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Final Year > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Diagnosis of diabetes

A

Fasting >7
Random/OGTT >11.1
HbA1c >48

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2
Q

Diagnosis of impaired glucose tolerance

A

Fasting 6.1-7
Random/OGTT 7.8-11.1
HbA1c 42-47

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3
Q

Normal fasting, random/OGTT, HbA1c

A

Fasting 4-5.4
Random/OGTT <7.8
HbA1c <42

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4
Q

Symptoms of hyperglycaemia

A 
Polyuria
Polydipsia
Blurred vision
Lethargy
Weight loss
Headache
Thrush
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5
Q

Symptoms of hypoglycaemia

A 
Hungry
Weak
Sweaty
Shaky
Confusion
Decreased GCS
Coma
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6
Q

What is LADA

A

Latent autoimmune diabetes of adulthood

Think of this in older patient with T1DM type presentation or not responding to anti-hyperglycaemic agents

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7
Q

What is MODY

A

Maturity onset diabetes of the young
Like T2DM but young
Will have a strong FH

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8
Q

What are HbA1c targets

A

48 if on one med
53 if on two or more meds or hypo risk
If >58 step up management
If >80 need insulin

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9
Q

What are the features of Charcot neuropathy

A

Pes cavus, claw toes, loss of transverse arch, rocker-bottom deformity

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10
Q

What are the features of diabetic retinopathy

A 
Hard exudates
Haemorrhage
Aneurysms
Macular oedema
Cotton wool spots
Neovascularisation
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11
Q

Which DM meds work by increasing insulin sensitivity

A

Metformin (biguanide)

Pioglitazone (thiazolidinedione)

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12
Q

Which DM meds work by increasing insulin secretion

A

DPP4 inhibitors (gliptin)
GLP1 agonists (glutide)
Meglitinides (glinide)
Sulphonylureas (zide)

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13
Q

Which DM med works by increasing renal excretion of glucose

A

SGLT2 inhibitors (flozin)

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14
Q

Name of DPP4 inhibitors

A

Gliptins
Linagliptin
Sitagliptin ect

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15
Q

Name of GLP1 agonists

A

Glutides
Dulaglutide
Liraglutide ect

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16
Q

Name of Metaglitinides

A

Glinides
Repaglinide
Nateglinide ect

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17
Q

Name of Sulphonylureas

A

Zide
Glipizide
Tolazamide
Tolbutamide

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18
Q

Name of SGLT2 inhibitors

A

Gliflozin
Dapagliflozin
Canagliflozin

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19
Q

Which DM meds increase weight

A

Sulphonylureas
Insulin
Pioglitazone

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20
Q

Which DM meds reduce weight

A

GLP1 agonists

SGLT2 inhibitors

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21
Q

Which DM meds have the highest risk of hypos

A

Insulin

Sulphonylureas

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22
Q

Which antibodies are associated with T1DM

A

ICA - islet cell antibodies

GAD - glutamic acid decarboxylase

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23
Q

What are the microvascular complications of diabetes

A

Retinopathy
Nephropathy
Neuropathy - peripheral and autonomic

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24
Q

What are the macrovascular complications of diabetes

A

Stroke
MI
Peripheral vascular disease

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25
Q

Which genes are associated with T1DM

A

HLA D3/4

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26
Q

Describe the pathophysiology of DKA

A

Associated with T1DM, develops quickly (<24hrs)
Insufficient insulin replacement or increased demand - hyperglycaemia but inability to utilise it
Increased vascular osmolality so urinary loss of fluids and electrolytes leads to dehydration and reduced total body potassium
Lipolysis leads to increased free fatty acids and lipolysis which causes metabolic acidosis with an increased anion gap

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27
Q

Signs and symptoms of DKA

A

Nausea, vomiting, abdo pain
Kussmaul breathing, sweet/fruity breath
Sx of hyperglycaemia
Sx of dehydration

