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Endo Flashcards

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1
Q

Medication used to treat hyperprolactinaemia

A

Dopamine agonist
Carbergoline or bromocriptine
Carb- cuts- milk

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2
Q

Medication used to treat acromegaly

A

Somatostatin analogs (octreotide)
Octopus- Stops - Growth

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3
Q

Diagnosing Addisons

A

Short Synathen test

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4
Q

When to add meds for T2DM

A

If Hba1c is 58
Add on therapy

Then add third if >58

If still not working with triple- replace one with GLP1

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5
Q

Symptomatic low T4 normal TSH mx

A

Pituitary MRI
As normal TSH and low T4- ?secondary cause

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6
Q

Complications and other features of acromegaly

A

raised prolactin in 1/3 of cases → galactorrhoea
6% of patients have MEN-1

Complications
hypertension
diabetes (>10%)
cardiomyopathy
colorectal cancer

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7
Q

Bloods for premature ovarian failure vs hypothalamic amennorhoea

A

POF- high FSH and LH
Low oestrogen

HA- low everything

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8
Q

Sick euthyroid bloods

A

Transient TFT changes during systemic illness
T3, T4, and TSH ALL LOW (or TSH inappropriately normal)

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9
Q

Marker of medullary thyroid cancer

A

parafollicular C cells of the thyroid gland, which produce calcitonin. Calcitonin serves as a highly specific tumour marker for MTC, and elevated levels strongly correlate with disease presence and burden.

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10
Q

Addisons investigations

A

synthACTHen test

Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.

If an ACTH stimulation test is not readily available (e.g. in primary care) then sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

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11
Q

Cushing syndrome tests

A

The three most commonly used tests are:
overnight (low-dose) dexamethasone suppression test
this is the most sensitive test and is now used first-line to test for Cushing’s syndrome
patients with Cushing’s syndrome do not have their morning cortisol spike suppressed

24 hr urinary free cortisol
two measurements are required

bedtime salivary cortisol
two measurements are required

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12
Q

When to change levothyroxine dose, and by what increments

A

When to increase dose:
TSH remains above target range (0.5-2.5 mU/l), indicating under-replacement.
Pregnancy: increase dose by 25-50 mcg immediately upon confirmation due to increased thyroid hormone requirements.
Weight gain or clinical symptoms of hypothyroidism persist despite normal TSH.

When to decrease dose:
TSH suppressed below normal range, indicating over-replacement.
Symptoms/signs of hyperthyroidism develop (e.g., palpitations, tremor).
In elderly patients or those with cardiac disease if signs of overtreatment occur.

Dose increments:
Adjust doses in small increments, typically 12.5-25 mcg at a time.
Titrate slowly, especially in elderly or cardiac patients, to avoid adverse effects.
Reassess thyroid function tests 8-12 weeks after any dose change before further adjustment.

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13
Q

Mx of HHS

A
  • Initial management focuses on fluid resuscitation with IV 0.9% sodium chloride to correct severe dehydration and reduce serum osmolality.
  • Insulin is only indicated if blood glucose levels fail to fall adequately after initial fluid replacement, typically when glucose remains >14 mmol/L despite rehydration.
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14
Q

Dx of HHS

A

There are no precise diagnostic criteria but the following are typically seen
hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)

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15
Q

if patient has hba1c of 42-47 what other test should you do

A

OGTT

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16
Q

Test differentiating between t1 and t2dm

A

C peptide
High in t2
Low in t1

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17
Q

Subclinical hypothyroidism

A

TSH raised but T3, T4 normal
no obvious symptoms

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18
Q

Subclinical hypothyroidism mx

A

TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range
if < 65 years consider offering a 6-month trial of levothyroxine if:
the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,and
there are symptoms of hypothyroidism

in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy is often used

if asymptomatic people, observe and repeat thyroid function in 6 months

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19
Q

MEN 1
MEN 2a
MEN 2b

A

MEN 1- parathyroid, pituitary, pancreas

2a- medullary, phaeo, parathyroid

2b-Medullary thyroid carcinoma – earlier onset, more aggressive
Pheochromocytoma
Mucosal neuromas – lips, tongue, GI tract
Marfanoid habitus

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20
Q

Hypogonadotrophic hypogonadism causes

A

Iron overload: Haemochromatosis causing pituitary iron deposition and dysfunction.

