Medicine - endocrine Flashcards
Treat all diabetic patients aged 40-75 with what regardless of any investigations
A statin
Statin indicated conditions
- Clinical atherosclerosis (MI, ACS, stroke, TIA, carotid disease, peripheral artery disease)
- Abdominal aortic aneurysm (>3 cm) or prev AAA surgery
- DM >40 yr -15 yr duration for age >30 yr (T1DM) -Microvascular disease
- Chronic kidney disease (age 50 yr) -eGFR <60 mL/min/1.73m2 or -ACR >3 mg/mmol 5. LDL-C 5.0 mmol/L
Diagnosis of diabetes (Diabetes Canada 2018 Clinical Practice Guidelines)
Any one of the following
FPG 7.0 mmol/L (Fasting = no caloric intake for at least 8 hours) or
HbA1C 6.5% (in adults) (Not for diagnosis of suspected T1DM, children, adolescents, or pregnant women) or
2hPG in a 75g OGTT 11.1mmol/L or Random PG 11.1 mmol/L
Mechanism of action of sulfonylureas
Increase endogenous insulin
In whom is Metformin contraindicated?
- >80
- Renal insufficiency
- Hepatic failure
- Heart failure
- Alcoholics
- Past history of lactic acidosis on metformin therapy
- Lactation
Tight glucose control in Type 1 DM decreases risk for micro or macrovascular complications?
Micro. The effect on macro (CVA/ MI) is unknown
What type of antibodies may be present in type 1 DM?
- Anti-islet cell
- Anti-GAD glutamic aid decarboxylase
- Anti-insulin
- Anti-Zn transporter
What may a type II with a glucose over 33 mmol/L present with
Hyperosmolar Hyperglycaemic state HHS
What is seen on kidney biopsy of diabetic nephropathy?
Kimmelstiel-Wilson nodules
Diagnostic HbA1c level for diabetes
>6.5%
Diagnostic criteria for metabolic syndrome
3 of 5
- Abdominal obesity > 40 inches (102cm) in men and 35 inches (88cm) in women
- Triglycerides >150mg/gL
- BP > 130/85 or a requirement for antihypertensives
- Fasting glucose > 100mg/dL
- HDL <40mg/dL in men and <50 in women
The single best test for screening of thyroid disease
TSH
Preferred screening test for thyroid hormone levels
Free T4
Purpose of a radioactive iodine uptake (RAIU) test and scan
To determine of a nodule is functioning or nonfunctioning and requires a biopsy for malignancy workup.
Three signs that are specific for Graves disease
- Exopthalmus
- Pretibial myxedema
- Thyroid bruits
Antibodies found in patients with Graves disease
TSH receptor stimulating antibodies
What to do when screening for TSH if it is a) normal b) high and c) low
a) normal- no further tests b) high- measure free T4 c) low- measure free T4 + T3
TSH, T4 and T3 in primary hypothyroidism
TSH ⬆︎ T4 ⬇︎ T3 ⬇︎
TSH, T4 and T3 in primary hyperthyroidism
TSH ⬇︎ T4 ⬆︎ T3 ⬆︎
TSH, T4 and T3 in secondary hypothyroidism
TSH ⬇︎ T4 ⬇︎ T3 ⬇︎
What happens to thyroid levels in pregnancy?
TBG increases resulting in reduced free T3/T4 levels and increased TSH
What is the natural history of impaired glucose tolerance (pre-diabetes)? ie in terms of progression
- 1-5% per yr go on to develop DM
- 50-80% revert to normal glucose tolerance
Genetic syndromes associated with DM
- Down’s syndrome
- Klinefelter’s syndrome
- Turner’s syndrome
Infections associated with DM
- Congenital rubella
- CMV
- Coxsackie
Target blood pressure Diabetes Canada 2018 Clinical Practice Guidelines
130/80
Target Fasting plasma glucose Diabetes Canada 2018 Clinical Practice Guidelines
4-7 mmol/L (72-126 mg/dL)
Target 2h post-prandial glucose Diabetes Canada 2018 Clinical Practice Guidelines
5-10 mmol/L (90-180 mg/dL) or 5-8 mmol/L (90-144 mg/dL) if not meeting target A1c and can be safely achieved
Pathology of Type I DM
Pancreatic cells are infiltrated with lymphocytes resulting in islet cell destruction 80% of cell mass is destroyed before features of DM present
Target HbA1c Diabetes Canada 2018 Clinical Practice Guidelines
<7%
Risk factors Type II DM
- Age >40 yr
- Schizophrenia
- Abdominal obesity/overweight
- Fatty liver
- First-degree relative with DM
- Hyperuricemia
- Race/ethnicity (Black, Aboriginal, Hispanic, Asian-American, Pacific Islander)
- Hx of impaired glucose tolerance or impaired fasting glucose
- HTN
- Dyslipidemia
- Medications e.g. 2nd generation antipsychotics
- PCOS
- Hx of gestational DM or macrosomic baby (>9 lb or >4 kg)
HbA1c reflects what?
