Endocrine Flashcards
Sheehan’s syndrome
Ischaemic pituitary necrosis due to severe post-partum haemorrhage.
Pathophysiology -
Pituitary is increased in pregnancy and this puts it at increased risk
Vasospasm, thrombosis and vascular compression of hypophyseal arteries with an enlarged pituitary gland and DIC are possible factors.
Clinical effects -
- Vasopression stores are depleted, resulting in initial polyuria
- ACTH secretion decreases, resulting in hypoadrenalism, with lethargy and hyponatremia
- TSH secretion decreases, also resulting in lethargy and hyponatremia
- Prolactin secretion cannot increase, resulting in failed lactation
Key issues in obesity management post op
Avoidance of opiate excess
Mechanical ventilation for the morbidly obese patient
- The weight of the chest wall contributes to a decreased respiratory compliance
- A higher PEEP and Paw is the expected norm.
- Still, one should try to keep the Pplat under 35 cmH2O
Staged extubation - esp if patient DI
Extubation on to NIV
Logistics of mobilisation postural positioning and pressure area care
How do you prescribe TPN?
Usually the bag is about 2L
Carbohydrate: fat ratio: 70:30.
Protein is also required: 1.5-2g/kg/day
Fat is supplied as 10% lipid emulsion, at 1.1 kcal/ml
Carbohydrate is supplied as 50% dextrose, at 3.4 kcal/ml
Protein is supplied as 10% amino acid solution, as 100g/L
Feeding in pancreatitis
For mild or moderate pancreatitis:
Fast for the first 3-4 days
Advance to normal diet after this
Only progress to enteral nutrition of the patient has been fasted for 5-7 days
For severe pancreatitis:
EN is preferable to PN
Tube position does not matter (gastric vs jejunal)
Elemental feeds are preferred
Nutritional requirements are 25-35kcal/kg/day, and 1.2-1.5g/kg/day of protein
When to use parentral nutrition? These guidelines are much less prescriptive than previous statements. “when EN is contraindicated or not well tolerated”, they say.
Treatment of thyrotoxic crisis and rationale
Halt synthesis
- carbimazole or PTU
Halt release
- iodine - only used 30mins after PTU as may stimulate synthesis before
Blocking peripheral action
- beta blockers block peripheral conversion
- steroids also work
Drugs that affect thyroid -
Inhibit peripheral conversion of t4 to t3
- amioderone
- propranolol
- steroids
Suppress TSH secretion
- steroids
- opioids
- dopamine
- dobutamine
- octreotide
Stimulate TSH Release
- metoclopramide
- antipsychotics
Inhibit thyroid synthetic function (t3 t4 synthesis)
- thiouracils - propylthiouracil
- inidazoles - carbinazole
- lithium
- amioderone
- thalidomide
Stimulate thyroid synthetic function
- inorganic iodine
- iodinated contrast
- anioderone
Increased thyroid hormone binding (decreased levels)
- oesteo gens
- heroine
- methodone
Decease binding -> increased levels
- steroids
Clearance of T4 increased
- phenytoin
- carbazepine
- rifampicin
Features of sick euthyroid syndrome
Low serum levels of thyroid hormones in clinically euthyroid patients with nonthyroidal systemic illness
Treatment is of underlying illness - thyroid replacement not indicated
Due to dysregulation of normal hormonal feedback in critical illness
Low T3 High rT3 (biologically inactive) Low T3/rT3 ratio High or normal T4 (because there is reduced conversion of T4 -> T3) High or normal TSH
Why does hyperglycaemia occur in diabetes
Increased glucogenesis
increased glycogenolysis
reduced peripheral glucose utilization
Diagnostic criteria of DKA
Hyperglycaemia (BSL >14, usually, <44)
Acidosis (pH <7.3, bicarb <15)
ketosis
Diagnostic criteria of HHS (hyperosmolar hyperglycaemic state) and prominent features
BSl >33 (often >55)
arterial pH >7.3
no ketones
osmolality >320
Severe fluid deifcit (up to 10L)
