Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PA MATRIX > ENDOCRINE + METABOLIC > Flashcards

ENDOCRINE + METABOLIC Flashcards

1
Q

What is diabetes mellitus?

A

Chronic hyperglycaemia due to insulin dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does Type 1 diabetes clinically present?

A

Young: 2-6 week history of thirst, polyuria and weight loss.

Ketoacidosis if not picked up earlier (fruity breath).

Older: Similar, but over longer period.
Additionally lack of energy and eye problems (blurred vision).
Neuropathy, eventually (glove and stockings).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does Type 2 diabetes clinically present?

A

Same as type 1 diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of type 1 diabetes:

A

Autoimmune destruction of the pancreatic beta cells.

Associated with HLA genetics, but triggered by one or more environmental antigens.

Autoantibodies directed against insulin and islet cell antigens predate the onset by several years.

Polyuria: Blood glucose exceeds renal tubular reabsorptive capacity (renal threshold) -> Osmotic diuresis

Weight loss: Fluid depletion, Insulin deficiency -> Muscle and fat breakdown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology of type 2 diabetes:

A

Polygenic.

Environmental factors (central obesity) trigger onset in genetically susceptible.

Beta cell mass reduced to 50% of normal.

Inappropriately low insulin secretion and peripheral insulin resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cause of type 1 diabetes

A

HLA-DR3/4 affected in >90%.

Autoimmune disease targeting islet cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cause of type 2 diabetes

A

Genetic susceptibility, but no HLA link.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Epidemiology of type 1 diabetes

A

Onset younger (<30 years).

Usually lean.

More north european ancestry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epidemiology of type 2 diabetes

A

Onset older (>30 years).

Usually overweight.

More common in African/ Asian.

More common in general.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnostic tests for diabetes

A

Plasma glucose (mmol/L) levels:

Fasting >7 (or random >11.1)

HbA1c: 6.5% / 48mmol/mol.

C peptide goes down in type 1, persists in type 2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment for type 1 diabetes

A

Glycaemic control through diet (low sugar, low fat, high starch),

insulin (twice daily and with meals).

Exercise encouraged.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment for type 2 diabetes

A

Diet and exercise changes.

If no change -> Biguanide (Metformin) -> + sulfonylurea (gliclazide) / DPP4I (sitagliptin) -> + insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Complications of diabetes (both types)

A

Diabetic ketoacidosis, diabetic nephropathy,

diabetic neuropathy (-> lack of sensation in feet -> occult foot ulcers),

diabetic retinopathy,

Hyperosmolar hyperglycaemic nonketotic coma (mostly in type 2s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Graves disease?

A

Hyperthyroidism due to pathological stimulation of TSH receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does Graves disease clinically present?

A

Rapid heart beat, tremor, diffuse palpable goiter with audible bruit.

Eye problems: bulging outwards and lid retraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathophysiology of Graves disease

A

Thyroid stimulating immunoglobulins recognise and bind to the TSH receptor which stimulates T4 and T3

  • > thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
  • > reduced release of TSH in a negative feedback look
  • > Very high levels of circulating thyroid hormones, with a low TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cause of Graves disease

A

Unclear.

Some genetic element.

Autoimmune disease. Associated with other autoimmune diseases, such as pernicious anaemia and myasthenia gravis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Epidemiology of Graves disease

A

Most common cause of hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diagnostic tests for Graves disease

A

High T3+T4,

Lower TSH than normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment for Graves disease

A

Antithyroid drugs (carbimazole or propylthiouracil) with either dose titration or ‘block and replace’.

Thyroidectomy. Radioactive iodine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complications of Graves disease

A

Thyroid storm: treat with propylthiouracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Hashimoto’s thyroiditis?

A

Hypothyroidism due to aggressive destruction of thyroid cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does Hashimoto’s thyroiditis clinically present?

A

Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on the neck.

Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pathophysiology of Hashimoto’s thyroiditis

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.

Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cause of Hashimoto’s thyroiditis

A

Unknown. Autoimmune. Some genetic element. Triggers; iodine, infection, smoking and possibly stress.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Epidemiology of Hashimoto’s thyroiditis

A

Most common in Japan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diagnostic tests for Hashimoto’s thyroiditis

A

TSH levels, usually raised in hypothyroidism.