Hypothalamic or pituitary tumours: e.g. craniopharyngioma, pituitary adenomas.

Trauma or surgery: Damage to hypothalamus or pituitary (e.g. neurosurgery, head injury).

Infiltrative diseases: Sarcoidosis, histiocytosis affecting hypothalamic-pituitary axis.

Radiation therapy: Cranial irradiation damaging hypothalamic-pituitary function.

Genetic causes: Kallmann syndrome

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21
Q

Graves antibodies

A

TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)

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22
Q

How to interpret OGTT

A

Same as random
2 hour post glucose
if >11.1- DM
If 7.8-11 Impaired glucose tolerance if fasting normal

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23
Q

First line treatment for thyroid storm

A

IV BB

Then
anti-thyroid drugs: e.g. methimazole or propylthiouracil
blocks new hormone synthesis
Lugol’s iodine (iodine solution)
prevents further thyroid hormone release.
glucocorticoids
reduce peripheral conversion of T4 → T3
IV hydrocortisone or dexamethasone

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24
Q

Testicular size and Precocious puberty

A

bilateral enlargement = gonadotrophin release from intracranial lesion
unilateral enlargement = gonadal tumour
small testes = adrenal cause (tumour or adrenal hyperplasia)

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25
Change of meds in pre existing T2DM if become pregnant
Existing T2DM who becomes pregnant → stop all medications except metformin and start insulin
26
Target Hba1c in DM
T2DM 48 if lifestyle or single drug 53 if multiple T1DM HbA1c every 3–6 months: aim <48 mmol/mol Capillary BMs: Waking: 5–7 mmol/L Pre-meal: 4–7 mmol/L
27
Differentiating between different thyroid cancers
Papillary Often young females - excellent prognosis Spreads early to cervical lymph nodes Check TG levels every3-6m for 3y then 6-12m Follicular Spreads to lungs and bones through blood Medullary Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2 Raised serum calcitonin and carcinoembryonic antigen (CEA) Anaplastic Not responsive to treatment, can cause pressure symptoms Lymphoma (rare) - Association: Hashimoto’s thyroiditis - Presentation: Rapidly enlarging thyroid mass with systemic symptoms
28
Primary hyperaldosterism features and treatment
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases adrenal adenoma: 20-30% of cases aldosterone is high renin is low hypertension hypokalaemia e.g. muscle weakness adrenal adenoma: surgery (laparoscopic adrenalectomy) bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
29
Treatment of hypocalcaemia
Oral- mild or asymptomatic IV- moderate-severe/symptomatic Mild hypocalcaemia: Corrected serum calcium 2.0–2.1 mmol/L Moderate hypocalcaemia: Corrected serum calcium 1.75–1.99 mmol/L. Symptoms such as paraesthesia, muscle cramps, or mild tetany may be present. Severe hypocalcaemia: Corrected serum calcium <1.75 mmol/L. Often symptomatic with tetany, seizures, cardiac arrhythmias, or laryngospasm.
30
Most common endogenous cause of Cushing
Pituitary adenoma
31
Diagnosing acromegaly
if a patient is shown to have raised IGF-1 levels, an oral glucose tolerance test (OGTT) with serial GH measurements is suggested to confirm the diagnosis
32
How to tell between poor compliance of levothyroxine vs needing higher dose
