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Phase 4 > Endo > Flashcards

Endo Flashcards

1
Q

What is Acromegaly?

A

A disorder of excessive growth hormone

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2
Q

what is the most common cause of acromegaly?

A

Pituitary adenoma - 95%

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3
Q

what is gigantism?

A

excessive GH secretion before epiphyseal closure, during childhood or adolescence leading to increased linear growth

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4
Q

what are 5 rarer causes of acromegaly?

A

Bronchial carcinoid tumour
Lung carcinoids
Pancreatic islet cell tumour
Phaeochromocytoma

Paraneoplastic syndrome due to ectopic growth hormone releasing hormone (GHRH) or growth hormone (GH) secretion

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5
Q

what 2 hormones inhibit the secretion of GH?

A

Dopamine
Somatostatin

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6
Q

what is the pathophysiology of acromegaly?

A

Increased GH => increased glucose release, muscles retain nitrogen causing them to grow => epiphyseal plates fused so can only grow in places where there is still growth => jaw, nose, hands, feet

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7
Q

5 symptoms of acromegaly?

A

Bigger hands, feet and face
excessive sweating
tiredness
weight gain
headache
deep voice/amenorrhoea

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8
Q

6 signs of acromegaly?

A

Bi-temporal hemianopia
spade like hands and feet
large tongue - macroglossia
Jaw protrusion - prognathism
interdental seperation
predominant forehead

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9
Q

what are 6 conditions related to acromegaly?

A

Hypertrophic heart
Hypertension
T2DM
Carpal tunnel syndrome
Colorectal cancer

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10
Q

what is the 1st line investigations for acromegaly?

A

Raised insulin like growth factor 1

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11
Q

What is the gold standard test for acromegaly to comfirm diagnosis after 1st line testing?

A

oral glucose tolerance test

  • in normal patients GH suppressed to <2 with hyperglycaemia
  • no suppression of GH in acromegaly
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12
Q

what scan can be used in acromegaly?

A

MRI pituitary - ?pituitary tumour

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13
Q

What is the 1st, 2nd and 3rd line management for acromegaly?

A

1st line - trans-sphenoidal surgery if pituitary adenoma

2nd line -
- Cabergoline (dopamine agonist)
- Somatostatin analogue (octreotide)
- Pegvisomant - GH receptor antagonist give SC OD

3rd line - Radiotherapy,

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14
Q

What are 5 complications of acromegaly?

A

T2DM
Arthritis and carpal tunnel
Cardiac - cardiomyopathy, heart failure, HTN
Colorectal cancer
Obstructive sleep apneoa

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15
Q

what visual field defect is associated with acromegaly?

A

Bitemporal hemianopia

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16
Q

what is the inheritance pattern for inherited multiple endocrine neoplasia?

A

autosomal dominant

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17
Q

what are the 3 different types of multiple endocrine neoplasia?

A

MEN1
MEN2A
MEN2B

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18
Q

what is the most common presentation of MEN1?

A

hypercalcaemia

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19
Q

what is the most common cancer associated with multiple endocrine neoplasia 1?

A

Pituitary adenoma - 60% of MEN1 patients

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20
Q

what is the cause of MEN1?

A

mutations in MEN1 tumour supressor gene

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21
Q

what is the presentation of multiple endocrine neoplasia (MEN) 1?

A

3Ps

Primary Hyperparathyroidism
Pancreatic neuroendocrine tumour (50%)
Pituitary Adenoma (70%)

Also adrenal and thyroid cancers

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22
Q
A
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23
Q

what causes Addison’s disease?

A

Autoimmune - adrenal gland or 21-hydroxylase antibodies

Also - TB, infectious disease, secondary to HIV infections

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24
Q

What are 4 risk factors for Addison’s?

A

Female
adrenal hemorrhage
autoimmune diseases
HIV/TB

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25
Q

What is the pathophysiology for Addison’s?

A

there is decreased adrenocortical hormones due to either destruction of all 3 layers of the adrenal cortex (GFR) or disruption of hormone synthesis

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26
Q

What are 7 clinical presentations of Addison’s?

A 
Hyper pigmentation
Fatigue and weakness
Weight loss/anorexia
salt craving 
loss of pubic hair (women)
Hypotension and tachycardia
nausea/vomiting
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27
Q

What are 2 investigations for Addison’s?

A

serum electrolytes - low Na+, elevated K+

morning serum cortisol levels - low

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28
Q

what is the gold standard test for Addison’s?

A

Adrenocorticotrophic hormone stimulation test (synacthen’s test) - low

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29
Q

What are 3 differentials for Addison’s?

A

Adrenal suppression due to corticosteroid therapy
haemochromatosis
hyperthyroidism

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30
Q

What is the management for Addison’s?

A

Hydrocortisone

Fludrocortisone

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31
Q

what are 3 complications of Addison’s?

A

Secondary Cushing’s syndrome (too much glucocorticoid replacement)
osteopenia/porosis
treatment related hypertension

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32
Q

What is the prognosis for Addison’s?

A

Replacement therapy for life, non-adherence to treatment is life threatening (generally good adherence due to uncomfortable symptoms with non-adherence)

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33
Q

What is Cushing’s syndrome?

A

the clinical manifestation of pathological HYPERcortisolism

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34
Q

is Cushing’s more common in women or men?

A

women

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35
Q

what are 4 causes of Cushing’s?

A

exogenous corticosteroid exposure (most common)
ACTH secreting pituitary adenoma/carcinoma
adrenal cortisol secreting adenoma/carcinoma (rarer)
gene mutation

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36
Q

What are 4 risk factors for Cushing’s?

A

Exogenous corticosteroid use
pituitary/adrenal adenoma
adrenal carcinoma
small cell lung cancer

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37
Q

What are 7 clinical manifestations of Cushing’s?

A 
facial redness + moon face
hypertension 
stretch marks + acne 
menstrual irregularities
osteoporosis/unexplained fractures
weight gain/central obesity
dorsocervical fat pad - buffalo hump
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38
Q

What are 3 investigations of Cushing’s?

A

late night salivary cortisol - elevated
overnight dexamethasone suppression test - elevated
24 hour urinary free cortisol - elevated

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39
Q

what is the gold standard test for Cushing’s?

A

late night salivary cortisol - elevated

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40
Q

What is the management of Cushing’s?

A

1st line - trans-sphenoidal pituitary adenectomy/ adrenalectomy

adjuncts - post surgery corticosteroid/non-corticosteroid replacement, chemo, radiotherapy on primary tumour

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41
Q

is reoccurrence common with Cushing’s?

A

Yes

untreated survival = 50%

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42
Q

what are 4 complications of Cushing’s?

A

osteoporosis
increased infection
DM
hypertension

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43
Q

What is DMT1?

A

a metabolic autoimmune disorder characterised by hyperglycaemia due to destruction of insulin producing beta cells in the pancreas, results in absolute insulin deficiency.

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44
Q

who is DMT1 most common in?

A

women + young people

5-10% of all diabetes patients

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45
Q

what are 4 risk factors for DMT1?

