Endocrinology & Breast Flashcards
Definition & Pathophysiology - T1DM
Autoimmune destruction of pancreatic beta cells leading to loss of insulin production
S&S - T1DM
4Ts - toilet (polydipsia), thin (W/L), thristy (polydipsia) & tired
nausea
vomiting
FTT
Diagnosis of T1DM
Clinical symptoms & random blood glucose >11 mmol/L
DKA - pathophysiology
Complete lack of insulin leads to a state of hyperglycaemia, glucose cannot be transported into cells as no insulin signal. Blood is hyperglycaemia but body/cells perceived as in a starvation state & so begin ketogenesis.
Over time the patient gets higher and higher glucose and ketones levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.
Over time the ketone acids use up the bicarbonate and the blood starts to become acidic
S&S - DKA
Polyuria & Polydipsia N&V Abdominal pain Leg cramps Headache Confusion Drowsiness Coma
Diagnosis of DKA
Hyperglycaemia - glucose >11mmol/L
Ketones - +++ on dipstick or cap >3mmol/L
Venous/arterial blood gas: pH < 7.3 or bicarbonate < 15 mmol/L
Management of DKA
FIG PICK Fluids resuscitation Insulin Glucose - monitor & add dextrose Potassium - monitor & correct Infection - treat underlying causes Chart - fluid balance Ketones - monitor
Causes of DKA
Non-compliance 25%
Inadequate/missed dose of insulin 13%
Infection (30-40%)
Undiagnosed T1DM 10-20%
Definition of Hyperthyroidism - types
Overproduction of thyroid hormone causing thyrotoxicosis
Primary - issue with thyroid, high T4/T3, low TSH
Secondary - issue with hypothalamic/pituitary, high T4/T3 & high TSH
Aetiology of Hyperthyroidism
Grave's Disease - autoimmune disease, TSHR-Abs Toxic multinodular goitre Solitary toxic adenoma 2 hyperthyroidism - pituitary adenoma Drugs - amiodarone, T4 overdose
Clinical Features - Hyperthyroidism
Goitre Palpitations Heat intolerance Weight loss Diarrhoea Amenorrhoea Reduced libido Gynaecomastia (in men) Fatigue Change in mood
Signs: Goitre, Sinus tachycardia/arrhythmias, Hair loss, Palmar erythema
Tremor, Thyroid bruit (Graves’), Myxoedema
Investigations - Hyperthyroidism
Bedside - observations, ECG (sinus tachycardia)
Bloods e.g. FBC (hb - anaemia for tiredness)
Thyroid function tests - fT3/fT4 & TSH
Autoantibodies - TSH-R
Imaging - USS, thyroid uptake scan
NICE also advises screening for T1DM, other AI conditions & new onset AF
Management - Hyperthyroidism
Thioamides (carbimazole or propylthiouracil)
Beta blockers - symptoms
Radioactive iodine
Thyroidectomy
Complications - Hyperthyroidism
A thyrotoxic crisis is rare but potentially fatal result of untreated/undertreated hyperthyroidism.
Beta-blockers
Thionamides: typically propylthiouracil, which in addition to its anti-thyroid effect also reduces the conversion of T4 to T3.
Corticosteroids: reduce the conversion of T4 to T3.
Definition & Types - Hypothyroidism
Definition: Underproduction of thyroid hormone
Primary - issue with thyroid, low T3/T4 but high TSH
Secondary - issue with pituitary, low T3/T4 & low TSH
Tertiary - issue with hypothalmus, low T3/T4 & low TSH
Causes - hypothyroidism
AI - Hashimoto’s thyroiditis
Iodine deficiency
Drugs - amiodarone, radioI
Congenital Hypothyroidism
Investigations - Hypothyroidism
Bloods • FBC - Hb (r/o anemia) • B12 & Folate • Autoantibodies - anti-TPO & anti-Tg Thyroid Function Tests • Primary - low T3/T4 & high TSH • Secondary - low T3/T4 & low TSH
Imaging
• USS + 2ww if suspicion of malignancy
Clinical features - hypothyroidism
• Weight gain • Tiredness/fatigue • Cold intolerance • Goitre • Hair loss ○ characteristically the outer third of the eyebrows • Bradycardia
• Dry skin
• Hair loss
• Reduced libido
o Menstrual irregularities
Management of Hypothyroidism
Replacement of thyroxine
• Levothyroxine & titrate for control
Complications - Hypothyroidism
Often results from acute decompensation during an intercurrent illness. Patients are hypotensive, hypothermic, bradycardic and demonstrate cognitive decline.
IV levothyroxine is the mainstay of management. Electrolyte imbalances and hypothermia should be addressed. IV hydrocortisone may be needed unless hypopituitarism is ruled out as a cause.
