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Hasnat Motive > Endocinology > Flashcards

Endocinology Flashcards

1
Q

What is T1DM?

A

Hyperglycaemia due to insulin deficiency.
By autoimmune destruction of beta cells of the pancreas.

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2
Q

Cause of T1DM?

A

Autoimmune
Genetic: HLA-DR3-DQ2 or HLA-DR4-DQ8
Enterovirus

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3
Q

Risk factors of T1DM (5)

A

Northern European
Family history (HLA)
Autoimmune diseases (Coeliacs, Addisons)
Enteroviruses
Vit D deficiency

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4
Q

Pathophysiology of T1DM

A

Autoantibodies destroy insulin-secreting Beta cells
Causes insulin deficiency
Leads to hyperglycaemia
Makes you thirsty
Lots of urine containing glucose
Can lead to diabetic ketoacidosis if no insulin given
Insulin is required to move glucose from blood into cells.
GLUT 4 (insulin regulated glucose transporter)

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5
Q

Signs & Symptoms of T1DM

A

Lean
Glucose + ketones in urine
Glove and stocking
Reduced visual acuity
Diabetic foot

Thirsty
Lots of urine
Weight loss
Lethargy

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6
Q

What effect does ketoacidosis have on the body?

A

Ketone bodies are strong acids:

lower the pH of the blood
impairs Hb ability to bind O2
acute kidney injury

reduced glucose supply to cells due to lack of insulin THUS ketones formed

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7
Q

Investigations of T1DM (4)

A

1- Blood glucose ≥11mmol/L
2- Fasting blood glucose:≥7.0 mmol/L

Two abnormal values are required in asymptomatic individuals

3- Oral glucose tolerance test:>11mmol/L
(two hours after a 75g oral glucose load)
7.8-11mmol/L suggests pre-diabetes.

4- HbA1C (uncommon as type 1 diabetes has fast onset)
Other: C-Peptide, Autoantibodies

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8
Q

When should you suspect MODY?
(maturity onset diabetes of the young)

A

Patients who are:
Non obese
Young
Family history of diabetes

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9
Q

How do you differentiate MODY from T1DM?

A

C peptide will be present, autoantibodies will be absent

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10
Q

Management for T1DM?

A

1- lifestyle (weight, smoking, alcohol, carb counting)
2- Basal - bolus

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11
Q

Complications of insulin therapy? (4)

A
  • Hypoglycaemia: (also caused by SULFONYLUREA - antidiabetic drug)
  • Injection site - lipohypertrophy
  • Insulin resistance
  • Weight gain: insulin makes people feel hungry
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12
Q

How do you manage T1DM?

A

HbA1c:measure every 3-6 months with a target of≤48 mmol/mol

Self monitoring

Annually diabetic review: retinopathy, renal function, diabetic foot, cardiovascular (BP), thyroid disease

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13
Q

What is T2DM?

A

production of insulin becomes insufficient due to insulin resistance.

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14
Q

What causes T2DM?

A

Combination of environmental and genetic factors, poor diet, lack of exercise and obesity.

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15
Q

Risk factors for T2DM?

A

Family history
Obesity
Hypertension
Increasing age
Gestational Diabetes
Low (HDL) & High triglycerides
Polycystic ovary syndrome
Drugs: corticosteroids, thiazide diuretics
Ethnicity - Middle Eastern, South-east Asian and Western pacific

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16
Q

What is the Pathophysiology of T2DM?

Hint: Starlings Curve

A

Insulin binds normally to its receptor on the surface of cells in DMT2 just like in healthy people

Circulating insulin levels are typically higher than in non-diabetics following diagnosis and tend to rise further, only to decline again after months or years due to eventual secretory failure - phenomenon is known as the Starling curve of the pancreas.

Initial compensatory mechanism is hyperplasia and hypertrophy of beta cells to secrete more insulin. This is then exhausted and leads to hypoplasia and hypotrophy.

Hyperglycaemia and lipid excess are toxic to beta cells

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17
Q

Signs & Symptoms of T2DM?

A

Acanthosis nigricans
Glove and stocking
Reduced visual acuity
Diabetic retinopathy
Diabetic foot disease
Increased thirst and urine
Recurrent infections
Lethargy

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18
Q

Investigations for T2DM?

Hint: same as T1DM investigations

A

Blood glucose: ≥11mmol/L is diagnostic

Fasting blood glucose:≥7.0 mmol/L

Oral glucose tolerance test:>11mmol/L

HbA1C: ≥48 mmol/mol

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19
Q

How to diagnose Patients with impaired fasting glucose (IFG)

A

raised fasting glucose and normal OGTT

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20
Q

How to diagnose patients with impaired glucose tolerance (IGT)?

A

raised OGTT, and may or may not have a raised fasting glucose

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21
Q

How to manage T2DM?

A

Lifestyle (diet and exercise)
Metformin if HbA1c rises above 48 mmol/mol(6.5%)

second anti-diabetic drug should be commenced if HbA1Crises above58 mmol/mol(7.5%)

Insulin based therapy

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22
Q

What are the side effects of metformin? (4)

A

anorexia
diarrhoea
nausea
abdominal pain

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23
Q

What is diabetic ketoacidosis? (3)

A

medical emergency that is characterised by hyperglycaemia, acidosis and ketonaemia.

Blood glucose > 11 mmol/L
Ketosis > 3 mmol/L
Acidosis pH < 7.3

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24
Q

Causes/ Risk factors for DKA?

A

Infection
Diabetes
Heart attack
Hypothyroidism & pancreatitis
Corticosteroids, diuretics, salbutamol

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25
Q

Sings and symptoms of DKA?

A

Smell of acetone (‘fruity’ breath)
Vomiting
Dehydration
Abdominal pain
Hyperventilation (Kussmaul; deep sighing)
Hypovolaemic shock
Drowsiness
Coma

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26
Q

What is the pathophysiology of DKA?

A

Lack of insulin = body unable to utilise glucose

More glycogenolysis + gluconeogenesis + lipolysis
Lipolysis —> FA’s —> ketogenesis)

Ketones = weak acids
Leads to dehydration and electrolyte imbalances (K+) + hyperglycaemia

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27
Q

How to diagnose DKA? (3)

A

Ketonaemia: 3mmol/L and over
Blood glucose over 11mmol/L
Bicarbonate below 15mmol/L or venous pH less than 7.3

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28
Q

How to manage DKA?

A

Mild = rehydrate + subcutaneous insulin injection

Moderate = IV fluids + insulin and glucose infusion + potassium replacement

Severe = ABCDE approach for emergency resuscitation

Cerebral oedema = Major Complication !!!

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29
Q

What is Hyperosmolar Hyperglycaemic State (HHS)?

A

occurs in people with type 2 diabetes who experience very high blood glucose levels

  • absence of significant ketoacidosis
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30
Q

Causes of HHS? (4)

A

Infection
Medications that cause fluid loss or lower glucose tolerance
Surgery
Impaired renal function

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31
Q

Pathophysiology of HHS?

A

lack of insulin is coupled with a rise in counter-regulatory hormones (e.g. cortisol, growth hormone, glucagon) that leads to a profound rise in glucose.

Enough insulin, which prevents the development of ketosis that epitomises DKA

excessive glucose (kidneys at max capacity) —> osmotic diuresis within the kidneys —> loss of electrolytes —> dehydration

Blood becomes thick and viscous

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32
Q

Diagnostic criteria for HHS? (3)

A
  1. severe hyperglycaemia (>=30mmol/L)
  2. hypotension
  3. hyperosmolality (usually >320 mosmol/kg).

No significant acidosis

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33
Q

Main difference between DKA and HHS?

A

DKA presents with acidosis and ketosis whereas HHS does not.

DKA in T1DM
HHS in T2DM

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34
Q

What are the signs and symptoms of HHS?

A

Nausea and vomiting
Lethargy
Weakness
Confusion
Dehydration
Coma
Seizure

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35
Q

Management of HHS? (4)

A

IV fluids
Insulin (if glucose doesn’t fall)
K+ replacement
Anticoagulants (VTE prophylaxis)

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36
Q

What are the Primary Causes of Hyperthyroidism?
(Caused by thyroid disfunction)

A

Graves disease
Toxic thyroid adenoma
Multinodular goitre
Silent thyroiditis
De Quervain’s thyroiditis (painful goitre)
Radiation

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37
Q

What are the Secondary Causes of Hyperthyroidism?

A

TSH producing Pituitary adenoma
Ectopic tumour
Gestational
Hypothalamic tumour
Lithium

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38
Q

Presentation of Hyperthyroidism?

A

Fine tremor
Finger clubbing
Sweating
Swollen arms and legs with plaques
Goitre (depending on cause)
Thyroid bruit
Protruding eyes & lid retraction
Atrial fibrillation
Diarrhoea
Muscle wasting
Tachycardia

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39
Q

How does Graves’ disease cause hyperthyroidism?

A

Anti TSH receptor antibodies which over stimulate thyroid gland

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40
Q

How does toxic adenoma / toxic multinodular goitre cause hyperthyroidism?

A

Iodine deficiency leads to compensatory TSH secretion

The excess TSH can cause the thyroid to enlarge and create a multinodular goiter.

Nodules can become TSH independent and secrete thyroid hormone

Toxic adenoma = 1 nodule

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41
Q

What causes Secondary Hyperthyroidism?

A

Benign Tumours
Pituitary - TSH secreting
Hypothalamic - TRH secreting
Ectopic - hCG secreting

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42
Q

How to diagnose hyperthyroidism?

A

Thyroid function test

Antibodies test (anti TSH receptor)
Ultrasound if palpable nodule

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43
Q

What are the TSH and T4 levels in someone with Primary Hyperthyroidism?

A

Low TSH
High T4

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44
Q

What are the TSH and T4 levels in someone with Secondary Hyperthyroidism?

A

High TSH and High T4

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45
Q

How to manage hyperthyroidism? (4)

A

Beta blocker (Propanol) for symptomatic relief
And carbimazole/ propylthiouracil to stop thyroid making hormones
Radio- iodine for goitres and adenomas
Thyroidectomy for recurrent goitres

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46
Q

How to manage a Thyroid storm? (4)

A

IV beta blocker (propanol)
IV Dijoxin (increases cardiac output but decreases HR)
Anti thyroid medication
Steroids

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47
Q

What is De Quervain’s thyroiditis?

A

Hyperthyroidism from acute inflammation of the thyroid gland, due to viral infection

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48
Q

Most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

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49
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune process associated withHLA-DR5andanti-TPO antibodies

Thyroid gland feels smooth but larger than normal

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50
Q

How does thyroiditis causes hypothyroidism?

A

Thyroiditis can also cause symptoms of hypothyroidism, or underactive thyroid. In some cases, after your thyroid is overactive for a period of time, it may become underactive.

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51
Q

What are the causes of hypothyroidism? (7)

A

Hashimoto’s
Autoimmune
Goitre (fibrous tissue)
Iodine deficiency
Postpartum
Viral (De Quervain’s)
Drugs (lithium)

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52
Q

How to diagnose Hypothyroidism?

A

Thyroid function test
- high TSH and low T4 = primary
- low TSH and low T4 = secondary

Test for antibodies

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53
Q

Management for Hypothyroidism?

A

Levothyroxine (manufactured thyroid hormone)

Risks include osteoporosis and cardiac arrythmias.

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54
Q

How to investigate a thyroid cancer? (4)

A

1- Ultrasound (malignant or benign)
2- Fine needle biopsy (malignant or benign)
3- Thyroid function tests (manage hypo/Hyperthyroidism first)
4- Laryngoscopy (paralysed vocal cord is highly suggestive of malignancy)

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55
Q

Papillary cancer is derived from which cells?
And what do these cells do?

A

Follicular cells

They secrete thyroglobulin and take up radioiodine

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56
Q

Follicular cancer is derived from which cells?
And what do these cells do?

A

Follicular cells

secretes thyroglobulin and takes up radioiodine

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57
Q

How does follicular cancer spread?

A

Early metastasis
vascular invasion
Distal spread more common

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58
Q

How to manage follicular cancer?

A

Lobectomy (with lymph removal)
Radioiodine
TSH suppression and Levothyroxine

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59
Q

Medullary cancer is derived from which cells?
And what do these cells do?

A

para-follicular cells
(aka C-Cells responsible for calcitonin production)
Very aggressive cancer

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60
Q

How to manage Medullary cancer?

A

Lobectomy

Thyroid hormone replacement for normal TSH (no TSH suppression)

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61
Q

What is the most aggressive thyroid cancer?

A

Anaplastic

Poor differentiation and Very aggressive

infiltrative to local structures, soft tissue of neck, widespread metastases, early mortality

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62
Q

How to manage Anaplastic cancer

A
  • Does not respond to radioactive iodine
  • If possible a total thyroidectomy is done
  • Combined chemotherapy and radiation - may be palliative
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63
Q

What is Cushing’s Syndrome

A

Hypercortisolism (excess glucocorticoids )

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64
Q

What causes Cushing’s syndrome? (4)

A

ACTH INDEPENDENT
Excess steroid use

adrenal adenoma or adrenal hyperplasia - secreting excess cortisol

ATCH DEPENDENT
pituitary adenoma secreting excess ACTH (Cushing’s disease )

Ectopic ACTH e.g. from small cell lung cancer

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65
Q

Signs and symptoms of Cushing’s syndrome?

A
  • Hypertension
  • Moon face
  • Buffalo hump
  • Central adiposity
  • Violaceous striae
  • Muscle wasting and proximal myopathy
  • Acne
  • Bloating and weight gain
  • Mood change & Tiredness
  • Menstrual irregularity & Reduced libido
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66
Q

How to investigate Cushing’s syndrome?
(Gold standard)

A

Overnight Dexamethasone suppression test (shows failure of cortisol suppression) GOLD

Plasma cortisol levels (could be unreliable)

Exclude excess steroid use

24-hour urinary free cortisol

67
Q

How does a dexamethasone suppression test distinguish between Cushing’s disease and an ectopic ACTH source?

A

Dexamethasone suppress ACTH production from the pituitary gland.
(Low dose DST = cortisol not suppressed)
After High dose DST: cortisol should be suppressed if its Cushing’s disease.
Cortisol will remain High if its an ectopic cause.

68
Q

Other investigations to localise the cause of Cushing’s syndrome?