A

geographic region - N Europe
FHx
Other autoimmune disease
dietary factors

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46
Q

what causes DMT1?

A

autoimmune pancreatic beta cell destruction

subclinical until 80-90% of beta cells have been destroyed

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47
Q

What are 6 clinical manifestations of DMT1?

A 
polyuria + polydipsia + hunger
blurred vision
fatigue/tiredness 
weight loss
FHx of autoimmune disorders 
KETOACIDOSIS
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48
Q

what is the gold standard test for diabetes?

A

HbA1c > 48 mmol/mol

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49
Q

what are 4 tests for DMT1?

A

Random glucose tolerance test (>11.1mmol/L)
Fasting plasma glucose - raised
2-hour plasma glucose - raised
plasma or urine ketones - raised

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50
Q

What is the management of DMT1?

A 
Basal-bolus insulin (insulin glargine s/c)
Pre-meal insulin correction dose
Amylin analogue (pramlintide)

2nd line: fixed insulin dose.

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51
Q

What are 3 side effects of insulin?

A

hypoglycaemia
weight gain
lipodystrophy

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52
Q

What are the 3 microvascular complications of Diabetes?

A

retinopathy
neuropathy
nephropathy

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53
Q

what are 3 macrovascular complications of diabetes?

A

IHD
cerebrovascular disease
peripheral artery disease

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54
Q

what are the legal requirements of a person with DMT1?

A

inform DVLA of insulin use => may not be allowed to drive

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55
Q

what is DMT2?

A

A metabolic disorder of hyperglycaemia due to a combination of insulin resistance and deficiency

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56
Q

when is DMT2 common?

A

populations with affluent lifestyles
older age
male
S asian, Afrocaribbean at greater risk

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57
Q

what causes DMT2?

A

Decreased insulin secretion and/or increased insulin resistance. Associated with obesity, lack of exercise, increase calorie intake and alcohol excess

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58
Q

What are 5 risk factors of DMT2?

A 
Family history (genetics)
increasing age
obesity
poor exercise
ethnicity
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59
Q

what is the pathophysiology of DMT2?

A

post receptor resistance
50% of beta cell mass usually lost => greater amounts of insulin produced by fewer beta cells => hyperglycaemia and lipid excess are toxic to beta cells.

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60
Q

What are 8 clinical manifestations of DMT2?

A 
polyuria, nocturia + polydypsia
weight loss and fatigue 
ketonuria 
glycosuria
acanthosis nigricans - black pigment on nape of neck and axillae 
visual blurring
candida infections
itchy vulva/swollen penis
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61
Q

what are 5 differentials for DMT2?

A 
DMT1
Pancreatitis 
neoplasia of pancreas
acromegaly
Drugs (thiazide diuretics, beta-blockers, immunosuppressives, thyroid hormone)
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62
Q

What is the 1st line management of DMT2?

A

LIFESTYLE

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63
Q

what is the monitoring for DMT2?

A

daily glucose monitoring

annual diabetic review, foot checks

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64
Q

what are 6 complications of DMT2?

A 
Staphylococcal skin infection
retinopathy
erectile dysfunction
peripheral arterial disease
CAD/IHD 
kidney disease
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65
Q

what are 3 contraindications to metformin prescription?

A

heart failure, liver disease, renal disease

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66
Q

What is Grave’s disease?

A

An autoimmune thyroid condition associated with hyperthyroidism and over production of thyroid hormones

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67
Q

are thyroid disorders and cancers more common in men or women?

A

women

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68
Q

what causes Grave’s disease?

A

thyroid hormone overproduction stimulated by TSH receptor antibodies
can be genetic

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69
Q

What are 4 risk factors for Grave’s disease?

A

FHx
Autoimmune disease
Stress
High Iodine intake

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70
Q

What is the pathophysiology for Grave’s disease?

A

TSH receptor autoantibodies cause thyroid hormone hyperproduction as well as thyroid hypertrophy and hyperplasia of thyroid follicular cells resulting in the clinical manifestations of hyperthyroidism and diffuse goiter.

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71
Q

What are 6 clinical presentations of Grave’s disease?

A

Thyroid acropachy - clubbing, and hand swelling
Thyroid bruit
Pretibial myxoedema
Diffuse goitre
Thyroid eye disease
Hyperthyroidism signs - heat intolerance, sweating, tremor

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72
Q

What is the diagnostic test for Grave’s disease?

A

serum TSH receptor antibodies - present

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73
Q

what are 4 differential diagnoses for Grave’s disease?

A

toxic nodular goitre
post-natal thyroiditis
TSH producing pituitary adenoma
Excessive thyroxine

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74
Q

What is the management of Grave’s disease?

A

1 - Carbimazole 15-40mg OD for 4-8 weeks then reduce gradually over 12-18 months

2 - Propylthiouracil 200-400mg OD till euthyroid then reduce over time

3 - radioactive iodine treatment, thyroidectomy

Beta blockers - propranolol 10-40mg T/QDS - for symptom control

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75
Q

what are 2 adverse effects of carbimazole?

A

Acute pancreatitis
Agranulocytosis (also propylthiouracil)

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76
Q

what are 6 complications of graves disease?

A

AF
Pregnancy related issues - miscarriage, prem, thyroid dysfunction of foetus
Sight threatening orbitopathy
Osteoporosis
Congestive heart failure
Thyroid storm

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77
Q

what is thyroid storm?

A

rare but life threatening sudden significant rise in thyroid hormone levels resulting in fever, profuse sweating, diarrhoea, vomiting, delerium, profound weakness, seizure, jaundice, raised HR, BP and temp and eventually coma

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78
Q

what are 4 complications of Grave’s disease?

A

bone mineral loss
AF/congestive heart failure
sight threatening complications
elephantiasis dermopathy

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79
Q

what is Hashimoto’s thyroiditis?

A

an autoimmune-mediated lymphocytic inflammation of the thyroid gland resulting in a destructive thyroiditis with release of thyroid hormone causing transient hyperthyroidism (for 2/3 months) then permanent hypothyroidism

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80
Q

what are 3 risk factors for Hashimoto’s thyroiditis?

A

Female
Autoimmune disease
genetics - Turner’s/Down’s

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81
Q

what antibodies cause Hashimoto’s thyroiditis and what do they do?

A

ant-Thyroid peroxidase antibodies

attack thyroid cells causing fibrosis and the release of stored thyroid hormone causing transient hyperthyroidism for a few months before stores run out and permanent hypothyroidism ensues

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82
Q

what are 3 features of hashimoto’s thyroiditis?

A

Hypothyroidism features
firm non-tender goitre
anti-TPO antibodies

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83
Q

what is the gold standard test for Hashimoto’s thyroiditis?

A

serum ant-Thyroid peroxidase antibodies

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84
Q

what is the management of Hashimoto’s?

A

levothyroxine

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85
Q

what are 3 complications of Hashimoto’s?

A

Atrial fibrillation
IHD/CHF
low risk of developing Grave’s disease

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86
Q

what is the prognosis for Hashimoto’s thyroiditis?

