Endocrine notes Flashcards
What are the causes of hypoK?
What are the indications for screening of Conns syndrome?
- Refractory hypertension: uncontrolled hypertension despite the use of at least 3 different classes of antihypertensives
- Young aget onset hypertension (below 40)
- Family history of associated young death
- HypoK and hypertension already has probability risk
What screening and confiramtory tests for conns syndrome?
check ABG: alkalosis (endocrine causes), acidosis (renal causes –> no time for renal compensation)
- Measure aldosterone renin ratio: >750 is confirmatory (if already 5 digits it is confirmatory of conns syndrome)
Confirmatory testing
* NS suppression test: infuse with 2L of NS, there should be suppression of aldosterone to less than 140
* Salt loading test: test for 24 hour urinary aldosterone (if still elevated = positive)
Less commonly used test: captopril suppression test, fludrocortisone suppression test
Localization test
After NS test, can do postural stimulation test to differentiate adenoma from hyperplasia
* Measure aldosterone at supine 8am than measure standing up after 4 hours
* Adenoma: ACTH stimulates production of aldosterone. ACTH is low in hte noon.
* Bilateral adrenal hyperplasia: ACE stimulates the bilateral adrenal hyperplasia when standing. Aldosterone will be will be low in the morning and high in the afternoon.
Afternoon cortisol level must be lower than morning cortisol due to ACTH.
What is the necessary diagnostics to proceed to surgery in Conns syndrome?
- NS test positive (elavated PAC despite test)
- Postural test is high
- CT imaging shows unilateral adrenal mass (if bilateral requires venous sampling to do lateralization test)
If during venous sampling the differene is 3-4x it points to lateralization and the side with more secretion can be removed. If ratio is less than 4 will not do surgery and just do medication.
If fulfill all 3 –> can proceed to surgery
How is adrenal venous sampling done for Conn syndrome?
- Using laterality index of >4 as cut off
- Administer ACTH than measure the cortisol level of IVC and adrenal vein
What are CT features that favor adrenal adenoma over malignancy?
What size is considered more likely malignant?
- Adenomas are small <3cm
- Round, or ovoid homogenous with low density and smooth borders
- Contain fat
- Non contrast imaging: <10 HFU
- Washout imaging (15 mins post contrast): >60% absolute washout, >40% relative washout
Phaeochromocytomas and hypervascular metastases such as RCC and HCC may have identical washout values. Hence if >120 HU on the portal venous phase, the washout value should be ignored, as the lesion is most likely a hypervascular metastasis (RCC/HCC) or phaeochromocytoma rather than a lipid-poor adenoma
What is treatment for thyrotoxic periodic paralysis vs hypoK periodic paralysis?
Thyrotoxic periodic paralysis:
Stabilize patient with K+ supplementation
Long term treatment:
if symptomatic should do RAI or thyroidectomy as with hypoK there is high risk of arrhythmia
Hypokalemic periodic paralysis (idiopathic)
K+ sparing diuretics (prevent urinary loss of K+): spironolactone
Acetazolamide
What Ix done for phaeochromocytoma?
- Urine catecholamines: metanephrine, normetanephrine, dopamine, and vanillylmandelic acid (VMA)
- CT scan
- MIBG scan: can be therapeutic via MIBG radionuclide therapy
- 68-Ga-DOTATE PET CT scan (phaeochromocytoma has malignant potential) which shows somatostatin receptor positive tumors: can use peptide receptor radionuclide therapy
In DM patient with thyroid associated orbitopathy, apart from eye exam what would you do?
Fundoscopy
* Choroidal flow signifies severity of thyroid eye disease
* See if DM retinopathy (impairing visual acuity)
In thyroid associated opthalmopathy patient what is the triad of signs to assess?
- Eye
- Acropachy (digital clubbing, soft tissue swelling of the hands and feet, periosteal new bone formation)
- Pretibial myxedema (dermopathy)
What are the risk factors for aggravation of graves opthalmopathy?
- Smoking: if patient has hyperthyroidism (therapeutic efficacy of PTU/methimazole will be impaired thus inducing hypothyroidism –> increasing TSH)
- Thyroid dysfunction: especially hypothyroidism (causes increased TSH: the eye has same TSHr as thyroid which causes them to bind to EOM inducing thickening and inflammation)
- Radioactive iodine: may induce chemical thyroiditis
- Trauma: prone to pretibial myxedema (myxedema can occur at any traumatic site e.g. BCG scar at arm)
What is the pathophysio of myxedema?
