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Endo Flashcards

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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:

Study These Flashcards
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?

Study These Flashcards
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:

Study These Flashcards
A

LEVOTHYROXINE THERAPY may shrink the goitre,

24
Q

Hypothyroidism Treatment:

Complication of hypothyroidsm and its Tx:

Study These Flashcards
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
THYROID CARCINOMA:
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
``` The adrenal glands are located above the kidney - retroperitoneal • Consist of ... Three layers of... (from outside in): secretes? mnemonic ``` Medulla:
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
Cushing’s syndrome:
- General term which refers to chronic excessive and inappropriate elevated levels of circulating CORTISOL whatever the cause - Alcohol excess mimics this
28
Cushing’s disease:
- Specifically refers to excess glucocorticoids resulting from inappropriate ACTH (adrenocorticotrophic hormone) secretion from the pituitary due to tumour
29
- Adrenal carcinoma: - Ectopic ACTH: RELATING TO CUSHING'S
• 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
GH controlling hormones
- Growth hormone releasing hormone (GHRH) stimulates GH secretion - Somatostatin(SST) inhibits GH secretion
31
• Gigantism vs Acromegaly:
- Excessive GH production in children BEFORE fusion of the epiphyses of the long bones - Excess GH in adults
32
ADDISON’S DISEASE: PRIMARY HYPOADRENALISM - | DEF.
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
ADDISON’S DISEASE: PRIMARY HYPOADRENALISM - Tx: - Adrenal crisis: Tx:
- 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
ADDISON's disesase: | SECONDARY HYPOADRENALISM: Tx
- Adrenals will recover if long-term steroids are slowly weaned off - but this is a long and difficult process - ORAL HYDROCORTISONE
35
DIABETES INSIPIDUS (DI): Ix: Tx:
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
SYNDROME OF INAPPROPRIATE SECRETION OF ADH (SIADH): DEF Tx:
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
DISORDERS OF CALCIUM METABOLISM: | DEF:
• 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
PTH has many actions - all serving to increase... by:
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
Calcitriol is the active form of ... and has many roles: (4) Calcitriol release is stimulated by: (3)
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
Primary hyperparathyroidism and malignancies are by far the MOST COMMON CAUSES (90%) of hypercalcaemia Tx for Acute severe hypercalcaemia:
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
HYPOCALCAEMIA & HYPOPARATHYROIDISM: | Clinical presentation:
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
HYPOCALCAEMIA & HYPOPARATHYROIDISM: Tx: incl. for VitD deficiency
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
HYPERKALAEMIA: | Def
* Serum K+ > 5.5 mmol/L | * Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!
44
Common Aetiology:
- 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
HYPERKALAEMIA Diagnosis Tx
- 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
ACUTE HYPERKALAEMIA
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
HYPOKALAEMIA: DEF Diagnosis
* 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
CARCINOID TUMOURS & CARCINOID SYNDROME: | Def +Tx:
• 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
Serotonin effects: (7)
- Bowel function - Mood - Clotting - Nausea - Bone density - Vasoconstriction - Increases force of contraction and heart rate
50
Carcinoid crisis: Def + Tx:
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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