A

Permanent hypothyroidism and treatment with levothyroxine

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87
Q

What is defined as hyperkalaemia?

A

high potassium >6 mol/L

small potassium changes have significant muscular and cardiac effects

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88
Q

what causes hyperkalaemia?

A

high intake and decreased renal excretion

extracellular redistribution of potassium - decreased cell entry/increased cell exit of potassium

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89
Q

what are 4 risk factors for hyperkalaemia?

A

Renal failure
diabetes
adrenal insufficiencies
drugs (ACEi, ARBs, Diuretics, NSAIDs)

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90
Q

what is the pathopysiology of hyperkalaemia?

A 
decreased excretion of potassium due to acute/chronic renal insufficiency 
reduction in plasma aldosterone 
pseudo hypoaldosteroism
congenital adrenal hyperplasia
lupus
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91
Q

what 7 drugs can cause hyperkalaemia?

A 
potassium sparing diuretics
NSAIDs
Trimethoprim/pentamidine
ACEi/ARBs
heparin
calcineurin inhibitors - ciclosporin
loop/thiazide type diuretics
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92
Q

what are the clinical manifestations of hyperkalaemia?

A 
muscle weakness
ECG changes
ascending paralysis
SOB
chest pain, nausea and vomiting
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93
Q

what ECG changes are present in hyperkalaemia?

A 
tall peaked (tented) T waves
prolonged PR interval (>0.2s)
loss of P wave 
widened QRS complex
ST segment depression
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94
Q

What are the 4 investigations for hyperkalaemia?

A

Basic metabolic panel (serum potassium, glucose, bicarb, urea, and creatinine)
serum calcium
FBC
ECG

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95
Q

what are 6 differential diagnoses for hyperkalaemia?

A 
CKD/acute kidney failure
diabetic ketoacidosis/HHS
drug related hyperkalaemia 
potassium supplementation + underlying renal dysfunction 
renal tubular acidosis
Addison’s disease
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96
Q

what is given in a hyperkalaemic emergency?

A

IV calcium gluconate/chloride

insulin/glucose infusion

nebulised salbutamol

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97
Q

what is a complication of hyperkalaemia?

A

life threatening arrhythmias

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98
Q

what is given in non-emergency hyperkalaemia?

A

patiruer and sodium ziconium cyclosilicate

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99
Q

What is the pathophysiology of Hyperosmolar Hyperglycaemic state?

A

Hyperglycaemia drives osmotic diuresis leading to fluid and electrolyte loss
Due to small amounts of insulin present lipolysis does not occur hence no ketoacidosis

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100
Q

what are 5 key features of HHS?

A

Hyperglycaemia
Hyperosmolality (>320 mosmol/Kg)
Dehydration
Electrolyte abnormalities
WITHOUT Ketoacidosis

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101
Q

what are 3 risk factors for HHS?

A

Infection
MI
Poor medication compliance

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102
Q

what are 5 clinical manifestations for HHS?

A

Weakness and leg cramps
Reduced GCS, confusion, lethargy, headache, seizure
polyuria/oliguria + polydipsia
Nausea, Vom ,abdo pain
Dehydration - tachy, hypotension, dry

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103
Q

what are the four 1st line investigations for HHS

A

Serum/urine glucose
U+Es
ABG
Blood/urinary ketones

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104
Q

what is the gold standard test for HHS?

A

serum osmolality - raised

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105
Q

How can serum osmolarity be calculated?

A

2(Na+) + Glucose + Urea

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106
Q

what is the diagnostic criteria for HHS?

A

Hyperglycaemia >30 mmol/L
Hyperosmolality >320 mOsmol/Kg
Hypovolaemia

NO hyperketonaemia
NO acidosis (pH >7.3, Bicarb >15)

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107
Q

what is the management for HHS?

A

1st line - fluid replacement (0.9% saline), potassium replacement if low

adjuncts - LMWH, restore electrolyte loss, insulin if needed

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108
Q

when should insulin be given in HHS?

A

only IF blood glucose stops falling with IV fluids alone

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109
Q

How slowly should plasma sodium fall in HHS?

A

no quicker than 10 mmol/24 hours

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110
Q

How quickly should plasma glucose fall in HHS?

A

4-6 mmol/hour

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111
Q

what are 4 complications of HHS?

A

CV - VTE, arrythmias, MI
Neuro - stroke, seizure
Renal - AKI
Iatrogenic - cerebral oedema/cerebral pontine myelinolysis

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112
Q

what are 5 causes of hyperthyroidism?

A

Grave’s disease (most common)
Toxic multinodular goitre
Thyroiditis
Thyroid cancer
subacute thyroiditis (granulomatous or De Quervain’s)

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113
Q

what are 8 risk factors for hyperthyroidism?

A

female
post-partum
60+
FHx
autoimmune diseases
radiation
lithium therapy
smoking

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114
Q

What are 5 symptoms of hyperthyroidism?

A

Heat intolerance/sweating
palpitations/tremor
irritability
menstrual irregularities/sexual dysfunction
Goitre

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115
Q

what are 5 signs of hyperthyroidism?

A

orbitopathy (Grave’s)
cardiac flow murmur (thyroid bruit)
scalp hair loss
acropachy (Grave’s)
weight loss

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116
Q

what is the gold standard investigation for hyperthyroidism?

A

serum free total T3/4

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117
Q

what are 3 investigations for hyperthyroidism?

A

TSH - high/low
TSH receptor antibodies - present in Graves
Serum free/total T3/T4 - high

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118
Q

what are 6 causes of primary hyperthyroidism?

A

Graves - most common
Toxic multinodular goitre
Toxic adenoma
Subclinical hyperthyroidism
Thyroiditis - de quervains, hashimotos, post partum
Drugs - amiodarone, lithium

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119
Q

what is toxic multinodular goitre?

A

Several autonomously functioning thyroid gland nodules resulting in hyperthyroidism - often benign but can be malignant

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120
Q

what are 3 causes of secondary hyperthyroidism?

A

Pituitary adenoma - secreting TSH
Ectopic tumour - hCG secreting tumour (choriocarcinoma)
Hypothalamic tumour

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121
Q

what is hypokalaemia?

A

serum potassium <3.5 mol/L

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122
Q

what can cause hypokalaemia?

A

GI losses - D+V, malabsorption, oral sodium phosphate solution
decreased intake
increased potassium entry into cells (increased pH, insulin etc)
increased potassium excretion (GI, burns, sweat)
Dialysis

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123
Q

what are 5 clinical manifestations of hypokalaemia?

A 
muscle weakness, cramps and pain
ECG changes and cardiac arrhythmia 
rhabdomyolysis
renal abnormalities 
psychological symptoms
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124
Q

what ECG changes are seen in hypokalaemia?

A

U waves
flattening and inversion of T waves (mild)
Q-T interval prolongation
mild ST depression (severe)

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125
Q

what are 4 investigations in hypokalaemia?

A

basic metabolic panel
ECG
U+E + creatinine levels
urine electrolytes

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126
Q

what are 4 differentials for hypokalaemia?

