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Phase 2a Medicine > endocrinology > Flashcards

endocrinology Flashcards

1
Q

What are the 7 major organs involved in the endocrine system

A

pituitary gland, thyroid, parathyroid, adrenal glands, pancreas, ovary and testes

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2
Q

What are the properties of water-soluble hormones

A

transport- unbound
cell interaction- bind to surface receptor
half-life- short
Clearance- fast

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3
Q

Are peptide hormones lipo or hydro-philic

A

hydrophilic

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4
Q

What are the properties of Fat-soluble hormones

A

transport- protein bound
cell interaction- diffuse into cell
half life- long
clearance- slow

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5
Q

Are steroid hormones lipo or hydrophilic

A

lipophilic

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6
Q

what form are peptide hormones in at different stages

A

Synthesis: preprohormone -> prohormone
Packaging: prohormone -> hormone
Storage: hormone
Secretion: hormone

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7
Q

Are thyroid hormones water soluble

A

Thyroid hormones are not water soluble, 99% is protein bound.

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8
Q

What is the process of T3 and T4 synthesis and secretion

A

Tyrosine molecules are incorporated with iodine to form iodothyrosines. These conjugate to give rise to T3 and T4 which are stored in colloid bound to thyroglobulin. T3 and T4 are cleaved from thyroglobulin when TSH stimulates the movement of colloid into secretory cell.

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9
Q

Which hormones have their receptor in the nucleus

A

oestrogen
thyroid hormone
vitamin D

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10
Q

Which class of hormone has its receptors in the cytoplasm

A

steriods

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11
Q

What are the features of vitamin D

A

Fat soluble
Enters cells directly to nucleus to stimulate mRNA production
Transported by vitamin D binding protein
cholesterol derivative

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12
Q

What are the features of adrenocortical and gonadal steroids

A

95% protein bound
After entering the cell, it passes to nucleus to induce response
Altered to active metabolite
Bind to a cytoplasmic receptor

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13
Q

What are the 5 steps of steroid action

A

Steroid hormone diffuse through plasma membrane and binds to receptor
Receptor-hormone complex enters nucleus
Receptor-hormone complex binds to GRE
Binding initiates transcription of gene to mRNA
mRNA directs protein synthesis

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14
Q

What are GREs

A

glucocorticoid-response elements, found in promoter regions of steroid sensitive genes

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15
Q

What is involved in the control of hormone secretion

A

Basal secretion – continuously or pulsatile
Release inhibiting factors – dopamine inhibiting prolactin, sum of positive and negative effects (GHRH and somatostatin on GH)
Releasing factors

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16
Q

What is involved in the control of hormone action

A

Hormone metabolism
Hormone receptor induction ( induction of LH receptors by FSH in follicle)
Hormone receptor down regulation
Synergism
Antagonism

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17
Q

What is the hypothalamo-pituitary-thyroid axis

A

Hypothalamus -> TRH -> anterior pituitary -> TSH -> thyroid gland -> thyroid hormones

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18
Q

What are the 5 functions of thyroid hormone

A

Accelerates food metabolism
Increases protein synthesis
Enhances fat metabolism
Brain development during foetal life and postnatal development
Growth rate accelerated

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19
Q

What is the endocrine role of the adrenal cortex

A

Produces steroids hormones:
Mineralocorticoids e.g. aldosterone
Glucocorticoids e.g. cortisol androgens
Androgens e.g. androstenedione and DHEA

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20
Q

What is the endocrine function of the adrenal medulla

A

Produces epinephrine and norephinephrine

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21
Q

What are the levels of BMI

A

<18.5 – underweight
18.5-24.9 – normal
25.0-29.9 – overweight
30.0-39.9 – obese
>40 – morbidly obese

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22
Q

How is BMI calculated

A

weight (kg) / height (m2)

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23
Q

What are 7 major risks of obesity

A

Type II diabetes
Hypertension
Coronary artery disease
Stroke
Osteoarthritis
Obstructive sleep apnoea
Carcinoma

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24
Q

What 4 carcinomas have an increased risk caused by obesity

A

Breast
Endometrium
Prostate
Colon

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25
Q

What is the effect of different nutrients on satiety

A

Highly refined sugar – quick and short satiety
Low glycaemic index foods – better
High protein – prolonged satiety
High fat – stimulate and entice people to eat more

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26
Q

Which region of the brain plays a central role in appetite regulation

A

Hypothalamus

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27
Q

What is the structure and action of peptide YY

A

36 amino acids
Structurally similar to NPY
Binds NPY receptors
Secreted by neuroendocrine cells in ileum, pancreas and colon in response to food
Inhibits gastric motility
Reduces appetite

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28
Q

what is NPY

A

Neuropeptide Y
It stimulates food intake, preferably carbohydrates

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29
Q

What is Cholecystokinin’s effect on appetite regulation

A

Receptors in pyloric sphincter
Delays gastric emptying
Gall bladder contraction
Insulin release
And via vagus – satiety

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30
Q

What 4 stimuli are involved in increasing appetite

A

Olfactory, gustatory, cognitive and visual stimuli

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31
Q

Which hormone stimulates food intake

A

Ghrelin

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32
Q

What is the role of stretch receptors in the stomach

A

increase satiety

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33
Q

What 4 hormones increase satiety

A

CCK, Glucagon like peptide-1 (GLP), insulin and Peptide YY

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34
Q

Define Diabetes Mellitus

A

A disease in which the body’s ability to produce or respond to the insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood.

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35
Q

Name 6 types of diabetes

A

Type 1
Type 2 – includes gestational and medication induced diabetes
Maturity-onset diabetes of the young (MODY)
Pancreatic diabetes
Endocrine diabetes – Cushing’s/ acromegaly
Malnutrition related diabetes

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36
Q

What is the pathology of diabetes

A

Chronic hyperglycaemia due to insulin dysfunction – can’t move glucose from blood into cells. Leads to low glucose in cells with starve of energy.

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37
Q

Define type 1 diabetes

A

an insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction.

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38
Q

Define type 2 diabetes

A

inappropriately low insulin secretion and peripheral insulin resistance

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39
Q

What is the disease process of diabetes

A

Lack of insulin drives the mobilisation of energy stores from muscles, fat and the liver
Glucose accumulates in the blood, causing hyperglycaemia
In the kidneys, the glucose reabsorption mechanism becomes saturated and glucose appears in the urine
Glucose within renal tubules draws water in by osmosis, leading to osmotic diuresis
The raised plasma osmolality stimulates the thirst centre
Over time, diabetes damages capillaries and markedly accelerates atherosclerosis

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40
Q

how does acromegaly cause secondary diabetes

A

excessive secretion of growth hormone. Insulin resistance rises.

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41
Q

How does cushing’s syndrome cause secondary diabetes

A

increased insulin resistance, reduced glucose uptake into peripheral tissues.

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42
Q

What is the process of drug-induced diabetes

A

glucocorticoids increase insulin resistance

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43
Q

What causes type 1 diabetes

A

initiated by genetic susceptibility and environmental triggers

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44
Q

What causes type 2 diabetes

A

combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

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45
Q

What causes MODY

A

single gene defect altering beta cell function

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46
Q

What are 6 subacute clinical presentations of diabetes

A

Thirst (osmotic activation of hypothalamus)
Polyuria (osmotic diuresis)
Weight loss and fatigue (lipid muscle loss due to unrestrained gluconeogenesis)
Hunger (lack of useable energy source)
Pruritis vulvae and balanitis
Blurred vision (due to uptake of glucose/ water into lens)

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47
Q

What are 5 suggestive features of type 1 Diabetes

A

Onset in childhood/ adolescence
Lean body habitus
Acute onset of osmotic symptoms
Prone to ketoacidosis
High levels of islet autoantibodies

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48
Q

What are 3 suggestive features of type 2 diabetes

A

Usually presents in over 30s
Onset is gradual
Diet, exercise and oral medication can often control hyperglycaemia

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49
Q

What are 4 suggestive features of MODY

A

Parents affected with diabetes
Absence of islet autoantibodies
Evidence of non-insulin dependence
Sensitive to sulphonyl urea

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50
Q

What are 3 investigations for diabetes

A

Fasting >7mmol/L plasma glucose
Random plasma glucose >11mmol/L
HbA1c 6.5%/ 48mmol/mol

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51
Q

What are 3 methods of neuropathy screening for diabetes

A

sensation (10mg monofilament), vibration perception (tuning fork), ankle reflexes.

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52
Q

What are the consequences of missing a type 1 diabetes diagnosis

A

It can lead to fat metabolism and the formation of ketone bodies.

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53
Q

What is the process of ketone body production in type 1 diabetes

A

reduced insulin leads to fat breakdown, forming free fatty acids, which:
Impair glucose uptake
Are transported to the liver, providing energy for gluconeogenesis
Are oxidised to form ketone bodies (acetone, beta-hydroxybutyrate)
Ketone bodies dissolve in the blood and release H+, causing acidosis.

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54
Q

What is the process of Ketoacidosis

A

Absence of insulin and rising counterregulatory hormones leads to increasing hyperglycaemia and rising ketones.
Glucose and ketones escape in the urine but lead to an osmotic diuresis and falling circulating blood volume
Ketones cause anorexia and vomiting

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55
Q

What is Diabetic Ketoacidosis (DKA) characterised by

A

hyperglycaemia, raised plasma ketones and metabolic acidosis

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56
Q

What are 4 symptoms of DKA

A

Polyuria and polydipsia
Nausea and vomiting
Weight loss
Abdominal pain

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57
Q

what are 6 signs of DKA

A

Hyperventilation
Dehydration
‘Fruity breath’
Hypotension
Tachycardia
Coma

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58
Q

What are the 4 steps in management of DKA

A

Rehydration
Insulin
Replacement of electrolytes (K+)
Treat underlying cause

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59
Q

What are 6 complications of diabetes

A

Leading cause of blindness in working age adults – diabetic retinopathy
Diabetic nephropathy – leading cause of end-stage renal disease
Peripheral vascular disease
Stroke
Cardiovascular disease – leading cause of mortality
Diabetic Peripheral Neuropathy – leading cause of non-traumatic lower extremity amputations

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60
Q

what are 4 ways that diabetes causes morbidity and mortality

A

Acute hyperglycaemia- metabolic emergencies, DKA, HHS
Hyperglycaemic hyperosmolar state
Chronic hyperglycemia- tissue complications
side effects of treatment- hypoglycemia

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61
Q

What are 4 features of Diabetic neuropathy

A

Pain – burning, paraesthesia
Autonomic – orthostatic hypotension, constipation, ED
Insensitivity – foot ulceration, Charcot foot, amputation
Peripheral neuropathy – glove and stocking sensory loss

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62
Q

What are 4 risk factors for diabetic neuropathy

A

hypertension, smoking, changes in HbA1c, diabetes duration

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63
Q

What are 3 treatment methods for diabetic neuropathy

A

good glycaemic control, anticonvulsants, opioids.

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64
Q

What are 3 features of diabetic retinopathy

A

Micro-aneurysms: pericyte and smooth muscle loss
Leakage: basement membrane thickening reduced junctional contact with endothelial cells
Ischaemia: pericyte loss

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65
Q

What is the treatment of diabetic retinopathy

A

laser therapy to stabilise changes, not improve sight.

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66
Q

What is the core aim to management of type 1 diabetes

A

Restore the physiology of the beta cell

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67
Q

What are the methods to management of type 1 diabetes

A

Insulin treatment (twice daily with meals)
Awareness of blood glucose lowering effect of exercise
Ability to judge CHO intake
DAFNE: dose adjustment for normal eating (reduces DKA and severe hypos)

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68
Q

What is the first line treatment for Type 2 diabetes

A

Weight loss and exercise are substantial and will reverse hyperglycaemia

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69
Q

What is the issue with the first line treatment for type 2 diabetes

A

Patients with type 2 diabetes don’t tend to respond to these lifestyle changes, due to their lifestyle choices.

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70
Q

What is the second line treatment for type 2 diabetes

A

Medication to control BP, blood glucose and lipids.
Metformin = weight loss
Metformin + sulphonyl urea but side effect of weight gain + chance of hypo
Insulin

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71
Q

What is Hyperglycaemic Hyperosmolar state (HHS) and who does it affect

A

A complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.
unwell patients with type 2 DM

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72
Q

What are 6 symptoms of HHS

A

Weakness
Leg cramps
Vision problems
An altered level of consciousness
marked dehydration
glucose >30mmol/L.