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28
Q

Diagnostic criteria of DKA

A

Ketonaemia >3 or ketonuria 2+
Hyperglycaemia >11 or known T1DM
Acidosis HCO3 <15 +/ venous pH >7.3

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29
Q

What are the potential triggers of DKA

A 
Infection
Lack of adherence to medication
Alcohol
Steroids
Injury/surgery
Pregnancy
Menstruation
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30
Q

How do you manage DKA

A

Lots of fluid replacement
Fixed rate short acting insulin
Potassium replacement if <5.5 and passing urine
When glucose falls below 14 start IV glucose 10%

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31
Q

Describe the pathophysiology of HHS

A

Associated with T2DM, develops slowly
Hyperglycaemia (>35) intravascular osmolality (>320) leading to severe dehydration and a thrombotic state
Develops as a result of illness/dehydration
Don’t get ketosis or acidosis like you do in DKA

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32
Q

How do you manage HHS

A

Rehydration
Prophylactic LMWH
Fixed rate insulin infusion

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33
Q

Management of hypoglycaemia

A

If able to swallow: 5-7 glucose tablets or 150ml lucozade and a long acting carb
If conscious but can’t swallow: 1.5-2 tubes of glucose gel around the teeth
Unconscious: 150ml 10% glucose STAT, IM glucagon, BM in 10 mins, give long acting carbohydrate when able to swallow

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34
Q

Indications for OGTT at 26 weeks

A 
BMI >30
Previous baby >4.5kg
1st degree relative DM
Family origin high risk
Previous FDIU or congenital malformations
PCOS
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35
Q

Indications for OGTT at 16 weeks

A

Previous GDM

PCOS

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36
Q

Describe the pathophysiology of GDM

A

Thought to be the placenta that causes increased insulin requirements and resistance, if the pancreas can’t compensate enough you get GDM

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37
Q

How does pregnancy affect women with existing DM

A

Insulin resistance increases so may need higher med doses, risk of hypos is higher, and complications (e.g. retinopathy) progress more quickly

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38
Q

What is the extra care for women with existing DM in pregnancy

A

5mg folic acid (NTD risk)
Aspirin (pre-eclampsia risk)
Growth scans 4wkly after 28/40

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39
Q

When do you aim to deliver for a woman with existing DM

A

37-39 weeks

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40
Q

When do you aim to deliver for a woman with GDM

A

Before 41 weeks

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41
Q

Diagnosis of GDM

A

Fasting 5.6

Random/OGTT 7.8

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42
Q

Glucose targets for GDM/EDM in pregnancy

A

4-7 throughout the day
<5.3 fasting
<7.8 after meals

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43
Q

What endocrine diseases can cause diabetes

A

Cushings
Acromegaly
Phaeochromocytoma

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44
Q

What is the difference between ACTH-dependant and ACTH-independant Cushings disease

A

ACTH-dependent disease — In these diseases, the body is making too much ACTH which leads to too much cortisol production. Pituitary tumors and ectopic ACTH producing tumors are examples. ACTH-independent disease — In this case, the adrenal gland is making too much cortisol and the ACTH is low.

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45
Q

What are the main hormones released by the adrenal glands

A

Aldosterone (mineralocorticoid)
Cortisol (glucocorticoid)
Androgens
Adrenaline/noradrenaline

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46
Q

What are the ACTH dependant causes of Cushings syndrome

A

Cushings disease (pituitary adenoma)
Ectopic ACTH production (SCLC)
Rarely - ectopic CRH (medullary thyroid cancer)

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47
Q

What are the ACTH independant causes of Cushings syndrome

A

Adrenal tumour

Adrenal nodular hyperplasia

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48
Q

Are ACTH levels low or high in ACTH-independant Cushings syndrome

A

Low - the problem is excess cortisol so ACTH is low due to negative feedback

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49
Q

Describe the possible outcomes of the dexamethasone suppression test

A

Decreased cortisol with low dose = normal
No change in cortisol with low dose = Cushings syndrome
Decreased cortisol with high dose = Cushings disease (pituitary tumour)
Normal cortisol with high dose = ectopic ACTH secretion