Insulin rarely needed
Common triggers for HHS
alochol and drug abuse anaesthesia burns GI haemorrahge infections - MOST common hypothermia MI pancreatitis PE intracranial event medications - antiepileptics, antihypertensives, beta blockers, steroids, diurecitcs
fluid considerations in DKA/ HHS
fluid and Na depletion present in both
Fluid administration is a priority
- this will replete the intravascular volume, reduce BSL and the counter regulatory hormones (catacholamines, cortisol, growth hormone)
- once insulin started -> drives fluid into intracellular compartment and worsens hypovolaemia
Correct osmolality no faster than 3/hr
Need caution with Na (is higher than appears due to glucose)
Initially given N/saline (1l over an hour)
0.45% slaine is likley suitable to reduce risk of hypercl acidosis
once BSL <15 - start 5% dextrose
targets of Mx in DKA, HHS
raise bicarb by 3mmol/l/hr reduce BSL by 3mmol/l/hr reduce ketones (blood) by 0.5mmol/l/hr maintain normal K
If BSL not falling - consider inadequate fluid resus
INsulin dose DKA/ HHS
insulin dose - 0.1 - 0.15 u/kg/hr - 10% will have resistance and need higher doses
reduce to 0.02-0.05u/kg/hr when BSL <12 DKA, <14 HHS
K Mx in DKA
grossly K deficient
if K levels are low - indicates profound depletion
- should be replaced immediately, before insulin started
PO4 Mx in DKA
deficit of >1mmol/kg normal
shift is from cells with subsequent urinary loss
serum levels are typically normal
low PO4 rarely causes problems, but may ->
- muscle weakness
- haemolytic anaemia
- impaied cardiac function
Not routinely replaced (can -> hypocalcaemia)
Should replace if < 0.4
why is there a delay in pH normalising after ketones have gone in DKA
bicarb needs to be restored by renal or hepatic mechanisms
Complications of DKA
early - low or high BSL, low K, hyperchloraemic acidosis (10%), hypoxia, non cardiogenic pulmonary oedema, MI, cerebral oedema (seen in 1%, mainly children, mortality 25%, morbidity 25%)
Intermediate -
reversible critical illness motor syndrome (reversible tetraplagia - seen in HHS)
- DVT/PE - more freuqent with DKA, but significant cause of mortality in HHS
Late - movement disorder can persisit after recovery from HHS
- effects of neuroglycopenia (defiicent glucose for the brain) -> amnesia, optic atrophy
Poor outcome in HHS associated with
older age
lower BP
low Na, pH and bicarb
high urea levels (strongest association)
Pathophysiology of DKA
due to a marked deficiency of insulin in the face of high levels of hormones that oppose the effects of insulin, particularly glucagon.
Other hormones that antagonise insulin effects -
- cortisol
- oestrogen
- growth hormone
- catecholamines
Precipitating factors for DKA
Lack of Insulin
- New diagnosis of diabetes
- Poor treatment compliance
- Dietary mismanagement
Drugs which trigger DKA
- Corticosteroids
- Phenytoin
- Diuretics
- Catecholamine inotropes
- TPN
Physiological stress
- Infection
- Systemic inflammatory response
- Myocardial infarction
- Surgery
- Substance abuse
mechanisms of ketosis
Stress, which produces changes in the use of metabolic substrates:
- Increased glycogenolysis
- Increased gluconeogenesis
- Increased lipolysis (and thus ketogenesis)
Lack of insulin
Resistance to insulin
Mechanism of ketone acidosis
Ketones are acidic.The ketone bodies - with the exception of acetone - are well dissociated at physiological pH, and produce a nice excess of hydrogen ions. The result is a depletion of the buffering systems, and a drop in pH.
a lactic acidosis can develop in association with ketoacidosis.
excess of free fatty acids in the bloodstream, which are also acidic (but which do not contribute extesnively to the acidosis per se.)
