Endocrine Flashcards
1
Q
define thyrotoxicosis
A
abnormal and excessive quantity of thyroid hormone in the body
2
Q
Primary hyperthyroidism
A
due to thyroid pathology
thyroid itself is behaving abnormally and producing excessive thyroid hormone
3
Q
Secondary hyperthyroidisim
A
condition where thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH
Pathology is the hypothalamus or pituitary
4
Q
Graves disease
A
autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism
TSH receptor antibodies are abnormal antibodies produced by the immune system that mimic TSH and stimulate TSH receptor on the thyroid
(MOST COMMON CAUSE OF HYPERTHYROIDISM)
5
Q
Toxic multinodular goitre
A
aka = Plummers disease
condition where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thryoid hormone
6
Q
What is exophthalmos and what causes it
A
bulging eyeball out of socket caused by graves disease
due to inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball out
Can be tested from behind patient and getting them to extend their head back to see if you can see the eyeballs bulging
Also if you can see the sclera above their iris
7
Q
What is pretibial myxoedema and what is it specific to
A
dermatological condition where there are deposits of mucin under the skin on the anterior aspect of the leg
Gives a discoloured, waxy, oedematous appearance to the skin over the area
specific to Graves disease and is a reaction to the TSH receptor antibodies
8
Q
Causes of hyperthyroidism
A
Graves disease
toxic multinodular goitre
solitary toxic thyroid nodule
thyroiditis (e.g. hashimotos, postpartum and drug induced)
9
Q
Universal features of hyperthyroidism
A
anxiety and irritability
sweating and heat intolerance
tachycardia
weight loss
fatigue
frequent loose stools
sexual dysfunction
10
Q
Unique features of Graves disease
A
Diffuse goitre
Graves eye disease
Bilateral exophthalmos
pretibial myoxedema
11
Q
Unique features of toxic multinodular goitre
A
goitre with firm nodules
most patients are over 50
second most common cause of thyrotoxicosis (after Graves)
12
Q
What is solitary toxic thyroid nodule
A
single abnormal thryoid nodule is acting alone to release thyroid hormone
nodules are usually benign adenomas
treated with surgical removal of the nodule
13
Q
De Quervain’s thyroiditis
A
Presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism
hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback
Self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief of hyperthyroidism is all that is necessary
14
Q
Thyroid storm
A
rare presentation of hyperthyroidism
Also known as thyrotoxic crisis
more severe presentation with pyrexia, tachycardia and delirium
requires admission for monitoring and is treated the same way as any other presentation of thyrotoxicosis
may need suppotive care with fluid resus, anti-arrhythmic meds and beta blockers
15
Q
Hyperthyroidism management
A
Carbimazole (first line) - successful in Graves disease (usually normal thryoid function after 4-8 weeks and full remission within 18months)
Propylthiouracil (second line) - small risk of severe hepatic reactions
Radioactive iodine - destroys some thyroid cells
beta blockers - block adrenalin related symptoms of hyperthyroidism
propanolol is a good option because it non selectively blocks adrenergic activity (particularly useful in thyroid storm)
Surgery - to removed whole thyroid or toxic nodules
will require levothyroxine replacement for life
16
Q
Hyperthyroidism management
A
Carbimazole (first line) - successful in Graves disease (usually normal thryoid function after 4-8 weeks and full remission within 18months)
Propylthiouracil (second line) - small risk of severe hepatic reactions
Radioactive iodine - destroys some thyroid cells
beta blockers - block adrenalin related symptoms of hyperthyroidism
propanolol is a good option because it non selectively blocks adrenergic activity (particularly useful in thyroid storm)
Surgery - to removed whole thyroid or toxic nodules
will require levothyroxine replacement for life
17
Q
Primary hypothyroidism
A
problem with thyroid gland itself -> autoimmune disorder affecting thyroid tissue
18
Q
Secondary hypothyroidism
A
due to a disorder with the pituitary gland or a lesion compressing th epituitary gland
19
Q
Congenital hypothyroidism
A
due to a problem with thyroid dysgenesis or thyroid dyshormonogenesis
20
Q
Hashimoto’s thyroiditis
A
most common cause in developed world for hyPOthyroidism
autoimmune disease associated with T1DM, addisons or pernicious anaemia
