Download File - Sheffield Peer Teaching Society

Endocrinology
Phase 2a Revision Session
Rhys Watkins and David Rutherford
27/3/17
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Glucose
Range: 3.5-8 mmol/L under all conditions
Liver
- Stores Glycogen
- Glycogenolysis
- Gluconeogenesis from fat, protein, glycogen
Taken into cells by GLUT receptors (comes in different
varieties based on location)
Insulin: GlucoseGlycogen, Glucose into cells, supppresses
glycogenolysis and gluconeogenesis
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Diabetes Mellitus (Type I)
• B-cell destruction in Islet of Langerhans
• Aetiology: Autoimmune
Acute presentation:
Polyuria
Polydipsia
Weight loss
Subacute presentation:
Fatigue
Polyuria/dipsia
Balanitis/candida
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DKA
Visual change
Type II – the metabolic syndrome
Central obesity
Elevated
cholesterol/triglycerides
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Raised
BP
Type II
Risk: Obese, advancing age, FH, certain ethnic groups
Major Immediate Complication: HHS (Previously HONK)
Major Long-term Complications: Kidney, Eye, Foot,
Neuropathy
Everything
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Diagnosis
HbA1C >48 (6.5%) -- Consider ‘pre-diabetes’ if 42-47
(6.1-6.4%)
Fasting glucose >7 (>6.5 = impaired GT)
Oral GTT @2hrs >7.8 (>6.1 = Impaired)
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Management
Stepwise
SULFONYLUREA
(caution glibenclamide/cholropropramide in eldery/renal impairment)
METFORMIN
DPP-4 INHIBITOR
PIOGLITAZONE
(avoid with biggest CVD risk)
Triple Therapy
Insulin
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Stop this from happening, please
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DKA
Features: Lethargy, polyuria, dehydration, confusion, coma,
abdo pain, Kussmaul breathing
Diagnose: Ketone ++, Glucose >11, venous pH <7.3, bicarb
<16
First priority: Fluid balance and dehydration. 0.9% saline
500ml bolus then replacement regime, typically 100ml/kg
(1L over 1hr, 2hr, 4hr, 6hr)
Second: Actrapid 0,1u/kg/hr IV. Avoid SC
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Resolution:
pH >7.3
Bicarb >18
Ketones <0.3
Ketones poorly discriminative
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THYROID DISEASE
THYROID ANATOMY
Thyroid cartilage
Isthmus
4th tracheal ring
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THYROID ANATOMY
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THYROID HISTOLOGY
Colloid
(thyroglobulin)
Cuboidal
epithelial
cells
Follicle
Basement
membrane
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THYROID PHYSIOLOGY
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HYPOTHYROIDISM: CAUSES
PRIMARY HYPOTHYROIDISM (↓T4)
-
Primary atrophic hypothyroidism
Hashimoto’s thyroiditis (anti-TSHR, anti-Tg, anti-TPO)
Iodine deficiency
Post-thyroidectomy / radioiodine / antithyroid drugs
Lithium / amiodarone
SECONDARY HYPOTHYROIDISM (↓TSH)
- Hypopituitarism
HYPOTHYROIDISM
SYMPTOMS
CVS: RS: Hoarse voice
