endocrine Flashcards
triad for pheochromocytoma
headache
sweating
tachycardia
a cause of 2ndary HTN in young px
what are the types of thyroid cancer + how do you differentiate them
PAPILLARY CANCER
- most common (70%)
- 30-40yrs
- more local invasion via lymphatics
- F
- v good prog
FOLLICULAR CANCER
- second most common
- more common in areas of low iodine + in women
- 30-60
- more likely to spread to lungs + bones haematologically
MEDULLARY CANCER
- Derived from calcitonin producing C-cells -> can present with hypocalcaemia and diarrhoea secondary to raised calcitonin.
- Assoc with Multiple endocrine neoplasia (MEN) syndrome type 2A + B although 75% are sporadic.
- Often metastasis to lymph nodes
- Prognosis worse
- Disease activity can be monitored with calcitonin levels.
ANAPLASTIC CANCER
- least common
- 60-70
- aggressive, presents with rapidly growing masses. pressure sx
- invasion of the trachea, recurrent laryngeal nerve or other local structures by the time of presentation.
- poor prognosis – median survival: 8 months
THYROID LYMPHOMA
- 10% of thyroid cancers
- Non-Hodgkins
- 50-80
- Assoc with Hashimoto’s thyroiditis
sx of prolactinoma (benign tumour of pituitary gland)
excess prolactin in women:
- amenorrhoea
- infertility
- galactorrhoea
- osteoporosis
excess prolactin in men:
- impotence
- loss of libido
- galactorrhoea
other symptoms:
- headache
- visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
- symptoms and signs of hypopituitarism
prolactinoma tx
dopamine agonists e.g. cabergoline, bromocriptine
(inhibit release of prolactin from pituitary)
surgery
what is a somatroph pituitary adenoma
pituitary adenoma that secretes growth hormone causing sx of acromegaly
diagnostic marker for carcinoid syndrome
urinary 5-hydroxyindoleacetic acid measurements (5 HIAA)
- measured in 24 hr urine collection
myxoedemic coma
rare, life-threatening clinical condition that represents severe hypothyroidism with physiologic decompensation
most common causes of hypercalcaemia
Malignancy and primary hyperparathyroidism
what is subacute thyroiditis (De Quervain’s thyroiditis)? + the phases
temp inflam of thyroid gland
There are typically 4 phases;
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR, flue-like illness
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal
what is a thyroid storm/thyrotoxic crisis + how does it present?
rare and more severe presentation of hyperthyroidism with high fever, tachycardia and delirium, high BP.
It can be life-threatening and requires admission for monitoring.
what is subclinical hyperthyroidism
normal T3 + 4 levels
low TSH level
what are the risks of subclinical hyperthyroidism
AF
osteoporosis
what is subclinical hypothyroidism
high TSH
normal T4
primary hyperthyroidism
thyroid behaves abnormally and produces excessive thyroid hormones.
high T3 and T4
low TSH level.
secondary hyperthyroidism
pituitary behaves abnormally and produces excessive TSH (e.g., pituitary adenoma), stimulating the thyroid gland to produce excessive thyroid hormones.
TSH, T3 and T4 will all be raised.
Primary hypothyroidism
thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH.
TSH is raised, and T3 and T4 are low.
Secondary hypothyroidism
pituitary behaves abnormally and produces inadequate TSH (e.g., after surgical removal of the pituitary), resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones.
TSH, T3 and T4 will all be low.