Poor compliance: Characterised by a persistently elevated TSH with normal or low-normal free T4. The patient may have fluctuating symptoms and inconsistent TSH levels on serial testing. A high TSH despite prescribed therapy suggests missed doses rather than inadequate dosing. Normal T4, high TSH The most likely explanation is that she started taking the thyroxine properly just before the blood test. This would correct the thyroxine level but the TSH takes longer to normalise. Need for higher dose: Typically presents with a persistently elevated TSH and low free T4 despite good adherence. Symptoms of hypothyroidism persist or worsen. Dose increase is indicated after confirming compliance.
33
When to offer GLP1 agonist
If triple therapy is ineffective, consider GLP-1 agonist (liraglutide) if: BMI > 35 or BMI < 35 but.. Weight loss would improve co-morbidities Insulin would have significant occupational implications (e.g. HGV driver)
34
GLP1 monitoring
GLP-1 Monitoring: Continue if: HbA1c falls ≥11 mmol/mol AND weight loss >3% at 6 months
35
When are SGLT2 inhibitors first line
CVD, HF, QRISK > 10% CKD + proteinuria
36
SE of gliclazide
SE: Hypoglycaemia, weight gain
37
SE of sitagliptin
SE: Pancreatitis
38
SE of SGLT2
UTI Genital candidiasis DKA (may be euglycaemic)
38
SE of GLP1
Adverse effects: Nausea, pancreatitis
39
Diagnostic criteria metabolic syndrome
Diagnosis requires 3 or more of the following: Increased waist circumference: Men >102 cm Women >88 cm Triglycerides > 1.7 mmol/L Low HDL cholesterol: Men <1.03 mmol/L Women <1.29 mmol/L Hypertension Insulin resistance: Fasting BM > 5.6 or diagnosis of T2DM
40
Management of obesity
Orlistat BMI > 30 BMI > 28 with risk factors Target: Must achieve ≥5% weight loss by 12 weeks to continue GLP1 Liraglutide (Saxenda) BMI ≥35 + non-diabetic hyperglycaemia + high CVD risk (secondary care only) Semaglutide (Wegovy) BMI ≥35 with at least 1 weight related comorbidity. Consider if BMI 30-34.9. Tirzepatide (Mounjaro) BMI ≥35 with at least 1 weight-related comorbidity
41
When to prescribe statin primary prevention
QRISK > 10% T1DM and: Age > 40 Diabetes > 10 years Nephropathy CKD
42
Target for statin and further management
Aim for >40% reduction in non-HDL in 3 months If not achieved - intensify treatment - increase statin dose If not met, consider adding ezetimibe
43
Yellow palmar creases - diagnosis and management
Palmar/tuberous xanthomas Remnant Hyperlipidaemia (Dysbetalipoproteinaemia) Fibrates
44
Diagnosis of familial hypdercholestrolaemia
TC > 7.5 + family history CVD <60 TC > 9 or Non-HDL > 7.5
45
What diagnosis Plasma aldosterone/renin ratio can give
Low renin = primary - bilateral adrenal hyperplasia (most common), conn’s adenoma Further invx: CT adrenals & AVS. High renin = secondary - renal artery stenosis Further invx: USKUB/MRA
46
Most common cause of primary hyperparathyroidism
solitary parathyroid adenoma, accounting for around 80–85% of cases.
47
Hungry bone syndrome
After removal of a hyperfunctioning parathyroid gland, the previously high bone turnover leads to rapid skeletal uptake of calcium and phosphate, resulting in profound post-operative hypocalcaemia. Symptoms: Tingling, tetany, muscle cramps, and positive Chvostek’s/Trousseau’s signs due to hypocalcaemia. Management: IV calcium initially if symptomatic, followed by oral calcium and active vitamin D
48
Management of hyperparathyroidism
1st line: Parathyroidectomy (total or subtotal) Conservative: Consider if calcium <0.25 above upper limit + age >50 + no end organ damage Alternative: Cinacalcet if unsuitable for surgery A calcimimetic - acts on the calcium-sensing receptors of the chief cells of the parathyroid gland, providing negative feedback for PTH secretion.
49
Toxic multinodular goitre features
Autonomously functioning thyroid nodules - produce excess T3/T4 thyrotoxicosis. Invx: Thyroid nuclear scintigraphy - patchy uptake
50
Mx of Toxic multinodular goitre
1st line = Radio-iodine
51
Toxic adenoma thyroid scintigraph
