Endocrinology Flashcards
1
Q
What are the properties of peptide hormones? How do they work?
A
- Made from short-chain amino acids (size is anything from few AAs to small protein)
- Pre-made and stored in cell, released and dissolved into blood when needed
- Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane
- Bind to receptors on cell membranes, triggering a second messenger to be released within cell - very quick
- Examples: Insulin, growth hormone, TSH, ADH
2
Q
What are the properties of steroid hormones? How do they work?
A
- Synthesised from cholesterol
- Not stored in cell, released as soon as they are made
- Not water soluble - must be bound to transport proteins to travel in blood
- Lipid soluble - can cross plasma membrane and bind to receptor inside cell - slow response
- Examples: Testosterone, oestrogen, cortisol
Pregnenolone is the precursor for all steroid hormones, and its formation represents the rate-limiting step of steroid synthesis. Conversion of cholesterol to pregnenolone takes place within mitochondria.
3
Q
Tell me about catecholamine hormones (amino acid derived)
A
- Synthesised from the amino acid tyrosine
- Acts same way as peptide hormone
- Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane, so released via exocytosis
- Examples: Adrenaline, dopamine
4
Q
What are the cell types and their functions within the islets of langerhans in the pancreas?
A
Alpha cells - produce glucagon
Beta cells - produce insulin and amylin
Delta/D cells - produce somatostatin
PP cells - produce pancreatic polypeptide
5
Q
What are the classes of hormones?
A
- Steroids
- Peptides
- Thyroid hormones
- Catecholamines
6
Q
Tell me about thyroid hormones
A
- Released via proteolysis
- T3 = triiodothyronine, T4 = thyroxine
- Take a day to act
- In blood bound to thyroglobulin binding protein (produced by liver)
7
Q
What is the blood supply to the thyroid gland?
A
- Superior thyroid artery - off thyrocervical trunk (subclavian)
- Inferior thyroid artery - off external carotid artery
8
Q
Where are the thyroid and parathyroid glands located?
A
- Thyroid gland sits at C5-T1
- Two lobes connected by an isthmus
- Parathyroid is 4 glands on the posterior surface of thyroid glands
9
Q
What effect does parathyroid hormone have on the kidneys?
A
- Increased conversion of 25-hydroxyvitamin D (inactive) to 1,25-dihydroxyvitamin D(active)
- At the DCT: Increased Ca2+ reuptake and PO43- excretion
10
Q
What effect does parathyroid hormone have on the gut?
A
Increased Ca2+ and PO43- absoroption
11
Q
What hormones does the adrenal gland produce?
A
Adrenal cortex:
- Zona glomerulosa - mineralocorticoids (eg: aldosterone)
- Zona fasciculata - glucocorticoids (eg: cortisol)
- Zona reticularis - adrenal androgens
Adrenal medulla:
- Catecholamines (eg: adrenaline)
12
Q
Draw out the process of phosphate regulation physiology
A
increased PTH:
increased phosphate—> increased FGF-23 (osteocyte)—-> less 25 dihydroxy vit D—> less inorganic phosphate absorption—-> less phosphate
increased FGF-23 then completes cycle above
Less inorganic phosphate absorption directly
PHEX leads to less phosphate
13
Q
What can pituitary tumours do?
A
- Press local structures - eg: optic chiasm -> bitemporal hemianopia
- Hypopituitarism
- Hyperpituitarism - acromegaly, Cushing’s disease, prolactinoma
14
Q
Hormones secreted by the hypothalamus and what they stimulate from the anterior pituitary
A
- GnRH -> FSH and LH
- CRH -> ACTH
- GHRH -> GH
- TRH -> TSH
- DA -> inhibits Prolactin
15
Q
What is always given to unresponsive hypoglcyemic patients?
A
IM glucagon
16
Q
Role of insulin
A
- Increase peripheral glucose uptake
- Glucose -> glycogen
17
Q
Biphasic release of insulin
A
- Glucose binds to GLUT2 receptors of pancreas on b cells, stimulating insulin release
- Insulin binds to peripheral insulin receptors:
- Activates intracellular tyrosine kinases + cascade
- Increase of Glut-4 channel expression on CSM
18
Q
Posterior pituitary hormones
A
- Oxytocin (paracentricular nucleus) - milk ejection + labour induction
- Vasopressin (supraorbital nucleus) = adh
19
Q
What does vasopressin do?
A
- Vasoconstricts blood vessels
- Increased APO II (aquaporin) expression in collecting duct
- Increased aldosterone
20
Q
Functions of cortisol
A
- Increases protein and carb breakdown
- Upregulates alpha 1 receptors on arterioles -> increased BP
- Suppresses immune response
- Increased osteoclast activity (osteoporotic)
- Increased insulin resistance
21
Q
GH/IGF-I axis
A
increased GHRH + decreased SMS - from hypothalamus
Leads to pituitary releasing GH
Liver then releases IGF -I which reduces hypothalamus releases of GHRH and SMS
22
Q
Insulin secretion by the beta cell
A
- Glucose enters via GLUT2 transporter
- K+ channels close and depolarise cell membrane
- Calcium channels open and Ca2+ enters cell and stimulates insulin secretory granules
- Insulin secreted
23
Q
Insulin action in muscle and fat cells
A
- Insulin enters via insulin receptors
- Intracellular signalling cascades cause GLUT4 vesicles to integrate into plasma membrane
- Glucose enters cell via GLUT4 transporter
24
Q
Alpha vs beta islet of Langerhans cells
A
Alpha cells: glucagon
- Increases hepatic glucose by increasing glycogenolysis and gluconeogenesis
- Stimulates lipolysis and muscle breakdown
- Reduces peripheral glucose output
Beta cells: insulin
- Suppresses hepatic glucose by decreasing glycogenolysis and gluconeogenesis
- Suppresses lipolysis and breakdown of muscle
- Increases glucose uptake into insulin sensitive tissues
25
Thyroid axis
Hypothalamus releases TRH, pituitary releases TSH then thyroid releases T4 & T3 which has a neg response on TRH and TSH.
26
Physiology of thyroid hormone production
- Iodine diffuses from follicular thyroid cells into the colloid (fatty empty space inbetween follicular cells)
- Iodine binds to tyrosine residues on molecule thyroglobulin
- Cleaved from long chains to form T3 or T4(active)
27
Physiology of thyroid hormone release-what hypothalamas nucleus?
