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
