Endocrinology Flashcards
1
Q
what does the anterior pituitary gland release?
A
TSH
ACTH
LH
GH
prolactin
2
Q
what does the posterior pituitary release?
A
oxytocin
ADH
3
Q
how is T3 and T4 released?
A
hypothalamus releases TRH which stimulates ant pit to release TSH which stimulates the thyroid glands to release T3 and T4, neg feedback of TRH and TSH
4
Q
when is cortisol highest and how is it released?
A
peaks in the morning
hypothalamus ->CRH-> ant pit-> ACTH->adrenal gland->cortisol
cortisol suppresses CRH and ACTH
5
Q
what are the actions of cortisol?
A
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
6
Q
how is IGF-1 released?
A
GnRH from hypothalamus -> ant pit-> GH ->liver -> IGF-1
7
Q
what are the actions of IGF 1?
A
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
8
Q
what are the actions of PTH?
A
increases no and activity of osteoclasts-> serum calcium increases
increase in calcium reabsoprtion in kidneys -> serum calcium increases
stimulates kidneys to convert vit D3-> calitriol -> calcium reabsorption from food in small intestines
9
Q
define RAAS system
A
Renin is a hormone secreted by the juxtaglomerular cells that sit in the afferent (and some in the efferent) arterioles in the kidney. They sense the blood pressure in these vessels. They secrete more renin in response to low blood pressure and secrete less renin in response to high blood pressure. Renin is an enzyme that acts to convert angiotensinogen (released by the liver) into angiotensin I. Angiotensin I converts to angiotensin II in the lungs with the help of an enzyme called angiotensin-converting enzyme (ACE).
Angiotensin II acts on blood vessels to cause vasoconstriction. This results in an increase in blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands.
Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts
When sodium is reabsorbed in the kidneys water follows it by osmosis. This leads to an increase in intravascular volume and subsequently blood pressure.
10
Q
define cushing’s syndrome and disease
A
syndrome - prolonged abnormal elevation of cortisol
disease - pituitary adenoma secretes ACTH
11
Q
what are the features of cushing’s syndrome?
A
Round “moon” face
Central Obesity
Abdominal striae
Buffalo Hump (fat pad on upper back)
Proximal limb muscle wasting
Hypertension
Cardiac hypertrophy
Hyperglycaemia (Type 2 Diabetes)
Depression
Insomnia
osteoporosis
easy bruising and poor skin healing
12
Q
what are the causes of cushing’s syndrome?
A
Exogenous steroids (in patients on long term high dose steroid medications)
Cushing’s Disease (a pituitary adenoma releasing excessive ACTH)
Adrenal Adenoma (a hormone secreting adrenal tumour)
Paraneoplastic Cushing’s - excess ACTH is released from a cancer (not of the pituitary) and stimulates excessive cortisol release, usually small cell lung cancer
13
Q
what is the first line investigation for cushing’s?
A
dexamethasone suppression test - If the low dose test is normal, Cushing’s can be excluded. If the low dose test is abnormal, then a high dose test is performed to differentiate between the underlying causes…see if dexamethasone suppresses normal morning spike of cortisol..if doesnt ->high dose, in cushing’s disease this suppresses cortisol,if adrenal adenoma - cortisol is produced independent of the pituitary so does not suppress it, however ACTH will be supressed as neg feedback on hypothalamus, if ectopic ACTH - neither cortisol or ACTH will be suppressed as independent of hypothalamus AND pituitary
14
Q
what other investigations are used for cushing’s?
A
24 hour urinary free cortisol
FBC - raised white cell, potassium low, MRI brain for pituiary adenoma, chest CT for small cell lung cancer, abdo CT for adrenal tumours
15
Q
how is cushing’s treated?
A
Trans-sphenoidal (through the nose) removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH
16
Q
define addison’s disease
A
primary adrenal insuffiency - reduces cortisol and aldosterone
most common cause - autoimmune
secondary adrenal insufficiency - inadequate ACTH stimulates adrenal gland so less cortisol due to damage to pituitary gland - due to surgery to remove a tumour, infection, loss of blood flow or radiotherapy or sheehan’s syndrome
tertiary adrenal insufficiency - inadequate CRH, usually due to long term steroids causing suppression of hypothalamus, steroids should be tapered
17
Q
what are the sx of addison’s?