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73
Q

What is the effect on ketonemia in HHS

A

There is no switch to ketone metabolism, so ketonemia stays <3MMOL/L AND PH >7.3.

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74
Q

What is the typical osmolality in HHS

A

> 320mosmol/kg.

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75
Q

What are the dangers of occlusive events in HHS

A

focal CNS signs, chorea, Disseminated intravascular coagulation (DIC), leg ischaemia

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76
Q

What is the management of HHS

A

Give LMWH prophylaxis to all unless contraindication
Rehydrate slowly with 0.9% saline IVI over 48h
Replace K+ when urine starts to flow

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77
Q

what are the 3 mechanisms for increased levels of thyroid hormone

A

Overproduction of thyroid hormone
Leakage of preformed hormone from thyroid
Ingestion of excess thyroid hormone

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78
Q

What are 5 causes of Hyperthyroidism

A

Grave’s disease
Toxic multinodular goitre
Toxic adenoma
Congenital hyperthyroidism
Thyroiditis

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79
Q

What are 7 symptoms of hyperthyroidism

A

Weight loss
Tachycardia
Anxiety
Heat intolerance
Sweating
Diarrhoea
Menstrual disturbance

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80
Q

What are 3 specific signs to graves’ disease

A

Diffuse goitre
Thyroid eye disease
Acropachy

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81
Q

What is the specific sign for adenomal hyperthyroidism

A

Solitary nodule

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82
Q

What is euthyroid hyperthyroxinemia

A

Euthyroid hyperthyroxinemia is defined as a condition in which the serum total T4 and T3 concentrations are increased, but the thyroid-stimulating hormone (TSH) concentration is normal and there are no clinical signs or symptoms of thyroid dysfunction.

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83
Q

What are 3 investigations for thyroid diseases

A

Thyroid function tests to confirm biochemical hyperthyroidism
Clinical history, physical signs usually sufficient for diagnosis
Supporting investigations – thyroid antibodies

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84
Q

What are 4 treatments for hyperthyroidism

A

Antithyroid drugs e.g. thionamides (carbimazole)
Beta blockers
Radioiodine
Surgery (partial/ subtotal thyroidectomy)

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85
Q

Define Graves’ disease

A

An autoimmune disease affecting the thyroid that causes hyperthyroidism and results in an enlarged thyroid.

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86
Q

What is the pathology of graves disease

A

The immune system is tricked into targeting receptors on the thyroid gland, causing it to become overactive - hyperthyroidism.
Increased levels of TSH receptor stimulating antibody (TRAb) which causes excess thyroid hormone secretion (low TSH in the blood stream, but high thyroid hormone levels (T3 and T4) due to the TRAb having the same effects as TSH on the thyroid).

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87
Q

What are 7 symptoms and signs of graves disease

A

Anxiety and irritability
A fine tremor of your hands or finger
Heat sensitivity and an increase in perspiration or warm, moist skin
Weight loss, despite normal eating habits
Enlargement of thyroid gland (goiter)
Bulging eyes – Graves’ ophthalmopathy
Thick, red skin usually on the shins or tops of the feet - Graves’ dermopathy

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88
Q

What is the core aim of management of graves disease

A

Inhibition of the production of thyroid hormones and to block the effect of the hormones on the body.

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89
Q

What are 5 methods involved in the management of graves disease

A

Radioactive iodine therapy – oral radioactive iodine. This destroys the overactive thyroid cells over time, causing the gland to shrink and to lessen symptoms gradually
Anti-thyroid medications – interfere with the thyroid’s use of iodine to produce hormones e.g. carbimazole
Beta blockers e.g. propranolol – provide rapid relief of irregular heartbeats, tremors, heat intolerance and muscle weakness
Ophthalmopathy – corticosteroids/ orbital decompression surgery
Thyroidectomy

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90
Q

Define primary Hypothyroidism

A

Subnormal activity of the thyroid gland due to intrinsic underactivity of the thyroid gland.

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91
Q

Define secondary hypothyroidism

A

Subnormal activity of the thyroid gland due to reduced stimulation of the gland caused by a deficiency of TSH due to disease of the pituitary gland

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92
Q

define tertiary hypothyroidism

A

Subnormal activity of thyroidgland due to low TRH caused by hypothalamic disease

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93
Q

What is the most common type of hypothyroidism, its proportion of all cases and is most common cause

A

Primary
>99%
Most cases due to Hashimoto’s thyroiditis (autoimmune hypothyroidism)

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94
Q

What are the 3 main causes of Adult primary hypothyroidism

A

Hashimoto’s thyroiditis
Thyroidectomy
Iodine deficiency

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95
Q

What is the main cause of adult secondary hypothyroidism

A

Pituitary tumour

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96
Q

What are the 3 main causes of child hypothyroidism

A

Neonatal hypothyroidism
Resistance to thyroid hormone
Isolated TSH deficiency

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97
Q

What are 14 symptoms of hypothyroidism

A

Fatigue, loss of energy, lethargy
Weight gain
Decreased appetite
Cold intolerance
Dry skin
Muscle pain, joint pain, weakness in the extremities
Depression
Emotional lability, mental impairment
Forgetfulness, impaired memory, inability to concentrate
Constipation
Menstrual disturbances, impaired fertility
Decreased perspiration
Paraesthesia and nerve entrapment syndromes
Blurred vision

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98
Q

What are 10 signs of hypothyroidism

A

Weight gain
Slowed speech and movements
Dry skin
Jaundice
Pallor
Coarse, brittle, straw-like hair
Loss of scalp hair, axillary hair, pubic hair, or a combination
Hoarseness
Bradycardia
Pericardial effusion

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99
Q

What are the differential diagnoses to hypothyroidism

A

Addison disease
Goiter
Chronic fatigue syndrome
Hypopituitarism
Iodine deficiency

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100
Q

What are the investigations for hypothyroidism

A

Sinus bradycardia, low pulse pressure, pericardial effusion, coronary artery disease
TSH and thyroxine tests

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101
Q

What are the outcomes of TSH and T3/T4 tests for primary hypothyroidism

A

Increased TSH, usually decreased free T4, decreased T3
T4/T3 may be below normal in positive titre of TPO antibodies in Hashimoto’s

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102
Q

What are the outcomes of TSH and T3/T4 tests for secondary hypothyroidism

A

TSH inappropriately low for reduced T4/T3 levels

103
Q

What are the 3 features of hypothyroidism management

A

Full replacement of 100 µg thyroid hormone (Levothyroxine) – titre according to TSH
Requirements vary according to cause e.g. higher disease in thyroid ablation
Monitoring treatment

104
Q

What are the 3 features of monitoring hypothyroidism treatment

A

Dose titrated until TSH normalises
T4 half-life is long – check levels 6-8 weeks after dose adjustment
In secondary/ tertiary hypothyroidism TSH will always be low, T4 is monitored

105
Q

What is Hashimoto’s thyroiditis

A

Hypothyroidism due to aggressive autoimmune destruction of thyroid cells. An autoimmune thyroid disease characterised by diffuse enlargement of the thyroid and high titres of thyroid autoantibodies.

106
Q

What are 5 risk factors for Hashimoto’s thyroiditis

A

Sex – women more likely
Age – most commonly during middle age
Heredity – family history of Hashimoto’s disease
Other autoimmune disease
Radiation exposure – (more common in Japan)

107
Q

What is the pathology of hashimoto’s disease

A

Inflammation from Hashimoto’s disease, chronic lymphocytic thyroiditis, often leads to an underactive thyroid gland – hypothyroidism.
Activated CD4+ helper T-cells recruit CD8+ cytotoxic T-cells which destroy thyroid follicular epithelial cells
Anti-thyroid autoantibodies produced by activated B-cells may also contribute

108
Q

What are 3 triggers for Hashimoto’s disease

A

Iodine
Infection
Smoking

109
Q

What are 10 signs and symptoms of Hashimoto’s disease

A

Fatigue and sluggishness
Increased sensitivity to cold
Constipation
Pale, dry skin
A puffy face
Brittle nails
Hair loss
Muscle weakness
Joint pain and stiffness
Unexplained weight gain

110
Q

What are the investigations for hashimotos disease

A

Diagnosis is based on signs and symptoms
Blood tests – thyroid hormone and TSH levels produced in the pituitary gland
Hormone test – underactive thyroid – level of thyroid hormone is low but TSH is elevated
Antibody test – Hashimoto’s disease involved the production of abnormal antibodies. Blood test confirm presence of antibodies against thyroid peroxidase (TPO antibodies).

111
Q

What is the treatment for hashimotos disease

A

Synthetic hormones – synthetic thyroid hormone levothyroxine
Resection of obstructive goitre

112
Q

What are the 5 types of Thyroid cancers and their prevalence

A

papillary (most common 60%), follicular (≤25%), medullary (5%), lymphoma (5%) and anaplastic (rare).

113
Q

What are the 2 aetiologies for thyroid cancers

A

Radiation exposure is a well-documented risk factor for thyroid carcinoma, most notably papillary carcinoma.
Iodine deficiency, particularly for follicular carcinomas

114
Q

What is the pathology of thyroid cancers

A

Epithelial tumours that originate from thyroid follicular cells.

115
Q

What are the 6 clinical presentations of thyroid cancers

A

Thyroid carcinoma most commonly manifests as a painless, palpable, solitary thyroid nodule.
Increased rate of malignancy in males
Nodular growth
Rapid growth: ominous sign
Usually painless; sudden onset of pain more strongly associated with benign disease
Hard and fixed nodules

116
Q

What are the 4 investigations for thyroid cancers

A

Thorough head and neck examination, including thyroid gland and cervical soft tissues
Fine-needle aspiration biopsy (FNAB)
Indirect laryngoscopy
Lab tests – serum calcitonin – elevated levels suggest medullary thyroid carcinoma

117
Q

What is the management of thyroid cancers

A

Malignancies require surgical intervention

118
Q

What are the features of papillary thyroid cancer

A

Younger patients
Spread – lymph nodes and lung

119
Q

What is the treatment of papillary thyroid cancer

A

total thyroidectomy to remove non-obvious tumour. Consider node excision/ radioiodine to ablate residual cells
Give levothyroxine to suppress TSH

120
Q

What are the features and treatment of follicular thyroid cancer

A

Middle age
Spreads early via blood (bone, lungs)
Treatment – total thyroidectomy + T4 suppression + radioiodine ablation

121
Q

What are the features and treatment of medullary thyroid cancer

A

Sporadic (scattered) or part of MEN syndrome (multiple endocrine neoplasia)
May produce calcitonin which can be used a cancer marker
Do not concentrate iodine
Treatment – thyroidectomy + node clearance
External beam radiotherapy may prevent regional recurrence

122
Q

What are the features and treatment of thyroid lymphomas

A

Female: male = 3:1
May present with stridor/ dysphagia
Do full staging pre-treatment (chemotherapy)
Assess histology for mucosa-associated lymphoid tissue (MALT)

123
Q

What are the features and treatment of anaplastic thyroid cancers

A

Female: male = 3:1
Elderly
Poor response to any treatment
Excision + radiotherapy may be tried

124
Q

What is Cushing’s disease

A

a tumour on the pituitary gland that causes the gland to produce too much ACTH, leading to high levels of cortisol production.

125
Q

What is Cushing’s syndrome

A

an abnormal condition caused by chronic excess levels of corticosteroids (particularly cortisol) in the body due to hyperfunction of the adrenal gland (often due to the use of corticosteroid medication).