causes of secondary adrenal insufficiency
inadequate ACTH due to loss or damage to pituitary -> lack of stim to adrenals -> low cortisol
- tumours (pituitary adenoma)
- surgery to pituitary
- radiotherapy
- sheehan’s syndrome (where major PPH -> AVN to pituitary)
- trauma
causes of tertiary adrenal insufficiency
inadequate CRH by the hypothalamus
usually result of px taking long-term oral steroids (>3wks) causing -ve feedback
when they are withdrawn the hypothalamus cannot release the amounts needed fast enough
therefore need to be tapered down
cause of primary adrenal insufficency
addison’s
damage to adrenals - AI
sx of adrenal insufficiency
Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido
signs of adrenal insufficiency
Bronze hyperpigmentation of the skin (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)
biochemical findings in adrenal insufficiency
hyponatraemia (low Na)
maybe:
hyperkalaemia
hypoglycaemia
raised creatinine + urea due to dehydration
hypercalcaemia
ix for adrenal insufficiency
short Synacthen test (ACTH stim test)
- failure of cortisol to double after dose of synthetic ACTH = addison’s / v signif atrophy of adrenals after long time w 2ndary
ACTH is high in primary and low in secondary
what autoantibodies might you see in addison’s
adrenal cortex antibodies
-21-hydroxylase
-17 alpha hydroxylase
mx of adrenal insufficiency
replacement steroids
- hydrocortisone (glucocorticoid) to replace cortisol
- fludrocortisone (mineralcorticoid) to replace aldosterone)
Give px a steroid card, ID tag + emergency letter
what to do in acute illness if steroid dependent
Double doses (to match normal steroid response to illness)
Px + close contacts to give IM hydrocortisone in emergency
if vomiting take it IM
presentation of adrenal crisis / Addisonian crisis
reduced conc
hypotension
hypoglycaemia
hyponatraemia + hyperkalaemia
cld be initial pres or triggered by infection, trauma, acute illness
mx of adrenal crisis
ABCDE
IM/IV hydrocortisone (initial dose = 100mg, followed by an infusion or 6 hrly doses)
IV fluids
Correct hypoglycaemia (IV dextrose)
monitor electrolytes + fluid balance
what is cushing’s disease
A pituitary adenoma secreting excessive ACTH -> excessive cortisol release from adrenals
what is cushing’s syndrome
the features of prolonged high levels of glucocorticoids in the body.
features of cushing’s syndrome
Round face (known as a “moon face”)
Central obesity
Abdominal striae (stretch marks)
Enlarged fat pad on the upper back (known as a “buffalo hump”)
Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
Male pattern facial hair in women (hirsutism)
Easy bruising and poor skin healing
Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
metabolic effects of cushing’s syndrome
Hypertension
Cardiac hypertrophy
Type 2 diabetes
Dyslipidaemia (raised cholesterol and triglycerides)
Osteoporosis
causes of cushing’s syndrome
C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome (when ACTH is released from a tumour somewhere other than the pituitary e.g. small cell lung cancer)
E – Exogenous steroids (patients taking long-term corticosteroids)
ix for cushing’s
dexamethasone suppression tests
low dose test
- cortisol decreased rules out cushing’s
- cortisol remains high -> cushing’s
measure serum ACTH
- if low due to an adrenal tumour (primary)
- if still high there is a secondary cause
high dose test
- cortisol now low = pituitary adenoma
- cortisol still high = ectopic ACTH secretion
tx of cushing’s syndrome
surgical removal of tumour (pituitary/adrenal/ectopic)
what does cortisol do in the body
Increases alertness
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
what does gastroparesis cause in T1DM
erratic blood glucose control
bloating
vomiting
diabetics can get gastroparesis due to neuropathy of the vagus nerve
tx of gastroparesis
metoclopramide, domperidone or erythromycin (prokinetic agents)
mx of DKA
- fluid replacement w isotonic saline FIRST (i.e 0.9% NaCl) (1L over 1 hr, 500ml over 5 mins if BP <90)
- IV insulin at 0.1 unit/kg/hr
once blood glucose is <14 mmol/l start an infusion of 10% dextrose as well as fluids - correction of electrolyte dist (K+) - monitor closely
treat underlying triggers such as infection
if the ketonaemia and acidosis have not been resolved within 24 hours then the patient should be reviewed by a senior endocrinologist
dx of DKA
Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
Ketosis (e.g., blood ketones above 3 mmol/L)
Acidosis (e.g., pH below 7.3)
what is SIADH
increased release of ADH (vaspressin) from the posterior pituitary increasing water reabsorption from the urine, diluting the blood + leading to hyponatraemia
urine becomes more conc
sx of SIADH
relate to low Na
can be asx
- headache
- fatigue
- muscle aches + cramps
- confusion
severe hyponatraemia can cause seizures + reduced conc
causes of SIADH
SIADH pneumonic
Small cell lung tumours
Infection
Abscess
Drugs (carbemazepine + antipsychotics)
Head injury
- post-operative after major surgery
- Lung infection, particularly atypical pneumonia and lung abscesses
- Brain pathologies, such as a head injury, stroke, intracranial haemorrhage or meningitis
- Medications (e.g., SSRIs and carbamazepine)
- Malignancy, particularly small cell lung cancer
- Human immunodeficiency virus (HIV)
diagnosis of SIADH
no single test
Euvolaemia
Hyponatraemia
Low serum osmolality
High urine sodium
High urine osmolality
exclude things
establish the cause
SIADH meds
Vasopressin receptor antagonists (e.g., tolvaptan)
- needs close monitoring
what is osmotic demyelination syndrome
or CPM
a comp of long-term severe hyponatraemia being treated too quickly (e.g., more than a 10 mmol/L increase per 24 hours).
what are the 2 diff ways diabetes insipidus can occur
CRANIAL - lack of ADH
NEPHROGENIC - lack of response to ADH
causes of cranial diabetes insipidus
Brain tumours
Brain injury
Brain surgery
Brain infections (e.g., meningitis or encephalitis)
Genetic mutations in the ADH gene (autosomal dominant inheritance)
Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
ix for DI
Low urine osmolality (lots of water diluting the urine)
High/normal serum osmolality (water loss may be balanced by increased intake)
More than 3 litres on a 24-hour urine collection
WATER DEPRIVATION TEST I.E. desmopressin stimulation test
cranial
low urine osmolarity after water deprivation
high urine osmolarity after synthetic ADH given
nephrogenic
urine osmolarity always low
MEN 1 tumours
3Ps
pArathyroid
p1tuitary
pAncreas
MEN 2
2a - 2Ps 1M
PTH
Phaeo
Medullary Ca
2b - 1 P 2Ms
Phaeo
Marfan
Medullary
how is MEN inherited
AD
MEN 2a
2a - 2Ps 1M
PTH
Phaeo
Medullary Ca
MEN 2b
2b - 1 P 2Ms
Phaeochromocytoma - adrenal tumour
Marfan
Medullary thyroid cancer
hypercalcaemia sx
bones, stones, groans, moans
polyuria, polydipsia
hypocalcaemia sx
CATs go numb
Convulsions
Arrythmias
Tetany
Chvostek’s (facial nerve spasm) and Trousseau’s (BF cuff causing wrist to flex + fingers to draw together) signs
ECG in hypocalcaemia
long QT
hypernatraemia sx
thirst + dehydration
weakness, lethargy, irritability, coma
hyponatraemia sx
N&V, headache, irritability, confusion, weakness, decreased CGS, seizures
ECG in hyperkalaemia
tall tented T waves
prolonged PR
wide QRS
small/absent P
hyperkalaemia sx
chest pain
rapid pulse
arrhythmias
headache
decreased power
hypokalaemia sx
muscle weakness
hypotonia
palpitations
ECG in hypokalaemia
you have no Pot, no Tea, but a long PR and a long QT
flat T waves
ST depression
U waves
prolonged PR
dosing regime for hydrocortisone in adrenal insufficiency
majority dosing in the morning, the remainder in the evening
what cancer is hashimotos thyroiditis assoc w
MALT lymphoma
what does metformin do
increases insulin sensitivity
decreases glucose production
hepatobiliary set of action + cleared renally
SEs metformin
GI sx - D&V
lactic acidosis (espesh in hepatic + renal failure but v rare)
when must you stop metformin
px not eating/drinking
AKI
raised lactate
prior to IV radiology contrast (risk of renal failure)
what do SGLT-2 inhibitors do (end in -gliflozin)
cause more glucose to be excreted in urine
when to add SGLT-2 inhibitors (end in -gliflozin) to metformin
when the px has CVD/HF
if their QRISK > 10%
e.g. Dapagliflozin
SEs of SGLT-2 inhibitors (end in -gliflozin)
increase urine output and frequency
UTIs
thrush
when to stop SGLT-2 inhibitors (end in -gliflozin)
everybody has their SGLT-2 withheld on admission to hx due to risk of EKA during acute illness
need senior review prior to restarting
examples of sulfonureas
GLICLAZIDE
tolbutamIDE
glibendamIDE
what does a sulfonylurea do (gliclazide)
stimulate insulin release from the pancreas
‘SPANK THE PANC’
SEs of a sulfonylurea (gliclazide)
weight gain
hypos
what does pioglitazone do (a thiazolidinedione)
increases insulin sensitivity (helps get insulin into the ZONE)
decreases glucose production
SEs of pioglitazone
weight gain
HF (don’t start it if px already has this)
fluid retention
increased fracture risk
increased risk of bladder cancer
when to stop pioglitazone
acute fluid overload (ie HF)
known or suspected bladder cancer
what do DPP-4 inhibitors do (end in -GLIPTIN)
enhance the incretin effect
increase insulin secretion + lower glucagon secretion
dont cause weight gain
SEs DPP-4 inhibitors (end in -GLIPTIN)
nausea
pancreatitis
STOP IN PANCREATITIS
what do GLP1 agonists do (exenaTIDE)
enhance the incretin effect
increase insulin secretion
inhibit glucagon secretion
delay gastric emptying
suppress appetitie
can result in weight loss
SEs GLP1 agonists (exenaTIDE)
nausea
pancreatitis
AKI
STOP IN PANCREATITIS/AKI
causes of nephrogenic DI
idiopathic
genetic:
- more common form affects the vasopression (ADH) receptor
x-linked recessive
- less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
- hypercalcaemia (HIGH Ca)
- hypokalaemia (LOW K+)
lithium
- lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
Kidney diseases (e.g., polycystic kidney disease)
what is pheochromocytoma
tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline) from chromaffin cells
releases it in bursts
what genetic disorders make pheochromocytoma more common
Multiple endocrine neoplasia type 2 (MEN 2)
Neurofibromatosis type 1
Von Hippel-Lindau disease
ix pheochromocytoma
Plasma free metanephrines
24-hour urine catecholamines
CT/MRI to look for tumour
mx pheochromocytoma
Alpha blockers (e.g., PHENOXYBENZAMINE or doxazosin)
Beta blockers, only when established on alpha blockers
or labetalol as it blocks alpha + beta receptors
Surgical removal of the tumour
what to do if there is difficulty distinguishing T1DM from other types
measure C-peptide
low in T1DM (as the pancreas is not making enough insulin precursor, which breaks down to form C-peptide and insulin)
normal or high in T2DM
or measure Anti-GAD (present in most px w T1DM)
what is Maturity onset diabetes of the young (MODY)
A group of inherited genetic disorders affecting the production of insulin
-> younger px developing sx similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
what is a hyperosmolar hypergycaemic state (HHS)
occurs in people with type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l)
med emergency
pathophysiology of hyperosmolar hypergycaemic state (HHS)
hyperglycaemia → ↑ serum osmolality (high conc stuff) → osmotic diuresis (wee) → severe volume depletion
precipitating factors for hyperosmolar hypergycaemic state (HHS)
intercurrent illness
dementia
sedative drugs
presentation hyperosmolar hypergycaemic state (HHS)
can come on over days (unlike DKA which is hrs)
consequences of vol less
- dehydration
- polyuria + polydipsia
systemic
- lethargy
- N&V
neuro
- altered conc
- focal neuro def
haem
- hyperviscosity
dx hyperosmolar hypergycaemic state (HHS)
hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)
mx hyperosmolar hypergycaemic state (HHS)
fluid replacement
insulin should not be given unless blood glucose stops falling while giving IV fluids (cld lead to CPM)
venous thromboembolism prophylaxis
normal range for BM
4-7
what is primary hyperparathyroidism
excess secretion of PTH resulting in hypercalcaemia
usually tumour in parathyroid glands
high PTH (or inappropriately normal)
high Ca
what is secondary hyperparathyroidism
insufficient VD or CKD reduces Ca absorption from the intestines, kidneys and bones. This results in hypocalcaemia.
The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone
Ca low or normal
PTH high
what is tertiary hyperparathyroidism
secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated
parathyroid gland hyperplasia has occured
when can you dx T2DM
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
or
HbA1c >48 mmol/mol (6.5%) in adults (less than this does not exclude as less sensitive that above tests)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
when to add a second drug in T2DM
titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%),
but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)
when is metformin CI
severe CKD
what is the most common cause of impaired hypoglycaemia awareness in T1DM
if longstanding - neuropathy of parts of the autonomous nervous system
Drug causes of gynaecomastia
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids
grave’s disease tx
initially: propranolol
refer to 2nday care
carbimazole if this does not control sx
side effects of glucocorticoids
Endocrine
- impaired glucose regulation
- increased appetite/weight gain
- hirsutism
- hyperlipidaemia
Cushing’s syndrome sx
Musculoskeletal
- osteoporosis
- proximal myopathy
- avascular necrosis of the femoral head
Immunosuppression
Psychiatric
- insomnia
- mania
- depression
- psychosis
Gastrointestinal
- peptic ulceration
- acute pancreatitis
Ophthalmic
- glaucoma
- cataracts
Suppression of growth in children
Intracranial hypertension
Neutrophilia
any change in vision w graves
urgent referral as risk of thyroid eye disease
acid-base imbalance in cushings
hypokalaemic metabolic alkalosis
what is sick euthyroid syndrome
a condition in which serum levels of thyroid hormones are low in patients who have nonthyroidal systemic illness but who are actually euthyroid
it is often said that everything (TSH, T4, T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3)
Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed.
causes of primary hyperaldosteronism
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases
adrenal adenoma (Conn’s syndrome): 20-30% of cases
unilateral hyperplasia
familial hyperaldosteronism
adrenal carcinoma
features of primary hyperaldosteronism
hypertension
hypokalaemia
e.g. muscle weakness
metabolic alkalosis
ix for primary hyperaldosteronism
1st line = plasma aldosterone/renin ratio
- shows high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
high-resolution CT abdomen and adrenal vein sampling
mx primary hyperaldosteronism
adrenal adenoma: surgery (laparoscopic adrenalectomy)
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
The Hba1c target for patients on a drug which may cause hypoglycaemia
53 mmol/mol
what can lead to lower than expected HbA1c levels
reduced red blood cell lifespan
Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodialysis
what can lead to higher than expected HbA1c levels
increased red blood cell lifespan
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
mx thyroid storm
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil (PTU)
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
calcitonin
Released from the parafollicular cells
Usually found in patients with medullary carcinoma of the thyroid
antibodies found in autoimmune disease affecting the thyroid (Hashimotos 100%) and Graves (70%)
Thyroid peroxidase (microsomal) antibodies
antibodies found in individuals with Graves disease (95%)
Antibodies to TSH receptor
antibodies to check as thyroid cancer follow up
Thyroglobulin antibodies for most
Calcitonin for medullary
ix thyroid nodules
TFTs
Ultrasonography
causes of benign thyroid nodules
Multinodular goitre
Thyroid adenoma
Hashimoto’s thyroiditis
Cysts (colloid, simple, or hemorrhagic)
causes of malignant thyroid nodules
Papillary carcinoma (most common malignant cause)
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Lymphoma
what is an insulinoma
a neuroendocrine tumour deriving mainly from pancreatic Islets of Langerhans cells
assoc w MEN-1
most common pancreatic endocrine tumour
features of insulinoma
1) hypoglycaemia with fasting or exercise
2) reversal of symptoms with glucose
3) recorded low BMs at the time of symptoms
skin lesions in grave’s disease
pretibial myxoedema - deposits of glycosaminoglycans under the skin on the anterior aspect of the leg
shiny, orange peel like
what can cause falsely low HbA1c readings
sickle cell anaemia
GP6D deficiency
hereditary spherocytosis
haemodialysis
as they reduce RBC lifespan
what can cause higher than expected HbA1c readings
VB12/folic acid deficiency
iron-deficiency anaemia
splenectomy
phaeochromocytoma presentation
triad of sweating, headaches, and palpitations in association with severe hypertension
Pheochromocytoma dx
urinary metanephrines
what is the incretin affect
the insulin response to oral glucose is much greater than the response to IV
this effect is diminished in T2DM
what is grave’s disease
AI condition where TSH receptor antibodies cause primary hyperthyroidism - they stim TSH receptors on the thyroid
most common cause hyperthyroidism
causes of hyperthyroidism
G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre
causes of thyroiditis
De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis
general course of thyroiditis
often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism)
presentation hyperthyroidism
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination
features of Grave’s disease
Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)
tx De Quervain’s Thyroiditis
self-limiting, sx tx
NSAIDs for symptoms of pain and inflammation
Beta blockers for the symptoms of hyperthyroidism
Levothyroxine for the symptoms of hypothyroidism
mx hyperthryroidism
Carbimazole
Once the patient has normal levels (within 4-8 weeks), they continue on maintenance carbimazole and either:
- The dose is titrated to maintain normal levels (known as titration-block)
- A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)
risk whilst taking carbimazole
agranulocytosis
acute pancreatitis
second line anti-thyroid drug (+ its risk)
Propylthiouracil
(small risk of severe liver reactions)
what can both anti-thyroid drugs cause
Agranulocytosis
- vulnerable to severe infections
- look out for px on these drigs w sore throat + get urgent FBC
how does radioactive iodine tx work
drink a single dose of radioactive iodine, the thyroid gland takes this up + the emitted radiation destroys a proportion of the thyroid cells -> decrease in thyroid hormone production. Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine
radioactive iodine tx rules
no preg / breastfeeding, must not get preg within 6 mths of tx
men must not father children within 4 mths tx
limit contact w ppl after the dose
most common cause of hypothyroidism in developed world
Hashimoto’s thyroiditis
antibodies assoc w Hashimoto’s thyroiditis
anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies
most common cause of hypothyroidism in developing world
iodine deficiency
what drugs can interfere w thyroid hormone production
lithium inhibits production
amiodarone interferes w production + metabolism
Causes of Secondary Hypothyroidism
Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma
hypothyroidism presentation
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation
iodine def causes goitre
mx hypothyroidism
Oral levothyroxine (synthetic T4 that metabolises to T3 in the body)
dose titrated based on TSH level, initially every 4 wks
what is acromegaly
the result of excessive growth hormone (GH)
causes of acromegaly
pituitary adenoma (GH produced by anterior pituitary gland)
can be 2ndary to cancer e.g. lung/pancreatic cancer w a tumour that secretes ectopic GH
acromegaly presentation
if space-occupying pituitary tumour:
- headaches
- visual field defect (bitemporal hemianopia)
excess GH:
Prominent forehead and brow (frontal bossing)
Coarse, sweaty skin
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)
other:
Hypertrophic heart
Hypertension
Type 2 diabetes
Carpal tunnel syndrome
Arthritis
Colorectal cancer
acromegaly ix
Insulin-like growth factor-1 (IGF-1) tested on blood sample - indicates GH level
(can’t test GH directly as fluctuated throughout the day)
OGTT ie GH suppression test (where glucose drink sld suppress GH level if normal) - do after IGF-1 test to confirm dx
pituitary MRI
acromegaly tx
Trans-sphenoidal surgery, through the nose and sphenoid bone, to remove the pituitary tumour
Surgical removal of ectopic tumours
medical options for reducing GH
Pegvisomant is a GH receptor antagonist given daily by a SC injection
Somatostatin analogues (e.g., octreotide) block GH release
Dopamine agonists (e.g., bromocriptine) block GH release
diabetic neuropathy
diabetes leads to sensory loss, typically glove + stocking distribution, lower legs affected first
can be painful
mx diabetic neuropathy
same way as all neuropathic pain
1 = amitriptyline, duloxetine, gabapentin or pregabalin
2 = swap to another ^
tramadol for rescue therapay
diabetic retinopathy
what does it cause + why
most common cause of blindness in adults aged 35-65 years-old
Hyperglycaemia damages the retinal small vessels and endothelial cells.
Increased vascular permeability -> leaking BVs, blot haemorrhages + hard exudates (yellow-white deposits of lipids and proteins in the retina)
Damage to BV walls -> microaneurysms and venous beading
Damage to nerve fibres -> cotton wool spots on retina
Intraretinal microvascular abnormalities (IRMA) = dilated + tortuous capillaries in the retina that act as a shunt between the arterial and venous vessels
Neovascularisation (dev of new BVs)
grading of diabetic retinopathy
Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots
Pre-proliferative – venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA)
Proliferative – NEOVASCULARISATION and vitreous haemorrhage
Diabetic maculopathy
Exudates within the macula
Macular oedema
comps of diabetic retinopathy
Vision loss
Retinal detachment
Vitreous haemorrhage (bleeding into the vitreous humour)
Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
Optic neuropathy
Cataracts
mx diabetic retinopathy
Non-proliferative = close monitoring and careful diabetic control.