Fluid regimen in DKA and HONK
- 15-20ml/kg in the first hour (and use colloid if they are shocked)
- 4-14ml/kg in the second hour (of 0.45% NaCl)
- 4-14ml/kg again in the third hour (use 0.9% NaCl if the sodium is low)
- When glucose is under 15mmol/L, Oh’s Manual recommends to start 5% dextrose 100-250ml/hr, as well as some other sort of sodium-containing fluid to prevent hyponatremia.
With this regimen, for a 70kg DKA/HONK patient, one ends up giving about 1.5-3L in the first 3 hours.
Advantages of N/saline in DKA
Isotonic saline is a cheap widely available fluid
Its high sodium content can promote the retention of fluid in the intravascular space
It is safe to use in most settings
Volume replacement will result in a more rapid resolution of ketoacidosis and lactic acidosis in DKA
Normal anion gap acidosis due to the extra chloride may be mild and transient
there is some evidence that lactate-containing solutions (eg. Harmanns) may delay the resolution of ketoacidosis and achievement of normoglycaemia by contributing substrate (lactate) for hepatic gluconeogenesis, and thus by contributing additional glucose to the already hyperglycaemic patient.
Disadvantages of saline in DKA
Normal anion gap metabolic acidosis may develop
Work of breathing may increase due to acidosis
Existing (already near-depleted) buffer systems may be further depleted by this NAGMA.
Causes of hypoglycaemia
Inadequate intake of carbohydrate (28%) Ingestion of alcohol (19%) Deliberate overdose of insulin (13%) Accidental overdose of insulin (6%) Strenuous exercise (7%)
Other causes - -Starvation - Hepatic failure - Cardiac failure - Renal failure - Sepsis - hypothyroidism - Adrenal insufficiency -Insulinoma - drugs - Insulin (duh) Glucagon Indomethacin Lithium ACE-inhibitors β-blockers Alcohol
Key distinction between DKA and HONK
in HONk, there is still enough insulin to overcome the ketogenic effects of glucagon.
Pathogenesis of HHS
Glucagon inhibits acetyl-CoA carboxylase, which normally converts acetyl-CoA into malonyl-CoA. Malonyl CoA inhibits acyl-carnitine synthesis; if this is uninhibited, it results in a stream of fatty acids being sucked up into the mitochondria to be converted into ketones.
-> a hyperglycaemic patient who remains reasonably asymptomatic because in them acidosis fails to develop (and thus, they are not short of breath).
They remain hyperglycaemic for some time.
As a result, they subject themselves to osmotic diuresis for a prolonged period, which allows them to become progressively more and more dehydrated.
The result is the hyperosmolar state which is usually associated with HONK.
This hyperosomolar hyperglycaemia is an intensely proinflammatory and prothrombotic state
Complications of HHS
HHS-specific physiological abnormalities
- Hypotension and shock
- Metabolic acidosis
- Coma
Complications arising from the HHS disease state:
- Cardiac arrest
- Cardiovascular collapse
- Myocardial infarction
- Pulmonray oedema
- Stroke
- Cerebral oedema and brain injury
- Venous thrombosis (DVT, PE)
- Aspiration
Complications of therapy for HHS:
- Dysnatraemia
- Hyperchloremia from saline administration.