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50
Q

Describe the possible outcomes of the CRH test

A

Big increase in plasma ACTH + cortisol = Cushings disease

Not much change = ectopic ACTH secretion

51
Q

Signs/symptoms of raised cortisol

A 
Weight gain/truncal obesity/facial fullness/dorsal fat pad
Low mood
Amenorrhoea
High BP 
Increased skin pigmentation
Red/purple striae
Gynaecomastia
Ance
Bruising
Osteoporosis
Hypokalaemia
Hirsutism
Muscle wasting
Infection susceptibility/poor wound healing
Proximal weakness
52
Q

What is Nelsons syndrome

A

A complication of bilateral adrenalectomy - really high ACTH and skin pigmentation

53
Q

What are the possible causes of primary adrenocortical insufficiency

A 
Addisons/Autoimmune (80%)
TB
HIV
Cancer
Adrenal bleed
54
Q

What is the cause of secondary adrenocortical insufficiency

A

Withdrawal of long term steroid therapy (you get suppression of pituitary-adrenal axis)

55
Q

Are cortisol and aldosterone high or low in Addisons disease

A

Low

56
Q

What does low cortisol cause

A

Hypoglycaemia

57
Q

What does low aldosterone cause

A

Low Na

High K

58
Q

What are the signs and symptoms of Addisons disease

A

Lean, tanned, tired/fatigued, weak, tearful, anorexia, dizzy/faints, flu-like aches and pains, low mood, nausea and vomiting, abdo pain, constipation/diarrhoea, pigmented palmar creases/buccal mucosa, postural hypotension

59
Q

What happens to Na, K and glucose in Addisons disease

A

Low Na
High K
Low glucose

60
Q

Explain the short synacthen test

A

Its an ACTH stimulation test
You give an ACTH analogue
If cortisol rises to >550 then this excludes Addisons
Because in adrenal insufficiency the adrenals don’t respond to ACTH

61
Q

9am ACTH levels in primary Vs secondary adrenal insufficiency

A

Inappropriately high in primary

Low in secondary

62
Q

Treatment for Addisons disease

A

Replace cortisol with hydrocortisone
Replace aldosterone with fludrocortisone
Add 5-10mg hydrocortisone before strenuous activity/exercise
Double steroids in febrile illness, injury or stress

63
Q

Precipitators of Addisonian crisis

A 
Infection
Trauma
Surgery
Missed medication
Bilateral adrenal haemorrhage
64
Q

Clinical features of Addisonian crisis

A

Hypovolaemic shock - low BP, high HR
High temp
Weak/confused/coma
Possible high K, low Na, low glucose

65
Q

Management of Addisonian crisis

A

Check cortisol and ACTH
Check Na and K and treat accordingly (consider rehydration and ECG)
Check blood glucose
Hydrocortisone 100mg IV STAT and fluid bolus

66
Q

Causes of primary hyperaldosteronism

A 
Conns syndrome (aldosterone producing adenoma)
Bilateral adrenocortical hyperplasia
67
Q

Causes of secondary hyperaldosteronism

A

Increased renin release secondary to decreased renal perfusion
Some causes of decreased renal perfusion are renal artery stenosis, accelerated HTN, diuretics, CCF, hepatic failure

68
Q

Features of hyperaldosteronism

A

Increased Na and H2O retention - high BP

Low K - weakness, cramps, paraesthesia, polyuria, polydipsia

69
Q

Describe the renin-angiotensin system

A

Decreased renal artery pressure/Na or sympathetic stimulation causes renin to be released by kidneys
Renin converts angiotensinogen from the liver to angiotensin I
ACE from the lungs converts ANGI to ANGII
ANGII causes vasoconstriction and aldosterone release from the adrenal cortex (to retain Na)

