ENDOCRINE + METABOLIC Flashcards
1
Q
What is diabetes mellitus?
A
Chronic hyperglycaemia due to insulin dysfunction.
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).
3
Q
How does Type 2 diabetes clinically present?
A
Same as type 1 diabetes.
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.
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.
6
Q
Cause of type 1 diabetes
A
HLA-DR3/4 affected in >90%.
Autoimmune disease targeting islet cells.
7
Q
Cause of type 2 diabetes
A
Genetic susceptibility, but no HLA link.
8
Q
Epidemiology of type 1 diabetes
A
Onset younger (<30 years).
Usually lean.
More north european ancestry
9
Q
Epidemiology of type 2 diabetes
A
Onset older (>30 years).
Usually overweight.
More common in African/ Asian.
More common in general.
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.
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.
12
Q
Treatment for type 2 diabetes
A
Diet and exercise changes.
If no change -> Biguanide (Metformin) -> + sulfonylurea (gliclazide) / DPP4I (sitagliptin) -> + insulin
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)
14
Q
What is Graves disease?
A
Hyperthyroidism due to pathological stimulation of TSH receptor
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.
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
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.
18
Q
Epidemiology of Graves disease
A
Most common cause of hyperthyroidism
19
Q
Diagnostic tests for Graves disease
A
High T3+T4,
Lower TSH than normal
20
Q
Treatment for Graves disease
A
Antithyroid drugs (carbimazole or propylthiouracil) with either dose titration or ‘block and replace’.
Thyroidectomy. Radioactive iodine.
21
Q
Complications of Graves disease
A
Thyroid storm: treat with propylthiouracil
22
Q
What is Hashimoto’s thyroiditis?
A
Hypothyroidism due to aggressive destruction of thyroid cells.
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.
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
25
Cause of Hashimoto's thyroiditis
Unknown. Autoimmune. Some genetic element. Triggers; iodine, infection, smoking and possibly stress.
26
Epidemiology of Hashimoto's thyroiditis
Most common in Japan
27
Diagnostic tests for Hashimoto's thyroiditis
TSH levels, usually raised in hypothyroidism.
Thyroid antibodies.
28
Treatment for Hashimoto's thyroiditis
Thyroid hormone replacement (Levothyroxine).
Resection of obstructive goitre.
29
Complications of Hashimoto's thyroiditis
Hyperlipidaemia and consequenceS
30
Sequelae of Hashimoto's thyroiditis
Hashimoto's encephalopathy
31
What is hypothyroidism?
Reduced action of thyroid hormone
32
What are the three types of hypothyroidism?
Primary, secondary and transient.
33
How does hypothyroidism clinically present?
Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on the neck.
Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating,
34
Note on primary hypothyroidism
Disease associated with the thyroid
35
Note on secondary hypothyroidism
Disease associated with the pituitary or hypothalamus.
36
Note on transient hypothyroidism
Disease associated with treatment withdrawal.
37
Pathophysiology of primary hypothyroidism
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
38
Pathophysiology of secondary hypothyroidism
Reduced release or production of TSH -> reduced T3 and T4 release.
39
Pathophysiology of transient hypothyroidism
The thyroid overcompensates until it can reestablish correct concentrations of thyroid hormone.
40
Cause of primary hypothyroidism
Autoimmune hypothyroidism (Hashimoto's),
iodine deficiency,
congenital defects
41
Cause of secondary hypothyroidism
Isolated TSH deficiency,
hypopituitarism (due to neoplasm, infection),
hypothalamic disorders (neoplasms, trauma).
42
Cause of transient hypothyroidism
Withdrawal of thyroid suppressive therapy such as radioactive iodine.
43
Epidemiology of primary hypothyroidism
12-20 times more frequent in women.
Most common cause of goitrous hypothyroidism.
44
Diagnostic test for hypothyroidism
Serum free T4 levels low, thyroid antibodies may be present.
45
Treatment for primary hypothyroidism
Thyroid hormone replacement (Levothyroxine).