- Phosphate depletion
- Hypokalemia
- Hypoglycaemia
Risk factors for cerebral oedema in HHS/DKA
Younger age (especially under 5’s)
Newly diagnosed diabetes
Severity of acidosis & hyperglycaemia
Severity of dehydration
Change in corrected [Na]
Speed of rehydration & correction of hyperglycaemia
Administration of bicarbonate
key issues with HHS Mx
Fluid resuscitation
Electrolyte replacement
Careful slow reduction of serum osmolality
Investigation for complications:
- Myocardial infarction
- Stroke
- Cerebral oedema and brain injury
- Venous thrombosis
Management of other possible precipitating causes:
- Infection, systemic inflammatory response
- Intracranial haemorrhage
- Hepatic encephalopathy
- Drugs, including illicit substances, steroids, phenytoin, diuretics, TPN, lithium
Causes of thyrotoxicosis
Graves disease - diffuse thyroid hyperplasia (85%) Exogenous thyroid hormone hyperfunctional multinodular goitre thyperfunctional adenoma of thyroid thyroiditis TSH secreting pituitary adenomas drugs
precipitants of thyroid crisis
stress
infection
surgery
if radio iodine therapy institutated without patient being euthyroid first
features of thyroid crisis
fever - most characteristic
CVS - initially HTN, then profound hypotension and shock
CNS - tremor, agitation, encephalopathy/coma
GI - D, N&V, may present with an acute abdomen, may have abnormal LFTs due to congestion (presence of jaundice = poor prognostic sign)
Respiratory considerations - dyspnoea common due to increased O2 consumption and CO2 production
lab findings in thyroid crisis
T3/T4 increased - levels do not correlate with severity
Hyperglycaemia
leucocytosis with left shift, even without infection
abnormal LFTs and increased bili
increase ca due to haemoconcentration
low K and Mg
serum cotrisol should be raised (if low, consider adrenal insufficiency)
Graves disease
- symtoms
- cause
Classical triad -
- hyperthyroidism
- infiltrative opthalmopathy
- pretibial myxoedema
An autoimmune disease caused by thyroid autoantibodies that bind to and stimulate the TSH receptor
Non-thyroidal illness states that affect thyroid function
starvation sepsis bone marrow transplant surgery Mi psychiatric illness acute porphyria cushings
cretinism
hypothyroidism developing in infancy or early childhood (usually secondary to inborn errors of metabolism)
-> impaired development of CNS and skeletal system
Have severe metnal retardation, short stature, coarse facial features, protruding tongue and umilical hernia
myxoedema
hypothyroidism developing in older child or adult
slowing of physical and mental activity
Symptoms -
- fatigue, apathy, mental sluggishness
- slowed speech and thought
- cold intolerant
- weight gain
- dry skin, brittle hair
- SOB and reduced exercise capacity
- oedema (myxoedema = non pitting oedema)
- tongue enlargement
precipitating factors of myxoedematous coma
infection cold environment burns stroke trauma chronic heart failure CO2 retention GI haemorrhage hypoglycaemia medications - amioderone, anaesthetic agents, beta blcokers, phenytoin, lithium
Benefits of giving T3 in severe hypothyroidism AND why it isn’t given
more biologically active
more rapid onset
bypasses the impaired de-iodination of T4 -> T3
Very expensive AND
if too much is given has been associated with increased mortality (therefore given T4 usually - allows a slow increase in T3)
treatment principles in myxoedema coma
thyroid hormone replacement
- usually levothyroxine 100-500mcg
steroid replacement
- hydrocortisone 100mg tds (take cortisol level first)
Supportive measures
- passive rewarming
- may need A/B support
- may need large doses of inotropes (beta adrenoceptor number reduced/ alpha preserved)
- Na usually corrects with thyroid replacement (is low)
Autoantibodies against thyroid antigens seen in Hashimotos thyroiditis
thyroglobulin
thyroid peroxidases
TSH receptor (blocks receptors - in Graves the receptor is stimulated by the antibody)
iodine transporter