A
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
18
Q
what are the signs of addisons?
A
Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension)
19
Q
which investigations are required for addisons?
A
electrolytes - hyponatraemia, hyperkalaemia
early morning cortisol levels - but sometimes falsely nromal
short synacthen test is test of choice
ACTH levels - high if primary, low if secondary,
adrenal autoantibodies - adrenal cortex antibdoies, 21-hydroxylase antibodies
CT/MRI adrenls
MRI pituitary
20
Q
how does ACTH stimulation test work?
A
short test - giving synacthen - which is synthetic ACTH, measure cortisol at baseline, 30 and 60 mins after administered, should have at least doubled…failure to do so = primary (addisons disease)
long test - primary = no cortisol response, in secondary = cortisol will rise
…nowadays simply measure ACTH
21
Q
how is addison’s disease treated?
A
replacement steroids - hydrocortisone for cortisol and fludrocortisone to replace aldosterone
pts given steroids card and emergency ID tag to alert emergency services
doses of steroids are doubled in acute illness
22
Q
define addisonian crisis
A
an acute presentation of severe Addisons, where the absence of steroid hormones leads to a life threatening presentation
23
Q
what are the sx of addisonian crisis?
A
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell
24
Q
what can trigger addisonian crisis?
A
sudden withdrawal of steroids
infection
trauma
illness
25
how is addisonian crisis managed?
Intensive monitoring if unwell
Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance
26
what are the biochemical results of hyperthyroidism?
TSH low, except if pituitary adenoma which TSH will be high,high T3 and T4
27
what are the biochemical results of primary hypothyroidism?
high TSH, low T3 and T4
28
what are the biochemical results of secondary hypothyroidism?
low TSH, low T3, T4 - pituitary or hypothalamic cause
29
what are the antibodies involved in thyroid diseases?
anti-TPO antibodies - grave's and hashimoto thyroiditis
antithyroglobulin antibodies - grave's, hashimotos thyroditis, and thyroid cancer
TSH receptor antibodies - autoantibodes that mimic TSH - grave's disease
30
which imaging is used in thyroid disease?
thyroid USS - thyroid nodules - cystic and solid nodules
radioisotope scans - The more gamma rays that are emitted from an area the more radioactive iodine has been taken up. Diffuse high uptake is found in Grave’s Disease, Focal high uptake is found in toxic multinodular goitre and adenomas, “Cold” areas (i.e. abnormally low uptake) can indicate thyroid cancer-
31
define grave's disease
autoimmune conditions ...primary hyperthyroidism. TSH receptor antibodies are abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid.
32
define plummer's disease
toxic multinodular goitre...nodules develop on thyroid gland and continuously produce excessive thyroid hormones
33
what are the sx of grave's disease and their cause?
exopthalmos - inflammation and hypertrophy of tissues behind eyeball
pretibial mxoedema - deposits of mucin under skin in pre tibial area
diffuse goitre
geave's eye disease
34
what are the causes of hyperthyroidism?
Grave’s disease
Toxic multinodular goitre
Solitary toxic thyroid nodule
Thyroiditis (e.g. De Quervain’s, Hashimoto’s, postpartum and drug-induced thyroiditis)
35
what are the universal features of hyperthyroidism?
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
36
what are the unique features of plummer's disease?
Goitre with firm nodules
Most patients are aged over 50
Second most common cause of thyrotoxicosis (after Grave’s)
37
define solitary toxic thyroid nodules and how it is treated?
single abnormal thyroid nodules relasing thyroid hormone
usually benign adenomas
surgical removal of nodule
38
define de quervain't thyroiditis, how it presents and how it is treated?
viral infection with fever, neck pain and tenderness, dysphagia and fx of hyperthyroidism
There is a hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback. It is a self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief
39
define thyroid storm
rare presentation of hyperthyroidism - thyrotoxic crisis
severe - pyrexic, tachycardic, delirium
admission for monitor
fluid resus, anti arrhytmic meds, beta blockers
40
how is hyperthyroid managed?
carbimazole - first line
propylthiouracil - second line (hepatic reactions, death)
radiactive iodine destroys thyroid cells (must no be preg or be in contact with children or preg women)
beta blockers - block adrenaline related sx
surgery - remove whole thyroid or toxic nodules, require levothyroxine replacement for life
41
what are the causes of hypothyroidism?
hashmito's thyroiditis = anti-TPO antibodies and antithyroglobulin antibodies...goitre then atrophy of thyroid gland
iodine deficiency
secondary to tx of hyperthyroidism - carbimazole etc
medications - lithium inhibits production of thyroid hormones as well as amiodarone
hypopituitarism - caused by tumours, infection, vascular causes or radiation
42
how does hypothyroisim present?