Thyroid antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment for Hashimoto’s thyroiditis

A

Thyroid hormone replacement (Levothyroxine).

Resection of obstructive goitre.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Complications of Hashimoto’s thyroiditis

A

Hyperlipidaemia and consequenceS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Sequelae of Hashimoto’s thyroiditis

A

Hashimoto’s encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is hypothyroidism?

A

Reduced action of thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the three types of hypothyroidism?

A

Primary, secondary and transient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does hypothyroidism clinically present?

A

Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on the neck.

Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Note on primary hypothyroidism

A

Disease associated with the thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Note on secondary hypothyroidism

A

Disease associated with the pituitary or hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Note on transient hypothyroidism

A

Disease associated with treatment withdrawal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pathophysiology of primary hypothyroidism

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.

Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH -> reduced T3 and T4 release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pathophysiology of transient hypothyroidism

A

The thyroid overcompensates until it can reestablish correct concentrations of thyroid hormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cause of primary hypothyroidism

A

Autoimmune hypothyroidism (Hashimoto’s),

iodine deficiency,

congenital defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Cause of secondary hypothyroidism

A

Isolated TSH deficiency,

hypopituitarism (due to neoplasm, infection),

hypothalamic disorders (neoplasms, trauma).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Cause of transient hypothyroidism

A

Withdrawal of thyroid suppressive therapy such as radioactive iodine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Epidemiology of primary hypothyroidism

A

12-20 times more frequent in women.

Most common cause of goitrous hypothyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Diagnostic test for hypothyroidism

A

Serum free T4 levels low, thyroid antibodies may be present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Treatment for primary hypothyroidism

A

Thyroid hormone replacement (Levothyroxine).

Resection of obstructive goitre.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Treatment for secondary hypothyroidism

A

Thyroid hormone replacement (Levothyroxine).

Treat underlying cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Treatment for transient hypothyroidism

A

Remits on its own.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Complications of hypothyroidism

A

Myxoedema coma: 20-50% mortality.

Reduced level of consciousness, seizures, hypothermia and hypothyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Cushing’s syndrome (Hypercortisolism)?

A

Persistently and inappropriately elevated circulating glucocorticoid (cortisol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How does Cushing’s syndrome (Hypercortisolism) clinically present?

A

Obesity (fat distribution central, buffalo hump),

plethoric complexion, rounded ‘moon face’,

thin skin, bruising, striae, hypertension, pathological fractures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Note on Cushing’s syndrome (Hypercortisolism)

A

Cushing’s disease: When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Pathophysiology of Cushing’s syndrome (Hypercortisolism)

A

Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae.

Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings’s), but resolves on alcohol recession

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Causes of Cushing’s syndrome (Hypercortisolism)

A

ACTH (adrenocortiotropic hormone) dependent disease: excessive ACTH from pituitary, ACTH producing tumour or excess ACTH administration

Non-ACTH dependent: adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration (most common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Epidemiology of Cushing’s syndrome (Hypercortisolism)

A

10/1,000,000.

Higher incidence in diabetes.

2/3 cases are Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Diagnostic test for Cushing’s syndrome (Hypercortisolism)

A

Confirm raised cortisol: 48 hour low-dose dexamethasone: Fail to suppress cortisol.

Urinary free cortisol over 24hrs. Late night salivary cortisol.

Establishing cause: CT and MRI of renal and pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Treatment for Cushing’s syndrome (Hypercortisolism)

A

Tumours: Surgical removal

Cortisol synthesis inhibition: metyrapone, ketoconazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Complications of Cushing’s syndrome (Hypercortisolism)

A

Hypertension, obesity, death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Sequelae of Cushing’s syndrome (Hypercortisolism)

A

Rare remission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is acromegaly?

A

Overgrowth of all organ systems due to excess growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does acromegaly clinically present?

A

Slow onset (old photos).

Larger hands/feet.

Large tongue, prognathism, interdental separation, spade-like hands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Note on acromegaly

A

If before fusion of epiphyseal plates (children); gigantism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Pathophysiology of acromegaly

A

GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor.