Causes of iatrogenic hypothyroidism
thyroidectomy(2-4 weeks after therapy) radioiodine treatment (months-years after therapy) radiation therapy to thyroid Drugs - - lithium - aioderone
Patients taking thyroxine may become hypothyroid again with the following drugs -
- phenyoin
- amioderone
De Quervain thyroiditis
subacute thyroiditis
due to a viral infection (usually an urti)
- triggers the formation of autoimmune cytotoxic T cells, which damage the thyroid follicular cells
Is self limited
Presents with pain in the neck, which may radiate to the upper neck/jaw/throat/ears
HYperthyroid for 2-6 weeks, then hypothyroid 2-8 weeks
What controls alodosterone secretion
angiotensin II
extracellular K and Na levels
ACTH (small influence)
Actions of cortisol
needed for synthesis of adrenergic receptors
CVS - increases BP by direct action on smooth muscle and via renal mechanisms
Renal - increase in GFR, Na retention and K loss
Stimulate lipolysis
Muscle - protein catabolism, reduced glucose uptake, increased beta oxidation of fatty acids
Liver - stimulates gluconeogensis, glycogenolysis and synthesis of plasma proteins
- overall - increases blood glucose and FFA in blood
Immune -
- reduces capillary permeability, reduces leukocyte migratin, t cell proliferation and phagocytosis, reduces cytokine release
GI - decreased PG synthesis = increased ulcer risk
Bone - increased osteoclastic activity
aldosterone vs cortisol
aldosterone = primary mineralocorticoid secreted by adrenal glands
Cortisol has 1/400 the potenency of mineralocorticoid action BUT is 1000x more concentrated in the plasma
effects of aldosterone
Na and water retention
increases K secretion
increased blood pressure
actions of angiotensin II
direct vasocontriction
stimulates aldosterone release from adrenal cortex
increase thirst and ADH secretion
potentiates the release of norad from post-ganglionic sympathetic fibres
increase Na reabsorption (direct effect on kidney)
net effects of ATII release
renal salt and water retention
increased peripheral vascular resistance
increased BP
increased CO
Addisons
primary adrenal insufficiency
- Autoimmune 80% cases
- may also be due to - infections, haemorrhage (waterhouse-fredrickson), infacrction, infiltration (lymphoma, mets, scaroid), drugs, congenital
Secondary adrenal insufficiecy
similar features to addisons, but no hyperpigmentation as ACTH not increased
- most common cause is cessation of exogenous glucocorticoids
- other causes - pituitary surgery, pituitary infacrtion (sheehan syndrome) and pituitary tumour
relative adrenal insufficiency
adrenal gland responds to stress, but magnitude isn’t suitable
Clinical presentation of addisonian crisis
undifferentiated shock, not responding to standard Mx
abdo pain may occur and -> mis diagnosis of acute surgical abdomen
suggestive features -
- hyperpigmentation
- hypoNa
- hyperK
- eosinophilia
Classical blood findings in Addisons
HypoNa
HyperK
mild metabolic acidosis
urea and creatinine elevated due to hypovolaemia
hypoglycaemia can occur after prolonged fasting
Cushing syndrome - types
- constellation of symptoms caused by several diseases
- most common cause is due to iatrogenic steroid therapy
ACTH dependent -
- high ACTH
- cushings disease
- ectopic secretion of ACTH
ACTH independent -
- iatrogenic
- adrenal adenoma
- bilateral adrenal hyperplasia
- McCunue-Albright syndrome
Clinical features of cushings
central obestiy moon face buffalo hump proximal muscle wasting thin skin striae poor wound healing PUD HTN VTE DM depression
Hyperaldosteronism causes
Conn’s syndrome
Bilateral adrenal hyperplasia
ectopic secretion - esp from renal, ovarian or adrenocorical carcinoma
adenoma - renin-responsive aldoserone secreting
Action of aldosterone
acts on distal tubules to retain Na and water and exrete K and H ions
Causes -
- hyperNa
- hypoK
- metabolic alkalosis
- HTN
Recognised indications for steroids in ICU