Reflects glycemic control over 3 mo and is a measure of patient’s long-term glycemic control
LDL-C cholesterol target for diabetics
LDL-C <2.0 mmol/L
Macro ratios for a diabetic diet
Daily carbohydrate intake 45-60% of energy Protein 15-20% of energy Fat <35% of energy
Continue lifestyle modifications in NIDDM for how long before treating?
2-3 months
Unless initial HbA1c >8.5% at the time of diagnosis, in which case initiate pharmacologic therapy with metformin immediately, and consider combination of therapies or insulin immediately
Clinical features of HHS Hyperosmolar Hyperglycaemic state
- Onset is insidious, preceded by weakness, polyuria, polydipsia
- History of decreased fluid intake
- History of ingesting large amounts of glucose containing fluids
- Dehydration (orthostatic changes)
- ⇣ LOC ⇢ lethargy, confusion, comatose due to high serum osmolality
- Kussmaul’s respiration is absent unless the underlying precipitant has also caused a metabolic acidosis
Clinical features DKA
Hyperglycemia (polyuria, polydipsia, weakness) • Acidosis (air hunger, nausea, vomiting, abdominal pain, Kussmaul’s respiration, acetone-odoured breath) • Precipitating conditions (insulin omission, new diagnosis of diabetes, infection, MI, thyrotoxicosis, drugs)
Serum abnormalities DKA
Serum • ⇡ BG (typically 11-55 mmol/L, ⇣ Na+ (2º to hyperglycemia - for every ⇡ in BG by 10 mmol/L there is a ⇣ in Na+ by 3 mmol/L)
- Normal or ⇡ K+, ⇣HCO3–, ⇡ BUN, ⇡ Cr, ketonemia, ⇣ PO43-
- ⇡ osmolality
- corrected sodium = current sodium + [0.3 x (current glucose -5)]
What is the best way to monitor the degree of ketoacidosis in DKA?
Anion gap is the most important endpoint used to monitor the resolution of the metabolic acidosis
Rehydration in DKA
-500 mL/h x4 h, then 250 mL/h x4 h NS if mild-moderate deficit, 1-2 L/h NS if severe deficit (shock)
– Switch to 0.45% NaCl once euvolemic (continue NS if corrected [Na+] is low or rate of fall of plasma osmolality 3 mosm/kg/h)
– once BG reaches 14.0 mmol/L add Dextrose 5% in water or D10W to maintain BG of 12-14 mmol/L
Insulin therapy in DKA
Critical to resolve acidosis, not hyperglycemia
- do not use with hypokalemia (see below), until serum K+ is corrected to >3.3 mmol/L
- use only regular insulin (R)
- maintain on 0.1 U/kg/h insulin R infusion
- check serum glucose hourly
Risk of MI in those with DM compared to age-matched controls
3-5x higher
HbA1c level is a significant and independent predictor of the risk of what in DM?
Stroke
Clinical features of diabetic retinopathy
macular edema: diffuse or focal vascular leakage at the macula
- non-proliferative (microaneurysms, intraretinal hemorrhage, vascular tortuosity, vascular malformation)
- proliferative (abnormal vessel growth) • retinal capillary closure
Percentage of diabetics who progress to neuropathy
Approximately 50% of patients within 10 yr of onset of T1DM and T2DM
Classical features of peripheral sensory neuropathy in DM
Paresthesias (tingling, itching), neuropathic pain, radicular pain, numbness, decreased tactile sensation
Bilateral and symmetric with decreased perception of vibration and pain/ temperature; especially true in the lower extremities but may also be present in the hands
Decreased ankle reflex
Distal-predominant – longest nerves affected first
Classic stocking-glove distribution
May result in neuropathic ulceration of foot
Candidates for bariatric surgery in Canada
BMI >35 and risk factors or BMI >40 Failing behavioural modication
For whom should free T3 be measured?