- Form of cutaneous and dermal edema secondary to increased deposition of connective tissue components
- Fibroblast stimulation by TSHr causes increased deposition of GAG which results in osmotic edema and fluid retention. Many cells responsible for forming connective tissue react to increases in TSH level (hence any trauma can form myxedema)
- Lymphocyte stimulation (trauma). Lymphocytes react against TSHr (present in mixed connective tissues) by inappropiately producing thyroid stimulating immunoglobulin –> tissue damage and scar tissue formation
What are the Ix done for thyroid eye disease?
- CBC
- TFT
- Anti TSHr (correlates with activity, used for monitoring response to drug treatment. If anti TSHr is still high after a year, cannot stop the antithyroid drug due to high risk of relapse)
- CT orbit
- MRI orbit for better delineation of periorbital EOM edema
What is the treatment for thyroid eye disease?
Aim for euthyroid status
* Eye lubricant (symptomatic relief)
* Selenium (mild eye disease): QoL and symptomatic relief
* IV pulse steroids (12 week regimen): 500mg 1x weekly for 6 weeks followed by 250mg 1x weekly for 6 weeks. Pulse steroids has better efficacy than oral steroids + less chance of cushingoid features
* MMF: synergistic effect combined with steroids –> eye prognosis better
* Tocilizumab
* Statin: atorvastatin (useful in moderate to severe eye disease): 2mg daily
- Orbital RT: has better efficacy when combined with IV pulse steroids –> helps improve diplopia (if no diplopia not done)
Contraindications - Young people <30 years (has carcinogenic effect)
- Diabetic retinopathy, hypertensive retinopathy
When steroids not successful
* Surgical decompression
* Rehabilitative surgery (1-2 years later in the fibrotic stage, not done in inflammatory stage. Tighten the muscles, improve the diplopia)
In thyroid eye disease short case how would you approach PE?
- Look at eye signs
- After I would like to look for clubbing (acropachy) and pretibial myxedema
- Than assess the thyroid status (e.g. AF, hand tremor)
If patient has thyroidectomy with graves ophtalmopathy, non drug compliance and high TSH with poor vision what should you suspect?
- Blindess due to compressive optic neuropathy
- Excess TSH due to hypothyroidism (no thyroxine taken) binds to TSHr in the eye causing compression
If there is unilateral eye opthalmoplegia what must you suspect apart from Graves opthalmopathy?
Euthryoid Graves disease is rare (+presents unilaterally). 95% of cases will present with bilateral proptosis.
Single eye involvement suspect other potential ddx
* Eye lymphoma
* Pseudotumor
* IgG4 related disease
Patient with ocular MG and graves opthalmopathy, how would you manage?
Stabilize the MG first
* Start on IVIG
* Followed by IV infusion pyridostigmine and pulse methylprednisolone (administered once a week for 6 weeks)
If given steroid first there is extremely high chance of inducing myasthenia crisis (bulbar symptoms and respiratory arrest). Hence given IVIG to protect.
In thyrotoxicosis and thyroid eye disease can you do thyroidectomy?
No as it will exacerbate the thyroid eye disease. Thyroidectomy is not a treatment for thyroid eye disease (only for after stabilizing eye for maintenance)
How to calculate thyroid hormone replacement?
If find that t4 is elevated after a long stable period what could this mean?
1.6kg x body weight
If there is full thyroxine replacement that means there is no remaining thyroid.
If there is a sudden rise in T4: the patient can may have reduced in weight.
How to ensure proper consumption of thyroxine replacement?
- Taken at empty stomach
- Can eat only 30 mins after
- See if taking any iron or calcium (will interfere with absorbance): can only be taken 3 hours before or after T4 consumption
TZD example and side effect/contraindications
eg. pioglitazone, rosiglitazone
Improve insulin sensitivity by activation of PPARgamma
AE
* Fluid retention (Edema) and congestive heart failure
* Bladder cancer
* Diabetic macular edema
* Fluid retention (Weight gain)
* Fractures
* Hepatotoxicity
* Increased ovulation and teratogenic effects
Contraindications for bisphosphonates
- Renal failure
- Esophageal erosions: GERD, benign strictures
- Hypocalcemia (will exacerbate as this is anti-resorptive agent)
Contraindications to use of teriparatide?