Excess causes uncontrolled growth of organ systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Cause of acromegaly

A

Usually excessive GH secretion by a pituitary tumour.

Other GH releasing tumours possible (hypothalamus, specific lung cancers).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Epidemiology of acromegaly

A

1/200,000.

Average 40 yrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Diagnostic test for acromegaly

A

Glucose tolerance test: IGF-1 raised.

GH raised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Treatment of acromegaly

A

Transsphenoidal resection surgery.

Dopamine agonists (cabergoline),

somatostatin analogues (octreotide)

and GH receptor antagonists (pegvisomant).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Complications of acromegaly

A

Hypertension, diabetes.

Untreated adenoma can impact the optic chiasm -> blindness, colorectal cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is Conn’s syndrome (primary hyperaldosteronism)?

A

High aldosterone levels independent of renin-angiotensin system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does Conn’s syndrome (primary hyperaldosteronism) clincially present?

A

Hypertension (possibly low urine output), hypokalaemic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Note on Conn’s syndrome (primary hyperaldosteronism)

A

Hyperaldosteronism due to high renin levels is called secondary hyperaldosteronism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Pathophysiology of Conn’s syndrome (primary hyperaldosteronism)

A

Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule.

Therefore, hyperaldosteronism causes increased reabsorption of sodium (and water) and excretion of potassium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Cause of Conn’s syndrome (primary hyperaldosteronism)

A

Adrenal adenoma secreting aldosterone in Conn’s syndrome (or possibly bilateral adrenal hyperplasia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Diagnostic test for Conn’s syndrome (primary hyperaldosteronism)

A

Plasma aldosterone and renin.

74
Q

Treatment of Conn’s syndrome (primary hyperaldosteronism)

A

Adenoma: Surgical removal

Hyperplasia: aldosterone antagonist (spironolactone).

75
Q

What is adrenal insufficiency (hypoadrenalism)?

A

Destruction of the adrenal cortex -> reduction in adrenal hormones.

76
Q

What are the two types of adrenal insufficiency (hypoadrenalism)?

A

Primary insufficiency (Addison’s disease).

Secondary

77
Q

How does primary insufficiency (Addison’s disease) clinically present?

A

Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.

Postural hypotension.

Thin, tanned, tired and tearful.

Hyperpigmentation.

78
Q

How does secondary adrenal insufficiency clinically present?

A

Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.

Postural hypotension.

Thin, tired and tearful.

79
Q

Note on primary insufficiency (Addison’s disease)

A

Destruction of adrenal cortex -> Less cortical products.

Excess ACTH -> stimulates melanocytes -> hyper pigmentation

80
Q

Note on secondary adrenal insufficiency

A

Reduction of adrenal cortex stimulation -> Less cortical products.

Low ACTH -> less melanocytes stimulation -> no pigmentation.

81
Q

Pathophysiology of primary insufficiency (Addison’s disease)

A

Autoimmune destruction of the entirety adrenal cortex.

Associated with other autoimmune conditions.

Loss of cortex -> reduction in ability to produce cortisol and/or aldosterone.

Excess ACTH stimulates melanocytes -> pigmentation.

82
Q

Pathophysiology of secondary adrenal insufficiency

A

Inadequate pituitary or hypothalamic stimulation of the adrenal glands.

No pigmentation, since ACTH levels are low.

83
Q

Cause of primary insufficiency (Addison’s disease)

A

Organ specific autoantibodies in 90% of cases.

Rarely; adrenal gland tuberculosis, surgical removal or haemorrhage.

84
Q

Cause of secondary adrenal insufficiency

A

Hypothalamic-pituitary disease or from long term steroid therapy leading to hypothalamic-pituitary-adrenal suppression.

85
Q

Epidemiology of primary insufficiency (Addison’s disease)

A

1/10,000

86
Q

Epidemiology of secondary adrenal insufficiency

A

200/1,000,000.

87
Q

Diagnostic test for primary insufficiency (Addison’s disease)

A

Sodium reduction, potassium elevation.

Cortisol taken across multiple time points.

88
Q

Diagnostic test for secondary adrenal insufficiency

A

Long ACTH test (synacthen test) to distinguish from primary: ACTH raised in primary, lowered in secondary.