70
Q

Where is ADH (vasopressin) released from and how does it work

A

Secreted by the posterior pituitary

Increases water reabsorption by the collecting ducts

71
Q

In what disease is ADH high and in which disease is ADH low

A

High in SIADH

Low in diabetes insipidus

72
Q

SIADH - high or low?: urine osmolality, serum osmolality, serum Na

A 
Urine osmolality > serum osmolality by at least 100
High urine osmolality
Low serum osmolality
Dilutional hyponatraemia (low serum Na)
Euvolaemic/Hypervolaemic

Decrease in volume and an increase in osmolality (concentration) of the urine excreted. The extra water that has been reabsorbed re-enters the circulatory system, reducing the serum osmolality.

73
Q

Diabetes insipidus - high or low?: urine osmolality, serum osmolality, serum Na

A

Low urine osmolality
High serum osmolality
Low serum Na

74
Q

Causes of SIADH

A

Primary brain injury – e.g. meningitis. subarachnoid haemorrhage (SAH), abscess, stroke, trauma, SLE, vasculitis
Malignancy – e.g. small-cell lung cancer, pancreas, prostate, thyroid, lymphoma
Drugs – e.g. opiates, psychotropics, carbamazepine, SSRIs, amitriptyline
Infectious – e.g. atypical pneumonia, cerebral abscess
Hypothyroidism
TB, pneumonia, abscess, aspergillosis

75
Q

Symptoms of SIADH

A

Mild – nausea, vomiting, headache, anorexia, lethargy
Moderate – muscle cramps, weakness, confusion, ataxia
Severe – drowsiness, seizures, coma

76
Q

Signs of SIADH

A

Decreased level of consciousness
Cognitive impairment – short-term memory loss, disorientation, confusion
Focal or generalised seizures
Brain stem herniation (severe acute hyponatraemia) – coma, respiratory arrest
Hypervolaemia – pulmonary oedema, peripheral oedema, raised JVP, ascites

77
Q

What criteria are required to make a diagnosis of SIADH

A

Concentrated urine: Na >20, osmolality >100
Hyponatraemia <125
Low plasma osmolality <260
Absence of: hypovolaemia, oedema, diuretics

78
Q

Causes of neurogenic diabetes insipidus

A

Diabetes insipidus can occur as a result of decreased circulating levels of vasopressin (ADH). Consider hypothalamic or posterior pituitary damage.
Familial mutations in the vasopressin gene (autosomal dominant)
Tumours - pituitary adenoas
Trauma
Neurosurgery
Infections - meningitis
Sheehan’s syndrome
Sarcoidosis (granuloma formation in pituitary)
Haemochromatosis (iron deposition in pituitary/hypothalamus_
Idiopathic

79
Q

Causes of nephrogenic diabetes insipidus

A

Familial mutations in ADH receptor gene (X linked recessive)
Familial mutation in aquaporin 2 gene (autosomal recessive)
Metabolic: hypercalcaemia, hyperglycaemia, hypokalaemia
Drugs: lithium, demeclocyline
Chronic renal disease
Amyloidosis
Post obstructive uropathy

80
Q

Signs and symptoms of diabetes insipidus

A 
Polyuria >3L/24hrs
Polydipsia
Nocturia
Dehydration - headache, dizziness, dry mouth
Hypotension
Dilute urine
Reduced cap refill
81
Q

Water deprivation test results for diabetes insipidus a) neurogenic b) nephrogenic c) primary polydipsia

A

Urine osmolality
Neurogenic: <300 after deprivation, >800 after desmopressin
Nephrogenic: <300 after deprivation, <300 after desmopressin
Primary polydipsia: >800 after deprivation, >800 after desmopressin