GI: Constipation
Int: Cold intolerance
Endo: Weight gain
UG: Menorrhagia
MSK: Myalgia, weakness
Neuro / Psych: Tired,
low mood, dementia
SIGNS
Bradycardic
Reflexes relax slowly
Ataxia (cerebellar)
Dry, thin hair / skin
Yawning / drowsy /
coma
Cold hands +/- ↓T°C
Ascites
Round puffy face
Defeated demeanour
Immobile +/- Ileus
CCF
HYPOTHYROIDISM
↓T3, ↓T4
=
↑TSH
INVESTIGATIONS:
(a) TFT
(b) Lipids/cholesterol
(c) FBC
(macrocytosis)
HYPOTHYROIDISM: ASSOCIATIONS
AUTOIMMUNE
Type 1 Diabetes Mellitus
Addison’s disease
Pernicious anaemia
Primary biliary cirrhosis
INHERITED
Turner’s syndrome
Down’s syndrome
Cystic fibrosis
HYPOTHYROIDISM: TREATMENT
• Levothyroxine (T4) – review at 12
weeks, adjust 6 weekly
• NB: give smaller doses if elderly as
risk of angina or MI
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The Peer Teaching Society is not liable for false or misleading information…
HYPERTHYROIDISM: CAUSES
1. GRAVES’ DISEASE:
- IgG autoantibodies bind to and stimulate TSH
receptors (triggers = infection, stress, childbirth)
- Eye disease, pretibial myxoedema, thyroid acropachy
- Autoimmune (vitiligo, type 1 DM, Addison’s)
2. TOXIC MULTINODULAR GOITRE
3. TOXIC ADENOMA
4. ECTOPIC THYROID TISSUE (mets / struma ovarii)
5. EXOGENOUS (Iodine / T4 excess)
6. DE QUERVAIN’S THYROIDITIS (post-viral)
Pretibial Myxoedema
Thyroid Acropachy
HYPERTHYROIDISM
SYMPTOMS
CVS: Palpitations
RS: GI: Diarrhoea
Int: Heat intolerance
Endo: ↓Weight, ↑appetite
UG: Oligomenorrhoea +/infertility
MSK: Neuro / Psych: Tremor,
irritability, labile emotions
SIGNS
HANDS:
- Palmar erythema; warm,
moist skin; fine tremor
PULSE:
- Tachycardia; SVT; AF
FACE:
Thin hair; lid lag / retraction
NECK:
Goitre; nodules; bruit
HYPERTHYROIDISM
↑T3, ↑T4
=
↓TSH
INVESTIGATIONS:
(a) TFT
(b) FBC (normocytic
anaemia)
(c) ESR (↑)
(d) Calcium (↑)
(e) LFT (↑)
(f) Thyroid autoantibodies
(g) Visual fields, acuity, eye
movements
HYPERTHYROIDISM: TREATMENT
(i) β-blockers:
- Propanolol (rapid control of symptoms)
(ii) Antithyroid medication:
- Titration (carbimazole: SE = AGRANULOCYTOSIS)
- Block and replace (carbimazole + thyroxine)
(iii) Radioiodine (131I)
(iv) Thyroidectomy
THYROID EYE DISEASE
• 25-50% have Graves’ disease
• Main risk factor = smoking
• Eye and thyroid disease may not correlate
SYMPTOMS: Eye discomfort, grittiness, diplopia
SIGNS: Exophthalmos, proptosis, ophthalmoplegia
TESTS: Clinical diagnosis +/- CT/MRI orbits
MANAGEMENT: Conservative measures (stop smoking,
sunglasses, Fresnel prism); IV methylprednisolone;
Surgical decompression; Eyelid surgery
CAUSE OF GOITRE
DIFFUSE
- Physiological
- Graves’ disease
- Hashimoto’s thyroiditis
- De Quervain’s
NODULAR
- Multinodular
- Adenoma / cyst
- Carcinoma
THYROID CANCERS
1. Papillary (60%)
2. Follicular (≤25%)
3. Medullary (5%)
4. Lymphoma (5%)
5. Anaplastic
EMERGENCIES
1. Myxoedema coma (↓T4)
2. Thyrotoxic storm (↑T4)
ADRENAL DISORDERS
ADRENAL GLANDS
ADRENALS HISTOLOGY
CUSHING’S SYNDROME
• CHRONIC glucocorticoid excess
• LOSS of normal feedback mechanisms
• LOSS of circadian rhythm.