Anabolic agent: PTH analogue
- Hypercalcemia
- Pagets disease
- Osteogenic sarcoma
- Previous irradiation to the skeleton
- Pregnancy or breast feeding
- Bone cancer to metastatic cancer to bone
DM drugs that reduce weight
- SLGT2i (dapagloflozin)
- DPP4 inhibitor (sitagliptin)
- GLP1 agonist (liraglutide)
What are the Ix for suspected diabetic ketoacidosis?
What parameters need to be monitored?
Ix
* Urine (fast) and blood glucose
* Urine (fast) +/- plasma ketones or BAHA
* Electrolytes (Na, K, PO4 +/-Mg), anion gap
* Urea, creatinine, Hb
* ABG
If indicated (Ix to detect underlying infections which are exacerbating condition –> easy to manage)
* CXR, ECG
* Blood and urine culture and sensitivity
* Urine and serum osmolality
* PT, aPTT
Parameters to monitor
* Clinical status for dehyderation: BP, pulse. respiratory rate, consious level, I/O charting
* Hourly urine and blood glucose
* Na, K, urea, AG (till blood glucose <14mmol/L
* Repeat ABG (if patient is in ketoacidosis: may just be hyperglycemic)
What are the ancillary measures for diabetic ketoacidosis?
- Aspirate stomach if patient unconsious or vomiting (protect airway with cuffed endotracheal tube if necessary)
- Catheterize bladder and set CVP as indicated
- Give antibiotics if evidence of infection
- Treat hypotension and circulatory failre
How to Mx diabetic ketoacidosis?
- Hydration with 1-2L 0.9% NS in the initial hour. 1L/hour or 2 hours as appropriate. If serum Na>150mmol/L use 0.45% NS. Fluid in first 12 hours should not exceed 10% BW, watch for fluid overload. When blood glucose <14mmol/L, change to D5
- Regular human insulin 0.15U/kg as IV bolus, followed by infusion. Aim at decreasing plasma glucose by 3-4mmol/L per hour, double insulin dose to achieve this rate of decrease in blood glucose if necessary. When BG <14mmol/L change to D5 and decrease dose of insulin to 0.05-0.1U/kg/hour
- K: 10-20mmol/hour in initial hour. Continue 10-20mmol/hour, change if K<3mmol/L, increase to 40mmol/hour. Aim at maintaining serum K between 4-5mmol/L. Must add K+ regardless if normal as insulin causes intracellular shift of K+.
- NaHCO3- if pH lower than 7. If pH between 6.9-7: give 50mmol in NaHCO3- in 1 hour. If pH <6.9 give 100mmol NaHCO3- in 2 hours. Recheck ABG after infusion, repeat every 2 hours until pH>7. Monitor serum K when giving NaHCO3-.
Normal saline will cause intravascular expansion and correct the hyperosmolar hypovolemic hyponatremia as it contains Na+.
What is a possible insulin regimen?
Basal to mimic and control the fasting glucose. Bolus is to control the meals glucose. If the patient is smart: patient can titrate their own prandial insulin. If large meal: more insulin. If no meal can skip insulin. Can do carbohydrate counting.
* Tresiba (insulin degludec: basal) 9 units SC AM
* Apidra (glulisine): 6U in the morning, 5 in afternoon, 3 in night
In DM what is the importance of assessing when hypoglycemia occurs in insulin replacement?
Will be able to know what insulin dosage to titrate
* If fasting hypoglycemia in the morning –> adjust basal insulin
* If happens before lunch –> adjust breakfast prandial dose
Find underlying cause: having extra dose, excessive excercise (without snack), eating half amount of food
How to confirm dx of DM with patient presenting with hyperglycemia?
- Fasting glucose (for quickest results)
- HbA1c (most accurate)
- Random glucose is not that good but done 1st line, haemstix
HyperPTH patient with high ALP, what would you suspect?
Osteitis fibrosa cystica
How to differentiate DKA vs HHS (hyperosmolar hyperglycemic state)?
Why would a T2DM patient be on insulin injection?
On presentation
* symptomatic
* Presenting with features of insulin deficiency e.g. DKA
* Very high glucose (fasting >13mmol/L, random >16.7mmol/L)
Poor glycemic control despite 2 OHAs
* Persistent symptoms
* HbA1c ?9%
How to make dx of DM?