89
Q

Treatment of primary insufficiency (Addison’s disease)

A

Hormone replacement (glucocorticoid (hydrocortisone)

and mineralocorticoid (fludrocortisone).

90
Q

Treatment of secondary adrenal insufficiency

A

Hormone replacement (just hydrocortisone).

If from steroid therapy; remove steroids very slowly.

91
Q

Complications of primary insufficiency (Addison’s disease)

A

Adrenal crisis, reduced QOL.

92
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products.

93
Q

How does adrenal hyperplasia clinically present?

A

In severe forms; salt loss.

Female: Ambiguous genitalia with common urogenital sinus.

Male: no signs at birth, bar subtle hyperpigmentation and possible penile enlargement.

94
Q

Note on adrenal hyperplasia

A

Low cortisol, maybe low aldosterone, high androgen.

95
Q

Pathophysiology of adrenal hyperplasia

A

Defective 21-hydroxylase -> disruption of cortisol biosynthesis.

This causes cortisol deficiency, with or without aldosterone deficiency and androgen excess.

In severe forms, aldosterone deficiency -> salt loss

96
Q

Cause of adrenal hyperplasia

A

Genetic 21-hydroxylase deficiency is the cause of about 95% of cases.

97
Q

Diagnostic test for adrenal hyperplasia

A

Serum 17-hydroxyprogesterone (precursor to cortisol) levels: high.

98
Q

Treatment of adrenal hyperplasia

A

Glucocorticoids: Hydrocortisone

Mineralocorticoids: Control electrolytes

If salt loss: Sodium chloride supplement.

99
Q

What is diabetes insipidus?

A

Hyposecretion or insensitivity to ADH

100
Q

What are the two types of diabetes insipidus?

A

Cranial and Nephrogenic

101
Q

How does diabetes insipidus clinically present?

A

Polyuria, compensatory polydipsia

102
Q

Note on cranial diabetes insipidus

A

It is due to hypo-secretion of ADH

103
Q

Note on nephrogenic diabetes insipidus

A

It is due to insensitivity to ADH

104
Q

Pathophysiology of cranial diabetes insipidus

A

Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production.

Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still ‘leak’ out.

105
Q

Pathophysiology of nephrogenic diabetes insipidus

A

Depends on the aetiology.

Can be due to disruption of the channels, damage to the kidney -> Lack of appropriate response to ADH.

106
Q

Cause of cranial diabetes insipidus

A

Neurosurgery, trauma, tumour, infiltrative disease, idiopathic

Genetic: Mutations in the ADH gene

107
Q

Cause of nephrogenic diabetes insipidus

A

Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease

Genetic: Mutation in ADH receptor.

108
Q

Epidemiology of diabetes insipidus

A

1/25,000

109
Q

Diagnostic test for diabetes insipidus

A

Urine volume: Confirm polyuria.

Water deprivation: Confirm DI.

U&Es: Confirm not a more common cause of polyuria

MRI of hypothalamus: Confirm CDI

110
Q

Treatment of cranial diabetes insipidus

A

Mild cases: thiazide diuretics, carbamazepine and chlorpropramide to sensitise the renal tubules to endogenous vasopressin.

Desmopressin.

111
Q

Treatment of nephrogenic diabetes insipidus

A

Treatment of the cause.

112
Q

What is syndrome of inappropriate ADH secretion (linked to hyponatraemia)?

A

Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.

113
Q

How does syndrome of inappropriate ADH secretion (linked to hyponatraemia) clinically present?

A

Nausea, irritability and headache with mild dilutional hyponatraemia.

Fits and coma with severe hyponatraemia.

114
Q

Pathophysiology of inappropriate ADH secretion (linked to hyponatraemia)

A

Ectopic production increases the amount of ADH produced, beyond mechanisms of control.

115
Q

Cause of inappropriate ADH secretion (linked to hyponatraemia)

A

Disordered hypothalamic-pituitary secretion, or ectopic production of ADH.

Neurological: Tumour, trauma, infection

Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis.

116
Q

Diagnostic test for inappropriate ADH secretion (linked to hyponatraemia)

A

FBC. Diagnose by serum concentrations.

117
Q

Treatment of inappropriate ADH secretion (linked to hyponatraemia)

A

Underlying cause.