126
Q

What are the two causes of Cushing’s syndrome

A

Iatrogenic – pharmacological use of steroids leads to increased cortisol in circulation
Cushing’s disease

127
Q

What are 5 symptoms of Cushings syndrome

A

Weight gain
Mood change – depression, lethargy, irritability
Proximal weakness
Gonadal dysfunction – irregular menstruation, erectile dysfunction
Acne

128
Q

What are 4 signs of Cushing’s Syndrome

A

Central obesity - round face, supraclavicular fat distribution
Skin and muscle atrophy
Purple abdominal striae
Osteoporosis

129
Q

What are 6 differential diagnoses for Cushings syndrome

A

Alcoholism
Anorexia nervosa
Bulimia nervosa
Depression
Obesity
Pseudo-Cushing syndrome

130
Q

What are the 2 investigations for Cushings syndrome

A

Overnight dexamethasone suppression test
If this test is positive, test for plasma ACTH

131
Q

What is the likely diagnosis for undetectable ACTH in a Cushing’s syndrome patient

A

Tumour adenoma of the adrenal glands

132
Q

How does the overnight dexamethasone suppresion test work for cushings syndrome

A

1mg dexamethasone at midnight, the take serum cortisol at 8am
Normally cortisol suppresses to <50nmol/L – NO suppression in Cushing’s syndrome

133
Q

Management of cushing’s syndrome

A

Iatrogenic – stop medications if possible
Cushing’s disease – selective removal of pituitary adenoma

134
Q

What is acromegaly

A

The abnormal growth of hands, feet and face due to overproduction of growth hormone.

135
Q

What is the pathophysiology of Acromegaly

A

growth hormone stimulates growth of bone and soft tissue, through secretion of Insulin-like growth factor-1.

136
Q

What are 10 symptoms of acromegaly

A

Acral enlargement (peripheries – hands and feet)
Arthralgias (joint pain)
Maxillofacial changes
Excessive sweating
Headache
Backache
Hypogonadal symptoms
Acroparaesthesia (burning, tingling sensations in the extremities)
Amenorrhoea (absence of menstruation)
Decreased libido

137
Q

What are 6 signs of acromegaly

A

Growth of hands
Coarsening face; wide nose
Macroglossia (big tongue)
Puffy lips, eyelids and skin
Obstructive sleep apnoea
Goitre

138
Q

What are 4 differential diagnoses for Acromegaly

A

Marfan syndrome
Precocious puberty
Prolactinoma
Gigantism

139
Q

What are the 3 investigations for acromegaly

A

IGF-1 test, GH test, glucose tolerance test

140
Q

Why cant solely GH tests be used for Acromegaly

A

GH cannot be relied on alone as the secretions are pulsatile and at peaks acromegalic and normal levels overlap. GH also increases during pregnancy, stress, and sleep.

141
Q

What are the 3 management options for acromegaly

A

1st line: Pituitary surgery (trans-sphenoidal surgery) – size of the tumour and the surgeon will determine the success of the surgery
Medical therapy – dopamine agonists e.g. cabergoline
Radiotherapy

142
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism: a disease of the adrenal glands involving excess production of aldosterone (independent of the renin-angiotensin system). It can cause high blood pressure.

143
Q

What is the pathology of Conn’s syndrome

A

Conn’s syndrome causes excess aldosterone production due to a solitary aldosterone-producing adenoma (linked to mutations in K+ channels).
Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule. Therefore, hyperaldosteronism causes increased reabsorption of sodium and excretion of potassium.

144
Q

What are the 7 symptoms of Conn’s syndrome

A

Often asymptomatic
Signs of hypokalaemia
Weakness
Cramps
Paraesthesia
Polyuria (excessive urine production)
Polydipsia (excessive thirst)

145
Q

What are the 3 signs of Conn’s syndrome

A

High blood pressure
May cause headaches, blurred vision, dizziness
Low potassium levels (not reliable as some patients will have normal levels)
This may cause fatigue, numbness, increased urination, increased thirst

146
Q

What are the 4 differential diagnoses of Conns syndrome

A

Congenital adrenal hyperplasia (autosomal recessive disorder)
Secondary hyperaldosteronism
Exogenous mineralocorticoid excess
Liddle syndrome

147
Q

What are 3 investigations for Conns syndrome

A

Investigate for suppressed renin and increased aldosterone
Adrenal vein sampling
U&E – potassium may be low or normal

148
Q

What is the management for Conns syndrome

A

Laparoscopic adrenalectomy
Spironolactone (25-100)mg for 4 weeks pre-op controls BP and K+.

149
Q

What is secondary hyperaldosteronism

A

excess aldosterone production due to a high renin from decreased renin perfusion e.g. in renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure.

150
Q

What is Adrenal insufficiency

A

A condition in which the adrenal glands do not produce adequate amounts of steroid hormone (mainly cortisol). (and aldosterone)

151
Q

What is the pathophysiology of adrenal insufficiency

A

Autoimmune destruction of the entire adrenal cortex. Loss of cortex leads to reduction in ability to produce cortisol and/or aldosterone. Excess ACTH stimulates melanocytes, resulting in the pigmentation.

152
Q

What is the primary cause of adrenal insufficiency

A

Addison’s disease
Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency.

153
Q

What is secondary adrenal insufficiency

A

Hypopituitarism/ long-term steroid therapy leading to suppression of the pituitary-adrenal axis.

154
Q

What are 9 symptoms of adrenal insufficiency

A

Fatigue
Weight loss
Dizzy
Faints
Poor recovery from illness
Adrenal crisis
Headache
Abdominal pain
Diarrhoea/ constipation

155
Q

What are 5 symptoms of adrenal crisis

A

Hypotension and cardiovascular collapse
Fatigue
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia

156
Q

What are 2 signs of adrenal insufficiency

A

Pigmentation and pallor
Primary – Hyperpigmentation
Secondary – no pigmentation
Hypotension

157
Q

What are the 5 differential diagnoses for adrenal insufficiency

A

Adrenal crisis
Eosinophilia
Hyperkalaemia
Sarcoidosis
Tuberculosis

158
Q

What is the investigation for adrenal insufficiency

A

Short ACTH stimulation test – give ACTH, if cortisol remains low then it diagnoses AI.

159
Q

What parts of the history are important in diagnosis of adrenal insufficiency

A

Past history
TB
Post partum bleed
Cancer
Family history
Autoimmunity – most common
Congenital disease
Any previous use of steroids

160
Q

What are the 3 treatment points for adrenal insufficiency

A

Replace the aldosterone with fludrocortisone (for primary AI)
Hydrocortisone 2/3 times daily to replace the cortisol
Mineralocorticoids to correct postural hypertension

161
Q

What is diabetes insipidus

A

A rare metabolic disorder in which the patient produces large quantities of dilute urine and is constantly thirsty. also known as argenine vasopressin insufficiency/resistance

162
Q

What is the pathology of diabetes insipidus

A

It is due to a deficiency of the pituitary hormone vasopressin (ADH), which regulates reabsorption of water in the kidneys. This means that the body can’t make enough concentrated urine and too much water is passed

163
Q

What is Cranial diabtetes insipidus

A

Most common type of diabetes insipidus
Not enough AVP in the body to regulate urine production
Caused by damage to the hypothalamus/pituitary gland e.g. after infection, operation, brain tumour or brain injury.

164
Q

What is nephrogenic diabetes insipidus and its causes

A

There’s enough AVP in the body, but the kidneys fail to respond to it.
It can be caused by kidney damage, or sometimes inherited as a problem
Congenital
Acquired - lithium (used to treat bipolar disorder) can cause nephrogenic diabetes insipidus by damaging the cells of the kidney

165
Q

What are the symptoms of diabetes insipidus

A

Polydipsia (extreme thirst)
Polyuria (excessive urine) – up to 20litres per day in severe cases
Tiredness (having to pass urine at night)
Irritability
Difficulty concentrating

166
Q

What are 5 differential diagnoses for diabetes insipidus

A

Histiocytosis
Hypercalcaemia
Hypokalaemia
Medullary cystic disease
Type 1 diabetes mellitus

167
Q

What are 3 investigations for diabetes insipidus

A

Water deprivation test
Vasopressin test
MRI scan

168
Q

How is the water deprivation test used to investigate diabetes insipidus

A

not drinking any liquid for 8 hours – in diabetes insipidus the body will still pass large amounts of dilute urine instead of small amount of concentrated urine.

169
Q

How is the vasopressin test used to investigate diabetes insipidus

A

inject small dose AVP. If it stops urine production = cranial DI (shortage of AVP). If urine production continues = nephrogenic DI (no response to AVP)

170
Q

how is an MRI scan used to investigate diabetes insipidus

A

view images of the brain to see if there is damage to the hypothalamus or pituitary gland.

171
Q

What are the 3 management options for diabetes insipidus

A

Treatment not always necessary – fluid intake must be increased to compensate for excess fluid lost through urine.
Medication called desmopressin can be used to replicate the functions of AVP (cranial DI)
Nephrogenic DI often treated with thiazide diuretics, which reduce the amount of urine the kidneys produce

172
Q

What is Syndrome of innapropriate secretion of ADH

A

The hyponatraemia and hypo-osmolality resulting from inappropriate, continued secretion or action of the ADH arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion.

173
Q

What are the 5 potential causes of Syndrome of inappropriate secretion of ADH

A

Malignancy – lung small-cell, pancreas, prostate, thymus, or lymphoma
CNS disorders – meningoencephalitis, abscess, stroke, subarachnoid/ subdural haemorrhage
Chest disease – TB. Pneumonia, abscess
Drugs – opiates, cytotoxics
Other – trauma, major abdominal surgery, symptomatic HIV

174
Q

What is the pathology of Syndrome of inappropriate secretion of ADH

A

Disordered hypothalamic -pituitary secretion or ectopic production of ADH.

175
Q

What is the affect of Syndrome of inappropriate secretion of ADH on Na+ and osmolality

A

Decreased Na+ with decreased or normal urea and creatinine
Decreased plasma osmolality
Increased urine osmolality
Increased urine Na+

176
Q

what are the signs and symptoms of Syndrome of inappropriate secretion of ADH

A

Nausea
Irritability and headache with mild dilutional hyponatraemia
Fits and coma with severe hyponatraemia

177
Q

What is the 1 differential diagnosis for Syndrome of inappropriate secretion of ADH

A

CSW (cerebral salt-wasting syndrome) – excessive ADH secretion caused by stimulation of the hypothalamus after trauma or ischaemia.

178
Q

What are the 2 investigations for Syndrome of inappropriate secretion of ADH

A

Full blood count
Diagnose by serum concentrations of sodium, potassium, chloride and bicarbonate
Hyponatraemia with corresponding hypo-osmolality
Concentrated urine (Na+>20mmol/L) and osmolality (>100mOsmol/Kg)

179
Q

What are the 3 management options for Syndrome of inappropriate secretion of ADH

A

Treat the cause and restrict the fluid
Consider salt +/- loop diuretic if severe.
Vasopressin receptor antagonists - Vaptan

180
Q

What is hyperparathyroidism

A

Excessive secretion of parathyroid hormone, usually due to a small tumour in one of the parathyroid glands. Results in hypercalcaemia. Primary is most common.

181
Q

What is the pathology of hyperparathyroidism

A

Primary – caused by a solitary adenoma, or occasionally hyperplasia of all glands.
Secondary – caused by decreased vitamin D intake or chronic renal failure
Tertiary – occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously after undergoing hyperplastic or adenomatous change.

182
Q

What is the physiology of PTH

A

Parathyroid hormone (PTH) is normally secreted in response to low ionized Ca2+ levels, by 4 parathyroid glands situated posterior to the thyroid. The glands are controlled by negative feedback via Ca2+ levels.

183
Q

What is the pathophysiology of hyperparathyroidism

A

Primary – adenoma or hyperplasia provides additional secretive tissue to provide excess PTH
Secondary – parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia
Tertiary – glands become autonomous, producing excess of PTH even after the correction of calcium deficiency

184
Q

What are the symptoms and signs of primary hyperparathyroidism

A

Often asymptomatic, occasionally bones, stones, groans, moans

185
Q

What are the symptoms and signs of secondary hyperparathyroidism

A

kidney disease, with skeletal or cardiovascular complications

186
Q

What are the symptoms and signs of tertiary hyperparathyroidism

A

bones, stones, groans, moans

187
Q

What is bones stones moans and groans in relation to hyperparathyroidism

A

Bones – osteitis fibrosa cystica, osteoporosis
Kidney stones
Psychic groans – confusion
Abdominal moans – constipation, acute pancreatitis

188
Q

What are 5 differential diagnoses for hyperparathyroidism

A

Adverse drug reaction to lithium/ thiazide diuretics
Cancers producing parathyroid hormone
Leprosy
Exogenous calcium intake
Multiple endocrine neoplasms

189
Q

What are the investigations and results for primary hyperparathyroidism

A

Increased Ca2+ and PTH
Increased Alkaline phosphatase (ALP) – from bone resorption

190
Q

What are the investigations and results for secondary hyperparathyroidism

A

Low serum calcium
Raised PTH

191
Q

What are the investigations and results for tertiary hyperparathyroidism

A

Raised calcium
Raised PTH

192
Q

What is the management for primary hyperparathyroidism

A

surgical removal of adenoma.

