Endocrine

First- Fifth

Everything you need to know ever about

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ENDOCRINOLOGY

index

8. Insulin

1. Growth Hormone

9. Androgens

2. ACTH

index

3. RAAS

4. Cortisol

5. ADH

6. TSH

7. PTH

Equal and opposite

- Cause and effect- Normal, high or low - Primary, secondary or tertiary - Not just hormones but electrolytes and sugars too - Loss of feedback

Foreword

Brain

Hypothalamus

Your hypothalamus, a structure deep in your brain, acts as your body's smart control coordinating center. Its main function is to keep your body in homeostasis. It does its job by directly influencing your autonomic nervous system or by managing hormones.

Hypothalamus

Found in the sphenoid process in the cavornous sius. Connected to the hypothalamus via the pituitary stalk

Anterior

Endocrine Tissue

Stimulated by hormones from the hypothalamusEndoncrine hormones:o Growth hormone: o Thyroid Stimulating Hormone (TSH) o Adrenocorticotrphic Hormone (ACTH) o Prolactin o LH/FSH

Pituitary

Posterior

Neuro tissue

Stimulated by impulses from the hypothalamusNeurohypophyseal hormones: o Oxytocin (OT): stimulates smooth muscles. o Anti-diuretic hormone (ADH) (aka Vasopressin).

Growth Hormone

SOMATOTROPIN Axis

the secretion of growth hormone (GH; somatotropin) from the somatotropes of the pituitary gland into the circulation and the subsequent stimulation of insulin-like growth factor 1 (IGF-1; somatomedin-1) production by GH in tissues such as, namely, the liver

Hormones

+ Info

TOO MUCH

GIGANTISM

ACROMEGALY

Adult pituitary adenoma secreting growth hormone, causeing excessive height, sweating, pressure on nerves (e.g. carpal tunnel syndrome), muscle weakness, excess sex hormone-binding globulin (SHBG), insulin resistance or even a rare form of type 2 diabetes, and reduced sexual function.

Childhood pituitary adenoma secreting growth hormone, causing excessive height

Pathology

TESTS

Oral glucosetolerence test Glucose should suppress growth hormone levels and Serum IGF-1

TOO LITTLE

PITUITARY DWARFISM

LARON SYNDROME

Laron syndrome, also known as growth hormone insensitivity or growth hormone receptor deficiency (GHRD), is an autosomal recessive disorder characterized by a lack of insulin-like growth factor due to a lack of sensitivity to Growth hormone

Growth hormone deficiency (GHD), also known as dwarfism or pituitary dwarfism, Children with GHD have abnormally short stature (below the 5th percentile) with normal body proportions. GHD can be present at birth (congenital) or develop later (acquired).

Pathology

TESTS

Measure serum growth hormone and 1-GLP

Adrenocorticotropic

Hypothalamic-Pituitary-Adrenal Axis

Increased production and release of cortisol and androgens by the cortex and medulla of the adrenal gland, respectively. ACTH is also related to the circadian rhythm in many organisms.ACTH and β-lipotropin are secreted from corticotropic cells. Causes the release of Cortisol and Aldosterone

Hormones

+ Info

RAAS SYTEM

RENIN ANTIOTENSIS ALDOSTERONE SYSTEM

Hormones

TOO MUCH

CUSHING'S

Too much Cortisol from the adrenal cortexCaused by steroid overuse or adenomas

TESTS

Pathology

Dexamethasone suppression test is used to test if cortisol production decreases with dexamethasone. Can be High dose or low dose.Cushing's syndrome caused by adrenal tumor Low dose: no change High dose: no change Cushing's Syndrome caused by pituitary tumor (Cushing's Disease) Low dose: no change High dose: normal suppression Cushing's syndrome related to ectopic ACTH-producing tumor Low dose: no change High dose: no change

TREATMENT

for ACTH-secreting adenomas, medical therapy may include cortisol synthesis inhibitors (e.g., ketoconazole, metyrapone) and neuromodulators transsphenoidal surgery the primary treatment for most pituitary adenomas is transsphenoidal surgery,

TOO MUCH

CONN'S

Too much Aldosterone from the adrenal cortex

TESTS

Pathology

Plasma aldosterone: renin ratio blood tests are used in the diagnosis of primary aldosteronism. This is a useful test in patients who present with hypertension, hypokalaemia, polyuria and polydipsia. Primary hyperaldosteronism - caused by a tumor is most often treated by removing the adrenal gland (unilateral adrenalectomy). Secondary hyperaldosteronism - is most often treated with drugs Bilateral hyperplasia is treated with diuretics (water pills), which help manage fluid buildup in the body

TOO MUCH

TESTS

PHEOCHROMOCYTOMIA

24-hour urine test. positive if the catecholamine levels exceed two times the upper limit of normal Clonidine suppression tests are second-line investigations to consider in pheochromocytoma. It involves the administration of clonidine to suppress catecholamine production - in pheochromocytoma, levels remain elevated.