A

vomiting and diarrhoea
diabetic ketoacidosis
drug/alcohol induced
primary aldosteronism

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127
Q

what is the management of hypokalaemia?

A

oral/IV potassium replacement (KCl)

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128
Q

what are 2 complications of hypokalaemia?

A

severe muscle weakness

paralysis

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129
Q

what can cause hypoparathyroidism?

A

post-surgery
genetic and autoimmune conditions - (di george syndrome)
iron and copper overload (haemochromatosis or Wilson’s disease)
idiopathic
Prolonged hypomagnesaemia can suppress PTH

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130
Q

what are 3 risk factors for hypoparathyroidism?

A

thyroid/parathyroid surgery, hypomagnesianism, transfusional iron overload (in thalassaemia)

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131
Q

what does parathyroid hormone do? (3)

A

Acts to increase serum calcium:

Increase renal calcium absorption and phosphate excretion

Increased production of 1,25-dihydroxyvitamin D in kidney

Increase bone calcium resorption

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132
Q

what is normal serum calcium?

A

2.2-2.6 mmol/L

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133
Q

what is the physiology of the parathyroid gland?

A

Chief call produce parathyroid hormone and store it in secretory granules

Serum calcium is detected by calcium sensing receptors on the cell surface which control the release of PTH

Higher serum calcium inhibits PTH release and low calcium leads to more PTH release

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134
Q

what is the physiology of PTH in bone?

A

increases activity and number of osteoclasts leading to calcium and phosphate release from the bone

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135
Q

What is the physiology of parathyroid action on the kidney? 3

A

1 - Stimulates calcium reabsorption in distal CT and collecting duct

2 - Decreases phosphate reabsorption in proximal CT

3 - stimulates conversion of 25-hydroxyvitamin D into the active for 1,25-dihydroxyvitamin D (CALCITRIOL)

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136
Q

what is the activation pathway of vitamin D?

A

Dietary vitamin D

Converted to 25-hydroxyvitamin D by liver 25-hydroxylase enzyme

Converted to 1,25-dihydroxyvitamin D in kidney by 1-hydroxylase enzyme

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137
Q

what is the name of the active form of vitamin D?

A

1,25-duhydroxyvitamin D

CALCITRIOL

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138
Q

How does active vitamin D (calcitriol) affect calcium, phosphate and parathyroid? 3

A

Increases calcium and phosphate absorption in small intestine

Increases calcium and phosphate reabsorption in kidneys

Inhibits PTH release through negative feedback

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139
Q

what is calcitonin?

A

a hormone excreted by thyroid parafollicular (C-cells) that acts opposite to PTH

Inhibits osteoclast activity in bone
inhibits calcium reabsorption in kidneys

140
Q

How does high phosphate affect calcium?

A

Phosphate ions bind to calcium ions to become calcium phosphate which the amount of free calcium in the blood

Lower phosphate leads to higher serum calcium

141
Q

What are 3 GI presentations of hypoparathyroidism?

A

malnutrition
malabsorption
diarrhoea

142
Q

what are 6 presentations of hypoparathyroidism?

A

muscle twitches/spasms
parasthesia, numbness and tingling
convulsions
irregular heartbeat
tachycardia
Trousseau’s and Chvostek’s signs

143
Q

what are the two examination signs for hypocalcaemia?

A

Trousseau’s sign – involuntary wrist spasm causing adduction of thumb, flexion of MCP joints and extension of interphalangeal joints with wrist flexion (Italian hand) when inflating BP cuff

Chvostek’s sign – twitching of facial muscle due to tapping over facial nerve (parotid)

144
Q

What are 3 differentials for hypoparathyroidism?

A

hypovitaminosis D
hypomagnaesaemia
renal failure/CKD

145
Q

a deficiency of what mineral exacerbates hypocalcaemia?

A

magnesium

146
Q

what are 3 complications of hypoparathyroidism?

A

Renal stones
Ectopic calcifications
Renal failure
Cataracts
arrythmia, cardiac arrest, tetany, death

147
Q

What are 5 investigations for hypoparathyroidism?

A

PTH
Calcium
phosphate
magnesium
Vitamin d

ECG - Long QT

148
Q

what are the 2 forms of thyroid hormone?

A

Triiodothyronine - T3
Thyroxine - T4

149
Q

what is the physiology of the thyroid gland?

A

Hypothalamus produces TRH

TRH stimulates anterior pituitary to secrete TSH

Thyroid gland produces T4+T3 in response to TSH by oxidising iodide to iodine and adding it onto tyrosine residues on thryroglobulin using thyroid peroxidase (TPO)

Most T3/4 is bound to thyroglobulin, only free T3/4 is active

Free thyroid hormones act on hypothalamus as -ve feedback

150
Q
A
151
Q

which thyroid hormone is produced more?

A

T4 > T3

Free T4 more reliable indicator of thyroid function on testing

152
Q

what is the half life of T4?

A

1 week - need to wait a few weeks before retesting T4

153
Q

what is primary hypothyroidism?

A

due to pathology affecting the thyroid gland (hashimotos) OR iodine deficiency

154
Q

what is secondary hypothyroidism?

A

due to pathology affecting the pituitary - pituitary apoplexy or tumour - OR hypothalamic disorders and drugs

155
Q

What are 6 causes of primary hypothyroidism?

A

Hashimotos (most common cause in developed world)
iodine deficiency
De Quervain’s thyoiditis
Post-partum thyroiditis
Riedel’s thyroiditis
Thyroidextomy/radiation
Drugs - amiodarone, lithium, antithyroid drugs (carbimazole)

156
Q

what is De Quervain’s thyroiditis?

A

Subacute thyroiditis occurring after viral infection

Phase 1 - 3-6 weeks of hyperthyroidism, painful goitre, raised ESR
phase 2 - 1-3 weeks euthyroid
phase 3 - weeks to month - hypothyroidism
phase 4 - back to normal

157
Q

what is seen on thyroid scintigraphy in de Quervain’s thyroiditis?

A

globally reduced uptake of iodine-131

158
Q

what are 5 causes of secondary hypothyroidism?

A

Tumours - pituitary adenoma
Surgery to pituitary
radiotherapy
Sheehan syndrome - major PPH causes avascular necrosis of pituitary
Trauma

159
Q

what are 3 drugs that can inhibit TSH secretion?

A

Cocaine
Steroids
Dopamine

160
Q

what are 7 risk factors for hypothyroidism?

A

Female
Middle age
Post-partum
radiotherapy
Autoimmune conditions - T1DM, coeliac
Genetic disorders - turners, downs
FHx

161
Q

What are 8 presentations of hypothyroidism?

A

lethargy
constipation
weight gain
dry/coarse skin and hair
bradycardia
Goitre
cold sensitivity
Menorrhagia, oligomenorrhoea and amenorrhoea

162
Q

what are 3 initial investigations for hypothyroidism?

A

Thyroid function tests - TSH increased and T3/4 low in primary, both low in secondary

Antibody tests - Anti-TPO in hashimotos

Inflammatory markers - raised in De Quervain’s thyroiditis

163
Q

what is the first line management of hypothyroidism?