A

MRI pituitary (pituitary adenoma)
CT chest, abdomen, pelvis (ectopic)

69
Q

What is the Cortisol pathway from the hypothalamus?

A

Hypothalamus secrets CRH
CRH causes the pituitary to secrete ACTH
ACTH causes adrenal cortex (Zona fassicularis) to secrete cortisol

70
Q

When does cortisol levels peak and what are its effects?

A

Peaks in the morning (circadian rhythm )
Cortisol
- ↑gluconeogenesis, proteolysis, lipolysis
- ↑ insulin levels
- ↑ sensitivity to catecholamines = vasoconstriction
- ↑ BP & fluid retention
- ↓gonadotrophin releasing hormone
- ↓ dampens immune response

71
Q

How to manage Cushing’s syndrome?

ACTH-dependent causes

A

ACTH-dependent causes
Cushing’s disease: trans-sphenoidal resectionof the pituitary tumour
Ectopic: Treat cancer
(glucocorticoid antagonists or radiotherapy)

72
Q

How to manage Cushing’s syndrome?

ACTH-INdependent causes

A

ACTH-INdependent causes

Review medications

Adrenal tumour:tumour resection
(replacement of glucocorticoids and mineralocorticoids)

73
Q

Excessive growth hormone secretion causes which condition?

A

Acromegaly

74
Q

What are the 3 main causes of acromegaly?

A

Pituitary adenomas (> 90% cases)
Hypothalamic tumour (excess GHRH)
Ectopic (GH/GHRH)

75
Q

What effects does Growth Hormone have?

A

Liver releases more glucose
Muscles retain Nitrogen for growth
Osteoblasts stimulated
More insulin resistance = ↑Blood glucose
Stimulates insulin like growth factor 1 production!

76
Q

What should growth hormone be suppressed by?

A

Somatostatin

77
Q

How does acromegaly cause type 2 diabetes and inappropriate growth?

A

Excess GH causes insulin resistance
Excess GH causes excessive IGF-1

78
Q

Signs and symptoms of acromegaly?

A

Large hands and feet
Outward growth of the jaw and head with increased inter dental spacing and macroglossia
Headaches
Erectile dysfunction
Voice change
Increased sweating
Mood disturbances
Polyuria

79
Q

How to investigate acromegaly?

A

Test to see if Serum insulin-like growth factor 1 (IGF-1) is raised.
Oral glucose tolerance test.
(Glucose load should suppress GH)
Pituitary MRI

80
Q

How to manage acromegaly?

A

trans-sphenoidal surgery - remove pituitary tumour

Somatostatin receptor ligands
GH analogue
Dopamine agonist

81
Q

What are some of the complications of acromegaly?

A

T2DM (insulin resistance from excess GH)
Cardiomyopathy
Carpel tunnel syndrome
Organomegaly
Arthritis

82
Q

Difference between acromegaly and gigantism?

A

Gigantism = Excess GH secretion in children (before fusion of the growth plates)

83
Q

What is Conns syndrome

A

Primary hyperaldosterone

84
Q

Which cells produce aldosterone, and what does it do?

A

Zona glomerulosa

↓K+
↑ Na+
↑BP

Aldosterone binds to DCT
Principal cells: ↑ Na/K pumps (more Na+ in blood)
Intercalated cells: ↑ ATPase pumps (more protons in urine = ↑pH)

85
Q

Causes of hyperaldosterone?

A

Primary:
Adrenal adenoma (Conns Syndrome)
Adrenal hyperplasia or carcinoma

Secondary (inappropriate activation of RAAS):
Renal artery stenosis
Heart failure

86
Q

Signs and symptoms of Hyperaldosterone?

A

Classically, the disease presents as refractory hypertension, hypokalaemia, and metabolic alkalosis. Hypernatraemia may or may not be seen.

  • Lethargy
  • Mood disturbance
  • Paresthesia and muscle cramps
  • Polyuria and nocturia
87
Q

How to investigate hyperaldosteronism?

A

Aldosterone/renin ratio

high aldosterone, with LOW renin in cases of primary hyperaldosteronism (Do CT after)
high aldosterone and HIGH renin in cases of secondary hyperaldosteronism.

Serum U+E
Blood gas
Adrenal venous sampling (measure corticosteroids secreted from each adrenal gland to see if uni or bilateral problem)

88
Q

How to manage Hyperaldosteroism?

A

Aldosterone antagonists
Adrenalectomy for unilateral adrenal adenoma/ hyperplasia

Potassium sparing diuretics (promotes Na+ excretion) for bilateral (Spironolactone)

For Secondary hyperaldosteronism - renal artery angioplasty to resolve renal artery stenosis

89
Q

What happens if a pituitary adenoma affects the mammotrophs?

A

hyperprolactinaemia caused by a prolactinoma.
(Prolactin causes breasts to grow and develop and causes milk to be made after a baby is born)

90
Q

What happens if a pituitary adenoma affects the somatotroph cells?

A

Acromegaly due to excess growth hormone.

