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Endocrinology Flashcards

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1
Q

Adrenal insufficiency/Addison’s definition

A

Adrenal glands do not produce enough steroid hormones (cortisol & aldosterone)

Addison’s disease = primary adrenal insuff. caused by autoimmunity

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2
Q

Primary adrenal insufficiency definition

A

Adrenal glands damaged, resulting in low cortisol and aldosterone secretion (inc. Addison’s; specifically autoimmune)

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3
Q

Secondary adrenal insufficiency definition

A

Inadequate ACTH resulting in a lack of stimulation of adrenal glands

Result of loss of/damage to pituitary from pituitary adenoma, surgery, radiotherapy or trauma

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4
Q

Tertiary adrenal insufficiency definition

A

Insufficient CRH release from hypothalamus

Usually from patients on long-term (>3 weeks) steroids not tapering doses correctly

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5
Q

Adrenal insufficiency presentation

A

Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido

Bronze hyperpigmentation of the skin, particularly in creases (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)

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6
Q

Adrenal insufficiency investigations

A

Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised creatinine and urea due to dehydration
Hypercalcaemia (high calcium)

Early morning cortisol often falsely low

ACTH measured directly may be high or low depending on primary/secondary/tertiary

Adrenal cortex or 21-hydroxylase antibodies may be present in Addison’s

CT or MRI of adrenal glands or MRI of pituitary may be helpful

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7
Q

Test for adrenal insufficiency

A

Short synacthen test

Synthetic ACTH given & cortisol checked after 30 and 60 minutes

Should double cortisol levels

If failure to double, either primary adrenal insufficiency or significant adrenal atrophy from prolonged secondary adrenal insufficiency

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8
Q

Management of adrenal insufficiency

A

Hydrocortisone to replace cortisol

Fludrocortisone to replace aldosterone if needed

When ill, double hydrocortisone dose to mimic body’s response to stressors, and attend A&E if vomiting

Will have medical ID bracelet and steroid card, and should carry emergency hydrocortisone injection

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9
Q

Adrenal crisis definition, presentation & management

A

Acute presentation of severe adrenal insufficiency

Present with:
Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

Manage with IV hydrocortisone, IV fluids, IV dextrose
ABCDE approach to management

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10
Q

Hyperthyroidism definition

A

Over-production of thyroid hormones, T3 & T4 by thyroid gland

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11
Q

Thyrotoxicosis definition

A

Effects of an abnormal/excessive amount of thyroid hormones on the body

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12
Q

Primary hyperthyroidism definition

A

Dysfunction of the thyroid gland itself, producing excessive thyroid hormone e.g. Grave’s disease, in which autoantibodies stimulate TSH receptors

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13
Q

Secondary hyperthyroidism definition

A

Dysfunction of the pituitary or hypothalamus and over-production of TSH e.g. from a pituitary adenoma

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14
Q

Sub-clinical hyperthyroidism definition

A

Thyroid hormones (T3/T4) are normal but TSH is suppressed/low

(May have mild or absent symptoms)

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15
Q

Grave’s disease definition

A

Form of primary hyperthyroidism in which anti-TSH receptor antibodies bind to the receptors on the thyroid and stimulate excessive thyroid hormone secretion

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16
Q

Plummer’s disease definition

A

Form of primary hyperthyroidism in which nodules develop on the thyroid gland which are unregulated by the thyroid axis and continually secrete thyroid hormones

(Most common in patients >50 years old)

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17
Q

Grave’s disease presentation

A

In addition to the universal symptoms of hyperthyroidism
Also present with Grave’s eye disease, which is evident via lid lag and exophthamos
Pretibial myxoedema (gives skin a discoloured, waxy, oedematous appearance)
Goitre

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18
Q

Hyperthyroidism presentation

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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19
Q

Thyroid storm presentation and management

A

Acute presentation of hyperthyroidism

Presents with fever, tachycardia and delirium

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone/hydrocortisone - blocks the conversion of T4 to T3

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20
Q

Hyperthyroidism management & drug contraindications

A

Carbimazole = first line drug
Propylthiuracil = second line drug

(Both can cause agranulocytosis, if suffering sore throat stop taking and see a doctor ASAP

Carbimazole is contraindicated in pregnancy)

Propranolol for symptomatic relief

Radioactive iodine can be used as a definitive treatment

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21
Q

Hyperparathyroidism definition

A

Overactivity of the 4 parathyroid glands, resulting in excessive secretion of PTH

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22
Q

Hyperparathyroidism presentation

A

Bones, moans, stones & groans

(bone pain, depression, delirium, kidney stones, abdominal moans [vomiting, nausea and constipation])

Categorised by hypercalcaemia

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23
Q

Primary hyperparathyroidism definition, biochem presentation and management

A

Uncontrolled PTH release from the parathyroid glands e.g. from a tumour

Presents with elevated PTH and calcium

Manage surgically

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24
Q

Secondary hyperparathyroidism definition, biochem presentation and management

A

Insufficient vitamin D or chronic kidney disease reduces calcium absorption, leading to hypocalcaemia

Presents with elevated PTH but low/normal calcium

Treat by correcting underlying condition

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25
Tertiary hyperparathyroidism definition, biochem presentation and management
Caused by hyperplasia of the parathyroid gland due to prolonged secondary hyperparathyroidism post-resolution Presents with high PTH and high calcium Treat by surgically removing part of parathyroid tissue
26
Hypothyroidism definition
Insufficient thyroid hormones, T3 & T4
27
Primary hypothyroidism definition & biochem
Thyroid behaves abnormally and produces inadequate thyroid hormones e.g. iodine deficiency Loss of negative feedback, hence presents with elevated TSH
28
Secondary hypothyroidism definition & biochem
Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by: Tumours (e.g., pituitary adenomas) Surgery to the pituitary Radiotherapy Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland) Trauma Low TSH, Low T3/4
29
Hashimoto's thyroiditis definition
Autoimmune condition associated with anti-TPO and anti-Tg Causes goitre followed by wasting/atrophy of thyroid gland
30
Hypothyroidism management
Oral levothyroxine = first-line treatment (synthetic T4) Liothyronine sodium = rarely used under specialist care (synthetic T3)
31
Hypothyroidism presentation
Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retention (including oedema, pleural effusions and ascites) Heavy or irregular periods Constipation Goitre for iodine deficiency
32
Cushing's syndrome & disease definition
Refers to prolonged high levels of glucocorticoids in the body (primarily cortisol) Cushing's disease refers specifically to high levels from a pituitary adenoma secreting excessive ACTH
33
Cushing's syndrome presentation
Round face (known as a “moon face”) Central obesity Abdominal striae (stretch marks) Enlarged fat pad on the upper back (known as a “buffalo hump”) Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms) Male pattern facial hair in women (hirsutism) Easy bruising and poor skin healing Hyperpigmentation of the skin in patients with Cushing’s disease
34
Causes of Cushing's mnemonic
CAPE Cushing's disease Adrenal adenoma Paraneoplastic syndrome (ACTH from tumour somewhere other than pituitary) Exogenous steroids
35
Cushing's syndrome diagnostic test
Dexamethasone suppression test First line = low dose overnight test, give dexamethasone at 11pm and check cortisol at 9am - suppressed normally For the low-dose 48-hour test, dexamethasone (0.5mg) is taken every 6 hours for 8 doses, starting at 9 am on the first day. Cortisol is checked at 9 am on day 1 (before the first dose) and 9 am on day 3 (after the last dose). A normal result is that the cortisol level on day 3 is suppressed. Failure of the dexamethasone to suppress the day 3 cortisol could indicate Cushing’s syndrome, and further assessment is required. The high-dose 48-hour test is carried out the same way as the low-dose test, other than using 2mg per dose (rather than 0.5mg). This higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), but not when it is caused by an adrenal adenoma or ectopic ACTH.
36
Cushing's syndrome management
Trans-sphenoidal (through the nose) removal of pituitary adenoma Surgical removal of adrenal tumour Surgical removal of the tumour producing ectopic ACTH (e.g., small cell lung cancer), if possible
37
Hyperaldosteronism/Conn's syndrome definition
Refers to high levels of aldosterone Conn's specifically refers to an adrenal adenoma producing too much aldosterone May be present in 5-10% patients with hypertension
38
Primary hyperaldosteronism definition and causes
Adrenal glands directly responsible for producing too much aldosterone Serum renin will be low due to negative feedback May be due to a bilateral adrenal hyperplasia, adrenal adenoma (aka Conn's) or familial
39
Secondary hyperaldosteronism definition and causes
Caused by excessive renin stimulating the release of excessive aldosterone Usually due to disproportionately lower blood pressure in the kidneys e.g. renal artery stenosis, liver cirrhosis, heart failure
40
Hyperaldosteronism biochem & investigatons
High aldosterone Low renin (primary) or high renin (secondary) Hypertension Hypokalaemia Alkalosis Adrenal vein sampling CT/MRI
41
Hyperaldosteronism management
Aldosterone antagonists - eplerenone & spironolactone Treating underlying cause e.g. surgical removal of tumour
42
Acromegaly definition
Result of excessive growth hormone Usually from pituitary adenoma Also linked to carpal tunnel syndrome
43
Acromegaly presentation
Headaches Bitemporal hemianopia Prominent forehead and brow (frontal bossing) Coarse, sweaty skin Large nose Large tongue (macroglossia) Large hands and feet Large protruding jaw (prognathism)
44
Acromegaly investigations
Insulin-like growth factor-1 can be tested on a blood sample Also glucose tolerance test Pituitary MRI
45
Acromegaly management
Trans-sphenoidal surgery Pegvisomant (growth hormone receptor antagonist given daily by a subcutaneous injection) Somatostatin analogues (e.g., octreotide) block growth hormone release Dopamine agonists (e.g., bromocriptine) block growth hormone release
46
Phaeochromocytoma definition
Tumour of the adrenal glands secreting unregulated and excessive amounts of catecholamines i.e. adrenaline
47
10% rule of phaeochromocytoma
10% bilateral 10% cancerous 10% outside adrenal gland
48
Phaeochromocytoma presentation
Anxiety Sweating Headache Tremor Palpitations Hypertension Tachycardia
49
Phaeochromocytoma diagnosis
Tests include plasma free metanephrines (breakdown products of catecholamines) & 24 hour urine catecholamines
50
Phaeochromocytoma management
Alpha blockers e.g. henoxybenzamine or doxazosin Beta blockers, only when established on alpha blockers Surgical removal of the tumour
51
Diabetes insipidus definition
Rare disease in which the body makes too much urine Can be cranial DI (lack of ADH) or nephrogenic DI (lack of response to ADH)
52
ADH function
Produced in hypothalamus & secreted by posterior pituitary gland Stimulates water reabsorption from the collecting ducts in the kidneys Lack of ADH results in polyuria and polydipsia
53
Primary polydipsia definition
Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria) - this is not diabetes insipidus
54
Nephrogenic diabetes insipidus definition and causes
Collecting ducts of the kidneys do not respond to ADH Idiopathic Medications e.g. lithium Familial (X-linked recessive inheritance for ADH rec gene) Hypercalcaemia Hypokalaemia Kidney diseases
55
Cranial diabetes insipidus definition and causes
Hypothalamus does not produce ADH for the pituitary gland to secrete Idiopathic Brain tumours Brain injury Brain surgery Brain infection Familial (ADH gene autosomal dominant inheritance) Wolfram syndrome
56
Diabetes insipidus presentation
Polyuria Polydipsia Dehydration Postural hypotension
57
Diabetes insipidus investigations results
Low urine osmolarity High/normal serum osmolarity >3l on 24-hr urine collection
58
Diabetes insipidus test
Water deprivation test/desmopressin stimulation test Patient avoids fluids for ~8hrs before test After water deprivation, urine osmolarity is measured. If low, synthetic ADH (desmopressin) is given, then urine osmolarity is measured over 2-4 hours after If high urine osmolarity after water deprivation - likely to be primary polydipsia & no ADH is given Cranial diabetes insipidus - patient lacks ADH, therefore after synthetic ADH given their osmolarity should increase and be high Nephrogenic diabetes insipidus - ADH will not have an effect therefore osmolarity will still be low
59
Diabetes insipidus management
Treat underlying cause Desmopressin for cranial DI, but monitor sodium for hyponatraemia Nephrogenic DI can be treated with thiazide diuretics, high dose desmopressin, NSAIDs and good access to water
60
Type 1 diabetes
Pancreas no longer able to produce adequate insulin, resulting in a loss of ability to absorb glucose from the blood
61
Type 1 diabetes presentation
Polyuria Polydipsia Weight loss (DKA)
62
DKA definition
Diabetic ketoacidosis is a consequence of inadequate insulin When body recognises low glucose due to lack of insulin signalling, ketogenesis occurs, producing ketones. Usually buffered by the kidneys to prevent ketone acids causing acidosis. But when diabetes causes excess ketones, causes life-threatening metabolic acidosis = DKA
63
DKA presentation & usual patients
The initial presentation of type 1 diabetes An existing type 1 diabetic who is unwell for another reason, often with an infection An existing type 1 diabetic who is not adhering to their insulin regime Ketoacidosis Dehydration Potassium imbalance Metabolic acidosis w low bicarb Hyperglycaemia Sweet smelling breath Hypotension Altered consciousness
64
DKA management
FIG-PICK Fluids - normal saline, 1L in first hr then 1L per 2hrs Insulin - fixed rate infusion Glucose - if blood glucose <14mmol/L Potassium Infection - treat underlying infection if applicable Chart fluid balance Ketones - monitor
65
Key complications from DKA treatment
Hypoglycaemia (low blood sugar) Hypokalaemia (low potassium) Cerebral oedema, particularly in children Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome
66
Autoantibodies in T1D
Anti-islet cell antibodies Anti-GAD antibodies Anti-insulin antibodies Serum C-peptide can give a measure of insulin
67
Long term T1D management
Subcutaneous insulin (rotate injection sites to avoid lipodystrophy) Monitor carb intake Monitor blood sugar Monitor for complications
68
T1D basal-bolus regime
Combination of background long-acting insulin injected once a day & short actin insulin injected 30 mins before carb intake
69
Insulin pump definition, pros & cons
Small device continuously infusing insulin at different rates to control blood sugar levels Cannula replaced every 2-3 days and insertion site rotated Pros: Better blood sugar control More flexibility with eating Fewer injections Cons: Difficulties learning to use the pump Having it attached at all times Blockages in the infusion set A small risk of infection
70
T2D risk factors
Non-modifiable: Older age Ethnicity (Black African/Caribbean & South Asian) Family history Modifiable: Obesity Sedentary lifestyle High carb diet
71
T2D presentation
Tiredness Polyuria Polydipsia Unintentional weight loss Opportunistic infection Slow wound healing Glycosuria Acanthosis nigricans HbA1c >48mmol/mol indicates T2D, repeated 1 month apart to confirm
72
Pre-diabetes definition & criteria
Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes An HbA1c of 42 – 47 mmol/L indicates pre-diabetes
73
T2D management
Education Low-glycaemic index, high fibre diet Exercise Weight loss Anti-diabetic drugs Monitor/manage complications
74
T2D treatment targets
HbA1c 48 mmol/mol for new type 2 diabetics 53 mmol/mol for patients requiring more than one antidiabetic medication
75
T2D medical management
First line = metformin Add SGLT-2 inhibitor if patient has CVD or heart failure or with QRISK >10% (side effect to be aware of = DKA) Second-line is to add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor. Third-line options are: Triple therapy with metformin and two of the second-line drugs Insulin therapy (initiated by the specialist diabetic nurses)
76
Metformin mechanism of action & side effects
Increases insulin sensitivity & decreases glucose production by liver GI symptoms, including pain, nausea, diarrhoea Lactic acidosis Try modified-release metformin if bad GI effects
77
SGLT-2 inhibitors mechanism of action & side effects
End with suffix -gliflozin Inhibits sodium-glucose co-transporter 2 protein, preventing reabsorption of glucose from urine Glycosuria Increased urine frequency and output Genital and urinary tract infections (e.g. thrush) Weight loss DKA (with moderately raised glucose) Fournier's gangrene (rare, severe infection of genitals or perineum)
78
Pioglitazone mechanism of action & side effects
Increases insulin sensitivity and decreases liver production of glucose Weight gain heart failure Small increased risk of bladder cancer Increased risk of bone fractures
79
T2D complications
Infections Diabetic retinopathy Peripheral neuropathy Autonomic neuropathy Chronic kidney disease Diabetic foot Gastroparesis Hyperosmolar hyperglycaemic state
80
T2D neuropathic pain management
Amitriptyline – a tricyclic antidepressant Duloxetine – an SNRI antidepressant Gabapentin – an anticonvulsant Pregabalin – an anticonvulsant
81
Hyperosmolar hyperglycaemic state definition, presentation & management
Characterised by hyperosmolality (water loss leads to very concentrated blood), hyperglycaemia and the absence of ketones, distinguishing it from ketoacidosis Presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion Manage with IV fluids and careful monitoring (involve seniors)
82
Hypoglycaemia definition
Blood glucose below 3.5 mmol/L
83
Hypoglycaemia presentation
Trembling Sweating Palpitations Hunger Headache Double vision Difficulty concentrating Slurred speech Confusion Coma
84
Hypoglycaemia causes
Drugs (insulin, sulphonylureas, GLP-1 analogues, DPP-4 inhibitors, beta blockers) Alcohol Acute liver failure Sepsis Adrenal insufficiency Insulinoma Glycogen storage disease
85
Mild hypoglycaemia management
ABCDE approach 15-20g of fast-acting carbohydrate Follow with slow-acting carbohydrate
86
Severe hypoglycaemia management
ABCDE approach 200ml 10% dextrose IV 1mg glucagon IM if no IV access (won't work if alcohol ingestion is cause) Manage seizures
87
Hypoglycaemia investigations
Whipple's triad: Plasma hypoglycaemia Symptoms attributable to a low blood sugar Resolution of symptoms when correcting blood sugar Measure insulin, C-peptide and proinsulin levels to differentiate between exogenous and endogenous insulin sources High C-peptide/proinsulin = endogenous Low C-peptide/proinsulin = exogenous Review medication history for drugs that may cause issue
88
Diabetic neuropathy definition
Refers to a variety of peripheral nerve disorders as a result of diabetes Primary causative factor is chronic hyperglycaemia Develops from both type 1 & type 2 DM
89
Diabetic neuropathy types and presentation
Distal Symmetrical Sensory Neuropathy Most common form Resulting from loss of large sensory fibres Sensory loss in a 'glove and stocking' distribution, typically affecting touch, vibration and proprioception Small-fibre Predominant Neuropathy Due to loss of small sensory fibres Deficits in pain and temperature sensation in a 'glove and stocking' distribution, with episodes of burning pain Diabetic Amyotrophy Originates from inflammation of the lumbosacral plexus or cervical plexus Severe pain around the thighs and hips, along with proximal weakness. Mononeuritis Multiplex Typically painful Defined as neuropathies involving two or more distinct peripheral nerves Autonomic Neuropathy Postural hypotension Gastroparesis Constipation Urinary retention Arrhythmias Erectile dysfunction
90
Diabetic neuropathy investigations
Neuro exam Nerve conduction studies Bloods - glucose levels, HbA1c, B12, thyroid function, liver function
91
Diabetic neuropathy management
Control blood glucose Pain control Manage complications
92
Chvostek's sign
Facial twitch obtained by tapping the distribution of the facial nerve in front of the tragus Caused by mechanical irritability of peripheral nerves Indicative of hypocalcemia and is the most reliable test for hypocalcemia
93
Hyperprolactinaemia definition and levels
Elevated serum prolactin Mildly increased levels (400-600mu/L) may be physiological and asymptomatic, higher levels usually pathological Very elevated levels (>5,000 mu/L) usually imply a prolactin-secreting pituitary tumour
94
Hyperprolactinaemia presentation
Amenorrhoea, oligomenorrhoea or anovulatory cycles Galactorrhoea Breast pain & enlargement Infertility Loss of libido Hirsutism For men: Impotence Loss of libido Decreased seminal volume Galactorrhoea Gynaecomastia
95
Hyperprolactinaemia investigations
MRI/CT Formal assessment of visual fields
96
Hypercalcaemia secondary to malignancy presentation
Hypercalcaemia Low PTH Low phosphate High PTHrP
97
Changes to hypothyroidism medication during pregnancy
increase dose by up to 50% in first 4-6 weeks of pregnancy
98
DM1 sick day rules
If on insulin, they must not stop it due to the risk of diabetic ketoacidosis Check blood glucose more frequently, for example, every 1–2 hours including through the night Consider checking blood or urine ketone levels regularly Maintain normal meal pattern if possible If appetite is reduced meals could be replaced with carbohydrate-containing drinks (such as milk, milkshakes, fruit juices, and sugary drinks) Aim to drink at least 3 L of fluid (5 pints) a day to prevent dehydration
99
DM2 sick day rules
Advise the patient to temporarily stop some oral hypoglycaemics during an acute illness Medication may be restarted once the person is feeling better and eating and drinking for 24-48 hours Metformin: stop treatment if there is a risk of dehydration, to reduce the risk of lactic acidosis Sulfonylureas: may increase the risk of hypoglycaemia SGLT-2 inhibitors: check for ketones and stop treatment if acutely unwell and/or at risk of dehydration, due to the risk of euglycaemic DKA GLP-1 receptor agonists: stop treatment if there is a risk of dehydration, to reduce the risk of AKI if on insulin therapy, do not stop treatment, as above monitor blood glucose more frequently as necessary
100
De Quervain's thyroiditis
Also known as subacute thyroiditis Hyperthyroid period followed by hypothyroidism, before returning to euthyroid Can present with antibodies Results in decreased isotope uptake Goitre is usually painful
101
Addison's steroid dosing/regime
the hydrocortisone dose is split with the majority given in the first half of the day
102
How many times a day should a type 1 diabetic check blood sugars?
At least 4 times a day, including before meals and before bed

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