Endocrine Flashcards
Jacky, 30, has had a range of persisting symptoms, which doctors believe is down to hypoadrenalism. Which symptom would distinguish between primary adrenal failure and secondary adrenal insufficiency?
Skin hyperpigmentation
Seen in primary adrenal insufficiency (as this will have high ACTH)
Not seen in secondary as this has low ACTH
Hyperpigmentation is caused by melanin stimulating hormone (which has same pre-cursor as ACTH)
Name 4 common features of multiple myeloma
CRAB C- hyperCalcaemia R- Renal failure A - Anaemia (and thrombocytopenia) B - Bone fractures or lytic lesions or bone pain
Investigate: Serum elecrophoresis looking for a monoclonal band
What presenting symptoms and investigation results characterise diabetes insipidus?
Polyuria and polydipsia
High serum osmolality and low urine osmolality
(High urine osmolality would rule out DI)
What steroids are highly mineralocorticoid and which highly glucocorticoid? What side effects do each have?
Mineralocorticoid = Fluid retention, HTN
- Fludrocortisone
Glucocorticoid = Immune suppresion plus all normal steroid SE (endocrine, GI, pysch, cushings etc)
- Dexamethosone
What is indicated by raised ferritin levels?
Either iron overload (10%)
OR
Inflammation (90%) - note ferritin is an acute phase protein
Transferin saturation <50% excludes iron overload
A 41-year-old woman presents with palpitations and heat intolerance. On examination her pulse is 90/min and a small, diffuse goitre is noted which is tender to touch. Thyroid function tests show the following:
Free T4 24 pmol/l
TSH < 0.05 mu/l
What is the most likely diagnosis?
Thyrotoxicosis with tender goitre = subacute (De Quervain’s) thyroiditis
Name 3 ECG changes associated with hyperkalaemia?
Prolonged PR
Wide QRS
Peaked/ tented T waves
What are the three categories and six most common causes of hyponatremia?
Na < 135
Hypovolemic: Diuretics or Addisons
Euvolemic: SIADH
Hypervolemic: Heart/ liver/ renal failure
How do you treat hyponatremia in acute and chronic situations?
PLUS TREAT UNDERLYING CAUSE Acute (<48hrs) = 3% hypertonic saline Chronic: - Hypovolemic = 0.9% isotonic saline - Euvolemic = Fluid restriction - Hypervolemic = Fluid restriction (plus furosemide if underlying condition warrants it)
What are the symptoms of hyponatremia? (5)
Confusion, headache, balance difficulty Altered mental status Seizures/ coma Orthostatic hypotension Low urine output, decreased JVP, dry mucus membranes, poor skin turgor
What are the most common causes of hypernatremia? (5)
Water loss
- Hyperglycemia
- Loop diuretics
- Diabetes insipidus (not enough ADH to reabsorb water)
- Severe diarrhoea, sweating, burns, vomitting etc
Not enough water gain
- Limited intake of water
Sodium gain
- Cushings (= increased glucose, sodium retention with the water retention)
- Primary aldosteronism (resets regulation of ADH secretion)
How do you manage hypernatremia?
Oral or IV fluids
Plus treat underlying cause
- If water loss may need desmopression (Diabetes insipidus)
- If excess sodium and fluid overload may need loop diuretic
What are the definitions of hyperkalaemia?
Mild - 5.5-5.9 mmol/L.
Moderate - 6.0-6.4 mmol/L.
Severe - >6.5 mmol/L.
What are the main causes of hyperkalaemia? (4 groups)
DRISP
Drugs (ACEI, ARBs, NSAIDS, heparin)
Renal (AKI/ CKD/ addisons)
Increase in production (Tumour lysis syndrome, trauma, burns)
Shift from intracellular to extracellular (DKA)
Pseudo (long tourniquet time, clenched fist, test tube haemolysis)
Name 3 symptoms of hyperkalaemia?
Usually non specific weakness and fatigue
Can get muscle paralysis, SOB and bradycardia
What investigations should be done on a patient with hyperkalaemia? (4)
Repeat K+ ECG Glucose FBC ABG
Name 3 changes on an ECG associated with hyperkalaemia?
Peaked T waves Prolonger PR (>200) Wide QRS (>120)
Hyperkalaemia can cause conduction disturbances!
How should hyperkalaemia be managed is K+ is 7.1?
SEVERE: Urgent ABCDE
- ABG to give immediate determination if true result, perform ECG
1) 10ml 10% Calcium gluconate to protect heart (works in 1-3mins, lasts 30-60mins). Keep giving upto 50ml until ECG improvement
2a) Insulin-glucose infusion (10units with 25g glucose) - moves K+ into cells. NB: K+ should come down 0.5-1 over 15mins
2b) Nebulised salbutamol (10-20mg should reduce K+ 0.5-1mmol/L in 15-30mins)
How should a K+ of 5.9 be treated?
Use calcium resonium (gets K+ out of GI tract, brings down by approx 1mmol but takes 2 hours so no use in acute setting)
How is hypokalaemia classified?
Mild - 3.1-3.5 mmol/L
Moderate - 2.5-3.0 mmol/L
Severe - <2.5 mmol/L
What are the three most common causes of hypokalaemia?
Increased water loss: - Diuretics - Vomiting/ diarrhoea Cellular shift: - Alkalosis - Insulin/ glucose Decreased K+ intake: - NBM - Anorexia
How does hypokalaemia present?
Generally asymptomatic
Can give weakness, muscle pain, constipation or paralysis
What are the findings in an ECG for a patient with a K+ of 2.9?
ECG changes in hypokalaemia:
- Flat T waves
- ST depression
- Prominant U waves
How is hypokalaemia managed? (2)
If mild: Dietary suppliments (40-120mmol/day)
If secondary care and severe:
- IV KCL (never bolus, give with normal saline). Needs careful monitoring
You are called to the ward to see a patient with high sugars, roughly how much does 1 unit of insulin cause a BM to drop?
1 unit drops blood glucose by approx 3mmol
Remember aiming around 8-10
Name 3 rapid acting insulins? When are they used?
Humalog
Novorapid
Apidra
Fiasp
All act rapidly (within 20mins) and have short action (<6hours)
Good for meal time insulin and correcting insulin
When should biphasic insulins be given?
At meal times
As contain rapid and intermediate acting insulins
What is the definition of hypoglycaemia?
Under 3mmol however in practice any under 4 should be treated
What is a phaeochromocytoma and how does it present?
Neuroendocrine tumor of the medulla of the adrenal glands
Present: Raised BP, palpitations, sweating, anxiety
What investigation is done for phaeocrhomocytoma?
24 hr urinary metanephrines
What is the treatment pathway for phaeochromocytoma?
A- Alpha blocker
B- Beta blocker
C- Cut it out (surgery)
How does congenital adrenal hyperplasia present and what is the most common cause?
Kid with precocious puberty and possible sex changes
Due to 21-hydroxylase deficiency
What investigation should be done for congenital adrenal hyperplasia?
17-hydroxyprogesterone
What is the function of vasopressin?
Vasopressin = ADH
Causes retention of water (solute free)
What is diabetes insipidus and how can causes be categorised?
Diabetes insipidus = not enough ADH (so no stopping of diuresis = lots of diuresis)
Therefore presents with polyuria and polydipsia
Cranial cause - Not producing ADH in post pituitary
Renal cause - Not responding to ADH
What is seen on plasma and urine osmolarity in diabetes insipidus?
Plasma osmolality = High
Urine osmolality = Low (as lots of fluid in urine so it’s dilute)
What is the first/ second line investigation of diabetes insipidus?
1) Water deprivation test
Would expect urine osmolality to rise, if it DOESN’T then this is DI (if it does probably pyschogenic cause of polydipsia)
2) Desmopressin test
- Giving ADH should put things back to normal (raised urine osmolarity). If it does then this is pituitary cause of the DI, if it doesn’t the kidneys aren’t responding to any ADH so renal cause
How do you manage diabetes insipidus?
Cranial cause = Give desmopression (ADH)
Renal cause = Supportive, protect kidneys, desmopression may help a bit
What is the action of aldosterone?
Promotes water reabsorbtion (via Na+ absorbtion and K+ excretion)
- So spironolactone which inhibits aldosterone causes less reabsorbtion (lowerBP) and less K+ excretion (which is why can cause hyperkalaemia)
What are the features of acromegaly (increased growth hormone 2ndry to pituitary adenoma)
Spade hands, increase show size
Large tongue
Excessive sweating and oily skin
Pituitary tumour > Headaches, bitemporal hamianopia
How do you investigate a patient for suspected acromegaly?
GH varies throughout day so not diagnostic
Do OGTT with serial GH measurements
- Normal = GH supressed <2 with hyperglycaemia
- Acromegaly = No supression of GH
How is acromegaly managed?
Trans-sphenoidal surgery
Can use somatostatin (GH inhibiting hormone) analogues (octreotide) as an adjunct before surgery
What are the diagnostic criteria for T2DM?
HbA1c > 48mmol/l
Fasting glucose > 7mmol/L
OGTT > 11.1mmol/L
1 result if symptomatic, 2 if asymptomatic
What are the result options for a fasting glucose?
<6.1 = Normal 6.1-7 = Impaired fasting glucose >7 = Diabetes
What are the result options for an OGTT?
<7.8 = Normal 7.8-11.1 = Impaired glucose tolerance >11.1 = Diabetes
What are the driving rules with diabetes?
Ok to drive but if more than 1 episode of hypo which required assistance need to contact DVLA
What are the characteristics of a DKA presentation?
Abdopain, polyuria, polydipsia, pear drop breath, kussmaul breathing, N+V, reduced GCS
Acidosis <7.3
Ketones in urine
Glucose >11mmol
(Diagnositic criteria)
How should DKA be treated?
ABCDE
Fluids (1L in 1hr, 1L in 2hrs, in 4hrs, in 8hrs)
Insulin (0.1/units/kg/hr)
- Once glucose under 15mmol/l start 5% dextrose also
Investigations for cause: FBC, blood cultures, CXR
CT head if reduced GCS
Note needs continually reassessing
What is the presentation of HHS?
General weakness, leg cramps, confusion, hypovolemia
Criteria:
Glucose >30mmol/l
Hyperosmotic >320mOs/l
Hypovolemia
Often no acidosis!
How is HHS treated?
Slow fluid rehydration
- Watch for reducing osmolarity
- Only use insulin if acidosis
Name 5 presenting symptoms of diabetes?
Polyuria Polydipsia Lethargy Pruritus Frequent infections
What are your first four steps in T2DM management?
1) Lifestyle
2) If HbA1c still over 48mmol/l = Start metformin
3) If HbA1c still over 58mmol/l = Start 2nd
- Sulfonylurea (Gliclazide, glipizide, glimepiride)
- DPP-4/Gliptins (Sitagliptin)
- Thiozolidianoes (Pioglitazone)
- SGLT-2 inhibitor (Dapagliflozin)
4) Add third drug from above
What is 5th line management in T2DM?
If HbA1c still >58mmol/L on 3 drugs
- If BMI <35 = Start exanitide (GLP-1 analouges)
OR
- Start insulin
What are pre and post prandial targets for T1DM?
Pre-prandial = 4-7mmol/l Post-prandial = <9mmol/l
What are the characteristics of MODY?
Young age T2DM Autosomal dominant (HNF-1alpha)
What is the best 1st line tx for MODY?
Sulfonylureas
(Gliclazide)
NOT metformin
What is the action of glucagon?
Increases glucose to increase blood sugar
What are the characteristics of SIADH?
No peeing (So high urine osmolarity) Diluted plasma (So low serum osmolarity) Often have hyponatermia
How is SIADH treated?
Depending on cause (Hypo/eu/hypervolemic)
What is addisons disease?
Primary adrenal insufficiency (low cortisol and low aldosterone)
What are the features of addisons disease?
Lethargy, weakness, N+V, weight loss, salt craving
Hyperpigmentation (raised ACTH)
Hypotension, hyperkalaemia, acidosis, hyponatremia (all due to low aldosterone)
Hypoglycemia (due to low cortisol)
How do you investigate possible adissons disease?
Short syncanthen test (give ACTH)
- Normal = Cortisol will rise >550 within 30mins
- Addisons = Adrenals not working so no rise in cortisol
How is addisons disease treated?
Replace glucocorticoid (hydrocortisone) Replace mineralocorticoid (fludrocortisone)
Other than addisons name three other causes of hypoadrenalism?
Primary (Mets, TB, HIV)
Secondary (Pituitary tumour, radiation)
EXOGENOUS GLUCOCORTICOID THERAPY
What is Conn’s syndrome?
Primary hyperaldosteronism CAUSED by an adrenal adenoma
i.e. all Conn’s is PH but not all PH is Conn’s
What are the three key features of primary hyperaldosteronism?
Hypertension
Hypokalaemia
Alkalosis
What is the first line investigation for primary hyperaldosteronism?
Aldosterone/ renin ratio
will be raised in primary hyperaldosteronism
How do you manage primary hyperaldosteronism?
If Conn’s = Surgery (take out adenoma)
If due to bilateral adrenocortical hyperplasia (70%) = Spironolactone
What are the components of the HPA axis?
Hypothalmus >(CRH)> Pituitary >(ACTH) > Adrenals > (Cortisol)
What are the 4 most common causes of cushings syndrome?
Exogenous = Iatrogenic (steroid therapy)
Endogenous: Cushing disease (80%) - Pituitary tumour releasing ACTH Adrenal adenoma (10%) Ectopic ACTH (5%) i.e. from SCLC
Name 5 features of cushing syndrome?
Weight gain Moon face Truncal obesity Easy brusiing Hirsuitism Proximal muscle weakness Facial plethora
What 2 investigations can be performed to diagnose cushing syndrome?
Urinary 24hr free cortisol (>280nmol/24hrs = CS)
Low dose (1mg) dext supression test Normal = Cortisol reduces CS = No reduction
How do you distinguish between pituitary or adrenal causes of cushing disease?
High dose (8mg) dex supression test
Pituitary cause = Decrease in ACTH and decrease in cortisol
Adrenal cause =
Decrease in ACTH but NO decrease in cortisol
What are the most common causes of an addisonian crisis? (3)
Sepsis
Surgery
Steroid withdrawal
How should an addisonian crisis be managed?
1) 1L saline over 1hr
(with dextrose if hypoglycemic)
2) IV hydrocortisone
What are the components of a diabetic foot exam?
Look (Skin, ulcers, swelling) Feel (Temp, cap refil, pulses) Move (+gait) \+ Sensation
Name 3 features of a hyperthyroid crisis (thyroid storm)?
Hyperpyrexia (>41)
Tachycardia (>140)
N+V, jaundice, diarrhoea, abdo pain, confusion, agitation
How should you treat a hyperthyroid crisis (thyroid storm)?
1) ABCDE (oxygen, fluids etc)
2) IV propanolol 5mg
3) Carbimazole or propylthiouracil PO
4) Hydrocortisone
If agitation - chlorpromazine
What is myxoedema coma?
Extreme manifestation of (usually untreated) hypothyroidism
> Hypothyroid features \+ Apathy, low mood, confusion, cognitive decline and possible coma Hypothermia (<35.5) Hypotension, bradycardia
How should myxoedema coma be managed?
ABCDE
- Early HDU/ ICU admission
- Immediate T4 and T3 given IV
- IV hydrocortisone
- Broad spectrum AB’s
Correct electrolyte and fluid abnormalities
Name 7 common hyperthyroid symptoms?
Weight loss Heat intolerance Tachycardia Diarrhoea Oligomenorrhoea Sweats Tremor Irritability and agitation
Name 7 common symptoms of hypothyroid?
Weight gain Cold intolerance Bradycardia Constipation Menorrhagia Myalgia/ cramps Weakness Thin hair Dry skin Low mood
What are the 4 most common causes of hyperthyroidism?
Graves (70%)
Toxic multinodular goitre
Subacute (DeQuevains) thyroiditis - post viral
Toxic adenoma
What are three common features of graves disease?
Age 40-60
Exopthalmos, opthalmoplegia, lid lag, pretibial myxoedema
(TSH receptor antibodies in 90%)
How do you manage hyperthyroidism?
Propanolol for rapid symptom relief
Then either:
A - Slowly titrate carbimazole (or propriothiouracil if preg) according to TFT’s
B- High dose carbimazole to block and levothyroxine to replace
Tx for 12-18months then slowly withdrawl
2nd line - Radioiodine
3rd line - Thyroidectomy
What are the 6 most common causes of hypothyroidism?
Primary atrophic thyroid
Hashimoto’s (Goitre + TPO antibodies)
Iodine deficiency (Worldwide most common)
Drugs/ surgery (amiodarone/ lithium)
Sick euthyroid (precipitated by illness) - Low TSH
Pituitary tumour - Low TSH
What is sub-clinical thyroid disease and how is it managed?
Low or high TSH with a normal T3/T4
- Treat if symptomatic, otherwise observe 6 monthly
How do you treat hypothyroidism?
Levothyroxine (0-100mcg)
- Half life is 7 days so wait 4 weeks between changing doses
What is the most useful marker to monitor progression of a thyroid carcinoma?
Serum thyroglobulin
What are the most common types of thyroid cancer?
Papillary carcinoma (70%) - Young females, excellent prognosis Follicular adenoma (20%)
How should papillary carcinomas or follicular adenomas of the thyroid be managed?
Total thyroidectomy
Followed by radioiodine
Yearly thyroglobulin levels to detect early recurrent disease
What is the typical bone profile and clinical features of primary hyperparathyroidism?
Bone profile:
- Raised PTH, raised Ca, low Phosphate
Clinical:
Asymptomatic or recurrent abdo pain (pancreatitis/ renal colic)
What is the most common cause of primary hyperparathyroidism?
Adenoma (80%)
What is the typical bone profile and clinical features of secondary hyperparathyroidism?
Bone profile:
- Raised PTH, low Ca, high phosphate, low VitD
Clinical features:
- Bone disease
(Secondary hyperparathyroid often due to CKD)
What is the most common cause of secondary hyperparathyroidism?
CKD
How is primary hyperparathyroidism managed?
Surgery
How is secondary hyperparathyroidism managed?
Medical
Calcium and vitD supplimentation
How do you differentiate between primary atrophic hypothyroid and hashimoto’s?
Primary - No goitre
Hashimoto’s- Goitre, likely TPO antibodies
What is the second line diabetic management drug (after metformin) most commonly for a) Obese patients and b) non-obese patients?
a) Sitagliptin (DPP-4 inhibitor) - weight neutral
b) Gliclazide (sulfonylurea) - normally best but can cause weight gain (so not in obese) also causes hypo’s so not those at high risk
Which acid causes acidosis in DKA?
β-hydroxybutyric acid
In the cori cycle, where is glucose converted to lactate and vice versa?
Glucose > lactate = In liver
Lactate > Glucose = In skeletal muscle