Free T should only be measured in the small subset of patients with hyperthyroidism and suspected thyrotoxicosis.
The first line tool for identification of thyroid nodules that require FNAB
Ultrasound
Investigation of choice for hyperthyroid patients with thyroid nodules
Radioisotope thyroid scan and RAIU
Indication for a radioisotope thyroid scan (Technetium-99)
if 1) one or more thyroid nodule(s) and 2) patient is hyperthyroid to determine whether nodules are hot (functioning excess thyroid hormone production) or cold (non-functioning)
What is the chance of malignancy in a hot nodule in a hyperthyroid patient?
Very low. Treat the hyperthyroidism
Cold nodules require a workup
Epidemiology of thyrotoxicosis
Epidemiology • 1% of general population have hyperthyroidism • F:M = 5:1
Graves Disease- genetic associations
Association with HLA-B8 and DR3
Pathophysiology of Graves
Autoimmune disorder due to breakdown in thyroid tolerance likely due to a combination of factors including autoreactive B lymphocytes and an imbalance favouring a 2 vs 1 immune response
• B lymphocytes produce thyroid-stimulating immunoglobulin (TSI) that binds and stimulates the TSH receptor and stimulates the thyroid gland
Graves Disease investigation findings
- low TSH
- increased free T4 (and/or increased T3)
- positive for TRAb (sensitivity and specicity of third gen TRAb tests that are available currently is > 98% allowing use for determining etiology of hyperthyroidism)
- increased radioactive iodine (I-131) uptake
- homogeneous uptake on thyroid scan
Treatment for Graves
Thionamides, radiodine (RAI), or surgery.
Name two thionamides and their mechanism of action
Thionamides (antithyroid medications): propylthiouracil (PTU) or methimazole (MMI) Inhibit TH synthesis by inhibiting peroxidase-catalyzed reactions, thereby inhibiting organification of iodide, blocking the coupling of iodotyrosines
Major side effects antithyroid meds
Hepatotoxicity (cholestasis, hepatitis), agranulocytosis, vasculitis
Note they are also teratogens
Symptomatic Rx hyperthyroidism
Beta-blockers
Risks of thyroidectomy
Hypoparathyroidism and vocal cord palsy
Painful Thyroiditis (DeQuervain’s, granulomatous) is strongly associated with what genetically?
Strongly associated with HLA-D35
Painful Thyroiditis (DeQuervain’s, granulomatous): presentation clinically
Painful swelling of the thyroid (may radiate to jaw and ears)
Transient vocal cord paresis
Malaise, Fatigue, myalgia, fever
Often preceded by URTI Painful condition lasts for a week to few months
Signs of hyperthyroidism during hyperthyroid phase (palpitations, tachycardia, stare)
Painful Thyroiditis (DeQuervain’s, granulomatous): Treatment options
-NSAID/prednisone for pain
𝝱-adrenergic blockage is usually effective in reversing most of the hypermetabolic and cardiac symptoms
If symptomatically hypothyoid, may treat short-term with thyroxine
Toxic Adenoma/Toxic Multinodular Goitre: Clinical features, and who tends to present with it
Clinical Features
- multinodular goitre
- tachycardia, heart failure, arrhythmia, weight loss, nervousness, weakness, tremor, and sweats
- seen most frequently in elderly people as opposed to Graves’ disease which is more common in younger ppl
Toxic Adenoma/Toxic Multinodular Goitre: Treatment
- use high dose radioactive iodine (I-131) to ablate hyperfunctioning nodules
- 𝜷-blockers often necessary for symptomatic treatment prior to definitive therapy
- surgical excision may also be used as 1st line treatment
Thyrotoxic crisis clinical features
hyperthyroidism
- Extreme hyperthermia (40°C), tachycardia, vomiting, diarrhea, hepatic failure with jaundice, AF, congestive heart failure
- CNS manifestations including agitation, delirium, psychosis, lethargy, seizures, coma
Thyrotoxic crisis bloods
- increased free T4 and T3, undetectable TSH
- ± anemia, leukocytosis, hyperglycemia, hypercalcemia, elevated LFTs
Thyrotoxic crisis Rx
- PTU is the anti-thyroid drug of choice and is used in high doses (200 mg q4h)
- Give iodide, which acutely inhibits release of thyroid hormone, 1 h after first dose of PTU is given
- Hydrocortisone 100 mg IV q8h or dexamethasone 2-4 mg IV q6h for the rst 24-48 h; inhibits peripheral conversion of T4 to T3
Foods that reduce absorption of thyroxine
Soybeans and coffee
Secondary hypothyroidism is caused by what?