Water restriction.

Demeoclocycline; inhibition of ADH

118
Q

What is hyperparathyroidism?

A

Excessive secretion of PTH

119
Q

What are the three types of hyperparathyroidism?

A

Primary, secondary and tertiary.

120
Q

How does primary hyperparathyroidism clinically present?

A

70-80% asymptomatic.

Bone pain, renal calculi, nausea, neuropsychiatric

(Bones, stones, abdominal groans and psychic moans)

121
Q

How does secondary hyperparathyroidism clinically present?

A

Kidney disease, with skeletal or cardiovascular complications.

122
Q

How does tertiary hyperparathyroidism clinically present?

A

Bone pain, renal calculi, nausea, neuropsychiatric

(Bones, stones, abdominal groans and psychic moans).

123
Q

Pathophysiology of primary hyperparathyroidism

A

Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH.

124
Q

Pathophysiology of secondary hyperparathyroidism

A

Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia.

125
Q

Pathophysiology of tertiary hyperparathyroidism

A

Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency.

126
Q

Cause of primary hyperparathyroidism

A

Single parathyroid adenoma or hyperplasia

127
Q

Cause of secondary hyperparathyroidism

A

CKD (any condition with hypocalcaemia, such as vitamin D deficiency).

128
Q

Cause of tertiary hyperparathyroidism

A

Develops from secondary hyperparathyroidism.

129
Q

Epidemiology of primary hyperparathyroidism

A

Third most common endocrine disorder.

130
Q

Diagnostic test for primary hyperparathyroidism

A

Bloods: Hypercalcaemia.

131
Q

Diagnostic test for secondary hyperparathyroidism

A

Bloods: low serum calcium.

132
Q

Diagnostic test for tertiary hyperparathyroidism

A

Bloods: Raised calcium, raised PTH

133
Q

Treatment of primary hyperparathyroidism

A

Surgical removal of adenoma.

Potentially bisphosphonates.

134
Q

Treatment of secondary hyperparathyroidism

A

Calcium correction.

Treat underlying condition.

135
Q

Treatment of tertiary hyperparathyroidism

A

Calcium mimetic (Cinacalcet),

total or subtotal parathyroidectomy.

136
Q

Complications of primary hyperparathyroidism

A

Hypercalcaemia

137
Q

Complications of secondary hyperparathyroidism

A

Development into tertiary hyperparathyroidism.

138
Q

Complications of tertiary hyperparathyroidism

A

Overtreatment with vitamin D -> hypercalcaemia.

139
Q

Note on primary hyperparathyroidism

A

One parathyroid gland produces excess PTH.

140
Q

Note on secondary hyperparathyroidism

A

Increased secretion of PTH to compensate hypocalcaemia.

141
Q

Note on tertiary hyperparathyroidism

A

Autonomous secretion of PTH, due to CKD.

142
Q

What is hypoparathyroidism?

A

Low levels of PTH.

143
Q

How does hypoparathyroidism clinically present?

A

Increased excitability of muscles and nerves.

Numbness around the mouth/extremities, cramps, tetany, convulsions.

Chvostek and Trousseau signs.

144
Q

Note on hypoparathyroidism

A

Hypocalcaemia and hyperphosphataemia.

145
Q

Pathophysiology of hypoparathyroidism

A

PTH stimulates the activation of vitamin D, which facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone.

Phosphate reabsorption is inhibited by PTH.

In disease, these processes do not occur.

146
Q

Cause of hypoparathyroidism

A

May be transient.

Most commonly follows anterior neck surgery.

Genetic: Can be due to defects in PTH gene.

Can be autoimmune.

147
Q

Epidemiology of hypoparathyroidism

A

Rare.

148
Q

Diagnostic test for hypoparathyroidism

A

Bloods: Calcium and PTH low, phosphate high.

149
Q

Treatment of hypoparathyroidism

A

Acute: IV calcium

Persistent: Vitamin D analogue (alfacalcidol).

150
Q

Complication of hypoparathyroidism

A

Overtreatment with vitamin D -> hypercalcaemia.

151
Q

What is hypercalcaemia?

A

Excess of calcium

152
Q

What is hypocalcaemia?

A

Deficiency of calcium

153
Q

How does hypercalcaemia clinically present?