Random glucose ≥ 11.1 + Symptoms of hyperglycemia
Fasting glucose ≥ 7.0 on two occasions in asymptomatic individuals
2 hour OGTT ≥ 11.1 during 75g OGTT
HbA1c ≥ 6.5%
Name the types of insulin
Insulin can be human insulin or insulin analog.
Inulin can be:
Ultrashort acting: Lispro, Aspart
Short acting: regular human insulin
Intermediate acting: neutral protamine hagedorn (NPH), lente
Long acting: ultralente, Detemir, Glargine, Degludec
Different preparations of premixed insulin
NPH insulin + Lispro insulin
NPH insulin + Aspart insulin
NPH insulin + regular insulin
When is HbA1c not reliable?
Falsely high - ↑ Glycation (chronic renal failure) + ↓ Erythropoiesis (iron def.) + Assay issues (↑ bilirubin).
Falsely low - ↓ RBC lifespan (blood loss, haemolysis, hypersplenism) + Blood transfusion
How to ix thyroid disorder?
- measure TSH
- Autoantibodies: anti TSH receptor Ab (TRAb), antithyroglobulin Ab, antimicrosomal Ab
- Radioactive iodine scan (diffuse uptake in graves)
- ECG
- For diplopia: MRI orbit
How to manage patient if thyrotoxic and opthalmopathy?
- Rapid control of thyroid dysfunction to euthyroid
- Immunosuppressants for infiltrative opthalmopathy –> steroids (IV pulse), cyclosporin A, plasmapharesis, Ig
- Teprotoumumab
- Orbital irradiation
- Surgery: orbital decompression or EOM surgery
NO RAI: release thyroid antigens and auto Ab –> increase risk of opthalmopathy
What is Whipple’s triad?
Hyperinsulenemic hypoglycemia
CT abdomen with contrast
Insulinoma
Co-existing diabetes and insulinoma
Very rare
What 2 tests needed to diagnose and manage DM?
- Random blood glucose >11.1 (random blood glucose will always be higher than fasting glucose)
- Fasting glucose used to determine severity and guide whether needs treatment (if 7 can do lifestyle modification, if 12 cannot decrease to 7 by lifestyle modification and requires medical treatment)
Only if random blood glucose is between 7-11.1 than the diagnosis is uncertain. Than requires a further fasting blood glucose test to confirm. If 2 patients with random fasting glucose presents –> cannot determine the severity as the pretest variability is different (could have had buffet, fasting)
How to achieve dx of CMV graft infection?
What is the difference between ganciclovir and valganciclovir?
AE of ganciclovir?
- Blood CMV pp65 via PCR
- Valganciclovir has a valine group in addition to ganciclovir –> is a prodrug, oral formulation
- bone marrow suppression, renal insufficiency
How to manage CAPD peritonitis?
- Rapid flushing with 3 bags of PD fluid with heparin 500 units/L to prevent recurrent peritonitis
- Empirical antibiotics (then change regimen based on culture and sensitivity results): intraperitoneal antibiotics ceftazidime (gram-ve) and vancomycin (gram +ve)
Haemodialysis complications
Cx related to vascular acess: vascular access stenosis, UL ischemia (trash arm), lymphedema
Cx related to catheter access: exit site infection, septicemia unrelated to catheter
Cx during haemodialysis: hypotension, cardiac arrhythmia, technical malfunction
Long term cx: amyloidosis, tertiary hyperparathyroidism, cardiovascular cx (HT, LVH, anemia, cardiac dysfunction)
Cx of PD?
- PD catheter exit site infection
- PD-related peritonitis
- Inadequate ultrafiltration
- Cx due to increased intraperitoneal pressure
- Metabolic disturbance due to glucose absorption
- Malnutrition
Long term complications of renal failure?
- CNS: decreased LOC, stupor, seizure
- CVS: cardiomyopathy, CHF, arrhythmia, pericarditis, atherosclerosis
- GI: peptic ulcer disease, gastroduodenitis, AVM
- Hematologic: anemia, bleeding tendency (platelet dysfunction), infections
- Endocrine: decreased testosterone, estrogen, progesterone , increased FSH, LH
- Metabolic
- Renal osteodystrophy: secondary increased PTH due to decreased Ca2+, high PO43-, and low active vitamin D: Osteitis fibrosa cystica
- Hypertriglyceridemia, accelerated atherogenesis
- Decreased insulin requirements, increased insulin resistance
- Dermatologic: pruritus, ecchymosis, hematoma, calciphylaxis (vascular Ca2+ deposition)
What basic PE to differentiate if kidney issue is due to DM to HT?
- Check fundi: both neuropathy and retinopathy are small vessel disease, so DM retinopathy signs should be seen if kidney problem due to DM
- DM retinopathy: cotton wool spots, hard exudates, dot and blot hemorrhage, microaneurysm, proliferative diabetic nephropathy
How to make dx of diabetic nephropathy?
When would a renal biopsy be indicated in suspected DM nephropathy?
Clinical dx (not done by renal biopsy: GBM thickening, hyaline deposition, glomerulosclerosis): persistent albuminuria (>30mg/day) or decreased GFR (<60ml/min)
Renal biopsy in suspected DM nephropathy indications
* Severely elevated albuminuria (>300mg/day)
* RBC casts ,dysmorphic RBC, WBC casts in urine sediment
* Presence of another systemic disease (SLE)
* Sudden increase in albuminuria or rapid decline in eGFR (atypical features of DM nephropathy)
What type of insulin given for DKA?
What drug given before discharge?
- Regular human insulin
- Basal long acting insulin (on top of this is bolus insulin prior to meal)
What is dawn phenemonon?
Somogyi effect?
How to differentiate?
How to mx?
Dawn phenomenon: night hormones such as cortisol and GH promp the liver to release glucose. More common in T1DM where there is no insulin to counteract the effect.
* Treatment: increase medication (increase basal insulin) or adjust timing to improve control
Somogyi effect: rebound hyperglycemia often in T1DM when there is excessive insulin injection at night causing hypoglycemia which results in rebound hyperglycemia.
* Decreasing medication (decrease evening insulin) or adjust timing to prevent hypoglycemia
Check blood sugar in middle of night (0300). High/normal indicates Dawn phenomenon, low indicates somogyi effect
Is HbA1c a valid monitoring of BG in type 1 DM?
HbA1c is a reflection of average blood glucose levels during the life of RBC: 120 days
* Glucose levels will fluctuate day to day so does not accurately reflect glycemic control hence why T1DM requires regular HBGM
If DM patient is not hypertensive, may give drug, what is it and why?
ACEI: inhibits ACEI which converts angiotensin I to angiotensin II which causes vasoconstriction as well as increased aldosterone secretion. Therefore there is vasodilation of the efferent and afferent glomerular arterioles reducing glomerular hydrostatic pressure –> blood flow and GFR are preserved.
Renoprotective effect: proteinuria
Symptoms of hypoglycemia?
Sweating, dizziness, hunger, sleepiness, anxiousness, headache
Complications of DM
Macrovascular
* Stroke
* Cardiovascular disease (not only MI)
* Peripheral vascular disease
Microvascular
* peripheral (glove and stocking)/autonomic neuropathy (postural hypotension)
* Retinopathy
* Nephropathy
Basal plus bolus regimen example
Long acting: detemir
Short acting: aspart and lispro
First sensation lost in DM
Vibration
ddx of selar masses?
- Pituitary adenoma
- Pituitary carcinoma: germ cell tumors, lymphoma
- Craniopharyngioma (children)
- Other tumros: meningioma, lymphoma, germ cell tumor
- Non neoplastic masses: Rathkes cleft cyst, arachnoid cyst, pituitary abscess, carotid cavernous fistula
Complications of pituitary lesion?
- Local mass effet: optic nerve compression, optic chiasm (bitemporal hemianopia)
- Pituitary apoplexy
- Affect secretion of pituitary hormones: hyperprolactinemia, diabetes insipidus
How to Ix DI?
What is use of 2nd test?
How to manage patient after pituitary surgery?
- Urine and serum osmolality. Urine osmolality will be inappropriately low (inability to concentrate the urine)
- Water deprivation test: no fluid for 8 hours, measuring urine and serum osmolality
2nd test to differentiate DI and psychogenic cause
Anterior pit: cortisol, T4 supplement, sex hormone (PO/IV testosterone)
Posterior: DDAVP (synthetic ADH that acts on distal tubules and colleting duct)
Pituitary sits on the sella turcica
Which pituitary tumor is associated with post DI?
Craniopharyngioma (70-90% post op)
Meningioma, germ cell tumor, suprasellar pituitary adenoma, lymphoma
What to exclude in bellsy palsy?
What is Mx for bells palsy?
Central CN7 palsy: stroke, malignancy
Peripheral: GBS,cerebellopontine tumors, parotid gland tumors (esp adenoid cystic carcinoma)
What treatment for acromegaly?
- Transphenoidal surgery
- Somatostatin analogue (inhibits GH secretion and relieves the OSA): octreotide/lanreotide
- GH receptor antagonis: pegvisomant
Complications of acromegaly?
- Coarsening of facial features, protruding supraorbital ridges, prognathism causing gap bite (tombstone appearance), broade nose
- Enlargement of visceral organs: Cardiomegaly, splenomegaly, hepatomegaly
- OSA
- Carpal tunnel syndrome, spade shaped hands and feet, thickened heel pads
- Goiter (usually non toxic)
- OA
- DM, HT, HL
Anatomy of carpal tunnel?
Demonstrate sign?
Contains median nerve, 9 flexor tendons of forearm musculature (FDP, FDS): carpal tunnel syndrome (complication of acromegaly0
Tests:
* Muscle wasting of thenar eminence
* Finger numbness in lateral 3.5 fingers palmar side
* Phalens sign: back of hands placed against each other to provide hypreflexion of the wrist
* Tinels sign: firm percussion over course of median nerve –> produce symptoms
* Durkans sign: apply presure over transverse carpal ligament
Complications of transphenoidal surgery?
DI due to damage/ excision of anterior pituitary/ stalk
Damage to parasellar structures
* CSF rhinorrhea
* ICA: massive hemorrhage
* Optic chiasm/nerves: direct damage/post op hemorhagae into residual adenoma causing compression
Common causes of hypertension with hypoK
- Essential hypertension with diuretics
- Primary aldosteronism
- Cushing syndrome
- Phaeochromocytoma
- Renal vascular disease
- Malignant hypertension
What is the screening test for cushing?
- Overnight dexamethasone suppression test
- 1mg dexamethasone at 11pm, measure morning cortisol (9am)
- Normal: cortisol <50nmol/L
- Positive for cortical excess: failure of suppression
How to perform a low dose dexamethasone suppression test?
- 0.5mg dexamethasone q6h for 48 hours: total 4mg
- e.g. 8am,2pm,8pm, 2am for 2 consecutive days
- Normal: cortisol <50nmol/L
What test for cushing syndrome?
- Exclude iatrogenic cushings: drug history, establish raised 9am cortisol in serum (confirm endogenous)
- Screening test: overnight dexamethasone suppression test (shows elevated cortisol at 9am)
- Confirmation: low dose dexamethasone test
- Differentiate ectopic and cushing disease: high dose dexamethasone test
How to manage cushing disease?
Cushing’s disease
1st line: transsphenoidal surgery + cortisol replacement
RT: for non-visible tumour / not treated by surgery / fertility concerns
Medications: adrenal enzyme inhibitors (ketoconazole, metyrapone); indicated if:
* If awaiting effect after RT
* Severe comorbidities
* Non-visible tumours
* High surgical risk
Ectopic ACTH
Medication for non-resectable tumours: adrenal enzyme inhibitors, adrenolytics, glucocorticoid-receptor antagonists
Surgical excision of tumour
What is antihypertensive and DM drugs?
Hypertension
* Start on ACEI/ARB
* Add on CCB/diuretics
* BB less effective
DM
* 1st line is metformin, sulphonylureas (glipizide)
* 2nd line considered if HbA1c >9%: GLP analogues (exenatide), DPP4 inhibitors (sitagliptin), Alpha glucosidase inhibitors, SGLT2 inhibitors (lose weight)
* Insulin considered adding when HbA1c >10% or HHs or DKA
* Basal plus bolug e.g. NPH insulin + humilin R or glargine + aspart
Multiple myelomap findings in serum/urine protein electrophoresis with immunofluorescence?
Paraprotein
Reduction of other immunoglobulins –> immunoparesis
How to interpret PTH, Ca and PO4 in hyerparathyroidism?
- Primary hyperPTH: high PTH, high Ca and low PO4 (increased urinary excretion)
- Secondary hyperPTH: high PTH, low to normal Ca (due to high PTH) and high PO4 (CKD causing impaired phosphate excretion)
- Tertiary hyperPTH: increased PTH, increased calcium (bone release and absorption from intestine), high phosphate (impaired excretion)
- PTHrP: decreased PTH, increased calcium
sestamibi scan for parathyroid lesion
AE of carbimazole?
- Rash –> treat with antihistamines
- Agranulocytosis
- Rare: cholestatic jaundice, arthralgia, vasculitis
Short term S/E of steroid?
Infection
HypoK: mineralocorticoid effect
Hyperglycemia
Cushings only in long term use
What is proximal muscle weakness in graves disease?
Duration of treatment for oral antithyroid drug treatment?
How often to assess thyroid function?
Autoimmune diseases associated?
- Endocrine myopathy
- 12-18 months
- 2 weeks (monitor the thyroid function and blood count for agranulocytosis), there is around >60% chance of recurrence
Associated autoimmune diseases
* T1DM
* MG
* RA
* Sjogrens
* Autoimmune hepatitis (rare)
What is exopthalmos?
What is lid retraction?
Thyroid hormone effect on CVS?
- Exophthalmos: protrusion of the sclera anterior to the supraorbital ridge when assessed from above
- Lid retraction: sclera visible between upper limbus and eyelid (it is not a sign of Graves opthalmopathy –> due to enhanced sympathetic nervous system in thyrotoxicosis)
Thyroid hormones have a permissive effect on catecholamines. It increases the expression of B receptors to increase HR, stroke volume, cardiac output and contractility.
What needs to be done before giving radioactive iodine for hyperthyroidism?
- Avoid iodine containing food, medicine >4 weeks before
- Avoid antithyroid medication 4 weeks before RAI (ensure effective uptake of radioactive iodine)
- Avoid pregnancy/breastfeeding >6 months after therapy
- Pregnancy test should be performed 48 hours before RAI
post RAI thyroid requires what monitoring and precautions?
Monitoring
* TFT: for hypoT or persistent hyperthyroidism. Normalization usually takes 4-10 weeks
Post treatment precautions
* Avoid close contact with children/pregantn women/sleeping in the same room with another person
* Female: Pregnancy related 4-6 months post RAI
* Male: contraception for 3-4 months to allow adequate sperm turnover
Hypopituitarism clinical presentations to elicit in history?
- ACTH deficiency: fatigue, malaise, anorexia, n/v, abdominal pain, dizziness/orthostatic hypotension (not as severe as PAI); adrenal crisis
- TSH deficiency: fatigue, cold intolerance, decreased appetite, constipation
- Gonadotropin deficiency: oligomenorrhea / infertility in women; decreased libido / energy in males
- GH deficiency: increased fat / reduced BMD
- Prolactin: cannot lactate after delivery
How to treat addisons disease?
- Glucocorticoid + mineralocorticoid replacement
- Steroid cover during acute stress: eg. Infection / surgery
hyperthyroid, what is sign
Thyroid acropachy: clubbing, periosteal new bone formation in metacarpals/phalanges
drugs causing hyperthyroidism
- Amiodarone
- IFNa
- Immune checkpoint inhibitors: PD-1 inhibitors–nivolumab, pembrolizumab
- Radiation based cancer therapy
How to elicit cushings, phaeo, hyperaldosteronism and increased sex hormones in history?
(Any Cushing)
* No DM/glucose intolerance, unaware of any osteopenia/osteoporosis, recent weight gain, thin extremities, easy bruising, proximal weakness, plethora, rounded moon face, purple striae, acne, or hirsutism.
(Any pheochromocytoma)
* No sudden HT, flushing, headache, palpitation, sweating, postural hypotension.
(Any hyperaldosteronism)
* No HT, some non-specific hypoK symptoms e.g. fatigue, cramps on bilateral lower limbs especially at toes several times per month, increased urinary frequency with nocturia 2x at night, unaware of any increase in urine amount; (no dysuria, no hematuria, no stone passage, no fever).
(Sex hormones):
* No breast tenderness, patient menopaused otherwise also can ask if any infertility
Conditions associaetd with PBC
- Thyroid disorder: hashimotos thyroiditis
- Rheumatological: sjogrens, scleroderma, RA
- Renal tubular acidosis
Location of paragangliomas (extraadreal phaeochromocytoma)?
Scan?