Insufficiency of pituitary TSH
Neurological signs of hypothyroidism
- Paresthesia
- Slow speech
- Muscle cramps
- Delay in relaxation phase of deep tendon reflexes (“hung reflexes”) -Carpal tunnel syndrome
- Asymptomatic increase in CK
- Seizures
Myxedema Coma: mortality rate
40%
Myxedema Coma: what is it?
medical emergency – severe hypothyroidism complicated by trauma, sepsis, cold exposure, MI, inadvertent administration of hypnotics or narcotics, and other stressful events
Myxedema Coma: Clinical Features
- hallmark symptoms of decreased mental status and hypothermia
- hyponatremia, hypotension, hypoglycemia, bradycardia, hypoventilation, and generalized non-pitting edema often present
Goitrogens- name some
• iodine deciency or excess • rogens: brassica vegetables (e.g. turnip, cassava) • drugs: iodine, lithium, para-aminosalicylic acid
Which layer of the adrenal cortex produces mineralocorticoids (aldosterone)?
Zona glomerulosa
Which layer of the adrenal cortex produces glucocorticoids (cortisol)?
Zona Fasciculata
Which layer of the adrenal cortex produces androgens (DHEA, androstenedione)
Zona Reticularis
Principle action of aldosterone
- a mineralocorticoid which regulates extracellular fluid volume through Na+ (and Cl–) retention and K+ (and H+) excretion (stimulates distal tubule Na+/K+ ATPase)
- regulated by the renin-angiotensin-aldosterone system and by hyperkalemia
Gold standard test used to diagnose adrenal insufficiency
Insulin tolerance test
Dexamethasone (DXM) Suppression Test assesses what?
HPA axis.
Principle: DXM suppresses pituitary ACTH, plasma cortisol should be lowered if HPA axis is normal
Overnight DXM Suppression Test: method
Oral administration of 1 mg DXM at midnight, then measure plasma cortisol levels the following day at 8 AM
Physiologic response: plasma cortisol <50 nmol (<1.8 μg/dL) Inappropriate response: failure to suppress plasma cortisol
Core features of primary hyperaldosteronism
Hypertension and Hypokalemia
Usual cause of hyperaldosteronism
Bilateral adrenocortical hyperplasia (60-70%)
Sometimes unilateral adrenal adenoma (Conn syndrome)
Hyperaldosteronism treatment
Adenoma: surgical resection
Bilateral hyperplasia: Aldosterone receptor antagonist
Pheochromocytoma is most commonly associated with which neoplastic syndromes?
MEN 2A and 2B
What type of tissue is a pheochromocytoma a tumour of?
Chromaffin tissue - secretes catecholamines)
Presenting features of pheochromocytoma
- 50% suffer from paroxysmal HTN; the rest have sustained HTN
- classic triad (not found in most patients): episodic “pounding” headache, palpitations/tachycardia, diaphoresis
- other symptoms: tremor, anxiety, chest or abdominal pain, nausea and vomiting, visual blurring, weight loss, polyuria, polydipsia
Best initial test for pheochromocytoma
24-urine catecholamines
After that do a CT
Most common cause of Cushing’s syndrome
Iatrogenic due to prolonged steroid therapy
Most common endogenous cause of Cushing’s syndrome
Hypersecretion of ACTH from a pituitary adenoma (Cushing’s Disease)
Diagnostic tests for Cushing’s (4)
- 24hr free cortisol (↑)
- Salivary cortisol - late night (↑)
- ACTH (↑)
- Dex suppression test morning cortisol level (low dose ↑ high dose ↓)- suppression is normal (no Cushing’s)
Acromegaly lab tests 1. to establish abnormality 2. to confirm Dx
1) IGF-1 levels (not growth hormone)
2) OGTT - GH levels will remain high despite glucose administration
Surgery for acromegaly
Transphenoidal surgical resection
Medical therapy for acromegaly
Ocreotide
Complications of acromegaly
- Diabetes from glucose intolerance dt XS GH secretion.
- Cardiomyopathy
- Carpal tunnel syndrome
- Bitemporal hemianopsia (optic chiasm/ pituitary adenoma)
- Sleep apnea
- Heart disease
Leading cause of death is cardiovascular
- congestive heart failure
Clinical features of acromegaly
- Skull enlargement
- frontal bossing
- wide spaced teeth
- Coarsening of facial features
- Large tongue
- Skin tags
Diabetes insipidus- essential problem
Inability to produce concentrated urine due to ADH dysfunction.
Central DI- posterior pituitary fails to secrete ADH, or
_Nephrogenic D_I- kidneys fail to respond to ADH
Diagnosis of diabetes insipidus
1) serum osmolality > urine osmolality, reduced urinary sodium, possible hypernatremia
2) water deprivation test - patients continue to excite high volume of dilute urine
3) desmopressin acetate suppression test (DDAVP) - DDAVP is synthetic analog of ADH. In Central DI it shows reduced urine output and increased urine osmolarity. _In nephrogenic DI there is no effec_t on urine output or osmolarity.
What are the three peaks of occurrence of physiologic gynecomastia?
Neonates Puberty Old age
Percentage of gynecomastia that is idiopathic
58%
Pathological causes of gynecomastia
- Hepatic cirrhosis
- Testicular carcinoma (not commonly though)
- Chronic kidney disease
- Lung cancers
- Klinefelter’s
- Certain meds
- Pituitary adenoma
ADH works where to do what?
At the collecting ducts of the nephron to bring back water from urine to the bloodstream therefore to dilute the serum. Serum osmolality and serum sodium drop.
What happens to plasma osmolality in SIADH?
Decreases
Best initial management of SIADH
Restrict fluid. This is the cornerstone of managing SIADH
Why do you have to correct hyponatremia slowly in SIADH?
To prevent osmotic demyelination syndrome
Management of persistent or symptomatic hyponatremia in SIADH
IV hypertonic saline therapy
ADH secretion does what to urine volume
Reduces it, producing concentrated urine
Some complications of Pagets Disease of Bone (PDB)
Nerve root compression
Spinal stenosis
Deafness
Pathological fractures
Secondary osteoarthritis
Osteosarcoma
High output cardiac failure
Classic radiologic findings of PDB
Thickening of the cortex
Accentuation of the trabecular pattern
Increased bone density
Skull X-Rays described as having ‘cotton wool’ appearance
X-Rays are diagnostic
The most sensitive way to differentiate primary from secondary causes of hyperaldosteronism?
Aldosterone to renin ratio
You can do the test with random sodium intake
Best test for adrenal function eg Addison’s
Cosyntropin stimulation test (inject cosyntropin iv and measure cortisol 60mins later)
aka the ACTH Test/ The Synacthen test
ACTH is injected and cortsol is measured
It is 97% sensitive and 95% specific for primary adrenal insufficiency
First line treatment PDB. And what supplements also need to be administered?
Bisphosphonates are first line
Also calcium and vitamin D
Signs of zinc deficiency
- Leukonychia
- Night blindness
- Impaired taste
- Impaired growth
- Alopecia
- Impaired immunity
- Anemia lethargy
- Poor wound healing
- Delayed puberty
Which substance can worsen Graves orbitopathy?
Radioactive iodine
Elevated parathyroid hormone levels are usually caused by what?
Single parathyroid adenoma in 80% cases
Calcium reference range
Calcium is maintained within a fairly narrow range from 8.5 to 10.5 mg/dl (4.3 to 5.3 mEq/L or 2.2 to 2.7 mmol/L).
Best screening test for diabetic nephropathy
Detection of microalbuminuria
HbA1c target
7%
Laboratory features of pheochromocytoma
Hyperglycemia
Hypercalcemia
Erythrocytosis
Renoprotective drugs for diabetic nephropathy
ACE inhibitors
Angiotensin receptor blockers
They delay the progression of chronic kidney disease in DMs with Microalbuminuria
In addition to the treatment of diabetes, insulin can also be used to manage severe what?
Hyperkalemia
Drugs that can cause SIADH
- Amiodarone
- Carbamazepine
- SSRIs
- Chlorpromazine
First line of management for severe hypercalcemia
Saline infusion
Hypercalcemia causes dehydration from vomiting and renal insufficiency. Hydration alone may lower calcium levels.
How do you monitor thyroxine overreplacement?
With TSH levels
Omega 3 fish oils have been shown to do what to reduce the risk of stroke after MI
Reduce triglycerides
Absolute contraindication to radio iodine Rx for Graves disease
Pregnancy
What do you have to do to antithyroid medication before radio iodine therapy?
Stop it
The most common cause of death in Marfan Syndrome
Dissecting aortic aneurysm
The screening tool of choice for Cushing’s
24-hour urinary cortisol
The most specific test for acromegaly
Measuring serum GH during OGTT
What is the WHO definition for ‘impaired fasting glucose’ (IFG)?
Fasting glucose 5.6-7 mmol/l.
Which tumours are associated with MEN2A (multiple endocrine neoplasia)?
Mnemonic TAP 1. Thyroid (medullary carcinoma). 2. Adrenal (phaeochromocytoma). 3. Parathyroid.
What is the function of parathyroid hormone (PTH)?
To increase serum Ca levels NOTES Acts at the bone (osteoclast stimulation) and kidneys (Ca absorption and PO4 excretion, calcitriol synthesis).
What is the mechanism of action of metformin?
- Decreases hepatic glucose production.
- Decreases intestinal glucose absorption.
- Increases insulin sensitivity.
Most serious side effect of metformin
Lactic acidosis
List 2 examples of rapid-acting insulin
- Humalog
- Novorapid
NOTES Usually taken just before a meal. Usually prescribed in type 1 diabetes. Increased risk of hypoglycaemic episodes.
List 2 examples of long-acting insulin
- Lantus (glargine).
- Levemir (determir).
- Hypurin bovine lente.
What is Kallman syndrome?
Hypogonadotropic hypogonadism with anosmia
NOTES
A genetic disorder, due to failure of migration of hypothalamic GnRH-secreting neurons. Represents a type of tertiary hypogonadism.
“What is the treatment for asymptomatic SIADH?”
Must consider and address the underlying cause, in the meantime:
- Conservative - Patient education. Fluid restriction e.g. 1500ml/day.
- Meds e.g. IV saline in severe hyponatraemia (consider).
NOTES SIADH = syndrome of inappropriate antidiuretic hormone. Slow correction of hyponatraemia minimises the risk of osmotic demyelination syndrome.
What is the treatment for hypocalcaemia?
Must consider and address underlying cause, in the meantime:
- Resus A+B - consider airway support and O2. C - IV access.
- Meds 20ml of 10% calcium gluconate IV.
First line treatment for acromegaly
Surgery
What are the clinical features of hypercalcaemia?
History
Neuro: tiredness, acute confusion.
Urinary: polyuria, polydipsia, may be renal stones.
GIT: constipation, nausea.
Skeletal: pathological fractures (demineralisation).
Examination: signs of delirium, dehydration. Palpation: may be abdo tenderness.
NOTES Mnemonic for features of hypercalcaemia: ““stones, bones, and groans””.
What is Chvostek’s sign?
Contraction of ipsilateral facial muscles on tapping the facial nerve anterior to the ear.
What is Trousseau’s sign?
Carpopedal spasm after application of a tourniqet to occlude the pulse for 3 min.
NOTES A sign of hypocalcaemia.
What is the treatment for Graves eye disease?
- Conservative e.g. smoking cessation; dark glasses; artificial tears.
- Meds e.g. prednisolone, consider rituximab.
- Radiotherapy (uncertain benefit).
- Surgery (orbital decompression).
Hypertension and hypokalemia together
Primary hyperaldosteronism ***
Pretibial myxoedema
Graves disease
Acromegaly
Cushing’s syndrome
Chvostek sign
Hypocalcemia
Paget’s disease with cotton wool appearance
Myxoedema
Causes of hyperprolactinaemia
- Pituitary or hypothalamic tumour compressing stalk infiltration
- Pregnancy or breast feeding
- Co-secretion of prolactin in acromegaly
- Hypothyroidism
- Stress
- Renal failure
- Drugs
Pheochromocytoma investigations
Plasma-free metanephrines and normetanephrines
Abdominal CT
Pheochromocytoma complications
- Hypertensive crisis- elevated systolic blood pressure (> 200 mmHg) that is unresponsive to traditional treatment and threatens end-organ damage
- Myocardial Ischemia/Infarction
- Toxic myocarditis
- Cardiomyopathy
- Stroke
- Headache
Biggest cause of Addison’s disease in the developing world
TB
Signs of primary adrenal insufficiency
- Gradual onset
- Hypotension
- Hyperpigmentation
- Fatigue
- Musce weakness
- Weight loss
What might this be?
Sudden penetrating pain in the legs, lower back, or abdomen
Severe vomiting and diarrhea, resulting in dehydration
Low blood pressure
Syncope
Hypoglycemia
Confusion, psychosis, slurred speech
Severe lethargy
Hyponatremia
Hyperkalemia
Hypercalcemia
Convulsions
Fever
An Addisonian crisis