A

levothyroxine 50-100mcg OD starting dose

Review every 3 months initially then annually once stable

start on 25 mcg OD in >64 or Hx of IHD

164
Q

What 2 drugs reduce absorption of levothyroxine?

A

Iron
alcium carbonate

should take >4 hours apart

165
Q

what happens to thyroxine demand in pregnancy?

A

Higher demand => dose usually increased 25-50 mcg

166
Q

what are 5 complications of hypothyroidism?

A

CVD - hypercholesterolaemia
Neruo - carpal tunel, peripheral neuropathy
Myxoedema coma - confusion, hypothermia, hypoglycaemia, hypoventilation, hypotension
Increased risk of lymphoma

167
Q

what is subclinical hypothyroidism?

A

Elevated TSH but normal T4 levels - can cause or not cause symptoms

requires regular monitoring

TSH >10 + T4 normal - consider thyroxine

TSH 5.5-10 and T4 normal - consider 6 month trial of thyroxine in <65 years

168
Q

What is phaeochromacytoma?

A

A tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla

169
Q

what are 4 side effects of thyroxine?

A

Hyperthyroidism
AF
Osteoporosis
Angina

170
Q

where can phaeochromacytomas be?

A

either in chromatin cells of adrenal medulla (90%) or extra-adrenal

171
Q

what are 4 risk factors for phaeochromacytomas?

A

MEN syndrome 2A/B
Von Hippel-Lindau syndrome
neurofibromatosis type 1
succinate dehydrogenase subunit B/D gene mutation

172
Q

what enzyme converts adrenaline and noradrenaline to their inactive forms? what are their inactive forms?

A

catechol-O-methyltransferase (COM)

metanephrine and normetanephrine

173
Q

are extra-adrenal phaeochromacytomas more common in children or adults and are they more likely to be malignant or not?

A

Children

more likely to be malignant

174
Q

what are 6 key presentations of phaeochromacytomas?

A 
headache 
palpitations
diaphoresis (sweating)
hypetension
impaired glucose tolerance 
panic attacks and sense of doom
175
Q

What are 4 investigations that can be done for phaeochromacytomas?

A

24 hour urine collection of catecholamines, metanephrines, normeanephrines and creatinine - elevated
serum free metanephrines and normetanephrines
plasma catecholamines
genetic testing

176
Q

what are 4 differentials of phaeochromacytomas?

A

anxiety and panic attacks
essential hypertension
hyperthyroidism
cardiac arrhythmias

177
Q

what is the management of phaeochromacytomas?

A 
control hypertension 
alpha blockers (phenoxybenzamine)
beta blockers 
calcium channel blockers 
high salt diet
surgical removal of tumour
radiation/ablation of tumour
178
Q

what are 4 complications of phaeochromacytomas?

A

hypertensive crisis
MI
hypotension
neurological complications

179
Q

what are 3 risk factors for pituitary adenomas?

A

MEN-1
familial associated pituitary adenoma
Carney complex

180
Q

What are 4 key presentations of pituitary adenomas?

A

compressive effects - headache, bitemporal hemianopia, cranial nerve palsy, DI
Cushing’s
Acromegaly
Prolactinoma - galactorrhea, lack of libido, erectile dysfunction

181
Q

What are 5 investigations that can be done in pituitary adenomas?

A 
MRI
testosterone/oestrodiol levels (low)
Morning cortisol - Low
TSH and free thyroxine - low
prolactin - may be elevated
182
Q

what are 3 differentials for pituitary adenomas?

A

infection
meningioma
rathke’s cleft cyst

183
Q

what is the management of pituitary adenomas?

A 
transsphenoidal surgery 
observation 
hormone replacement 
radiotherapy
dopamine agonist
184
Q

what are 3 complications of pituitary adenomas?

A

meningitis
Diabetes insipidus
hypopituitarism

185
Q

what is primary hyperparathyroidism?

A

Excess secretion of PTH leading to hypercalcaemia

usually due to a parathyroid adenoma

186
Q

what causes primary hyperparathyroidism?

A

80% due to benign parathyroid adenoma

Genetics -
MEN1/2A/4 , hyperparathyroidism jaw tumour syndrome, familial isolated primary hyperparathyroidism

<1% due to parathyroid malignancy

187
Q

what are 4 risk factors for primary hyperparathyroidism?

A

female
Older age - >50-60
FHx
MEN 1/2A/4

188
Q

what is the pathophysiology of primary hyperparathyroidism?

A

PTH is inappropriately not suppressed in normal or high calcium levels leading to over stimulation of bone resorption, kidney absorption and vitamin D conversion causing calcium levels to rise

189
Q

What are the 4 clinical presentations of primary hyperparathyroidism?

A

Most commonly asymptomatic

Symptoms of hypercalcaemia - bones, stones, moans, groans

Polyuria, parasthesia, muscle cramps

190
Q

what are 3 investigations of primary hyperparathyroidism?

A

Serum calcium
Serum PTH
Kidney function tests - CKD can lead to secondary/tertiary hyperparathyroidism
Vitamin D

US neck
Sestamibi scan
4D CT neck

191
Q

what are 4 differentials for primary hyperparathyroidism?

A

secondary/tertiary hyperparathyroidism

familial hypocalciuric hypercalcaemia

Malignancy - multiple myeloma

medications - thiazides

192
Q

what is the management of primary hyperparathyroidism?

A

1 - parathyroidectomy, monitoring

Calcitonin
Cinacalcet - mimics calcium to cause negative feedback
Desunomab
Bisphosphonates

193
Q

what are 4 complications of primary hyperparathyroidism?

A

Osteoporosis + fractures
Kidney stones and injury
Hypertension and CVD
GI disorders - peptic ulcers, pancreatitis, gall stones

194
Q

what are 4 indications for parathyroidectomy in primary hyperparathyroidism?

A

Symptomatic disease - hypercalcaemia, osteoporosis, renal stones
>50 years
serum calcium >2.85
eGFR <60

195
Q

what is secondary adrenal insufficiency?

A

decreased cortisol production as a result of negative feedback on the hypothalamic-pituitary-adrenal axis, caused by excess glucocorticoids

196
Q

what kind of patients is secondary adrenal insufficiency common in?

A

those treated with glucocorticoids - asthma, COPD, arthritis

197
Q

what 3 causes of secondary adrenal insufficiency?

A

exogenous glucocorticoids
glucocorticoid secreting adrenal adenomas
hypothalamic pituitary disease

198
Q

what are 2 risk factors for secondary adrenal insufficiency?

A

glucocorticoids

medroxyprogesterone use

199
Q

what is the pathophysiology of secondary adrenal insufficiency?

A

Exposure to excess glucocorticoids => negative feedback to hypothalamus-pituitary-adrenal axis => patients may have Cushing’s symptoms due to excess glucocorticoids

200
Q

What are 5 clinical presentations of secondary adrenal insufficiency?

