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Endo Flashcards

1
Q

Endocrinology is the study of

A

hormones (and their gland of origin), their receptors,

the intracellular signalling pathways, and their associated diseases

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2
Q

DEF Endocrine (within/separate):

A

• These glands ‘pour’ secretions directly into the blood stream, without ducts, e.g. thyroid, adrenal and beta cells of pancreas

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3
Q

DEF Exocrine (outside):

A

• These glands ‘pour’ secretions through a duct to site of action e.g. submandibular, parotid and pancreas - amylase & lipase

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4
Q

DEF Hormone action:
• Endocrine
• Paracrine
• Autocrine

A
  • Endocrine - blood-borne, acting a distant sites
  • Paracrine - acting on nearby adjacent cells
  • Autocrine - feedback on same cell that secreted hormone - acts on itself
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5
Q

Hypophysiotropic hormones:

A
  • Corticotropin-releasing hormone (CRH):
    • Stimulates the release of adrenocorticotropic hormone (ACTH)
  • Growth hormone-releasing hormone (GHRH)
    • Stimulates the release of growth hormone (GH):
    • Somatostatin (SST) - INHIBITS release of GHRH
  • Thyrotropin-releasing hormone (TRH)
    • Stimulates the release of thyroid stimulating hormone (TSH)
  • Gonadatropin-releasing hormone (GnRH):
    • Stimulates the release of luteinising hormone (LH) & follicle stimulating hormone (FSH)
  • Dopamine (DA):
    • INHIBITS the release of prolactin
    - Prolactin is under negative control by dopamine thus if the pituitary connecting stalk/infundibulum was destroyed then that would results in an increase in the secretion of prolactin as its negative pressure would not be able to reach it
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6
Q

Hormones of the anterior pituitary:
Secretes?

mnemonic

A
  • Secretes 6 PEPTIDE hormones:
    1. Follicle-stimulating hormone (FSH):
  • Produced in gonadotrophs
    2. Lutenizing hormone (LH):
  • Prodcued in gonadotrophs
    3. Adrenocorticotropic hormone (ACTH - also known as corticotropin):
  • Produced in corticotrophs
    4. Thyroid-stimulating hormone (TSH - also known as thyrotropin):
  • Produced in thyrotrophs
    5. Prolactin:
  • Produced in lactotrophs
    6. Growth hormone (GH - also known as somatotropin):
  • Produced in somatotrophs
  • FLATPIG:
    • FSH
    • LSH
    • ACTH
    • TSH
    • Prolactin
    • Ignore
    • GH
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7
Q

ALL pituitary & hypothalamic hormones act on

A

G-PROTEIN COUPLED

RECEPTORS

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8
Q

(TREAT Prolactinoma - increased prolactin:)

A

using dopamine agonist which in turn will inhibit prolactin release e.g. CABERGOLINE

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9
Q 
DIABETES MELLITUS (DM):
• Definition:
A
  • Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both
  • Hyperglycaemia results in serious microvascular (retinopathy, nephropathy, neuropathy) or macrovascular (strokes, renovascular disease, limb ischaemia and above all heart disease) problems
  • So think of DM as a vascular disease
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10
Q

CLINICAL PRESENTATION DMT1 & 2:

A

• Polyuria and nocturia:
- Since glucose draws water into the urine by osmosis - not enough glucose can be reabsorbed as kidneys have reached the renal maximum reabsorptive capacity
- This results in high levels of glucose in tubule urine and thus lots of water resulting in polyuria and nocturia
• Polydipsia (thirst):
- Due to the loss of fluid and electrolytes from excess glucose and thus water being in the urine
• Weight loss:
- Due to fluid depletion and the accelerated breakdown of fat and muscle secondary to insulin deficiency

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11
Q

DIAGNOSIS DMT1 & 2:

A

• Random plasma glucose > 11.1mmol/L = DIABETES DIAGNOSIS
• Fasting plasma glucose > 7mmol/L = DIABETES DIAGNOSIS
- For both tests one abnormal value is DIAGNOSTIC in symptomatic individuals
- Two abnormal values are required in asymptomatic individuals
• For borderline cases:
- Oral glucose tolerance tests (OGTT):
• Fasting > 7mmol/L = DIABETES DIAGNOSIS
• 2 hrs after glucose > 11.1 mmol/L = DIABETES DIAGNOSIS
• Can also detect impaired glucose tolerance (IGT) - a risk factor for future diabetes and cardiovascular disease:
- Fasting < 7mmol/L
- 2 hrs after glucose 7.8-11.0mmol/L
• Haemoglobin A1c:
- Measures amount of glycated haemoglobin - thus tells us blood glucose
concentration
- HbA1c > 6.5% normal (48mmol/mol) = DIABETES DIAGNOSIS

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12
Q

Treatment of DMT 1+2

A

-hypertension with ACE-inhibitors e.g. RAMIPRIL (or angiotensin receptor blocker e.g. CANDESARTAN if ACE intolerant - usually cough) for patients
with one other major cardiovascular risk factor
(target below 130/80 mmHg)
-hyperlipidaemia with statins e.g. SIMVASTATIN
(+ oral metformin ( biguanide))
- risk factors for long term complication
(orlistat for obesity)

If HbA1c > 53mmol/L 16 weeks later then add a sulfonylurea e.g. ORAL GLICLAZIDE: safest drug in the very elderly is ORAL TOLBUTAMIDE
If at 6 months the HbA1c > 57mmol/L consider adding:
- ISOPHANE INSULIN or a long-acting analogue
- Or a glitazone e.g. ORAL PIOGLITAZONE (replaces
metformin or sulfonylurea ^ insulin sensitivity)
- Or could use sulfonylurea receptor binders e.g. ORAL
NATEGLINIDE
- Or could use glucagon-like peptide analogues (GLP) (promotes insulin release after oral glucose load) e.g. SC EXENATIDE:

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13
Q 
DIABETIC KETOACIDOSIS (DKA) - DIABETIC METABOLIC EMERGENCY!:
 insulin amount?
A

INSULIN MAY NEED ADJUSTING UP OR DOWN BUT SHOULD NEVER BE

STOPPED!!

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14
Q 
DIABETIC KETOACIDOSIS (DKA) - DIABETIC METABOLIC EMERGENCY!:
Diagnosis:
A
  • Hyperglycaemia - blood glucose > 11mmol/L
  • Raised plasma ketones > 3mmol/L - measured using a finger prick sample and near-patient meter that measure Beta-hydroxybutyrate (major ketone)
  • Acidaemia - blood pH < 7.3
  • Metabolic acidosis with bicarbonate < 15mmol/L
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15
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE:

A
  • This is a life-threatening emergency characterised by marked hyperglycaemia, hyperosmolality and mild or no ketosis
  • This is the metabolic emergency characteristic of uncontrolled type 2 diabetes mellitus
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16
Q

Diabetic neuropathy treatment

A
  • Good glycaemic control
  • Treated with PARACETAMOL
  • Tricyclic antidepressant e.g. AMITRIPTYLINE
  • Anticonvulsants e.g. GABAPENTIN or PREGABALIN
  • Opiates e.g. TRAMADOL
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17
Q

HYPOGLYCAEMIA DEF-

A

commonest endocrine emergency:

• Defined as plasma glucose < 3mmol/L

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18
Q

HYPOGLYCAEMIA In non-diabetics

A
  • EXPLAIN:
    • Ex -Exogenous drugs - insulin, oral hypoglycaemic, alcohol binge with no food
    • P - Pituitary insufficiency
    • L - Liver failure
    • A - Addison’s disease
    • I - Islets cell tumour (insulinoma) & immune hypoglycaemia
    • N - Non-pancreatic neoplasm e.g. fibrosarcomas and haemangiopericytomas
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19
Q

HYPOGLYCAEMIA treatment

A

Oral sugar and long-acting starch e.g. toast

  • If cannot swallow then give 50% GLUCOSE IV
  • Or IM GLUCAGON if no IV access
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20
Q

Hyperthyroidism:
Graves’ disease:
*Graves’ opthalmopathy Tx:

A

Treated with IV METHYLPREDNISOLONE and surgical

decompression or eyelid surgery

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21
Q

Hyperthyroidism Tx:

A
  • Beta-blockers e.g. PROPRANOLOL for rapid control of symptoms
  • Anti-thyroid drugs
    • PROPYLTHIOURACIL (PTU) stops the conversion of T4 to T3
    • E.g. ORAL CARBIMAZOLE which blocks thyroid hormone biosynthesis
    and also has immunosuppressive effects (which will affect Graves’
    disease process)
    • 2 strategies:
  • Titration e.g. ORAL CARBIMAZOLE for 4 wks then reduce doses
    according to thyroid function tests (TFTs; TSH, T3 & T4)
  • Block-replace therapy e.g. ORAL CARBIMAZOLE + THYROXINE (T4) which has less risk of developing hypothyroidism
    RADIOACTIVE I(131)
22
Q

Thyroid crisis or thyroid storm:

- MEDICAL EMERGENCY! Tx?

A
  • ORAL CARBIMAZOLE
  • ORAL PROPRANOLOL
  • ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
  • IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to
    T3)
23
Q

Hypothyroidism:

Hashimoto’s thyroiditis:

A

LEVOTHYROXINE THERAPY may shrink the goitre,

24
Q

Hypothyroidism Treatment:

Complication of hypothyroidsm and its Tx:

A
  • Lifelong thyroid hormone replacement e.g. ORAL LEVOTHYROXINE (T4)

• Myxoedema coma:
MEDICAL EMERGENCY and given IV/ORAL T3 & glucose infusion as well as gradual rewarming

25
Q

THYROID CARCINOMA:

A

Treatment:

  • Thyroid LOVES iodine- readily takes up radioactive iodine = locally irradiates cancer = little radiation to surrounding structures
  • LEVOTHYROXINE (T4) to keep TSH reduced as this is a growth factor for the cancer!
26
Q 
The adrenal glands are located above the kidney - retroperitoneal
 • Consist of ...
Three layers of... (from outside in):
secretes?
mnemonic

Medulla:

A

cortex and medulla

  • Zona glomerulosa (G): - Mineralocorticoids e.g. Aldosterone
  • Zona fasciculata (F): - Glucocorticoids e.g. Cortisol
  • Zona reticularis (R): - Androgens (sex hormones) which have a weak effect until peripheral conversion to testosterone and dihydrotestosterone
  • Can remember as GFR - Makes Good Sex
  • Under sympathetic control and secretes catecholamines e.g.adrenaline and noradrenaline
27
Q

Cushing’s syndrome:

A
  • General term which refers to chronic excessive and inappropriate elevated levels of circulating CORTISOL whatever the cause
  • Alcohol excess mimics this
28
Q

Cushing’s disease:

A
  • Specifically refers to excess glucocorticoids resulting from inappropriate ACTH (adrenocorticotrophic hormone) secretion from the pituitary due to tumour
29
Q
  • Adrenal carcinoma:
  • Ectopic ACTH:

RELATING TO CUSHING’S

A

• Adrenalectomy (doesn’t cure cancer) so radiotherapy and adsrenolytic drugs e.g. MITOTANE

  • Surgery if tumour is located and hasn’t spread
  • Drugs that inhibit cortisone synthesis e.g. METYRAPONE, KETOCONAZOLE and FLUCONAZOLE are used pre-op or if awaiting effects of radiation
30
Q

GH controlling hormones

A
  • Growth hormone releasing hormone (GHRH) stimulates GH secretion
  • Somatostatin(SST) inhibits GH secretion
31
Q

• Gigantism vs Acromegaly:

A
  • Excessive GH production in children BEFORE fusion of the epiphyses of the long bones
  • Excess GH in adults
32
Q

ADDISON’S DISEASE: PRIMARY HYPOADRENALISM -

DEF.

A

A in Addison’s = Adrenal issue!
• Destruction of the entire adrenal cortex resulting in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and sex steroid (androgens - precursors of
sex hormones) deficiency

33
Q

ADDISON’S DISEASE: PRIMARY HYPOADRENALISM -
Tx:

  • Adrenal crisis:
    Tx:
A
  • seriously ill or hypotensive:
    • IV HYDROCORTISONE
    • IV 0.9% SALINE
    • GLUCOSE infusion if there is hypoglycaemia
  • Replace steroids with daily - 3x a day to mimic circadian rhythm:
    • Glucocorticoids e.g. ORAL HYDROCORTISONE or ORAL PREDNISOLONE
    • Mineralocorticoids e.g. ORAL FLUDROCORTISONE
    • Warn against abrupt stopping steroids!!
    • Give steroid drug card and bracelet
  • Adrenal crisis:
    • Nausea, vomiting, abdominal pain, muscle cramps and confusion
    • IV HYDROCORTISONE IMMEDIATELY!
34
Q

ADDISON’s disesase:

SECONDARY HYPOADRENALISM: Tx

A
  • Adrenals will recover if long-term steroids are slowly weaned off - but this is
    a long and difficult process
  • ORAL HYDROCORTISONE
35
Q

DIABETES INSIPIDUS (DI):
Ix:
Tx:

A

To differentiate between nephrogenic or cranial - give IM DESMOPRESSIN:
- Urine will not be concentrated in nephrogenic DI but it will in cranial DI

  • Cranial DI:
    • MRI of head and test anterior pituitary (tumour affecting posterior pituitary)
    • synthetic analogue of ADH e.g. ORAL DESMOPRESSIN:
  • Has long duration of action and has no vasoconstrictive effects
  • Nephrogenic DI:
    • Treat cause - usually renal disease
    • Give thiazide diuretics (work in the DISTAL CONVOLUTED TUBULE) e.g. ORAL BENDROFLUMETHIAZIDE - produces mild hypovolaemia encouraging the kidneys to take up more Na+ and water in the PROXIMAL TUBULE, thereby offsetting water losses
    • NSAIDs e.g. IBUPROFEN which will lower urine volume and plasma Na+ by inhabiting prostaglandin synthase - prostaglandins locally inhibit the action of ADH
36
Q

SYNDROME OF INAPPROPRIATE SECRETION OF ADH (SIADH):
DEF
Tx:

A

Continues secretion of ADH despite of plasma being very dilute leading to retention of water and excess blood volume and thus hyponatraemia (as Na+
becomes less concentrated)

ORAL DEMECLOCYCLINE daily: Induces nephrogenic DI (inhibits that action of ADH on the kidney) -
very potent inhibitor of ADH but takes 2-3 days for onset of effects
Vasopressin antagonist e.g. ORAL TOLVAPTAN (V2 blocker) daily:
• Promotes water excretion with no loss of electrolytes - effective in treating hyponatraemia
- Salt and loop diuretic e.g. ORAL FUROSEMIDE:
• If severe to prevent circulatory overload

37
Q

DISORDERS OF CALCIUM METABOLISM:

DEF:

A

• Serum Ca2+ is mainly controlled by parathyroid hormone (PTH) and vitamin D
• Hypercalcaemia is much more common than hypocalcaemia and is frequently
detected incidentally with channel biochemical assays

38
Q

PTH has many actions - all serving to increase… by:

A

plasma Ca2+

  • Increasing osteoclastic resorption of bone - occurs rapidly
  • Increasing intestinal absorption of Ca2+ - slow response
  • Activation of 1,25-dihydroxyvitamin D (calcitriol) in the kidney
  • Increasing renal tubular reabsorption of Ca2+
  • Increasing excretion of phosphate
39
Q

Calcitriol is the active form of … and has many roles:
(4)
Calcitriol release is stimulated by:
(3)

A

vitamin D

  • Increased Ca2+ and phosphate absorption in the gut
  • Inhibits PTH release - negative feedback
  • Enhanced bone turnover by increasing numbers of osteoclasts
  • Increased Ca2+ and phosphate reabsorption in the kidney’s
  • Low plasma Ca2+
  • Low plasma phosphate
  • PTH
40
Q

Primary hyperparathyroidism and malignancies are by far the MOST COMMON CAUSES (90%) of hypercalcaemia

Tx for Acute severe hypercalcaemia:

A

Acute severe hypercalcaemia = MEDICAL EMERGENCY:
• Rehydrate with IV 0.9% saline fluids - to prevent stones
• Give bisphosphonates (to prevent bone resorption by inhibiting osteoclasts) after rehydration e.g. IV PAMIDRONATE
• Measure serum U&E’s daily and serum Ca2+ 48hrs after initial treatment
• Can give glucocorticoid steroids e.g. ORAL PREDNISOLONE in myeloma, sarcoidosis and vitamin D excess

41
Q

HYPOCALCAEMIA & HYPOPARATHYROIDISM:

Clinical presentation:

A

SPASMODIC:
• Spasms - carpopedal spasms = Trousseau’s sign
• Perioral paraesthesia
• Anxious, irritable, irrational
• Seizures
• Muscle tone increases in smooth muscle hence wheeze
• Orientation impaired and confusion
• Dermatitis
• Impetigo herpetiformis - reduced Ca2+ and pustules in pregnancy
• Chvostek’s sign, Cataract, Cardiomyopathy

42
Q

HYPOCALCAEMIA & HYPOPARATHYROIDISM:
Tx:
incl. for
VitD deficiency

A

Acute e.g. with tetany (intermittent muscle spasms/ cramps):
• Give IV CALCIUM GLUCONATE
- Vitamin D deficiency:
• Given ORAL COLECALCIFEROL (vitamin D3 - occurs in food and also formed in the skin) or can be given ORAL ADCAL (calcium + vitamin D3)- ineffective for hypoparathyroidism as PTH is needed for conversion of vitamin D3 to 1,25 dihydroxyvitamin D
- Hypoparathyroidism:
• calcium supplements + CALCITRIOL (active vitamin D)

43
Q

HYPERKALAEMIA:

Def

A
  • Serum K+ > 5.5 mmol/L

* Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!

44
Q

Common Aetiology:

A
  • Decreased exertion:
    • Acute kidney injury (AKI) or oliguric renal failure (
    small amount of urine produced) - COMMON
    • Drugs:
  • Potassium-sparing diuretics e.g. spironolactone - COMMON
  • ACE inhibitors (interfere with RAAS) e.g. ramipril - COMMON
  • NSAIDs - COMMON
45
Q

HYPERKALAEMIA
Diagnosis
Tx

A
  • Serum K+:
    • Over 5.5 mmol/L is hyperkalaemic
    • Over 6.5 mmol/L is a MEDICAL EMERGENCY!
  • Progressive abnormalities on ECG:
    • Tall tented T waves, small P waves and wide QRS complex

POLYSTYRENE SULFONATE RESIN. It binds K+ in the gut reducing absorption

46
Q

ACUTE HYPERKALAEMIA

A

Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!
Urgent - K+ > 7.0mmol/L - MEDICAL EMERGENCY:
• Stabilise cardiac membrane:
- IV 10ml 10% CALCIUM GLUCONATE - reduces the excitability of cardiomyocytes
Drive K+ into cells:
- Give soluble insulin e.g. IV ACTRAPID - facilitates glucose uptake into cell which brings K+ with it
- Must be accompanied by GLUCOSE to avoid hypoglycaemia
- IV or nebulised SALBUTAMOL - also drive K+ into cells

47
Q

HYPOKALAEMIA:
DEF
Diagnosis

A
  • Serum K+ < 3.5 mmol/L
  • Serum K+ < 2.5 mmol/L = URGENT TREATMENT!

see above
- ECG: Small or inverted T waves, prominent U waves (after T waves), a long PR interval, depressed ST segments

48
Q

CARCINOID TUMOURS & CARCINOID SYNDROME:

Def +Tx:

A

• These tumours originate from the enterochromaffin cells (neural crest) and by
definition are capable of producing serotonin (5HT)

  • OCTREOTIDE or LANREOTIDE which are somatostatin analogues that block release of tumour hormones and counters peripheral effects
  • Surgical resection =only cure - so essential to find primary!!
49
Q

Serotonin effects: (7)

A
  • Bowel function
  • Mood
  • Clotting
  • Nausea
  • Bone density
  • Vasoconstriction
  • Increases force of contraction and heart rate
50
Q

Carcinoid crisis:

Def + Tx:

A

tumour outgrows its blood supply or is handled too much during surgery - mediators flow out
• = LIFE-THREATENING:
- Vasodilation caused by bradykinin
- Hypotension - caused by ACTH which causes increased cortisol
- Tachycardia caused by serotonin
- Bronchoconstriction caused by bradykinin
- Hyperglycaemia caused by glucagon and ACTH
• Treated with a high dose somatostatin analogue e.g. OCTREOTIDE which reduces tumour hormone secretion

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