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15
https://t.me/med1917
ENDOCRINOLOGY
Diabetes mellitus ....................................................................16
Pituitary disorders .................................................................20
Adrenal disease ........................................................................22
ABBREVIATIONS
Abs – Antibodies
ACEi – Angiotensin-converting enzyme
inhibitor
ACTH – Adrenocorticotrophic hormone
ADH – Antidiuretic hormone
AKI – Acute kidney injury
Ald – Aldosterone
ALP – Alkaline phosphatase
ARB – Angiotensin receptor blocker
ARDS – Acute respiratory distress
syndrome
BG – Blood glucose
BNP – B-type natriuretic peptide
Ca – Calcium
CAH – Congenital adrenal hyperplasia
Carb – Carbohydrate
CBG – Capillary blood glucose
CF – Cystic fibrosis
CKD – Chronic kidney disease
CRH – Corticotrophin-releasing hormone
CV – Cardiovascular
CVD – Cardiovascular disease
DA – Dopamine
DHEA(-S) – Dehydroepiandrosterone
(sulfate)
DKA – Diabetic ketoacidosis
DM – Diabetes mellitus
DPP4 – Dipeptidyl-peptidase 4
FNA – Fine needle aspiration
FSH – Follicle-stimulating hormone
GC – Glucocorticoid
GH – Growth hormone
GLP1 – Glucagon-like peptide 1
HHS – Hyperglycaemic hyperosmolar state
HPA axis – Hypothalamic–pituitary–
adrenal axis
HPT – Hyperparathyroidism
HRT – Hormone replacement therapy
ICP – Intracranial pressure
IGF – Insulin-like growth factor
IHD – Ischaemic heart disease
KB – Ketone bodies
LA – Long-acting
LH – Luteinising hormone
MC – Mineralocorticoid
NA – Noradrenaline
Thyroid disease ........................................................................26
Parathyroid disease ..............................................................29
Sodium imbalance .................................................................31
02
Na – Sodium
OGTT – Oral glucose tolerance test
OSA – Obstructive sleep apnoea
Osm – Osmolality
PCOS – Polycystic ovarian syndrome
PO4 – Phosphate
PSA – Prostate-specific antigen
PTH – Parathyroid hormone
RAI – Radioactive iodine
SA – Short-acting
SGLT2 – Sodium-glucose transport
protein2
SLE – Systemic lupus erythematosus
SNS – Sympathetic nervous system
SSRI – Selective serotonin reuptake
inhibitor
T1DM – Type 1 diabetes mellitus
T2DM – Type 2 diabetes mellitus
TPO(Ab) – Thyroid peroxidase (antibodies)
TRAb – Thyroid receptor antibodies
TSH – Thyroid-stimulating hormone
vit D – Vitamin D
16 Chapter 2: Endocrinology
https://t.me/med1917
Diabetes mellitus
Type 1 (8%) Type 2 (90%)
Pathogenesis Autoimmune beta cell destruction
= absolute insulin deficiency
Age of onset Peak 12y (can be any age) Peak in 70s (getting younger)
Associations • Autoimmune condition (islet Abs)
• FHx (50% twin concordance)
Symptoms Rapid onset: often present with DKA
• polydipsia, polyuria
• weight loss / thin
• fatigue, infections
Treatment Lifelong insulin Lifestyle, oral medication, insulin, bariatric surgery
Other types of diabetes mellitus (2%)
1. Genetic e.g. MODY (mature onset diabetes of young) – presents like T2DM but
