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IMSCP2 - Pathology > Calcium Metabolism and Adrenal Pathology > Flashcards

Calcium Metabolism and Adrenal Pathology Flashcards

1
Q

Consequences of hypercalcaemia and hypocalcaemia?

A

Hypercalcaemia:

  • Urolithiasis
  • Renal impairment
  • Muscle weakness
  • Arrhythmias

Hypocalcemia

  • Tetany, hyperreflexia
  • Paresthesia (pins and needles)
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2
Q

What are the two types of indices for serum calcium?

What is the difference between them?

A

Total calcium (unadjusted, albumin adjusted)

Ionised calcium (uncorrected, pH corrected)

Ionised calcium is the form that is metabolically active. Protein bound calcium is not.

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3
Q

What is the relationship between albumin and total calcium?

A

IF albumin is low, correct the calcium upwards.

If albumin is high, correct the calcium downwards.

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4
Q

What is the purpose of pH adjustment of ionised calcium?

A

AFter the sample is taken:

  • RBC metabolism produces acid, lowering pH
  • Uncapped sample or ‘headspace’ may cause CO2 to evaporate, increasing pH

IF there is a chance of a pH change, use the adjusted value. If not, the unadjusted value is the correct value.

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5
Q

What is the relationship between pH and calcium-albumin binding?

A

Hydrogen ions also binds to albumin

Low pH = more H+ ions bound to albumin, less calcium can bind and ionised calcium increases.

Vice versa for high pH

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6
Q

What is the relationship between parathyroid hormone levels and hypercalcaemia?

A

High PTH indicates primary hyperparathyroidism (e.g. parathyroid adenoma) causing high calcium

Low PTH indicates hypercalcaemia (e.g. from malignancy) driving PTH levels down.

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7
Q

Hypophosphataemia is the hallmark sign of which syndrome?

What is the mechanism of action behind the hypophosphataemia?

A

Refeeding syndrome

Follows carbohydrate intake (refeeding) to treat nutrient deficiency.

The sudden spike in insulin causes an intracellular shift of phosphate, magnesium and potassium.

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8
Q

What are the consequences of refeeding syndrome

A

Hypophosphataemia driven

  • Muscle weakness
  • Rhabdomyolysis via ATP depletion and the consequent inability of muscle cells to maintain membrane integrity.
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9
Q

Causes and consequences of hyperphosphataemia?

A

Causes:

  • Kidney disease
  • Rhabdomyolysis
  • Hypoparathyroidism

Consequences:

  • Secondary hyperparathyroidism with chronic kidney disease
  • Renal stones
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10
Q

Describe the normal function of the adrenal gland and what type of control they are undre

A

Paired glands, one on each pole of kidney

Cortex (90%) - produce corticoid hormones under endocrine control

Medulla - produce catecholamines under autonomic nervous system control

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11
Q

What are the three groups of steroid hormones produced by adrenal cortex and where are they produced?

A

Mineralocorticoids - Zona glomerulosa

Glucocorticoids - Zona fasciculata

Sex steroids - Zona reticularis

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12
Q

What is the main function of mineralocorticoids and the most important example?

A

Aldosterone

Maintain normal intravascular volume and pH through sodium retention and elimination of K+ and H+ ions.

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13
Q

What are the main actions of glucocorticoids?

What control are they under?

A

Under pituitary control - ACTH

Functions: Metabolic regulation (protein/carb/fat)

  • Inhibit protein synthesis and increase protein breakdown
  • Inhibit glucose uptake by cells and increase gluconeogenesis
  • Redistribute fat
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14
Q

Describe the three important groups of sex steroids

A

Oestrogens - development and regulation of female repro system, feminising secondary sex characteristcs

Progestogens - menstrual cycle, pregnancy, lactation

Androgens - Spermatogenesis, masculinising secondary sex characteristics

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15
Q

What are the three major syndromes of hyperfunction of the adrenal cortex?