193
Q

What is the management for secondary hyperparathyroidism

A

calcium correction; treat underlying cause

194
Q

What are 3 other management options for hyperparathyroidism

A

Calcium mimetic, total or subtotal parathyroidectomy

195
Q

What is Hypoparathyroidism

A

Subnormal activity of the parathyroid glands, causing a fall in the blood concentration of calcium and muscular spasms.

196
Q

What are the 4 causes of hypoparathyroidism

A

genetics, autoimmune (polyglandular type 1), infiltration of the parathyroid glands by iron overload (haemochromatosis), surgery (parathyroidectomy)

197
Q

What is the pathology 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.

198
Q

What are the 7 symptoms and signs of hypoparathyroidism

A

increased excitability of muscles and nerves. Numbness around the mouth/ extremities, cramps,
tetany,
convulsions.
Chvostek sign- facial twitch of touching
Trousseau sign- hand and foot spasm under ischaemia

199
Q

What is Pseudohypoparathyroidism

A

A genetic defect that causes lack of response to parathyroid hormone.

200
Q

What are the 5 symptoms of Pseudohypoparathyroidism

A

short stature, obesity, round faces, mild learning difficulties, short fourth metacarpals

201
Q

What is the treatment for Pseudohypoparathyroidism

A

calcium and vitamin D can reverse most of the features.

202
Q

What is Pseudopseudohypoparathyroidism

A

a condition in which all the symptoms of pseudohypoparathyroidism are present, but the patient’s response to parathyroid hormone is normal.

203
Q

What is Hypercalcaemia of malignancy

A

A higher-than-normal level of calcium in the blood due to a malignancy secreting parathyroid hormone-related protein.

204
Q

What is the pathology of Hypercalcaemia of malignancy

A

Malignancies of the lung, oesophagus, skin, cervix, breast and kidney can be a cause. The tumour secretes parathyroid hormone-related protein which results in increased calcium levels.
Another cause is local osteolysis.
Main cause is primary hyperparathyroidism.

205
Q

Name 16 signs and symptoms for Hypercalcaemia

A

Bones – osteitis fibrosa cystica, osteoporosis
Kidney stones
Psychic groans – confusion
Abdominal moans – constipation, acute pancreatitis
Weight loss
Anorexia
Nausea
Polydipsia
Polyuria
Constipation
Abdominal pain
Dehydration
Weakness
Confusion
Seizure – short QT interval on ECG
Coma

206
Q

What are 2 differential diagnoses for hypercalcaemia

A

Hyperparathyroidism
Hypernatremia

207
Q

What are the investigations and results for hypercalcaemia of malignancy

A

Raised Ca2+
Decreased albumin
Decreased Cl-
Alkalosis
Decreased K+
Increased PO43-

208
Q

What are the 3 management options for hypercalcaemia of malignancy

A

Aggressive rehydration
Bisphosphonates e.g. zoledronic acid IV, usually normalize calcium within 3 days and can be given as a repeated infusion
Long term – control of underlying malignancy

209
Q

what is hypocalcaemia

A

An abnormally low calcium concentration in the blood.

210
Q

What are 5 causes for hypocalcaemia

A

HAVOC
hypoparathyroidism, acute pancreatitis, vit D deficiency, Osteomalacia, CKD

211
Q

What are the clinical presentations of hypocalcaemia

A

SPASMODIC
spasms, paraesthesiae, anxious, seizures, muscle tone increase, orientation impaired, dermatitis, impetigo herpetiformis, cardiomyopathy

212
Q

What are 5 differential diagnoses for hypocalcaemia

A

Hypoparathyroidism
Hypoalbuminemia
Metabolic alkalosis
Acute kidney injury
Acute pancreatitis

213
Q

What are 5 complications of hypocalcaemia

A

Dysphagia
Wheezing; bronchospasm
Syncope
Congestive heart failure
Angina

214
Q

What are 5 investigations for hypocalcaemia

A

Measure serum albumin levels to rule out hypoalbuminemia
Chvostek’s sign – tap over facial nerve and look for spasm of facial muscles
Trousseau’s sign – compression of brachial artery causes carpopedal spasm (wrist and fingers flex)
eGFR to look for chronic kidney disease
PTH and vitamin D levels

215
Q

What in the history can be used to diagnose hypocalcaemia

A

Family history
Lack of sun exposure
Low-calcium diet
Drugs – antibiotics, loop diuretics, oestrogen

216
Q

What is the management plan for hypocalcaemia

A

Mild symptoms
Give calcium 5mmol/6 hours, with daily plasma Ca2+ levels
Severe symptoms
10ml of 10% calcium gluconate IV over 30min.
Hypoparathyroidism – alfacalcidol
correct resp. alkalosis if thats the cause

217
Q

What is hyperkalaemia

A

An abnormally high concentration of potassium in the blood, usually due to failure of the kidneys to secrete it.