in <25y → monogenic inheritance
2. Gestational DM – usually temporary
3. Secondary DM
• Pancreatic failure: pancreatitis, CF, cancer
• Endocrine: Cushing’s, acromegaly
• Drugs: corticosteroids, beta-blockers, thyroid hormone
→ 4.7 million people (1 in 15) in UK with DM
→ INCREASING PREVALENCE
Gradual beta cell decline due to prolonged hyperglycaemia
= relative insulin deficiency + insulin resistance
• Obesity, sedentary, age
• FHx (90% twin concordance)
Gradual onset: often no Sx / present with complications
• polyuria, polydipsia
• may lose weight, but overweight to start with
• fatigue, infections
Evaluating glucose control:
• Finger prick = capillary blood glucose
• HbA1C = reflects 3–4m glucose control –
check every 6m
• Continuous monitoring e.g. freestyle LIBRE /
Dexcom
HbA1c targets: individualised
T1DM: <48
T2DM (lifestyle ± single agent): <48
T2DM (gliclazide or 1 agent or insulin): <53
Diagnosis of DKA:
1. Blood glucose >11mmol/L or known DM
2. Capillary ketones >3mmol/L or urinary +++
3. Venous pH <7.35 or HCO
= metabolic acidosis with anion gap
Triggers of DKA:
• new diagnosis / non-compliance
• concurrent illness / SURGERY
• binge drinking / starvation
NB: continue patient’s normal long-acting
SC insulin while on IV insulin
–
<15mmol/L
3
Diagnosis
→ Symptoms + 1 positive lab test OR
→ Asymptomatic + 2 positive lab tests
*OGTT = 75g glucose & wait 2h
Normal Impaired Diabetes
Fasting mmol/L <6.1 6.1–6.9 ≥7.0
OGTT* mmol/L <7.8 7.8–11.0 ≥11.1
HbA1c mmol/mol <42 42–47.9 ≥48
DO NOT USE HbA1c for Dx if:
• Child / suspect T1DM
• Symptoms <2m
• Acute illness, anaemia, CKD
• Pregnancy
• Diabetes-inducing medications
If HbA1c 42–48 suggests
→ do fasting glucose test
↳ If diagnosed, screen for target organ damage:
fundoscopy, urine dip & BP, U&Es, PNS exam
pre-diabetes
Acute complications of DM
DKA T1DM: insufficient insulin causes compensatory metabolic changes to
glucose (fatty acids oxidised to KBs)
Symptoms: N&V, abdo pain, leg cramps, hyperventilation (Kussmaul), confusion,
drowsiness, collapse
→ causes of death = cerebral oedema, hypokalaemia, ARDS, AKI, cardiac arrhythmia
Management1: see Chapter 16: Critical illness
1. IV fluids 0.9% saline IV (1L in 1h)
2. High dose, fixed rate insulin 0.1 units/kg/h (continue until cap. ketones <0.6)
3. Potassium replacement: early (from 2nd bag fluids)
4. Glucose replacement: 10% dextrose when glucose <14mmol/L
5. Careful monitoring (may need HDU): glucose, ketones, VBG, U&Es, neuro status
Medicine
1
Diabetes UK (2021) Management of diabetic ketoacidosis in adults
Chapter 2: Endocrinology 17
https://t.me/med1917
HHS T2DM: severe hyperglycaemia causes hyperosmolar state WITHOUT
SIGNIFICANT KETOSIS → leads to SEVERE DEHYDRATION
Symptoms: onset over 3–14d
• Osmotic diuresis / polydipsia + signs of dehydration
• Nausea & vomiting
• Neuro signs (confusion, seizures, aphasia, hemianopia)
• Consciousness with osmolality
Complications: seizures, cerebral oedema, MI/CVA, DVT/PE, foot complications
Management2: see Chapter 16: Critical illness
