Deck 3 Flashcards
Anterior pituitary secretes
GH (GHRH) - Measure by IGF-1. Growth, glucose, FFA
TSH (TRH) - >basal met rate
ACTH (CRH)
FSH (follicular growth/spermatogenesis - GnRH)
LH (testosterone/progesterone - GnRH)
Prolactin (dopamine inhibits)
Posterior pituitary scretes
Vasopressin (ADP - released if ECF hyperosmolarity. Acts on CD and arteriolar smooth muscle)
Oxytocin
Macroadenoma
Pituitary adenoma >10mm.
Causes local effects (headache, bitemooral heminaopia, diplopia, disconnection prolactinaemia, pituitary apoplexy, hydrocephlus (3rd ventricle compression), sphenoid sinus invasion (CSF rhinorrhoea), hypothalamous compression (altered appetite, thirst, sleep cycle)
Can also cause systemic effects (hyperprolactinaemia (galactorrhoea, amenorrhoea, hypogonadism), acromegaly, Cushings.
Can also hypopituitarism (ACTH loss gives addisons symptoms, gonadotrophin loss causes lethargy, libido loss, hair loss, ED, infertility, amenorrhoea. GH loss gives lethargy. TSH loss gives hypothyroid symptoms. Vasopressin loss gives diabetes insipidus)
Microadenoma
Unlikely to cause local effects, often secreting hormones (or rarely causing hypopituitarism)
Pituitary tumour
May be associated with MEN1 (tumours of PT gland, endocrine GI tumours)
Classed by size, function and histology
Chromophobes (70%) secrete prolactin or non-functional. 30% have local pressure effects
Acidophils (15%) secrete GH or prolactin. 10% local pressure
Basophils (15%) tend to secrete ACTH - rarely cause local pressure issue
Hyperprolactinaemia
Galactorrhoea, oligo/amenorrhoea, decreased libido, subfertility, arrested puberty.
Long term, can give osteoporosis.
Distinguish from drug induced, idiopathic or stress. Diagnose by MRI and raised serum prolactin
Acromegaly
Almost always pit tumour in adults, but can be rare paraneoplastic tumour secretion.
Diagnose by raised IGF-1 (gives 24h GH correlation) and OGTT (>2mcg/mL GH at 2h)
Growth symptoms, headaches, diabetes, interdental separation, large tongue, HTN, excessive sweating, tiredness
Cushings (exogenous)
Exogenous is more common.
Can also be Adrenal adenoma (5-10%, carney complex (syndrome with cardiac myxoma) and micronodular adrenal dysplasia (very rare)
Endogenous cushings
80% are cushing’s disease (pituitary tumour) 5-10% are ectopic ACTH (small cell lung cancer is most common)
Pseudocushing’s
Mimic’s cushings. Often due to alcohol excess or severe depression. Causes FP dex suppression test and raised 24h urine cortisol. Distinguish with insulin stress test
Note that alcohol excess can give cushingoid appearnace
Cushing’s S+S
Central weight gain, depression, insomnia, poor libido, thin skin/easy bruising, hirsutism, acne, diabetes symptoms, moon face, frontal balding, striae, HTN, pathological fractures, dorsal fat pad, proximal myopathy.
Predisposes to CVD, diabetes and osteoporosis
Cushing diagnosis
Overnight dex suppresion test (1mg at midnight)
48h dex suppresion test
24h urinary cortisol
Midnight cortisol
Plasma ACTH (if N/D, adrenal cause liekly and CT needed)
In high ACTH, try high dose dexa suppression (will reduce if pituitary, but not in ectopic secretion).
Note that if ACTH or CRH is high then Cushing’s disease, otherwise syndrome
Adrenal gland
Cortex has: Zona glomerulosa (aldosterone) Zona Fasicula (cortisol and some sex hormones) Zona reticularis (testosterone and some cortisol)
Medulla secretes catecholamines (Adrenaline is alpha (vasoconstriction) and beta (tachycardia, insulin resistance and skeletal muscle vasodilation) agonist. NA is alpha)
Conns
More common in young females
Primary is adrenal hyperplasia or adrenal adenoma
Secondary is RAAS overactivation in renal artery stenosis or JGA tumour
HTN, muscle weakness/cramps, paraesthesia, polyuria, headaches.
Hypernatraemia, hypokalaemia, alkalaemia (met alkalosis), acidic urine, raised aldosterone:renin ratio
Addison’s definition and causes
Primary andrenocortisol insufficiency
80% in UK are autoimmune, TB is most common cause worldwide
Can also be adrenal met (lymphoma).
Secondary adrenocortisol insufficiency
Not addisons.
Occurs in steroids withdrawal or pituitary apoplexy with reduced ACTH release)
Note will not see hyperpigmentation in this case
Addison’s signs and symptoms
Fatigue, muscle weakness, anorexia, weight loss, diarrhoea, N&V, hyperpigmentation, depression/irritability, myalgia, arthalgia, postural hypotension, faints, loss of body hair.
Crisis is abdo pain, vomiting, shock and coma.
Addison’s biochemistry
Hyperkalaemia (cardiac arrythmia risk), hyponatraemia, high ACTH, low cortisol, 21 hydroxylase adrenal autoantibodies, CXR for TB, adrenal CT
Addison’s management
fludrocortisone for aldosterone, hydroxycortisol.