218
Q

What are the boundaries for mild, moderate and severe hyperkalaemia

A

Mild: 5.5-6.0mEq/L
Moderate: 6.1-7.0mEq/L
Severe: ≥7.0mEq/L

219
Q

What are the 6 potential causes of hyperkalaemia

A

Renal impairment
Rhabdomyolysis (muscle injury – death of muscle fibres that release their contents into the bloodstream)
Metabolic acidosis
Addison’s disease (primary adrenal insufficiency)
Drugs interfering with potassium excretion e.g. ACEi
Burns

220
Q

What are 7 signs and symptoms of hyperkalaemia

A

A fast, irregular pulse
Chest pain
Weakness
Palpitations
Light-headedness
Dyspnoea
Paraesthesia
Frank muscle paralysis

220
Q

What are the 3 differential diagnoses for hyperkalaemia

A

Metabolic acidosis
Rhabdomyolysis
Acute tubular necrosis

220
Q

What are the 4 investigations for hyperkalaemia

A

Plasma potassium >6.5mmol/L – emergency, needs urgent assessment
Bloods: check potassium, recheck unexpected result
ECG: tall tented T waves, small P waves, wide QRS complex and ventricular fibrillation
Urine potassium, sodium and osmolality

221
Q

What is involved in the treatment of a hyperkalaemic crisis

A

Calcium gluconate – protects heart (prevents ventricular fib)
Insulin + dextrose (drives potassium into cells)
Salbutamol nebulised
Calcium resonium

222
Q

What are the 4 management options for hyperkalaemia

A

Treat underlying causes, review medications
Polystyrene sulfonate resin, binds K+ in the gut, preventing absorption and bringing K+ levels down over a few days.
If vomiting – 30g enema, followed by a 9 hour colonic irrigation
Dietary potassium and loop diuretic

223
Q

What is hypokalaemia

A

Abnormally low levels of potassium in the blood: occurs in dehydration.

224
Q

What are the 7 potential causes for hypokalaemia

A

Diuretics - hyperaldosteronism
Vomiting and diarrhoea
Pyloric stenosis
Intestinal fistula
Cushing’s syndrome/ steroids/ ACTH
Conn’s syndrome
Alkalosis

225
Q

What are 8 clinical presentations for hypokalaemaia

A

Muscle weakness
Hypotonia
Hyporeflexia
Cramps
Tetany (intermittent muscular spasms)
Palpitations
Light-headedness (arrhythmias)
Constipation

226
Q

What are 3 differential diagnoses for hypokalaemia

A

Bartter syndrome (inherited defect that causes low potassium levels)
Hyperthyroidism and thyrotoxicosis
Metabolic alkalosis

227
Q

What are 3 investigations for hypokalaemia

A

If potassium <2.5mmol/L, urgent treatment is required.
ECG: T wave inversion, prominent U wave
Urine potassium, sodium and osmolality

228
Q

What is the treatment for mild hypokalaemia

A

Mild (>2.5mmol/L)
Oral K+ supplement
Review after 3 days

229
Q

What is the treatment for severe hypokalaemia

A

Severe (<2.5mmol/L)
IV potassium (no more than 20mmol/h and 40mmol/L)
Do not give K+ if oliguric.

230
Q

What are neuroendocrine tumours

A

Tumours that form from cells that release hormones into the blood in response to a signal from the nervous system.

231
Q

What are 3 vital signs for diagnosing neuroendocrine tumours

A

Pressure on local structure e.g. optic nerves – bitemporal hemianopia
Pressure on normal pituitary – hypopituitarism
Functioning tumour – prolactinoma, acromegaly, Cushing’s disease

231
Q
A
232
Q

What is a prolactinoma

A

Lactotroph cell tumour of the pituitary

233
Q

at what size does a microadenoma become a macroadenoma

A

tumour >1cm

234
Q

What is the clinical presentation of a prolactinoma caused by its local effects

A

macroadenoma
Headache
Visual field defect (bi-temporal hemianopia)
CSF leak (rare)

235
Q

What are 5 clinical presentations of prolactinomas

A

Menstrual irregularity/ amenorrhoea
Galactorrhoea
Infertility
Loss of libido
Low testosterone in men

236
Q

What 4 investigations can be used to find prolactinomas

A

Ultrasound
CT
MRI
PET

237
Q

What is the management plan for prolactinomas

A

Management is medical rather than surgery – use dopamine agonists such as cabergoline.
Remarkable shrinkage usual with macroadenoma – sight saving
Microadenoma – usually respond to small doses of cabergoline just once or twice a week

238
Q

What is a Pheochromocytoma

A

Catecholamine (adrenaline) secreting tumour.

239
Q

What is the pathology of Pheochromocytomas

A

Tumours of the chromaffin cells of the medulla that produce catecholamine

240
Q

What are 9 clinical presentations of pheochromocytomas

A

Episodic
Headaches
Palpitations
Sweating
Tremor
Anxiety and nausea
Hypertension
Tachycardia
Pallor

241
Q

What are 2 investigations for pheochromocytomas

A

24 hour urine collection for urinary catecholamines and metabolites
Plasma catecholamines

242
Q

What is the management plan for pheochromocytomas

A

Surgery – this must be preceded by alpha and beta blocker to stagger adrenaline loss

243
Q

What are carcinoid tumours

A

Neuroendocrine tumours that particularly affect the small bowel, large bowel or appendix.

244
Q

What is the pathophysiology of carcinoid tumours

A

Carcinoid tumours are a group of tumours of enterochromaffin cell origin, capable of producing 5HT. They secrete bioactive compounds e.g. serotonin and Kallikrein which cause carcinoid syndrome.
GI carcinoid tumours only cause this if they metastasise to liver.

245
Q

What is the clinical presentation of carcinoid tumours

A

Initially, few GI tumours can cause appendicitis, intussusception or obstruction. Hepatic metastases may cause RUQ pain.
then clinically present as expected based on location

246
Q

What is carcinoid syndrome

A

the collection of symptoms some people get when a neuroendocrine tumour (usually hepatic involvement) releases hormone such as serotonin into the blood stream.

247
Q

What are 4 symptoms and signs of carcinoid tumours

A

Bronchoconstriction
Diarrhoea
Skin flushing
Carcinoid crisis – when a tumour outgrows its blood supply, mediators flood out. Life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia occur.

248
Q

What are 4 investigations for carcinoid tumours

A

Increased 24h urine 5-hydroxyindoleacetic acid (5HIAA)
CXR + chest/pelvis MRI/CT to help locate primary tumours
Echocardiography can be used to investigate carcinoid heart disease
Liver ultrasound – confirm metastases

249
Q

What is the treatment of carcinoid syndrome

A

Octreotide; blocks release of tumour mediators and counters peripheral effects.

250
Q

What is the management of carcinoid tumours

A

Loperamide for diarrhoea
Tumour resection is only cure for carcinoid tumours – vital to find primary site.
Debulking, embolisation or radiofrequency ablation of hepatic metastases can decrease symptoms

Phase 2a Medicine (10 decks)

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