Endocrine Flashcards

1
Q

Sheehan’s syndrome

A

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
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2
Q

Key issues in obesity management post op

A

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

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3
Q

How do you prescribe TPN?

A

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

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4
Q

Feeding in pancreatitis

A

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.

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5
Q

Treatment of thyrotoxic crisis and rationale

A

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
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6
Q

Drugs that affect thyroid -

A

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
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7
Q

Features of sick euthyroid syndrome

A

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
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8
Q

Why does hyperglycaemia occur in diabetes

A

Increased glucogenesis
increased glycogenolysis
reduced peripheral glucose utilization

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9
Q

Diagnostic criteria of DKA

A

Hyperglycaemia (BSL >14, usually, <44)
Acidosis (pH <7.3, bicarb <15)
ketosis

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10
Q

Diagnostic criteria of HHS (hyperosmolar hyperglycaemic state) and prominent features

A

BSl >33 (often >55)
arterial pH >7.3
no ketones
osmolality >320

Severe fluid deifcit (up to 10L)
Insulin rarely needed

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11
Q

Common triggers for HHS

A
alochol and drug abuse
anaesthesia
burns
GI haemorrahge
infections - MOST common
hypothermia
MI
pancreatitis
PE
intracranial event
medications - antiepileptics, antihypertensives, beta blockers, steroids, diurecitcs
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12
Q

fluid considerations in DKA/ HHS

A

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

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13
Q

targets of Mx in DKA, HHS

A
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

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14
Q

INsulin dose DKA/ HHS

A

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

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15
Q

K Mx in DKA

A

grossly K deficient
if K levels are low - indicates profound depletion
- should be replaced immediately, before insulin started

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16
Q

PO4 Mx in DKA

A

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

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17
Q

why is there a delay in pH normalising after ketones have gone in DKA

A

bicarb needs to be restored by renal or hepatic mechanisms

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18
Q

Complications of DKA

A

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

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19
Q

Poor outcome in HHS associated with

A

older age
lower BP
low Na, pH and bicarb
high urea levels (strongest association)

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20
Q

Pathophysiology of DKA

A

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
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21
Q

Precipitating factors for DKA

A

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
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22
Q

mechanisms of ketosis

A

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

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23
Q

Mechanism of ketone acidosis

A

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.)

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24
Q

Fluid regimen in DKA and HONK

A
  • 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.
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25
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.
26
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.
27
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 ```
28
Key distinction between DKA and HONK
in HONk, there is still enough insulin to overcome the ketogenic effects of glucagon.
29
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
30
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
31
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
32
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
33
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 ```
34
precipitants of thyroid crisis
stress infection surgery if radio iodine therapy institutated without patient being euthyroid first
35
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
36
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)
37
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
38
Non-thyroidal illness states that affect thyroid function
``` starvation sepsis bone marrow transplant surgery Mi psychiatric illness acute porphyria cushings ```
39
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
40
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
41
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 ```
42
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)
43
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)
44
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
45
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
46
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
47
What controls alodosterone secretion
angiotensin II extracellular K and Na levels ACTH (small influence)
48
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
49
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
50
effects of aldosterone
Na and water retention increases K secretion increased blood pressure
51
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)
52
net effects of ATII release
renal salt and water retention increased peripheral vascular resistance increased BP increased CO
53
Addisons
primary adrenal insufficiency - Autoimmune 80% cases - may also be due to - infections, haemorrhage (waterhouse-fredrickson), infacrction, infiltration (lymphoma, mets, scaroid), drugs, congenital
54
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
55
relative adrenal insufficiency
adrenal gland responds to stress, but magnitude isn't suitable
56
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
57
Classical blood findings in Addisons
HypoNa HyperK mild metabolic acidosis urea and creatinine elevated due to hypovolaemia hypoglycaemia can occur after prolonged fasting
58
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
59
Clinical features of cushings
``` central obestiy moon face buffalo hump proximal muscle wasting thin skin striae poor wound healing PUD HTN VTE DM depression ```
60
Hyperaldosteronism causes
Conn's syndrome Bilateral adrenal hyperplasia ectopic secretion - esp from renal, ovarian or adrenocorical carcinoma adenoma - renin-responsive aldoserone secreting
61
Action of aldosterone
acts on distal tubules to retain Na and water and exrete K and H ions Causes - - hyperNa - hypoK - metabolic alkalosis - HTN
62
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 ```
63
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)
64
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)
65
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
66
Steroids in head injury
CRASH trial 10,000 patients increased mortality at 14 days and 6/12, increased risk of severe disability
67
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
68
Steroids in pneumonia
may increase mortality in ICU (esp with influenza) SHOULD use in PJP and exac COPD
69
Steroids in meningitis
clear benefit esp in - - children with H influenzae - adults with pneumococcal
70
Side effects of steroid therapy
``` adrenal suppresion hypoK glucose intolerance truncal obesity myopathy mood alterations HTN PUD glaucoma hyperlipids aseptic necrosis of femoral head ```
71
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
72
investigation for phaeochromocytoma
plasma levels f free metanephrines 24hours urinary levels of fractionated metanephrines Metanephrines are produced continually , while catecholamines are produced episodically
73
treatment of phaeo
control of HTN - alpha blockade first, then beta blckers open adrenalectomy recurrence rate is upto 16% and so annual monitoring needed
74
thiamine deficiency diagnosis
levels of red cell transketolase
75
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
76
Laboratory features of hypothyroidism
``` Decreased T4 and T3 Increased TSH Hyperlipidaemia Hyponatremia Normochromic normocytic anaemia ```
77
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
78
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
79
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
80
stress induced hyperglycaemia
Transient hyperglycaemia during acute illness –usually restricted to patients without prior evidence of diabetes with reversion to normal after discharge.
81
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.
82
Implications of stress induced hyperglycaemia
Increased mortality Pro-inflammatory effects Increased susceptibility to infection
83
complications of phaeo
``` Malignancy •Death •Myocardial infarction •Arrhythmias •Seizures •Stroke ``` Discussion
84
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
85
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