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Endo Flashcards

1
Q

Commonest cause of a diffuse Goitre

A

Grave’s Disease

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2
Q

Plummer’s Disease

A

Single toxic nodule (adenoma) which is present on a background of a suppressed multinodular goitre

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3
Q

De Querviains Thyroiditis Tx

A
  • NSAIDS

- Corticosteroids

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4
Q

Hashimoto’s antibodies

A

antibodies against thyroid peroxidase

Large firm swelling

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5
Q

Drugs Causing Hypothyroidism

A

Lithium
Iodine
Amiodarone

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6
Q

Most common Thyroid Cancer

A

Papillary Carcinoma (80%)

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7
Q

Things to look for in Papillary Carcinomas

A 
RF = radiation exposure, Young people
Excellent prognosis
Papillary pattern
Calcified rings = Psamomma bodies
Clear nuclei  = ‘Orphan Annie Eye nuclei’
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8
Q

Calcified rings = Psamomma bodies

Clear nuclei = ‘Orphan Annie Eye nuclei’

A

Papillary Carcinoma

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9
Q

3 Facts about follicular thyroid carcinoma

A

Tend to metastasize to lung and bone
Presentation with Hurthle cells
Middle age

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10
Q

Hurthle cells

A

Follicular Thyroid Carcinoma

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11
Q

Medullary Thyroid Carcinoma

A

Familial pattern of inheritances
Associated with MEN 2A
Arises from parafollicular cells – C Cells
Increased secretion of calcitonin

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12
Q

MEN2A

A

Parathyroid hyperplasia
Medullary Thyroid carcinoma
Pheochromocytoma

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13
Q

MEN1

A

Pituitary adenoma
Parathyroid Hyperplasia
Pancreatic tumors

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14
Q

MEN2B

A

Mucosal Neuromas
Marfanoid body habits
Medullary Thyroid Cancer
Phaeochromocytoma

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15
Q

Oral Glucose Tolerance Test

A 
2 Hours after an oral load of 75g glucose
Diagnostic cut off is >11.1 mmol/L
Impaired OGTT :
Fasting plasma glucose is < 7.0 mmol/L
With OGTT of 7.8 – 11.0 mmol/L
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16
Q

HbA1c Cut off

A

Diagnostic is >48 mmol/mol (6.5%)

Remember two values
6% = 42 mmol/mol
7% = 53 mmol/mol
Addition of 11 mmol/mol

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17
Q

DKA management rational

A

Progression to a point where there is an impairment of normal function
Hyperglycaemia
Acidotic
Hyperglycaemia leads to an osmotic diuresis
This can potentiate dehydration
Acidity may cause vomiting, diarrhoea which worsens dehydration
Treat dehydration and glucose level
Dehydration provides greatest risk so treat this with fluid management

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18
Q

Sulphonylurea

A

Mechanism of action relates to increased secretion of insulin
Glibenclamide
Chlorpropamide
Tolbutamide
Often in those with uncontrolled Type 2 diabetes who are NOT obese

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19
Q

Alpha Glucosidase Inhibitors

A

Acarbose
Act as competitive inhibitors to that digest carbohydrates
Prevent digestion of carbohydrates such as starch or sugar
Reduce amount of glucose entering blood
Particular use in:
Those not tolerating other medication
Those suffering with post-prandial hyperglycaemia

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20
Q

Hypoglycaemia management

Group 1 – Adults who are conscious and orientated

A
  1. Give 15-20g of Quick Acting Carbohydrate such as Fruit Juice, Lucozade or sugar in water
  2. Repeat Capillary Blood Glucose and repeat until it reaches 4.0mmol/L or more
  3. If remains below 4mmol/L – Get Help! Consider 1mg Glucagon IM or IV 10% Glucose at 100ml/Hr
  4. Once above 4.0mmmol/L give a long acting Carbohydrate such as biscuits, slice of toast or 200-300mL milk
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21
Q