82
Q

Describe the pathway for thyroid hormone release

A

Hypothalamus releases TRH
Anterior pituitary releases TSH
Thyroid releases T4
T4 converted to T3 in the periphery and bound to thyroxine binding globulin

83
Q

Signs and symptoms of hyperthyroidism

A

Increased HR, irregular pulse, warm/moist skin, fine tremor, fine hair, palmar erythema, lid lag, lid retraction, goitire, thyroid nodules, bruit
Diarrhoea, weight loss, increased appetite, sweating, proximal myopathy, heat intolerance, palpitations, tremor, irritability, oligomenorrhoea/amenorrhoea/infertility

84
Q

Causes of hyperthyroidism

A 
Graves disease
Toxic multinodular goitre
Toxic adenoma
Drugs - amiodarone, interferon
Sub-acute De Quervain's thyroiditis
85
Q

Antibody associated with Graves disease

A

TSH receptor stimulating antibodies

86
Q

Three features that are unique to Graves disease

A

Eye disease - exophthalmos, ophthalmoplegia
Pretibial myxoedema
Thyroid acropachy - clubbing, painful swellings on fingers and toes

87
Q

Treatment options for hyperthyroidism

A

Carbimazole - titrate vs block and replace
Radioiodine
Thyroidectomy

88
Q

What is the main risk you need to warn patients about regarding carbimazole

A

Agranulocytosis - so seek medical advice if sore throat/signs of infection

89
Q

Features of hyperthyroid crisis/thyrotoxic storm

A

Increased temperature, agitation, confusion/coma, tachycardia, AF, diarrhoea and vomiting, goitre, thyroid bruit, heart failure

90
Q

Three medications you can use to treat thyroid storm

A

Propanolol
Carbimazole
Hydrocortisone/dexamethasone (stops peripheral conversion of T4 to T3)

91
Q

Signs and symptoms of thyroid eye disease

A

Exophthalmos (appearance of protrusion), proptosis (protrusion beyond the orbit), ophthalmoplegia, conjunctival oedema
Discomfort, grittiness, increased tear production, photophobia, diplopia, decreased acuity, afferent pupillary defect if optic nerve is compressed

92
Q

Causes of a nodular goitre

A

Toxic multinodular goitre
Toxic adenoma
Carcinoma

93
Q

Causes of a diffuse goitre

A

Physiological
Graves disease
Hashimotos thyroiditis
De Quervains thyroiditis (painful)

94
Q

Signs and symptoms of hypothyroidism

A

Tired/lethargic, low mood, cold intolerance, weight gain, constipation, menorrhagia, hoarse voice, decreased memory/cognition, myalgia, cramps, weakness
Bradycardia, reflexes relax slowly, cerebellar ataxia, dry/thin hair and skin, cold, round/puffy face, goitre

95
Q

Causes of hypothyroidism

A

Primary atrophic hypothyroidism
Hashimotos thyroiditis
Post-thyroidectomy/radioiodine
Drugs - amiodarone, lithium, iodine, antithyroid meds
De Quervains thyroiditis (second phase)
Secondary hypothyroidism due to pituitary disease

96
Q

Which antibodies are associated with Hashimotos thyroiditis

A

Anti-TPO

Anti-Tg

97
Q

What problems can hypothyroidism cause in pregnancy

A 
Eclampsia
Anaemia
Prematurity
Low birth weight
PPH
Stillbirth
98
Q

Medication used to treat hypothyroidism

A

Levothyroxine

99
Q

Features of myxoedema coma

A

Typical hypothyroid features plus low temperature, decreased reflexes, low blood glucose, bradycardia, coma, seizures, HF, cyanosis, hypotension

100
Q

What is sick euthyroidism and what would TFTs be like

A

Asymptomatic deranged TFTs in a systemic illness

Typical pattern is for everything to be low

101
Q

What is De Quervains thyroiditis and what would TFTs be like

A

Post-viral thyroiditis
Painful goitre
Initial hyperthyroidism then hypothyroidism

