Critical care endocrine Flashcards by Eliot Carrington-windo

What do blood tests show in addisons?

Low sodium
High potassium
High ACTH
Low cortisol

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How would you confirm diagnosis of addison’s?

Short synacthen test
Synacthen (ACTH analogue) normally causes increase in cortisol
Does not occur in addison’s

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How would you manage hypotensive pt with suspected addison’s?

Resuscitate according to CCRISP protocol
15L O2
IV access, bloods (FBC, U+E, CRP, ACTH, Cortisol–> if possible before starting tx
IVI
IV hydrocortisone
Monitor blood glucose

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What are the causes of addison’s disease?

Addison’s disease
-Congenital adrenal hyperplasia
-autoimmune adrenalitis

Addisonian crisis
-Iatrogenic (e.g. withdrawal high dose steroids)
-Surgery
-Trauma
-Infection

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Describe layers of adrenal gland and function

Zona glomerulosa (mineralocorticoids–> aldosterone)
Zona reticularis (glucocorticoids –> cortisol)
Zona fasciculata (oestrogens and androgens –> oestriol, progesterone, testosterone)

Medulla (catecholamines–> adrenaline)

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Where is ACTH released from?

Anterior pituitary

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What is addison’s disease?

-Also known as primary adrenal insufficiency
-Characterised by inadequate production of aldosterone and cortisol by two outer layers adrenal cortex

Addison’s disease, also known as primary adrenal insufficiency,[4] is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands (adrenal cortex), causing adrenal insufficiency
-Addison’s refers specifically to primary adrenal insufficiency rather than iatrogenic

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What hormones are produced by pituitary?

Anterior: growth hormone, ACTH, TSH, FSH, LH, prolactin

Intermediate lobe: MSH (melanocyte stimulating hormone)

Posteiror: ADH, oxytocin

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Describe actions of glucocorticoids:

Cardiovascular:
–> increases myocardial contractility
–> increases vasoconstriction

Immune system
–> antiinflammatory
–> immunosuppressive

Metabolism:
–Increases gluconeogenesis and glycogenolysis during fasting
-Increases glycogen storage during feeding

Bones
–Increases bone resorption and risk of fracture

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Pituitary axis for cortisol and thyroid hormone

Hypothalamus –> Pituitary –> adrenal cortex
CRH –> ACTH –> cortisol
TRH–> TSH –> T3, T4

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What would be your differential for pathological fracture with hypercalcaemia?

-Hypercalcaemia secondary to hyperparathyroidism
-metastases
-Multiple myeloma

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Which cells release PTH?

Chief cells within parathyroid gland

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What are the actions of PTH?

Kidney:
–> Increased calcium absorption in distal tubule
–> Decreased phosphate absorption in proximal and distal tubule
–> Increased 1 alpha hydroxylase, causing production 1,25 dihydroxyvitamin D: increased calcium resorption in small intestine

Bone:
–> increased action of osteoclasts: increased release of calcium and phosphate from bone

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What is primary hyperparathyroidism?

-Excess parathyroid production by parathyroid gland
-May be due to adenoma or carcinoma
-PTH produced regardless of calcium level

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What is secondary hyperparathyroidism?

-Excess PTH production in response to low calcium state e.g. renal failure
-PTH production in response to low ca

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What is tertiary hyperparathyroidism

-Caused by hyperplasia parathyroid gland following secondary hyperparathyroid
-PTH produced in response to normal ca

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What are functions of calcium

-Bone formation and maintenance
-Muscle contraction

-Any process involving exocytosis
-cofactor for certain clotting factors
-Regulation of intracellular proteins

Why can you have temporary hypocalcaemia following parathyroidectomy for hyperparathyroid?

-‘hungry bone disease’
-Excess PTH causes leaching of calcium from bone
-When stimulus removed bone ‘mops up’ excess calcium, leading to temporary hypocalcaemia

Describe symptoms high calcium

Stones, bones, moans, thrones, muscle tone
-Kidney stones
-Bone pain
-Abdominal pain
-Constipation and excessive urination
-Muscle weakness

Also
-Dehydration
-Vomiting
-Renal failure
-Dro

Symptoms low calcium

“CATs go numb”
-convulsions
arrhythmias
-tetany
-numbness in the hands and feet and around the mouth

What are the causes hypercalcaemia

Hypercalcaemia of malignancy
Multiple myeloma
Hyperparathyroid

Familial Hypocalcuric hypercalcaemia
Paget’s disease
Sarcoidosis

What would you get on hypercalcaemia vs hypocalcaemia ecg?

Hyper: u have no pot and no t but a long pr and short qt

Shortened qt

Hypo

U have no pot and no t but a long pr and qut

U wave
T wave inversion
Long PR
Long QT

Describe DKA

-Breakdown of fatty acids due to lack of insulin
-Causes production of ketone bodies
-Produces triad of hyperglycaemia, acidosis and ketosis

Describe management of DKA

-Manage according to ccrisp protocols
-fixed rate insulin infusion (0.1 unit/kg/hr)
-Give IVI
-Hourly monitoring of blood glucose and ketones
-Regular monitoring electrolytes and ph
-Monitor conscious level (deterioration may be sign of co2 rise or cerebral oedema)
-VTE prophylaxis
-Contact diabetes team

What are causes DKA?

Sepsis Surgery MI stress (e.g. trauma) Non compliance with insulin therapy

How would you manage pt with T1 diabetes in pre, perioperative and post operative setting?

Pre op: First on list, VRII from midnight if missing >1 meal, regular monitoring BMs Intra op: Continue VRII, regular monitoring BMs, Post op: regular monitoring BMs, continue VRII until eating and drinking normally

What are the functions of pancreas?

Exocrine: proteolytic, lipolytic enzymes and amylase Endocrine: secrete insulin, glucagon, somatostatin

Where are endocrine hormones produced in pancreas?

4 types of islets of langerhans -Beta cells: insulin -Alpha cells: glucagon -Delta cells: somatostatin -gamma cells: pancreatic polypeptide

What is addison's disease?

-primary adrenal insufficiency -Characterised by inadquate production of cortisol and aldosterone by two outer layers adrenal cortex Addison's disease, also known as primary adrenal insufficiency,[4] is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands (adrenal cortex), causing adrenal insufficiency

What are the features of myxoedema coma?

-Altered mental state/coma -Hypothermia -Bradycardia -Hypoglycaemia

What are the causes of myxoedema coma?

Undiagnosed hypothyroidism Failure to comply with regular levothyroxine

How do patient's with hypothyroidism present?

Symptoms -Weight gain -Cold intolerance -Decreased appetite -Constipation -Depression -Fatigue Signs -Bradycardia -Dry skin -Loss of outer 1/3rd of eyebrow

What would you find on examination in hypothyroidism?

Bradycardia Slowed reflexes Goitre Dry skin Loss outer 1/3rd eyebrow

Describe anatomy of thyroid gland

Structure -2 lobes with isthmus overlying 2nd-4th tracheal rings -Each lobe is 5-6cm in length, 2.5-3cm in width. C5-T1 vertebral levels -Surrounded by pretracheal fascia Blood supply -Superior thyroid artery, branch of external carotid -Inferior thyroid, branch of thyrocervical trunk -Occasionally thyroid IMA from brachiocephalic trunk or aortic arch Venous drainage: -Superior and middle thyroid veins --> drain to internal jugular vein -Inferior thyroid vein --> drains to brachiocephalic vein

Name hormones produced by thyroid gland:

-Thyroxine -Tri-iodothyronine -Calcitonin

Describe mechanism of action of thyroxine and tri-iodothyronine

Metabolic -Increased basal metabolic rate -Increased protein catabolism -Increased glycogenolysis Cardiac -Increased heart rate (increased sensitivity of beta receptors to catecholamines) -Increased cardiac output CNS: -enhances sympathetic activity -Aids development of CNS GI: -Increased glucose absorption from GI tract -Increased GI motility -Increased GI secretions

Describe mechanism of action of calcitonin

Inhibits calcium release from bone when serum calcium is high

Where is calcitonin produced?

Parafollicular C cells of thyroid

Which type of thyroid ca produces calcitonin?

Medullary thyroid carcinoma

Where is TSH released from?

Anterior pituitary

Where is TRH released from? What is its function?

-Hypothalamus -TRH stimulates anterior pituitary to release thyroid stimulating hormone and prolactin

How are thyroid hormones synthesised?

-Iodide absorbed into follicular cell--> iodine by thyroid peroxidase -Iodine + thyroglobulin out, combined with tyrosine--> iodotyrosine or diiodotyrosine -iodotyrosine/diiodotyosine in: T3 and T4 out -Iodide is absorbed form plasma into thyroid follicular cell where it is converted to iodine by thyroid peroxidase -Iodine secreted from thyroid follicular cell with thyroglobulin is combined with tyrosine to form iodotyrosine or di-iodotyrosine -Iodotyrosine/di-iodotyrosine is transported back into thyroid follicular cell -Two di-iodotyrosines or one di-iodotyrosine and one iodotyrosine to form T3 and T4 respectively -T3 and T4 are secreted into bloodstream and transported bound to proteins