Too much Adrenaline- Pheochromocytoma is a type of neuroendocrine tumor that grows from cells called chromaffin cells. High blood pressure Headache Heavy sweating Rapid heartbeat Tremors Pallor Shortness of breath Panic attack-type symptoms

Pathology

TREATMENT

The primary treatment for a pheochromocytoma is surgery to remove the tumor.The patient must first however be stabilized with medical management: alpha-blocker (e.g. phenoxybenzamine), given before a beta-blocker (e.g. propranolol)

TOO LITTLE

PRIMARY ADRENAL INSUFFICIENCY - ADDISONS

SECONDARY ARENAL INSUFFICIENCY

Suppressed production of ACTH due to an impairment of the pituitary gland or hypothalamus by a Tumour or ischeamia. Similar to primary but no ACTH

The adrenal glands don’t make enough cortisol and aldosterone

• Hyponatremia
• Hyperkalaemia
• Hypotension

Treatment: give hydrocortisone and flucortisone to replace the missing hormones (2:1:1 dose to mimic Circadian rhythm), double hydrocortison with sick.

Pathology

TESTS

Tests for adrenal insufficiency primarily involve measuring cortisol levels, both at baseline and after stimulation, and may include imaging studies to assess the adrenal glands and pituitary gland. The most common test is the ACTH stimulation test (Synacthen test), which evaluates the adrenal glands' ability to produce cortisol in response to synthetic ACTH.

Anti-Diuretic Hormone

Posterior Pituitary

Increases water reabsorption, concentrates urine, by activating Aquaporins in the collecting tubule.Released in response to a increase in blood plasma osmolality. Maintains blood volume and electrolyte concentration

Hormones

TOO MUCH

Syndrome of Inappropriate ADH

Too much ADH so massive water retation causing systemic dilution - hyponatremia Caused by Neurological - hypothalamus, Paraneoplastic tumours or medications - SSRIs Treat with restriction of fluid intake, using salt tablets (sometimes with diuretics), urea supplements, or increasing the protein intake.[2] The vasopressin receptor 2 blocker tolvaptan may also be used.

Pathology

TESTS

Urea & electrolytes: serum sodium is low in SIADH (<130 mmol/L). Plasma osmolality: reduced in SIADH (due to low serum sodium). Urine is concentrated with high sodium.

TOO LITTLE

DIABETES INSIPIDUS

Neurogenic diabetes insipidusPituitary doesn't produce ADH due to damage the hypothalamus or posterior pituitary Nephrogenic diabetes insipidus The kidney becomes insennsitive to ADH Can be caused by lithium Dipsogenic diabetes insipidus Occurs as a result of hypothalamic disease or trauma resulting in loss of thrist regulation so the patient is always thirsty

Diabetes insipidus (DI) is a disease characterised by the passage of large volumes (>3L/24hrs) of dilute urine (osmolality <300 mOsmol/Kg)Hypernatremia is common Excessive urination (>3L/24hrs) Excessive thirst (especially for ice-cold water) Nocturia Dehydration – headache/dizziness/dry mouth Give desmopressin and mesure serum osmolality

Pathology

TESTS

The patient is deprived of fluids for up to eight hours or 5% loss of body weight, following which desmopressin is given and then osmolality is taken 8 hours later

Diabetes Insipidus

What is what?

situation

THYROID STIMULATING

Hypothamic - Pituitary - Thyroid Axis

The hypothalamus release thyroid-releasing hormone (TRH). This causes thyrotrope cells in the anterior pituitary to release thyroid-stimulating hormone (TSH). The thyroid responds to the TSH by releasing T4 and T3. T4 inhibits the pituitary and hypothalamus in a negative feedback loop. The thyroid maintains metabolic action Normal: Thyroid function tests (TFTs) TSH (0.4 – 4 mU/L) Free T4 (9 – 25 pmol/L) Free T3 (3.5 – 7.8 nmol/L)

Hormones

TOO MUCH

SECONDARY HYPERTHYROIDISM

PRIMARY HYPERTHYROIDISM

Too much action by the Pituitary overproducing TSH and therefore T3 and T4.