102
Q

What is subacute hyper/hypothyroidism and what would TFTs be like

A

Asymptomatic

TSH changed but normal T3/T4

103
Q

What are the 5 types of thyroid cancer

A 
Papillary 
Follicular 
Medullary
Anaplastic
Lymphoma
104
Q

What is the typical presentation of papillary thyroid cancer

A

Young woman with lymph node metastases

105
Q

In which thyroid cancer would serum calcitonin be raised

A

Medullary carcinoma

106
Q

What is the typical presentation of anaplastic thyroid cancer

A

Elderly women, rapid growth and local invasion

107
Q

What is the typical presentation of follicular thyroid cancer

A

Middle aged, solitary thyroid nodule, may have spread to lung and bone

108
Q

What are the 5 possible FNAC results of thyroid biopsy

A 
Thy 1 - non-diagnostic
Thy 2 - benign
Thy 3 - intermediate
Thy 4 - suspicious
Thy 5 - malignancy
109
Q

Describe the action of parathyroid hormone

A

Released by the parathyroid glands in response to low serum calcium

  1. increases osteoclast activity
  2. increases renal Ca reabsorption and PO4 excretion
  3. increases VitD levels

So overall increases serum calcium and decreases serum phosphate

110
Q

What are the 4 types of hyperparathyroidism

A

Primary
Secondary
Tertiary
Malignant

111
Q

What are the causes of primary hyperparathyroidism

A

Solitary adenoma
Parathyroid gland hyperplasia
Parathyroid gland cancer (<1%)

112
Q

What are the symptoms of primary hyperparathyroidism

A

Increased serum calcium: weak, tired, depressed, polydipsia, polyuria, dehydration, renal stones, abdo pain, pancreatitis, peptic ulcers
Bone reabsorption: pain, fractures, osteopenia, osteoporosis
Increased BP

113
Q

What medication can be used to reduce PTH levels

A

Cinacalcet

114
Q

What are the causes of secondary hyperparathyroidism

A

It’s a physiological/appropriate response to low serum Ca. So causes include low vitamin D intake and chronic renal failure

115
Q

What is tertiary hyperparathyroidism

A

Inappropriately high PTH despite high serum Ca
Happens when you have had secondary hyperparathyroidism for a very long time which causes the parathyroid glands to undergo hyperplasia and start to act autonomously from serum Ca so you have high PTH unlimited by negative feedback. Seen in chronic renal failure

116
Q

What is malignant hyperparathyroidism

A

When you get parathyroid-related-protein (PTHrP) produced by a cancer (SCLC, breast, renal cell carcinomas).
PTHrP increases Ca.
PTH serum levels wouldn’t be increased because PTHrP doesn’t show up on the assay so you need to order a special test

117
Q

What can cause primary hypoparathyroidism

A

Autoimmune

Congenital

118
Q

What can cause secondary hypoparathyroidism

A

Radiation
Surgery
Low Mg

119
Q

Signs/symptoms of hypocalcaemia

A

Cramps, perioral numbness, muscle spasm, confusion, seizures, Chvostek sign (twitching of facial muscles if you tap over the facial nerve)

120
Q

What are the 6 anterior pituitary hormones

A 
Growth hormone
FSH and LH (gonadotrophins)
TSH
ACTH
Prolactin
121
Q

What can cause raised prolactin levels

A

Pregnancy/breastfeeding
Medications - antipsychotics, dopamine antagonists
Hypothyroidism

122
Q

What are the signs/symptoms of high prolactin

A

Raised prolactin causes low LH/FSH/testosterone/estrogen

Hypogonadism, infertility, osteoporosis, amenorrhoea/oligomenorrhea, decreased libido, anorgasmia, erectile dysfunction

123
Q

Which medications are used to treat high prolactin

A

Dopamine agonists - Cabergoline/Bromocriptine

Final Year (4 decks)

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