• Most common cause = IATROGENIC
• If due to pituitary adenoma = Cushing’s DISEASE
• “Lemon on sticks” appearance
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CUSHING’S SYNDROME: CAUSES
ACTH DEPENDENENT
(↑ACTH)
CUSHING’S DISEASE
Bilateral adrenal hyperplasia from
ACTH-secreting pituitary adenoma
ECTOPIC ACTH PRODUCTION
Small cell lung Ca and carcinoid
tumours
ACTH INDEPENDENT
(↓ACTH DUE TO
NEGATIVE
FEEDBACK)
ADRENAL ADENOMA /
CARCINOMA
Abdo pain +/- virilisation in females
ADRENAL NODULAR
HYPERPLASIA
ECTOPIC CRH PRODUCTION
IATROGENIC
Thyroid medullary and prostate
cancers
Steroids (common)
CUSHING’S SYNDROME
SYMPTOMS
Int: Acne
Endo: ↑ Weight
UG: Gonadal dysfunction
MSK: Proximal weakness
Psych: Mood change
SIGNS
FAT DISTRIBUTION:
- Central obesity
- Moon face
- Buffalo neck hump
- Supraclavicular fat distribution
SKIN CHANGES:
- Skin and muscle atrophy
- Bruises
- Purple abdominal striae
OTHER:
- Osteoporosis
- Hypertension, hyperglycaemia
- Infection-prone / poor healing
BASIC RULES OF ENDOCRINOLOGY:
1. EXCESS hormone – INHIBIT the gland
2. LOW hormone – STIMULATE the gland
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The Peer Teaching Society is not liable for false or misleading information…
CUSHING’S SYNDROME: INVESTIGATIONS
1. Bloods (↑plasma cortisol)
2. Overnight dexamethasone suppression test
- Dexamethasone 1mg PO at 00:00
- Measure serum cortisol at 08:00
- Normal <50nmol/L (no suppression in Cushing’s)
3. 48h dexamethasone suppression test
- Dexamethasone given qds for 2 days
- Measure cortisol at 0h and 48h
- No suppression in Cushing’s
LOCALISING THE LESION
• If above tests +ve → PLASMA ACTH
• ACTH undetectable → ADRENAL TUMOUR → CT
ADRENAL GLANDS
• ACTH detectable → PITUITARY vs ECTOPIC:
- 48h HIGH-DOSE dexamethasone suppression test
- CRH TEST (measure cortisol at 120 mins)
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CUSHING’S SYNDROME: TREATMENT
• Iatrogenic – stop steroids
• Cushing’s disease – trans-sphenoidal surgery or
bilateral adrenalectomy (caution Nelson’s syndrome)
• Adrenal adenoma – adrenalectomy
• Adrenal carcinoma – adrenalectomy, RT and
adrenolytics (mitotane)
• Ectopic ACTH – surgery (if localised)
YOU HAVE NO ADRENAL
GLANDS
ADDISON’S DISEASE
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ADDISON’S DISEASE
• Primary adrenocortical insufficiency
• Destruction of adrenal cortex
• ↓Glucocorticoids and ↓Mineralocorticoids
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ADDISON’S DISEASE: CAUSES
• Autoimmune (80%) – commonest in UK
• TB – commonest worldwide
•
•
•
•
•
Adrenal metastases (lung, breast, kidney)
Lymphoma
Opportunistic infections in HIV (e.g. CMV)
Adrenal haemorrhage (e.g. SLE, APS)
Congenital adrenal hyperplasia (late-onset)
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ADDISON’S DISEASE
SYMPTOMS
GI: N/V, abdo pain,
constipation / diarrhoea
Int: Tanned skin
Endo: Lean build
MSK: Weakness, flu-like
arthralgias, myalgias
Neuro: Dizzy, faints
Psych: Tired, tearful,
anorexia, depression,
psychosis
SIGNS
SKIN:
- Pigmented palmar
creases and buccal
mucosa
-
Vitiligo
CVS:
- Postural hypotension
-
Shock (↑BP, ↓HR, coma)
BASIC RULES OF ENDOCRINOLOGY:
1. EXCESS hormone – INHIBIT the gland
2. LOW hormone – STIMULATE the gland
The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
ADDISON’S DISEASE: INVESTIGATIONS
1. Bloods:
- FBC (anaemia, eosinophilia)
- U&E (↓Na+, ↑K+, ↑Ca2+, ↑Urea)
- BM (↓)
2. Short ACTH Stimulation Test:
- Measure plasma cortisol before and 30mins after IM
Tetracosactide (SynACTHen)
- Addison’s excluded if 30min cortisol >550nmol/L
3. 9AM ACTH levels: inappropriately high in Addison’s
4. 21-hydroxylase adrenal autoantibodies
ADDISON’S DISEASE: TREATMENT
• Replace steroids with 15-25mg Hydrocortisone daily
• Replace mineralocorticoids with Fludrocortisone