Definition - Cushing’s Syndrome & Disease
Syndrome associated with chronic inappropriate elevation of free circulating cortisol
Aetiology - Cushing’s
ACTH-Dependent (80%)
• Excess ACTH secreted from pituitary adenoma –> Cushing’s Disease
• ACTH secreted from ectopic source e.g. small cell lung carcinoma
ACTH-Independent (20%)
• Excess cortisol secreted from benign adrenal adenoma
• Excess cortisol secreted from adrenal carcinoma
Exogenous Steroids
Clinical Features - Cushing’s
'’SWEDISH’’ - spinal tenderness/osteoporosis, weight gain, easy bruising, T2DM, intracapsular fat pad, striae, hypertension
Moon Face Hyperpigmentation Central obesity Hiritisum Acne Frontal Balding Oligo/amenorrhea Poor wound healing Recurrent infections
Investigations - Cushing’s
Bloods
• Early morning cortisol
• Low dose dexamethasone (1mg) suppression test
○ if cortisol still high then +ve = Cushing’s
Urine
24 hour urinary cortisol; levels 3-4x normal
Localising
- plasma ACTH (high = acth dependent)
- high dose dexamethasone (suppressed - pituitary, unsuppressed - ectopic)
Management - Cushing’s
Surgery - transsphenoidal resection of pituitary adenoma
T2DM - Risk Factors
Obesity Family hx PCOS HX of GDM Diet Low birth weight
T2DM - Clinical Features
Tiredness/lethargy Polyuria Polydipsia Weight gain Recurrent infections
T2DM - Diagnosis
Clinical symptoms + HbA1c >48 or fasting glucose >7
T2DM - Management
Lifestyle modifications
Metformin (1st line) - if HbA1c stays >58 then + 2nd line
2nd line: sulphonylurea, GLP1 agonists, DDP4i, SLGT2i
Insulin
Classes & Examples of Diabetic Drugs
Metformin Sulphonylurea - gliclazide GLP1 agonists - liraglutide DPP4i - sitagliptin SLGT2i - empaglifozin
Breast Cancer - risk factors
• Genetics - BRCA • Family history • Early menarche & late menopause • Age • Nulliparity • Increased age of first pregnancy • Combined oral contraceptive (still debated, effect likely minimal if present) • Hormone replacement therapy • White ethnicity Exposure to radiation
Breast Cancer - Types
ductal (in ducts) or lobular (in lobes)
invasive or in situ (not invaded basement membrane)
Breast Cancer - Clinical Features
• Breast lump - often hard, irregular, immobile
• Axillary lump
• Changes to skin - change to normal experience, skin tethering, peau d’orange, oedema
Nipple changes - new inversion, discharge (bloody = scarier), dilated veins
Breast Cancer - 2WW Criteria
• Aged 30 or over with breast lump (with or without pain)
• Aged 50 or over with any of the following in one nipple
○ New inversion
○ Discharge
○ Other changes of concern
• Anyone with skin changes worrying for breast cancer
• Aged 30 or over with axillary lump
Breast Cancer - Investigations
TRIPLE ASSESSMENT
• History & Examination by specialist
• Imaging - mammogram or USS
○ <40s tend to have USS as breast tissue is too dense
○ USS also used if patient has had recent mammogram
• Histopathology
FNA or Core biospy
Breast Cancer - Management Options
• Surgical
○ Local resection +/- lymph nodes
○ Mastectomy +/- lymph nodes
• Radiotherapy - often used adjunctively (after surgery) ○ Local ○ Whole breast ○ Lymph nodes • Chemotherapy & Biologics ○ Before surgery ○ Chemotherapy regimes ○ Herceptin (Trastuzumab) in those with HER2 positive breast cancer • Endocrine therapy - usual course is for 5yrs ○ Tamoxifen or Aromatase inhibitors
Aetiology - Mastitis
Infective - bacteria enters breast via nipple, commonly staph aureus
Non-infective - obstruction of milk ducts & accumulation of breast milk
Mastitis - Risk Factors
• Poor attachment to breast ○ Cleft palate ○ Short frenulum • Reduced feeding (in no. or duration) ○ Rapid weening ○ Unilateral feeding ○ Breast tenderness • Pressure on breast ○ Seat belt ○ Tight Bra Sleeping position
Clinical features - Mastitis
Red hot swollen painful breast - usually unilateral
lymphadenopathy
Signs of systemic upset - malaise, myalgia, pyrexia, tachycardia
Management - Mastitis
Conservative
• Patient education regarding risk factors
• Encourage to continue breast feeding/expressing
• Analgesia - paracetamol, ibruprofen
Warm compresses & warm bathing
• Some may require antibiotic treatment • If no improvement with conservative management or if infection is suspected e.g. fever Flucloxacillin QDS 10-14days
Benign Breast Disease
Fibroadenoma: Result from hyperplasia of a breast lobule and contain both normal epithelial and connective tissue elements.
Fat necrosis: Irregular and necrotic adipocytes, amorphous material and inflammatory cells, including foreign body giant cells, can mimic malignancy.