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Heavy or irregular periods
Constipation
43
which investigations are required to diagnose hypothyroidism?
TSH, T3, T4 levels - see previous flashcard
44
how is hypothyroidism managed?
Replacement of thyroid hormone with oral levothyroxine - synthetic T4, and metabolises to T3 in the body. have to measure TSH leevls months until stable
if too high - dose is too low , if tsh low, dose is too high
45
define ketogenesis
insufficient glucose supply and glycogen - fatty acids are converted to ketones which can cross BBB
can be measured in urine dipstick and in blood using ketone meter
acetone breath
if diabetic - can not buffer the acidity...DKA which is lifethreatening
46
define the pathophysiology of type 1 DM
pancreas stops producing insulin
genetic or triggered by virus such as enterovirus
47
when does DKA occur/
not enough insulin to process glucose
48
what occurs as a result of DKA?
acidosis of blood due to ketogenesis
dehydration - due to osmotic diuresis caused by hyperglycaemia...polyuria and polydipsia
potassium imbalance - without insulin, potassium is not added to and stored in cells, so hypokalaemia...arrhythmias
49
how does DKA present?
life threatening!
Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered Consciousness
They may have symptoms of an underlying trigger (i.e. sepsis)
50
how is DKA diagnosed?
Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)
51
how is DKA treated?
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)
52
how is type 1 DM managed long term?
education
monitor
subcut insulin regimes - background, long acting insulin given once a day and a short acting insulin injected 30 minutes before intake of carbohydrate
monitor carb intake
monitor blood sugar
monitor for and manage complications
cycle their injection sites - lipodystrophy stops absorption
53
what are the short term complications of incorrect insulin management?
hypoglycaemia - tremor, sweat, irritable, dizzy, pallor, reduced consciousness, coma and death
....treated with rapid acting glucose and slower acting carbs such as biscuits for when rapid acting glucose is used by, if severe - IV dextrose and IM glucagon
hyperglycaemia - insulin is required
54
what are the long term complications of chronic exposure to hyperglycaemia?
Macrovascular Complications-
Coronary artery disease
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension
Microvascular Complications-
Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis
Infection Related Complications-
Urinary Tract Infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis
55
how is DM monitored?
HbA1c - glycated Hb, measured every 3-6 months as red cells last 3-4 months
capillary blood glucose
flash glucose monitoring - sensor on skin that measures glucose level of interstitial fluid
56
what is the pathophysiology of type 2 DM?
Repeated exposure to glucose and insulin makes the cells in the body become resistant to the effects of insulin. It therefore requires more and more insulin to produce a response from the cells and get them to take up and use glucose. Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less
57
what are the risk factors for type DM?
Non-Modifiable-
Older age
Ethnicity (Black, Chinese, South Asian)
Family history
Modifiable-
Obesity
Sedentary lifestyles
High carbohydrate (particularly refined carbohydrate) diet
58
how does type 2 DM present?
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine
59
how is type 2 DM diagnosed?
oral glucose tolerance test - baseline fasting plasma glucose then giving a glucose drink and measure 2 hours later
HbA1c
60
how is prediabetes diagnosed?
pre diabetes
HbA1c – 42-47 mmol/mol
Impaired fasting glucose – fasting glucose 6.1 – 6.9 mmol/l
Impaired glucose tolerance – plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT
61
what is the criteria for diabetes to be diagnosed?
HbA1c > 48 mmol/mol
Random Glucose > 11 mmol/l
Fasting Glucose > 7 mmol/l
OGTT 2 hour result > 11 mmol/l
62
how is type 2 DM managed?
dietary = veg and oily fish, low glycaemic and high fibre diet, low carb diet
optimise risk fx = exercise and weight loss, stop smoking, tx for hypertension, hyperlipidaemia, CVD
monitor for complications = retinopathy, kidney disease, diabetic foot
63
what are the treatment targets for type 2 DM?
48 mmol/mol for new type 2 diabetics
53 mmol/mol for diabetics that have moved beyond metformin alone
64
what is the 1st line medical management of type 2 DM?
metformin
65
what are the 2nd and 3rd line medical management of type 2 DM?
second line - sulfonylureas, piglitazone, DPP-4 inhibitors, SGLT-2 inhibitors
third line - triple therapy with metformin and two of second line, or metformin plus insulin
66
what are the guidelines for tx of type 2 DM with CVD?
SGLT-2 inhibitors and GLP-1 mimetics
67
metformin
biguanide - increases insulin sensitivity and decreases production of glucose
weight neutral
sx - diarrhoea and abdo pain, lactic acidosis
68
pioglitazone
increases insulin sensitivity and decreases production of glucose
sx - weight gain, fluid retenion, anaemia, HF, increased risk of bladder cancer
69
sulfonylurea
gliclazide - stimulates insulin release
sx - weight gain, hypoglycaemia, increased risk of CVD, MI
70
DPP-4 inhibitors
sitagliptin - inhibits DPP4 enzyme and increases GLP1 activity
sx - GI upset, URTI, pancreatitis
71
GLP-1 mimetics
exenatide - inhibit glucagon production, increased insulin, slow absorption by GI tract
sx - GI upset, weight loss, dizzy, low risk of hypoglycaemia
72
SGLT-2 inhibitors
canagliflozin/dapagliflozin - causes glucose to be excreted in urine
- also reduces risk of CVD, HF and death
sx - glucoseuria, increased no of UTI, weight loss, DKA, lower limb amputation
73
insulin
rapid acting - novorapid, humalog, apidra
short acting - actrapid, humulin S, insuman rapid
intermediate acting - insulatard, humulin I, insuman basal
long acting - lantus, levemir, degludec
combination - humalog 20, 50, novomix 30
74
define acromegaly
excessive growth hormone by anterior pituitary...usually caused by pituitary adenoma or from cancer such as lung or pancreatic which secretes ectopic GHRH or growth hormone
75
define bitemporal hemianopia
pituitary adenoma can press on optic chiasm..loss of vision on outer half of both eyes
76
how does acromegaly present?
space occuping lesion - headaches, bitemporal hemianopia
overgrowth of tissues - prominent forehead and brow, large nose, tongue, hands and feet, protruding jaw, arthritis
organ dysfunction - hypertrophic heart, hypertension, type 2 DM, colorectal cancer
new skin tags
profuse sweating
77
which investigations are required for acromegaly?
IGF-1 - initial test to see if raised
oral glucose tolerance test - growth hormone, high glucose should suppresses growth hormone
MRI brain - pituitary adenoma
refer for opthalmology for visual field tests
78
how is acromegaly treated?
trans-phenoidal surgical removal of pituitary tumour = if pituitary adenoma
GH antagonist - pegvisomant, somatstatin analogue - ocreotide, dopamine agonist - bromocriptine
79
what are the sx of hypercalcaemia?
Renal stones
Painful bones
Abdominal groans refers to symptoms of constipation, nausea and vomiting
Psychiatric moans refers to symptoms of fatigue, depression and psychosis
80
how is primary hyperparathyroidism treated?
hypercalcaemia - so surgically removes the tumour
81
what is the cause of secondary hyperparathyroidism and how is it treated?
insufficient vit D or chronic renal failure - low absoprtion of calcium, so PTH released, so calcium is low/normal but Pth is high
treated by correcting with vit D deficiency and renal transplant if renal failure
82
what is teritiary hyperparathyoidism caused by and how is it treated?
when secondary continues for a long period of time...so pth increases from hyperplasia, and remains high when secondary hyperparathyroidism is treated...so hypercalcaemia
treated surgically removing pth tissue
83
RAAS
In the afferent arteriole in the kidney there are special cells called juxtaglomerular cells. They sense the blood pressure in these vessels. When they sense a low blood pressure in the arteriole they secrete a hormone called renin. This liver secretes a protein called angiotensinogen. Renin acts to convert angiotensinogen to angiotensin I. Angiotensin I converts to angiotensin II in the lungs with the help of angiotensin converting enzyme (ACE). Angiotensin II stimulates the release of aldosterone from the adrenal glands.
84
define primary hyperaldosteronism and the causes
when adrenal gland produce too much aldosterone
serum renin will be low as it suppressed by high BP
- bilateral adrenal hyperplasia, adrenal adenoma secreting aldosterone (conn's syndrome), familial hyperaldosteronism type 1 and 2, adrenal carcinoma
85
define secondary hyperaldosteronism
excess renin stimulates adrenal gland to produce more aldosterone, renin will remain high
- renal artery stenosis, renal artery obstruction, heart failure
86
what is the main cause of renal artery stenosis and how is it diagnosed?
atherosclerosis
doppler USS, CT angiogram, MRA
87
which investigations are required for hyperaldosteronism?
renin/aldosterone ratio - whether primary or secondary
BP - hypertension, serum electrolytes - hypokalaemia, blood gas - alkalosis
if high aldosterone, require CT/MRI or renal dopplerCT angiogram
88
how is hyperaldosteronism managed?
aldosterone antagonist- eplerenone, spironolactone
treat underyling cause - surgical removal of adenoma, percutaneous renal artery angioplasty
89
what is the most likely cause of secondary hypertension?
hyperaldosteronism - bp wont respond to treatment
check renin:aldosterone ratio
(may also have low potassium)
90
define euvolaemic hyponatraemia
excessive water reabsorption is not usually significant enough to cause a fluid overload from SIADH
91
what are the sx of SIADH?
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
92
what are the possible causes of SIADH?
Post-operative from major surgery
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis
93
define SIADH
Anti-diuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”. ADH stimulates water reabsorption from the collecting ducts in the kidneys. SIADH is a condition where there is inappropriately large amounts of ADH.
94
which investigations are required to diagnose SIADH?
clinical exam - euvolaemia
U+E - hyponatraemia
urine sodium and osmolality high
other causes to be excluded - short synacthen test to exclude adrenal insufficiency, no diuretic use, no diarrhoea/vomit/burns/sweat, no excessive water intake, no CKD/AKI
a new medication, a chest infection or recent major surgery. This can be confirmed by treating the underlying cause and assessing whether the hyponatraemia resolves
chest x ray - pneumonia, lung abscess, lung cancer
suspect malignancy with persistent hyponatraemia, hx of smoking, weight loss etc
95
how is SIADH managed?
stop causative medications
correct sodium slowly to prevent central pontine myelinolysis
fluid restriction - 500mls to 1l
tolvaptan - adh receptor blocker
demeclocycline - tetracycline abx which inhibits ADH
close monitoring of sodium
96
define central pontine myelinolysis
or osmotic demyelination syndrome
a complication of long term severe hyponatramia being treated too quickly
if the hyponatraemia has been present and severe for a long time the brain cells will also have a low osmolality. This is not a problem until the blood sodium levels rapidly rise. When this happens water will rapidly shift out of the brain cells and into the blood:
- 1st phase = electrolyte imbalance - encephalopathic and confused, headache, N+V
- 2nd phase = demyelination of neurones - spastic quadriparesis, pseudobulbar palsy, CBT, risk of death
....must prevent, some neurological deficit, supportive tx
97
define diabetes insipidus
lack of ADH or lack of response to ADH...sp kidneys can not concentrate the urine..polyuria and polydipsia
either nephrogenic or cranial
different to primary polydipsia has ADH is normal but drinking excess water
98
define nephrogenic diabetic insipidus
when collecting ducts of kidneys do not respond to ADH
caused by drugs (lithium used in bipolar), mutations in AVPR2 gene on X chromosome, intrinsic kidney disease, hypokalaemia and hypercalcaemia
99
define cranial diabetes insipidus
when hypothalamus does not respond to ADH
can be idiopathic or caused by brain tumours, head injury, brain malformations and infection, brain surgery or radiotherapy
100
how does diabetes insipidus present?
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatraemia
101
which investigations are requires for diabetes insipidus?
low urine osmolality
high serum osmolality
water deprivation test - no fluid for 8 hours then urine osmolality measured and synthetic ADH...in cranial - urine osmolality remains low , when ADH is given, kidneys response and urine osmolality will be high. in nephrogenic - urine osmolality will remain low even with ADH as can not respond to it. in primary polydipsia will remain high even before ADH is given
102
how is diabetes insipidus managed?
treat underlying cause
conservative management
desmopressin - cranial and nephrogenic (neph has to be in higher doses)
103
define phaeochromocytoma
tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline...this stimulates the SNS
25% are familial and associated with multiple endocrine neoplasia type 2
10% bilateral, 10% cancerous, 10% outside of adrenal gland
104
how is phaeochromacytoma diagnosed?
24 hr urine catecholamines - how much adrenaline is being secreted by tumour over 24 hr period
plasma free metanephrines - longer half life, less prone to fluctuations and more reliable
105
how does phaechromacytoma present
sx fluctuate -
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation
106
how is phaeochromacytoma managed?
alpha blockers - phenoxybenzamine
beta blockers
adrenalectomy
107
kallmans syndrome
allman's syndrome is an X-linked recessive condition, causing failure of GnRH (gonadotropin-releasing hormone) secreting neurons migrating to the hypothalamus. This results in hypogonadotropic hypogonadism. It presents with delayed puberty and anosmia in a male, who are often average/ above average height.
108
hyperparathyroid tx
The definitive treatment for primary hyperparathyroidism is a total parathyroidectomy however conservative management may be used if specific severity markers are absent or if the patient is not fit for surgery (as in this patient). For these cases the medication cinacalcet maybe use
109
diabetic neuropathy manageemtn
first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as 'rescue therapy' for exacerbations of neuropathic pain
110
type 1 v type 2 DM results
In type 1 diabetes, we would expect a low or undetectable level of plasma C-peptide due to absolute insulin deficiency. The elevated levels here point towards type 2 diabetes.
111
adrenal venous sampling
Adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia in primary hyperaldosteronism
112
Klinefelters
Klinefelter's syndrome causes high LH and low testosterone
above average height and infertility
113
Sick euthryoid
Sick euthyroid is common in unwell, elderly patients and often needs no treatment
114
Toxic multi nodular goitre
Radioactive iodine therapy is the correct answer. The patient in the vignette has features of hyperthyroidism (flushing, weight loss, palpitations). The rough lump in her neck and the patchy uptake seen on nuclear scintigraphy point to a toxic multi-nodular goitre (TMN) diagnosis, for which radioiodine therapy is the appropriate treatment. Radioiodine is taken up by and ablates any autonomous nodules, leaving healthy tissue intact.
115
Cause of cranial diabetes insipidus
Recent transsphenoidal is a well-documented cause for cranial diabetes insipidus and would be most relevant given the water deprivation findings above.
116
Primary polydipsia
Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high
117
Falsely high hba1c
Splenectomy can give a falsely high HbA1c level due to the increased lifespan of RBCs
118
Mxodermic coma
Myxoedemic coma is treated with thyroxine and hydrocortisone
119
causes of hypothyroidism apart from hashimotos
Subacute thyroiditis (de Quervain's)
associated with a painful goitre and raised ESR
Riedel thyroiditis
fibrous tissue replacing the normal thyroid parenchyma
causes a painless goitre
Postpartum thyroiditis
Drugs
lithium
amiodarone
Iodine deficiency
120
causes of hyperthyroidism apart from graves
Toxic multinodular goitre
autonomously functioning thyroid nodules that secrete excess thyroid hormones
Drugs
amiodarone
121
what conditions both have low TSH and T3 and T4?
sick euthyroid and secondary hypothyroidism
122
subclinical hypothyroidism v poor compliance with thyroxine
subclinical hypo - normal T3/4 but high TSH
poor compliance - norma but high TSH
123
what is the first line investigation for thyroid nodules?
ultrasonography
124
what are the associations of hashimotos?
other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto's thyroiditis is associated with the development of MALT lymphoma
125
how does hashimotos present?
firm, non tender goitre
126
diabetic retinopathy
non-proliferative diabetic retinopathy (NPDR) - blot hamaeorrhages, cotton wool spot vs proliferative retinopathy (PDR) - vascularisation and maculopathy
127
hypocalcaemia sign
Trousseau's sign: carpal spasm on inflation of BP cuff to pressure above systolic
Trousseau's sign = hypocalcaemia, often occurs after 2 minutes of cuff inflation above systolic pressure
128
PCOS
High oestrogen - not pulsatile - ineffective ovaries
So Amenorrhoea or irregular
Endometrial protection rather than bone protection required
129
AIS
Male with female features as gonads not respond
130
Turner’s syndrome
Female, visual changes (but not more androgenous) - neck changes
Lack of oestrogen to cause Amenorrhoea
131
Ovarian v pituitary cause
Ovarian - high FSH, LH and low oestrogen
Pituitary - low FSH, LH and low oestrogen
132
Primary ovarian failure
Autoimmune
Mostly idiopathic
Turner’s (requires karyotyping)
133
If low oestrogen all life v if sudden drop
If low all life - not get sx such as hot flushes but still given oestogej for bone and CVS health
If sudden change(ie menopause) - symptomatic Tx as well as bone protection, stop at 50 to decide whether to continue
134
Congenital adrenal hyperplasia
Male fx, failure to thrive
High androgens, low cortisol and aldosterone
135
If not had withdrawl bleed with pill
Anatomical abnormalities ie absent uterus
136
Goitre v nodule
Goitre - more general term but can define mutlunodular
Nodule
137
Hyperthyroidism tx outline
Carbimazole 12-18 months, regular monitoring of dose changes required
If nodule - radioactive idiome ro target or remove all together
Both results in hypothyroidism - so requires levothyroixine but can be on this lifelong
138
When is propyluracil indicated?
In 1st trimester of pregnancy
If carbimazole nor suited
139
Measure T4 or T3?
T4 (ratio is 14:1)
140
How do you detect malignancy of the thyroid gland?
USS
Clinically not have fx of hypo or hyper, gland functionally not a problem
141
Monitor of hypo and hyper
Hypo - TSH
Hyper - T4 for dose changes as 3monthe for TSH ro adjust
142
What social fx must be asked about in relation to grave’s?
Smoking - risk of eye disease
143
How effective carbimazole?
Resolve
Or resolve and come back
Or struggled to get off drug and require definitive tx
144
Hyperparathyroidism
Primary - serum and urinary calcium high - resulting in stones
Secondary - chronic kidney disease related, calcium low or normal, vit D low - look at kidney function and vit D
FFH (familial…). - serum calcium high and urine calcium low - low risk of stones
Treat,ent - calcium binder and monitor or surgery to remove if symptomatic and able to undergo surgery
145
Post partum thyroiditis
Hyper then hypo then normalises
146
de quervain's thyroditis - uptake of iodine
De Quervain's thyroiditis: initial hyperthyroidism, painful goitre and globally reduced uptake of iodine-131
147
dapafliflozin side effects
fourniers gangrene
148
type 2 t manageemnt
1. metformin, if not tolerated - modified release metformin
2. SGLT2 inhibitor if risk of CVD, DP4 inhibitor or pioglitazone if not
149
tertiary hyperaparathyroidism
high phosphate
150
tertiary hyperparathyoidism
high phosphate
151
primary hyperparathyroidism
normal PTH
152
hyperglycaemia hyperosmolar state v DKA
Clues to the correct diagnosis of hyperglycaemic hyperosmolar state are hyperglycemia with increased serum osmolarity and no ketosis
153
maturity-onset diabetes of the young
Maturity-onset diabetes of the young (MODY) is characterised by the development of type 2 diabetes mellitus in patients < 25 years old. It is typically inherited as an autosomal dominant condition
154
dka treatment
A fixed rate intravenous insulin infusion of 0.1 units/kg/hour is recommended to treat diabetic ketoacidosis.
155
first line pharmacological tx of phaemochromacytoma
phenoxybenzamine, an alpha-receptor block
156
asx diabetic patients
Asymptomatic patients with an abnormal HbA1c or fasting glucose must be confirmed with a second abnormal reading before a diagnosis of type 2 diabetes is confirmed
157
type 2 dm - titrated up metformin what % HBA1C requiring another agent
7.5%
158
hot solidary nodule
toxic adenoma
159
pappillary thyroid cancer
Papillary thyroid cancer is the most common type of thyroid cancer and are the more common in females (M:F=1:3). Papillary tumours are more likely to develop lymphatic spread than follicular tumours.