May cause transient thryotoxicosis in acute phase
5-10 times more common in women
21
Q
Drugs that cause hypothyroidism
A
lithium
amiodarone
22
Q
TSH and free T4 levels in thyrotoxicosis (graves)
A
low tsh
high free t4
23
Q
TSH and free T4 levels in primary hypothyroidism (hashimotos)
A
high tsh
low free t4
24
Q
TSH and free t4 levels in secondary hypothyroidism
A
low tsh
low free t4
25
tsh and free t4 levels in sick euthyroid syndrome
low tsh
low free t4
common in hospital inpatients
changes are reversible upon recovery from systemic illness and no treatment is usually needed
26
TSH and free T4 levels in subclinical hypothyroidism
high tsh and normal free T4
27
TSH and free t4 levels in someone with poor compliance with thyroxine
high tsh and normal free t4
patients who are poorly compliant may tae their thyroxine the day before a routine blood test
the thyroxine levels are hence normal but the TSH lags and reflects longer term low thyroxine levels
28
Thyroid autoantibodies that can be tested
Anti-thyroid peroxidase (anti TPO) antibodies
TSH receptor antibodies
thyroglobulin antibodies
29
Source of growth hormone
anterior pituitary
30
What is growth hormone responsible for
stimulating cell reproduction and growth of organs, muscles, bones and height
stimulates release of insulin like growth factor (IGF-1) by the liver which is also important in promoting growth in children and adolescents
31
Congenital growth hormone deficiency
Results from disruption to growth hormone axis (at hypothalamus or pituitray gland)
can be due to genetic mutation of GH1 or GHRHR(growth hormone releasing hormone receptor)
or due to empty sella syndrome (where pituitary is under developed or damaged
32
Acquired growth hormone deficiency
secondary to trauma, infection or interventions such as surgery
33
Presentation of growth hormone deficiency in neonates and older infants
neonates = micropenis, hypoglycaemia and severe jaundice
older infants = poor growth (usually stopping/severely slowing from 2-3). short stature, slow devlopment of movement and strength and delayed puberty
34
growth hormone stimulation test
involves measuring medications that normally stimulate release of GH (like glucagon, insulin, arginine adn clonidine)
GH levels are monitored for 2-4 hours after administering medication to asses hormonal response
in GH deficiency their will be poor response to the stimulus
35
Other investigations for GH deficiency
other associated hormone deficiencies (thyroid and adrenal deficiency)
MRI brain for structural pituitary or hypothalamus abnormalitites
genetic testing - associated conditions like turner syndrome or prader willi syndrome
Xray of wrist or DEXA scan can determine bone age and help predict final height
36
Treatment of GH deficiency
daily s/c injections of GH (somatropin)
Treatment of other associated hormone deficiencies
close monitoring of height and development
36
Treatment of GH deficiency
daily s/c injections of GH (somatropin)
Treatment of other associated hormone deficiencies
close monitoring of height and development
37
Most common case of hypothyroidism in developing world
iodine deficiency
38
Source of cortisol
zona fasciculata of adrenal cortex
39
Functions of cortisol
increases BP - permits normal response to angiotensin II and catecholeamine by up regulating alpha 1 receptors on arterioles
inhibits bone formation - decreases osteoblasts, decreases type 1 collagen, decreases absorption of clacium from the gut, increases osteoclastic activity
increases insulin resistance
inhibits inflammatory and immune responses
maintains functions of skeletal and cardiac muscles
40
Regulation of cortisol
Increases secretion:
ACTH from the pituitary gland, itself stimulated by CRH (corticotrophin releasing hormone) released by the hypothalamus
stress
41
Glucagon source
alpha cells of pancreas
42
Function of glucagon
glycogenolysis
gluconeogenesis
lipolysis
(opposite metabolic effects to insulin)
43
What increases secretion of glucagon
hypoglycaemia
stresses (infections, burns, surgery)
Increased catecholeamines + sympathetic nervous system stimulation
increased plasma amino aicds
44
What decreases secretion of glucagon
hyperglycaemia
insulin
somatostatin
increased free fatty acids and keto acid
45
SGLT-2 inhibitors (-gliflozins)
mechanism of action
route
main side effects
notes
inhibits reabsorption of glucose in the kidney
oral
UTI
typically result in weight loss
46
Insulin
mechanism of action
route
main side effects
notes
direct replacement for endogenous insulin
s/c