Sclerosing adenosis: Is an aberration of normal involution.
Duct ectasia: Occurs when central ducts become dilated with duct secretions; if leakage occurs into periductal tissue, this causes an inflammatory reaction (periductal mastitis).
Adrenal Insufficiency - Definition
Deficiency of adrenal hormones - glucocorticoids, mineralocorticoids & androgens
Adrenal Insufficiency - Types & Aetiology
o Primary AI; issues with adrenal glands
- 80% of cases are due to autoimmune causes - Addison’s
- Other causes: infection (TB), metastasis, hemorrhage or sepsis
o Secondary AI; issue with pituitary gland
- Lack of ACTH released resulting in low cortisol - Can be due to pituitary tumour, infection, loss of blood flow (Sheehan's syndrome)
o Tertiary AI; issue with hypothalamus
- Lack of CRH released usually due to suppression of HPA axis - Usually due to long term use of steroids
Clinical Features - Adrenal Insufficiency/Addison’s
• Fatigue/tiredness • Abdominal pain • Nausea & vomiting • Cramps Reduced libido
• Hyperpigmentation • Postural hypotension • Hypotension Loss of body hair (women)
Diagnosis & Investigations - Adrenal Insufficiency/Addison’s
U&Es - can show hypoNa & hyperK
Serum cortisol - measured 8-9am
Short synacthen test; synacthen given - cortisol measured, should double in normal patients
Imaging - CT/MRI Adrenals
Can be used if structural pathology suspected
Management of Adrenal Insufficiency/Addisons
Replacement of steroids - titrated based on S&S & electrolytes
• Hydrocortisone - replaces cortisol
• Fludrocortisone - used in aldosterone in need of replacment
Patient education
• Recognition of Addisonian Crisis (managed with IV hydrocortisone & fluid rehydration)
• Steroid Card & ID tag
Sick day rules - double doses in acute illness
Complications of Addison’s
Addisonian Crisis – severe dehydration, severe n&v, pale, cold, clammy skin, sweating, rapid, shallow breathing, dizziness, coma
Treat with IV steroids (hydrocortisone), fluids & glucose if needed
Types of Hyperparathyroidism & causes
Primary = increased PTH (independent on Ca level) due to adenoma, leads to hyperCa
Secondary = increased PTH due to hypoCa, usually as a result of chronic renal failure or vit D deficiency
Tertiary = increased PTH leading to hyperCa due to hyperplasia of gland due to long term secondary HPTH
Clinical features of hyperCa vs hypoCa
HyperCa - renal stones, bone pain, constipation, N&V, confusion, fatigue
HypoCa - pins & needles, spasms, cramps, wheeze, stridor
Causes of hyperCa
Primary or Tertiary HPTH Malignancy Ectopic Vit D production - sarcoidosis Thyrotoxicosis Drugs - OTC Ca or Vit D or thiazide diuretics
Investigations for hyperparathyroidism
Bloods - U&Es, calcium, ALP (bone profile), albumin, phosphate, VitD
- Serum Ca - high = HPTH
- Measure PTH - high = HPTH, low = other cause e.g. malignancy,
Primary HPTH = high PTH, high Ca
Secondary = high PTH, normal/low Ca
Tertiary = high PTH, mega high Ca
Can also consider urine Ca (r/o familial hypocalcuric hyperCa)
Imaging - USS or Xray
Management of Hyperparathyroidism
Primary HPTH - surgery to remove adenoma or conservative treatment (maintain adequate hydration)
Secondary HPTH - treat cause e.g. renal failure or Vit D supplements
Management of hyperCa
IV fluids x2
Bisphosphonates
'’Rehydrate, rehydrate, bisphosphonates’’
Hyperaldosteronism - Types & Causes
Primary hyperaldosteronism (Conn’s Syndrome)
- Due to issue with adrenal glands, acting independently of RAS
- Causes include: bilateral idiopathic hyperplasia, adrenal adenoma, familial (rare) & adrenal carcinoma (rare)
- –> High aldosterone, low renin
Secondary hyperaldosteronism
- Dysfunctional RAS causes overproduction of aldosterone
- Causes include: renal artery stenosis, renal artery obstruction & heart failure
- –> High aldosterone, high renin
Clinical features of hyperaldosteronism
HypoK
Hypertension
Alkalosis
Investigations & Diagnosis - Hyperaldosteronism
Serum aldosterone & renin ratios
○ Primary = high aldosterone, low renin
○ Secondary = high aldosterone, high renin
Bloods - U&Es to show hypoK
BP - hypertension
Imaging
o CT/MRI adrenals - adenoma
o Renal doppler - renal a. stenosis
Management of Hyperaldosternonism
- Aldosterone antagonists - spironolactone & eplerenone
* Surgical options to treat cause e.g. removal of adenoma or renal a. angioplasty repair