A

tachycardia
hypotension
Cushingoid examination features
shock - fatigue, abdo pain, weakness, vomiting, hypotension

201
Q

What are 5 investigations for secondary adrenal insufficiency?

A

serum chemistry panel - electrolyte abnormalities
serum a.m cortisol - low
salivary am cortisol - low
FBC - WBCs may be elevated
thyroid function test - possible elevated free thyroxine

202
Q

what is the gold standard test for secondary adrenal insufficiency?

A

ACTH stimulation test - cortisol levels won’t rise enough in secondary adrenal insufficiency

203
Q

what are 4 differentials for secondary adrenal insufficiency?

A

primary adrenal insufficiency
pituitary compression
tumour
head trauma

204
Q

what is the treatment for primary adrenal insufficiency ?

A

hydrocortisone - in crisis
double dose corticosteroid in minor crisis
corticosteroid taper in stable patients
supportive measures

205
Q

what are 2 complications of primary adrenal insufficiency?

A

corticosteroid dependence

permanent recurrence of adrenal crisis

206
Q

What is syndrome of inappropriate ADH?

A

Continues secretion of ADH despite plasma being very dilute leading to retention of water, excess blood volume and hyponatraemia

207
Q

what is the most common electrolyte disorder?

A

hyponatraemia

208
Q

What can cause SIADH?

A 
neuro - meningitis, stroke, trauma 
Malignancy - small cell most commonly 
infections - TB, HIV, pneumonia
endocrine 
Drugs - chemo, antidepressants, recreational, diuretics, ACEI, SSRIs
209
Q

what are 6 risk factors for SIADH?

A

50+
pulmonary conditions
malignancy
Drugs

210
Q

what are 6 clinical manifestations of SIADH?

A 
altered mental status
seizures
coma 
nausea, vomiting, headache
absence of hypovolaemia
211
Q

what are 5 investigations for SIADH?

A 
Serum sodium - low
Serum osmolality - low
serum urea - usually low
urine osmolality - high
urine sodium - high
212
Q

what are 4 differentials for SIADH?

A

psudohyponatraemia due to hyperglycaemia
hyperlipidaemia
renal failure
Addison’s disease

213
Q

what is the plasma osmolality equation?

A

plasma osmolality = 2 (Na+) + 2(K+) + glucose + urea (all in mol/L)

214
Q

what is the management for SIADH?

A

1st - IV hypertonic saline, vasopressin receptor antagonist (vaptans)

adjuncts - frusomide, treat underlying

215
Q

what is a complication of SIADH?

A

central pontine myelinolysis

216
Q

what can cause central pontine myelonolysis?

A

rapid sodium serum correction >12mEq/L/Day

217
Q

what is the most common endocrine malignancy?

A

thyroid cancer

218
Q

when is thyroid cancer most common?

A

early adulthood - 30s-40s

219
Q

what are the 4 most common thyroid cancers?

A

papillary
follicular
anapaestic
medullary

220
Q

what are 3 risk factors for thyroid cancer?

A

head and neck irradiation
female
FHx

221
Q

What are 6 presentations of thyroid cancer?

A 
palpable thyroid nodule 
hoarse voice
dyspnoea  (SOB)
dysphagia 
rapid neck enlargement 
tracheal deviation
222
Q

what are 4 investigations for thyroid cancer?

A

Thyroid function test
Neck ultrasound - nodules
fine needle biopsy
larangoscopy

223
Q

what are 2 differentials for thyroid cancer?

A

benign thyroid nodule

goitre

224
Q

what is the management of thyroid cancer?

A

surgery - lobectomy
radioactive iodine ablation
TSH suppression
chemo

thyroid replacement after

225
Q

what are 4 complications of thyroid cancer?

A

hypocalcaemia (parathyroid injury)
airway obstruction
recurrent laryngeal nerve injury
secondary tumours

226
Q

where is erythropoietin produced and what does it do?

A

kidneys (peritubular cells)

stimulates maturation of erythrocytes

227
Q

What is the blood supply to the adrenal glands?

A

superior adrenal artery - from inferior phrenic
middle adrenal artery - from abdominal aorta
inferior adrenal artery - from renal artery

228
Q

what does the zone glomerulosa produce?

A

Mineralocorticoids - ALDOSERONE

229
Q

what does the zona fasiculata produce?

A

Glucocorticoids - CORTISOL

230
Q

what does the zona reticularis produce?

A

ANDROGENS

231
Q

what are corticosteroids?

A

mineralocorticoids + glucocorticoids (aldosterone + cortisol)

232
Q

what do mineralocorticoids do?

A

regulate body electrolytes

aldosterone - maintain salt balance, BP, RAAS

233
Q

what triggers the secretion of aldosterone?

A

release of renin by juxtaglomerular cells in afferent arterioles of kidneys

234
Q

what is the function of cortisol?

A

suppresses immune system
inhibits bone formation
increases metabolism - protein catabolism & lipolysis, gluconeogenesis, increases alertness.

235
Q

what triggers secretion of cortisol?

A

stress => hypothalamus => corticotrophin releasing hormone (CRH) => anterior pituitary => adrenocorticotropic releasing hormone (ACTH) => cortisol release from adrenal cortex

236
Q

what does adrenaline release stimulate?

A 
gluconeogenesis 
lipolysis 
tachycardia
redistribution of circulating volume
vasoconstriction
vasodilation (due to less noradrenaline)
237
Q

what vertebral level is the thyroid located at?

A

C5-T1

238
Q

what is the connection called in the thyroid?

A

isthmus

239
Q

what arteries supply the thyroid?

A

superior and inferior thyroid arteries

240
Q

what week in utero does thyroxine begin to be releases?

A

18-20 weeks

241
Q

what is produced in the parafolicular cells/ C cells?

A

calcitonin

242
Q

what is produced in the follicular cells of the thyroid?

A

T3 and T4

243
Q

what does the follicle of the thyroid contain?

A

thyroglobulin - iodine store

244
Q

what embryological tissue is the anterior pituitary formed from?

A

Ectoderm - Rathke’s pouch

245
Q

what embryological tissue if the posterior pituitary formed from?

A

floor of the 3rd ventricle

246
Q

what 6 hormones are released by the hypothalamus?

A 
corticotropin releasing hormone - CRH 
GHRH
thyrotropin releasing hormone - TRH
Gonadatrophin releasing hormone - GnRH 
Dopamine
247
Q

what 6 hormones are released by the anterior pituitary?

A

FSH - follicle stimulating hormone
LH - luteinizing hormone
Adrenocorticotrophic hormone - ACTH
TSH - thyroid stimulating hormone
Prolactin
Growth Hormone

FLAT PG

248
Q

What 2 hormones are released from the posterior pituitary?

A

Anti-diuretic hormone

Oxytocin

249
Q

Where in the brain is the ADH release stimulated from in the brain?

A

supraoptic nucleus

250
Q

Where in the brain is the oxytocin release stimulated from in the brain?

A

paraventricular nucleus

251
Q

what do delta cells in the pancreas release?

A

somatostatin

252
Q

What is thyroid storm?