- Supraventricular nucleus of hypothalamus releases TRH
- TSH released from thyrotrophs in anterior pituitary
- Binds to TSH-receptors on thyroid
- Causes T3/T4 to diffuse from colloid to follicular cells then to the bloodstream
28
PTH regulation
- Tightly regulated by body Ca2+ to prevent hyper/hypocalcaemia
- Directly inhibited by calcitonin - from parafollicular C cells fo the thyroid
29
Testing gonadal axis: men
- Low testosterone, high LH/FSH: Primary hypogonadism
- Low testosterone, normal/low LH/FSH: Hypopituitarism
- Low testosterone and low LH: Anabolic use
Measure 9hr fasted testosterone (morning) and LH/FSH in pituitary disease
30
Testing gonadal axis: women
- Low oestradiol, high LH and FSH (FSH greater) = Primary ovarian failure
- Low oestradiol, normal/low LH and FSH, oligo/amenorrhoea = Hypopituitarism
31
Normal gonadal levels in women
Before puberty:
- Low oestradiol
- Low LH/FSH
Puberty:
- Increased oestradiol
- Increased pulsatile LH
Post menarche:
- Monthly menstrual cycle with LH/FSH
- Mid-cycle surge in LH and FSH
- Levels of oestradiol increases through cycle
32
What does the pituitary gland control?
- Thyroid
- Adrenal cortex
- Testis
- Ovary
Not the adrenal medulla
33
What hormones have a circadian rhythm
- Cortisol
- Testosterone
- DHEA
- 17OH Progesterone
Not T4
34
Which hormones suppress appetite?
- Peptide YY
- CCK
- GLP 1
- Glucose
35
What is the main adipose signal to the brain?
Leptin
36
Typical features of hypogonadism in males
- Joint and muscular aches
- Decreased sexual appetite
- Decreased hair growth
- Asymptomatic
37
What is satiety?
The physiological feeling of no hunger
38
What does ghrelin do?
Stimulates hunger
39
What do long term corticosteroid medications lead to?
- Suppression of the adrenal glands
- Long term atrophy of the adrenal glands - can't produce enough corticosteroids
- Adrenal insufficiency if medication is stopped
40
Differential diagnoses for presentation of polyuria and polydipsia
- Diabetes mellitus
- Diabetes insipidus
- SIAD - Syndrome of Inappropriate Antidiuretic Hormone Secretion.
- Primary polydipsia
- Hypercalcaemia
41
Side effects of dopamine agonists such as bromocriptine
Impulsiveness, so can lead to addictions
42
Link between acromegaly and prolactinoma
50% of acromegaly tumours are associated with prolactinoma
43
Primary adrenal insufficiency
- Addison's disease
- Pathology is at the adrenal glands
- Decreased producion of adrenocortical hormones (cortisol and aldosterone)
- High ACTH, low adrenocortical hormones
44
Secondary adrenal insufficiency
- Pathology is in the pituitary
- Inadequate ACTH released from pituitary
- Leading to low release of adrenocortical hormones from the adrenal gland
- Low ACTH, low adrenocortical hormones
45
Why do patients with primary adrenal sufficiency present with bronzed skin?
High ACTH stimulates melanocytes, resulting in hyperpigmentation
46
Aetiology of primary adrenal insufficiency
- Developed world: Autoimmune adrenal destruction (21-hydroxylase present in 60-90% of people)
- Developing world: TB (+ sarcoidosis)
47
Risk factors for adrenal insufficiency
- Female
- Adrenocortical antibodies
- Other autoimmune disease
48
Other causes of adrenal insufficiency
- Adrenal metastasis (lung, liver, breast)
- Adrenal haemorrhage (eg: meningococcal septicaemia)
49
Symptoms of adrenal insufficiency
- Weight loss
- Nausea and vomiting
- Lethargy and generalised weakness
- Salt cravings
50
Signs of adrenal insufficiency
- Bronze hyperpigmented skin, particularly in palms (only in Addison's)
- Postural hypotension
- Hypoglycaemia
- Change in body hair distribution - Loss of pubic hair in women
- Associated autoimmune condition
51
Signs of adrenal crisis
- Hyponatraemia
- Hyperkalaemia
- Profound fatigue
- Dehydration
- Vascular collapse (low BP)
52
Treatment of Addisonian/adrenal crisis
- Immediate 100mg hydrocortisone
- IV solve + dextrose (if hypoglycaemia)
- Without cortisol, you will die from adrenal crisis if you have an infection
53
Diagnosis of adrenal insufficiency
- First line: 8-9am cortisol
- Gold standard: ACTH stimulation test (short Synacthen test)
RESULTS
- Low cortisol, high ACTH, poor response to synacthen = Primary adrenal insufficiency
- Low cortisol, low/normal ACTH, poor response to synacthen = Secondary adrenal insufficiency OR hypopituitarism
54
Other investigations for adrenal insufficiency
- U+E to test for hyponatraemia and hyperkalaemia
- Aldosterone:renin ratio
- Adrenal CT or MRI
- Test bloods for 21-hydroxylase adrenal antibodies
55
Treatment for Adrenal insufficiency
- Hydrocortisone - glucocorticoid to replace cortisol
- Fludrocortisone - mineralocorticioid to replace aldosterone if necessary
- Double the dose of hydrocortisone in trauma/infection
56
Tertiary adrenal insuffiiency
- Caused by inadequate CRH released by the hypothalamus
- Usually a result of long term oral steroids
57
Complications of adrenal insufficiency
- Addisonian crisis (experiences by 40% of patients) - life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium.
- Cushing's syndrome
58
What are carcinoid tumours?
- Poorly malignant tumours of enterochromaffin cells which produce 5-HT/serotonin
- Mostly in the GI tract at the appendix and terminal ileum
- Can also be in the lungs
59
Carcinoid tumours vs syndrome
- Tumours - only the neoplastic cell, no/v little symptoms
- Syndrome - when tumour metastasises to the liver
60
Presentation of carcinoid syndrome
- Diarrhoea
- Flushing
- Tricuspid incompetence (valve lesion)
- Right upper quadrant pain- hepatic metasteses.
- Bronchospasm
61
What does carcinoid syndrome tend to express?
Somatostatin receptors
62
Diagnosis of carcinoid syndrome
- High volume of 5-hydroxyindoleacetic acid (breakdown of serotonin) in urine
- Metabolic panel and LFTs
- Liver ultrasound to confirm metastases
- CT/MRI to locate primary tumour
63
Treatment for carcinoid syndrome
- Surgically excise primary tumour
- Peri-operative ocreotide (SST analogue) infusion to block tumour hormones
- For metastases: above + radiofrequency ablation
64
Carcinoid crisis treatment
- Life threatening
- Treated with high dose SST analogue (octeotride)
65
Symptoms of HHS
- Generalised weakness and leg cramps
- Confusion, lethargy, hallucinations, headaches
- Visual disturbance
- Polyuria and polydipsia
- Nausea, vomiting and abdo pain (more common in DKA)
Hyperosmolar hyperglycemic syndrome (HHS) is a clinical condition that arises from a complication of diabetes mellitus.
66
Epidemiology of HHS
- Less than 1% of diabetes admissions
- 5-15% mortality
Risk factors:
- Infection
- MI
- Poor medication compliance
67
Pathophysiology of HHS
- Rise in counter-regulatory hormones (glucagon, Ad, cortisol, GH)
- Causes hyperglycaemia ans hyperosmolality
- Electrolytes in blood overflow into urine -> excessive loss of water and electrolytes
68
Characteristics of HHS
- Marked hyperglycaemia
- Hyperosmolality
- Profound dehydration
- Electrolyte abnormalities
69
Diagnosis of HHS
Diagnostic:
- Hyperglycaemia ≥30mmol/L without a metabolic acidosis or significant ketonaemia
- Hyperosmolality ≥320mOsmol/kg
- Hypovolaemia
Other tests:
- Urine dipstick: heavy glycosuria
- U+E: low total body K+, high serum K+
70
How can HHS be differentiated from Diabetic ketoacidosis?
DKA
- T1DM
- Patients younger and leaner
- Ketoacidosis
- Develops over hours to a day
HHS
- T2DM
- No ketoacidosis
- Significantly higher mortality rate
- Develops over a longer time - days to a week
71
Treatment of HHS
- IV fluid 0.9% saline
- IV insulin only if there is ketonaemia or IV fluids aren't working
- LMWH to anticoagulate patient as they have thicker blood
- Electrolyte loss (K+)
72
What are complications of HHS treatment with insulin?
- Insulin-related hypoglycaemia
- Hypokalaemia
73
Signs of HHS
- Reduced GCS
- Dehydration
- Hemiparesis (can be confused for a stroke)
- Seizures
74
Why is there no acidosis in HHS?
- Small amounts of circulating insulin in T2DM
- So lipolysis doesn't occur
75
Complications of HHS
- Cardiovascular - venous thromboembolism, arrhythmias, MI
- Neuro - stroke and seizures
- AKI
76
Causes of hypoglycaemia
- Diabetic drugs: sulfonylureas or insulin
- Non diabetic: oral, liver failure, Addison's, increasing age
77
Symptoms of hypoglycaemia on the brain
- Cognitive dysfunction
- Blackouts
- Seizures
- Comas
- Psychological effects
78
Treatment for hypoglycaemia
If not serious, food to release blood sugars
- IV glucose or oral glucose gel
- If no access, IM glucagon (only if alpha cells are working)
- Check Blood sugar after 5 mins and if it’s increased give food
79
Symptoms of hypoglycaemia on the heart
- Increased risk of MI
- Cardiac arrhythmias
80
Symptoms of hypoglycaemia on the musculoskeletal system
- Falls
- Accidents (inc. driving)
- Fractures
- Dislocations
81
Symptoms of hypoglycaemia on circulation
- Inflammation
- Blood coagulation abnormalities
- Haemodynamic changes
- Endothelial dysfunction
82
Blood glucose of patient with hypoglycaemia
<3.5mmol/L
83
Epidemiology of Diabetic Ketoacidosis
4% of T1DM patients develop each year
84
Risk factors for DKA
- Poorly managed/undiagnosed T1DM
- Infection/illness
- Characteristic in patients around 20 years old
85
Pathophysiology of DKA
- Absolute immune deficiency = unrestrained lipolysis and gluconeogenesis and decreased peripheral glucose uptake
- Not all glucose from gluconeogenesis is usable so converted to ketone bodies, which is acidic
86
Describe Kussmaul's breathing
Deep and rapid breathing in acidosis to expel acidic carbon dioxide
87
Signs of DKA
- Kussmaul's breathing
- Pear drop breath
- Reduced tissue turgar (hypotension + tachycardia)
88
How to investigate DKA
- Ketones > 3mmol/L
- RPG > 11.1mmol/L (hyperglycemic)
- pH < 7.3 or HCO3- < 15mmol
- Urine dipstick glyosuria/ketonuria
89
What are common differentials of DKA?
- HHS
- Lactic acidosis - identical presentation, normal serum glucose and ketones
- Starvation ketosis - physiologically appropriate lipolysis
90
Treatment for DKA (in order)
- ABCDE
- IV fluids FIRST 0.9% saline
- IV insulin 0.1units/kg/hour - once glucose level <14mmol add 10% glucose
- Restore electrolytes, eg: K+
91
Complications of DKA
- Coma
- Cerebral oedema
- Thromboembolism
- Aspiration pneumonia
- Death
- Dehydration
- MI
92
Symptoms of DKA
- Nausea and vomiting
- Weight loss
- Drowsy/confused
- Abdominal pain
93
Define T1DM
Absolute insulin deficiency, usually resulting from autoimmune destruction of the insulin-producing beta islet cells in the pancreas
- Type 4 hypersensitivity
94
Which genes are linked with increased risk of developing T1DM?
HLA-DR2 and HLA-DQ3
or
HLA-DR4 and HLA-DQ8
95
Environmental factors that can increase the risk of developing T1DM
- Diet
- Vitamin D deficiency
- Early-life exposure to viruses associated with islet inflammation (eg: enteroviruses)
- Decreased gut-microbiome diversity
96
Epidemiology of T1DM
- Young (usually between 5-15 years)
- Lean
- North European descent
- 10% of diabetes is type 1
97
Macrovascular complications of T1DM
Atherosclerosis, which leads to:
- CVD
- Stroke
- Peripheral arterial disease
98
Microvascular complications of T1DM
- Nephropathy
- Retinopathy -> glaucoma, cataracts
- Neuropathy -> diabetic foot disease
99
Other autoimmune conditions that can result from T1DM (most to least common)
- Thyroid disease
- Autoimmune gastritis
- Pernicious anemia
- Coeliac diease
- Vitiligo
- Addison's disease
100
Psychological complications of T1DM
- Anxiety
- Depression
- Eating disorders
Also in children:
- Behavioural and conduct disorders
- Family/relationship difficulties
- Risk-taking behaviour
101
Signs of T1DM
- BMI < 25kg/m2
- Failure to thrive in children
- Glove and stocking sensory loss
- Reduced visual acuity
- Diabetic retinopathy
- Diabetic foot disease
102
Symptoms of T1DM
- Polyuria
- Polydipsia
- Weigt loss
- Lethargy
- Recurrent infections
- Evidence of complications - eg: blurred vision or parasthesia
103
At what level of blood glucose can it no longer be absorbed?
10mmol/L
Thirsty and develop polyuria - body attempts to remove excess glucose
104
At what level of Beta cell destruction does hyperglycaemia develop?
80-90%
105
Diagnosis of T1DM
Random blood glucose ≥11mmol/L
Fasting blood glucose ≥7mmol/L
- One abnormal value diagnostic in symptomatic patients
- Two abnormal values diagnostic in asymptomatic patients
106
What is the most accurate test for T1DM?
HbA1C - measures glycated haemoglobin
>48 mmol/mol or >6.5% suggest hyperglycaemia over 3 months
107
Optimal targets for glucose self monitoring
- FBG: 5-7mmol/L on waking
- Plasma glucose 4-7mmol/L before meals at other times of the day
- If testing after meals: 5-9mmol/L at least 90 minutes after
108
How can T1DM be differentiated from Latent Autoimmine Diabetes in Adults (LADA)?
- In LADA age of onset is >30 yrs
- Low to normal C-peptide
109
How can T1DM be differentiated from Neonatal diabetes?
In neonatal diabetes:
Genetic testing shows mutation in genes coding ATP K+ channel and insulin gene
110
How can T1DM be differentiated from Monogenic diabetes?
In monogenic diabetes:
- C-peptide present
- Autoantibodies absent
111
First line treatment for T1DM
Basal-Bollus regimen
Basal - Long acting (either given twice or once daily)
Bollus - Short before meals
112
Pathophysiology of T1DM
- Beta islet cell destruction
- Hyperglycemia
- Low cellular glucose (increased lypolysis and gluconeogenesis)
- Hyperkalemia even though there is a low body K+ (enters cells via Na+/K+ ATPases)
113
NICE diagnostic criteria for T1DM
- Clinical features and evidence of hyperglycaemia
- Ketosis
- Rapid weight loss
- < 50 years
- BMI < 25 kg/m2
- Personal and/or family history of autoimmune disease
114
Other treatments for T1DM after basal-bollus
- Mixed insulin regimen
- Continuous insulin infusion
115
Mixed insulin regimen
- A mixture of short or rapid acting and intermediate-acting insulin
- Twice daily
- For those who can't tolerate multiple injections for basal bollus
116
Continuous insulin infusion
- If patient has disabling hypoglycaemia
- or persistently hyperglycaemic (HbA1c > 69mmol/mol) on multiple injection insulin therapy
117
Pathophysiology of T2DM
- Peripheral insulin resistance with partial insulin deficiency
- Decreased GLUT4 expression - impaired insulin secretion
- Lipid and beta amyloid deposits in pancreas, progressive b cell damage
118
Epidemiology of T2DM
- Presents later on in life (usually 30+ years)
- Males > females
- People of Asian, African and Afro-Carribean ethnicity are 2-4x more likely to develop T2DM than white people
119
Clinical presentation of T2DM
- Obese hypertensive older patient
- Polydipsia
- Nocturia
- Polyuria
- Glycosuria
- Recurrent thrush
120
Diagnosis of T2DM
- Same as T1DM
- fbg and random
- Prediabetes exists this time
121
Risk factors for T2DM
- Genetic link (stronger than T1DM)
- Obesity
- Alcohol excess
- Hypertension
- Gestational diabetes
- PCOS
- Drugs: corticosteroids, thiazides
122
Last line of treatment for T2DM if all else fails
Insulin treatment
123
Treatment for T2DM
Initial: Biguanide (metformin)
Second line: Carry on Metformin and add either:
- DPP-4 inhibitor
- Pioglitazone
- Sulfonylurea
- SGLT-2 inhibitor
124
Prediabetic states
FBG: 6.1-6.9
2nd post prandial: 7.8-11.0
HbA1c: 42-47 (6.0-6.4%)
125
First treatment for Type 2 diabetes and prediabetes before drugs
Lifestyle change - diet, exercise, modify RFs
126
Main complication of T2DM
Hyperosmolar hyperglycaemic state
127
Types of Insulin
- Rapid: aspart, lisporo, novorapid, glulisine
- Short: regular insulin
- Intermediate: NPH (half a day)
- Long: detemir, lantus, glargine
128
How can you get ketoacidosis in T2DM?
- Happens later on in the disease
- Because initially, micro secretions of insulin are sometimes still present, inhibiting glucagon
129
Why are thiazolidinediones (pioglitazone) not commonly given as a diabetic drug?
- Increase weight
- Increase risk of heart failure
- Increase risk of fractures
130
Advantages of basal insulin in T2DM
- Patient adjusts insulin themselves, based on fasting glucose measurements
- Carries on with oral therapy, combination therapy is common
- Less risk of hypoglycaemia at night
131
Advantages of premixed insulin in diabetes
- Both basal and prandial together
- Can cover insulin requirements though most of the day
132
Disadvantages of pre-mixed insulin
- Requires consistent meal and exercise pattern
- Cannot seperately titrate individual insulin components
- Increased risk of nocturnal and fasting hypoglycaemia
133
Disadvantages of basal insulin in T2DM
- Doesn't cover meals
- Best used with long-acting insulin analogues (expensive)
134
Signs of T2DM
- Acanthosis nigricans
- Glove and stocking sensory loss
- Diabetic retinopathy
- Diabetic foot disease
135
Side effects of other diabetic medication
- SGLT-2 inhibitor - genitourinary infections
- GLP-1 analogue - weight loss
- Thiazide diuretics - weight gain
136
Two types of diabetes insipidus
- Cranial - Low ADH secretion
- Nephrogenic - Low response to ADH
137
Aetiology of cranial diabetes insipidus
- ADH gene mutation
- Pituitary adenomas
- Brain infections
- Idiopathic
138
Aetiology of nephrogenic diabetes insipidus
- Renal tubular acidosis
- ADH-R mutation
- Drugs (lithium)
- Electrolyte disturbance
139
Presentation of diabetes insipidus
- Polyuria
- Polydipsia
- Hypernatremia
- Lethargy confusion coma
- Severe dehydration
140
How much urine a day will make you suspect diabetes insipidus?
Over 3L
141
Water deprivation test for diabetes insipidus
- No fluid for 8 hours
- Normally serum osmolality stays normal, urine osmolality increase
- DI = serum osmolality rises while urine osmolality unchanged
142
Desmopressin test for diabetes insipidus
Cranial urine osmolality:
After deprivation: Low
After desmopressin: High
Nephrogenic urine osmolality:
After deprivation: Low
After desmopressin: Low
Primary polydipsia
After deprivation: High
After ADH: High
143
Treatment for diabetes insipidus
Cranial - Desmopressin
Nephrogenic - Thiazides (+ treat underlying cause)
144
High and low values for urine osmolality
< 300 = low
>800 = high
145
Aetiology of hypercalcaemia (90% of cases)
90%:
- Hyperparathyroidism
- Malignancy: bone mets, myeloma, PTHrP, lymphoma
146
ECG in hypercalcaemia
Short QTc
147
Symptoms of hypercalcaemia and hyperparathyroidism
- Bones - excess resorption, ostopoenia
- Stones - kidney
- Groans - abdominal pain, constipation
- Psychedelic moans - confusion, depression, anxiety
- Thrones - polyuria and polydipsia
148
How does hypercalcaemia affect muscles
Low muscle tone and contractions as Ca2+ inhibits fast Na+ influx
149
What happens to PTH in hypercalcaemia
It will decrease due to negative feedback
(except in hyperparathyroidism)
150
Other causes of hypercalcaemia (other than top 90%)
- Multiple myeloma
- Granulomatous diseases (eg: TB and sarcoidosis)
- Dehydration
- Drugs
151
Drugs that can cause hypercalcaemia
- Thazides
- Diuretics
- Lithium
- Excessive Vit D or A intake
152
Treatment of hypercalcaemia
- Aggressive IV fluids
- Consider IV bisphosphonates if no response
- Treat underlying cause
153
Definition of hyperkalaemia and hypokalaemia
Hyper ≥ 5mmol/L
Emergency hyper = ≥ 6.5mmol/L
Hypo < 3.5mmol/L
154
Presentation of hyperkalaemia
- Muscle weakness and cramps
- Parasthesia
- Palpitations
- Tachycardia (arrhythmias)
155
Aetiology of hyperkalaemia
Increased intake of potassium
- IV therapy
- Increased dietary intake
Decreased excretion of potassium
- AKI and CKD
- Drugs (NSAIDs, spironolactone, ACE inhibitors)
- Renal tubular acidosis (T4)
- Addison's disease
Potassium shifted to extracellular
- Metabolic acidosis/DKA
- Rhabdomyolysis
Other: trauma and burns
156
Effect of hyperkalaemia on types of muscle
- Smooth muscle cramping
- Skeletal mucle weakness due to overcontraction
- Cardiac arrythmias and arrest
157
Effect of hyperkalaemia on Insulin, pH and Beta 2 receptors
- Insulin deficiency as not enough K+ flows into the cell
- Acidosis (H+ in and K+ out)
- Beta blocker - inhibits pumping of K+ into cell
158
Complications of hyperkalaemia + ecg
Cardiac arrhythmias and arrest
- Hyperkalaemia is associated with broadening QRS complex
159
Pathophysiology of hyperkalaemia
- High K+ decreases action potential
- Easier depolarisation
- Abnormal heart rhythms
160
Diagnosis of hyperkalaemia
- High K+ on U+Es
ECG:
- Absent P waves
- Prolonged PR
- Tall tented T waves
- Wide QRS
- Bradycardia
161
Treatment for hyperkalaemia
If urgent: Calcium gluconate to stabilise cardiac membrane if there are heart problems, then insulin dextrose
Non-urgent: Insulin (+dextrose)
162
Aetiology of hypocalcaemia
- CKD (due to decreased Vit D activation)
- Severe Vit D deficiency
- Primary hypoparathyroidism
- Acute pancreatitis
163
Symptoms of hypocalcaemia and hypoparathyroidism
Parasthesia
- Tetany (involuntary muscle contractions)
- Chvostek sign -face twitch
- Trousseau sign - forearm wrist twitch
164
How does hypocalcaemia affect muscle?
Muscle spasms: hands, feet, larynx, premature labour
165
How does hypocalcaemia affect PTH?
- Always increases
- Except in hypoparathyroidism
166
How to calculate corrected calcium levels
total serum calcium + (0.02* (40-serum albumin))
167
Why may serum calcium levels be inaccurate?
- Low serum albumin causes a low total serum calcium
- But this is not a low ionised calcium
- Need to do corrected calcium equation
168
Drugs that can cause hypocalcaemia
- Bisphosphonates
- Phenytoin
- Loop diuretics
- Cinacalcet
169
Treatment of hypocalcaemia
- Oral calcium replacement or IV calcium gluconate
- Treat the cause
170
ECG in hypocalcaemia
Longer QTc and ST segment
171
Presentation of hypokalaemia
- Hypotonia
- Hyporeflexia
- Arrhythmias (especially AF)
- Muscle paralysis and rhabdomyolysis
172
Aetiology of hypokalaemia
Decreased intake of potassium
Increased excretion of potassium
- Thiazides + loop diuretics
- Renal disease
- GI loss
- Increased aldosterone (Conn's syndrome)
Potassium shifted to intracellular
- Insulin
- Salbutamol
- (other drugs)
173
Treatment for hypokalaemia
- K+ replacement
- Aldosterone antagonist (spironolactone)
- Treat underlying cause
- Other electrolyte defficiencies
174
Diagnosis of hypokalaemia
- Low K+ in U+E
ECG:
- Small inverted T waves
- Prominent U waves
- ST depression
- PR prolongation
175
Effect of hypokalaemia on types of muscle
- Smooth muscle constipation
- Skeletal muscle weakness and cramps
- Cardiac arrythmias and palpitations
176
Effect of hypokalaemia on insulin, pH and beta 2 receptors
- Excess insulin as too much K+ flows into cell
- Alkalosis (H+ out and K+ in)
- B2 agonist - Increase B2 pumping of K+ into cell
177
Aetiology of hyperaldosteronism
2/3 - Adrenal adenoma (Conn's)
1/3 - Bilateral adrenal hyperplasia
Also (rare):
- Familial hyperaldosteronism type 1 and 2
- Adrenal carcinoma
178
Secondary hyperaldosteronism
Excessive renin stimulates the adrenal glands to produce more aldosterone
Causes:
- Renovascular disease
- Renin-secreting tumour
179
Pathophysiology of hyperaldosteronism
- Excess aldosterone(😱)
- Increased sodium and water reabsorption and potassium excretion in kidneys
- Hypertension and hypokalaemia
180
Symptoms of hyperaldosteronism
- Resistant hypertension (unfixable with ACE inhibitors or beta blockers)
- Hypokalaemia (lethargy mood disturbance, parasthesia, muscle cramps)
- Polydipsia + polyuria
181
Diagnosis of hyperaldosteronism
1st line: Aldosterone:renin ratio
High ratio = Primary (do CT)
Low rato = Secondary
Diagnostic: High serum aldosterone not suppressed with 0.9% IV saline or fludrocortisone
Also: Hypokalaemic on U+E and ECG
182
Treatment of hyperaldosteronism
- Single benign adrenal tumour -> unilateral adrenalectomy
- Bilateral adrenal hyperplasia -> Aldosterone antagonist (spironolactone)
183
How to determine if hyperaldosteronism is unilateral or bilateral
Adrenal venous sampling
- Measures the amount of corticosteroid secreted from each adrenal gland
184
Primary hyperparathyroidism
- Usually caused by a parathyroid adenoma
- Causes hypercalcaemia
185
Secondary hyperparathyroidism
- Caused by parathyroid hyperplasia
- Secondary to CKD + Vit D deficiency
186
Tertiary hyperparathyroidism
- After many years of secondary
- Most common cause is CKD
- Glands act autonomously and release PTH regardless of Ca conc.
187
Malignant causes of hyperparathyroidism
- Neoplasms
- (Squamous cell lung cancer, breast, renal)
- Secrete PTHrP, ectopically mimics PTH
188
Diagnosis of primary hyperparathyroidism
- High PTH
- Very high calcium
- Low phosphate
- High ALP- due to high bone turn over.
189
Diagnosis of secondary hyperparathyroidism
- High PTH
- Low Calcium- Secondary hyperparathyroidism is when the glands are fine but a condition, like kidney failure, lowers calcium levels and causes the body to react by producing extra parathyroid hormone.
- High phosphate - In kidney disease, your blood phosphate level can be high because your kidneys cannot remove phosphate in your urine.
- High ALP
190
Diagnosis of tertiary hyperparathyroidism
- High PTH
- High Calcium
- High phosphate
- High ALP
191
Other tests for hyperparathyroidism
- Xr KUB for kidney stones
- DEXA scan for bone density
- U+E to assess renal function
- Short QT on ECG
192
Treatment for hyperparathyroidism
- Primary: Removal of PTH adenoma/parathyroidectomy of all 4 glands :( (most definitive)
- Secondary and tertiary: Treat cause
- Tertiary: Removal of parathyroid glands
- Malignant: Remove tumour!
193
Complication of hyperparathyroidism
- Acute severe hypercalcaemia
- Give IV fluids + bisphosphonates
194
Diagnosis of pseudohyperparathyroidism
- High PTH
- Low calcium
- High phosphate
195
What does hypercalcaemia of malignancy do to PTH and phosphate levels?
- PTH levels decrease
- Phosphate levels stay the same
196
Epidemiology and risk factors of hyperparathyroidism
- Female
- Radiation therapy to neck
- Severe Vit D or Calcium deficiences
- Familial rare conditions: MEN1 and 2A
197
Primary vs secondary hypoparathyroidism
Primary: PTH gland failure, a number of causes
Secondary: After surgery (parathyroid/thyroid ectomy)
198
Causes of primary hypoparathyroidism
- Di George syndrome
- Genetic
- Radiation
- Autoimmune
- Infiltration
- Magnesium deficiency
199
Pseudohypoparathyroidism pathophysiology and what it's associated with?
- Very rare
- End-organ PTH resistance due to defect in G protein signalling
Associated with:
- Low IQ
- Short stature
- Small 4th/5th metacarpals
- Obesity
200
What is the Chvostek sign?
Twitching of facial muscles when facial nerve is trapped over parotid
201
What is the Trousseau sign?
Carpopedal spasm when tourniquet is applied to forearm
202
Diagnosis of hypoparathyroidism
- Low PTH
- Low Calcium
- High phosphate
- ECG = longer QTc
203
Treatment for hypoparathyroidism
Calcium and Vitamin D suppements (AdCalD3)
204
Diagnosis of pseudohypoparathyroidism
- High PTH
- Low Calcium
- High Phosphate
Pseudopseudohypoparathyroidism also exists, but levels for everything are normal
205
What is a phaeochromocytoma?
An adrenal medullar tumour of chromaffin cells that secrete catecholamines (NAd, Ad)
206
Aetiology of phaeochromocytomas
- 25% familial and associated with MEN 2a+2b
- Neurofibromatosis 1 (tumours deposited along myelin sheath)
- Von-Hippel Lindau disease
207
Tumour patterns in phaeochromocytomas
- 10% bilateral
- 10% cancerous
- 10% familial
- 10% extra-adrenal (mc location: organ of Zuckerkandl at aortic bifurcation)
208
Signs of phaeochromocytomas
- Hypertension (90%)
- Hypertensive retinopathy
- Tachycardia
209
Symptoms of phaeochromocytomas
- Episodic headache
- Profuse sweating
- Palpitations
- Anxiety
210
Diagnosis of phaeochromocytoma
- 24 hour urine metanephrine collection
- Plasma free metanephrines
- CT abdomen and pelvis
211
Why are metanephrines measured to diagnose pheochromocytoma?
- Adrenaline has a very short half life in blood (only a few minutes)
- Metanephrines are a breakdown product of adrenaline and have a longer half life
212
Treatment of phaeochromocytoma
Peri-operative
- Alpha blocker first (eg: phenoxybenzamine)
- Then beta blocker (eg: atenolol, propanolol)
- This prevents reactive vascoconstriction
Surgical
- Laproscopic adrenalectomy
213
Pheochromocytoma hypertensive crisis
- BP higher than 180/120
- Causes: XR contrast, TCA, opiates
- First line treatment: phentolamine (alpha blocker)
214
Acromegaly in children
- Called gigantism
- Occurs before epiphyseal fusion
- Hypopituitarism causes inhibition of puberty as gonadotrophs cannot be released
215
Aetiology of acromegaly
Functional pituitary adenoma
216
Pathophysiology of acromegaly
- Excess GHRH
- GHRH -> GH -> High IGF-1 (produced by liver)
217
Signs of acromegaly caused by space occupying lesion
- Bitemporal hemianopia
- Headaches
218
Signs of acromegaly to do with overgrowth of tissues
- Prominent forhead and brow
- Large nose, tongue, hands and feet
- Large, protruding jaw
- Arthritis
219
Signs of acromegaly to do with GH causing organ dysfunction
- Hypertrophic heart
- Hypertension
- Impaired glucose tolerance
- Colorectal cancer
220
Other symptoms suggesting active raised growth hormone
- Development of new skin tags
- Profuse sweating
221
Diagnosis of acromegaly
- 1st line: IGF-1 serum levels (high)
- Gold standard: OGTT: Oral glucose tolerance test (failure of GH suppression 2 hours post 75g glucose load)
222
First line treatment for acromegaly
Transsphenoidal resection of pituitary adenoma
223
Other treatments for acromegaly
- Somatostatin analogue to block GH (eg: ocreotide)
- Dopamine agonist (eg: bromocriptine)
- GH antagonist (eg: pegvisomant)
- Radiotherapy
224
Complications of acromegaly
- T2DM caused by impaired glucose tolerance
- Obstructive sleep apnoea
- Cardiomyopathy
- Hypertension
- Arthropathy
- Carpal tunnel syndrome
225
Why can acromegaly cause sleep apnoea?
Pressure around the neck due to enlargement
226
Peak ages craniopharyngiomas occur
- 5 to 14 years
- 50 to 74 years
227
Pathophysiology of craniopharyngioma
- Squamous epithelial remnants of Rathke's pouch
- Benign, slow growing tumour infiltrates to surrounding structures
- Mixed solid and cystic parts
- Doesn't spread to other parts of the body but puts pressure on suprasellar region of skull
228
Adamantinous vs squamous papillary craniopharyngioma
Adamantinous: Cyst formation and calcification
Squamous papillary: Well circumscribed
229
Presentation of craniopharyngioma
- Raised ICP
- Visual disturbances (bitemporal hemianopia)
- Growth failure
- Pit. hormone deficiency
- Weight increase
230
Pathophysiology of Cushing's syndrome
Chronic excess of cortisol released by the adrenal glands
231
Aetiology of Cushing's syndrome
ACTH dependent causes
- Cushing's disease
- Ectopic ACTH production
- ACTH treatment
ACTH independent causes
- Iatrogenic (steroid use) - mc
- Adrenal adenoma
232
What is Cushing's disease?
Pituitary adenoma secreting excess ACTH
233
Signs of Cushing's syndrome
- Hypertension
- Moon face
- Central obesity
- Abdominal striae
- Buffalo hump (fat pad on upper back)
- Proximal limb muscle wasting
- Ecchymoses and fragile skin
234
Symptoms of Cushing's syndrome
- Bloating and weight gain
- Mood change
- Increased susceptibility to infection
- Menstrual irregularity
- Reduced libido
- Hyperglycaemia
235
Pseudo-Cushing's
- Cushingoid features and abnormal cortisol levels, but not associated with HPA pathology
- Common causes: alcohol excess, severe depression, obesity, pregnancy
- Results in a false positive dexamethasone suppression test and 24hr free cortisol
- Differentiated using an insulin stress test
236
Diagnosis of Cushing's syndrome
- Dexamethasone suppression test OR midnight salivary cortisol
- If positive, test plasma ACTH to see if ACTH dependent
- If independent, see if it is pituitary or ectopic GH release
237
How to do dexamethasone suppression test
- Measure cortisol at 12am, before giving dexamethasone
- Measure cortisol 8 hours later, at 8am
- Non-Cushing's -> suppression >50nmol/L
- Cushing's -> little/no suppression
238
Plasma ACTH test
- Test at 9am
- High = ACTH dependent cause -> Do high dose dexamethasone suppression test
- Low = ACTH independent cause -> CT adrenals to look for pathology
239
Treatment for Cushing's syndrome caused by Cushing's disease
Transsphenoidal resection or bilateral adrenalectomy
240
Complication of bilateral adrenalectomy
Nelson's syndrome
- Pituitary tumour will continue to enlarge with no negative feedback from adrenals
- High ACTH and skin hyperpigmentation
241
Treatment for Cushing's syndrome caused by adrenal adenoma
Tumour resection or unilateral adrenalectomy
242
Treatment for Cushing's syndrome caused by ectopic ACTH
Treatment of underlying cancer, such as surgical removal of SCLC
small cell lung cancer
243
Complications of Cushing's syndrome
- Osteoporosis
- T2DM
- Hypertension and ischaemic heart disease
244
Risk factors for hyperprolactinaemia
- Females
- High serum prolactin (released from lactotrophs in the ant. pituitary)
245
Aetiology of hyperprolactinemia
- Prolactinoma
- Drugs (ecstacy)
246
Symptoms of hyperprolactinoma
- Secondary amenorrhoea
- Galactorrhoea 🪐🌌
- Sexual dysfunction (M+F)
- Gynecomastia, low testosterone
247
Diagnosis of hyperprolactinemia
- High serum prolactin
- >1000mIU/L
- or 500-1000mIU/L on two occasions
248
Best treatment for hyperprolactinemia
- Dopamine agonists
- eg: cabergoline or bromocriptine
- Massively shrinks prolactinoma (tumour) as dopamine is an inhibitor of prolactin
249
How common are meningiomas?
Most common tumour of region after pituitary adenoma
250
Cause of meningiomas
Complication of radiotherapy
251
Complications of meningioma
- Loss of visual acuity
- Visual field defects
- Endocrine dysfunction
252
What is SIAD?
- Overdiagnosed cause of hyponatremia
- Inappropriately released ADH, dilute euvolemia
- Excess ADH = more water retention = compensatory Na+ excretion to maintain euvolemia
Syndrome of Inappropriate Antidiuretic Hormone Secretion.
253
Aetiology of SIAD
- Cancers - SCLC and others
-Infection/immunosuppression, eg: TB, pneumonia, meningitis
- Abscesses
- Drugs: SSRIs, carbamazepine, sulfonylureas
- Head trauma
254
Pathophysiology of SIAD
- High ADH independent of RAAS
- Increased vasoconstriction
- APO-II expression of collecting duct
- Lead to high BP
- Excess H2O retained means more dilute blood and more Na+ loss
255
Symptoms of hyponatremia
- Vomiting
- Headache
- Decreased GCS
- Muscle weakness
256
Symptoms of extreme hyponatremia
- Seizures
- Neurological complications
- Brainstem herniation
257
Diagnosis of SIAD
- Decrease in serum Na+ and normal serum K+
- High urine osmolality
- Skin turgor and jugular venous pressure test
258
Differential diagnosis of SIAD
Na+ depletion
- Give 0.9% saline
- Na+ depletion -> serum will normalise
- SIAD -> serum fails to normalise
259
Treatment for hyponatraemia secondary to SIAD
- Asymptomatic/mild symptoms: Fluid restrict; vaptans (vasopressin antagonist)
- Severe symptoms: 3% hypertonic saline to concentrate blood
260
Which conditions do you need to rule out before confirming SIAD?
- Hypothyroidism
- Hypervolaemia
- Adrenal insufficiency
- Diuretic use
261
Treatment of chronic cases of SIAD
- Furosemide
- Vasopressin antagonist (tolvaptan)
- Demeclocycline (inhibits ADH)
262
Cancers that can cause SIAD
- SCLC (small cell carcinoma)
- Prostate cancer
- Pancreatic cancer
- Lymphomas
- Cancer of the thymus
263
Normal water sodium distribution vs SIADH
equal na+ and h20 = normal
siadh= lots of h20 not much na+
euvolemia with hyponatremia
264
How can hyponatremia cause brain stem herniation?
- Low Na+ means high compensatory H2O
- Enters skull, high ICP
- Causes hyponatremic encephalopathy
- Risk of brainstem herniating through foramen magnum (tentorial herniation)
265
Signs of thyroid storm
- Hyperpyrexia, often >40°C
- Tachycardia, often >140bpm, with or without atrial fib
- Reduced GCS
266
Diagnosis of thyroid storm
- TFTs: High T3 and T4, suppressed TSH
- ECG
- Blood glucose (perform in all patients with reduced consciousness)
267
Treatment of thyroid storm
High dose propylthiouracil and KI
268
What is thyroid storm/thyrotoxic crisis?
- Endocrine emergency often seen in patients with Graves’ disease or toxic multinodular goitre
- Secondary to precipitating factor such as infection or trauma
- 10-20% mortality
269
Treatment for DeQuervain’s thyroiditis
- NSAIDs for pain and inflammation
- Beta blockers for symptomatic relief
270
Difference between primary and secondary hyperthyroidism?
- Primary: Pathology is in the thyroid
- Secondary: Pathology is in the hypothalamus/pituitary
271
TFTs for hyperthyroidism
- Low TSH, high T4 = primary hyperthyroidism (Graves')
- High TSH, high T4 = secondary hyperthyroidism OR thyroid hormone resistance
272
Graves' specific hyperthyroid signs
- Exophithalmos or ephthalmoplegia - eye issues
- Pretibial myxedema due to deposits of mucin under the skin (may also be seen in Hashimoto’s)- scaly skin, leg swelling
- Thyroid acropachy
273
Epidemiology and risk factors of hyperthyroidism
- Middle aged women
- Family history
- Autoimmune diseases
274
Pathophysiology of Graves' disease
- Immune system produces TSH receptor antibodies that mimic TSH and stimulate the TSH receptors on the thyroid
- Increased T3 increases metabolic rate, CO, bone resorption and activates the sympathetic nervous system
275
Symptoms of hyperthyroidism
- Heat intolerance and sweating
- Weight loss
- Palpitations
- Oligomenorrhoea
276
What is toxic multinodular goitre? (also known as Plummer's disease)
Nodules develop on the thyroid gland and produce excessive thyroid hormone
277
Symptoms of thyroid storm
- NDV
- Abdo pain
- Jaundice
- Confusion, delirium or coma
278
Diagnosis of hyperthyroidism
First line: TFT (thyroid function test)
- Anti-TSH receptor antibodies positive in Graves'
- Anti TPO antibodies in 80% of cases (but much more in hypo)
- Thyroid ultrasound
279
First line treatment for hyperthyroidism
- Carbimazole
- Blocks synthesis of T4
- Normal thyroid function after 4-8 weeks (euthyroidism)
- SE: agranulocytosis, presents as sore throat/mouth ulcers
- + beta blocker (eg: propanolol) alongside for rapid symptom relief
280
Second line treatment for hyperthyroidism
- Propylthiouracil
- Prevents T4->T3 conversion
- Small risk of severe hepatic reaction, including death
281
Radioactive iodine treatment for hyperthyroidism
- First line definitive treatment for Grave’s disease and toxic multinodulae goitre
- Destroys excess thyroid tissue
- Remission can take 6 months
- Patient must not be pregnant or planning to get pregnant within 6 months, must also avoid close contact with children and pregnant women for 3 weeks
- Also limit contact with anyone for several days after receiving the dose
282
Last resort treatment for hyperthyroidism
Surgery or radioactive iodine
283
How to stop patients from becoming hypothyroid after hyperthyroidism treatment
Give them levothyroxine
284
Who would you not want to give carbimazole to?
Women wanting to get pregnant as it’s teratogenic (causes fetal abnormalities)
285
What to do after euthyroidism is achieved in hyperthyroid treatment
Maintenance carbimazole using either:
- Titration block regimen
- Block and replace regimen
Complete remission achieved after 18 months of treatment (remission rate 50%)
286
Risk factors of hyperthyroidism
- Smoking
- Stress
- HLA-DR3
- Female 20-40 years
- Other autoimmune diseases
287
General signs of hyperthyroidism
- Postural tremor
- Palmar erythema
- Hyperreflexia
- Goitre
- Lid lag and retraction
288
Most common cause of hypothyroidism in the developed world
- Hashimoto's thyroiditis
- Autoimmune inflammation of the thyroid gland - initially cause a goitre
- Associated with anti-TPO antibodies and antithyroglobulin antibodies
289
Most common cause of hypothyroidism in the developing world
Iodine deficiency
290
What is postpartum thyroiditis
- Same mechanism as Hashimoto's
- Acute: presents during pregnancy
- Resolves by itself within 1 year of symptoms
291
Other causes of hypothyroidism
- DeQuervain’s thyroiditis
- Post-thyroidectomy or post-radioiodine
- Drugs; amiodarone, lithium, carbimazole
292
Causes of secondary hypothyroidism (pathology at pituitary gland)
- Compression from a pituitary tumour
- Sheehan syndrome
- Drug: cocaine, steroids, dopamime (all inhibit TSH secretion)
293
Symptoms of hypothyroidism
- Cold intolerance
- Constipation
- Weight gain
- Lethargy
- Menorrhagia
294
Signs of hypothyroidism
- Hair loss, dry and cold skin
- Bradycardia
- Goitre
- Decreased deep tendon reflexes
- Carpal tunnel syndrome
295
Diagnosis of hypothyroidism
- TFT (thyroid function test)
- Anti-TPO antibodies high
- Tyically anaemic (any type)
296
TFTs for hypothyroidism
- High TSH, low T4 = primary hypothyroid
- Low TSH, low T4 = secondary hypothyroid
- Normal/low TSH, Low T4 = hypopituitarism
297
Treatment for hypothyroidism
- Levothyroxine (T4)
- Titrate dose so you don't induce iatrogenic hyperthyroidism
298
Complication of hypothyroidism
Myxedema coma
- Often infection precipitated
- Rapidly drops T4
- Loss of consciousness, heart failure
299
Treatment for myxedema coma
- Levothyroxine
- Antibodies
- Hydrocortisone
300
Epidemiology of hypothyroidism
- Mainly >40 years
- F>M 6:1
301
Types of thyroid carcinoma
- Papillary - 70%
- Follicular - 25%
- Anaplastic (worst prognosisas as it metastasises the most)
- Lymphoma
- Medullary cell
302
Most common metastasis sites for thyroid carcinoma
- Lung - 50%
- Bone - 30%
- Liver - 10%
- Brain - 5%
303
How does thyroid carcinoma usually present?
- As hard and irregular thyroid nodules
- May have local compression (eg: hoarse voice)
304
Treatment for thyroid carcinoma
- Papillary and follicular = thyroidectomy or radioactive iodine
- Anaplastic = mostly palliative :(
305
Diagnosis of thyroid carcinoma
- Fine needle aspiration biopsy
- TFTs
- Thyroid ultrasound
306
De Quervain's thyroiditis
- Follows a viral prodrome and can also present with a transient thyrotoxic state
- Painful goitre with raised inflammatory markers. Usually self limiting