Nuclear scintigraphy shows a well defined area of increased uptake.
52
GH deficiency features
Delayed puberty, short height, low muscle mass, truncal obesity, ‘chubby’ face.
53
Diagnosis and management of GH deficiency
Diagnosis: Insulin tolerance test. Management: rHGH
54
Testing for hypopituitarism
Dynamic Testing: Triple bolus test (insulin, TRH, GnRH) Cortisol/GH → should rise with insulin-induced hypoglycaemia TSH/Prolactin → should rise with TRH LH/FSH → should rise with GnRH
55
Pituitary apoplexy symptoms
Sudden headache, visual loss, and hypotension in known adenoma
56
Sheehan's syndrome sx
Failure to lactate post-partum + amenorrhoea
57
Mx of carcinoid
1st line: Octreotide (somatostatin analogue) Cyproheptadine for diarrhoea (serotonin antagonist)
58
Features and ix for carcinoid
Flushing Diarrhoea Bronchospasm Tricuspid valve stenosis (mid-diastolic murmur) Investigations 24hr urinary 5-HIAA (serotonin metabolite)
59
Autoimmune Polyendocrine Syndrome (APS) APS Type 1
Oral candidiasis Addison's disease Primary hypothyroidism +/- Vitiligo
60
APS Type 2
Addison's disease Type 1 diabetes mellitus OR Hashimoto's thyroiditis +/- Vitiligo
61
Diagnosing insulinoma
Supervised prolonged fast (+/- CT pancreas)
62
Dosing of levo
Most patients: Start at 50–75 mcg OD Elderly/IHD: Caution required - start at 25–50 mcg Pregnancy: Increase dose by 25–50 mcg early in pregnancy Monitoring: TSH every 6–8 weeks until stable
63
Hashimoto’s Thyroiditis features
anti-TPO and anti-thyroglobulin Firm, non-tender goitre Commonly occurs alongside other autoimmune conditions: Vitiligo, coeliac, T1DM ↑ Risk of MALT lymphoma (common MCQ)
64
Riedel’s Thyroiditis
Hard, fixed, painless goitre Symptoms of hypothyroidism
65
Pendred syndrome
Bilateral sensorineural hearing loss Goitre Congenital hypothyroidism
66
Myxoedema Coma features and treatment
Severe hypothyroidism Hypothermia, bradycardia, reduced GCS IV Hydrocortisone + IV Levothyroxine
67
Dex suppression testing results meaning
If cortisol suppressed to < 50 nmol/L - Cushing’s excluded. If cortisol not suppressed - further investigations include midnight + 9am ACTH levels Low ACTH suggests an ACTH independent cause - e.g. adrenal adenoma High dose dexamethasone suppression test - 8mg Cortisol level suppressed = Cushing’s disease Cortisol NOT suppressed = Ectopic ACTH production (e.g. small cell lung cancer)
68
Rapidly enlarging thyroid mass, normal LFTs
Anaplastic
69
Thyroid Nodule/mass? 1st line investigation
Ultrasound +/- biopsy
70
Thyroid lymphoma features
History of Hashimoto’s + rapidly growing thyroid mass
71
Pale, empty nuclei on biopsy of thyroid mass
("Orphan Annie eyes") Papillary Thyroid Cancer- most common
72
Management of papillary thyroid cancer
Total thyroidectomy Followed by radioactive iodine (I-131) ablation Monitor thyroglobulin levels: Every 3-6 months for the first 2 years Then every 6-12 months
73
Low libido, headaches, low BP, irregular periods
Non secretory pituitary adenoma
74
Congenital hypothyroidism features
Baby with prolonged jaundice & macroglossia Hypotonia Puffy face
75
Elevated fasting gastrin and peptic ulcer symptoms
Zollinger–Ellison syndrome
76
Diagnosis of Androgen Insensitivity Syndrome
Chromosomal analysis
77
Mx of Graves in Pregnancy
First trimester is propylthiouracil (PTU), then switched to carbimazole fro 2nd and 3rd because of the risk of PTU-induced hepatotoxicity with prolonged use.
78
Cause of low ACTH with round and plethoric fave, HTN, hyperglycaemia
Low ACTH levels suggest ACTH-independent Cushings Causes include: Exogenous steroids, adrenal adenoma/carcinoma, carney complex.
79
Primary vs secondary vs pseudo hypoparathyroid
Primary hypoparathyroidism Aetiology: Thyroidectomy CFs: Hypocalcaemia (tetany, cramps, paraesthesia) O/E: Trousseaus, chvosteks Secondary hypoparathyroidism – Term generally refers to low PTH due to suppression by hypercalcaemia (e.g. from vitamin D excess), not surgical loss. Pseudohypoparathyroidism – Target organ resistance to PTH; low calcium, high phosphate, but high PTH.
80
TSH is high, T3/4 low. Thyroid scintigraphy shows a globally reduced uptake. Anti-TPO and thyroglobulin antibodies are negative.
De Quervain
81
Blood gas Cushing
Hypokalaemic metabolic alkalosis
82
Step investigation for Cushing
Step 1: Confirm glucocorticoid excess Test: 1mg Overnight Dexamethasone Suppression Test Take 1mg dexamethasone at 11pm Measure serum cortisol at 9am next morning ✅ Normal: cortisol suppressed to < 50 nmol/L ❌ Cushing’s likely: cortisol > 50 nmol/L Step 2: Determine if ACTH-dependent or independent Measure plasma ACTH: Low ACTH = ACTH-independent (likely adrenal cause: adenoma/carcinoma or iatrogenic steroids) High ACTH = ACTH-dependent (likely Cushing’s disease or ectopic ACTH from SCLC etc.) Step 3: Localise the source if ACTH-dependent High-dose Dexamethasone Suppression Test (8mg overnight or 2mg q6h for 2 days): Cushing’s disease (pituitary): Cortisol suppression > 50% MRI Brain to identify pituitary adenoma Ectopic ACTH (e.g. small cell lung cancer): No significant suppression
83
What to do if high TSH, but normal T3/4
Reapeat TFT in 3 months
84
Mx of prolactinoma
Medical treatment is often 1st line (DAs - bromocriptine, cabergoline) Surgery may be indicated if Intolerance or resistance to medical therapy Tumour compressing optic chiasm or rapidly growing
85
Steps of T2DM mx
Step 1 Metformin 1st line (titrate slowly) In addition, add SGLT-2i 1st line if: CVD, HF, QRISK > 10% CKD + proteinuria Step 2 If HbA1c ≥ 58: add second agent DPP-4i (sitagliptin) Sulfonylurea (gliclazide) Thiazolidinediones (pioglitazone) SGLT-2i (dapagliflozin, empaggliflozin) Step 3 If HbA1c ≥ 58: Triple oral therapy OR start insulin Step 4 If triple therapy is ineffective, consider GLP-1 agonist (liraglutide) if: BMI > 35 or BMI < 35 but.. Weight loss would improve co-morbidities Insulin would have significant occupational implications (e.g. HGV driver)
86
MODY features
autosomal dominant Presents <25yrs, not overweight, family history Ketosis usually absent Most common = MODY3 (HNF1-α mutation)
87
MODY tx
1st line Tx: Sulfonylureas (e.g. gliclazide)
88
Low TSH, normal T3/T4
Subclinical Hyperthyroidism ⚠️ Complications Atrial fibrillation, osteoporosis 💊 Management Refer to endocrinology for investigation/management if: 2 x TSH <0.1 >3 months apart AND symptoms of thyrotoxicosis or goitre or positive antibodies Consider carbimazole if high risk - to reduce risk of AF/osteoporosis
89
FRII units per hour
FRIII = 0.1 units/kg/hour
90
Most common cause of hyperparathyroid
primary hyperparathyroidism (around 80–85% of cases) is a solitary parathyroid adenoma.
91
When to admit for high Ca
Admit patients with severe symptoms or severe hypercalcaemia (>3.4 mmol/L) for management with IVI +/- IV bisphosphonates
92
Bony pain, polyuria and constipation. He was admitted last month with pancreatitis. PTH is normal. Phosphate is low.
solitary parathyroid adenoma.
93
Mx of SIADH
1st Line: Fluid restriction. Other: Demeclocycline, Vaptans
94
Test of phaeo
Plasma metanephrines
95
Sx of prolactinoma
Women Galactorrhoea Amenorrhoea or oligomenorrhoea Infertility Decreased libido Men Erectile dysfunction Decreased libido Galactorrhoea (less common) Infertility
96
Targets ranges in T1DM
HbA1c every 3–6 months: aim <48 mmol/mol Capillary BMs: Waking: 5–7 mmol/L Pre-meal: 4–7 mmol/L
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