• Drug card and bracelet
• DOUBLE dose if febrile illness, injury or stress
• IV fluids if dehydrated
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SECONDARY ADRENAL INSUFFICIENCY:
• Lack of ACTH (and therefore cortisol)
• Commonest cause = IATROGENIC
• Long-term steroid therapy suppresses HPA axis
• Other rare causes include hypothalamo-pituitary
disease (no hyperpigmenation as ↓ACTH and
mineralocorticoid levels normal)
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CONN’S SYNDROME
•
•
•
•
Excess aldosterone independent of RAAS
Solitary aldosterone-producing adenoma
↑ retention of Na+ and water
Often asymptomatic. May have signs of ↓K+
• Ix: U&E, renin, aldosterone
• Tx: Laparoscopic adrenalectomy. Spironolactone for
4 weeks pre-op to control BP and K+
ACROMEGALY
• Excess GH from pituitary tumour (99%) or
hyperplasia (e.g. ectopic GHRH carcinoid tumour)
• Male : Female = 1:1
• 5% associated with MEN-1
• If before epiphyses fuse – GIGANTISM
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ACROMEGALY
SYMPTOMS
CVS: RS: Snoring
GI: “Wonky bite”
(malocclusion)
Int: ↑Sweating
Endo: ↑Weight
UG: ↓libido; amenorrhoea
MSK: Arthralgia; backache
Neuro: Acroparaesthesia;
headache
SIGNS
Skin darkening
Acanthosis nigricans
Big supraorbital ridge
Interdental separation
Macroglossia
Prognathism
Laryngeal dyspnoea
OSA
Spade-like hands and feet
Tight rings
Carpal tunnel syndrome
ACROMEGALY: COMPLICATIONS
• Impaired glucose tolerance (40%) and Diabetes
Mellitus (15%)
• Vascular: HTN; LVH; cardiomyopathy; arrhythmias;
IHD; stroke
• Colon cancer
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ACROMEGALY: INVESTIGATIONS
• GOLD STANDARD = IGF-1 and OGTT
• Don’t rely on random GH: pulsatile secretion
• ↑Glucose, ↑Ca2+, ↑PO43• MRI pituitary fossa, visual field and acuity
• Old photos
ACROMEGALY: TREATMENT
• Trans-sphenoidal surgery to remove tumour
• Somatostatin analogue (SSA) – e.g. IM octreotide or
lanreotide (NB GI side effects)
• Radiotherapy
• Pegvisomant (recombinant GH analogue)
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ADH (AVP)
Action of ADH
Collecting duct
300
This is the collecting duct
in water-rich conditions
H20
1200
ADH (2)
Action of ADH
Collecting duct
300
ADH increases expression
of Aquaporins in collecting
duct and therefore the
retention of water
H20
1200
Diabetes Insipidus
Lack of ADH
Diabetes Insipidus
Lack of ADH
Collecting duct
300
Water not sufficiently
reabsorbed from
collecting duct
H20
Large amounts of undilute
urine
1200
Diabetes Insipidus
Lack of ADH
= Polydipsia
= Polyuria
• Glucose metabolism
preserved
• Dehydration
• Hypernatremia
Fluid restriction has minimal
effect on urination
Diabetes Insipidus
Urine output falls, osmolarity increases
Desmopressin stimulation
Central = lack of ADH
No change
Rare causes
(dipsogenic, gestational)
Nephrogenic DI
Diabetes Insipidus
Treat with Desmopressin if neurogenic (central)
Thiazide diuretics (hydrocholorothiazide) and amiloride
are useful if nephrogenic
And of course, if there’s a detectable underlying cause,
you should treat that too
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SIADH
It’s exactly the opposite of DI  excessive ADH production
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SIADH
Excess ADH production
Collecting duct
300
Very small volumes of
concentrated urine
H20
1200
SIADH - symptoms
Varied and generic
Anorexia/nausea
Aches and weakness
Neuromuscular (myoclonus, reflex changes, tremor, ataxia…)
Respiratory (cheyne-Stokes respiration, apparently)
Neurological
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SIADH - Causes
Natural causes fall into three main camps
Central Nervous System
Pulmonary
Paraneoplastic
Infection
Infection
Mass/bleed
GBS/MS
Really rare stuff
First described in small
cell lung cancer
Other types too e.g.
Ewing Sarcoma, GI and
GU
Abcess
Asthma
CF
DRUG SIDE EFFECTS
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Diagnosis & Treatment
Euvolaemic with Hyponatraemia
Urine osmolarity > 100mOsm/kg
Urine Sodium >40mEq/L
Fluid restriction – increases Na concentration
Tolvaptan – V2 vasopressin blocker
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I hope you all like arrows
(I’m very sorry)
Calcium Homeostasis
Bone deposition
Thyroid releases Calcitonin
Ca
absorption
decreased
Calcium falls
Calcium rises
Serum Calcium
Approx 9-10mg/dL
Calcium falls
Calcium rises
Bone resorption
Increased GI uptake
Ca absorption up
Vit D production up
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PTH level rises
Calcium Homeostasis
Serum Calcium
Approx 9-10mg/dL
Calcium falls
Calcium rises
PTH level rises
Bone resorption
Increased GI uptake
Ca absorption up
Vit D production up
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Calcium Homeostasis (PTH only)
Serum Calcium
Approx 9-10mg/dL
Calcium falls
Calcium rises
PTH level rises
Bone resorption
Increased GI uptake
Ca absorption up
Vit D production up
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Hyperparathyroidism
Primary
80% due to adenoma
Serum calcium RAISED – STONES BONES MOANS GROANS, as well as
weakness and fatigue, muscle symptoms polyuria, polydipsia
Asymptomatic actually most common
Lab results
PTH High Calcium High
Phosphate (usually) low Phosphatase (usually) High
Treat underlying cause (usually surgical) if symptomatic or asymptomatic with
grossly abnormal test results (urine calcium or bone weakess)
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Hyperparathyroidism
Secondary
PTH is high to attempt to correct persistently low calcium levels
CKD and vit D deficiency most common – GI disease such as bypass and
Crohn’s are also possible
PTH High
Calcium Low
Phosphate High Phosphatase High
Usually asymptomatic in early stages  ymptoms are predominantly bony –
osteomalacia, joint pain
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Hyperparathyroidism
Tertiary
After many years of uncorrected secondary hyperparathyroidism
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Hyperparathyroidism
Differentiating blood results
PTH
Calcium
Phosphate Alk Phos
Primary




Secondary




Tertiary




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Hypoparathyroidism
LOW CALCIUM --- Parasthaesia (especially around mouth and lips)
--- Tetany (Chvostek’s sign & Trousseau’s sign)
--- Increased reflexes
--- QT elongation as well as reduced rate and contractility
Convulsions
Arrhythmia
Tetany
Go numb
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Yes, this was available with a simple Google search
Hypoparathyroidism
Surgical  the big one
Autoimmune
DiGeorge (and other, rarer causes of Parathyroid absence)
Haemochromatosis
Familial forms
Pseudohypoparathyroidism – PTH
levels OK, peripheral resistance
Pseudopseudo (RARE) – skeletal
defects, inherited via father,
biochemically normal
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Thanks, Wiki
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Oh, whilst we’re here
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Hypocalcaemia
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Hypocalcaemia
There are an unbelievable number of possible causes
Drug therapy – bisphosphonates calcitonin included, as well as other weird stuff
REDUCED INTAKE
Dietary insufficiency
Malabsorption
Alkalosis
Because the albumin dissociates
from hydrogen and picks up calcium
Reduced Vit D
Lack of sunlight
Vit-D dependent rickets
Anticonvulsant therapy
Kidney failure
Rhadomyolysis
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Hypocalcaemia
I wrote all that then found that Derbyshire NHS trust has conveniently already done this…
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Hypocalcaemia
Admit if severe - <1.8mmol or <2.0mmol/L with symptoms
Calcium replacement with calcium glucoronate – IV for
severe
Out in general practice everyone* takes Adcal (Calcium +
Vit D3)
*I’m exaggerating, obviously**
**Although not much
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HYPOKALAEMIA
• K+ < 3.5mmol/L (severe <2.5mmol/L)
• Muscle weakness, cramps, ↓tone, ↓reflexes,
palpitations, arrhythmias, constipation
• ECG: In ↓K+, U have no Pot and no Tea but a long PR
and a long QT
• Causes = Diuretics; V/D; Cushing’s; Conn’s; Pyloric
stenosis; Alkalosis
HYPERKALAEMIA
• K+ > 5.5mmol/L (severe >6.5mmol/L)
• Myocardial excitability → VF and cardiac arrest
• ECG: Tall tented T waves, small P waves, wide QRS
(eventually becoming sinusoidal), VF
• CAUSES: Oliguric renal failure; K-sparing diuretics;
Rhabdomyolysis; Addison’s; Burns; Metabolic
acidosis (DM); ACEi
HYPERKALAEMIA: TREATMENT
NON-URGENT:
- Treat underlying cause, review meds, polystyrene
sulfonate resin (binds K+ in gut)
EMERGENCY:
- Stabilize cardiac membrane: 10ml 10% Calcium
Gluconate
- Drive K+ into cells: 10U Actrapid (insulin) in 50ml
20% glucose (salbutamol nebs, NaHCO3-)
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CARCINOID TUMOURS
• Diverse group of tumours of enterochromaffin cell
(neural crest) origin
• Produce 5HT (serotonin)
• May also secrete bradykinin, tachykinin, substance P,
VIP, insulin, etc
• Appendix (45%), ileum (30%), rectum (20%)
• Consider all as malignant
QUESTION 1
A 46-year-old woman is referred to endocrine with a tender neck swelling. Blood
results are as follows:
TSH
<0.1 mU/l
T4
188 nmol/l
Hb
14.2 g/dl
Plt
377 * 109/l
WBC
6.4 * 109/l
ESR
65 mm/hr
Technetium thyroid scan shows decreased uptake globally
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QUESTION 1
What is the most likely diagnosis?
(a) Sick thyroid syndrome
(b) Acute bacterial thyroiditis
(c) Hashimoto’s thyroiditis
(d) Subacute thyroiditis
(e) Toxic multinodular goitre
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QUESTION 1
What is the most likely diagnosis?
(a) Sick thyroid syndrome
(b) Acute bacterial thyroiditis
(c) Hashimoto’s thyroiditis
(d) Subacute thyroiditis
(e) Toxic multinodular goitre
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QUESTION 1: RATIONALE
• Subacute thyroiditis (also known as De Quervain’s
thyroiditis) is suggested by the tender goitre,
hyperthyroidism and raised ESR.
• The globally reduced uptake on technetium thyroid
scan is also typical
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QUESTION 2
QUESTION 2
What does the ECG show?
(a)
(b)
(c)
(d)
(e)
Hypokalaemia
Hyperkalaemia
Hypercalcaemia
Hyponatraemia
WPW syndrome
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QUESTION 2
What does the ECG show?
(a)
(b)
(c)
(d)
(e)
Hypokalaemia
Hyperkalaemia
Hypercalcaemia
Hyponatraemia
WPW syndrome
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RATIONALE FOR QUESTION 2
This ECG displays many of the features of
hyperkalaemia:
• Prolonged PR interval.
• Broad, bizarre QRS complexes — these merge with
both the preceding P wave and subsequent T wave.
• Peaked T waves.
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QUESTION 2
QUESTION 3
QUESTION 3
What does the ECG show?
(a)
(b)
(c)
(d)
(e)
Hypokalaemia
Hyperkalaemia
Hypercalcaemia
Hyponatraemia
WPW syndrome
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QUESTION 3
What does the ECG show?
(a)
(b)
(c)
(d)
(e)
Hypokalaemia
Hyperkalaemia
Hypercalcaemia
Hyponatraemia
WPW syndrome
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RATIONALE FOR QUESTION 3
Hypokalaemia:
•
•
•
•
ST depression.
T wave inversion.
Prominent U waves.
Long QU interval.
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QUESTION 3
QUESTION 4
Patient comes in with:
-
Low sodium
Raised potassium
Raised calcium
Eosinophilia
What is the diagnosis?
QUESTION 4
Addison’s disease
RATIONALE:
Destruction of the adrenal cortex leads to loss of
mineralocorticoid and corticosteroid production.
Sodium is therefore not retained as normal and
potassium not expelled.
QUESTION 5
What is the treatment for
HYPERthyroidism?
HYPERTHYROIDISM: TREATMENT
(i) β-blockers:
- Propanolol (rapid control of symptoms)
(ii) Antithyroid medication:
- Titration (carbimazole: SE = AGRANULOCYTOSIS)
- Block and replace (carbimazole + thyroxine)
(iii) Radioiodine (131I)
(iv) Thyroidectomy