1. IV fluids 0.9% saline IV (over 24h to rehydrate)
2. Fixed rate insulin*: 0.05 units/kg/h = HALF DOSE DKA
3. K+ replacement: if K+ drops <5.5mmol/L
*only once glucose
falling by <5mmol/L/h
4. Prophylactic anticoagulation: LMWH for full duration of admission
HYPOGLYCAEMIA: blood glucose <4mmol/L in diabetics (otherwise
<3.5mmol/L with symptoms)
Symptoms:
• Autonomic: sweating, tremor, palpitations
• Neurogenic: confusion, aggression, anxiety, drowsiness, seizures
Management:
• If conscious: 15–20g fast-acting carb → repeat if CBG <4 in 10min (up to 3x)
→ long-acting carb once glucose >4
• If unconscious: 1mg IM glucagon or 100ml 20%
glucose IV → long-acting carb once glucose >4
Once hypo is treated: identify cause/RFs & address these to avoid future episodes
IV glucose is better as can be repeated
& effective in malnourished / liver
disease / alcoholic binge
Metabolic acidosis may be present if
dehydration leads to AKI
Diagnosis of HHS:
1. Blood glucose >30mmol/L
2. Capillary ketones <3mmol/L
3. Venous pH >7.3 or HCO
–
>15mmol/L
3
4. Osmolality >320 mosmol/kg
Triggers of HHS:
• poor control / glucose intake
• illness / infection / MI
• drugs (thiazides, steroids, BBs)
Triggers of hypoglycaemia in DM:
• SE of sulphonylureas & insulin therapy
• food, exercise, insulin
• alcohol
Chronic complications of DM
MICROVASCULAR
• Nephropathy: ×5 risk dialysis or transplant
▶ BP & glycaemic control = KEY
▶ Start ACEi/ARB or SGLT2 if microalbuminaemia → target BP <130/80
• Retinopathy/maculopathy:
▶ Retinopathy: no retinopathy (R0) → background (R1) → pre-proliferative
(R2) → proliferative (R3)
▶ Maculopathy: no maculopathy (M0) maculopathy (M1)
• Neuropathy: risk of neuropathic ulcers & Charcot joint
▶ Peripheral: symmetrical glove & stocking distribution → amitriptyline/
duloxetine/gabapentin/pregabalin if painful
▶ Autonomic: postural hypotension, tachycardia, or sweating,
gastroparesis, bladder dysfunction, erectile dysfunction
▶ Diabetic amyotrophy: progressive, painful muscle wasting (quadriceps &
shoulders)
MACROVASCULAR
• CVD / stroke / vascular dementia: ×2 risk stroke
• IHD/HTN: ×3–4 risk MI
• Peripheral vascular disease: ×20 amputation (gangrene)
If not nephropathy, BP targets are the same as normal:
→ <140/90 CBPM or <135/85 HBPM
Avoid SGLT2 in T1DM as can
cause ketoacidosis
RFs for chronic complications of DM
• long DM duration
• poor control
• smoking
• HTN
• pregnancy
Annual diabetic review:
→ Glycaemic control: med R/V & compliance
→ Retinopathy screening
→ Nephropathy screen: BP, urinalysis, U&Es,
Alb:Cr
→ Foot checks & care: early referral if needed
→ Assess CVD risk (QRisk): statin/antiplatelet
if needed
→ Education/advice: smoking, contraception/
pregnancy
Alb:Cr = albumin–creatinine ratio (needs to
be early morning sample)
2
Diabetes UK (2012) Management of the hyperosmolar hyperglycaemic state (HHS) in adults with diabetes
Medicine
18 Chapter 2: Endocrinology
https://t.me/med1917
Breakfast LunchDinner
Short acting
Plasma
insulin
level
Long acting
Time
Fig. 2.1 Action of SA & LA insulin.
CAUTION PRESCRIBING INSULIN
Ensure you have:
• the correct type (many similar names)
• the correct dose (always write UNITS in full)
• the correct times
Management of T1DM: INSULIN
SA = short acting LA = long acting
1. Basal-bolus: 1 or 2 LA injections PLUS SA with each meal
• Closer to natural insulin secretion pattern
• More flexible with food/exercise → CARB COUNTING
2. Biphasic / twice daily: 2 doses of mixed insulin (with breakfast & dinner)
3. Insulin pump: via cannula → basal rate set + bolus dose with meals
• Avoids multiple injections each day
TYPES OF INSULIN:
Type Peak Example
Rapid acting 1–2h NovoRapid, Humalog
Short acting 2–4h ActRapid, Humulin S
Intermediate acting 5–8h Insulatard, Humulin I
Long acting Relatively peakless Lantus / Levemir / Tresiba
Disadvantages of insulin:
• weight gain
• hypos
• regular monitoring
• injections
Mx complications/RFs:
1. BP = <140/90
(if nephropathy <130/80)
2. Statin if QRISK >10% or presence of
microvascular disease
3. ACEi if microalbuminuria
Sick day rules:
1. Continue normal insulin / oral hypoglycaemic
2. Check BG 4 hourly / more often
3. Encourage fluids (sugary drinks if unable
to eat)
Management of T2DM
3
LIFESTYLE: aim for HbA1c <48 (6.5%)
1. Diet: low glycaemic index carbs, fat, fibre
2. Weight loss: calorie restriction AND exercise (20–30min/d)
3. Reduce smoking/alcohol
Education to enable self-management is key:
1. Dietitian access
2. Websites / support groups
3. Importance of compliance / risk of complications
PHARMACOLOGICAL
Lifestyle
HbA1c >48
Monotherapy
HbA1c >58
Dual therapy
HbA1c >58
Triple therapy
HbA1c >58
Insulin therapy or
GLP1 mimetic
Less frequently used
2nd line agents:
Glitazones (pioglitazone)
Meglitinides (repaglinide)
METFORMIN
(biguanide)
+ Gliclazide (if not driving) OR
+ DPP4 inhibitor / SGLT2 inhibitor
(if renal impairment / CVD) OR
+ SGLT2 (if high BMI)
usually once daily regimen: LAatbreakfast or bed
LIFESTYLE MODIFICATION
(diet, exercise, weight control)
Trial for 3 months
HbA1c >58
INSULIN THERAPY
or GLP1 mimetic
(if BMI >35 or insulin not tolerated/practical)
HbA1c >58
+ DPP4 inhibitor / SGLT2
(if renal impairment / CVD) OR
If metformin
contraindicated,
e.g.poor renal
function, tissue
hypoxia
GLICLAZIDE
(sulphonylurea)
inhibitor
+ SGLT2 (if high BMI)
Medicine
Fig. 2.2
3
NICE (2015, updated 2022) Type 2 diabetes in adults [NG28]
Medication side-eects
https://t.me/med1917
Hypoglycaemic Advantages Disadvantages
Metformin (biguanides)
Gliclazide (sulphonylurea) • rapid effect
Glitazones • low risk of hypos
SGLT2 inhibitors • weight loss
Sitagliptin (DDP4 inhibitors) • low risk of hypos • nausea & acute pancreatitis
GLP1 mimetics • weight loss
• CV risk
• no weight gain
• cheap
• improve lipid profile & CVD risk
• reduce SBP & CVD risk
• good in renal disease
• CV risk if CVD
• GI upset (bloating/diarrhoea)
• not if eGFR <35
• hypos
• weight gain
• weight gain
• bone fractures
• risk fluid retention
• UTIs / candidiasis
• euglycaemic ketoacidosis
• nausea & acute pancreatitis
Chapter 2: Endocrinology 19
Stop metformin if
eGFR <30 or Cr >150 (as risk lactic acidosis)
Glitazones contraindicated in:
CCF, elderly, bladder cancer
Medicine
20 Chapter 2: Endocrinology
(GH-RH)
(TRH)
(CRH)
(GnRH)
(SRIF)
factor
(DA)
&
Testosterone
https://t.me/med1917
Pituitary disorders
The pituitary gland sits below the hypothalamus & optic chiasm
Mass effects of pituitary adenoma:
• Bitemporal hemianopia = from pressure on
optic chiasm
• Ocular palsies = from pressure on cavernous
sinus (CN 3,4,6)
• Headache from ICP
• Altered appetite/thirst/sleep = from pressure
on hypothalamus
• Hypopituitarism from destruction of
functional tissue
• Hyperprolactinaemia from stalk effect
‘The stalk effect’
→ Dopamine released from hypothalamus
reaches pituitary gland via pituitary stalk
→ Normally dopamine INHIBITS prolactin
→ Damaged/compressed stalk = DA =
inhibition = HYPERPROLACTINAEMIA
→ Secretory prolactinoma plus compression
effects = MASSIVE PROLACTIN (>10,000)
Pituitary adenoma: BENIGN
1. Microadenoma <1cm
2. Macroadenoma >1cm = mass effects
• Functioning: secrete hormones (70–80%)
• Non-functioning: not secretory (20–30%)
Growth hormone-releasing hormone
Thyrotropin-releasing hormone
Corticotropin-releasing hormone
Gonadotropin-releasing hormone
Somatotropin release inhibiting
/ somatostatin inhibitor
Dopamine
Bones,
muscles
Breasts
Fig. 2.4 Functions of the pituitary gland.