Hypoglycaemia management

Group 2- Adults who are Conscious but confused, disorientated, unable to cooperate, aggressive but able to swallow

A
  1. If possible, follow Group 1
  2. If uncooperative but able to swallow give 1.5 – 2 tubes of glucogel squeezed onto the gums
  3. If unable to do this consider 1mg Glucogon IM
  4. If does not raise CBG to 4mmol/L consider IV 10% Glucose infusion at 100ml/hr and call for help
  5. Once above 4.0mmol/L give a long acting carbohydrate
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22
Q

Hypoglycaemia management

Group 3 - Adults who are unconscious or experiencing seizures

A
  1. Must take an ABC approach first
  2. Stop any current insulin infusion
  3. Consider 1 of the following 3 based on local guidelines
    1mg Glucagon IM
    75-80mL 20% Glucose IV over 10-15mins
    150-160 10% Glucose IV
  4. Raise CBG to over 4.0mmol/L and regaining consciousness give a long acting carbohydrate meal
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23
Q

What does calcitonin do?

A

Reduces Ca levels by opposing the effects of PTH

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24
Q

Cushing’s Causes

A
  1. ACTH dependent (raised ACTH)
    Cushing’s disease – pituitary adenoma secreting ACTH
    Ectopic ACTH production – eg. small cell lung cancer
  2. ACTH independent (suppressed ACTH)
    Iatrogenic (most common) – pharmacological doses of steroids
    Adrenal adenoma/cancer – secreting cortisol
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25
Q

BP and electrolyte changes in Cushing’s

A

Hypertension (80%) and hypokalaemia

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26
Q

Cushing’s Tx

A

Conservative
Iatrogenic: decrease steroid dose

Surgical
Cushing’s disease: remove tumour trans-sphenoidally
Ectopic ACTH production: removal of tumour or bilateral adrenalectomy if spread
Adrenal adenoma: unilateral adrenalectomy

Radiotherapy
If tumour can’t be removed eg. adrenal carcinoma
Pre-op to reduce size

Pharmacologically
Inhibit cortisol synthesis (ketoconazole)

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27
Q

Drug that decreases cortisol synthesis

A

ketoconazole

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28
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism is excess production of aldosterone, causing increased potassium excretion, increased sodium and water retention, and decreased renin release.

If caused by aldosterone-producing adenoma = Conn’s syndrome

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29
Q

Causes of primary hyperaldosteronism

A
  1. Conn’s syndrome

2. Bilateral adrenal hyperplasia

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30
Q

Conn’s signs and symptoms

A 
Symptoms: Asymptomatic?
Oedema
Signs of hypokalaemia 
Weakness
Cramping 
Paraesthesia
Polyuria/polydipsia

Signs
Hypertension
Hypokalaemia or alkalosis
Hypernatraemia (can be normal)

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31
Q

Conn’s Tx

A
  1. Medical
    Spironolactone for 4 weeks pre-op to control BP and K
    Androgen receptor antagonist and a K-sparing diuretic
    Side effects: gynaecomastia, menstrual disturbances
  2. Surgical
    Laparascopic adrenalectomy
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32
Q

Phaeo symptom triad

A

Triad of PHEochromocytoma
Palpitations (episodic tachycardia)
Headache
Episodic sweating (diaphoresis)

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33
Q

Phaeo Tx

A

Management
Hypertensive crisis: α and β blockade (α first), such as short-acting IV α-blocker PHENTOLAMINE

Long-term
α -blockade eg. PHENOXYBENZAMINEP
β –blockade eg. Propanolol
Surgery

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34
Q

Hypoadrenal Diseases

A
  1. Addison’s

2. Congenital adrenal hyperplasia

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35
Q

Addisons definition and causes

A

Primary adrenocortical insufficiency: destruction of the adrenal cortex leading to glucocorticoid and mineralocorticoid deficiency.

Causes
Autoimmune (80% in UK)
TB (most common worldwide)
Iatrogenic (damage)

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36
Q

Addiosonian Crises Px

A 
Vomiting
Abdominal pain
Weakness
Hypoglycaemia 
Hypovolaemic shock
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37
Q

Addisons Tx

A

Management
Rehydration
Replace glucocorticoid: hydrocortisone (need more in infection/stress)
Replace mineralocorticoid: fludrocortisone

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38
Q

Causes of hyperprolactinaemia

A

physiological (pregnancy), drugs (eg. Metoclopramide) and due to disease (prolactinoma)

39
Q

Cushing’s Ix

A
  1. 9am and 12 midnight cortisol levels
  2. Low dose dexamethasone suppression test:
    0.5mg dexamethasone every 6 hours for 48 hours
    Cannot distinguish between different causes
  3. High dose dexamethasone test:
    2.0mg dexamethasone every 6 hours for 48 hours
    Distinguishes between Cushing’s disease and other causes
  4. 24 hour urine collection for urinary free cortisol (will be raised in disease)
  5. In Cushing’s disease, cortisol will be SUPPRESSED
  6. Imaging
    Adrenal MRI/CT
    Pituitary MRI/CT
40
Q

Conn’s Ix

A
  1. Plasma aldosterone:renin ratio
    In Conn’s syndrome, aldosterone will be raised and renin decreased
  2. Adrenal MRI/CT
41
Q

Phaeo Ix

A

24 hour urinary catecholamines
Plasma catecholamine levels
Imaging (CT/MRI)

42
Q

Addisons Ix

A
  1. Morning serum cortisol (between 8-9am)
  2. Plasma ACTH level
  3. Short synACTHen test:
    Cortisol and ACTH levels measured at the start
    IM injection 250 micrograms synthetic ACTH administered
    Cortisol measured 30 and 60 minutes post-injection
    In Addison’s disease, cortisol will NOT rise
43
Q

Acromeglay Ix

A
  1. Plasma GH hormone levels before and after oral glucose load (oral glucose tolerance test):
    Normal – glucose causes GH levels to DROP
    Acromegaly – GH levels remain HIGH
  2. IGF-1 levels (will be HIGH in acromegaly)
  3. Imaging: pituitary MRI
44
Q

Hyperprolactinaemia Ix

A

Prolactin levels (>6000 confirms diagnosis)
Urinary HCG – rule out pregnancy!
TFTs
Pituitary MRI

45
Q

Bone disorders:

Cause of Hypercalcaemia

A

Primary hyperparathyroidism
Malignancy

Causes
PTH suppressed: malignancy, rarer causes e.g. sarcoidosis, vitamin D excess
PTH raised or inappropriately normal: primary hyperparathyroidism

46
Q

Bone disorders:

Cause of Hypocalcaemia

A

Osteomalacia
Renal disease

Non-PTH driven: vitamin D deficiency, chronic kidney disease, PTH resistance (pseudohypoparathyroidism)
Due to low PTH: iatrogenic (post-thyroidectomy), autoimmune hypoparathyroidism, congenital absence of parathyroid glands (DiGeorge syndrome)

47
Q

Bone disorders:

Cause of normal calcium and other abnormality

A

Neutral
Osteoporosis
Paget’s disease

48
Q

Hypercalcaemia symptoms

A 
Symptoms 
STONES: renal stones
BONES: bone pain
GROANS: abdominal pain, nausea and vomiting
THRONES: constipation, polyuria
MOANS: confusion, psychosis, depression
Fatigue
49
Q

High Ca, low phosphate, high/normal PTH, normal Vit D, normal/raised ALP

A

Primary Hyperparathyroidism

50
Q

Primary Hyperparathyroidism causes

A

Parathyroid adenoma (85-90%)
Chief cell hyperplasia
Parathyroid carcinoma

51
Q

Hypercalcaemia of malignancy Tx

A

Treatment
IV fluids to combat volume depletion
Bisphosphonates eg pamidronate, or calcitonin
Treat underlying disease

52
Q

Hypocalcaemia symptoms

A

Muscle twitching/spasms
Tingling
Numbness
Hyper-reflexia
Chvostek’s sign (tapping on the cheek causes facial twitching)
Trousseau’s sign (applying a blood pressure cuff causes carpal spasm)

53
Q

Low/N Ca, low /N phosphate, high PTH, low Vit D, raised ALP

A

Osteomalacia/Ricketts

54
Q

Low Ca, high phosphate, high PTH (negative feedback), normal Vit D and Raised/normal ALP

A

CKD

55
Q

CKD

A

Decreased calcium reabsorption and decreased phosphate excretion
Hypocalcaemia and hyperphosphataemia
Results in secondary hyperparathyroidism
Due to lack of negative feedback, there is increase of PTH
Can progress to tertiary hyperparathyroidism (autonomous parathyroid glands resulting in hypercalcaemia)

56
Q

Osteoporosis Tx

A

Treatment
Conservative: smoking cessation, reduce alcohol intake, weight-bearing exercise
Medical: calcium/vitamin D supplements, bisphosphonates, teriparatide (recombinant PTH), HRT

57
Q

Osteoporosis RF

A
  1. Reduced oestrogen exposure: Late menarche, Early menopause, Amenorrhoea e.g. anorexia nervosa
  2. Nutritional: Low BMI e.g. anorexia nervosa, Malabsorption e.g. coeliac disease, IBD, gastric surgery
  3. Endocrine: Cushing’s syndrome, Hyperthyroidism, Hyperparathyroidism, Diabetes mellitus
  4. Musculoskeletal: Immobility, Rhematoid arthritis
  5. Iatrogenic: STEROIDS, Heparin, Anti-epileptics, PPIs
58
Q

Normal Ca, phosphate, PTH and Vit D. Raised ALP

A

Paget’s Disease

59
Q

Tx of Acromeglay

A
  1. Transphenoidal surgery

2. Somatostatin analogue: octreotide

60
Q

Carcinoid Syndrome

A

Constellation of symptoms caused by systemic release of humoral factors (amines, prostaglandins, polypeptides) from carcinoid tumors (neural crest origin).
Release of serotonin, histamine, and other vasoactive peptides causing systemic circulation

61
Q

Mainly gut tutors, high mets risk

A

carcinoid syndromes

62
Q

Carcinoid Syndrome

A

Syndromes: flushing, diarrhoea, wheeze, bronchoconstriction, sweating, palpitations

Sings: facial flushing, telangiectasia, RHS murmurs, signs of RHF

63
Q

High dose dexamethasone suppression test suppresses what in Cushings

A

suppreses cortisol when the cause is pituitary tumour.

64
Q

Diabetes Insipidus Tests

A
  1. serum and urine osmolarity
  2. water deprivation test
  3. AVP stimulation test
65
Q

Management of Diabetes Insipidus

A
  • Cranial: vasopressin

- Nephrogenic: Thiazide diuretics to stimulate RAS , Na/K restrict

66
Q

Retinopathy All stages

A

Background: microanurysems, blot haemorrhages, hard exudates
Pre-Proliferative: retinal haemorrhages, cotton wool spots
Proliferative: revascularization, fibrosis
Maculopathy: hard exudates involving macula

67
Q

Background Retinopathy

A

Background: microanurysems, blot haemorrhages, hard exudates

68
Q

Pre-proliferative Retinopathy

A

Pre-Proliferative: retinal haemorrhages, cotton wool spots

69
Q

Proliferative Retinopathy

A

Proliferative: revascularization, fibrosis

70
Q

Maculopathy

A

hard exudates involving macula

71
Q

DKA Management

A

Problem: inceased glucose and ketones, decreased pH

  1. Fluids IV infusion pump (NaCl soln 0.9%)
  2. IV insulin infusion
  3. Asses basic jobs of pt
  4. Aim to maintain K in normal range
72
Q

Complications of DKA

A
  • hyper/hypokalaemia
  • cerebral odema
  • hypoglycaemia
  • pulmonary odema
73
Q

Management of Type II DM

A
  1. Monotherapy (metformin unless contraindicated lactic acidosis or CKD )
  2. Dual therapy
  3. Triple therapy or start insulin
74
Q

SIADH is characterised by what?

A
  • hypotonic hyponatermia
  • concentrated urine
  • euvolemic shock

headaches, nausea and vomiting, muscle crams, irratibility, confusion, coma

75
Q

Tx of SIADH

Acute and Chronic

A

Acute:
1. IV hypertonic saline and fluid restrict
+/- treat underlying cause, vasopressin antagonist, frusemide

Chronic:

1st: fluid restrict, treat underlying cause
2nd: tolvaptan
3rd: sodium chloride and fruosemide

76
Q

Delayed sexual development and small testes and gynecomastia

A

Klienfelter’s (XXY)

77
Q

isloated GnRH deficiency, with anosmia and colourbliness

A

Kallman’s

78
Q

Loss of critical region on ch15, causing obesity, short stature, almond shaped eyes, learning difficulty and postnatal hypotonia

A

Prader-Willi

79
Q

Obesity, polydactyly, retinitis, pigmentosa, learning difficulty

A

Laurence-moon-biedi syndrome

80
Q

Short stature, high arched palate, widely spaced nipples, lowe posterior hairline,

A

Turners sundrome

81
Q

Pituitary apoplexy

A

haemorrhage/infarction of pituitary tutor

lofe threatening: headache, visual loss, CN palsies

82
Q

Sheen’s Syndrome

A

pituitary infarction, haemorrhage, necrosis following post part haemorrhage

83
Q

Myxodema Coma

A 
hypothermia 
hypoventilation 
hyponatemia 
HF 
confusion 
coma 
SLOWLY RELAXING REFLEXES
84
Q

Myxodema Coma Tx

A 
oxygen 
rewarming therapy 
rehydrated 
IV T3 
IV hydrocortisone
85
Q

Obesity definition

A

BMI > 30

86
Q

Hypokalaemia signs

A

muscle weakness, cramps, parasthesia, tetany

87
Q

PCOS diagnostic criteria

A

Rotterdam (2003) pt must have 2 of the following:

  • hyperandrogemism +/or hyperandrogenaemia
  • oligo or anovulation
  • polycystic ovaries on US
88
Q

Thiazolidinediones work by

A

activating peroxisome proliferator-activated
receptor-γ, which regulates the expression of several genes involving metabolism, and work by enhancing the actions of endogenous insulin.
They are used as a third-line therapy in combination with metformin and
sulphonylurea, however they cause sodium and fluid retention and should
not be used in patients with cardiac failure, such as in this case.

89
Q

Thiazolidinediones are used as..

A

third-line therapy in combination with metformin and
sulphonylurea, however they cause sodium and fluid retention and should
not be used in patients with cardiac failure, such as in this case.

90
Q

Thiazolidinediones are contraindicated in

A

cardiac failure pts

91
Q

The most common cause of hypocalcaemia is .

A

hypoalbuminaemia with a normal ionised calcium concentration (hence why it is important to
correct calcium concentrations according to serum albumin). Other causes include alkalosis, vitamin D deficiency, chronic renal failure,
pseudohypoparathyroidism, acute pancreatitis and hypomagnesaemia.

92
Q

Pseudohypoparathyroidism is an autosomal dominant condition

characterised by end-organ resistance to parathyroid hormone. Features include

A

…. mental retardation, short stature and short fourth and fifth metacarpals, accompanied by a low PTH, low calcium and high phosphate levels.

Pseudopseudohypoparathyroidism describes the condition where
you get all the phenotypic features of pseudohypoparathyroidism but in
conjunction with a normal biochemistry

93
Q

phaeocytochroma Ix

A

24-hour urinary vanillylmandelic acid

An abdominal CT will help localize the tumour.

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