hypoglycaemia, weight gain, lipodystrophy
used in all patients with T1DM and some patients with poorly controlled T2DM
47
Metformin
mechanism of action
route
main side effects
notes
increases insulin sensitivity and decreases hepatic gluconeogenesis
oral
GI upset, lactic acidosis
first line medication in management of T2DM
cannot be used in patients with an eGFR <30ml/min
48
Sulfonylureas
mechanism of action
route
main side effects
notes
stimulate pancreatic beta cells to secrete insulin
Oral
Hypoglycaemia, weight gain, hyponatraemia
examples include gliclazide and glimepiride
49
Thiazolidinediones
mechanism of action
route
main side effects
notes
activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
oral
weight gain, fluid retention
only available one is pioglitazone
50
DPP-4 inhibitors (-gliptins)
mechanism of action
route
side effects
notes
increases incretin levels which inhibit glucagon secretion
oral
generally well tolerated but increased risk of pancreatitis
51
primary hyperparathyroidism characteristically has hypocalcaemia or hypercalcaeia
hypercalcaemia
52
Pseudohyperkalaemia
rise in serum potassium that occurs due to excessive leakage of potassium from cells during or after blood is taken
laboratory artefact and does not represent the true serum potassium
In this case potassium is released as the large number of platelets aggregate and degranulate
53
Causes of pseudohyperkalaemia
haemolysis during venepuncture (excessive vacuum of blood drawing, prolonged tourniquet use or too fine a needle gauge)
delay in processing of blood specimen
abnormally high number of platelets, leukocytes or erythrocytes (such as myeloproliferative disorders)
familial causes
54
Compartment syndrome
particular complication that may occur following fractures
characterised by raised pressure within a closed anatomical space
raised pressure eventually compromises the tissue perfusion resulting in necrosis
two main fractures that cause this are supracondylar fractures and tibial shaft fractures
55
Features of compartment syndrome
pain, especially on movement
paraesthesiae
pallor
arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
paralysis of muscle group
56
How is a diagnosis of compartment syndrome made
measurement of intracompartmental pressure measurements
pressure in excess of 20mmHg are abnormal and >40mmHg is diagnostic
57
Treatment for compartment syndrome
prompt and extensive fasciotomies
in lower limb deep muscles may be inadequately decompressed by inexperienced operator
myoglobinuria may pccur following fasciotomy and result in renal failure (require aggressive IV fluids)
Death of muscle groups occur within 4--6 hours
58
first hormone secreted in hypoglycaemia
glucagon
59
Community management of hypoglycaemia
oral glucose 10-20g in liquid, gel or tablet form
alternatively quick acting carbohydrate like GlucoGel or DextroGel
HypoKit may be prescribed which contains a syringe and vial of glucagon IM or SC injection
60
Hospital management of hypoglycaemia
quick acting carbohydrate (GlucoGel or DextroGel) if alert
if unalert Sc/IM injection of glucagon
alternatively IV 20% glucose solution through a large vein
61
Carcinoid syndrome
occurs when metastases are present in liver and release serotonin into systemic circulation
may also occur with lung carcinoid as mediators are not cleared by liver
62
Features of carcinoid tumours
flushing
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis
ACTH and GHRH may be secreted resulting in cushings
63
Investigations for carcinoid tumours
urinary 5-HIAA
plasma chromogranin A y
64
management of carcinoid tumours
somatostatin analogues (octreotide)
for diarrhoea cyproheptadine may help
65
How does loperamide slow down bowel movements
acts on mu opioid receptors in the myenteric plexus of the large intestine
66
features of hypocalcaemia
tetany - muscle twitching, cramping and spasm
perioral paraesthesia
if chronic - depression, cataracts
ECG: prolonged QT interval
67
Trousseau's sign
sign of hypocalcaemia
carpal spasm if brachial artery occluded by inflating BP cuff and maintaining pressure above systolic
seen in around 95% patients
68
Chvostek's sign
sign of hypocalcaemia
tapping over parotid causes facial muscles to twitch
69
Second line therapy for patients who are unable to tolerate side effects of statins
ezetimibe
70
what is ezetimibe
lipid-lowering drug which inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in small intestine
71
What medication acutely prescribed may cause issues with diabetic control?
