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HUMAN HEALTH AND DISEASE > Endocrinology I & II: Diabetes Mellitus and Acromegaly > Flashcards

Endocrinology I & II: Diabetes Mellitus and Acromegaly Flashcards

1
Q

What is glucagon?

A

-Peptide from alpha cells in Islets of Langerhans

-Secreted in response to lowered glucose levels

-Action is to oppose insulin

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2
Q

What are catecholamines?

A

Secreted by adrenal medulla in response to stress which raises blood glucose levels

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3
Q

What is glucocorticoid?

A

Cortisol which promotes gluconeogenesis, gyconeolysis and protein catabolism

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4
Q

What are hypoglycaemic and hyperglycaemic hormones?

A

Hypoglycaemic: Hormone that drops glucose levels e.g insulin

Hyperglycaemic: Hormone that encourages increase in glucose levels e.g Glucagon, cortisol, catecholamines and growth hormone

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5
Q

What is diabetes Mellitus?

A

Group of conditions characterised by chronic hyperglycaemia resulting from reactive insulin deficiency, peripheral tissue resistance or both.

Is usually primary and classified as insulin dependent (type 1)

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6
Q

Compare type I vs type II diabetes

A

slides

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7
Q

What values suggest someone has diabetes mellitus (glucose tolerance test)?

A

> 6.7 mmol/l fasting
10 mmol/l two hours after glucose

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8
Q

What is the treatment for diabetes?

A

Type I - insulin such as actrapid, monotard, mixtard

Diet - fat reduced to 30% of total energy intake

Drugs - sulphonylureas, gibenclamide, tolbutamide, biguanides (metformin)

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9
Q

How do you measure the control of blood glucose levels?

A

-Fingerprick glucose
-Urine dipstick
-Lab serum glucose
-Glycosylated Hb

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10
Q

What is acute hypoglycaemia?

A

Blood glucose is less than 2.2 mmol/l (dental emergency)

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11
Q

What are the signs and symptoms of acute hypoglycaemia?

A

Increased sympathetic tone causes hunger, sweating, pallor and tachycardia

Later changes include aggression and peripheral tingling and altered sensations

Fits, hemiparesis and ultimately coma

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12
Q

What is the treatment of acute hypoglycaemia?

A

If patient is conscious, rapid ingestion of sugar (IV glucose, 50ml 50% dextrose or glucagon, 1mg IM)

If unconscious or depressed, gag reflex then

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13
Q

What is diabetic ketoacidosis (DKA)?

A

A condition where raised metabolism is required to fight illness which needs more insulin.

Reduced doses kill by causing relative hypoglycaemia

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14
Q

What is the pathophysiology of DKA?

A

Insulin deficiency leads to uncontrolled catabolism (cells cannot access glucose)

High blood sugar levels produce glycosuria (a condition characterized by an excess of sugar in the urine, typically associated with diabetes or kidney disease), osmotic diuresis (Osmotic diuresis is increased urination due to the presence of certain substances in the fluid filtered by the kidneys) and dehydration

Tissues that can’t get sugar from the blood start to break down into acidic ketones.

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15
Q

What are the clinical features of DKA?

A

Profound dehydration due to renal water and electrolyte losses

Low BP and air hunger (breathlessness) to compensate for metabolic acidosis

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16
Q

What are the complications of diabetes?

A

-Heart disease
-Peripheral vascular disease
-Atheroma
-Stroke
-Increased risk of UTI and skin infections

-Macrovascular: accelerated atheroma leading to stroke, ischaemic heart disease or ischaemic limbs

-Microvascular: diabetic retinopathy can lead to blindness, diabetic nephropathy can lead to renal failure, diabetic neuropathy can lead to loss of sensation

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17
Q

What are the two parts of the adrenal gland and what are their functions?

A

Medulla - catecholamine production

Cortex - steroid hormone production

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18
Q

What is Addison’s disease?

A

Hypoadrenalism-underfunction of adrenal gland

(Disease is rare but syndrome is more common)

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19
Q

What is Addison’s syndrome?

A

Endogenous steroid production is suppressed by exogenous therapeutics

Far more common

20
Q

What are the clinical signs of Addison’s disease?

A

Lethargy

Anorexia and weight loss

Hypotension (usually postural)

Hyperpigmentation of buccal mucosa, skin creases and scars

Can present as crisis (in disease and syndrome) which involves: abdominal pain, low Na, high K, hypoglycaemia and hypovolaemic shock with no bleeding

21
Q

What is the management of Addison’s disease?

A

Supplementation for life using hydrocortisone twice daily or fludrocortisone

22
Q

What is an Addisonian crisis?

A

Patient on steroid excess treatment has had the drug withdrawn too quickly

Patient cannot produce adequate cortisol to go along with the adrenaline in stressful situations so must receive supplementation to facilitate adrenaline’s action to maintain blood pressure

23
Q

What is the supplementation for Addisonian crisis?

A

100-200mg hydrocortisone if pre short procedure (multi uses if long operation)

IV access is mandatory during procedures

24
Q

What is Cushing’s syndrome?

A

Persistent raised plasma cortisol levels

Mostly from exogenously supplied steroid (different to Cushing’s disease)

25
Q

What are the clinical features of Cushing’s syndrome?

A

Obesity - fat centrally distributed (trunk, abdomen, buffalo hump on neck)

Plethoric complexion and thin skin which easily bruises (protein catabolic effect)

Moon face

Purple striae on abdomen, breasts and thighs

Pigmentation (melanin)

26
Q

What are the investigations of Crushing’s syndrome?

A

-Surgical removal of pituitary

-Metyrrapone inhibits cortisol release in cases not amenable to surgery

-Pituitary irradiation as salvage for impossible or failed surgery.

-Iatrogenic Crushing’s disease responds to reduction/cessation of steroid if possible.

27
Q

Whats cushing’s disease?

A

Glucocorticoid excess secondary to inappropriate ACTH secretion only

28
Q

What are the features of aldosterone?

A

Driven primarily by renal renin-angiotensin system

Increased by low plasma Na or low blood pressure

High K stimulates aldosterone secretion directly

29
Q

What are mineralocortcoids?

A

Steroid hormones that promote renal sodium reabsorption and K excretion

e..g aldosterone

30
Q

What is Conn’s syndrome?

A

Hyperaldosteronism which drives excess fluid retention, low K (hypokalaemia) and secondary hypertension

31
Q

What is the management of Conn’s syndrome?

A

Surgical resection of an adenoma

Hypertension from hyperplasia can be combatted using spironolactone (aldosterone antagonis

32
Q

What are the endocrine causes of hypertension?

A

-Excess renin production
-Excess aldosterone production
-Adrenal adenoma or hyperplasia
-Excess production of other steroid
-Excess catecholamines
-Oral contraceptive pill

33
Q

What is the growth hormone?

A

-Substance secreted by the adenohypophysis (anterior pituitary)

-Effects mediated via insulin like growth factor synthesised in liver

-GH deficiency in childhood produced a pituitary dwarf

-Excess GH in childhood leads to gigantism

34
Q

What is acromegaly?

A

Growth hormone excess that happens in adulthood typically from a benign anterior pituitary acidophil adenoma.

35
Q

What are the clinical features of acromegaly?

A

-Enlarging head, hands and feet

-Chin enlarges- dentures too small

-Cranial nerves pinched in bony foraminae

36
Q

What is the management of acromegaly?

A

Surgery

Radiotherapy

Drugs - octreotide (long acting somatostatin analogue) or bromocriptine (elderly)

37
Q

What is thyroid disease?

A

Hyper or hypo thryoidism

38
Q

What is hypothyroidism?

A

Typically a primary disease of the thyroid tissue where thyroid gland produces too little thyroid

39
Q

What are the clinical features of hypothyroidism?

A

-Normocytic/Macrocytic anaemia

-Hypercholesterolaemia

-Hyponatraemia (a lower than normal level of sodium in the bloodstream.)

-Hard to diagnose in elderly

40
Q

What is the management of hypothyroidism?

A

Lifelong replacement therapy with thyroxine (T4)

Assess efficacy and adjust dose on clinical resolution of symptoms and thyroid function tests

41
Q

What complication can severe hypothyroidism cause?

A

-Hypothermia
-Hypoventilation
-Cardiac failure
-Confusion and coma
-Depression common in elderly

42
Q

What is the most common cause of hyperthyroidism?

A

Graves’ disease

43
Q

What is hyperthyroidism?

A

Overactive thyroid which produced too much thyroid hormone (everything happens quick).

44
Q

What is the aetiology of hyperthyroidism?

A

-Grave’s disease
-Solid toxic nodules
-Toxic multi nodular goitre

45
Q

What are the clinical features of hyperthyroidism?

A

If cause is Grave’s disease:, clubbing, swollen fingers, perinatal new bone formation, eye signs like exophthalmos, limited eye movement, lid lag and corneal scarring
Atrial fibrillation and heart failure

46
Q

What is the management of hyperthyroidism?

A

Drugs~

Carbimazole - inhibits formation of thyroid hormones, mild immunosuppresive powers

Beta blockers - used to control sympathetic symptoms

Radioiodine - localised radiotherapy

Surgery

47
Q

What is hyperparathyroidism

A

Involves increased secretion of parathyroid hormone (PTH) that leads to hypercalcemia and hypophosphatemia.

HUMAN HEALTH AND DISEASE (58 decks)

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