Surgical removal

59
Q

What parts of the adrenal gland make the different hormones?

A

Medulla- noradrenaline (phaeochromacytoma)
Cortex- GFR

GFR Miner GA:
Glomerulosa- mineralcorticoid
Fasciculata- glucocorticoids
Reticularis- androgens

60
Q

What is Takotsubo cardiomyopathy?

A

Stress or catecholamine-induced cardiomyopathy (broken heart syndrome)

Sudden chest pain, mimicking an MI
ECG shows ST elevation
Echo- Apical ballooning during catecholamine surges
Can occur with phaeochromocytoma

61
Q

Causes of primary adrenocortical insufficiency (Addison’s disease):

A

Vascular: Waterhouse-Friderichsen’s syndrome of bilateral adrenal haemorrhage from meningococcal sepsis where endotoxin activates inflammatory and clotting cascades (DIC) or SLE, antiphospholipid syndrome

Infection: TB (commonest cause worldwide), opportunistic HIV
(T)
Autoimmune: 80% on UK
(M)
Iatrogenic
Neoplasia: mets, lyphoma
62
Q

How does Addison’s present?

A

PC:
Tired, weak, dizzy, myalgia, arthralgia
Depression, psychosis
N+V, abdo pain, constipation or diarrhoea

EHx:
Hands- pigmented palmar creases, vitiligo, pigmented skin
Shock- hypotensive, tachycardic, pyrexial, coma

63
Q

Patient has low Na+, high K+, low glucose, high Ca+, low Hb

What needs to be excluded and how?

A

Low Na+ and high K+ is lack of aldosterone
Low glucose may be due to low cortisol
So Addison’s disease:

Short ACTH stimulation test (synACTHen test)- check cortisol levels in response to ACTH, will remain low as no ability to make cortisol.

9am ACTH level (high if primary adrenocortical insufficiency)

64
Q

Test for Addison’s?

A

Primary adrenocortical insufficiency

  1. U+E: low Na, high K, high Ca, low glucose
  2. Short ACTH synacthen test- cortisol low after ACTH
  3. 9am ACTH level- low = secondary cause (ACTH-dependent cause)
  4. Plasma renin and aldosterone- measure mineralocorticoid status
65
Q

Which antibody is raised in autoimmune Addison’s disease?

Responsible for 80% of Addison’s in the UK

A

21-hydroxylase adrenal autoantibodies

66
Q

Rx of Addison’s disease?

A

Hydrocortisone in 2-3 doses- may cause insomnia if given late
Fludrocortisone OD

Steroid rules apply- no stopping suddenly, double in illness, extra for exercise, IM if vomiting, have steroid card or bracelet

67
Q

How does secondary adrenal insufficiency differ from Addison’s disease (primary adrenal insufficiency)?

A

Mineralocorticoid production remains intact- U+Es normal

ACTH is low rather than high
No hyperpigmentation- no excess ACTH

Commonly due to suppression of pituitary-adrenal axis from exogenous steroids

68
Q

Which hormones does ACTH stimulate production of?

A

Cortisol- fasciculata
Androgens- reticularis (GFR minerGA)

Rarely in glucocorticoid-remediable aldosteronism it can stimulate aldosterone release due to gene fusion

69
Q

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

A

Cushing’s syndrome- clinical state produced by chronic glucocorticoid excess and loss of normal feedback mechanisms in the axis.
Primarily due to exogenous steroids.

Cushing’s disease- pituitary adenoma secreting ACTH leads to bilateral adrenal hyperplasia, a specific and rare cause of Cushing’s syndrome

70
Q

What are the ACTH dependent and independent causes of Cushing’s syndrome?

A

ACTH dependent:
Pituitary adenoma (Cushing’s disease)
Ectopic ACTH production- small cell lung cancer, carcinoid tumours
Ectopic CRF (Corticotrophin Releasing Factor)- medullary and prostate cancers

ACTH independent:
Oral exogenous steroids
Adrenal nodular hyperplasia
Adrenal adenoma/cancer
Carney complex (pigmented, myxoma, schwannoma, endo tumours)
McCune-Albright syndrome (fibrous dysplasia of bone, pigmented)

71
Q

What type of cancer’s produce ectopic ACTH and which rarely can produce CRF?

A

ACTH- small cell lung cancer and carcinoid tumours

CRF- medullary thyroid and prostate cancer

72
Q

How does ectopic ACTH production in Cushing’s syndrome cause a hypokalaemic metabolic alkalosis?

A

Very high cortisol mimics mineralocorticoid activity = hyperaldosteronism

So more K+ exchanged for Na+ and more activation of proton ATPase leading to proton excretion

73
Q

How to investigate suspected Cushing’s syndrome:

A
  1. Late night cortisol
  2. Overnight Dexamethasone suppression test
    Dex at midnight, serum cortisol at 8am, no suppression
  3. 48 hour high dose Dex suppression test
    (halves cortisol in pituitary adenoma, Cushing’s disease)
  4. Plasma ACTH= dependent or independent cause
74
Q

How are ACTH dependent causes of Cushing’s syndrome investigated differently from independent causes once the ACTH dependency is established?

A

So after plasma cortisol,overnight dex test, high dose suppression test, ACTH levels

ACTH high:
Suppressed by high dose dex (pituitary cause) > head MRI
Not suppressed > CT chest, abdo, pelvix with contrast ± MRI

ACTH low:
CT adrenal glands
No mass > adrenal vein sampling or adrenal scintigraphy

75
Q

Rx of Cushing’s disease or ectopic ACTH production:

A

Pituitary adenoma secreting ACTH: transphenoidal removal of adenoma

Ectopic ACTH production: excision of tumour, ketoconazole and fluconazoe reduce cortisol pre-op if high
If ACTH causing psychosis may need cortisol receptor antagonist (mifespristone)

76
Q

Effects of PTH?

A 
Secreted in response to low ionised Ca+
Increases osteoclast activity
Increases Ca+ reabsorption in the kidney
Reduced PO4 reabsorption by kidney
Increases active Vit-D3 production
77
Q

Causes of primary hyperparathyroidism?

A

80% parathyroid adenoma
19% hyperplasia
0.5% cancer

78
Q

What can cause a high calcium and high or inappropriately normal PTH?

A

Primary hyperparathyroidism- adenoma, hyperplasia
Thiazides + lithium
Familial hypocalciuric hypercalcaemia (check 24hr urine Ca+)
Tertiary hyperparathyroidism (autonomous production of PTH after long period of secondary PTHism)

79
Q

Management of primary hyperparathyroidism?

A 
Conservative: 
Increase fluid (prevents stones)
Avoid thiazides
Ensure good vit D + calcium intake

Medical:
2nd post surgery Cinacalcet reduces PTH glands sensitivity to Ca+

Surgical:
US or MIBG might isolate a adenoma for removal
Or parathyroid gland excision if high Ca+, osteoporosis or renal damage
SEs: reccurent laryngeal nerve damage, low Ca+

80
Q

If secondary/tertiary hyperparathyroidism is caused by CKD how will this look different from primary parathyroidism?

A

Secondary has low Ca and high PTH
low Vit D means low Ca absorption in gut and low Ca

Primary would have high Ca and high PTH

Tertiary has high Ca and very high PTH because glands are acting autonomously without any feedback

81
Q

Which type of cancer rarely produces PTH related peptide?

A

Squamous cell lung cancers

Breast + renal cell carcinomas

82
Q

Patient has short 4th and 5th metacarpals, low IQ, high PTH and short stature. Cause?

A

Pseudohypoparathyroidism

Genetic loss of target cell response to PTH

83
Q

Differences between MEN1, MEN2a and MEN2b?

A

MEN1 - 3P’s
Parathyroid, Pituitary (prolactinoma or GH), Pancreas (VIPoma,
insulinoma)

MEN2a - 2P, 1M
Parathyroid, Phaeochromocytoma, Medullary thyroid

MEN2b- 1P, 2M
Phaeochromocytoma, Medullary thyroid, Marfanoid appearance/ mucosa neuroma

84
Q

Name 7 Multiple Endocrine Neoplasia syndromes and their characteristic features:

A

Autosomal dominant syndromes A with hormone-producing tumours

  1. Neurofibromatosis
    Type 1- cafe au lait spots, skin fold freckling, neurofibromas, Lisch nodules in eyes
    Type 2- cafe au lait spots, schwannoma causing acoustic neuroma
  2. MEN1: Parathyroid, Pancreas (VIPoma, insulinoma etc), Pituitary (prolactinoma, GH-producing)
  3. MEN2a: Parathyroid, phaeochromocytoma, medullary thyroid
  4. EN2b: Phaeochromocytoma, medullary thyroid, Marfainoid
  5. Von Hippel Lindau: renal cysts, phaeo, cerebellar haemangioma
  6. Peutz Jeghers: lip, mucosa, hand + feet freckling, GI polyps
  7. Carney complex: pigmentation, myxoma, schwannoma, adrenal and pituitary tumours
85
Q

In MEN1 syndrome, what types of pancreatic hormonal tumours may arise and their symptoms?

A

Gastrinoma (Zollinger Ellison): multiple + distal peptic ulcers, chronic diarrhoea as pancreatic enzymes are inactivated

Insulinoma: hypoglycaemia- faint, sweaty, tremor, palpitations

Somatostatinoma: DM, steatorrhoea, gallstones

VIPoma: diarrhoea and low K+, acidosis, high Ca+, low Mg+

Glucagonoma: migrating rash, glossitis, anaemia, weight loss

86
Q

Symptoms of hypothyroidism

A

Tired, sleepy, lethargic, depressed, reduced memory, dementia
Weight gain, constipation
Myalgia, cramps, neuropathy, myopathy, weakness
Menorrhagia, hoarse voice

87
Q

Causes of hypothyroidism:

A

Primary autoimmune:
Atrophic
Hashimoto’s- goitre from lymphocyte infiltration

Iodine deficiency
Iatrogenic- radioiodine or thyroidectomy
Drugs- Amiodarone, lithium, antithyroid drugs
Post viral- Subacute de Quervain’s
Secondary- very rare, pituitary insufficiency

88
Q

Rx of hypothyroidism, and things to watch out for with treatment:

A

Levothyroxine
Half life 7ds, so wait to check effects when changing dose
Susceptible to more metabolism when enzyme inducers given

89
Q

What is subacute hypothyroidism and how is it managed?

A

TSH raised, T4 normal
Risk of progression to hypothyroidism

Can try a trial of medication if TSH >4 to see if patient functions better

90
Q

Signs specific to Graves disease:

A

Eye disease- exopthalmos, opthalmoplegia
Pretibial myxoedema
Thyoid acropachy

Bruit, mild neutropenia

91
Q

What type of antibodies are associated with Graves disease?

A

TSH R antibody (Graves)
Thyroid peroxidase antibody (Graves or Hashimoto’s)

Thyroglobulin antibody (Hashimoto’s or thyroid cancer)

92
Q

If someone has hyperthyroidism and you give them contrast for a CT scan, what happens?

A

Thyroid storm

93
Q

Causes of hyperthyroidism and how they differ on isotope scan?

A

Graves- autoantibodies, global uptake of isotope
Toxic multinodular goitre- in elderly or iodine deficient, focal nodules
Toxic adenoma- hot nodule, rest supressed

Ectopic thyroid tissue- follicular thyroid cancer or ovarian
Iodine excess, amiodarone, levothyroxine
Subacute de Quervain’s- low isotope uptake (NSAIDs help)
Post-partum

94
Q

Management of hyperthyroidism:

A

Propranolol for symptoms

Carbimazole- either titrated up or block completely + give thyroxine
For 1-1.5 years, then withdraw.

Thyroidectomy or radio iodine (CI: pregnancy) if relapse.

95
Q

Main risk factor for Graves eye disease?

A

Smoking

96
Q

Symptoms of Graves eye disease?

A

Grittiness, tear production
Discomfort, photophobia
Diplopia, reduced acuity, afferent pupillary defect*

*optic nerve compression eek!

Exopthalmos = appearance of protruding eye, proptosis = eye extends beyond orbit

97
Q

Management of Graves eye disease

A

Conservative: if mild, artificial tears, sunglasses, elevate bed at night, Fresnel prism for diplopia

Medical: if severe, high dose steroids
Surgical: if sight threatening, decompression or cosmetic

98
Q

A painful goitre amounts to what typically:

A

Subacute De Quervain’s thyroiditis (viral)

99
Q

What is sick euthyroidism?

A

TSH and T4 all low
Following a systemic illness, TFTs may become deranged temporarily

If repeated when recovered, should not see this

100
Q

What test can you do if suspecting self-induced hyperthyroidism in a patient?
(Administering levothyroxine)

A

Thyroglobulin- the thyroid protein precursor to T4 will be low as endogenous T4 production is suppressed

101
Q

Which patients should be screened for thyroid abnormality?

A 
AF
Hyperlipidaemia
DM, Addison's disease
Type 1 DM + pregnant
Down's, Turner's syndrome
102
Q

When is surgery warranted for a thyroid problem?

A

Refractory hyperthyroidism (have withdrawn carbimazole after 1.5 years and still hyperthyroid)

Nodule is too big >3cm or compression
Rapid growth
Dominant nodule on scintigraphy, hypoechoic nodule

103
Q

Causes of hypoglycaemia:

A

EXPLAIN

EXogenous drugs- insulin, oral hypoglycaemics
Alcohol, ACEi, aspirin poisoning, bblockers, insulin (body builders)
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours- insulinoma, anti-insulin R abs in Hodgkins
Non-pancreatic neoplasms

Post-prandial hypoglycaemia:
After gastric or bariatric surgery IHx: prolonged OGTT

104
Q

Tests if a patient has hypoglycaemia?

A

Blood glucose- laboratory (monitors may not be reliable at low values)
Insulin level
C peptide- waste product of endogenous insulin production
Plasma ketones

105
Q

What causes hypoglycaemia, low insulin and no excess ketones?

A

Rarely
Anti-insulin receptor antibodies (in Hodgkin’s lymphoma)

Non-pancreatic neoplasms- fibrosarcoma, secreting an peptide downstream from insulin with a similar effect like insulin growth factor

106
Q

A patient has hypoglycaemia, how does the level of insulin determine the likely cause?

A

High insulin:
Insulinoma, sulphonylurea, insulin injection

Low insulin, high ketones:
Alcohol, pituitary insufficiency, Addison’s disease

107
Q

Patient has had a gastric bypass and has been found to be hypoglycaemic after meals, what specific test do they require?

A

Prolonged oral glucose tolerance test lasting 5 hours

108
Q

Rx of hypoglycaemia?

A
  1. Sugar or long-acting carb if possible
    2a. 200mL glucose 10% IV (less vein damage than 50% glucose)
    2b. Glucagon IM in no IV access
109
Q

What are Whipple’s triad of symptoms for fasting hypoglycaemia:

A

Occurs in insulinomas (sporadic or part of MEN1)

  1. Symptoms associated with fasting or exercise
  2. Recorded hypoglycaemia with symptoms
  3. Symptoms relieved with glucose
110
Q

Different tests if suspecting insulinoma?

A

Screening: Insulin level and glucose level during a fast

Suppressing: IV insulin + measure C-peptide
Normally exogenous peptide suppresses C peptide production

Imaging: CT/MRI

111
Q

Which signs distinguish ischaemia from peripheral neuropathy on the foot exam?

A

Ischaemia: critical toes (ulcers, gangrene), absent dorsalis pedis

Peripheral neuropathy: injury or infection over pressure points (like metatarsal head)

NB: most patients have both

112
Q

Signs of peripheral neuropathy in the diabetic foot:

A

Inspect:
Charcot foot- absent pes cavus, claw toes, loss of transverse arch, rocker bottom sole
Absent ankle jerks
Reduced sensation in a stocking distribution

113
Q

Points to educate someone with a diabetic/ischaemic foot on:

A
  1. Daily foot inspection
  2. Good shoes- soft leather, increased depth, no barefoot walking, cushioning insoles
  3. Regular chiropody- remove calluses
  4. Fungal infection treatment
  5. Surgery referral potentially
114
Q

What are the 4 things to examine or investigate with a diabetic foot ulcer?

A

Assess degree of:

  1. Neuropathy- clinically
  2. Ischaemia- clinically, doppler ± angiography
  3. Bony deformity(Charcot joint)- clinically + xray
  4. Infection- swabs, blood culture, ulcer probe (depth) + xray (osteomyelitis)
115
Q

Rx of diabetic neuropathy of the feet

A

Bed rest to relieve high pressure areas
Therapeutic shoes
Regular chiropody

Abs for infection- benzylpenicillin, flucloxacillin, metronidazole
Considerations for surgery

116
Q

What are the 4 types of neuropathy someone with diabetes might get?

A
  1. Peripheral sensory neuropathy- glove + stocking
  2. Mononeuritis multiplex- if sudden or severe, immunosupression can be tried
  3. Amyotrophy- painful wasting of quadraceps
  4. Autonomic- postural BP drop, gastroparesis, urine retention, ED
117
Q

How should gastroparesis be proved in a diabetic patient who is experiencing early satiety, post-prandial N+V and bloating?

A

99-technetium labelled meal

Rx: antiemetics, erythromycin or gastric pacing

118
Q

Complications of diabetes:

A

Macrovascular- MI, stroke, peripheral arterial disease
Statin advised + clopidogrel if PAD
Microvascular- nephropathy, neuropathy, retinopathy
ACEi i microproteinuria

119
Q

Stages of diabetic retinopathy:

A

Nonproliferative retinopathy: mild, moderate and severe
Mild- dots + blots
Moderate- dots, blots, hard exudates
Severe- blots, cotton wool spots, venous beading + loops

Proliferative retinopathy:
New vessel formation (floaters, visual loss)

Maculopathy:
Exudate (from vessel leaks) or retinal thickening within an optic disc

120
Q

Rx of maculopathy?

A

Sudden vision loss-
Intravitreal steroids
Laser photo-coagulation (to destroy peripheral ischaemic vessels releasing anti-VEGF)
Anti- angiogenic agents

121
Q

What is the stepwise approach to oral glycaemic agents in T2DM?

A

HbA1c >48: lifestyle measures
HbA1c
>48: metformin
>58: meformin + other drug* (Aim <53)

> 58: metformin + 2 other drugs (often 1 sulfonylurea) or insulin

*sulfonylurea, gliptin, SGLT2i, pioglitazone

122
Q

Under what circumstances is a GLP-2 mimetic indicated? (Exenatide)

A

If triple therapy of metformin + 2 other drugs is not tolerated

AND BMI >35

= metformin + sulfonylurea + GLP1 mimetic

123
Q

What is needed to diagnose diabetes?

A 
Symptoms + fasting glucose >6.9
Symptoms + random glucose >11
2 occasions of abnormal glucose
HbA1c >48 
1 abnormal glucose + abnormal OGTT (>11 at 2 hours)
124
Q

Which HLA groups is diabetes mellitus type 2 associated with?

A

HLA DR3 (3 little pigs and a straw shack)-

HLA DR4- rheum for dad and mum (DM)

125
Q

What are the untypical forms of type 1 and 2 DM?

A

Latent autoimmune diabetes of adults- T1DM onsetting later in life
Mature onset diabetes of the young- T2DM onsetting earlier in life (autosomal D)

126
Q

Features of metabolic syndrome:

A

Central obesity (waist circumference or BMI >30) + 2 of:

1. Hypertension 
   >130/85
2. Insulin resistance 
   DM or fasting glucose >5.5  
3. Low HDL levels
4. Hypertriglyceridaemia
  >1.6 mmol
127
Q

How does tubular dysfunction cause a difference in U+Es results than low eGFR?

A

Tubular dysfunction: low K+, low urate, low phosphate, high H+
May be polyuric with all sorts in the urine

Low eGFR: high K+, high urate, high phosphate, low H+
May be oliguric

128
Q

What pattern of U+Es do thiazides and loop diuretics cause?

A

Low Na+, low K+, high bicarbonate

Thiazide- high Ca in blood (the-HIGH-azide)
Loop diuretics- low Ca (Lowoop)

129
Q

How quickly can potassium be given in a peripheral line?

A

20mmol an hour

But 40mmol per bag max

130
Q

how does ma differ depending on whether someone has osteopenia or osteoporosis?

A

Osteopenia (T score from -2.5 to -1): lifestyle advice
Stop smoking, reduce alcohol
Weight bearing exercise, tai chi, calcium rich diet, OT input at home

Osteoporosis (T score below -2): lifestyle and Rx

131
Q

Causes of osteomalacia:

A

Vit D deficiency or resistance (inheritable)
Renal osteodystrophy
Liver failure- needed to convert Vit D also
Drug induced- anticonvulsants

132
Q

What is Paget’s disease and the complications of it?

A

Increased numbers of osteoclasts and osteoblasts + remodelling causing bone enlargement + deformity.

Asymptomatic 70%
Bony pain + deformity > pathological fractures, osteoarthritis
High Ca
Nerve compression from bone overgrowth (deafness)
High output CCF
Osteosarcoma <1%

133
Q

Rx of Paget’s disease:

A

Analgesia

Bisphosphonates

134
Q

Commonest type of porphyria and how it manifests:

A

Acute intermittent porphyria- autosomal dominant

Neurovisceral symptoms:
Abdo pain, vomiting, constipation, fever, WCC
Peripheral neuropathy, seizures, psychosis
High BP + HR, low BP

135
Q

How do acute and chronic porphyrias present differently?

A

Acute: neurovisceral symptoms with photosensitivity in the less common type (variegate prophyria)

Chronic: cutaneous photosensitivity alone- may have increased facial hair or hyperpigmentation (prophyria cutanea tarda, erythropoeitic protoporphyria)

136
Q

What is the inheritance and cause of primary hyperlipidaemia?

A

Autosomal dominant

Mutations in LDL receptors impairs exchange of LDLs

Heterozygotes- cardiovascular disease

137
Q

What are the four types of primary hypertriglyceridaemia?

A
  1. Familial hypertriglyceridaemia
    Xantomata, high VLDLs
  2. Familial dysbetalipoproteinemia
    Elevated intermediate DLs + chylomicrons
  3. Lipoprotein lipase deficiency
    Chylomicron metabolism
  4. Apo CII deficiency
    Needed to activate lipoprotein lipase
138
Q

What are secondary causes of elevated LDLs?

A

Hypothyroidism
Liver disease
Nephrotic syndrome

Thiazides, glucocorticoids, ciclosporin

139
Q

What are secondary causes of elevated triglycerides?

A

Obesity, diabetes, proegesterone, acute hepatitis

Alcohol, oestrogens, antifungals

140
Q

What are eruptive xanthomata and what do they occur in?

A

Itchy crops of lipid nodules found in primary hypertriglyceridaemia

141
Q

MEN2A+ 2B patients with medullary thyroid cancer have what gene mutation?

A

RET gene mutation- gain of function

MEDICINE NEW (22 decks)

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