Endocrinology p1 Flashcards
1
Q
What is DM?
A
A multi system disease resulting from inadequate action of the hormone insulin
2
Q
what is the pathophysiology of T1DM?
A
autoimmune disease with autoantibodies targeted against the insulin secreting beta cells of the pancreas, leading to cell death and inadequate insulin secretion
3
Q
What is the clinical presentation of T1DM?
A
presents in childhood / adolescence with a 2-6 week history of:
polyuria - high sugar content in urine leading to osmotic diuresis
polydipsia - due to resulting fluid loss
weight loss: fluid depletion plus fat / muscle breakdown
DKA = common first presentation
4
Q
What is the pathophysiology of T2DM?
A
Insensitivity of body tissues to insulin
‘insulin resistance’
Eventually, Beta cells decompensate and can no longer produce excess insulin, leading to hyperglycaemia
5
Q
What are the causes of T2DM?
A
Age genetic factors obesity high fat diet sedentary lifestyle
6
Q
What is the clinical presentation of T2DM?
A
polyuria
polydipsia
weight loss
lack of energy
visual blurring: glucose induced refractive changes
pruritus vulvae / balanitis due to candida
7
Q
What complications arise as a result of T2dm?
A
retinopathy
polyneuropathy
erectile dysfunciton
arterial disease: MI / peripheral vascular disease
8
Q
What is the metabolic syndrome?
A
T2DM
central obesity
dyslipidaemia: Low HDL cholesterol, hyptertriglyceridae,ia
9
Q
What are the secondary causes of T2DM?
A
Pancreatic disease: CF, chronic pancreatitis, pancreatic carcinoma
Endocrine disease: Cushing’s disease, acromegaly, thyrotoxicosis, PCC, glucagonoma
Drug induced: thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals
Congenital disease: insulin receptor abnormalities, myotonic dystrophy, friedreicqh’s ataxia
10
Q
What are the diagnostic criteria for T2DM?
A
usually diagnosed by Hba1c of 48mmol/mol or more in a symptomatic individual
Assess blood glucose over the last 8-12 weeks
11
Q
In which populations is HbA1c inappropriate in?
A
haemoglobinopathies haemolytic anaemia untreated iron deficiency anaemia suspected gestational diabetes children HIV chronic kidney disease people taking medication that may cause hyperglycaemia (for example corticosteroids)
12
Q
If you can’t use Hba1c, what is diagnostic of diabetes?
A
Fasting plasma glucose of 7mmol/l or creater
13
Q
How should diabetes diagnosis be done on an asymptomatic individual?
A
Never be based on a single abnormal HbA1c or fasting plasma glucose - at least 1 additional abnormal Hba1c or plasma glucose level is essential
If the second test results = normal, arrange regular review
14
Q
What are the normal ranges for fasting and after OGTT?
A
normal: fasting <7mmol/L
2h glucose: <7.8mmol/l
15
Q
What are the results of impaired glucose tolerance?
A
Fasting <7 and 2h glucose 7.8-11.0mmol/L
16
Q
What are the results of diabetes mellitus?
A
Fasting glucose >7mmol/L
2h glucose >11.0mmol/L
17
Q
How is T1DM diagnosed?
A
Random blood glucose of >11.0mmol/L in symptomatic individual
18
Q
What is the lifestyle management of T2DM?
A
Education
Screen for complications: fundoscopy, nephropathy
first pass morning urine for albumin:creatinine
serum creatinine for eGFR
Foot check: neuropathy, ischaemia, ulcers, deformity
Monitor CV risk: control blood pressure
Assess Qrisk2 score: atorvastatin for those >10%
Lifestyle advice: diet
Weight loss
Exercise: 20-30mins/day
Stop smoking
Alcohol reduction
19
Q
What dietary advice is given in T2DM?
A
High in low GI carbohydrates
limit foods high in sugar and saturated fats
diabetic specific foods not required
can see nutritionist to help with meal plans
20
Q
What is the HBA1c target for T2DM?
A
6.5% or 48mmol/L is the target HbA1c initially
53mmol/L = target for all patients on insulin / taking a drug associated with hypoglycaemia
21
Q
At what level for HbA1c should you start drug treatment?
A
58mmol/mol or higher
22
Q
What should be offered as the first drug in T2DM?
A
Biguanide such as standard release metformin unless contra-indicated (creatinine clearance below 60) titrated upwards (overweight)
Sulphonylurea in underweight
23
Q
What dose of metformin should be given initially?
A
500mg with breakfast for one week
500mg with breakfast and dinner for one week
500mg with breakfast, lunch and dinner thereafter
24
Q
What should be given if metformin is not tolerated or contra-indicated?
A
A gliptin (DPP-4 inhibitor): sitagliptin, lanagliptin
A thiazolidinedione (PPAR-Gamma activator: pioglitazone
A sulphonylurea: gibenclamide, gliclazide
25
What if metformin alone is not effective?
Metformin and one second drug
| If metformin contraindicated - any two of the drugs listed above
26
What if combination therapy is not effective?
Triple therapy:
metformin
a sulphonylurea
A gliptin / pioglitazone
If metformin contra-indicated, consider insulin regimens
27
Give an example of a biguinaide?
Metformin
28
How do biguinaides work?
Decrease hepatic glucose production and increase peripheral insulin sensitivity
(do not pose a risk of hypoglycaemia when used as mono therapy)
29
What level of renal function is needed at least, in order to start metformin treatment?
Do not start if eGFR is less than 30mL/min/1.73m2
| Review the dose if it is less than 45
30
What are the contraindications of metformin?
eGFR <30 for standard release or <45 for modified release
alcohol addiction
people at risk of lactic acidosis e.g. DKA
People at risk of tissue hypoxia: e.g. cardiac / resp failure
31
What are the side effects of metformin?
GI effects: nausea, vomiting, abdominal pain, loss of appetite
Generally resolve spontaneously
lactic acidosis: rare but serious, occurs due to drug accumulation
insidious onset with non-specific symptoms
more common when combined with alcohol
Vitamin b12 deficiency
32
Give examples of sulphonylureas
Tolbutamide, gliclazide, glibenclamide
33
How do sulphonylureas work?
Increase insulin secretion
| Thus only work if some residual function of pancreatic B cells
34
Which of the sulphonylureas are short, medium and long acting?
Tolbutamide = short acting
Gliclazide = medium acting
Glibenclamide = long acting
35
what is the indication for glibenclamide over the others?
if there is a risk of hypoglycaemia
36
what groups need cautious prescribing for sulphonylureas?
elderly: risks of hypoglycaemic events
obese: encourages weight gain
37
What are the side effects of sulphonylureas?
GI disturbances, liver dysfunction
38
Give examples of thiazolidinediones
Pioglitazone
39
What is the action of a thiazolidinedione?
PPAR-Gamma activators - increase peripheral insulin sensitivity
40
What are the side effects of thiazolidinediones?
Weight gain: redistribution of ectopically stored lipid
Fluid retention: contraindicated in CCF
Liver dysfunction: monitor LFTs
Association with bladder cancer: assess risk factors
41
Give an example of a gliptin
Sitagliptin
42
How do gliptins work?
DPP-4 inhibitors, thus increase post-prandial insulin release
43
In which patients should gliptins be avoided?
cardiac, hepatic or renal dysfunction
44
What are the side effects of gliptins?
GI disturbances
| rarely - acute pancreatitis
45
Give an example of a GLP-1 mimetic
enaxatide
46
In what circumstances would you give a GLP-1 mimetic?
If triple therapy is ineffective, then the gliptin / pioglitazone can be replaced by GLP-1 mimetic if:
Patient has a BMI >35 or
Patient has a BMI <35 and weight loss would benefit other co-morbitidies
insulin therapy would have negative occupational impacts
n.b. given by SC injection
47
What are the indications for insulin therapy?
All patients with T1DM that present below the age of 40 and all patients with T2DM that fail to respond to full medical treatment or are unsuitable for medical treatments
48
Describe the principles of management of T1DM?
Individualised care plan
Structured education programme
DAFNE: dose-adjustment for normal eating
Screen for complications: less common in early onset disease as not enough time to develop
Lifestyle advice:
Diet: carbohydrate counting is the most important advice as taught in DAFNE
Advice for how to adjust diet / insulin for exercise and consuming alcohol
Insulin regimen
Annual review
49
What are the three types of insulin available in the UK
human insulin
human insulin analogues
animal insulin
50
How is human insulin produced?
recombinant DNA technology - and have the exact same amino acid sequence as human insulin
Produced in the same way as human insulin but the insulin is modified to produce a specific desired kinetic characteristic e.g. an extended duration of action or faster absorption
51
Give examples of rapid acting insulin
Novorapid
Humalog
Apidra
These start working after around 10 minutes and last around 4 hours
52
How are short acting insulins used?
Injected with, or after food
Routine use after food should be discouraged
Onset of action = 15 minutes
Duration of action = 2-5 Hours
53
Give examples of short acting insulin
Actrapid
Humulin S
Insuman Rapid
These start working in around 30 minutes and last around 8 hours
54
How are soluble insulins used?
| short acting insulins
Generally injected 30 minutes before food
Onset of action 30-60 minutes
Duration of action up to 8 Hours
55
What are examples of intermediate acting insulins?
Insulatard
Humulin I
Insuman Basal
These start working in around 1 hour and last around 16 hours
56
Give examples of intermediate acting insulins?
Humulin I, Insulatard
57
How are intermediate acting insulins used?
Onset of action 1-2 hours
Maximal effects between 4-12 hours
Duration of action up to 16-35 hours
58
What Is the purpose of long acting insulins?
Mimic basal insulin secretion
59
Give examples of Long acting insulins
These starts working in around 1 hour and lasts around 24 hours:
Lantus
Levemir
Degludec (lasts over 40 hours)
60
How are long acting insulins used?
Used once/twice per day, achieved a steady state level after 2-4 days
61
What is novomix?
Combination insulin - These containing a rapid acting and an intermediate acting insulin.
62
Describe the typical insulin regime for T1DM
Basal bolus regimes recommended
Twice daily long-acting insulin: Detemir
Rapid acting insulin with each meal: Novorapid
If this is not possible, twice-daily mixed insulin regimens can be tried
If the patient cannot achieve HbA1c <8.5%, insulin pumps can be considered by a specialist team
63
wHat is the insulin regime for T2DM?
Continue metformin treatment to prevent excess weight gain
Intermediate acting insulin injected once/twice daily according to need
Biphasic preparations cane used if patient's HbA1c is particularly high
64
What considerations are there if there is poor diabetic control on insulin?
```
Non-adherence to treatment
Poor injection technique
Non-rotation of injection sites
Inappropriate dose titration
Psychosocial issues
Organic causes (?CKD)
```
65
What are the complications of insulin therapy?
General: weight Gain, avoided by DAFNE
Insulin resistance can develop
At the injection site: Pain, redness, swelling
Injection site abscess
lipohypertrophy:can result in erratic insulin absotrption
66
How is blood glucose monitored on a day to day?
Patients are asked to take four finger prick glucose readings on two days each week
Optimal targets are:
fasting: 5-7mmol on waking
Plasma glucose: 4-7 mmol/L before meals at other times of the day
Plasma glucose: 5-9mmol/L 90 minutes after eating
67
What are the sick day rules for diabetes?
Do not stop insulin therapy - seek advice from diabetes team on how to adjust insulin doses
monitor blood glucose more frequently: every 3-4 hours including overnight
consider blood/urine ketone monitoring
Maintain normal meal pattern where possible - replace meals with sugary drinks if appetite reduced
Drink at least 3L fluid/day. Seek advice if unable to do this due to nausea/vomiting
IV fluids may be required
68
In what circumstances would a patient need to inform the DVLA about their diabetes?
2 episodes of severe hypoglycaemia within the last 12 months
Reduced awareness of hypoglycaemic episodes
They are on insulin therapy
If on insulin, they must test their blood glucose every 2 hours on long journeys and carry appropriate glucose stores in case of hypoglycaemic events
69
What are the essential components of an annual diabetic review?
```
Assess cardiovascular risk: Macrovascular complications:
BMI
BP
Smoking
Blood lipid
```
```
Microvascular complications:
History: ED / neuropathic pain
Foot exam: neurovascular status
Fundoscopy: retinal involvement
Urine dip, first pass urine and plasma creatinine: renal involement
```
Assess diabetic control: Self monitoring and Hba1c
Assess concordance to diet/lifestyle advice
Assess for adverse events: hospitalisation, symptoms of hypoglycaemic episode, medication side effects, injection site reaction
Depression and anxiety
70
What is DKA?
Diabetic ketoacidosis
Metabolic emergency in which hyperglycaemia is associated with metabolic acidosis due to greatly raised ketone levels
Associated with T1DM
71
Describe pathophysiology of DKA
ABSOLUTE insulin deficiency
Ketoacidosis - uncontrolled catabolism: ketogenesis
higher and higher glucose and ketones levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH, but this is overwhelmed
Dehydration- Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis.
Potassium Imbalance
Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells.
72
Describe how renal perfusion is affected in DKA
Increased excretion of sodium and potassium
Despite a significant total body deficit of K+, initial serum K+ is typically normal or even elevated (pseudo-hyperkalaemia)
Serum K+ will then usually fall during treatment as the exogenous insulin drives K+ into cells
If serum K+ is not monitored and replaced as needed, life-threatening hypokalaemia may develop
73
Why do you get normal K+ initially in DKA?
Extracellular migration of K+ in response to acidosis and insulin deprivation
74
What are the common reasons for DKA development?
Previously undiagnosed diabetes
Interruption of insulin therapy
The stress of intercurrent illness/surgery
75
What are the clinical presentations of DKA?
```
NEED A KFC
N: nausea and vomiting
E: excessive thirst
E: excessive urination
D: dehydration
```
A: Abdominal pain
K: Kussmaul respiration
F: Fruity breath
C: Coma and death
76
How is diagnosis of DKA done?
ALL 3 of:
1. Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
2. Ketosis (i.e. blood ketones > 3 mmol/l)
3. Acidosis (i.e. pH < 7.3)
77
What are the essential investigations for DKA?
U+Es, creatinine, blood glucose
Venous blood gas: arterial puncture not generally required
Metabolic acidosis with raised anion gap
ECG, Chest Xray, cultures, pregnancy test based on clinical suspicion
N.B. raised WCC Is common, as is raised amylase
78
How is severity of DKA determined?
Mild: pH >7.3
Moderate: pH 7.1-7.3
Severe: pH <7.1
79
What is the immediate treatment of DKA?
ABCDE
+ FIGPICK
F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1
Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)
80
When should critical care review be sought in DKA?
Severe DKA, drowsy, pregnant, sats <94% on 40% O2 or persistent hypotension (<90SBP) after 2L of sodium chloride
81
What is the further treatment of DKA?
Continue fixed rate insulin at 0.1units/kg/hr and continue normal long acting insulin
Aim for blood glucose fall of >3mmol/L/hour until <14mmol/L
if not glucose is not falling, check dosage, pump operation, patient weight, reassess concomitant illness
Increase rate by 1 unit / hour every hour ifneccessary
Continue IV 0.9% NaCL
When glucose is <14mmol/L add 10% glucose at 125ml/hour
Potassium: if Plasma K <5.4, add 40mmol KCL per litre NaCl
consider after the first litre of fluid has run through
clinically reassess the patient hourly
regular lab monitoring of glucose, ketones, K+ and HCO3 is required
82
How should fluid be given in DKA?
```
1L STAT.
First bag: 1L over 1 hour
Second bag: 1L over 2 hours
Consider KCL from second bag onwards
Third bag: 1L over 2 Hours
Fourth bag: 1L over 4 hours
```
83
How should DKA be managed when the patient has recovered?
Transfer to SC insulin once the patient is able to eat and drink normally and venous pH is >7.3
Stop the IV infusion 1 hour after the next SC injection of insulin
Refer all patients to the diabetes team prior to discharge
84
What is HHS?
Complication of T2DM:
severe hypergycaemia causes a hyperosmolar state in the absence of severe ketosis
even a small amount of insulin is enough to prevent ketosis
85
What are the precipitants of HHS?
Consumption of glucose-rich fluids
Medications: thiazide diuretics, steroids, B-blockers
Intercurrent illness: infection / MI
86
What are the features of HHS?
Patients may be more severely dehydrated than DKA patients but there will be no raised ketones
Can be a lactic acidosis, but is generally mild
Features: dehydration, stupor, coma, seizures
Evidence of an underlying illness
87
How is diagnosis of HHS done?
Calculating osmolality:
2(Na+) + urea + glucose
88
What is the normal osmolality?
| What value suggests HHS?
Normal: 280-295
| Values >320 suggest HHS
89
What is the management of HHS?
Aggressive IV fluids: 1L 0.9% NaCL over 1 hour
Aim for positive balance of 3-6L over 12 hours
Low dose fixed dose IV insulin infusion
If ketones -treat as DKA and start immediately
If no ketones: add insulin once fall in glucose is <5mmol/L/hr
Consider potassium replacement: if 3.5-5.5 - 40mmolL
Regular monitoring
90
How long will normalisation of fluids and electrolytes take in HHS?
How should patients be managed in recovery?
may take 72 hours
Transfer to SC insulin when eating and drinking and normal biochemistry
Stop IV infusion 1 hour after starting SC insulin
91
What is hypoglycaemia?
Plasma glucose <3mmol/L, but individual thresholds for symptoms are variable
Symptoms are autonomic or neuroglycopenic
92
What are the autonomic symptoms of hypoglycaemia?
```
Sweating
Anxiety
Hunger
Tremor
Palpitations
```
93
What are the neuroglycopenic symptoms of hypoglycaemia?
Confusion
Drowsiness/Coma
Seizures
94
How does the pancreas react to hypoglycaemia?
alpha cells of pancreas will release glucagon, which work to:
increase glycogenolysis
Increase gluconeogenesis
inhibit glycogen synthesis
In T1dm, the alpha cells become insensitive to falls in glucose, thus becoming increasingly vulnerable to hypoglycaemia
95
How does hypoglycaemia occur?
Excess insulin:
inhibits hepatic gluconeogenesis and glycogenolysis
either exogenous or insulinoma
Depletion of hepatic glycogen: malnutrition, fasting, exercise or alcohol
liver failure can also cause this
pituitary insufficiency, adrenal insufficiency and non-pancreatic neoplasm can also cause hypoglycaemia
96
What is the management of hypoglycaemia if the patient can swallow?
If able to swallow: 10-20g of a fast acting form of carbohydrate: liquid
Recheck blood glucose after 10-15 minutes
should be reversed in 10 minutes
if inadequate response, repeat as above and check again. When symptoms improve, the patient should eat some long acting carbohydrate
97
What is the management of hypoglycaemia If the patient cannot swallow?
IM glucagon immediately
If <8 years, 500 micrograms
if >8 years, 1mg
If glucagon not available / person consumed alcohol / patient does not respond - 999
Intake of long acting carb when able to
98
How should hypoglycaemia recovery be managed
Vomiting common: precipitate further episodes --> ?hosptial for IV. can also give 20% glucose IV in hospital
Following recovery, never omit insulin in patients with T1DM
99
What is microvascular disease in diabetes?
Small vessels of the retina, glomeruli and nerve sheaths are particularly affected
100
What are the different types of diabetic eye disease?
Diabetic retinopathy - either proliferative or non-proliferative:
NPDR
PDR (more common in T2DM)
Diabetic maculopathy
CATARACTS
Glaucoma
101
What are the risk factors for diabetic retinopathy?
Poor control, smoking, HTN, pregnancy
102
What are the symptoms / signs of NPDR?
Usually asymptomatic, and always occurs at some severity after 8-10 years of DM
Features on fundoscopy:
Micro-aneurysms
Exudates: due to leaky vasculature
Haemorrhages: dot, blot, flame shaped
Cotton wool spots (>5 indicated pre-proliferative retinopathy)
Axoplasmic accumulation due to nerve fibre infarcts
Can progress into proliferative
103
What is the Mx of NPDR?
good glycemic control
104
What is PDR?
Development of new vessels on the optic disc or retina as a response to significant retinal ischaemia
Ischaemia leads to VEGF production
Vessels = fragile and likely to bleed, can give pre-retinal or vitreous haemorrhage
105
What are the symptoms of PDR?
Sudden deterioration in acuity
| Can also cause AACG due to iris neovasculariasation
106
What is the management of PDR?
Laser photocoagulation
Anti-VEGF medications such as ranibizumab and bevacizumab
Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
107
In which type of diabetes is diabetic maculopathy more common?
T2DM
108
What is diabetic maculopathy?
Specific type of retinopathy that affects the macula
| Typically presents as blurring of the vision
109
What are the subtypes of diabetic maculopathy?
Focal, diffuse and ischaemic
110
What is the management of diabetic maculopathy?
Mx with focal laser to stop focal leaks but mixed maculopathies require more complex treatment
111
What kind of cataracts develop in diabetics?
Posterior sub-capsular cataracts
112
Which type of glaucoma is more common in diabetics?
Progressive open angle glaucoma
113
What are the neurological complications of DM?
```
Symmetrical polyneuropathy
Acute painful neuropathy
Mononeuropathy
Diabetic amyotrophy
Autonomic neuropathy
```
114
what is a symmetrical neuropathy?
'glove and stocking' sensory loss, with vibration, deep pain and temperature lost first
patients complain of losing balance when their eyes are closed e.g. when washing face - decreased proprioception
Walking on cotton wool
Interrosseous wasting of the small mm of feet = foot shape + ulcers
Neuropathic arthropathy can also develop: Charcot's foot
115
What is acute painful neuropathy?
Painful burning in feet, shins and anterior thighs
Associated with poor glycemic control
Typically worse @ night
Usually remits after 3-12 months of good glycemic control
116
What is mononeuropathy?
Isolated nerve lesions: E.G.
CN lesions - mainly III, IV and VI: ocular palsies
Isolated peripheral nerve lesions can also occur: e.g. Carpal tunnel syndrome
Foot drop - sciatic nerve
When more than one affected = mono neuritis multiplex
117
What is diabetic amyotrophy?
Progressive wasting of muscle tissues
Rare, usually developing in middle aged men
In diabetes, presents as painful wasting of the quadriceps
118
What is autonomic neuropathy?
Sympathetic dysfunction leads to postural hypotension, ejaculatory failure, reduced sweating and Horner's syndrome
Parasympathetic dysfunction leads to erectile dysfunction, constipation, urinary retention and a Holmes-Adie pupil
119
How does diabetes affect the kidneys?
Diabetic nephropathy
CKD
120
How should diabetic patients be monitored for renal complications?
blood pressure control
test every patient 6 monthly for microalbuminurea i.e. negative urine dip but early morning albumin:creatinine ratio >3
Every patient with microalbuminurea should be started on an ACEi, regardless of blood pressure
121
How does diabetes affect atherosclerosis?
Risk factor for atherosclerosis:
2x increased risk of stroke
4x increased risk of MI
50x increased risk of amputation for gangrene
Treatment for DM only has a modest effect on CV risk
Risk are the same as for generalised atherosclerosis in non-diabetics, however are increased with increasing age, increasing duration of symptoms and also in poor control
122
What is a goitre?
Painless enlargement of the thyroid gland.
123
What characteristics are described with a goitre?
Diffuse vs nodular; pattern of swelling
simple vs toxic: is it actively secreting thyroid hormone
Benign vs malignant
124
What are the ddx for a diffuse goitre?
```
Physiological - puberty, pregnancy
autoimmune - graves, hashimotos
thyroiditis - subacute, reidel's
endemic - iodine deficiency
drugs - anti-thyroid drugs, lithium, iodine excess amiodarone
```
125
What are the ddx for a nodular goitre?
multinodular: toxic multi nodular goitre, subacute thyroiditis
Solitary nodule: follicular adenoma, benign nodule, thyroid malignancy, lymphoma, metastasis
infiltration (rare): TB, sarcoid
126
Wha investigations should be done for a thyroid swelling?
FBC: related anaemia
ESR: may indicate thyroiditis / autoimmune disease
TFTs: TSH, free T4
Thyroid autoantibodies: autoimmune disease
CT neck and thorax (if pressure symptoms)
USS
FNAC if concerned about malignancy
127
What is the management of a goitre
Depends on if hyper, hypo or euthyroid
| in euthyroid, treatment is not required for a non-malignant nodule unless it is causing pressure symptoms
128
What is thyrotoxicosis?
clinical disorder resulting from raised circulating levels of thyroid hormone
Affects 1% of the population
far more common in women 5:1
129
What are the causes of thyrotoxicosis?
Grave's disease:
toxic multi nodular goitre
```
Solitary toxic adenoma
Thyroiditis
drug-induced
excess iodine intake
hashitoxicosis
```
Rare - TSH secreting pituitary adenoma
Resistance to thyroid hormone
130
What are the symptoms of hyperthyroidism?
```
Anxiety/irritability
Heat intolerance/sweating
Increased appetite
Palpitations
weight loss
tremor
loose motions
fatigue/weakness
```
131
What are the signs of hyperthyroidism?
```
lid retraction / lid lag
Graves' ophthalmopathy*
Goitre/bruit*
systolic hypertension
tachycardia / AF
tremor
hyper-reflexia
warm peripheries
acropachy*
proximal weakness
pre-tibial myxoedema*
```
132
What is Graves ophthalmopathy?
Inability to close eyes completely
Exophthalmos / proptosis: bulging eyes
ophthalmoplegia - especially affecting upwards and lateral gaze
Periorbital oedema
133
What is a thyroid storm?
Rare presentation of hyperthyroidism, in people with untreated disease in periods of stress: infection, surgery, childbirth:
Hyperpyrexia
Severe tachycardia
Profuse sweating
Confusion / psychosis
If untreated, coma and death may ensue
134
What is the treatment of thyroid storm?
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol's iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
135
What are the investigations for hyperthyroidism?
TSH: fully suppressed - unless in the rare case of pituitary adenoma
Free T3/T4: elevated (typically both but sometimes just T3 and not T4)
TSH receptor antibody: sensitive and specific for graves disease
Technetium uptake scan: can distinguish from Grave's disease, toxic multinodular goitre, toxic adenoma or thyroiditis
CT/MRI of the orbit:
136
Describe the patterns of uptake of technetium scanning
Diffuse pattern of uptake in Graves' disease
One of more 'hot' nodules in toxic multinodular goitre
reduced/absent uptake in thyroiditis
137
What is the management of hyperthyroidism in primary care?
B-blocker: 20-40mg tds for rapid relief of symptoms
May be the only treatment required for cases of thyroiditis
Refer to a specialist endocrinologist
138
What is the management of hyperthyroidism in secondary care?
Antithyroid drugs, radioactive iodine therapy, or surgical management for Grave's disease
1st line: CARBIMAZOLE
2nd line: Propylthiouracil
Block and replace
High dose and titrate down until the patient is euthyroid
RAI or surgical management for other pathologies
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What is the first line antithyroid drug?
Carbimazole
| then Propylthiouracil
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How do antithyroid drugs use?
Act as Preferred substate for thyroid peroxidase, the key enzyme in thyroid hormone synthesis
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What are the side effects of anti-thyroid drugs?
Skin rashes
agranulocytosis/thrombocytopenia
Carbimazole can cause cholestatic jaundice
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Describe the uses of RAI therapy?
Used first line in non-Grave's pathology, or following failure of drug therapy in Grave's
Taken up by thyroid cells and induces DNA damage and cell death
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How should a patient beginning RAI therapy be counselled?
Contraindicated in pregnancy and in active Grave's ophthalmopathy
Can cause worsening of eye symptoms
Patients should avoid prolonged contact with children for three weeks after treatment and should not attempt to conceive for 6 months
Rarely can cause worsening of symptoms and thyroid storm
Slight increased risk of thyroid acnes
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What surgeries are done for hyperthyroidism and what are the indications?
Total or sub-total thyroidectomy
Indicated if the above measures have failed or are contraindicated
if there is a suspicion of malignancy, or to manage a large toxic goitre
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What are the post-op complications of thyroidectomy?
Haematoma formation causing asphyxia
emergency removal of sutures
Hypothyroidism (10%)
Hypocalcaemia: due to hypoparathyroidism (often transient)
Vocal cord paresis
