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202 > Clinical > Flashcards

Clinical Flashcards

1
Q

WHO classification of diabetes mellitus?

A

Fasting glucose >7mmol/l
2 hours post-prandial >11.1mmol/l

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2
Q

How many people in the UK have diabetes?

A

4.7 million

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3
Q

Peak age of onset for type-1 diabetes?

A

12 years old

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4
Q

What percentage of diabetes is type-1?

A

8%

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5
Q

What percentage of diabetes is type-2?

A

90%

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6
Q

Gestational diabetes is present in what percentage of pregnancies?

A

4-5%

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7
Q

Rarer forms of diabetes mellitus?

A

Monogenic forms of diabetes
Endocrinopathies

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8
Q

Other names for type-1 diabetes?

A

Autoimmune diabetes
Insulin-dependent diabetes Mellitus
Juvenile onset diabetes

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9
Q

Main cause of type-1 diabetes mellitus?

A

T-cell mediated autoimmune destruction of the pancreatic beta-cells

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10
Q

Clinical presentation of type-1 diabetes?

A

Hyperglycaemia
Glycosuria
Polyuria
Polydipsia
Weight loss
Pear drop breath

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11
Q

What is glycosuria?

A

High levels of glucose in the urine

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12
Q

Why is glycosuria present in type-1 diabetes?

A

When the renal threshold of a substance is exceeded, re-absorption of the substance by the proximal convoluted tubule is incomplete so part of the substance remains in the urine

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13
Q

How to test for glycosuria?

A

Clinical dipsticks

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14
Q

What is polyuria?

A

Abnormally large quantities of urine

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15
Q

Why is polyuria present in type-1 diabetes?

A

Exceeding renal threshold creates osmotic drag in the urine and increases diuresis

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16
Q

What is polydipsia?

A

Increased thirst

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17
Q

Why is polydipsia present in type-1 diabetes?

A

Polyuria leads to increased thirst due to the resulting loss of fluid and electrolytes

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18
Q

Why is weight loss present in type-1 diabetes?

A

Accelerated breakdown of fat and muscle in the absence of glucose uptake

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19
Q

What causes diabetic ketoacidosis?

A

The liver produces ketone bodies from fat. These can be used as a temporary fuel source

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20
Q

Ways to test for diabetes?

A

Random plasma glucose test
Fasting plasma glucose test
Oral glucose tolerance test
HbA1c
Urinary C-peptide
Diabetes specific antibodies
Genetic testing (MODY)

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21
Q

What does HbA1c measure?

A

The amount of glycated haemoglobin in the blood influenced by glucose levels over a period of 2-3 months

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22
Q

Normal HbA1c level?

A

<42mmol/mol (6%)

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23
Q

Pre-diabetic HbA1c level?

A

42-47mmol/mol (6-6.4%)

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24
Q

Diabetic HbA1c level?

A

> 48mmol/mol (6.5%)

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25
Q

When was insulin discovered?

A

1921

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26
Q

Who discovered insulin?

A

Frederick Banting and Charles H Best

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27
Q

Insulin was discovered in the pancreatic extracts of what animal?

A

Dog

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28
Q

Who helped develop insulin for human use?

A

B Collip and JJR Macleod

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29
Q

Which pharmaceutical company first manufactured insulin?

A

Eli lilly

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30
Q

When was the first large-scale manufacture of insulin?

A

1923

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31
Q

When was the first biosynthetic insulin available?

A

1982

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32
Q

Which was the first biosynthetic human insulin?

A

Humulin

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33
Q

Management of type-1 diabetes?

A

Insulin
Transplantation
Dietary considerations

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34
Q

Types of transplantation for type-1 diabetes?

A

Pancreas transplantation
Islet transplantation

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35
Q

Dietary considerations in type-1 diabetes?

A

Glycaemic index
Increase complex carbohydrates
Reduced saturated fat intake
Decrease salt intake

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36
Q

What can cause hypoglycaemia?

A

Too much insulin
Not enough food
Too much exercise
Too much alcohol

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37
Q

Symptoms of hypoglycaemia?

A

Shakiness
Anxiety
Tiredness/drowsiness
Weakness
Sweating
Hunger
A feeling of tingling on the skin
Dizziness/light-headedness
Headache
Difficulty speaking
Blurry vision
Confusion
Loss of consciousness

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38
Q

Diagnosis of DKA?

A

Ketones in blood or urine with hyperglycaemia

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39
Q

Which ketone bodies are produced in DKA?

A

Beta-hydroxybutyrate and acetoacetate

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40
Q

DKA is most common in which type of diabetes?

A

1

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41
Q

Symptoms of DKA?

A

Pear drop smell on breath
Nausea and vomiting
Belly pain
Rapid breathing
Feeling sluggish
Trouble paying attention
Coma
Death

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42
Q

Treatment of DKA?

A

Fluid and electrolyte replacement
Insulin

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43
Q

Long-term microvascular complications of hyperglycaemia?

A

Retinopathy
Nephropathy
Neuropathy
Foot ulcers
Sexual dysfunction

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44
Q

Long-term macrovascular complications of hyperglycaemia?

A

Heart disease
Stroke

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45
Q

Common types of autoantibodies involved in type-1 diabetes?

A

Proinsulin (IAA)
Glutamic acid decarboxylase (GAD)
Insulinoma-associated (IA-2)
Zinc transporter (ZnT8A)

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46
Q

Environmental triggers of type-1 diabetes?

A

Viruses- coxsackie-B, rubella, mumps
Toxins- streptozotocin and alloxin
Diet- cows milk, smoked fish (nitrosamines)
Vitamins- low vitamin D

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47
Q

What are the four T’s of type-1 diabetes?

A

Toilet
Thirsty
Tired
Thinner

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48
Q

Why is HbA1c not essential for type-1 diabetes diagnosis?

A

Would not be raised in patients with classic acute onset as glucose will not have had time to bind to haemoglobin

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49
Q

Reasons to test for diabetic autoantibodies?

A

Not needed for diagnosis
But helpful if unclear clinical picture
For coding
For access to health technologies

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50
Q

C-peptide is most clinically useful to distinguish?

A

Between forms of diabetes in those on insulin
To identify misdiagnosis

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51
Q

What does low C-peptide, high glucose show?

A

Insulin deficient (type-1)

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52
Q

What does high C-peptide, high glucose show?

A

Insulin resistance (type-2/MODY)

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53
Q

What does low C-peptide, low glucose show?

A

Possible complex pathology (such as insulinoma)

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54
Q

Advantages of C-peptide test?

A

Cheap
Fast as can be done at local labs

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55
Q

Goals of type-1 diabetic therapy?

A

Glycaemic management
Prevention of microvascular and macrovascular complications
Management of cardiovascular risk factors
Minimising psychosocial burden

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56
Q

Types of very rapid-acting insulin?

A

Fiasp
Lyumjev

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57
Q

Type of rapid-acting insulin?

A

Humalog
Novorapid
Apidra
Trurapi
Admelog

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58
Q

Types of analogue biphasic insulin?

A

Novomix 30
Humalog mix 25
Humalog mix 50

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59
Q

Types of short-acting insulin?

A

Actrapid
Humulin S
Hypurin neutral

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60
Q

Types of isophane biphasic insulin?

A

Humulin M3
Hypurin 30/70 mix

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61
Q

Types of intermediate-acting insulin?

A

Insulatard
Humulin I
Hypurin isophane

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62
Q

Types of long-acting insulin?

A

Lantus
Levemir

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63
Q

Types of long-acting biosimilar insulin?

A

Absalagar
Semglee

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64
Q

Types of ultra-long-acting insulin?

A

Tresiba
Toujeo

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65
Q

When to take short-acting insulin?

A

10-30 minutes pre-meal
In secondary care for hyperglycaemic correction

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66
Q

Short-acting insulin action of onset?

A

30-60 minutes

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67
Q

Short-acting insulin peak of action?

A

1-3 hours

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68
Q

Short-acting insulin duration of action?

A

6-8 hours

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69
Q

When to take rapid-acting/very rapid-acting insulin?

A

Mealtimes and when required for sick day management or hyperglycaemic correction doses

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70
Q

Rapid-acting insulin onset of action?

A

10-20 minutes

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71
Q

Rapid-acting insulin peak of action?

A

1 hours

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72
Q

Rapid-acting insulin duration of action?

A

4 hours

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73
Q

Very rapid-acting insulin onset of action?

A

5-10 minutes

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74
Q

Very rapid-acting insulin peak of action?

A

1 hour

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75
Q

Very rapid-acting insulin duration of action?

A

3 hours

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76
Q

When to take intermediate-acting insulin?

A

Twice daily. Usually 30 minutes pre-meal or bedtime

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77
Q

Intermediate-acting insulin onset of action?

A

60-90 minutes

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78
Q

Intermediate-acting insulin peak of action?

A

4-6 hours

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79
Q

Intermediate-acting insulin duration of action?

A

12-20 hours

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80
Q

When to take analogue biphasic insulin?

A

Two or three times daily, always with meals

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81
Q

Analogue biphasic insulin onset of action?

A

10-20 minutes

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82
Q

Analogue biphasic insulin peak of action?

A

1 hour

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83
Q

Analogue biphasic insulin duration of action?

A

12-24 hours

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84
Q

When to take isophane biphasic insulin?

A

Twice daily, always with meals

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85
Q

Isophane biphasic insulin onset of action?

A

30-60 minutes

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86
Q

Isophane biphasic insulin peak of action?

A

1-4 hours

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87
Q

Isophane biphasic insulin duration of action?

A

12-24 hours

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88
Q

When to take long-acting insulin?

A

Once or twice daily

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89
Q

Long-acting insulin onset of action?

A

2-4 hours

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90
Q

Long-acting insulin peak of action?

A

Either no peak or 6-14 hours depending on brand

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91
Q

Long-acting insulin duration of action?

A

16-24 hours depending on brand

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92
Q

When to take ultra-long-acting insulin?

A

Once daily

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93
Q

Ultra-long-acting insulin onset of action?

A

30-90 minutes

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94
Q

Ultra-long-acting insulin peak of action?

A

No peak

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95
Q

Ultra-long-acting insulin duration of action?

A

24-42 hours

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96
Q

Safety standards for prescribing insulin?

A

Prescribe by brand
Beware of sound-alike drugs
Correct device
Correct dose
Do not abbreviate units
Correct time
Correct strength

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97
Q

Types of insulin regimens?

A

Basal bolus
Two or three times daily biphasic
5 minutes for insulin

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98
Q

What types of insulins are used for basal bolus regimens?

A

3 rapid-acting and 2 intermediate-acting OR 3 rapid-acting and 1 long-acting

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99
Q

Advantages of basal bolus regimens?

A

More flexibility with meal times
Tighter glycaemic control
Less chance of nocturnal hypoglycaemia

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100
Q

Disadvantages of basal bolus regimen?

A

Multiple injections required
Can lead to more weight gain
Increased risk of hypoglycaemia
Requires patient compliance and responsibility

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101
Q

What does DAFNE stand for?

A

Dose adjustment for normal eating

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102
Q

What is DAFNE?

A

A course for ages 17 years and over to learn the necessary skills to count carbohydrates and inject the right amount if insulin

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103
Q

In an individual with the correct background and no resistance, how much insulin is needed for 10g of carbohydrates?

A

1 unit

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104
Q

Calculation for insulin needed?

A

ICR is usually 1 unit to 10g
ISF is sensitivity to insulin
IOB is insulin on board

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105
Q

What is insulin involved in two or three times daily insulin injection regimens?

A

2 or 3 analogue or isophane biphasic injections

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106
Q

Advantages of two or three times daily injections regimen?

A

Simple
Convenient
Can be provided by community nurses for those unable to administer their own insulin

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107
Q

Disadvantages of two or three times daily injections regimen?

A

Limited flexibility with timing of meal times
May require inter-meal snacks
Overnight blood sugar control issues
Difficult to treat hypers
Less tight glycaemic control

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108
Q

What insulins are used in 5 minutes for insulin regimen?

A

1 true long-acting and 1 analogue biphasic

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109
Q

Advantages of 5 minutes for insulin regimen?

A

Increased patient compliance
No time spent thinking about diabetes
Keeps patient out of DKA/HHS

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110
Q

Disadvantages of 5 minutes for insulin regimen?

A

Facilitates disengaged behaviour
No glucose control other than keeping patients out of the danger zone
Usually progress towards diabetic-related complications
Reduced life expectancy

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111
Q

Does size matter for an insulin needle?

A

No

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112
Q

Why may a patient ask for a different size insulin needle?

A

Incorrect injection technique
They may be injecting in the same area that has become thickened, they may do this as the area will not have any pain on injection

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113
Q

Regular monitoring for type-1 diabetes?

A

HbA1c
Blood pressure
Cholesterol
Eye screening
Foot examination
Kidney function
Urinary albumin
BMI
Smoking review

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114
Q

NICE recommends diabetic patients should aim for a HbA1c of?

A

53mmol/mol but targets should be individualised for patients

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115
Q

Criteria for a continuous glucose monitor?

A

Formal diagnosis of type-1 diabetes

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116
Q

Disadvantages of HbA1c?

A

Not useful to diagnose type-1 diabetes
Only should average glucose levels, not necessarily time in range

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117
Q

Usual time in range target?

A

> 70%

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118
Q

Time in range target for older people and those at risk of hypoglcaemia?

A

> 50%

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119
Q

Time in range target for pregnant women?

A

> 70%

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120
Q

What blood glucose level is defined as hypoglycaemia?

A

<4mmol/mol

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121
Q

Why is repeating glucagon administration not beneficial?

A

Glucagon causes release of glucose from the liver, this can only happen once

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122
Q

Driving and type-1 diabetes?

A

Must inform DVLA
Blood glucose must be more than 5mmol/mol before driving
If less then treat as hypo and wait at least 45 minutes after level is about 5mmol/mol
Test levels every two hours

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123
Q

When may the DVLA revoke a license in a type-1 diabetic patient?

A

When they have more than 1 severe hypo, whilst awake, in a 12-month period. It can be reapplied for three months later

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124
Q

How long does a type-1 diabetic patients driving license last?

A

1-3 years

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125
Q

How can alcohol affect type-1 diabetes?

A

Effect on blood glucose
Hypoglycaemia may be mistaken for being drunk
Harder to manage
More likely to forget insulin

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126
Q

Threshold for offering blood pressure management in type-1 diabetic patients?

A

135/85mmHg
OR 130/80mmHg in the presence of albuminuria

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127
Q

First-line antihypertensive for all type-1 diabetic patients?

A

ACE inhibitor

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128
Q

Second-line antihypertensive for all type-1 diabetic patients?

A

Calcium channel blocker

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129
Q

Third-line antihypertensive for all type-1 diabetic patients?

A

Thiazide like diuretic

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130
Q

Target total cholesterol level for type-1 diabetics?

A

<4mmol/l

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131
Q

Target LDL level for type-1 diabetics?

A

<2mmol/l

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132
Q

What statin to recommend for the primary prevention of CVD?

A

Atorvastatin 20mg

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133
Q

Jdjsjs

A

Jxdhd

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134
Q

When should a statin be offered to type-1 diabetics?

A

> 40 years old
Diabetic for >10 years
Established nephropathy
Other CVS risk factors

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135
Q

What statin should be recommended for secondary prevention of CVD in type-1 diabetics?

A

Atorvastatin 80mg

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136
Q

What causes peripheral vascular disease?

A

Atherosclerosis in arteries that feed the feet and legs

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137
Q

Therapy for peripheral vascular disease?

A

Statins
Clopidogrel
Naftidrofuryl

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138
Q

What causes neuropathic pain in type-1 diabetes?

A

High glucose levels destroy the small blood vessels that feed the peripheral nerves

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139
Q

Symptoms of diabetic neuropathic pain?

A

Initial pain: burning, stabbing, shooting, aching, electric shock-like
Later there is a complete loss of sensation

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140
Q

Treatment for diabetic neuropathic pain?

A

Amitriptyline, duloxetine, gabapentin, pregabalin, topical capsaicin

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141
Q

Types of diabetic retinopathy?

A

Nonproliferative
Proliferative

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142
Q

What causes diabetic retinopathy?

A

High blood glucose levels damage the retina

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143
Q

Treatment for diabetic retinopathy?

A

Laser treatment
Eye injections
Steroid eye implants
Eye surgery

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144
Q

Drugs used for diabetic retinopathy eye injections?

A

Ranibizumab
Aflibercept

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145
Q

Causes of diabetic nephropathy and kidney disease?

A

High blood glucose destroys blood vessels surrounding nephrons reducing ability to filter waste
Advanced glycation end products can damage glomerulus
High blood pressure and dyslipidaemia narrow and weaken renal blood vessels

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146
Q

ACR stands for?

A

Urine albumin to creatinine ratio

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147
Q

Diagnosis of diabetic kidney disease?

A

ACR of >30mg/g
Creatine clearance <60ml/min

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148
Q

Types of diabetic emergencies?

A

Severe hypoglycaemia
Acute diabetic foot
Diabetic ketoacidosis
Hyperosmolar hyperglycaemic state

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149
Q

Features of DKA?

A

Hyperglycaemia
Ketonaemia
Metabolic acidosis

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150
Q

Ketone levels in DKA?

A

> 3mmol/l in blood
4mmol/l in urine OR ++ on standard urine stick

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151
Q

When may euglycaemic diabetic ketoacidosis occur?

A

In type-2 diabetes treated with SGLT2 inhibitors

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152
Q

DKA triggers?

A

New onset diabetes
Poor sick day management
Non-adherence to insulin
Infection
MI
Stroke
Illegal drugs
Pregnancy
Drugs
Acute stresses

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153
Q

What should be checked before starting insulin in DKA?

A

Potassium levels

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154
Q

Brand names of biphasic insulin aspart?

A

Novomix 30

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155
Q

Brand names of biphasic insulin lispro?

A

Humalog mix 25
Humalog mix 50

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156
Q

Brand names of biphasic isophane insulin?

A

Humulin M3
Insuman comb 25
Hypurin Porcine 30/70

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157
Q

Brand names of insulin soluble?

A

Actrapid
Humulin S
Hypurin Porcine Neutral
Insuman Rapid

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158
Q

Brand names of insulin aspart?

A

Novorapid
Fiasp
Trurapi

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159
Q

Brand names of insulin degludec?

A

Tresiba

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160
Q

Brand names of insulin detemir?

A

Levemir

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161
Q

Brand names of insulin glargine?

A

Toujeo
Lantus
Semglee
Abasaglar

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162
Q

Brand names of insulin glulisine?

A

Apidra

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163
Q

Brand names of insulin lispro?

A

Humalog
Admelog
Lyumjev

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164
Q

Brand names of insulin isophane?

A

Humulin I
Insulatard
Insuman Basal
Hypurin Porcine Isophane

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165
Q

What does the thyroid gland secrete?

A

Thyroid hormones
Calcitonin

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166
Q

What does the parathyroid secrete?

A

Parathyroid hormone

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167
Q

What does parathyroid hormone do?

A

Maintenance of serum calcium and phosphate levels

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168
Q

Outline thyroid hormone synthesis?

A

1) iodide moved into follicular cells by active transport
2) thyroglobulin formed in follicular ribosomes and placed in secretory vesicles
3) thyroglobulin exocytosed into follicle lumen
4) iodination of thyroglobulin, MIT and DIT created
5) MIT and DIT couple for form T3 or T4
6) iodinated thyroglobulin endocytosed back into follicular cell. T3 or T4 then released

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169
Q

What is thyroglobulin?

A

A large protein rich in tyrosine

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170
Q

Important element in regards to the thyroid?

A

Iodine

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171
Q

What enzyme makes iodide reactive?

A

Thyroid peroxidase

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172
Q

How does iodide bind to thyroglobulin?

A

On the benzene ring of tyrosine residues

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173
Q

What does MIT stand for?

A

Monoiodotyrosine

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174
Q

What does DIT stand for?

A

Diiodotyrosine

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175
Q

What is produced when MIT and DIT couple?

A

T3

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176
Q

What is produced when DIT and DIT couple?

A

T4

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177
Q

Which thyroid hormone is produced more?

A

T4

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178
Q

Cardiac symptoms of hypothyroidism?

A

Bradycardia
Diastolic hypertension
Pericardial effusion

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179
Q

Gastrointestinal symptoms of hypothyroidism?

A

Weight gain
Decreased appetite
Abdominal distension
Constipation

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180
Q

Neuromuscular symptoms of hypothyroidism?