• TSH-secreting tumour
• Chorionic-gonadotropin secreting tumours (hCG secreting)
• Thyroid hormone resistance: TSH is resistant to T3/T4 negative feedback.

Too much action by the Thyroid overproducing T3 and T4, TSH is low in response.

• Graves’ disease (75% of all cases)
• Toxic multinodular goitre
• Toxic adenoma
• Iodine-induced (rare)
• Trophoblastic tumour (very rare)

Pathology

TESTS

Testing TSH, T3 and T4

TOO LITTLE

SECONDARY HYPOTHYROIDISM

PRIMARY HYPOTHYROIDISM

Too little action by the Pituitary underproducing TSH and therefore T3 and T4.Pituitary of hypothalmic tumor

Too little action by the Thyroid overproducing T3 and T4, TSH is high in response.

• Autoimmune thyroiditis (Hashimoto's)
• iodine deficiency

Pathology

Hypometabolic state, pretibial myxoedemaPeaches and cream complexion

SUB-ACUTE THYROIDITIS

DE QUERVAIN'S THYROIDITIS

Viral Illness De Quervain’s thyroiditis is believed to be caused by a viral infection and the inflammatory process associated Acute Phase - Hyperthyroid Fever, heat intolerance Anxiety Euthyroid Phase - Normal Hypothyroid Phase Fatigue, Dry skin, Swollen eyes, Intolerance to cold Constipation

Inflammation of the thyroid characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by a return to euthyroidism

Pathology

TREATMENT

hyperthyroid (thyrotoxic) phase 1ST LINE – supportive care with thyroid pain and tenderness PLUS –analgesic or corticosteroid with tachycardia or anxiety or tremor PLUS –beta-blocker or calcium-channel blocker with severe thyrotoxicosis PLUS –potassium iodide plus prednisolone hypothyroid phase 1ST LINE – observation and regular reassessment CONSIDER –levothyroxine

EUTHYROID SICK SYNDROME

EUTHYROID PATIENTS

Euthyroid sick syndrome is a condition in which serum levels of thyroid hormones are low in patients who have nonthyroidal systemic illness but who are actually euthyroid. Diagnosis is based on excluding hypothyroidism. Treatment is directed toward the underlying illness; thyroid hormone replacement is not indicated.

Pathology

PARATHYROID HORMONE

Parathyroid

Controls Calcium and Phosphate metabolism Calcium concentration = PTH MODULATION This is mediated by a calcium sensing receptor (CaR) on the surface of the parathyroid. (small changes in calcium => large changes in PTH). Low calcium more PTH Secreted Magnesium is needed for PTH secretion, Low Magnesiummore PTH Secreted High levels of phosphate in the blood will increase the complexed fraction of calcium causing hypocalcemia High Phosphate more PTH Secreted

Hormones

TOO MUCH

• Too much PTH, so high phosphate, low calcium and low magnesium
• Weak bones that break easily (osteoporosis)
• Kidney stones
• Excessive urination
• Stomach (abdominal) pain
• Tiring easily or weakness
• Depression or forgetfulness
• Bone and joint pain
• Frequent complaints of illness with no clear cause
• Nausea, vomiting or loss of appetite

HYPERPARATHYROIDISM

Pathology

TESTS

Measure Calcium and PTH to determine type Is it a Production or a Detection issue?

TOO MUCH

SECONDARY HYPERPARATHYROIDISM

PRIMARY HYPERPARATHYROIDISM

Parathyroid issue A noncancerous adenoma, this is the most common cause. Two or more parathyroid glands hyperplasia Radiation treatment to the neck area. Inherited conditions, such as multiple endocrine neoplasia type 1. Cancer of a parathyroid gland (rare).

A kidney issueSecondary hyperparathyroidism is when the glands are fine but a condition, like kidney failure, lowers calcium levels and causes the body to react by producing extra parathyroid hormone.

Pathology

TREAT

Cinacalcet - signaling the parathyroid glands to produce less PTH. intended for secondary hyperparathyroidismBisphosphonates. HRT in postmenopausal women Removeal of growths/treating the underlying disorder

TOO LITTLE

• A tingling sensation (paraesthesia) in fingertips, toes and lips
• Twitching facial muscles
• Muscle pains or cramps,
• Mood changes, such as feeling irritable, anxious or depressed
• Dry, rough skin
• Coarse hair that breaks easily and can fall out
• Fingernails that break easily

HYPOPARATHYROIDISM

• low parathyroid hormone levels
• low calcium levels
• high phosphorus levels

The most common cause of hypoparathyroidism is removal of or accidental injury to the parathyroid glands during surgery to the neck. Other causes include: Autoimmune conditions, – such as Addison's disease and pernicious anaemia Being born without parathyroid glands or with glands that don't work properly – DiGeorge syndrome can have underdeveloped parathyroid glands Radiotherapy to treat throat or neck cancer Low blood magnesium levels – for example, because of alcohol misuse

Pathology

TREAT

Calcium supplements

INSULIN AND GLUCAGON

Blood Glucose Homeostasis

Through its various hormones, particularly glucagon and insulin, the pancreas maintains blood glucose levels within a very narrow range of 4–6 mM. This preservation is accomplished by the opposing and balanced actions of glucagon and insulin, referred to as glucose homeostasis.

Hormones

+ Info

TOO LITTLE

TYPE 2 DIABETES

TYPE 1 DIABETES

Autoimmune distruction of pancreatic beta cells Young patients Low blood sugar

Loss of Insulin sensitivityAdult patients High and low blood sugar

Pathology

COMPLICATIONS

NeuropathyRetinopathy Nephropathy

COMPLICATIONS

DKA - T1DMHHS - T1DM

TEST

HbA1c - 3 month overveiwCBG - Sugar snapshot

Diabetes

+ Info

INSULIN REGIMES

What is what and when to use what

Fixed Rate InfusionDKA

Medications

Variable Rate Infusion Control/ NBM

InsulinDaily maintinace

Diabetes

+ Info

TYPE 2 MEDICATION

What to use, when and how aka SGLT2i are amazing, The standard HbA1c target in type 2 diabetes mellitus is 48 mmol/mol unless hypo risk

Type 1 diabetics may benefit form Metformin treatment aswell if BMI >25

MetforminFirst line, everyone gets

Medications

SGLT-2 inhibitorsSecond line, Great for HF

DPP4 inhibitorsSecond line, Elderly

SulphonyureasThird line, mimics insulin

GLP-1 inhibitorsThird line, weight loss

InsulinForth line, it just works

+ Info

MALE ANDROGENS

Male hypothalamo-pituitary-gonad Axis

GnRH FSH stimulates Sertoli cells in the testis, which then secrete androgen binding protein and inhibin = ↑ testosterone concentration in seminiferous tubules to stimulate spermatogenesis. Inhibin works via -ve feedback to inhibit further release of FSH.LH stimulates Leydig cells in testis, which then secrete testosterone. Testosterone also acts on Sertoli cells to ↑ ABP secretion, Testosterone works through -ve feedback to inhibit furtherrelease of LH.

Hormones

FEMALE SEX HORMONES

Female hypothalamo-pituitary-gonad Axis

At beginning of a menstrual cycle, level of GnRH slowly ↑, whichcauses ↑ secretion of LH and FSH from the gonadotrophs in anterior pituitary. FSH travels to ovaries, where it promotes follicular growth. It is ↑ follicular growth that promotes oestrogen production.Eventually oestrogen levels peak and stimulate surge of LH release. LH surge causes ovulation

Hormones

+ Info

TOO LITTLE

MENOPAUSE

Hot flushes

Pathology

COMLICATIONS

Osteoporosis

TREATMENT

HRTSertraline

TEST

Plasma LH and FSH are used in the investigation of menopause

Androgen Insensitivity

GENETIC MALES WITH FEMALE CHARACTERISTICS

No reaction to testosteron. X-linked recessive condition, resulting in an overall resistance to testosterone. The patient will have a male karyotype (46XY) with an external female phenotype. External female genitalia will be present and breasts may develop at puberty, due to the conversion of testosterone to oestradiol. However, there will be no internal female organs, it can present with primary amenorrhoea.Growth hormone deficiency can cause delayed puberty in males. However, it will not result in the hormone profile included in this scenario.