A

A rare but life threatening condition of untreated thyrotoxicosis (hyperthyroidism) causing irritability, high systolic and low diastolic BP, tachycardia, nausea, vomiting and diarrhoea

253
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism causing excessive sodium reabsorption leading to hypertension and suppression of angiotensin II.

254
Q

what are 2 causes of Conn’s syndrome?

A

genetics

adrenal adenoma

255
Q

what are 2 risk factors for Conn’s syndrome?

A

FHx

FHx of early onset hypertension/stroke

256
Q

What is the pathophysiology of Conn’s syndrome?

A

Aldosterone producing adenoma => Excessive aldosterone production => increased sodium absorption from distal tubule => if severe hypokalaemia and metabolic acidosis

257
Q

what are 6 clinical manifestations of conns syndrome?

A 
refractory hypertension
hypokalaemia  
nocturia/polyuria 
lethargy
muscle weakness/cramps 
difficulty concentrating and mood disturbances
258
Q

what are 3 investigations for Conn syndrome?

A

aldosterone:renin ratio - low
adrenal CT
U+E - hypokalaemia

259
Q

what are 3 differentials for conn syndrome?

A

essential hypertension
Liddle syndrome
renal artery stenosis

260
Q

what is the treatment of Conn syndrome?

A

aldosterone antagonist - spironolactone

Adrenalectomy

261
Q

what are 2 complications of conn syndrome?

A

hyperkalaemia and metabolic alkalosis

perioperative complications - stroke, MI, heart failure, AF

262
Q

what are the normal levels of blood glucose?

A

3.5-8 mmol/L

263
Q

how much glucose is prodded every day?

A

200g

264
Q

what organ is the major consumer of glucose in the body?

A

the brain

265
Q

what are 3 hormones that increase glucose production in live and reduce utilisation in fat and muscle?

A

cortisol
adrenaline
GH

266
Q

what chromosome codes for insulin?

A

11

267
Q

what peptide isn’t present in synthetic insulin?

A

C peptide

268
Q

what transported proteins allow beta cells to sense glucose levels in the blood?

A

GLUT 2

269
Q

what is a diagnostic random blood glucose value for diabetes?

A

> 11 mmol/L

270
Q

what is a diagnostic fasting blood glucose level for diabetes?

A

> 7 mmol/L

271
Q

what is a diagnostic oral glucose tolerance test level for diabetes?

A

> 11 mmol/L

272
Q

what is the name of a basal insulin?

A

Levemir

273
Q

what is the name of a bolus insulin?

A

Humalog

274
Q

what is the leading cause of death in diabetic patients?

A

CVD

275
Q

what is the 1st line treatment for DMT2 with HbA1c >48 mmol/mol?

A

Metformin

276
Q

above what HbA1c level is metformin 1st line in DMT2?

A

48

277
Q

what are 4 side effects of metformin?

A

anorexia
diarrhoea
nausea
abdominal pain

278
Q

what vertebral levels are the thyroid glands located between?

A

C5-T1

279
Q

what is the connection between the 2 lobes of the thyroid gland called?

A

isthmus

280
Q

what 3 disease have diffuse goitres?

A

Grave’s
Hashimotos
De Quervain’s

281
Q

What 3 conditions have nodular goitres?

A

Multi-nodular
Adenomas/cysts
Carcinomas

282
Q

what is the most common type of thyroid carcinoma?

A

papillary

283
Q

what is thyrotoxicosis?

A

clinical manifestation of excess thyroid hormone action at the tissue level due to high circulating thyroid hormone concentrations.

284
Q

what is the antibody is grave’s disease?

A

Anti TSH antibody

285
Q

what is the treatment of a thyroid storm?

A

IV fluids
antithyroid drugs - Propylthiouracil/carbimazole
IV hydrocortisone
B Blockers

286
Q

what thyroid disorder has raised inflammatory markers?

A

De Quervain’s

287
Q

what 3 things does ACTH stimulate the release of from the adrenals?

A

mineralocorticoids
glucocorticoids
gonadocorticoids

288
Q

what does the zone glomerulosa respond to?

A

RAAS system

289
Q

what is the action of aldosterone?

A

works on kidney to increase blood volume, increase BP. May also cause hypernatraemia.

290
Q

what is the action of cortisol?

A

suppresses immune system, inhibits bone formation, increases metabolism - protein catabolism & lipolysis, gluconeogenesis, increases alertness.

291
Q

what is the action of gonadocorticoids?

A

production of oestrogen and testosterone. Main role is controlling libido.

292
Q

when are cortisol levels at their highest?

A

7-9 am

293
Q

what hormone inhibits GH secretion?

A

somatostatin

294
Q

what hormone stimulates the release of GH?

A

Ghrelin

295
Q

what is an adrenal crisis?

A

acute insufficiency of adrenocortical hormones usually caused by infection or MI causing hypotension, shock and coma

296
Q

what is the management for an adrenal crisis?

A

IV fluids
Corticosteroids - hydrocortisone IV
treat underlying cause

297
Q

what is diabetes insipidus?

A

a metabolic disorder characterised by an absolute or relative inability to concentrate urine, resulting in the production of large quantities of dilute urine.

298
Q

what are 3 nephrogenic causes of DI?

A

drugs
genetics
intrinsic kidney disease

299
Q

what are 3 cranial causes of DI?

A

brain tumours
infections
TRAUMA

300
Q

what are 3 risk factors for DI?

A

pituitary surgery
brain injury
autoimmune disease

301
Q

what are 5 manifestations of DI?

A 
postural hypotension 
hypernatraemia 
polyuria
polydipsia 
dehydration
302
Q

what is the gold standard investigation for DI?

A

water deprivation desmopressin suppression test

303
Q

what are 3 first line investigations for DI?

A

U+E - hypernatraemia
Serum glucose
urine osmolality - low

304
Q

what are 3 differentials for DI?

A

DM
hypercalcaemia
primary polydipsia

305
Q

what are 2 management options for DI?

A 
desmopressin (if cranial)
thiazide diuretics (bendroflumethiazide) - encourages kidneys to take up more Na+ and thus water
306
Q

what are the 2 most common causes of hypercalcaemia?

A

Primary hyperparathyroidism - most common

Malignancy

307
Q

what are 3 reasons malignancy can cause hypercalcaemia?

A

PTH related hormone released from tumours - small cell lung cancer, breast, renal

Bony mets

Multiple Myeloma - due to increased osteoclastic bone resorption

308
Q

what are 7 other causes of hypercalcaemia?

A

Sarcoidosis (also other granulomas)
Vitamin d intoxication
acromegaly
thyrotoxicosis
Drugs - thiazides, calcium containing antacids
Dehydration
Addison’s disease

309
Q

what are 5 manifestations of hypercalcaemia?

A

Bones, Stones, Groans Moans

Bone pain

Renal stones

GI groans - nausea, vom, constipation, anorexia

Psychic moans - confusion, lethargy, coma

also HTN, short QT and cardiac arrhythmias

310
Q

what may be seen o/e in hypercalcaemia?