21 alpha hydroxylase deficiency
congenital adrenal hyperplasia. Enzyme needed for cortisol and aldosterone, but not sex hormones so see hypergonadism and raised 17 alpha hydroxyprogesterone levels
phaeochromocytoma
Chromaffin tumour.
Secretes catocholaemines. Can be in medulla or ectopid (e.g. abdominal).
10% malignant, 10% extra adrenal, 10% bilateral, 10% familial (MEN2a/2b, neurofibromatosis, von Hippel Lindau syndrome)
Causes headache, diaphoresis, tachycardia, episodic severe HTN, orthostatic HTN, heat intolerance.
Gives arrythmias/MI, tremor
Horner’s syndrome, tremor, CNS haemorrhage
Diarrhoea, vomiting, abdominal pain
Hyperglycaemia
Sweating, flushing, heat intolerance
Pallor
Symptoms can be worsened by stress, exercise, drugs (beta blockers without alpha blockade causes massive HTN)
See raised metadrenaline in plasma and urine, raised WCC
Surigcally managed
DM definition
Metabolic disorder with hyperglycaemia in the absence of treatment
Insulin inhibitors
alpha adrenergics, beta blockers and adrenaline
T1DM
Autoimmune
Associated with PA, addison’s, autoimmune thyroid diseases
Typical features are 2-6 week polyuria, polydipsia and weight loss
T2DM
metabolic state
Pancreatic insulin insufficiency and insulin resistance.
Strong hereditary factor.
Associated with hyperlipidaemia, obesity, sleep apnoea, and CVD
Longer onset, polydipisa/polyuria/weight loss may be present, but more commonly see fatigue, visual blurring, pruritis vulvae/balanitis.
mAY FIRST PRESENT WITH COMPLICATIONS
mody
Autosomal dominant diabetes
Defective beta cells
May or may not need insulin
Mimics T2DM, usually <25years
Other diabetes mellitus conditions
Type A insulin resistance
Rabson Menderhall syndrome
Down syndrome
Leprechainism/donohue syndrome
Secondary diabetes causes
Pancreatic disease, endocrinopathies (Acromegaly, Cushing's, phaeochromocytoma) Drug induced (steroids, thiazide, beta blockers) Infections (congenital rubella, CMV, mumps), Gestational
Glucose homeostasis
Insulin allows glucose uptake and promotes glycolysis (glucose to ATP) and reduces gluconeogenesis.
Acts on GLUT
Glucagon promotes gluconeogenesis and glucose release
GLUT2
beta cell sensing
GLUT4
skeletal muscle/adipose tissue uptake
DKA
Dehydration, elevated FFA with acidosis.
Compensatory hyperventilation
and vomiting
Renal perfusion falls, reduced acid and ketone secretion. Get gastric ileus.
Hyponatraemia, and hyperkalaemia (but may get pseudohyperkalaemia as it exhanges out of the cell)
Can be precipitated by MI or infection.
Acidosis, reduced bicarb <15), ketosis
Give fluids, ACTRAPID insulin.
If K <5.4 then 40mmol/L
If <3.4 then critical care.
Can give glucose (10% at 125mL/hour) once glucose <14
HONK/HSS
More insidious.
Can occur in glucose consumption, thiazide diuretics, steroids, beta blockers, infection/MI
Hypovolaemia, hyperglycaemia (>30), no significant ketonaemia, no significant acidosis, osmolarity >320 (2Na+glucose +urea)
May get hypernatraemia, may get mild lactic acidosis.
High thrombosis risk
Hypoglycaemia
<3mmol/L
Sweating, anxiety, hunger, trmor, palpitations, neuroglycopoenic (confusion, drowsiness, seizures)
Alpha pancreas cells can become insensitive. Can also be due to too much insulin, or depletion of hepatic glycogen (malnutrition, alcohol, liver failure).
Give 10-20g of fast acting carb if able to swallow, otherwise glucagon and 100mL 20% dlucose.
Diabetes complications
Macrovascular (Cardio/cerebrovascular disease, Peripheral arterial disease)
Microvascular:
Retinopathy, nephropathy, sensorimotor issues, peripheral neuropathy
Diabetic foot
Combination of micro and macro vascular problems, leading to peripheral neuropathy , ulcers, rocker bottom foot and infections
Diabetic neuropathy
Sensory neuropathy (loss of protection against minor injury) Autonomic neuropathy (lack of sweating - dry fissured skin allowing bacterial entry) Motor neuropathy - msall muscle wasting gives loss of arches and abnormal pressure areas
Tend to get stabbing pains in feet but still has warmth and colour (in contrast to PAD)
Impact of diabetes mentally etc
Diabulaemia (avoid insulin to avoid weight gain)
Lipohypertrophy (repeated finger prick and insulin injections)
DVLA notified if insulin or hypoglycaemia inducing meds, or have reduce hypo awareness
Must inform if 2 hypos in 12 months
Diabetic retinopathy
Can be NPDR - asymptomatic. Often see aneurysms, exudates, haemorrhages and cotton wool spots.
pDR is new vessel growth due to ischaemia, but new vessels are fragile and bleed (pre-retinal or vitreous haemorrhage). Can cause fibrosis or retinal detachment.