Kallman's syndorme

Pathology

No LH or FSH

Kallman's syndrome is caused by the failure of gonadotropin-releasing hormone (GnRH) secreting neurons migrating to the hypothalamus. It results in hypogonadotropic hypogonadism. Therefore, hormone profile will show a low testosterone and a low/ inappropriately normal LH and FSH. It presents with delayed puberty and anosmia in a male, who may be normal or above average height.

Klinefelter syndrome

Chromosome confusion

Klinefelter syndrome refers to the karyotype 47XXY, resulting in hypergonadotropic hypogonadism. Although it can present with delayed puberty in male, the hormone profile would show elevated levels of FSH and LH, with low testosterone.

2024

Endocrine

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Insulin

IIn newly diagnosed adults with type 1 diabetes, the first-line insulin regime should be a basal–bolus using twice‑daily insulin detemir

Metformin

This drug works by reducing the release of glucose & improving sensitivity to insulin. It therefore should not cause hypoglycaemia.

• Causes a massive reduction in macrovascular complications
• Reduces blood pressure & cholesterol
• Weight neutral (or slightly weight loss in some people)

Risks include:

• Lactic acidosis (sick day rules: metformin should held if a patient is acutely unwell, dehydrated or if the patient has or is at risk of AKI)
• Gastrointestinal side effects when first started which settle quickly

Contraindications:

• eGFR <30 ml/min (dose reduction to 500 mg twice daily if eGFR <45 ml/min)
• Liver failure or cirrhosis
• Severe advanced heart failure

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Sulphonyureas = Gliclazide

This drug works by making your pancreas release insulin (regardless of the blood sugar). As it causes the release of insulin, it usually causes weight gain & can cause significant hypoglycaemia.Starting sulphonylureas: If the HbA1c remains above 53 mmol/mol, depending on when the patient is hyperglycaemic 40 mg once or twice daily of Gliclazide will be started and titrated based on response. For example, if the patient’s morning/fasting CBG was elevated above the target, we would add in or increase the dose with dinner. For gliclazide, the dose can go up to 160 mg twice daily. Be particularly careful when using sulphonylureas in:

• Elderly patients (as they can get potent hypoglycaemia increasing risks of falls & injuries)
• Impaired renal function as they can accumulate and cause profound hypoglycaemia that is sometimes prolonged up to 72 hours
• Patients on insulin. In most circumstances, the sulphonylurea should be stopped due to poorly predictable hypoglycaemia & insulin is much easier to titrate

Sick day rules: Sulphonylureas should be held if the patient is not eating & drinking

How to tell what's what

Primary hyperparathyroidism is when there's a problem within the parathyroid gland itself, usually a benign (non-cancerous) tumour of the gland. Secondary hyperparathyroidism is when the glands are fine but a condition, like kidney failure, lowers calcium levels and causes the body to react by producing extra parathyroid hormone. Tertiary hyperparathyroidism is when long-standing secondary hyperparathyroidism starts to behave like primary hyperparathyroidism.

GLP-1 = 'tides

This is typically started as a third-line therapy that works by promoting insulin secretion with meals & increasing satiety thereby reducing caloric intake & weight. As it increases insulin secretion associated with meals, it is not expected to cause hypoglycaemia. The aim is to achieve a reduction of HbA1c of 11 mmol/mol and/or 3% weight loss within 6 months. As it has such favourable outcomes & is more frequently being used privately to help weight loss, we tend to start it earlier in patients to reduce the risk of long term complications. Key things to consider:

• It should not be used in conjunction with DPP4 inhibitors
• Warn the patient about transient nausea & GI side effects
• Contraindicated in severe renal impairment
• Rare risk of pancreatitis (therefore shouldn’t be initiated in patients who have had or otherwise are at high risk of pancreatitis)

Sick day rules: GLP-1 analogues should be held if the patient is unwell/at risk of dehydration

DPP4 i = 'gliptins

These work by stopping the breakdown of GLP-1. They are less potent than GLP-1 analogues causing increased insulin secretion with meals but typically not weight loss. They should not be used alongside GLP-1 analogues as they have no additive benefit. They are useful in the elderly and in obese patients. Commonly used agents include linagliptin, sitagliptin & alogliptin. Of these, linagliptin can be used without dose adjustment in even severe renal failure. Sick day rules: Usually can be continued without concern

SGLT-2i = 'flozins

These work by blocking glucose reabsorption in the kidneys, therefore, causing urination of glucose & fluid. They are not expected to cause hypoglycaemia. They seem to be very effective at not only diabetic control but the progression of cardiovascular & cerebrovascular disease as well as exacerbations of heart failure (diuretic effect). Furthermore, they cause weight loss. Even without diabetes, they reduce the risk of cardiovascular outcomes & exacerbations of heart failure.

• Key points to consider:
• Due to glycosuria can cause increased risk of UTIs
• There is a risk of euglycaemic ketoacidosis which is dangerous as with the normal glucose, it could be easily missed! Therefore this drug is contraindicated in anyone who develops ketoacidosis.
• There is a possibility of an increased risk of diabetic foot ulcers & complications. If a patient develops this, you should discuss whether the treatment should continue with the diabetes team

Sick day rules: These drugs should be stopped if a patient is unwell due to the risk of severe dehydration & hypotension

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FRIII

Fixed rate intravenous insulin infusion (FRIII) not only reduces blood glucose levels, but just as importantly, suppresses further ketogenesis, as well as correcting the electrolyte disturbance. Hour 1 - Give 0.1 units/kg (usually 7 units) with 1L Glucose over 1 hour Hour 2 - Reassess and add or keep or remove a unit depending on CBG Give 0.1 units/kg (usually 7 units) with 1L Glucose over 2 hours + KCl Hour 4 - Reassess and add or keep or remove a unit depending on CBG Give 0.1 units/kg (usually 7 units) with 1L Glucose over 2 hours + KCl Hour 6 - Reassess and add or keep or remove a unit depending on CBG Give 0.1 units/kg (usually 7 units) with 1L Glucose over 4 hours + KCl Hour 10 - Reassess and add or keep or remove a unit depending on CBG Give 0.1 units/kg (usually 7 units) with 1L Glucose over 4 hours + KCl Hour 14 - Reassess and add or keep or remove a unit depending on CBG Give 0.1 units/kg (usually 7 units) with 1L Glucose over 6 hours + KCl

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VRIII

Aim for a target blood glucose of 6.0mmol/l to 11.0mmol/l. When blood glucose is >11.0mmol/l for 2 consecutive readings, change to a higher regimen to give more insulin. Give with glucose

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DKA

HHS

Without enough insulin, the body can't use sugar to make the energy it needs. This causes the release of hormones that break down fat for the body to use as fuel. This also produces acids known as ketones. Ketones build up in the blood and eventually spill over into the urine

Hyperosmolar hyperglycemic state (HHS) is a life-threatening complication of diabetes — mainly Type 2 diabetes. HHS happens when blood glucose (sugar) levels are too high for a long period, leading to severe dehydration and confusion. HHS requires immediate medical treatment. Without treatment, it can be fatal.

Insulin

Insulin is usually started when the HbA1c remains above 58 mmol/mol despite maximum tolerated oral agents. If insulin is started, sulphonylureas like gliclazide are usually stopped due to the risk of profound hypoglycaemia There are multiple potential regimes:

• Basal only (once or twice daily injection) given at a set time to give a long-acting insulin lasting at least 12-16 hours
• Biphasic (or pre-mixed) insulin given twice daily with meals which contains short-acting & long-acting insulin mixed into one vial
• Basal-bolus insulin where there is a long-acting basal agent with short-acting bolus doses with each meal

Patients will be usually started on a basal-only regime with insulin types such as NPH insulin (Humulin I), Insulin Glargine (Lantus/Abasaglar), or Insulin Detemir (Levemir) t In T1DM, most patients will be on a basal-bolus regime as this allows greater flexibility of meal times & doses can be adjusted for each meal. We usually start around 0.3 units/kg/day to begin with and titrate this up to around 0.7-1 unit/kg/day Sick day rules: Never stop insulin as illness often results in increased insulin requirement.

Nelson Syndrome

Nelson's syndrome occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing's syndrome. Removal of both adrenal glands eliminates the production of cortisol, and the lack of cortisol's negative feedback can allow any pre-existing pituitary adenoma to grow unchecked. Continued growth can cause mass effects due to physical compression of brain tissue. Increased production of adrenocorticotrophic hormone (ACTH) can result in increased melanocyte stimulating hormone (MSH) which can result in hyperpigmentation. Nelson's syndrome is now rare because bilateral adrenalectomy is now only used in extreme circumstances.