GH
Prolactin
Ovaries &
testes
Oestrogen
Progesterone
Hypopituitarism
LH
FSH
Ant
ACTH
Adrenal
gland
Aldosterone
cortisol
Fig. 2.3 Visual fields in
bitemporal hemianopia.
NEUROSTIMULATION
Post
Oxytocin
ADH
TSH
Thyroid
gland
Kidneys
& T
T
3
Breasts
uterus
4
Hypopituitarism:
• Sx = vague & non-specific
• General Mx = HORMONE REPLACEMENT
• Ix & Tx of specific cause
DDx hypopituitarism:
Pituitary Hypothalamic
• Non-functioning
adenoma
• Metastatic tumour
• Surgical resection of
• Craniopharyngioma
• Infarction
• Infection
• Sarcoid
gland
• Apoplexy (vascular
insult)
Hormone
Clinical effects Management
lacking
GH Children: short stature
GH analogue
Adults: no Sx / abnormal body
composition / fatigue
LH/FSH ( sex
hormones)
Children: delayed puberty
Adults: no Sx / hypogonadism /
Testosterone (males)
or HRT (females)
amenorrhoea
TSH ( T3/T4)
ACTH ( cortisol) Lethargy, weight loss, glucose, Na
Typical order of hormone loss
Hypothyroidism (cold, weight loss, tired) Thyroxine
Hydrocortisone/prednisolone
PROLACTIN Failed lactation –
ADH Diabetes insipidus (polyuria/polydipsia) Desmopressin
INVESTIGATIONS:
1. History & examination: including visual fields & cranial nerves
2. Pituitary hormones:
• All except prolactin: LOW/normal
• PROLACTIN
→ 500–1000: (micro-prolactinoma) or (non-functioning tumour
compressing stalk) or (other cause of prolactin*)
→ >1000: (micro-prolactinoma AND stalk compression)
or (macroprolactinoma)
3. Effector gland hormones: LOW (T3/T4, FSH*, IGF-1, 9am cortisol)
*FSH should be high if post-menopausal as oestradiol (no more follicles)
• Renal impairment
• Antipsychotics
• Pregnancy/OCP
Medicine
4. Stimulation tests: LOW / no response
https://t.me/med1917
• For ACTH deficiency: insulin
stress test (IST)
• For acromegaly: OGTT → GH
When given insulin, blood glucose
drops → hypoglycaemia triggers ACTH
release – no ACTH suggests deficiency
suppression
• For non-pituitary cause of
adrenal disease: Synacthen test
5. Imaging: CT/MRI – determine
pathology
When given glucose in OGTT, GH
should be suppressed
No suppression suggests acromegaly (check
IGF-1 levels)
Secretory/functional adenomas
→ can produce >1 hormone
Type of adenoma Hormonal effect Symptoms Treatment
Prolactinoma 35%
(F:M = 5:1)
GH-secreting 20% ACROMEGALY/GIGANTISM
ACTH-secreting 10% CUSHING DISEASE
TSH-secreting rare HYPERTHYROIDISM
HYPERPROLACTINAEMIA
basal prolactin
IGF-1 & glucose
cortisol
T3/
4
• Galactorrhoea (+ female amenorrhoea)
• Fertility, libido, hypogonadism
• Complications: osteoporosis
• Size hands/feet slow onset
• Coarse facies, wide-spaced teeth
• Vision loss
• Tired, headache, sweaty, libido
• Complications: DM, HTN, OSA
• Weight, DM, libido
• Hair, striae, hump
• Weight, fatigue
• Hot, sweaty, palpitations
DA agonist*
• carbergoline
• bromocriptine
1. Surgery: transsphenoidal
2. Radiotherapy
3. Medical
• DA agonist
• somatostatin analogue
Chapter 2: Endocrinology 21
*
SE:
pulmonary
fibrosis (need CXR)
Raised TSH & T4 usually indicates poor compliance with LT4 treatment
LH-/FSH-secreting adenoma = VERY RARE
Medicine
22 Chapter 2: Endocrinology
https://t.me/med1917
Adrenal disease
→ Adrenal cortex produces steroid hormones
Zona glomerulosa
Zona fasciculata
Zona reticularis
Medulla
Cortex
Fig. 2.5 Adrenal gland structure.