Resection of obstructive goitre.
46
Treatment for secondary hypothyroidism
Thyroid hormone replacement (Levothyroxine).
Treat underlying cause.
47
Treatment for transient hypothyroidism
Remits on its own.
48
Complications of hypothyroidism
Myxoedema coma: 20-50% mortality.
Reduced level of consciousness, seizures, hypothermia and hypothyroidism.
49
What is Cushing's syndrome (Hypercortisolism)?
Persistently and inappropriately elevated circulating glucocorticoid (cortisol)
50
How does Cushing's syndrome (Hypercortisolism) clinically present?
Obesity (fat distribution central, buffalo hump),
plethoric complexion, rounded 'moon face',
thin skin, bruising, striae, hypertension, pathological fractures.
51
Note on Cushing's syndrome (Hypercortisolism)
Cushing's disease: When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary.
52
Pathophysiology of Cushing's syndrome (Hypercortisolism)
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
53
Causes of Cushing's syndrome (Hypercortisolism)
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)
54
Epidemiology of Cushing's syndrome (Hypercortisolism)
10/1,000,000.
Higher incidence in diabetes.
2/3 cases are Cushing's disease
55
Diagnostic test for Cushing's syndrome (Hypercortisolism)
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
56
Treatment for Cushing's syndrome (Hypercortisolism)
Tumours: Surgical removal
Cortisol synthesis inhibition: metyrapone, ketoconazole.
57
Complications of Cushing's syndrome (Hypercortisolism)
Hypertension, obesity, death.
58
Sequelae of Cushing's syndrome (Hypercortisolism)
Rare remission.
59
What is acromegaly?
Overgrowth of all organ systems due to excess growth hormone
60
How does acromegaly clinically present?
Slow onset (old photos).
Larger hands/feet.
Large tongue, prognathism, interdental separation, spade-like hands.
61
Note on acromegaly
If before fusion of epiphyseal plates (children); gigantism.
62
Pathophysiology of acromegaly
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.
63
Cause of acromegaly
Usually excessive GH secretion by a pituitary tumour.
Other GH releasing tumours possible (hypothalamus, specific lung cancers).
64
Epidemiology of acromegaly
1/200,000.
Average 40 yrs.
65
Diagnostic test for acromegaly
Glucose tolerance test: IGF-1 raised.
GH raised.
66
Treatment of acromegaly
Transsphenoidal resection surgery.
Dopamine agonists (cabergoline),
somatostatin analogues (octreotide)
and GH receptor antagonists (pegvisomant).
67
Complications of acromegaly
Hypertension, diabetes.
Untreated adenoma can impact the optic chiasm -> blindness, colorectal cancer.
68
What is Conn's syndrome (primary hyperaldosteronism)?
High aldosterone levels independent of renin-angiotensin system.
69
How does Conn's syndrome (primary hyperaldosteronism) clincially present?
Hypertension (possibly low urine output), hypokalaemic.
70
Note on Conn's syndrome (primary hyperaldosteronism)
Hyperaldosteronism due to high renin levels is called secondary hyperaldosteronism.
71
Pathophysiology of Conn's syndrome (primary hyperaldosteronism)
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.
72
Cause of Conn's syndrome (primary hyperaldosteronism)
Adrenal adenoma secreting aldosterone in Conn's syndrome (or possibly bilateral adrenal hyperplasia).
73
Diagnostic test for Conn's syndrome (primary hyperaldosteronism)
Plasma aldosterone and renin.
74
Treatment of Conn's syndrome (primary hyperaldosteronism)
Adenoma: Surgical removal
Hyperplasia: aldosterone antagonist (spironolactone).
75
What is adrenal insufficiency (hypoadrenalism)?
Destruction of the adrenal cortex -> reduction in adrenal hormones.
76
What are the two types of adrenal insufficiency (hypoadrenalism)?
Primary insufficiency (Addison's disease).
Secondary
77
How does primary insufficiency (Addison's disease) clinically present?
Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.
Postural hypotension.
Thin, tanned, tired and tearful.
Hyperpigmentation.
78
How does secondary adrenal insufficiency clinically present?
Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.
Postural hypotension.
Thin, tired and tearful.
79
Note on primary insufficiency (Addison's disease)
Destruction of adrenal cortex -> Less cortical products.
Excess ACTH -> stimulates melanocytes -> hyper pigmentation
80
Note on secondary adrenal insufficiency
Reduction of adrenal cortex stimulation -> Less cortical products.
Low ACTH -> less melanocytes stimulation -> no pigmentation.
81
Pathophysiology of primary insufficiency (Addison's disease)
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
Pathophysiology of secondary adrenal insufficiency
Inadequate pituitary or hypothalamic stimulation of the adrenal glands.
No pigmentation, since ACTH levels are low.
83
Cause of primary insufficiency (Addison's disease)
Organ specific autoantibodies in 90% of cases.
Rarely; adrenal gland tuberculosis, surgical removal or haemorrhage.
84
Cause of secondary adrenal insufficiency
Hypothalamic-pituitary disease or from long term steroid therapy leading to hypothalamic-pituitary-adrenal suppression.
85
Epidemiology of primary insufficiency (Addison's disease)
1/10,000
86
Epidemiology of secondary adrenal insufficiency
200/1,000,000.
87
Diagnostic test for primary insufficiency (Addison's disease)
Sodium reduction, potassium elevation.
Cortisol taken across multiple time points.
88
Diagnostic test for secondary adrenal insufficiency
Long ACTH test (synacthen test) to distinguish from primary: ACTH raised in primary, lowered in secondary.
89
Treatment of primary insufficiency (Addison's disease)
Hormone replacement (glucocorticoid (hydrocortisone)
and mineralocorticoid (fludrocortisone).
90
Treatment of secondary adrenal insufficiency
Hormone replacement (just hydrocortisone).
If from steroid therapy; remove steroids very slowly.
91
Complications of primary insufficiency (Addison's disease)
Adrenal crisis, reduced QOL.
92
What is adrenal hyperplasia?
Defective enzymes mediating the production of adrenal cortex products.
93
How does adrenal hyperplasia clinically present?
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
Note on adrenal hyperplasia
Low cortisol, maybe low aldosterone, high androgen.
95
Pathophysiology of adrenal hyperplasia
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
Cause of adrenal hyperplasia
Genetic 21-hydroxylase deficiency is the cause of about 95% of cases.
97
Diagnostic test for adrenal hyperplasia
Serum 17-hydroxyprogesterone (precursor to cortisol) levels: high.
98
Treatment of adrenal hyperplasia
Glucocorticoids: Hydrocortisone
Mineralocorticoids: Control electrolytes
If salt loss: Sodium chloride supplement.
99
What is diabetes insipidus?
Hyposecretion or insensitivity to ADH
100
What are the two types of diabetes insipidus?
Cranial and Nephrogenic
101
How does diabetes insipidus clinically present?
Polyuria, compensatory polydipsia
102
Note on cranial diabetes insipidus
It is due to hypo-secretion of ADH
103
Note on nephrogenic diabetes insipidus
It is due to insensitivity to ADH
104
Pathophysiology of cranial diabetes insipidus
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
Pathophysiology of nephrogenic diabetes insipidus
Depends on the aetiology.
Can be due to disruption of the channels, damage to the kidney -> Lack of appropriate response to ADH.
106
Cause of cranial diabetes insipidus
Neurosurgery, trauma, tumour, infiltrative disease, idiopathic
Genetic: Mutations in the ADH gene
107
Cause of nephrogenic diabetes insipidus
Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease
Genetic: Mutation in ADH receptor.
108
Epidemiology of diabetes insipidus
1/25,000
109
Diagnostic test for diabetes insipidus
Urine volume: Confirm polyuria.
Water deprivation: Confirm DI.