A

Dehydration
Hypertonia or hyporeflexia
Bone tenderness/deformity
Abdo pain/tenderness
Psychiatric abnormalities

311
Q

what is a differential for hypercalcaemia?

A

hyperalbuminaemia

312
Q

what are the 3 classifications of hyperparathyroidism?

A

Primary - due to hyperparathyroidism or malignancy usually - due to excessive PTH release leading to increased calcium reabsorption

Secondary - occurs in response to hypocalcaemia usually due to CKD, leads to parathyroid hyperplasia

Tertiary - parathyroid glands become autonomous and secrete PTH despite normal/high calcium due to persistent parathyroid hyperplasia

313
Q

what is the management for hypercalcaemia?

A

Rehydration
Bisphosphonates

Corticosteroids - if due to granulomatous disease or lymphomas
Calcitonin
Loop diuretics - furosemide
Dialysis

314
Q

what are 4 causes of hypocalcaemia with hyperphosphataemia?

A

CKD
hypoparathyroididsm
pseudohypoparathyroidism
acute rhabdomyolysis

315
Q

what are 4 causes of hypocalcaemia with normal phosphate?

A

vitamin D deficiency
osteomalacia
acute pancreatitis
over hydration

316
Q

what are 8 manifestations of hypocalcaemia?

A

SPASMODIC

Spasms - troussau’s
Paraesthesia
anxious
seizures
Muscle tone increase
Orientation impaired
Dermatitis
Impetigo herpetiformis
Chvosteks sign - facial muscle twitches after facial nerve tapped

317
Q

what are the ECG signs of hypocalcaemia?

A

prolonged QT

ST
arrhythmia
torsade de pointes
AF

318
Q

what is the management for hypocalcaemia?

A

IV calcium suplements - calcium gluconate
10ml in 100ml NaCl over 10-20 mins
Then slow IV 10% 50ml/hour

vitamin D supplements - alfacalcidol

319
Q

what are 5 manifestations of neuroendocrine tumours?

A

diarrhoea
SOB
flushing
itching
RUQ pain - hepatic metastases

Worsened by ALCOHOL

320
Q

how is insulin secreted?

A

hyperglycaemia leads to increased glucose uptake by cells/. Glucose metabolism leads to increased levels of ATP within the cell which causes K+ channels to close leading to the depolarisation of the cell membrane. Ca2+ channels open and calcium enters the cell. Increased calcium leads to exocytosis of insulin containing vesicles so insulin is released from the pancreatic beta cells into the blood stream.

321
Q

What part of the adrenal glands are the different adrenal hormones secreted from?

A

GFR Makes Good Sex

Zona Glomerulosa - Mineralocorticoids - Aldosterone

Zona Fasiculata - Glucocorticoids - Cortisol

Zona Reticularis - Androgens - testosterone, dihydrotestosterone

322
Q

what is used for the diagnosis of toxic multinodular goitre?

A

Clinical features
TFTs - low TSH, raised T3/4

Radioisotope scan - multiple hot and cold areas

323
Q

what is the management of toxic multinodular goitre?

A

1 - Radioactive iodine

2 - Thyroidectomy

324
Q

what are 4 contraindications and 3 cautions with radioactive iodine treatment?

A

Contraindication
- pregnancy
- <16 years
- breastfeeding
- established eye disease

Caution
- no close contact with pregnant women and children for 3 weeks
- Avoid pregnancy for 6 months
- Avoid fathering children for 4 months

325
Q

what are toxic thyroid nodules?

A

AKA toxic thyroid adenoma

a singular benign autonomously functioning thyroid nodule

326
Q

what is the main risk factor for toxic thyroid nodule?

A

iodine deficiency

327
Q

how are toxic thyroid nodules investigated?

A

TFTs
TSH receptor and TPO antibodies

1 - Thyroid US

2 - Radioisotope scanning

fine needle biopsy may be needed

328
Q

what is the management of toxic thyroid nodule?

A

Radioactive iodine therapy
Thyroidectomy

329
Q

what are 3 complications of thyroidectomy?

A

Recurrent laryngeal nerve injury
Transient hypocalcaemia
Hypothyroidism

330
Q

what are 4 benign causes of thyroid nodules?

A

Multinodular goitre
Thyroid adenoma
Hashimoto’s
Cysts

331
Q

what are 5 malignant causes of thyroid nodules?

A

Papillary carcinoma - most common
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Lymphoma

332
Q

what is the 1st line investigation of thyroid nodules?

A

Ultrasound

333
Q

what investigations can be done of thyroid nodules?

A

US
Radiolabelled iodine uptake scan
Fine needle aspiration
core needle biopsy
TFTs

334
Q

what is classed as hypoglycaemia?

A

BG <4.0 mmol/L

335
Q

what are 6 causes of hypoglycaemia?

A

Self administration of insulin/sulphonylures
Liver failure
Addison’s disease
Alcohol - causes exaggerated insulin secretion
Insulinoma
Nesidioblastosis

336
Q

what is the physiological response to hypoglycaemia?

A

Decreased insulin secretion
Increased glucagon release
Increased GH and cortisol release

Increased adrenergic and cholinergic neurotransmission in peripheral autonomic nervous system and CN system

337
Q

what is the usual presentation of mild-moderate hypoglycaemia (2.8-3.3)?

A

Sweating
Shaking
Hunger
Anxiety
Nausea

338
Q

what is the presentation of severe hypoglycaemia (usually <2.8)?

A

Weakness
Vision changes
Confusion
Dizziness
Convulsions
Coma

339
Q

what is C-peptide a marker of?

A

Endogenous insulin production - released from pancreas in same molar amounts as insulin

340
Q

what are 2 potential causes of high insulin, high c-peptide hypoglycaemia?

A

Endogenous insulin production

Insulinoma
Sulfonylureas

341
Q

what is the cause of high insulin, low c-peptide hypoglycaemia?

A

Exogenous insulin - overdose or factitious disorder

342
Q

what are 5 causes of low insulin, low c-peptide hypoglycaemia?

A

Alcohol induced
Critical illness - sepsis
Adrenal insufficiency
Growth hormone deficiency
Fasting/starvation

343
Q

what is the initial management of hypoglycaemia in an awake patient?

A

Oral glucose 10-20g liquid, gel or tablet

Other quick acting carbohydrate

Recheck BMs in 10-15 mins

Repeat up to 3 times!

344
Q

What is the management of hypoglycaemia in an unresponsive patient?

A

IM glucagon

IV 20% dextrose - 75-100ml

345
Q

what should be given after acute management of hypoglycaemia when BMs return to >4?

A

Long acting carbohydrate - biscuits, bread, milk, normal carbohydrate containing meal

346
Q

what is Whipple’s triad of hypoglycaemia?

A

Symptoms of hypoglycaemia
low serum glucose
resolution of symptoms with administration of glucose

347
Q

what is 1 caution to IV glucose administration?

A

Thiamine deficiency - IV glucose can precipitate wernike’s encephalopathy

Administer with B1 (thiamine)/pabrinex

Phase 4 (22 decks)

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