91
Q

What happens if a pituitary adenoma affects the Corticotroph cells?

A

excess cortisol (Cushing’s syndrome) through excess production ofACTH.

92
Q

What is Addisons Disease?

A

primary adrenal insufficiency caused by destruction or dysfunction of the adrenal cortex.

Results in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and gonadocorticoid (androgens) deficiency

93
Q

What causes Addisons Disease? (5)

A

Autoimmune
Infection (TB,HIV)
Infarction
Congenital
Medication

94
Q

What does a reduction in glucocorticoids, mineralocorticoids, and androgens have?

A

↓glucocorticoids = ↓cortisol, weight loss, fatigue,
(No -ve feedback so more CRH & ACTH = more prolactin)

↓mineralocorticoids = ↓Na+, ↓H2O, ↓BP, tachycardia

↓androgens = ↓ libido

95
Q

Signs and symptoms of Addison’s disease?

A

Hypotension and tachycardia
Fatigue and weakness
Nausea and vomiting
Syncope
Pigmentation (due to an increase in ACTH pre-cursors)

96
Q

How to investigate Addison’s disease?

A

Morning Cortisol levels (less than 100nmol/L = highly suggestive)

ACTH stimulation test (Synacthen): failure of adequate rise = highly suggestive

Check for adrenal antibodies, U+E’s
CT adrenals

97
Q

How to manage Addison’s disease?

A

Corticosteroid replacement:
(Hydrocortisone & Flurocortisone)
Androgen replacement for women

98
Q

1- What is Addisons crisis?
2- Signs and symptoms?
3- Management?

A

1- Adrenal crisis due to a a drop in corticosteroids
Severe Metabolic acidosis, hyperkalaemia, hyponatraemia.

2- Hypotension, hypovolemic shock, confusion, nausea, abdo pain, Trigger (e.g infection)

3- IV fluids and Hydrocortisone, treat underlying cause

99
Q

What is Secondary Adrenal Insufficiency?

A

Adrenal insufficiency due to insufficient pituitary or hypothalamic action on the adrenal glands. (lack of ACTH)

100
Q

Causes of Secondary Adrenal Insufficiency?

A

Long term steroid use

Hypothalamic pituitary disease - resulting in reduced ACTH production

Removal of pituitary tumour - remaining ACTH-secreting cells in the pituitary gland may be sluggish in their recovery

101
Q

Difference between clinical manifestation of primary and secondary adrenal insufficiency?

A

Similar presentation to Addison’s disease.

However in Secondary = no hyperpigmentation as there is no excess ACTH

Primary = High ACTH
Secondary = Low ACTH

Note: In Secondary Mineralocorticoid production remains intact.

102
Q

What will a patient with Secondary Adrenal Insufficiency levels be like for:

1- Cortisol,
2- ACTH
3- Mineralocorticoids

A

Cortisol = low
ACTH = low
Mineralocorticoids = normal

103
Q

How to manage Secondary Adrenal Insufficiency? (2)

A

Adrenals will recover if long-term steroids are slowly weaned off

Oral hydrocortisone

104
Q

Where is ADH produced?
Where is ADH stored?
When is ADH released?
What does ADH do?

A

magnocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus

Stored and released by the posterior pituitary

In response to rising plasma osmolality

ADH acts on the DCT and collecting duct to increase water reabsorption independent of sodium. Insertion of aquaporin-2 channels allowing the free entry of water.

105
Q

What is SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)?

A

ADH excess
Reduced diuresis
Increased total body water
Hyponatremia

106
Q

Pathophysiology of SIADH?

A

Increased ADH release

water retention by increased insertion of aquaporin 2, butnotthe reabsorption of solutes. This increases blood volume and decreases serum osmolarity.

Increase in blood volume leads to stretching of heart muscle and release of ANP and BNP (natriuretic peptide). This inhibits renin release and activity. This promotes natriuresis (excretion of sodium). This leads to sodium and water excretion

euvolaemic state rather than a hypervolaemic state, coupled with hyponatraemia.

Overall, patients will have high urine Na+ levels and low serum Na+ levels. They will be euvolaemic due to compensatory mechanisms.

107
Q

Causes of SIADH?

A

Neurological - meningitis, cranial haemorrhage, stroke
Malignancy
Infections - TB, HIV, Pneumonia
Endocrine - Hypothyroidism, Hypopituitarism
Drugs - CARDISH - chemo, antidepressants, recreational drugs, diuretics, inhibitors e.g. ACEI & SSRIs, sulfonylurea, hormones e.g. desmopressin)

108
Q

Signs and symptoms of SIADH?

A

Hyponatraemic and euvolaemic

Mild(130-135 mmol/L):
- Nausea, vomiting, headache, lethargy, anorexia

Moderate (125-129 mmol/L):
- Weakness, muscle aches, confusion, ataxia, asterixis

Severe(< 125 mmol/L):
- Reduced consciousness, seizures, myoclonus, respiratory arrest

109
Q

How to investigate SIADH? (2)

A

Blood test (low plasma osmolary)
Urine test (high osmolarity and Na+)

Clinical euvolaemia

110
Q

How to manage SIADH? (3)

A

Fluid restriction (up to 750ml/day) and treat underlying cause
ADH antagonists (e.g. tolvaptan, deomeclocycline)
Oral sodium and furosemide (diuretic)

Treat acute fast and chronic slow
Rapid correction = central pontine myelinolysis (brain shrinks)

111
Q

How does insulin, adrenaline, and aldosterone affect K+ homeostasis?

A

Insulin & Adrenaline: causes an intracellular shift of K+
Aldosterone: promotes K+ excretion

112
Q

At what serum concentration is a patient considered hyperkalemic?

A

A serum level >5.5 mmol/L is considered to be hyperkalaemia

A serum level > 6.5mmol/L = MEDICAL EMERGENCY!

113
Q

Drugs which can cause Hyperkalaemia? (6)

A
  • Potassium-sparing diuretics e.g. spironolactone - COMMON
  • ACE inhibitors (interfere with RAAS) e.g. ramipril - COMMON
  • NSAIDs - COMMON
  • Heparin
  • Beta-antagonists: inhibit cellular entry of potassium
  • Digoxin: inhibitor of Na+/K+ ATPase causing reduced cellular entry of potassium
114
Q

Causes of Hyperkalaemia?

A

IMPAIRED EXCRETION
Kidney injury
Addison’s disease (reduced aldosterone causes K+ excretion)
Hypoaldosteronism
Drugs

INCREASED K+ RELEASE FROM CELLS
Lactic acidosis (acidosis swap H+ from blood with K+ in cells)
Insulin deficiency (insulin activates Na/K pumps)
Haemolysis

115
Q

How does high levels of K+ affect action potential?

A
  • When K+ levels in the blood rise - this reduces the difference in electrical potential between cardiac myocytes and outside of the cells meaning the threshold for action potential is significantly decreased resulting in increased abnormal action potential and thus abnormal heart rhythms that can result in ventricular fibrillation and cardiac arrest
  • In smooth muscle it can cause cramping - due to depolarisation and contraction
  • In skeletal muscle it can cause weakness and flaccid paralysis - resting potential is too high, which means muscle can’t repolarise and then contract again
116
Q

What are the Signs and Symptoms of Hyperkalaemia?

A

Tachycardia (arrhythmia)
ECG differences - tall tented T waves, small P waves, wide QRS

Muscle weakness
Lightheadedness
Muscle cramps
Paresthesia (tingling in skin)
Palpitations
Chest pain

117
Q

How to investigate Hyperkalaemia?

A

ECG ( flat P waves, short QT interval, broad QRS, ST depression, and tented T waves)

U&E’s

Lithium heparin sample: rule out pseudohyperkalaemia. This is where thrombus formation and haemolysis causes falsely elevated potassium concentration

VBG: check for acidosis which may be causing the hyperkalaemia

118
Q

How to manage Hyperkalaemia?

A

Calcium gluconate (calcium protects cardiac membranes)

Insulin

Salbutamol

119
Q

At what plasma concentration is a Pattie to described as Hypokalaemic?

A

plasma K+ concentration < 3.5 mmol/L.

Severe: < 2.5 mmol/L

120
Q

Causes of Hypokalaemia?

A

Inadequate intake

Increased excretion (diuretics, excess mineralcorticoids, Cushing’s, Conns, Nephrotic syndrome, steroid use, diarrhoea)

Shift from extracellular to intracellular (alkalosis, excess insulin, Activation of beta-adrenergic receptors)

121
Q

How does low K+ affect Cardiac, Smooth, Skeletal, and Respiratory muscles?

A

Diminished contraction.

  • Cardiac - arrhythmias and cardiac arrest
  • Smooth muscle - constipation
  • Skeletal muscle - weakness, cramps and flaccid paralysis
  • Respiratory muscles - respiratory depression
122
Q

Signs and Symptoms of Hypokalaemia?

A

Arrhythmias
Muscle paralysis
Hypotonia
Hypoflexia

Fatigue
Generalised weakness
Light headedness
Muscle cramps and pain
Tetany
Palpitations
Constipation

123
Q

How to diagnose and manage Hypokalaemia?

A

Measure plasma K+ conc (<3.5mmol/L)
ECG (Prolonged PR, ST segment depression, flattening of T wave, U wave present)

Treat underlying cause
Review meds
K+ replacement (orally or K+ sparing diuretics)

124
Q

What is Diabetes Insipidus?

A

The patient is unable to make ADH or respond to ADH.
Resulting in the production of large quantities of dilute urine.
Inability to concentrate urine.

125
Q

Causes of Diabetes Insipidus?

A

NEPHROGENIC:
Drugs (lithium)
Genetic
Electrolyte imbalances
Renal disease

CRANIAL:
Head trauma
Meningitis
Inflammation (sarcoidosis)
Vascular (sickle cell)

126
Q

Difference between central and nephrogenic DI?

A

Central DI results from any condition that impairs the production, transportation, or release of ADH.

Nephrogenic DI results from conditions that impair the renal collecting ducts’ ability to respond to ADH.

127
Q

Signs and symptoms of DI?

A

Postural hypotension
Hypernatraemia
Lots of urine
Thirsty
Dehydration

128
Q

How to investigate DI?

A

Water deprivation test (desmopressin)
- cranial: after desmopressin urine osmolarity increases
- nephrogenic: after desmopressin, no effect to urine osmolarity

U&E’s (high Na+)
Serum glucose (exclude DM)
Urine osmolarity (low)
Serum osmolarity (high)

MRI for cranial DI

129
Q

How to manage DI?

A

Cranial DI = Desmopressin.
Sodium should be monitored routinely due to the risk of hyponatraemia.

Nephrogenic DI= Thiazade diuretics
correct any metabolic abnormality and stopping any offending drugs.

130
Q

At what plasma concentration are patients referred as Hypercalcemic?

A

> 10.5mg/dL

131
Q

How is calcium homeostasis maintained?

A

The parathyroid glands, specifically the chief cells in the glands, produce parathyroid hormone in response to low calcium.

The parathyroid hormone causes:
The bones to release calcium

The kidneys to reabsorb more calcium so it’s not lost in the urine (as well as excrete more phosphate)

The kidneys to synthesise calcitriol/ active Vitamin D. Active Vitamin D then goes on to cause the gastrointestinal tract to increase calcium absorption.

132
Q

What causes Hypercalcemia?

A

Acidosis- promotes less binding between albumin and calcium. This causes less bound calcium and more free ionised calcium

Hyperparathyroidism
Malignant Tumours (secrete PTHrP)
Excess Vit D
Sarcoidosis
Milk-alkali syndrome
Drugs - thiazides diuretics, lithium

133
Q

How does High levels of Calcium affect neurones?

A

High levels of extracellular Ca, voltage-gated sodium channels are less likely to open up, which makes it harder to reach depolarisation, and makes the neuron less excitable.

Slower or absent reflexes, muscle contraction

134
Q

Signs and symptoms of Hypercalcemia?

A

Abdominal pain
Vomiting
Constipation
Dehydration
Polydipsia and polyuria
Muscle weakness
Confusion + hallucinations
Pyrexia

135
Q

How to investigate Hypercalcemia?

A

Blood test (Ca, PTH, Vit D, Albumin, Phosphorus, Mg)
Urine test (High Ca)
ECG + imaging

136
Q

How to manage Hypercalcaemia?

A

Rehydration
Loop diuretics (inhibit calcium reabsorption in the loop of Henle)
Glucocorticoids (Decrease calcium absorption from GI tract)
Calcitonin + Biphophonates (reduce bone resorption)
Chemo for malignancy

137
Q

At what plasma concentration is a patient described as Hypocalcaemic?

A

Ca < 8.5mg/dL or 2.1mmol/L

138
Q

Causes of Hypocalcaemia?
(1) With increased phosphate
(2) with normal/ low phosphate

A

Chronic kidney diseases (lack of reabsorption)
Hypoparathyroidism
Acute rhabdomyolysis: large numbers of cells die and release phosphate. The phosphate binds to the ionised calcium and forms calcium phosphate, making it insoluble

Vit D deficiency (osteomalacia)
Acute pancreatitis: free fatty acids end up binding to ionised calcium, which is insoluble
Respiratory alkalosis: high pH (alkalosis) causes more binding between albumin and calcium

139
Q

How does low Calcium affect neurones?

A

Low levels of calcium, voltage-gated sodium channels are more likely to open up, which allows the cell to depolarise more easily, and makes the neurone more excitable. This can trigger tetany.

140
Q

Signs and Symptoms of Hypocalcaemia?
SPASMODIC

A

S – Spasms (Trousseau’s sign)
P – Perioral parasthaesia
A – Anxiety/Irritability
S – Seizures
M – Muscle tone increase (colic, dysphagia)
O– Orientation impairment (i.e. confusion)
D – Dermatitis
I – Impetigo herpetiformis
C – Chvostek’s sign

141
Q

How to investigate Hypocalcaemia?

A

Blood test: (Ca, PTH, Vit D, albumin, phosphorus, Mg)
ECG (prolonged QT, prolonged ST segment, and arrhythmias)
X-ray (suspected osteomalacia)

142
Q

How to manage Hypocalcaemia?

A

Calcium and Vit D supplements
Calcium gluconate (spasms/ ECG changes)
Correct alkalosis if present

143
Q

How is Primary Hyperparathyroidism caused?

A

Uncontrolled PTH produced directly by a tumour of the parathyroid glands. Can lead to Hypercalcemia

144
Q

How is Secondary Hyperparathyroidism caused?

A

There is increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease.

The glands become more bulky.

The serum calcium level will be low or normal but the parathyroid hormone will be high.

145
Q

How is Tertiary Hyperparathyroidism caused?

A

Autonomous secretion of PTH, usually because of chronic kidney disease (CKD).

when the cause of the secondary hyperparathyroidism is treated the parathyroid hormone level remains inappropriately high. hypercalcaemia.

146
Q

Signs and Symptoms of Hyperparathyroidism?

A

Moans, Stones, Groans and Psychiatric Moans

Painful Bones
Renal Stones
Abdominal Groans - GI symptoms: Nausea, Vomiting, Constipation, Indigestion
Psychiatric Moans – Effects on nervous system: lethargy, fatigue, memory loss, psychosis, depression

147
Q

Causes of Hyperparathyroidism?
Primary, secondary and tertiary

A

Adenomas

Vit D deficiency
Pancreatitis, rhabdomyolysis
Calcium malabsorption/ deficiency
CKD

Prolonged secondary hyperparathyroidism
The glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected.

148
Q

How to investigate Hyperparathyroidism?

A

Blood test (PTH, Ca, Vit D, Phosphate)
Primary and tertiary (High PTH and Ca)
Secondary (High PTH and LOW Ca)

Urine test (raised Ca)

149
Q

How to manage Hyperparathyroidism?

A

Primary: remove tumour, reduce Ca intake, Calcimimetics (mimics Ca and binds to receptors on parathyroid cells)

Secondary: Vit D, phosphate binders, Renal transplant if renal failure.

Tertiary: Surgical removal of parathyroid tissue

150
Q

What cause Primary and Secondary Hypoparathyroidism?

A

Autoimmune
DiGeorge syndrome
Autosomal dominant hypoparathyroidism (mutation in the parathyroid cell’s calcium-sensing receptor.)

Removal of parathyroid glands during surgery
Low Mg - Mg needed for PTH secretion

151
Q

Signs and symptoms of Hyperparathyroidism?

A

Chvostek’s sign: facial muscles twitch after the facial nerve is lightly tapped.
Trousseau’s sign: muscle spasm that makes the wrist and metacarpophalangeal joints flex.
Arrhythmias

Tetany
Pins and needles
Seizures

152
Q

How to investigate Hyperparathyroidism?

A

Blood test: (Low PTH, low Ca, Low Vit D, High Phosphate)
ECG: prolonged QT, prolonged ST segment, and arrhythmias

153
Q

How to manage Hyperparathyroidim?

A

Calcium and vitamin D supplements
Recombinant human parathyroid hormone

154
Q

What is a carcinoid tumour?

A

tumour of the neuroendocrine cells, resulting in excessive release of certain hormones.

Neuroendocrine cells release….
amines: serotonin and histamine
polypeptides: bradykinin and prostaglandins = Vasodilators

155
Q

What is carcinoid syndrome?

A

Carcinoid syndrome occurs when there is a buildup of hormones produced by the neuroendocrine cells as the liver is no longer able to metabolise them.

Increased histamine and bradykinin: can cause vasodilation leading to flushing

Increased histamine: can cause itching

Increased serotonin: can cause thickening of fibrosis, particularly in the heart valves leading to heart dysfunction

156
Q

Signs and symptoms of a carcinoid tumour?

A

Abdominal pain
Diarrhoea
Flushing
Wheeze
Pulmonary stenosis

  • effects of excess serotonin
157
Q

How to investigate a carcinoid tumour?

A

24 hr urine 5-hydroxyindoleacetic acid (high levels)
X ray/ MRI/ CT to identify location
Plasma chromogranin A (marker for the tumour)
Ostreoscan (binds to somatostatin receptor on tumour)

158
Q

How to manage Carcinoid Tumours?

A

Decreasing emotional stress and alcohol consumption
Somatostatin analogues (Octreotide)
Surgical resection
Radiofrequency ablation of hepatic metastases

159
Q

What is a Pheochromocytoma?

A

tumour (usually benign) arising from chromaffin cells in the adrenal medulla resulting in the overproduction of catecholamines

Catecholamines ie adrenaline

160
Q

Sign and symptoms of pheochromocytoma?

A

Hypertension
Tachycardia
Palpitations
Anxiety
Sweating
Hypersensitive retinopathy

161
Q

How to investigate Pheochromocytoma?

A

Plasma metanephrines and urinary metenephrines
(Metenephrines = breakdown product of catecholamines)

Adrenal imaging
PET scan

162
Q

How to manage Pheochromocytoma?

A

Alpha blockade - BP and heart rate to normalise
Beta blockade - for BP control and expand Blood volume

Remove the tumour

163
Q

How to diagnose Pre-Diabetes?

A

HbA1c between 42-47 mmol/mol

Hasnat Motive (1 decks)

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