A

Fatigue
Increased sensitivity to cold
Low mood
Impaired cognition
Paraesthesia
Peripheral neuropathy
Muscle weakness or pain
Joint pain
Delayed relation of deep tendon reflexes

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181
Q

Reproductive symptoms of hypothyroidism?

A

Irregular menstrual cycle
Menorrhagia
Infertility

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182
Q

Appearance symptoms of hypothyroidism?

A

Hoarse voice
Dry, flaking, thickened skin
Goitre
Reduced sweating
Yellow complexion
Facial swelling (particularly eyelids)
Brittle nails
Thin hair
Hair and eyebrow loss

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183
Q

Causes of hypothyroidism?

A

Autoimmune thyroiditis
Iodine deficiency
Post thyroidectomy
Post-radioactive iodine treatment
Drug-induced
Peripheral resistance to thyroid hormone
Congenital disease

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184
Q

How to diagnose hypothyroidism?

A

Symptoms
Biochemical test: TSH and free T4

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185
Q

What does high TSH and low free T4 show?

A

Overt primary hypothyroidism

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186
Q

What does slightly raised FSH and normal free T4 show?

A

Subclinical primary hypothyroidism

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187
Q

What does low TSH and low free T4 show?

A

Secondary hypothyroidism (hypothalamic or pituitary dysfunction)

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188
Q

What can rT3 testing be used for?

A

To ascertain peripheral T4 to T3 conversion. Low levels can show peripheral hypothyroidism

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189
Q

Which thyroid antibodies can be tested for?

A

Thyroid peroxide antibodies (TPOAb)
Thyroglobulin antibodies (TgAb)
Thyroid stimulating hormone receptor antibodies (TSHRAb/TRAb)

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190
Q

First line treatment of hypothyroidism?

A

Levothyroxine

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191
Q

Usual starting dose of levothyroxine?

A

1.6mcg/kg rounded to nearest 25mcg

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192
Q

When to use a reduced levothyroxine starting dose?

A

> 65 years old
Pre-existing CVD

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193
Q

What deficiency should be corrected before starting levothyroxine?

A

Glucocorticoid

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194
Q

Congenital hypothyroidism dose?

A

10-15mcg/kg for three months of life and then adjust according to TSH

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195
Q

How often to monitor TFTs?

A

Every three months until stable and then annually

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196
Q

Levothyroxine counselling?

A

Life-long compliance
30-60 minutes before food
Interactions: milk, calcium, PPIs etc
Monitoring requirements

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197
Q

side effects of levothyroxine?

A

Flushing
Restlessness
Palpitations
Insomnia
Angina
Thyroid crisis

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198
Q

What is liothyronine?

A

Synthetic form of T3

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199
Q

What is liothyronine used for?

A

Rarely used due to lack of clinical evidence apart from myxoedema coma

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200
Q

How to manage hypothyroidism in pregnancy?

A

Should consult GP/specialist when planning pregnancy to have frequent TSH levels checked
Once pregnant dose should be increased by 25-50mcg and TSH levels checked
Monitor every 4-6 weeks
2-4 weeks after birth TSH should be checked and most patients can return to previous stable dose

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201
Q

Can levothyroxine be used in pregnancy?

A

Yes- increased monitoring

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202
Q

Can levothyroxine be used when breastfeeding?

A

Yes

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203
Q

Normal TSH levels?

A

0.38-5.33mU/l

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204
Q

Normal free T4 levels?

A

7.9-14.4pmol/l

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205
Q

Target TSH in first trimester of pregnancy?

A

<2.5mU/l

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206
Q

Target TSH in third trimester of pregnancy?

A

<3mU/l

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207
Q

Common levothyroxine drug interactions?

A

Amiodarone
Lithium
Antacids
Colestyramine
Warfarin
Beta-blockers
Ferrous sulphate

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208
Q

What is myxoedema crisis?

A

a rare life-threatening clinical condition in patients with longstanding severe untreated hypothyroidism

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209
Q

Symptoms of myxoedema crisis?

A

Hypothyroidism symptoms and:
Hypothermia
Macroglossia (swollen tongue)
Ptosis (upper eyelid droop)
Periorbital swelling
Puffy face

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210
Q

What can precipitate myxoedema crisis?

A

Stress
Infection
Trauma
Possible drugs

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211
Q

In hyperthyroidism what does a symmetrical enlargement of the thyroid gland suggest?

A

Graves disease

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212
Q

In hyperthyroidism what does a unilateral enlargement of the thyroid gland suggest?

A

Nodular disease

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213
Q

Cardiac/respiratory symptoms of hyperthyroidism?

A

Tachycardia
Shortness of breath
Reduced exercise tolerance
Palpitation
AF
Decline in pre-existing cardiac disease

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214
Q

Gastrointestinal symptoms of hyperthyroidism?

A

Weight loss
Increased appetite
Diarrhoea

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215
Q

Neuromuscular symptoms of hyperthyroidism?

A

Insomnia
Restlessness
Iritability
Mood swings
Muscle weakness
Fine motor tremor
Rapid deep tendon reflexes
Psychosis

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216
Q

Reproductive symptoms of hyperthyroidism?

A

Reduced fertility
Reduced libido
Reduction/loss of periods
Gynaecomastia in males

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217
Q

Skin symptoms of hyperthyroidism?