Proliferative
- Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels
- Anti-VEGF medications by intravitreal injection
- Surgery (e.g., vitrectomy) may be required in severe disease
why do you get diabetic foot disease
- neuropathy - so loss of protective sensation
- PAD
what is charcot’s arthropathy
syndrome in patients who have peripheral neuropathy, or loss of sensation, in the foot and ankle
presentation diabetic foot disease
neuropathy: loss of sensation
ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
when to screen px w DM for diabetic foot dis + how
annually
screen for ischaemia - palpate for both the dorsalis pedis pulse and posterial tibial artery pulse
screen for neuropathy - a 10 g monofilament is used on various parts of the sole of the foot
when to screen to diabetic nephropathy + how
Annually
urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria
mx diabetic nephropathy
dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACEi or ARB should be start if urinary ACR of 3 mg/mmol or more
control dyslipidaemia e.g. Statins
what is secondary hyperaldosteronism caused by
excessive renin stimulating release of excessive aldosterone
excessive renin may be released due to disproportionately lower BP in the kidneys
- renal artery stenosis
- HF
- liver cirrhosis + ascites
insulin sick day rules
if a patient is on insulin, they MUST NOT STOP IT due to the risk of DKA
check blood glucose more frequently (e.g. every 1–2 hours including through the night)
consider checking blood or urine ketone levels regularly
maintain normal meal pattern if possible
if appetite is reduced meals could be replaced with carbohydrate-containing drinks (such as milk, milkshakes, fruit juices, and sugary drinks)
aim to drink at least 3 L of fluid (5 pints) a day to prevent dehydration
when to add 10% dextrose infusion in DKA mx
once blood glucose is < 14 mmol/l
blood results if poor compliance w meds in px w primary hypothyroidism
TSH level will be high implying that over recent days/weeks the body is thyroxine deficient.
If px starts taking meds properly just b4 appt free T4 will be within normal range. As thyroxine level wld be corrected but the TSH takes longer to normalise.
what to give everyone when prescribing insulin
glucagon kit for emergencies
what is a sliding scale + what must you accompany it w
variable rate IV insulin infusions (act rapid) - according to capillary blood glucose measurements
always accompanied by an infusion of fluid containing GLUCOSE + potassium to prevent insulin induced hypoglycaemia + hypokalaemia
- so 2 cannulas
when to use a sliding scale
px w know DM unable to take oral food + for whom their own insulin regime is not poss
vomiting (first exclude DKA/HHS)
NBM + who will miss more than one meal (ie pre-surgery, want them to be 1st on list)
severe illness + need to achieve good glycaemic control
reduced GCS
what monitoring is needed whilst a px is on a sliding scale
actual need for it - daily
CBG - hourly
if hypo -> tx + swap to insulin sensitive regime
U&Es - daily
monitor K
fluid status - daily
no overload concern -> 5% glucose (w K) 125ml/hr
overload concern -> 83ml/hr
v elderly/frail -> 42ml/hr
if hepatic/renal impairment -> insulin sensitive regime
what to stop / ctu whilst a sliding scale is running
stop all oral hypoglycaemic agents
i.e. no diabetets tablets
stop all short acting insulins
stop all pre-mixed insulins (all the ones w a number in)
ctu all long-acting + basal insulins (levemir)
when to come off a sliding scale
asap
when px has normal biochem
px is E+D
give the next meal related long-acting insulin dose, wait for 1 hr, then remove sliding scale (imp as it only has a half-life of 5 mins)
restart all other DM meds + review them
hypoglycaemia definition
glucose < 4
less than 4 on the floor
start tx if sx - seating, pallor, trmor, irritable
tx hypoglycaemia conscious + orientated
oral glucose load
- lucozade, orange juice, glucose gel
tx hypoglycaemia lower GCS w access
IV 10% glucose
-200 mls over 10 mins
-or 100mls 20% glucose stat
tx hypoglycaemia lower GCS no access
1mg IM glucagon
how often to monitor blood glucose in diabetic px
4x/day
when to omit insulin
NEVER in T1DM
(even if hypo!!!!)
criteria for GLP1 agonists (exenaTIDE) therapy
if triple therapy not effective/CI then give metformin + sulfonurea + GLP1 agonist if:
- BMI > 35 w obesity related probs
- BMI < 35 + insulin wld have serious occupational implications / not tolerated
when to consider insulin in T2DM
Hba1C > 58 after 3 mths of dual oral therapy
sld be intermediate-acting (due to hypo risk)
what is usual total daily dose of insulin
0.5units per kg
best insulin regime for T1DM
basal-bolus
split long and short acting 50/50
1-2 long acting
3 short acting w meals
round down not up
can knock some off as hypo risk
mx nephrogenic DI
thiazide diuretics
low salt/protein diet
mx cranial DI
desmopressin
Endocrine parameters reduced in stress response:
Insulin
Testosterone
Oestrogen