Addisonian crisis Anaphylacis asthma/COPD with resp failure PCP pneumonia bacterial meningitis Croup hypercalcaemia fulminant vasculitis idiopthic thromboyctopaenic purpura Myasthenic crisis myxoedema coma organ transplant thyroid storm
potential benefits of glucocorticoid therapy in critically ill
anti-inflammatory effects decreased cytokine production inhibition of arachidonic acid synthesis improved vascular tone improved catecholamine responsiveness
Also - a proportion of critically ill patients have
- relative adrenal insufficiency OR
- acquired glucocorticoid resistance (as high as 60% in septic shock)
Steroids in septic shock
Why they may be helpful -
- oppose systemic inflammation
- induce Na retention -> increased intravascular volume
- reduce production of nitric oxide synthetase and COX -> reduced systemic vasodilatation
- increase sensitivity of alpha 1 receptors
- pre treatment of cardiac muscle protects against sepsis induced cardiomyopathy
Studies -
French study in 2002: improved mortality (severe sepsis, mortality ~ 70%)
CORTICUS: no improvement in mortality (“mild” sepsis)
Disagreement among meta-analysis authors (Annane vs Sligl)
Supported by the Surviving Sepsis Guidelines (GRADE 2B)
Steroids in spinal injury
NASCIS II and III - looked at high dose steroids
Methylpred may have a role in early spinal cord injury
well designed RCT needed
Steroids in head injury
CRASH trial
10,000 patients
increased mortality at 14 days and 6/12, increased risk of severe disability
Steroids in ARDS
confilciting
Pros - earlier vent wean, imporved arterial oxygenation and increased resp compliance
Cons - higher rate of return to assisted ventilation and neuromusc weaknss
No overall mortality benefit
Steroids in pneumonia
may increase mortality in ICU (esp with influenza)
SHOULD use in PJP and exac COPD
Steroids in meningitis
clear benefit esp in -
- children with H influenzae
- adults with pneumococcal
Side effects of steroid therapy
adrenal suppresion hypoK glucose intolerance truncal obesity myopathy mood alterations HTN PUD glaucoma hyperlipids aseptic necrosis of femoral head
Clinical features of phaeochromocytoma
paroxysms of
- headahce
- sweating
- palpitations
- flushing
- anxiety or panic attacks
HTN - may be paroxysmal or sustained
- accompanied by secondary volume depletion -> large postural drop
investigation for phaeochromocytoma
plasma levels f free metanephrines
24hours urinary levels of fractionated metanephrines
Metanephrines are produced continually , while catecholamines are produced episodically
treatment of phaeo
control of HTN
- alpha blockade first, then beta blckers
open adrenalectomy
recurrence rate is upto 16% and so annual monitoring needed
thiamine deficiency diagnosis
levels of red cell transketolase
Causes of hyperglycaemia in ICU
Insulin resistance
- NIDDM
- Stress response
- Corticosteroid therapy
- Cushings disease
Inadequate insulin levels
- Under-supplemented
- Stress response
- Pancreatitis
- Haemochromatosis
- Insulin antibodies
Excessive endogenous glucose release
- Catecholamine infusion
- Stress response
- Glucagon administration
Excessive exogenous glucose supplements
- TPN with 50% dextrose
- Inappropriately sugary IV fluids
- Overfeeding with enteric nutrition
- Glucose-containing peritoneal dialysis fluid
Laboratory features of hypothyroidism
Decreased T4 and T3 Increased TSH Hyperlipidaemia Hyponatremia Normochromic normocytic anaemia
ICU management of hypothyroidism
Specific -
replacement of thyroid hormone (usually as T4 50 – 200 mcg/day).
Elderly, especially with heart disease require a more gradual introduction (eg. 25 mcg).
Intravenous T3 (5-20mcg initially) may also be used in the treatment of myxoedema coma.
Other treatment -
- need for intubation in the context of a decreased level of consciousness
- supportive care (ventilation, fluid and electrolyte management, temperature control)
- corticosteroids (eg. hydrocortisone 100 mg tds) in severe cases until adrenal insufficiency excluded.