Corticosteroids like prednisolone
72
How does Antidiuretic hormone promote water reabsorption
by the insertion of aquaporin-2 channels in the collecting ducts of the kidneys
73
Causes of hypercalcaemia
CHIMPANZEES
Calcium supplementation
Hyperparathyroidism
Iatrogenic (drugs: thiazides)
Milk Alkali syndrome
Paget disease of the bone
Acromegaly and Addisons disease
Neoplasia
Zollinger Ellison syndrome
Excessive vitamin D
Excessive vitamin A
Sarcoidosis
74
First sign of male puberty
testicular enlargement
75
What might happen if you abruptly stop someone's long term steroids
Longer-term systemic corticosteroids suppress the natural production of endogenous steroids. They should therefore not be withdrawn abruptly, as this may precipitate an Addisonian crisisAddisonian crisis is characterised by vomiting, hypotension, hyperkalaemia, and hyponatremia.
76
Where is prolactin secreted
Anterior pituitary gland
77
Function of prolactin
stimulates breast development
stimulates milk production
decreases GnRH pulsatility at the hypothalamic level and to a lesser extent, blocks the action of LH on the ovary or testis.
78
What increases the secretion of prolactin
thyrotropin releasing hormone
pregnancy
oestrogen
breastfeeding
sleep
stress
drugs, metoclopramide and antipyschotics
79
What decreases secretion of prolactin
dopamine
dopaminergic agonists
80
What is Leptin
Leptin is a hormone secreted by adipose tissue, playing an important role in satiety and fullness. Mutations that disrupt leptin signalling have been implicated in monogenic obesity, manifesting clinically as severe childhood-onset obesity.
81
What is Ghrelin
Ghrelin is known as the 'hunger hormone', mediating feelings of hunger. Decreased ghrelin synthesis would result in diminished hunger and does not manifest clinically as obesity.
82
What is mydriasis
dilation of pupils
83
What increases secretion of ADH
ECF osmolality increase
Volume decrease
pressure decrease
angiotensin II
84
What decreases secretion of ADH
ECF osmolality decrease
volume increase
temperature decrease
85
How does carbimazole work
blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production
86
Parathyroid hormone effects on the bone
Binds to osteoblasts which signal to osteoclasts to cause resorption of the bone and release calcium
87
Parathyroid hormone effects on the kidneys
Active reabsorption of calcium and magnesium from the distal convoluted tubule
decreases reabsorption of phosphate
88
Parathyroid hormone effects on the intestine via the kidneys
Increases intestinal calcium absorption by increasing activated vitamin D
Active vitamin D increases calcium reabsorption
89
What do SGLT-2 inhibitors do
reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
Examples include canagliflozin, dapagliflozin and empagliflozin.
90
Important adverse effects of SGLT-2
urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored
91
What does an excess of growth hormone increase the risk of
developing diabetes mellitus type 2
This is because the hormone mobilises glucose from fat stores (to build muscle), thus increasing its concentration in the blood. Subsequently, the pancreas has to secrete greater amounts of insulin to combat the increased levels of glucose.
92
Symptoms of excess growth hormones
Other symptoms of excess growth hormone may include thickened skin, enlarged hands and feet, a prominent jaw, carpal tunnel syndrome, tiredness, muscle weakness and hypertension.