U&Es: Confirm not a more common cause of polyuria
MRI of hypothalamus: Confirm CDI
110
Treatment of cranial diabetes insipidus
Mild cases: thiazide diuretics, carbamazepine and chlorpropramide to sensitise the renal tubules to endogenous vasopressin.
Desmopressin.
111
Treatment of nephrogenic diabetes insipidus
Treatment of the cause.
112
What is syndrome of inappropriate ADH secretion (linked to hyponatraemia)?
Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.
113
How does syndrome of inappropriate ADH secretion (linked to hyponatraemia) clinically present?
Nausea, irritability and headache with mild dilutional hyponatraemia.
Fits and coma with severe hyponatraemia.
114
Pathophysiology of inappropriate ADH secretion (linked to hyponatraemia)
Ectopic production increases the amount of ADH produced, beyond mechanisms of control.
115
Cause of inappropriate ADH secretion (linked to hyponatraemia)
Disordered hypothalamic-pituitary secretion, or ectopic production of ADH.
Neurological: Tumour, trauma, infection
Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis.
116
Diagnostic test for inappropriate ADH secretion (linked to hyponatraemia)
FBC. Diagnose by serum concentrations.
117
Treatment of inappropriate ADH secretion (linked to hyponatraemia)
Underlying cause.
Water restriction.
Demeoclocycline; inhibition of ADH
118
What is hyperparathyroidism?
Excessive secretion of PTH
119
What are the three types of hyperparathyroidism?
Primary, secondary and tertiary.
120
How does primary hyperparathyroidism clinically present?
70-80% asymptomatic.
Bone pain, renal calculi, nausea, neuropsychiatric
(Bones, stones, abdominal groans and psychic moans)
121
How does secondary hyperparathyroidism clinically present?
Kidney disease, with skeletal or cardiovascular complications.
122
How does tertiary hyperparathyroidism clinically present?
Bone pain, renal calculi, nausea, neuropsychiatric
(Bones, stones, abdominal groans and psychic moans).
123
Pathophysiology of primary hyperparathyroidism
Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH.
124
Pathophysiology of secondary hyperparathyroidism
Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia.
125
Pathophysiology of tertiary hyperparathyroidism
Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency.
126
Cause of primary hyperparathyroidism
Single parathyroid adenoma or hyperplasia
127
Cause of secondary hyperparathyroidism
CKD (any condition with hypocalcaemia, such as vitamin D deficiency).
128
Cause of tertiary hyperparathyroidism
Develops from secondary hyperparathyroidism.
129
Epidemiology of primary hyperparathyroidism
Third most common endocrine disorder.
130
Diagnostic test for primary hyperparathyroidism
Bloods: Hypercalcaemia.
131
Diagnostic test for secondary hyperparathyroidism
Bloods: low serum calcium.
132
Diagnostic test for tertiary hyperparathyroidism
Bloods: Raised calcium, raised PTH
133
Treatment of primary hyperparathyroidism
Surgical removal of adenoma.
Potentially bisphosphonates.
134
Treatment of secondary hyperparathyroidism
Calcium correction.
Treat underlying condition.
135
Treatment of tertiary hyperparathyroidism
Calcium mimetic (Cinacalcet),
total or subtotal parathyroidectomy.
136
Complications of primary hyperparathyroidism
Hypercalcaemia
137
Complications of secondary hyperparathyroidism
Development into tertiary hyperparathyroidism.
138
Complications of tertiary hyperparathyroidism
Overtreatment with vitamin D -> hypercalcaemia.
139
Note on primary hyperparathyroidism
One parathyroid gland produces excess PTH.
140
Note on secondary hyperparathyroidism
Increased secretion of PTH to compensate hypocalcaemia.
141
Note on tertiary hyperparathyroidism
Autonomous secretion of PTH, due to CKD.
142
What is hypoparathyroidism?
Low levels of PTH.
143
How does hypoparathyroidism clinically present?
Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.
144
Note on hypoparathyroidism
Hypocalcaemia and hyperphosphataemia.