Zones of the adrenal gland
Zona Glomerulosa Mineralocorticoids
Zona Fasciculata Glucocorticoids
Zona Reticularis Androgens
Medulla Adrenaline
(aldosterone)
(cortisol)
(DHEA, DHEA-S)
Noradrenaline
Na+ & K+ balance
= BP regulation
Response to stress
= glucose metabolism, inflammation
Stimulate masculinisation
Response to stress
= stimulate SNS
ALL STEROID HORMONES
−ve feedback = ACTH & renin (& CRH)
NB 2° adrenal insufficiency
steroids because long-term
→
ONLY LOW CORTISOL (aldosterone = normal)
if withdraw long-term
ACTH suppression
Addisonian crisis:
• Hypotension & tachycardia
• Severe weakness
• Abdo pain, N&V
• Hypoglycaemia, confusion
→ Illness/injury can be a trigger
Sick day rules: double dose hydrocortisone/
prednisolone when unwell
Addison’s disease
→ 1° adrenal insufficiency due to autoimmune destruction of cortex
CAUSES OF GLAND DESTRUCTION:
→ Autoimmune
→ TB
→ Surgery
→ Severe sepsis
→ Adrenal mets
CLINICAL FEATURES:
Symptoms = non-specific Signs
• Weight loss
• Malaise/myalgia/weakness
• Fatigue/depression
• Abdo pain / N&V
• Syncope
INVESTIGATIONS:
1. U&Es: K+ & Na+, urea & creatinine
2. Serum ACTH & cortisol: ACTH, cortisol, renin
3. SHORT SYNACTHEN TEST: 250mcg Synacthen given
• measure serum cortisol at 0 & 30min
• positive test = cortisol doesn’t over 420nmol/L
4. Adrenal autoantibodies
5. Adrenal imaging: USS/CT
MANAGEMENT4:
1. ACUTE CRISIS
→ 100mg IV hydrocortisone + 1L 0.9% IV saline
→ ± dextrose if low glucose
• Pigmentation ( ACTH = melatonin)
• Postural hypotension ( aldosterone)
• Dehydration ( urea & Cr) ( aldosterone)
• K+ & Na+ ( aldosterone)
• Glucose ( cortisol)
Medicine
2. LONG-TERM: lifelong hormone replacement
→ Glucocorticoid (GC): hydrocortisone (TDS – higher dose in morning)
→ Mineralocorticoid (MC): fludrocortisone (monitor BP, oedema, U&Es, renin)
4
NICE (2020) CKS: Addison’s disease
Chapter 2: Endocrinology 23
https://t.me/med1917
Congenital adrenal hyperplasia
→ auto-recessive enzyme deficiency for steroid synthesis
→ 21-hydroxylase = most common deficiency
Results in:
1. cortisol & aldosterone synthesis (in 80% 21-hydroxylase deficiency)
2. Backlog of precursors (progesterone)
3. Increased conversion to androstenedione = sex hormones
CLINICAL PRESENTATION:
Classical (salt-losing) Non-classical (non-salt losing)
Age of presentation First few days of life Teenagers / young adults
Symptoms Hyperandrogenism:
ambiguous genitalia
Similar to Addison’s crisis
• hypotension & dehydration (LOC)
• N&V, FTT, poor feeding
K+ & Na+, Glucose
Investigations 1. Steroid hormones & precursor levels 2. U&Es & glucose
Management Lifelong MC & GC replacement
(hydrocortisone & fludrocortisone)
Hyperandrogenism:
early puberty, menstrual irregularity, hirsutism
Enough enzyme to avoid salt loss
Minimum dose GC replacement
(enough to androgen production but not enough to cause Cushing’s)
mineralocorticoids & glucocorticoids
androgens
Conn’s syndrome
→ 1° hyperaldosteronism resulting in Na+ & H2O retention and K+ loss
CAUSES:
→ Adrenal adenoma (1/3)
→ Unilateral adrenal hypersecretion without adenoma (1/3)
→ Bilateral adrenal hyperplasia (1/3)
CLINICAL PRESENTATION:
→ Hypertension (headaches if severe)
→ Hypokalaemia (possible weakness, cramps, tetany)
INVESTIGATIONS:
1. BP = high
2. U&Es = Na+ & K
+
3. Aldosterone:renin ratio = high ( aldosterone : renin)
→ aldosterone : normal renin = 2° hyperaldosteronism
→ Second line testing = saline infusion or captopril challenge
4. Adrenal gland imaging: CT/MRI abdomen
5. Localisation: with adrenal venous sampling
DIAGNOSTIC
MANAGEMENT:
1. Adrenal adenoma: gland resection
2. Bilateral hyperplasia: medication (as cannot remove both glands)
• Spironolactone/eplerenone (= aldosterone antagonists)
usually asymptomatic
ALDOSTERONE
−ve feedback on renin–angiotensin system =
renin
NB
2° hyperaldosteronism
&
high renin
e.g. chronic liver disease, heart failure, renal
artery stenosis
= high aldosterone
Suspect Conn’s in younger patients (30–50y)
with hypertension plus hypokalaemia
Medicine
24 Chapter 2: Endocrinology
ACTH-dependent
ACTH = cortisol
Ectopic ACTH
= ACTH secretion
from elsewhere
e.g. small cell lung cancer
Cushing’s disease (80%)
= ACTH secretion
from pituitary
e.g. adenoma
ACTH-independent
Cortisol = ACTH
Adrenal tumour
= secretes cortisol
Exogenous
steroids
Loss of circadian
08.00 24.00
https://t.me/med1917
Adrenaline/NA
Syndromes associated with
phaeochromocytoma:
• MEN-II – medullary thyroid carcinoma,
hyperparathyroidism
• Von Hippel-Lindau – renal cell carcinoma,
haemangioblastoma, retinal angioma
• Neurofibromatosis – café-au-lait spots,
neurofibromas
→ Suspicion of syndrome if bilateral tumours
CORTISOL
Cushing‘s syndrome
is umbrella term for all
causes of raised cortisol
Cushing‘s disease is specific
problem of increased ACTH
secretion from pituitary
Phaeochromocytoma
→ catecholamine-secreting tumour ofadrenal medulla (chromaffin cells)
CLINICAL PRESENTATION: hypertension + classic triad
TRIAD: headache + tachycardia + sweating (dizzy/palpitations/tremor)
INVESTIGATIONS:
1. 24h urinary metanephrines ×2 OR plasma metadrenalines
2. Adrenal imaging:
• CT/MRI
• octreotide scan if abnormal CT/MRI
3. Genetic testing:
• if suspicious
MANAGEMENT:
Surgery (pre-op BP control with alpha- & beta-blockers)
Cushing’s syndrome
→ symptoms of increased glucocorticoids
CAUSES:
Medicine
CLINICAL PRESENTATION: cortisol has some MC activity so may see K
+
, Na
Symptoms Signs
• Central obesity (+ diabetic Sx)
• Acne & excess hair
• Thin skin & bruising
• Depression & insomnia
• Reduced libido
• Amenorrhoea
• Moon face & frontal balding
• Buffalo hump
• Abdominal striae
• Proximal myopathy
• Pathological fractures
• Hypertension/DM
INVESTIGATIONS:
Screening tests for Cushing’s syndrome:
1. Low dose dexamethasone suppression test (1mg) = measure 8am cortisol
→ dexamethasone = a GC so should cause ACTH and therefore morning
cortisol
→ no suppression in morning cortisol = Cushing’s syndrome
2. 24h urinary or midnight salivary cortisol: lost circadian rhythm
rhythm
Normal cortisol
cycle
Fig. 2.6 24h cortisol levels.
+
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