A

Can be asymptomatic.

More severe: malaise, depression, bone pain, abdominal pain, nausea, constipation.

Occasionally renal calculi and CKD.

Polyuria and polydipsia.

154
Q

How does hypocalcaemia clinically present?

A

Increased excitability of muscles and nerves.

Numbness around the mouth/extremities, cramps, tetany, convulsions.

Chvostek and Trousseau signs.

155
Q

Note on hypercalcaemia

A

Shortening of the QT interval

156
Q

Note on hypocalcaemia

A

QT prolongation (primarily by prolonging the ST segment).

157
Q

Pathophysiology of hypercalcaemia

A

Ectopic secretion of PTH is very rare.

Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity, direct invasion of bone and production of local factors for calcium mobilisation.

158
Q

Pathophysiology of hypocalcaemia

A

CKD -> Increased phosphate

  • > Microprecipitation of calcium phosphate in tissues
  • > Low serum level of calcium.

CKD -> Inadequate production of active vitamin D.

159
Q

Cause of hypercalcaemia

A

> 90% of cases; primary hyperparathyroidism and malignancy.

Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia.

160
Q

Cause of hypocalcaemia

A

Increased serum phosphate: Chronic kidney disease (most common), Phosphate therapy

Reduced PTH function: Post thyroidectomy and parathyroidectomy

Vitamin D deficiency: Reduced exposure to sunlight

161
Q

Epidemiology of hypercalcaemia

A

30/100,000

162
Q

Diagnostic test for hypercalcaemia

A

Bloods: Raised calcium

163
Q

Diagnostic test for hypocalcaemia

A

History. eGFR to search for CKD. PTH, Vitamin D.

164
Q

Treatment of hypercalcaemia

A

Loop diuretic to return calcium to normal.

Primary hyperparathyroidism: surgical removal.

165
Q

Treatment of hypocalcaemia

A

Acute: IV calcium

Persistent: In vitamin D deficiency, vitamin D supplement.

If hypoparathyroidism; alfacalcidol.

166
Q

Complications of hypocalcaemia

A

Death

167
Q

What is hyperkalaemia?

A

Excess of potassium.

168
Q

What is hypokalaemia?

A

Deficiency of potassium.

169
Q

How does hyperkalaemia clinically present?

A

Few symptoms until it can cause MI.

Impaired neuromuscular transmission (muscle weakness and paralysis).

170
Q

How does hypokalaemia clinically present?

A

Usually asymptomatic, possibly muscle weakness.

Increased risk of cardiac arrhythmias.

Polyuria.

171
Q

Note on hyperkalaemia

A

Tall tented T waves

172
Q

Note on hypokalaemia

A

T wave inversion, prominent U wave(?)

173
Q

Pathophysiology of hyperkalaemia

A

Renal impairment can lead to retention of potassium in the nephron.

This is possible with potassium sparing diuretic.

174
Q

Pathophysiology of hypokalaemia

A

Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy.

GI fluid loss -> less chloride

  • > increase in aldosterone
  • > Decreased potassium reabsorption
175
Q

Cause of hyperkalaemia

A

Renal impairment (most common) and drug interference with potassium excretion.

Elevated without either of these may be artefactural.

176
Q

Cause of hypokalaemia

A

Diuretic treatment and hyperaldosteronism.

Possibly due to loss of GI fluids by constant vomiting/diarrhoea.

177
Q

Diagnostic test for hyperkalaemia

A

Bloods: Check potassium.

Recheck unexpected result.

ECG: peaked T waves, prolonged PR, widened QRS and reduced P

178
Q

Diagnostic test for hypokalaemia

A

Bloods: low magnesium and potassium

ECG: Flat T waves, ST depression, prominent U waves.

179
Q

Treatment of hyperkalaemia

A

Dietary potassium restriction and loop diuretic.

180
Q

Treatment of hypokalaemia

A

Treat underlying cause.

Withdraw harmful medication.

Normalise magnesium as well as potassium.

181
Q

Complication of hyperkalaemia

A

Myocardial infarction -> Death

182
Q

Complication of hypokalaemia

A

Cardiac arrhythmia and sudden death.

PA MATRIX (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions