Endocrinology Flashcards

(64 cards)

1
Q

Causes of cranial diabetes insipidus?

A

Causes of AVP Deficiency (Cranial DI)

Head trauma
Inflammatory conditions (e.g., sarcoidosis)
Cranial infections such as meningitis
Vascular conditions such as sickle cell disease
Rare genetic causes

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2
Q

Causes of nephrogenic diabetes insipidus?

A

Causes of AVP Resistance (Nephrogenic DI)

Drugs (e.g., lithium)
Metabolic disturbances (e.g., hypercalcaemia, hypokalaemia, hyperglycaemia)
Chronic renal disease
Rare genetic causes (e.g., Wolfram’s syndrome)

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3
Q

common causes of osteoporosis?

A

history of glucocorticoid use
rheumatoid arthritis
alcohol excess
history of parental hip fracture
low body mass index
current smoking

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4
Q

Medications that may worsen osteoporosis (other than glucocorticoids)

A

SSRIs
antiepileptics
proton pump inhibitors
glitazones
long term heparin therapy
aromatase inhibitors e.g. anastrozole

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5
Q

further investigations for osteoporosis?

A

History and physical examination
full blood count
urea and electrolytes
liver function tests
bone profile
CRP
thyroid function tests
Bone densitometry ( DXA)
myeloma screen + Bence Jones proteins

PSA
Prolactin

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6
Q

adverse effects of bisphosphonates?

A

oesophagitis/ ulcers
osteonecrosis of the jaw -> needs dental check
increased risk of atypical stress fracture
acute phase reactant-> myalgia, fever, arthralgia

Hypocalcaemia/vitamin D deficiency should be corrected before giving bisphosphonates.

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7
Q

investigations for gestational diabetes?

A

Diagnosis of GDM is based on a 75g OGTT:

-Fasting blood glucose level (fasting glucose ≥5.6 mmol/L)
-2-hour plasma glucose level (2-hour glucose ≥7.8 mmol/L)

This can be remembered as ‘diagnosis of GDM is as easy as 5678’

Additional tests may include:

HbA1c: Helpful in distinguishing between gestational and pre-existing diabetes early in pregnancy
Urinalysis: To check for glycosuria

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8
Q

maternal complications of gestational DM?
foetal complications of gestational DM?

A

Maternal:
HNT and pre-eclampsia

Foetal:
Macrosomia -> shoulder dystocia-> c-section
Sacral agenesis
NRDS
Neonatal hypoglycaemia

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9
Q

Management of gestational DM?

A

-Lifestyle
-Metformin
-If fasting glucose levels are ≥7 mmol/L, insulin therapy with or without metformin is often the first-line treatment.
-Postpartum management includes glucose testing to ensure resolution of GDM and long-term follow-up due to the increased risk of future type 2 diabetes.

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10
Q

Causes of smooth goitre?

A

Grave’s disease
Hashimoto’s
Lithium
Amiodarone
Iodine deficiency/ excess
De Quervain’s thyroiditis

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11
Q

Causes of nodular goitre?

A

Toxic solitary adenoma
Non-functional thyroid adenoma
Multinodular goitre
Thyroid cyst
Thyroid Ca

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12
Q

Investigations for goitre?

A

TFTs
Thyroid USS
Thyroid FNA biopsy

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13
Q

Management for goitre?

A

Observation: Small, asymptomatic goitres may simply be observed.

Pharmacotherapy: Anti-thyroid drugs for hyperthyroidism, levothyroxine for hypothyroidism.

Radioiodine treatment: Used in hyperthyroid conditions or large goitres.

Surgery: Considered for large goitres causing compressive symptoms, suspicious or malignant cytology on FNA, or for cosmetic reasons.

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14
Q

causes of hypoglycaemia?

A

Causes of hypoglycaemia include:

Drugs: Insulin, Sulphonylureas, GLP-1 analogues, DPP-4 inhibitors, Beta-blockers
Alcohol
Acute liver failure
Sepsis
Adrenal insufficiency
Insulinoma
Glycogen storage disease

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15
Q

management for hypoglycaemia?
conscious pt
unconscious pt

A

Mild Hypoglycaemia (Patient is conscious):

-ABCDE approach
-Consume 15-20g of fast-acting carbohydrates (e.g., glucose tablets, non-diet soda, sweets, fruit juice).
Avoid chocolate due to slower absorption.
-Follow up with slower-acting carbohydrates (e.g., toast).

Severe Hypoglycaemia (e.g. Seizures, Unconsciousness):

ABCDE approach
-Administer 200ml 10% dextrose IV (alternatively dextrose 20% can be administered via a large vein).
-Administer 1mg glucagon IM if no IV access (Note: this won’t work if alcohol ingestion is the cause due to its action blocking gluconeogenesis).
Manage prolonged or repeated seizures.

Aftercare:

Consider medication changes.
Investigate non-drug causes if necessary.

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16
Q

Common SE of metformin?

A

Gastrointestinal side-effects
Lactic acidosis

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17
Q

Common SE of sulfonylureas?- Gliclazide

A

Hypoglycaemic episodes
Increased appetite and weight gain
Syndrome of inappropriate ADH secretion
Liver dysfunction (cholestatic)

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18
Q

Common SE of Glitazones?- pioglitazone

A

Weight gain
Fluid retention
Liver dysfunction
Fractures

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19
Q

Common SE of Gliptins?- sitagliptin

A

Pancreatitis

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20
Q

HbA1c target if on sulfonylurea?

A

53mmol/mol

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21
Q

What are SGLT2 inhibitors pose risk to cause?

A

sodium-glucose co-transporter 2 inhibitor (SGLT2 inhibitor) which reduces blood glucose concentrations by increasing urinary excretion of glucose. While an effective treatment for type 2 diabetes, SGLT2 inhibitors increase the risk of urinary tract infections (UTIs) as there is more glucose in the bladder and urine than normal.

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22
Q

When should T1DM monitor their glucose?

A

In type 1 diabetics, recommend monitoring blood glucose at least 4 times a day, including before each meal and before bed

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23
Q

Stepwise management for DKA?

A
  1. Fluid replacement- isotonic saline
  2. Insulin:
    IV infusion should be started at 0.1 unit/kg/hour
    once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
  3. Correct electrolytes- potassium
  4. long-acting insulin should be continued, short-acting insulin should be stopped
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24
Q

MOA of DPP-4 inhibitors?- Gliptins

A

Gliptins (DPP-4 inhibitors) reduce the peripheral breakdown of incretins such as GLP-1

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25
BP target for T2DM patients?
NICE recommends a blood pressure target of < 140/90 mmHg for type 2 diabetics
26
Sick day rules for T1DM patients?
do not stop insulin- risk of DKA check BMs every 1-2 hours check blood and urine ketones regularly maintain normal meal patterns
27
Sick day rules for T2DM patients?
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
28
Causes of Cushing's? CAPE
C- Cushing's disease (high ACTH caused by pituitary adenoma) A- adrenal adenoma P- paraneoplastic syndrome causing ectopic ACTH E- exogenous steroids
29
Investigation for Cushing's?
Dexamethasone suppression test 24 hour urinary free cortisol (to confirm) If >50% suppression -> pituitary adenoma If <50% suppression -> ectopic ACTH secreting tumour, may need MRI MRI: pituitary adenoma CT CAP: SCLC, adrenal tumour
30
Management for Cushing's?
1. Cushing’s caused by pituitary adenoma- trans-sphenoidal surgical resection + glucocorticoid support 2. Ectopic tumour cause- surgical adrenalectomy 3. Radiotherapy for pituitary- can affect other hormones and takes time work 4. Medically- metyrapone- cortisol supressing tablets 5. Chemotherapy/ radiotherapy for SCLC- if it’s the cause Surgery: removal of: pituitary adenoma adrenal adenoma SCLC
31
Primary, secondary and tertiary causes of hypothyroidism?
Primary: Hashimoto's thyroiditis (auto Abs that attack thyroid gland) Iodine deficiency Surgical removal/ radioactive iodine treatment Secondary: Pituitary adenomas Tertiary: Hypothalamic disease can result in diminished secretion of TRH, leading to reduced stimulation of the pituitary gland and subsequently lowered release of thyroid-stimulating hormone (TSH). Medications: lithium, amiodarone
32
Antibodies found in: Grave's disease- hyperthyroidism Hashimoto's- hypothyroidism
Grave's: TSH-receptor abs- 90% anti-TPO- 70% Hashimoto's: anti-TPO anti-thyroglobulin
33
Scans for hypothyroidism?
USS Nuclear scan
34
Management of hypothyroidism?
50-100mcg Levothyroxine (lower dose of 25mcg in elderly and IHD) if pregnant increase dose due to extra demand if change in dose then check TFTs after 8-12 weeks
35
Treatment for myxoedema coma? Features?
IV thyroid replacement- levothyroxine IV fluid IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded) electrolyte imbalance correction Myxoedema coma typically presents with confusion and hypothermia.
36
Management for hyperthyroidism?
-Carbimazole (propylthiouracil if pregnancy in 1st trimester, carbimazole in 2/3 trimester) -Beta-blocker (propranolol) symptomatic relief Radio-iodine: Considered for definitive treatment, especially for relapsed disease or when ATDs are not suitable. Not suitable for 40 years - risk of cancer Will need lifelong HRT due to hypothyroidism Surgery (Thyroidectomy): An option for those with large goiters causing compression, suspicion of malignancy, or when other treatments are contraindicated or refused. Requires preparation with ATDs to achieve euthyroid state before surgery to minimize risks.
37
SE of carbimazole?
Carbimazole can cause agranulocytosis, a severe and potentially life-threatening condition characterized by a significant decrease in white blood cells (neutrophils). Patients should be advised to seek immediate medical attention if they experience symptoms like fever, sore throat, mouth ulcers, or other signs of infection while taking Carbimazole.
38
Features of a thyroid storm?
Thyroid storm is a rare but life-threatening medical emergency caused by untreated or inadequately managed hyperthyroidism. It is often precipitated by stressors like surgery, trauma, or infection. Key features of thyroid storm include: Restlessness and agitation High-output heart failure Profound tachycardia Fever Delirium and altered mental status
39
Management for thyroid storm via the 3 principles? 1. Counteract Peripheral Action of Thyroid Hormone 2. Inhibit Thyroid Synthesis 3. Supportive Care
1. IV propranolol and digoxin -> control heart rate and manage cardiac symptoms 2. Propylthiouracil (PTU) through a NG tube and Lugol's iodine are administered to reduce thyroid hormone production 3. Supportive measures include intravenous fluids, cooling measures for fever, and addressing any precipitating factors (infection).
40
Antibodies found in Grave's disease?
IgG TSH-receptor Abs- 90% Anti-TPO- 75%
41
Investigations for acromegaly? Bloods/ bedside Imaging
Serum IGF-1 levels- first line OGTT- confirm diagnosis MRI: pituitary adenoma secreting excess GH
42
Management for acromegaly?
Trans-sphenoidal surgery is the first-line treatment for acromegaly in the majority of patients If the tumour is inoperable/ surgery is unsuccessful: -octreotide- somatostatin analogue which inhibits GH -pegvisomant GH receptor antagonist -dopamine agonists- bromocriptine
43
Investigation for Adrenal insufficiency (Addison's) and other/ imaging?
-Short synacthen test (ACTH stimulation test)- gold standard -9am serum cortisol if Synacthen test no available Testing for adrenal auto-antibodies Chest X-ray CT scan of the adrenal glands MRI of the brain
44
Investigation for diabetes insipidus??
Water depravation test
45
Investigations for pheochromocytoma?
24hr urinary metanephrines
46
Investigations for SIADH?
Serum and urine osmolarity
47
Electrolyte abnormalities in Addison's?
hyperkalaemia hyponatraemia hypoglycaemia metabolic acidosis
48
Management for Addison's?
Addison's disease: usually given both glucocorticoid and mineralocorticoid replacement therapy. This usually means that patients take a combination of: hydrocortisone + fludrocortisone
49
Features of adrenal crisis and management?
An acute life-threatening condition characterised by severe hypotension, hypoglycaemia, and altered mental status. Immediate treatment: IV hydrocortisone, fluids, and electrolyte correction is crucial.
50
Causes of hyperparathyroidism?
Primary hyperparathyroidism is caused by excess secretion of PTH resulting in hypercalcaemia 85%: solitary parathyroid adenoma 10%: hyperplasia 4%: multiple adenoma 1%: carcinoma
51
Features of hyperparathyroidism? 'stones, bones, abdominal groans and psychic overtones'
'Stones' - increased risk of kidney stones (17%) 'Bones' Bone pain (35%) Osteopenia and osteoporosis (40%) 'Abdominal groans' Abdominal pain Constipation Nausea + vomiting 'Psychic overtones' Fatigue Depression (10%) Memory impairment (18%) Other features include polyuria, paraesthesia and muscle cramps. As calcium levels rise more serious symptoms develop. In severe cases, cardiac and metabolic disturbances, delirium or even coma may occur.
52
Investigations for primary hyperparathyroidism? Bloods Imaging Genetic and why?
Bloods: FBC, serum calcium, PTH, U&Es, eGFR, vitD Imaging: -Sestamibi Scan: This is a nuclear medicine study that uses Technetium-99m sestamibi which preferentially accumulates in overactive parathyroid tissue. -USS neck -4D CT scan In patients with familial primary hyperparathyroidism or those diagnosed at a young age, genetic testing may be considered to identify mutations associated with hereditary hyperparathyroidism syndromes such as Multiple Endocrine Neoplasia type 1 (MEN1), MEN2A, and Hyperparathyroid-Jaw Tumour Syndrome (HPT-JT).
53
Management for primary hyperparathyroidism?
Surgical parathyroidectomy following indications: Symptoms of hypercalcaemia Osteoporosis and/or fragility fractures Renal stones or nephrocalcinosis Age <50 years Serum adjusted calcium of 2.85 mmol/L or above eGFR of less than 60 If surgery CI: Calcitonin which reduces serum calcium concentrations Cinacalcet which is a calcimimetic and acts to reduce serum calcium concentrations while not affecting bone density or urinary calcium concentrations Desunomab which also impairs calcium resorption Bisphosphonates
54
Complications of primary hyperthyroidism? Not treated Following treatment
Complications of untreated hypercalcaemia include: Osteoporosis and fragility fractures Kidney stones and kidney injury Hypertension and heart disease Numerous gastrointestinal disorders including peptic ulcer disease, pancreatitis and gall stones Complications of parathyroidectomy: General surgical complications (reduced risk with good surgical practice) Infection Thrombosis Scarring Procedure specific complications Damage to the recurrent or superior laryngeal nerves Post operative hypocalcaemia can result after the removal of too much parathyroid tissue Failure to identify adenoma or persistence of disease post-surgery
55
Features of Addison's?
lethargy, weakness, anorexia, nausea & vomiting, weight loss, 'salt-craving' hyperpigmentation (especially palmar creases) vitiligo loss of pubic hair in women hypotension hypoglycaemia hyponatraemia and hyperkalaemia may be seen crisis: collapse, shock, pyrexia
56
What is affected in Addison's?
Primary HYPO-aldosteronism caused by reduced production of cortisol and aldosterone
57
Advice for taking calcium and levothyroxine?
Iron / calcium carbonate tablets can reduce the absorption of levothyroxine - should be given 4 hours apart
58
Dose adjustments for Addison's disease patients during a period of illness?
Addison's patient with intercurrent illness → double the glucocorticoids, keep fludrocortisone dose the same Hydrocortisone- double dose (2-3 doses with majority given in the AM) Fludrocortisone- keep the same dose
59
How to treat adrenal crisis in the community/ crisis kit?
patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
60
What will the following up-take scans show: De Quervain's thyroiditis Grave's Toxic nodular Goitre Subacute thyroiditis Toxic adenoma
De Quervain's thyroiditis- faint diffuse uptake Grave's- increased homogenous uptake Toxic nodular Goitre- areas of intense/ patchy uptake interspersed with some reduced activity Subacute thyroiditis- no uptake at all Toxic adenoma- single hot nodule with the rest of the gland suppressed
61
Cushing's vs Addison's ABG?
Cushing's syndrome - hypokalaemic metabolic alkalosis Addison's disease - hyperkalaemic metabolic acidosis
62
Complication of over-replacement with levothyroxine?
Osteoporosis
63
What is psudo-cushing's? Causes Investigations
mimics Cushing's often due to alcohol excess or severe depression causes false positive dexamethasone suppression test or 24 hr urinary free cortisol insulin stress test may be used to differentiate
64
What cancer is associated with Hashimoto's thyroiditis?
MALT lymphoma