93
Difference between a pancreatic psuedocyst and a pancreatic cyst
A pseudocyst is surrounded in granulation tissue, as opposed to a true cyst which is surrounded with epithelial tissue
94
what do Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. Vildagliptin, sitagliptin) do
dipeptidyl peptidase-4, DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown
95
Pretibial myxoedema
localised skin lesion
classically on the skin in front of the tibia
development is due to an increase of glycosaminoglycans in the pretibial dermis
associated with grave's disease
96
Sulfonyureas mechanism of action
Increase stimulation of insulin by pancreatic B cells and decrease hepatic clearance of insulin
97
Where is ACE produced
pulmonary endothelium
98
Features of addisons
lethargy, weakness, anorexia, nausea and vomiting, weight loss, salt craving
hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia
99
Primary causes of hypoadrenalism
TB
metastases (bronchial carcinoma)
Meningococcal septicaemia (Waterhouse-Fredrichsen syndrome)
HIV
Antiphospholipid syndrome
100
Empagliflozin mechanism of action
SGLT-2 inhibitor - reversibly inhibit sodium-glucose co-transporter 2 in the renal proximal convoluted tubule
101
Insulin and potassium
decreases serum potassium through stimulation of the sodium potassium ATPase pump
102
Pathophysiology of DKA
Caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies
103
Most common precipitating factors of DKA
Infection
missed insulin
MI
104
Features of DKA
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
acetone smelling breath
105
Management of DKA
Fluid replacement: isotonic saline is used initially (even if severly acidotic)
Insulin: IV infusion at 0.1unit/kg/hour
Once glucose < 15mmol/l 5% dextrose infusion should be started
Correction of electrolyte disturbance: serum potassium is often high on admission despite total body potassium being low
potassium supplements may be needed
Long acting insulin should be continued and short acting insulin should be stopped
106
DKA resolution
Defined as
pH >7.3
blood ketones <0.6mmol/L
Bicarbonate >15mmol/L
107
Complications
gastric stasis
thromboembolism
arrythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
ARDS
AKI
108
Magnesium and parathyroid hormone
enables secretion and function of parathyroid hormones
levels must be sufficient to allow parathyroid hormone to exert its effects
109
Which metabolic disorder is hyperkalaemia associated with
Addisons
110
Klinefelter's syndrome
associated with karyotype 47, XXY
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia
elevated gonadotrophin levels but low testosterone
Diagnosis by karyotype
111
What decreases the secretion of prolactin
dopamine
dopaminergic agonists
112
Where are phaeochromocytomas found
adrenal medulla
113
What are phaeochromoctomas associated with
MEN type II
neurofibromatosis
von hippel-lindau syndrome
114
Features of phaeocromocytomas
hypertension
headache
palpitations
sweating
anxiety
115
Tests for phaeochromocytomas
24hr urinary collection of metanephrines
(has replaced 24hr urinary collection of catecholamines)
116
Management of phaeochromocytomas
surgery is definitive management
must first be stabilized with medical management
alpha blocker (phenocybenzamine) given before a beta blocker (propranolol)
117
Kallmann's syndrome
Recognised cause of delayed puberty secondary to hypogonadotropic hypogonadism
usually inherited as an X-linked recessive trait
thought to be caused by failure of Cn-RH secreting neurons to migrate to the hypothalamus
118
Typical clue of kallmann's syndrome in questions
associated with a lack of smell (anosmia) in a boy with delayed puberty
119
Features of Kallmann's syndrome
delayed puberty
hypogonadism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height
120
Source of prolactin
anterior pituitary
121
Source of somatostatin
Delta cells of the pancreas, pylorus and duodeum
122
Graves pathophysiology
Formation of IgG antibodies on the TSH receptors on the thyroid gland
123
How can corticosteroids worsen diabetic control
due to their anti-insulin effects
124
Example of minimal glucocorticoid activity but very high mineralocorticoid activity
fludrocortisone
125
Example of glucocorticoid activity and high mineralocorticoid activity
hydrocortisone
126
Example of predominant glucocorticoid activity and low mineralocorticoid activity
prednisolone
127
Example of very high glucocorticoid activity and minimal mineralocorticoid activity