145
Pathophysiology of hypoparathyroidism
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
Cause of hypoparathyroidism
May be transient.
Most commonly follows anterior neck surgery.
Genetic: Can be due to defects in PTH gene.
Can be autoimmune.
147
Epidemiology of hypoparathyroidism
Rare.
148
Diagnostic test for hypoparathyroidism
Bloods: Calcium and PTH low, phosphate high.
149
Treatment of hypoparathyroidism
Acute: IV calcium
Persistent: Vitamin D analogue (alfacalcidol).
150
Complication of hypoparathyroidism
Overtreatment with vitamin D -> hypercalcaemia.
151
What is hypercalcaemia?
Excess of calcium
152
What is hypocalcaemia?
Deficiency of calcium
153
How does hypercalcaemia clinically present?
Can be asymptomatic.
More severe: malaise, depression, bone pain, abdominal pain, nausea, constipation.
Occasionally renal calculi and CKD.
Polyuria and polydipsia.
154
How does hypocalcaemia clinically present?
Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.
155
Note on hypercalcaemia
Shortening of the QT interval
156
Note on hypocalcaemia
QT prolongation (primarily by prolonging the ST segment).
157
Pathophysiology of hypercalcaemia
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
Pathophysiology of hypocalcaemia
CKD -> Increased phosphate
- > Microprecipitation of calcium phosphate in tissues
- > Low serum level of calcium.
CKD -> Inadequate production of active vitamin D.
159
Cause of hypercalcaemia
>90% of cases; primary hyperparathyroidism and malignancy.
Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia.
160
Cause of hypocalcaemia
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
Epidemiology of hypercalcaemia
30/100,000
162
Diagnostic test for hypercalcaemia
Bloods: Raised calcium
163
Diagnostic test for hypocalcaemia
History. eGFR to search for CKD. PTH, Vitamin D.
164
Treatment of hypercalcaemia
Loop diuretic to return calcium to normal.
Primary hyperparathyroidism: surgical removal.
165
Treatment of hypocalcaemia
Acute: IV calcium
Persistent: In vitamin D deficiency, vitamin D supplement.
If hypoparathyroidism; alfacalcidol.
166
Complications of hypocalcaemia
Death
167
What is hyperkalaemia?
Excess of potassium.
168
What is hypokalaemia?
Deficiency of potassium.
169
How does hyperkalaemia clinically present?
Few symptoms until it can cause MI.
Impaired neuromuscular transmission (muscle weakness and paralysis).
170
How does hypokalaemia clinically present?
Usually asymptomatic, possibly muscle weakness.
Increased risk of cardiac arrhythmias.
Polyuria.
171
Note on hyperkalaemia
Tall tented T waves
172
Note on hypokalaemia
T wave inversion, prominent U wave(?)
173
Pathophysiology of hyperkalaemia
Renal impairment can lead to retention of potassium in the nephron.
This is possible with potassium sparing diuretic.
174
Pathophysiology of hypokalaemia
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
Cause of hyperkalaemia
Renal impairment (most common) and drug interference with potassium excretion.
Elevated without either of these may be artefactural.
176
Cause of hypokalaemia
Diuretic treatment and hyperaldosteronism.
Possibly due to loss of GI fluids by constant vomiting/diarrhoea.
177
Diagnostic test for hyperkalaemia
Bloods: Check potassium.
Recheck unexpected result.
ECG: peaked T waves, prolonged PR, widened QRS and reduced P
178
Diagnostic test for hypokalaemia
Bloods: low magnesium and potassium
ECG: Flat T waves, ST depression, prominent U waves.
179
Treatment of hyperkalaemia
Dietary potassium restriction and loop diuretic.
180
Treatment of hypokalaemia
Treat underlying cause.
Withdraw harmful medication.
Normalise magnesium as well as potassium.
181
Complication of hyperkalaemia
Myocardial infarction -> Death
182
Complication of hypokalaemia
Cardiac arrhythmia and sudden death.