A
  1. Cushing syndrome (hypercortisolism)
  2. Conn syndrome (hyperaldosteronism)
  3. Adrenogenital or virilsing syndrome (hyperandrogenism)
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16
Q

What are the 3 important types of adrenal cortex hypofunction?

A
  1. Primary acute adrenal insufficiency
  2. Primary chronic adrenal insufficiency (Addison disease)
  3. Secondary adrenal insufficiency (ACTH deficiency)
17
Q

Cause and 4 mechanisms to Cushing syndrome?

Are they ACTH dependent or independent?

A

Caused by excess glucocorticoid levels

  1. Exogenous - e.g. corticosteroids. ACTH independent
  2. Endogenous - ACTH from hypothalamus/pituitary = Too much cortisol production. Known as cushing disease - ACTH depedent
  3. Endogenous - Ectopic ACTH (e.g. small cell carcinoma of lung) = ACTH dependent
  4. Endogenous - adrenal cortical adenoma or primary cortical hyperplasia, ACTH is normal. ACTH independent
18
Q

Symptoms of Cushing syndrome?

A
  • Cataracts
  • Ulcers
  • Stria, skin thinning
  • Hypertension
  • Immunosuppression
  • N
  • Gain weight
  • Osteoporosis
  • Impaired wound healing
  • Depression
19
Q

Symptoms of Cushing syndrome?

A
  • Cataracts
  • Ulcers
  • Stria, skin thinning
  • Hypertension
  • Immunosuppression
  • N
  • Gain weight
  • Osteoporosis
  • Impaired wound healing
  • Depression
20
Q

Two primary and two secondary causes of hyperaldosteronism.

What is the conseuqnece of this disease?

A

Primary

  • Bilateral adrenal hyperplasia
  • Adenoma - Conn syndrome

Secondary: Renin-angiotensin activation

  • Decreased renal perfusion
  • Arterial hypovolaemia
21
Q

What is Conn syndrome?

A

Adenoma of the adrenal cortex (zona glomerulosa), resulting in overproduction of mineralocorticoids (aldosterone)

22
Q

What are two causes of adrenogenital syndrome?

A

Excess androgens caused by:

  • ADrenocortical neoplasms
  • Congenital adrenal hyperplasia
23
Q

Two mechanisms of adrenocortical sufficiency and the three patterns of disease?

A
  1. Primary hypoadrenalism
  2. Secondary hypoadrenalism - deficiency in ACTH

Three patterns

  1. Primary acute adrenocortical insufficiency
  2. Primary chronic adrenocortical insufficiency
  3. Secondary adrenocortical insufficiency
24
Q

How does adrenocortical insufficiency present?

A

Hypoglycaemia, dehydration, weight loss

Weakness, tiredness, hypotension.

25
Q

What is Addison’s disease?

What is a hallmark presentation?

A

Primary chronic adrenocortical insufficiency.

Presents with patchy, hard tanning of the skin

26
Q

When might primary acute adrenocortical insufficiency airse?

A
  • Sudden withdrawal of exogenous corticosteroids
  • Adrenal haemorrhage
27
Q

Causes of Addison’s disesae?

A

Rare:

  • Autoimmune
  • TB
  • Metastatic malignancy
28
Q

What ist he most common cause of secondary adrenocortical insufficiency?

A

Secondary adrenocortical insufficiency is caused by reduced ACTH output.

This is most common seen after prolonged administration of exogenous glucocorticoids causing pituitary atrophy through negative feedback.

29
Q

Production of which corticoid hormones are impacted in secondary adrenocortical insufficiency?

A

Cortisol and adrenogens will be deficiency.

Aldosterone production will be normal, because it is controlled by the renin-angiotensin system rather than ACTH.

30
Q

WHat is adrenal phaeochromocytoma?

A

Neoplasm of the adrenal medullary neuroendocrine cells.

Most are benign

Can be functional - more adrenaline/noradrenaline production.

31
Q

What are the symptoms of adrenal phaeochromocytoma?

A

Due to increased A/NA production:

  • Hypertension
  • Sweating
  • Palpitations
  • Headache

IMSCP2 - Pathology (27 decks)

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