How to manage if malignant hypertension
4 types of paragangliomas
* Branchiomeric: carotid body, laryngeal ganglia, subclavian ganglion
* Intravagal: jugular ganglion, nodose ganglion
* Aortosympathetic: sympathetic nerves of ganglia
* Visceral autonomic: nervous system of heart, digestive tract, liver hilus
MIBG scan for phaeochromocytoma
Alpha blocker by phenoxybenzamine than wait for a few weeks than add propranolol to avoid unopposed vasoconstriction by unopposed alpha action (normally B2 action causes vasodilation, if you control BP by blocking the beta first then the alpha vasoconstriction action will be full blown)
Tell me about MEN1/2
MEN1: parathyroid, pituitary, pancreas
MEN2a: parathyroid, phaeochromocytoma, MTC
MEN2b: neurom/gangliomas, parathyroid, phaeochromocytoma
MEN1: MEN1 gene
MEN2: RET gene
PE in HT and heart failure?
Thrusting apex due to LVH, late stage = displaced
S3 gallop associated with left atrial pressure >20mmHg and increased LV end diastolic pressure
Late stage = S4
Test for conns syndrome?
- Exclude other causes of hypoK, ensure reasonable Na intake
- Stop diuretics / BB / ACEI 2 weeks before dynamic biochemical tests
- Serum renin and aldosterone
Renin: primary (reduced), secondary (increased)
Aldosterone:renin ratio (ARR)
Primary: high >20
Secondary: low < 10 - Salt loading / infusion test
Give 0.9% NaCl 500 ml for 4 hours
Normal: suppression of renin + aldosterone
Primary hyperaldosteronism - Postural test
Give Na diet for 4 days, measure at supine (8 am) and 4 hours after ambulation (12 nn)
Normal: increased aldosterone due to drop in BP
Adrenal hyperplasia: exaggerated increase in in aldosterone (more sensitive to angiotensin)
Adrenal adenoma: not increased (more sensitive to ACTH)
Features of addisons
Mineralcorticoid deficiency
* HypoNa + dehydration —> nausea and vomiting, fatigue, postural hypotension
* HyperK + acidosis —> muscle weakness, palpitations
* Hypoglycaemia —> hunger, dizziness, sweating, palpitations
Glucocorticoid deficiency
Androgen deficiency (women)
* Decreased axillary and pubic hair, loss of libido
* Amenorrhea
Hyperpigmentation: skin, palmar creases, oral mucous membranes
Mx of severe hypoglycemia?
- D50 40cc IV stat followed by D10 drip
- 1mg IM glucagon (if cannot establish vascular access)
Which DM drugs causing hypoglycemia?
- Sulphonylurea: glipizide (diamicron)
- Meglitinides: rapaglinide, nateglinide
Rheumatological disorders associated with lymphomas?
- RA associated with non hodgkin lymphoma (DLBCL)
- SLE associated with NHL
How does basal plus bolus regimen work?
Basal taken at night time to maintain standard blood sugar overnight
Long acting insulin (detemir, glargine or degludec) usually injected night
Preprandial rapid acting insulin (lispro, aspart, glulisine)
Pros and cons of sliding scale insulin
Pros: patient involvement in his/her therapy, can be used to supplement scheduled insulin doses
Disadv: treats hyperglycemia insteadf of preventing it as there is lag time to onset of insulin. Poor glycemic control. Patient adherence and competency required.
Apart from HBGM what new device is there?
Continous glucose monitoring: freestyle libre
What DM drug cannot be used in renal impairment?
What drugs can be used?
Metformin as metabilized in kidney –> if renal function bad will result in lactic acidosis
SGLT2i (empagliflozin or canagliflozin) discontinued if eGFR <45ml/min
Sulphonylureas stimulate release of insulin release in pancreas (risk of hypoglycemia): discontinued if eGFR <60ml/min
Can be used in renal impairment
Insulin
Meglitinides: repaglinide (stimulate endogenous insulin production) can be used
AE of tacrolimus (FK)?
Tacrolimus is immunosuppressant used in renal transplant as well
Nephrotoxicity (Type IV RTA with hyperchloremic NAGMA), hypertension, hyperlipidemia, hyperglycemia, neurotoxicity.
AE of MMF
GI upset, pancytopenia, hypertension, hyperglycemia.
Less nephrotoxic and neurotoxic than calcineurin Inhibitors (e.g., tacrolimus)
Associated with invasive CMV infection.