To also consider -
delay in weaning from ventilation due to untreated hypothyroidism
increased sensitivity to sedating agents
decreased sensitivity to inotropes and vasopressors
Causes of adrenal insufficiency
Vascular aetiologies
- Infarction due to arterial embolism
- Infarction due to AAA
- Postpartum pituitary necrosis
Infection
- Sepsis
- Tuberculosis
- Histoplasmosis
- Cytomegalovirus
- Coccidiomycosis
- Menigococcal sepsis, purpura fulminans
- HIV
Neoplastic invasion
- Renal cell carcinoma
- Adrenal carcinoma
- Breast carcinoma
- Lung (NSCLC)
- Malignant melanoma
- Pituitary tumour
Drugs
- Corticosteroid withdrawal
- Etomidate (causes primary adrenal insufficiency)
- Azole antifungals - Fluconazole, ketoconazole
- Rifampicin (increases steroid metabolism)
- Phenytoin (increases steroid metabolism)
Infiltrative systemic disease
- Amyloid
- Sarcoidosis
- Haemochromatosis
Congential causes
- Adrenal dysgenesis
- Impaired steroidogenesis
Autoimmune destruction
- Addisons’s disease
Traumatic destruction
- Trauma is a major cause of adrenal insufficiency
Environmental factors
- Hypothermia
Causes of raised plasma catecholamine levels
Malignancy
- Phaeochromocytoma (adrenaline)
- Neuroblastoma (DOPA)
- Malignant melanoma (DOPA)
- Menke’s disease (dopamine)
Decreased clearance
- MAO A/B inhibition
- Altered COMT activity
- Tricyclic antidepresant use
- Hepatic insufficiency
Autonomic nervous system
- Normal stress response
- Asphyxiation
- Morbid obesity
- Hypoglycaemia
- Intracranial haemorrhage (eg. SAH)
- Acute clonidine withdrawal
Spurious results
- Anti-parkinsonian medications
- Amphetamine use
- Methyldopa
stress induced hyperglycaemia
Transient hyperglycaemia during acute illness –usually restricted to patients without prior evidence of diabetes with reversion to normal after discharge.
Mechanisms of stress induced hyperglycaemia
Increased glucose synthesis is due to the following mechanisms:
Increased lipolysis due to catecholamine activity
Increased gluconeogenesis due to catecholamine activity
Increased glycogenolysis due to catecholamine activity
Increased insulin resistance is due to the decreased sensitivity of skeletal muscle to insulin, via the effects of the following hormones:
- Catecholamines
- Growth hormone
- Cortisol
- TNF-α
Additional effects are the direct inhibition of insulin release by adrenaline, and the activation of hepatic glycolysis by glucagon.
Implications of stress induced hyperglycaemia
Increased mortality
Pro-inflammatory effects
Increased susceptibility to infection
complications of phaeo
Malignancy •Death •Myocardial infarction •Arrhythmias •Seizures •Stroke
Discussion
management of phaeo
Attention to the airway, oxygenation and ventilation
Control of hypertension
- Rapidly acting alpha-1 antagonist: phentolamine
- Slowly acting non-competitive alpha-1 antagonist: phenoxybenzamine
- Beta-antagonist
Maintenance of circulating volume in the face of vasodilation:
- IV fluid replacement
Control of AF
- Verapimil, diltiazem, or amiodarone
Assessment of myocardial damage
- ECG
- TTE
- CK and troponin
Carcinoid syndrome
- features and Dx
slowly growing neuroendocrine tumours of upper GI origin
facial flushing AND right heart valve damage (effect of the vasoactive substances secreted by the tumour on the myocardium, resulting in fibrotic changes) is pathognomonic
Diagnosed with -
- 24 hour urinary HIAA (5-hydroxyindoleacetic acid) OR Serum chromogranin-A