dexamethasone
betmethasone
128
Glucocorticoid endocrine side effects
impaired glucose regulation
increased appetite/weight gain
hirsutism ( where women have thick, dark hair on their face, neck, chest, tummy, lower back, buttocks or thighs. )
hyperlipidaemia
129
Glucocorticoid cushings side effect
moon face
buffalo hip
striae
130
Glucocorticoid MSK side effects
Osteoporosis
proximal myopathy
avascular necrosis of the femoral head
131
Glucocorticoid immunosuppresion side effects
increased susceptibility to severe infection
reactivation of TB
132
Glucocorticoid psychiatric side effects
Insomnia
mania
depression
psychosis
133
Glucocorticoid Gi side effects
Peptic ulceration
acute pancreatitis
134
glucocorticoid ophthalmic side effects
glaucoma
cataracts
135
T2DM medication that doesnt typically cause weight gain or hypoglycaemia
Metformin
Gliptins (DPP-4 inhibitors)
136
What is leptin secreted by
adipose tissue
137
DPP-4 inhibitors mechanism
work by inhibiting enzyme dipeptidyl peptidase 4
this enzyme acts to break down endogenos incretins such as GLP1 and GIP
in the body these molecules are released in response to food (they decrease appetite, increase insulin secretion and inhibit glucagon secretion to lower blood glucose levels)
as DPP 4 inhibitors inhibit the breakdown of these molecules their effect is increased leading ot the anti-diabetic role of this medication
138
What step is essential for the formation of all steroid hormones?
conversion of cholesterol to pregnenolone
pregnenolone is precursor for all steroid hormones
takes place within mitochondria
139
Primary hypogonadism (Klinefelter's syndrome)
Lh and testosterone levels
LH - high
testosterone Low
140
Hypogonadotrophic hypogonadism (Kallman's syndrome)
LH and testosterone levels
LH-low
testosterone - low
141
Androgen insensitivity syndrome
LH and testosterone levels
LH high and testosterone normal/high
142
Testosterone-secreting tumour
LH and testosterone levels
LH low
Testosterone high
143
How does orlistat work and what is it used for
reduces fat digestion by inhibiting lipase
anti-obesity agent
144
What are these examples of?
gliflozin (dapagluflozin)
tolbutamide
exenatide
linagliptin
pioglitazone
gliflozin - SGLT-2 inhibitor
tolbutamide - sulfonylurea
exenatide - glp-1 receptor agonist
linagliptin is a DPP 4 inhibitor
piolitazone is a thiazonlidinedione
145
What can you use to assess endogenous insulin production
C-peptide is secreted in proportion to insulin
146
What is fragment E
fibrinogen degradation product produced alongside D dimer upon break down of a clot
147
What is Addison's disease
Specific condition where the adrenal glands have been damaged, resulting in reduced secretion of cortisol and aldosterone. Most common cause is autoimmune
148
Symptoms of Addison's disease
- Fatigue
- Nausea
- Cramps
- Abdominal pain
- Reduced libido
149
Signs of Addison's disease
- Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
- Hypotension (particularly postural hypotension)
150
Investigations for Addison's disease
FBC & U&Es - hyponatraemia and hyperkalaemia
Short synacthen test - first line to diagnose adrenal insufficiency
ACTH - ACTH is high
Adrenal autoantibodies - adrenal cortex antibodies and 21-hydroxylase antibodies
151
Short synacthen test
Synacthen is synthetic ACTH
Test used to diagnose adrenal insufficiency (like for Addison's)
Ideally performed in the morning
Blood cortisol is measure at baseline, 30 & 60 mins after synacthen administration
Synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and the cortisol level should at least double
Failure of this process is indicative of primary adrenal insufficiency (Addison's)
152
Treatment for Addison's
Replacement steroids titrated to signs, symptoms and electrolytes
Hydrocortisone to replace cortisol
Fludrocortisone to replace aldosterone (if needed)
Patients also given steroid card and emergency ID for emergency services to know they are on long term steroids
153
How does an Addisonian crisis typically present
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Patients can be very unwell
154
Do you do investigations for someone presenting in an addisonian crisis
you don't wait for a definitive diagnosis before treating because it is life threatening
155
Management for addisonian crisis
intensive monitoring
parenteral steroids (IV hydrocortisone 100mg stat then 100mg every 6 hours)
Iv fluid resus
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance
