ENDO Flashcards
6Oyo Male pt presents with tiredeness, weight loss, polyuria, polydipsia and irritation on the tip of his penis.
What are you thinking?
T2DM
Why do you have polyuria and polydipsia in t2dm?
It results from osmotic diuresis that results from elevated blood glucose.
What is an irritation on the tip of the penis in a diabetic picture?
Candida
causing balantis in males
causing pruritus vulvae in females
It’s an opportunistic infection activated in subacute diabetic presentations.
What is diagnostic for symptomatic diabetes?
Single raised plasma glucose reading.
What is diagnostic for asymptomatic diabetes?
2 abnormal readings in fasting plasma glucose
or 2 random plasma values
PC of hypothyroidism
Tiredeness Cold intolerance Depression Constipation Weight gain
What are the main causes of hypothyroidism
Iodine deficiency
Autoimmune pathology - Hashimotos thyroiditis
Post partum thyroiditis
A 33yo obese female pt just gave birth and is feeling depressed, gained weight, has anorexia, tiredness.
What are you thinking?
And what should you not get tricked into thinking by Karim Meeran?
Think hypothyroidism
Dont think post-partum depression, its a trick.
Post partum depression should only have psychological signs including: confusion, low mood, delusional thought (think their child is evil), anhedonia, anergia. Anorexia and weight gain aren’t matching the picture.
When do you use urinary catecholamines?
In diagnosing a phaeochromocytoma
Recognise the presenting symptoms of Cushing’s syndrome
- Increasing weight “my jeans keep getting tighter”
- Fatigue
- Muscle weakness
- Myalgia
- Thin skin
- Easy bruising
- Poor wound healing
- Fractures
- Hirsuitism
- Acne
- Frontal balding
- Oligomenorrhoea/amenorrhoea
- Depression or psychosis
Whats the first investigation you do when a patient presents with cushingoid symptoms?
LOW dose dexamethasone test
give 0,5mg of dexamethasone every 6 hrs for 48 hrs
measure serum cortisol after 48hrs
CUSHINGS = RAISED cortisol (even after supression test)
Normal = lower cortisol
What’s the next step when the cortisol is raised after a low dose dexamethasone test?
HIGH dose dexamethasone test
give 8mg of dexamethasone
ACTH dependent disease aka cushings disease = LOW cortisol –> indicating pituitary adenoma or ectopic acth from lung cancer.
ACTH independent disease aka cushings syndrome = HIGH cortisol –> indicating benign adrenal carcenoma or adrenal carcinoma
49yo male pt has difficulty sleeping
reports tiredeness, weakness, weight gain, sweats very easily lately, dizzines, visual changes.
OE: coarse facial features
What are you thinking?
Classic acromegaly
Explanation:
Difficulty sleeping is due to enlargement of the soft tissues in the pharynx which collapse during sleep causing obstructive sleep apnoea. Hence the tiredness and weakness.
Weight gain - people usually report “tighter shoes” “tighter watch” in acromegaly
Add all the above + sweats = acromegaly for sure.
Visual changes happen because the most common cause of acromegaly is a pituitary tumour and it can compress the optic chiasm causing bilateral quadranopia or hemianopia in progressive disease. This is also the cause of dizziness.
What’s the most common cause of acromegaly?
Pituitary adenoma
Whats the gold standard test for acromegaly?
Oral glucose supression test
You give 75mg oral glucose and you expect GH to be supressed
Its not in pts with acromegaly.
What is a screening test for acromegaly?
serum IGF-1 is raised
A 42yo female pt presents with visual disturbance - double vision
She also reports being breathless very easily and having palpitations
OE: painless lesions on her shins
What is this
Hypothyroidism - classic
Explanation:
visual disturbances because antibodies which bind to the tsh receptor causing an increase in th can also bing to the extraoculer muscles leading to gaze abnormalities.
The same antibodies can also bind to the shins causing raised lesions known as ‘pretibial myxoedema’
What type of antibodies are bind to the TSH receptor in graves?
IgG
16yo female pt presents with swelling in her neck
She is feeling more irritable but this is transient
OE: there is diffuse swelling
There is no bruit on auscultation of the bruit
What are you thinking?
Simple idiopathic goitre
don’t get tricked into thinking hyperthyroidism or things like that because the irritability is due to her being a teenager - transient is the key word
Absence of a thyroid bruit = not hyperthyroidism
What should you suspect with a major haemodynamic collapse?
Acute adrenal failure
What is the reason for the increased pigmentation in addison’s
ACTH is derived from POMC and so is MSH (melanocyte-stimulating hormones) thats why you get pigmentation.
What do you expect with the shortsynacthen test in addisons?
Giving ACTH should normaly increase serum cortisol production.
In adrenal failure giving ACTH will not increase serum cortisol (<550nmol/L serum cortisol)
Whats the dose of the short synacthen test?
tetrocosactrin 250μg IM
What is the purpose of the long synacthen test?
To differentiate between 1’,2’ and 3’ adrenal insufficiency
What results of the long synacthen test do you expect for 1’ adrenal insufficiency?
There is no increase in cortisol after the 6th hour measurment
How does the long synacthen test work?
1 mg synthetic ACTH administered
Measure serum cortisol at 0, 30, 60, 90 and 120 minutes Then measure again at 4, 6, 8, 12 and 24 hours
What’s the mx of chronic addison’s
Hydrocortisone (to replace glucocorticoids, and increase dose during stress)
Fludrocortisone (to replace mineralocorticoids)
Wear med alert bracelet, have gc with you, have steroid warning card.
What are the complications of addisons?
HYPERkalemia
Addisonian crisis
What do you expect in u&e’s in addisonian crisi?
Low Na+
High K+
Whats the mx of addisonian crisis
RAPID iv fluid rehydration
50ml of 50% dextrose
IV hydrocortisone 200mg (and give every 6hrs until bp is stable)
What do you expect in a water deprivation test normally and what is the result for diabetes insipidus?
Normally you expect to get a rise in urine osmolarity and normal range serum osmolarity
In DI you get high serum osmolarity with no compensation in the urine part - so you get dilute urine as well.
What do you do to differentiate between cranial and nephrogenic DI?
You administer desmopressin
If the pt responds to desmopressin = cranial
if the pt doesn’t respond to desmopressin = nephrogenic
Whats the normal response to the plantar reflex?
Downwards response of toes
aka: negative babinski
aka: flexor plantar reflex
Whats an abnormal response of the plantar reflex?
Upwards response of toes and fanning
aka: positive babinski
aka: extensor plantar reflex
What does a positive babinski sign indicate?
upper motor neuron lesion cerebral palsy strokes brain injury or brain tumors spinal cord tumor or injury multiple sclerosis (MS) meningitis severe hyponytraemia *
What are some causes of SIADH?
Brain: haemorrhage, meningitis, tumour, Guillain-Barre
Lung: pneumonia, TB
Tumours: leukaemia, small cell lung cancer, lymphoma
Drugs: opiates, Carbamezapine (anti-convulsant)
Metabolic: alcohol withdrawl, porphyria, Hypothyroidism, Addisons
What are the PC of moderate/severe SIADH
Hyponatremia symptoms: headache nausea and vomiting muscle cramps muscle weakness irritability confusion drowsiness convulsions coma
What are the signs OE for hyponatremia?
Hyporeflexia
Positive babinski sign
Patients are euvolemic - no signs of oedema
What results give you a diagnosis of SIADH?
LOW plasma osmolality
LOW serum Na+
HIGH urine osmolality
HIGH urine Na+
What’s the mx of SIADH?
Treat underlying cause
Fluid restriction
VP receptor antagonists
Severe case: slow IV hypotonic saline + furosemide
What are complications of SIADH?
Convulsions
Coma
Death
Central pontine myelinosis *
What is central pontine myelinosis
When you correct hyponatremia way too fast
- quadriparesis (weakness in all 4 limbs)
- respiratory arrest
- fits
50% mortality
What is the prognosis of SIADH?
Na+ below 110 has a hight mortality and morbidity
50% mortality with central pontine myelinosis
54yo female presents to gp complaining of change in her breathing sound
She has noticed numbness in her toes and ginfers
She is snoring in her sleep
While taking her BP you notice her wrist flexing
What are you thinking?
Hypocalcemia
BP cuff inflation causing her wrist to flex.
Which sign is this?
Trosseau’s sign
Facial muscle twitching when taping on the facial nerve
Which sign is this?
Chvostek’s sign
What is stridor?
Stridor is a high-pitched, wheezing sound caused by disrupted airflow.
Stridor may also be called musical breathing or extrathoracic airway obstruction.
Airflow is usually disrupted by a blockage in the larynx (voice box) or trachea (windpipe).
What do you expect on an ECG of hypocalcemia?
Prolonged QT interval
What is the most common cause of hypocalcemia?
Renal failure
Others: pancreatitis Vit D deficiency Hyperparathyroidism Tumour Lysis Syndrome
What are the symptoms of hypercalcemia?
Hypercalcaemia symptoms: • Constipation • Polyuria/polydipsia • Depression • Kidney stones • Fatigue
” Stones Moans Groans “
Causes of hypercalcemia
Hyperparathyroidism * Lung Cancer Prostate Cancer Acromegaly complications PTH malignancies
What is Conn’s syndrome
Hyperaldosteronism arising from an adrenal tumour
Define primary hyperaldosteronism
Characterised by autonomous aldosterone overproduction from the adrenal gland with
subsequent suppression of plasma renin activity
What are the causes for primary hyperaldosteronism
- Adrenal adenoma (Conn’s syndrome) - responsible for 70% of cases
- Adrenal cortex hyperplasia (30% of cases)
• RARE:
o GlucocorticoidMsuppressible hyperaldosteronism
o Aldosterone producing adrenal carcinoma
Whats the pathophysiology of 1’ hyperaldosteronism
o Excess aldosterone leads to increased Na+ and water retention
o This leads to hypertension
o It also causes increased renal K+ loss leading to hypokalaemia
o Renin is suppressed due to NaCl retention
Summarise the epidemiology of primary hyperaldosteronism
- 1-2% of hypertensive patients
* Conn’s syndrome is more common in WOMEN and YOUNG patients
Recognise the presenting symptoms of primary hyperaldosteronism
- Usually ASYMPTOMATIC
- Tends to be an incidental finding on routine blood tests
• Symptoms of Hypokalaemia o Muscle weakness o Polyuria and polydipsia (due to nephrogenic DI) o Paraesthesia o Tetany
Recognise the signs of primary hyperaldosteronism on physical examination
- Hypertension **
- Complications of hypertension (e.g. hypertensive retinopathy)
Hypertension with nothing else think of conn’s
Identify appropriate investigations for primary hyperaldosteronism
• Screening Tests
o Low Serum K+ ****
• NOTE: Serum Na+ is usually normal because the Na+ reabsorption is matched by water reabsorption
o High Urine K+ ****
o High Plasma Aldosterone Concentration ****
o High aldosterone: renin activity ratio **
• Confirmatory Tests
SALT LOADING:
• Failure of aldosterone suppression following salt load confirms primary hyperaldosteronism
POSTURAL TEST
• Measure plasma aldosterone, renin activity and cortisol when the patient is lying down at 8 am
• Measure again after 4 hrs of the patient being upright
= Aldosterone-producing adenoma - aldosterone secretion decreases between 8 am and noon
= Bilateral adrenal hyperplasia - adrenals respond to standing posture and increase renin production leading to increased aldosterone secretion
o CT/MRI
o Bilateral adrenal vein catheterisation
• Measures adrenal vein aldosterone levels and allows you to distinguish between Conn’s syndrome and bilateral adrenal hyperplasia
o Radio-labelled cholesterol scanning
• Unilateral uptake in adrenal adenomas
• Bilateral uptake in bilateral adrenal hyperplasia
Generate a management plan for primary hyperaldosteronism
• Bilateral Adrenal Hyperplasia
o Spironolactone
o Eplerenone can be used INSTEAD OF spironolactone if its side-effects are intolerable
o Amiloride (potassium-sparing diuretic)
o Monitor serum K+, creatinine and BP
o ACE inhibitors and CCBs may also be added
• Aldosterone Producing Adenomas
o Adrenalectomy
• Adrenal Carcinoma
o Surgery
o PostMoperative mitotane (antineoplastic)
Whats spironolactone?
A steroid drug which promotes sodium excretion and is used in the treatment of certain types of oedema and hypertension.
Identify possible complications of primary hyperaldosteronism
• Complications of hypertension
Summarise the prognosis for patients with primary hyperaldosteronism
- Surgery may cure hypertension
* Or it may make the hypertension easier to treat with anti-hypertensive medication
Why would you do a 24ABPM if you are suspecting Conn’s in a patient with HTN?
To eliminate essential hypertension first
What is a phaeochromocytoma?
• Catecholamine= ADRENALINE -producing tumours that usually arise from chromaffin cells of the adrenal medulla but are extra-adrenal in about 10% of cases.
o 10% are bilateral
o 10% are malignant
o Extra-adrenal phaeochromocytomas are referred to as paragangliomas
10,10,10 - extra adrenal, bilateral, malignant.
Explain the aetiology/risk factors of phaeochromocytoma
• Sporadic cases are of unknown aetiology
• Familial in up to 30%
• Familial cases are seen in patients with:
o MEN2a
o von Hippel-Lindau syndrome
o Neurofibromatosis type 1
Recognise the presenting symptoms of patients with phaeochromocytoma
- PAROXYSMAL episodes
- Headache (due to malignant hypertension)
- Sweating
• Cardiorespiratory Symptoms
o Palpitations
o Chest pain
o Dyspnoea
• GI Symptoms
o Epigastric pain
o Nausea
o Constipation
• Neuropsychiatric Symptoms
o Anxiety *
o Weakness
o Tremor
Recognise the signs of phaeochromocytoma on physical examination
- Hypertension
- Postural hypotension *
- Pallor
- Tachycardia
- Fever
- Weight loss
Identify appropriate investigations for phaeochromocytoma
- 24 hr urine collection - check for catecholamine levels (and check for fractionated metanephrine levels) = metanephrines are metabolites of adrenaline
- Plasma free metanephrines
- Tumour localisation (MRI or CT)
- I-MIBG scintigraphy (another way of visualising the tumour)
- Screen for associated conditions
- Genetic testing
What is LADA and how would it typically present?
Atypical presentation of t1dm
Latent Autoimmune Diabetes of Adults
So its a t1dm presentation but latent - 45yo for eg.
PC: weight loss, hyperglycaemia, ketonuria, family history, polyuria, polydipsia,
Whats the very first step in t2dm mx
Lifestyle advice:
Diet and exercise advice
smoking cessation encouragement
What is the first thing that comes to your mind with a diabetic patient presenting with altered sensation in their hands and feet
Symmetrical Sensory Neuropathy
What is symmetrical sensory neuropathy
Early loss of vibration, pain and temperature sense in a GLOVE and STOCKING pattern.
In advanced disease pt’s will also lose their balance and complain of altered sensations
How does painful neuropathy typically present in a diabetic pt?
With burning sensations or painful parasthesia of their feet, shins or thighs.
How does diabetic amyotrophy usually present?
Painful wasting of the patients QUADRICEPS muscles and is usually asymmetrical.
Controlling glucose levels resolves this over time.
How does autonomic neuropathy typically present?
It’s rarely symptomatic.
Can present with a number of different problems of the sympathetic and parasympathetic systems.
Vagal neuropathy - tachycardia at rest, gastroparesis which can lead to vomiting, erectile dysfunction and atonic bladder.?
A t1dm patient presents with a raised smooth lump that is firmo on palpation on the lower abdomen
What is it?
Lipohypertrophy
Build up of adipose tissue in injection sites creating smooth firm lumps.
Patients should be encouraged to alternate injection sites: buttocks, abdomen, thigh, shoulder.
15yo pt presents with headaches which are getting gradually more and more frequent over the past 6w. She has white discharge from her nipples No other symptoms What are you thinking? What is the first test you want to do?
Hypeprolactinaemia
Serum prolactin measurement
What are the 4 types of prolactinomas
o Microadenomas: < 1 cm
o Macroadenomas: > 1 cm
o Giant Pituitary Adenomas: > 4 cm
o Malignant Prolactinoma (RARE)
o Risk of tumour enlargement in pregnancy
• NOTE: microprolactinomas rarely expand to become macroprolactinomas
What is the most common cause of hyperpolactinaemia?
Prolactinoma - pituitary adenoma causing stalk compression or hypothyroidism.
Recognise the presenting symptoms and signs of prolactinoma on physical examination
• Women o Amenorrhoea/oligomenorrhoea * o Galactorrhoea * o Infertility o Hirsuitism o Reduced libido
• Men o Symptoms are subtle and develop slowly o Reduced libido o Reduced beard growth o Erectile dysfunction
• Symptoms caused by tumour size o Headache * o Visual disturbance (bitemporal hemianopia) o Cranial nerve palsies o Signs and symptoms of hypopituitarism
Identify appropriate investigations for prolactinoma
- Serum prolactin level ** (extremely high levels (> 5000 mU/L) suggests true prolactinoma)
- TFTs - hypothyroidism –> high TRH –> stimulates prolactin release
- MRI
- Assessment of pituitary function
- Exclude pregnancy
Generate a management plan for prolactinoma
• Goals o Treat cause o Relieve symptoms o Prevent complications o Restore fertility
• Dopamine Agonists - CABERGOLINE and BROMOCRIPTINE
o Effective in most patients
o Usually need to be continued on a long-term basis
• If dopamine agonists are ineffective:
o Surgery
o Radiotherapy
Identify possible complications of prolactinoma
Complications of hypogonadism
o Osteoporosis
o Reduced fertility
o Erectile dysfunction
Complications of tumour size o Visual loss o Headache o Pituitary apoplexy o CSF rhinorrhoea
Summarise the prognosis for patients with prolactinoma
- Microprolactinomas will spontaneously resolve in about 1/3 cases
- Dopamine agonist withdrawal is usually attempted after about 2-3 years if prolactin levels have normalised and tumour volume is reduced
- High rates of recurrence
What is Kallman’s syndrome
A secondary hypogonadism cause
Its a congenital GnRH deficiency
What are some features of Kallman’s syndrome
Anosmia **
Undescended testes
Abnormal/Delayed pubertal development
“scarce pubic hair in 18yo male”
What is the most appropriate first line investigation in hypothyroidism?
TSH levels
What are the causes of primary hypothyroidism?
ACQUIRED
• Hashimoto’s thyroiditis (autoimmune)
• Iatrogenic (post-surgery, radioiodine, hyperthyroid medication)
• Severe iodine deficiency
• Iodine excess (WolffMChaikoff effect)
• Thyroiditis
CONGENITAL
• Thyroid dysgenesis
• Inherited defects in thyroid hormone biosynthesis
What are the cause of secondary hypothyroidism?
o Pituitary and Hypothalamic Disease M resulting in reduced TSH and TRH and, hence, reduced stimulation of thyroid hormone production
Only 5% is 2’
Whats the chronic mx for hypothyroidism?
LEVOTHYROXINE (25-200 mcg/day)
- IMPORTANT: rule out underlying adrenal insufficiency before starting thyroid hormone replacement
- Thyroid hormone replacement in the context of adrenal insufficiency can precipitate an Addisonian crisis
- Adjust dose based on clinical picture and TFTs
Identify possible complications of hypothyroidism
- Myxoedema coma
* Myxoedema madness (psychosis with delusions and hallucinations or dementia)
58yo female pt presents with an acutely painful neck and fever
The pain has been getting gradually worst over the past 2 weeks
She also has palpitations and weight loss
These symptoms subside and the pt presents again complaining of intolerance to the cold temperatures
What is this?
De Quervain’s thyroiditis
Classic “swing” from hyper to hypo thyroidism.
What happens in de quervain’s thyroiditis
Thyroid hormones are released because viral organisms infect the thyroid cells
Then they will suffer from hypothyroidism because the thyroid hormone gets completely depleted, until they get euthyroid again.
How does DKA clasically present
Nausea Vomiting Dehydration Abdominal pain* Kussmaul breathing (trying to compensate the acidosis) Sweet/ketotic breath (acetone)
45yo man wich cushing’s who had a bilateral adrenalectomy 1 year ago presents with dull headache, peripheral visual disturbances and increasing pigmentation of the skin creases of both hands.
What is this
Nelson syndrome
Classic: Addisonian symptoms POST bilateral adrenalectomy.
What is nelson syndrome?
locally aggressive pituitary tumour causing skin pigmentation due to ACTH
secretion)
29yo female patient is found unconscious and brought to a&e
She is t1dm and has a very well controlled insulin injection regime.
Blood biochemistry shows: moderately raised insulin
She is currently having a very stressful week at work and probably missing meals
what is this
hypoglycaemic coma
missing meals + taking insulin regularly
What is the most appropriate measurment taken to monitor diabetics?
HbA1c
aka: glycated haemoglobin
When conservative managment fails in newly diagnosed t2dm pts what do you give?
MEDICAL:
metformin for uncomplicated pt
sulphonylurea for obese pts with high fasting glucose and hba1c
33yo male pt complains of tingling in his arms when he is sleeping and this wakes him up
He also gained weight and his wedding ring is tight
OE: he is sweating, has a large jaw, furrowed tongue, large hands. BP - 142/91
Whats your next step?
Glucose Tolerance Test
You give 75g oral glucose which should normally supress GH but it’s raised when you measure it afterwards
IGF-1 is a screening test not a diagnostic test for acromegaly.
What is the first line treatment for acromegaly?
trans sphenoidal hypophysectomy
you give medical if surgery is contraindicated or transfused.
How is the anion gap interpreted in metabolic acidosis?
First of all you determine that this is metabolic acidosis by looking at the ABG
Then you calculate: (Na + K) - (Cl + HCo3)
so the cations minus the anions
Normally this should be = 10-18mmol
In metabolic acidosis this indicates that there is retention of H+/Cl- or loss of Na+/hco3- due to things like diarrhoea, renal tubular acidosis, hyperparathyroidism
If you have an elevated anion gap this can indicatesthat an unmeasured anion is present in increased wuantities such as a lactate or a ketone due to things likee lactic acidosis, ketoacidosis and excess salicylates.
38yo female presents with changes in her appearance and weight gain
Her clothes are tight especially around her waist
Her face seems puffy and flushed
Whats the most likely diagnosis?
Acromegaly
Not hypothyroidism
BECAUSE: “change in her appearance”
And its not hypothyroidism because there’s nothing like cold intolerance, constipation.
She is flushed - wouldn’t happen in hypothyroidism.
57yo lady presents with dull-grey brown patches in her mouth and the palms of her hand
She also gets very dizzy when rising from a seated position and is continually afraid of fainting
What’s the most likely diagnosis?
Addison’s
EXPLANATION: increased pigmentation (due to rise in MSH)
also CLASSIC: postural hypotension = addison’s