A

Wet skin
Thin hair
Hair loss
Increased sweating and heat sensitivity

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218
Q

How do the eyes look in graves disease?

A

Eyelids retract
Bulging eyes
Eye redness

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219
Q

Most common cause of hyperthyroidism?

A

Graves disease

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220
Q

What causes graves disease?

A

Autoimmune condition where the thyroid is attacked leading it to become overactive

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221
Q

What can cause hyperthyroidism?

A

Graves disease
Nodular disease
Thyroiditis
Pituitary disease

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222
Q

Risk factors for graves disease?

A

Young and middle-aged women
Can run in families
Smoking

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223
Q

What are thyroid nodules?

A

Lumps develop on thyroid. They are usually non-cancerous but can contain thyroid tissue resulting in excess production of thyroid hormones

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224
Q

Age group most likely to be affected by thyroid nodules?

A

> 60 years old

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225
Q

Why can amiodarone cause hyperthyroidism?

A

It contains iodine

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226
Q

How to diagnose hyperthyroidism?

A

Symptoms
Biochemical tests: TSH, free T3 and T4, TSH receptor antibodies

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227
Q

What does low TSH but high FT3 and FT4 suggest?

A

Hyperthyroidism of thyroidal origin (possibly thyroiditis)

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228
Q

What does high TSH and high FT3 and FT4 suggest?

A

Hyperthyroidism of extrathyroidal origin (hypothalamic or pituitary disease)

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229
Q

What does this thyroid likely show?

A

Graves’ disease

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230
Q

What does this thyroid likely show?

A

Normal thyroid

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231
Q

What does this thyroid likely show?

A

Thyroiditis

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232
Q

What does this thyroid likely show?

A

Single nodular (overactive)

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233
Q

What does this thyroid likely show?

A

Single nodular (under active)

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234
Q

What does this thyroid likely show?

A

Toxic multi nodular

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235
Q

Treatments for hyperthyroidism?

A

Anti thyroid drugs
Radioactive iodine
Thyroidectomy

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236
Q

When to use anti-thyroid drugs first line in graves disease?

A

When remission is likely

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237
Q

When to use radioactive iodine first line for graves disease?

A

When remission is unlikely

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238
Q

When to use thyroidectomy first line in graves disease?

A

Concerns regarding compression or malignancy

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239
Q

Can radioactive iodine be given in pregnancy?

A

No

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240
Q

What does GREAT stand for? (Thyroid)

A

Graves recurrent events after therapy

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241
Q

What does the GREAT score take into account?

A

Age
Sex
Smoking
Genetics
Goitre size
Biochemical tests
Pathology
Extrathyroidal involvement

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242
Q

How to grade a goitre?

A

Using the WHO goitre grading system

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243
Q

First-line anti-thyroid drug?

A

Carbimazole

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244
Q

First-line anti-thyroid drug in pregnancy?

A

Propylthiouracil

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245
Q

How long does it take to show benefit with anti-thyroid drugs?

A

6-8 weeks

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246
Q

Types of anti-thyroid regimens?

A

Titration
Block and replace

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247
Q

Carbimazole mechanism of action?

A

Inhibition of the organification of iodide and thyroglobulin and the coupling of iodothyronine residues which in turn suppress the synthesis of thyroid hormones

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248
Q

Initial dose of carbimazole?

A

20-60mg daily in divided doses

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249
Q

Titration carbimazole regimen?

A

Initial dose and then:
5-15mg daily
Regular TFT checks and dose adjusted according to response

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250
Q

Block and replace carbimazole regimen?

A

Continue high starting dose to completely block production
Levothyroxine started alongside which is titrated until TSH, T3 and T4 are in range

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251
Q

Carbimazole side effects?

A

Macropapular rash
Bone marrow suppression

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252
Q

What to counsel patients on when starting carbimazole?

A

Signs and symptoms of blood dyscrasias:
Sore throat: Bruising, Bleeding, Mouth ulcers, Fevers, Malaise
May need extra medication for symptoms management (beta-blocker)
Contraception in women of childbearing age

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253
Q

Monitoring requirements for carbimazole?

A

FBCs every six months
TFTs

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254
Q

Carbimazole/propylthiouracil contraindications?

A

Severe hepatic impairment
Pre-existing blood disorders
History of pancreatitis

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255
Q

Why can carbimazole not be used in severe hepatic impairment?

A

Carbimazole is a pro-drug so the liver needs to be able to metabolise it into the active form, methimazole

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256
Q

Carbimazole drug interactions?

A

Warfarin
Digoxin
Trimethoprim
Drugs that cause myelosuppression

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257
Q

Propylthiouracil mechanism of action?

A

Inhibits organification of iodide and the coupling of iodothyronine residues suppressing thyroid hormone production
Inhibits conversion of T4 to T3 in peripheral tissues supressing thyroid hormone action

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258
Q

Propylthiouracil inhibits what enzyme?

A

Peroxidase

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259
Q

What does propylthiouracil take 4 weeks to take effect?

A

All the pre-formed hormones need to be used up before circulatory concentrations fall

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260
Q

Initial dose of propylthiouracil?

A

200-400mg once daily

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261
Q

Titration dose regimen for propylthiouracil?

A

Once levels in range then give 50-150mg daily. Regular TFT tests and adjust dose according to response

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262
Q

Block and replace regimen dose for propylthiouracil?

A

Continue high starting dose to completely block production
Levothyroxine started alongside which is titrated until TSH, T3 and T4 are in range

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263
Q

1mg of carbimazole is roughly equivalent to how much propylthiouracil?

A

10mg

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264
Q

Side effects of propylthiouracil?

A

Macropapular rash
Severe hepatic reactions
Bone marrow suppression

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265
Q

Counselling for propylthiouracil?

A

Signs and symptoms of blood dyscrasias:
Sore throat: Bruising, Bleeding, Mouth ulcers, Fevers, Malaise
May need extra medication for symptoms management (beta-blocker)
Hepatic reactions: jaundice, dark urine, abdomen pain, pruritis, nausea, vomiting

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266
Q

Aim of radioactive iodine treatment?

A

Resolve hyperthyroidism without post-ablation hypothyroidism

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267
Q

Advice for patients after radioactive iodine treatment?

A

Avoid close contact (2m) for longer than one hour with anyone for 14 days
Avoid complete contact with children and pregnant women for 24 days

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268
Q

How long does radioactive iodine treatment take to have effect?

A

2-3 months

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269
Q

What is thyroid crisis (thyrotoxic storm)?

A

A rare, extreme manifestation of thyrotoxicosis due to over production of thyroid hormones

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270
Q

What can precipitate thyroid crisis?

A

Infection
Trauma
Medications e.g. Amiodarone
Radioactive iodine treatment
Sudden cessation of anti-thyroid drugs
Some anaesthetics
Surgery

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271
Q

Symptoms of thyroid crisis?

A

Hyperthyroidism symptoms with:
Hyperthermia
Tachycardia
Atrial arrhythmias
Hypotension
Swearing
Nausea
Vomiting
Diarrhoea
Jaundice
Abdominal pain
Confusion
Seizures

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272
Q

How to diagnose thyroid storm?

A

Using the scoring system
>45 indicates storm

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273
Q

Drugs used for thyroid storm?

A

Carbimazole or propylthiouracil
Iodine/lugols/lithium (very rarely)
Beta-blocker (usually propranolol)
Glucocorticoids
Can also use cholestyramine to bind free thyroid hormone

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274
Q

What is infertility?

A

A failure to conceive after a year of regular intercourse without contraception

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275
Q

What is virility?

A

The quality of having strength, energy and a strong sex drive

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276
Q

What is primary infertility?

A

One who has never conceived a child

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277
Q

What is secondary infertility?

A

One who has had a child before

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278
Q

Questions to ask patients trying to conceive?

A

Previous pregnancies/children
Trial timeframe
Sex life
Contraception
Medical history
Current medications
Lifestyle

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279
Q

Physical examination for females trying to conceive?

A

Weight
Pelvic examination: PID, fibroids, lumps, tenderness

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280
Q

Physical examination for males trying to conceive?

A

Weight
Penial/testicular examination for abnormalities

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281
Q

Five test to diagnose infertility?

A

Sperm test
Blood test to check ovulation
Chlamydia test
X-ray of Fallopian tubes
Trans-vaginal ultrasound scan

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282
Q

What is a normal sperm count?

A

15-150 million/ml AS LONG AS the total ejaculate sperm count is over 22 million

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283
Q

What is oligozoospermia?

A

Low sperm count
<15 million/ml

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284
Q

What is azoospermia?

A

No sperm count

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285
Q

What can cause azoospermia?

A

Problems with production
Blockage so cannot reach ejaculate

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286
Q

What factors can damage sperm production?

A

Untreated STIs
Excess heat
Alcohol
Smoking
Recreation drugs

287
Q

What is a fallopian tube X-ray called?

A

Hysterosalpingogram (HSG)

288
Q

Process of fallopian tube x-ray?

A

Opaque dye injected through the cervix. Dye helps to see if there are any blockages

289
Q

Treatment options for infertility?

A

Drug therapy
Surgery
Assisted conception

290
Q

Common drugs prescribed to women with infertility?

A

Clomifene
Tamoxifen
Metformin
Gonadotrophins
Dopamine agonists (bromocriptine, cabergoline)

291
Q

How does metformin work for infertility?

A

Stimulates ovulation
Encourages monthly periods
Reduced risk of miscarriage

292
Q

How do gonadotrophins help male infertility?

A

Improve sperm production

293
Q

Why is folic acid important for pregnancy?

A

Reduces the risk of neural tube defects such as spina bifida and anencephaly

294
Q

What dose of folic acid is recommended during pregnancy?

A

400mcg daily or 5mg daily if increased risk, for the first 12 week whilst the baby’s spine is developing

295
Q

Risk factor for neural tube defects in pregnancy?

A

Either parent having a neural tube defect
Previous pregnancy affected by a neural tube defect
Either parent have a family history of neural tube defects
Women with diabetes
Women with epilepsy

296
Q

Dietary sources of folic acid?

A

Green, leafy vegetables
Brown rice
Granary bread
Fortified cereals

297
Q

Why is liver not safe to eat in pregnancy?

A

High in vitamin A

298
Q

Types of combined hormonal contraceptives?

A

Pill
Patch
Ring

299
Q

How do combined hormonal contraceptives work?

A

Act on hypothalamopituitary-ovarian axis to suppress LH and FSH to inhibit ovulation

300
Q

Types of progesterone only contraceptives?

A

Pill
Patch
Ring
Implant

301
Q

How do progesterone only contraceptives work?

A

Inhibit ovulation and thicken cervical mucus

302
Q

Combined oral contraceptives are generally not recommended after what age?

A

50 years old

303
Q

Risks of combined hormonal contraception?

A

VTE
MI
Stroke
Breast cancer
Cervical cancer

304
Q

Health benefits of combined hormonal contraception?

A

Reduce menstrual pain and bleeding
Reduce PMS symptoms
Reduce risk of endometriosis reoccurrence
Reduce acne
Reduce hirsutism
Reduce some irregularity associated with PCOS
Reduction in endometrial and ovarian cancer
Reduced risk of colorectal cancer

305
Q

How to assess if suitable for combined hormonal contraception?

A

Medical history
Current medication
BMI
Blood pressure

306
Q

What BMI is combined hormonal contraception not recommended for?

A

> 35

307
Q

Symptoms that should prompt urgent medical attention when using combined hormonal contraception?

A

Calf pain, swelling or tenderness
Chest pain
Breathlessness
Hemoptysis
Loss of motor or sensory function

308
Q

Symptoms that should prompt medical review when using combined hormonal contraception?

A

Breast changes
Unilateral nipple discharge
New onset sensory/motor symptoms one-hour preceding onset of migraine
Persistent unscheduled vaginal bleeding

309
Q

Types of combined hormonal contraception regimens?

A

Standard or tailored

310
Q

What is standard combined hormonal contraception regimen?

A

Using the contraception for 21 days and then having a seven-day break to induce a bleed

311
Q

What is a tailored combined hormonal contraception regimen?

A

Reducing or completely stopping having a break in contraception so a bleed is not induced

312
Q

Negative of tailored combined hormonal contraception regimen?

A

Not licensed but it is supported by the Faculty of Sexual and Reproductive Health (FSRH)

313
Q

Negatives of standard combined hormonal contraception regimen?

A

Withdrawal bleed
Symptoms such as headache and nodo changes
Potential risk of pregnancy

314
Q

Should combined oral contraceptives be stopped before surgery?

A

Yes prior to major elective surgery, surgery to legs and surgery that involved prolonged immobilisation of lower limbs

315
Q

How long should combined oral contraceptives be stopped for before surgery?

A

4 weeks

316
Q

When can combined oral contraceptives be restarted after surgery?

A

At least two weeks after full mobilisation

317
Q

What happens if the combined oral contraceptive is not stopped before surgery?

A

Thromboprophylaxis required

318
Q

When may combined oral contraception be contraindicated?

A

High VTE risk
Heavy smokers
BP above 160/95
Valvular heart disease
Diabetes with complications
Migraine with aura

319
Q

Progestogen-only contraceptive mechanism of action?

A

Alter cervical mucus to prevent sperm entry and may inhibit ovulation

320
Q

What is the pregnancy prevention programme?

A

Helps to stop women exposed to teratogenic drugs from becoming pregnancy

321
Q

Drugs with high teratogenic potential?

A

Isotretinoin
Sodium valproate

322
Q

Which drugs can lower the efficacy of hormonal contraception?

A

Most antiepileptics (metabolic enzyme-inducing drugs)
Carbamazepine
Phenytoin
Phenobarbital

323
Q

Recommended contraception for women taking enzyme-inducing antiepileptics?

A

Long-acting reversible contraceptives such as depot injections, IUD and IUS

324
Q

What is defined as a missed contraceptive pill?

A

Combined: >24 hours
Progestogen-only: 3 hours
Deogesterel: 12 hours

325
Q

Common hormonal contraception drug interactions?

A

Carbamazepine
Phenytoin
Nevirapine
Ritonavir
St John’s wort
Rifampicin

326
Q

How long to use barrier contraception after taking ulipristal?

A

Combined and parenteral progestogen only: 14 days
Progestogen-only pill: 9 days
Qlaira: 16 days

327
Q

What happens if you miss a progestogen-only pill and have had unprotected intercourse in the last 5 days?

A

Emergency contraception recommended
Take pill next day as normal
Barrier contraception for 48 hours

328
Q

What happens if you miss a progestogen-only pill and have NOT had unprotected intercourse in the last 5 days?

A

Take one pill as soon as possible then continue at that time daily
Use barrier methods for 48 hours

329
Q

How long to use barrier methods for is combined pill is missed?

A

7 days

330
Q

What to do if vomiting occurs within two hours of taking the contraceptive pill?

A

Take another

331
Q

What if a patient has vomiting or diarrhoea for more than 24 hours whilst taking the contraceptive pill?

A

Class it as a missed pill
Use barrier methods for 7 days

332
Q

What does LAM stand for?

A

Lactational amenorrhea method

333
Q

What is the Lactational amenorrhea method?

A

Avoids pregnancy through the natural reduction in gonadotrophins caused by breastfeeding

334
Q

How effective is Lactational amenorrhea method?

A

98% if all criteria fulfilled

335
Q

Criteria for Lactational amenorrhea method?

A

Less than six months postpartum
No vaginal bleeding after the first 56 days postpartum
Fully breastfeeding: at least every four hours during the day and at least every six hours during the night

336
Q

Why does anti-epileptics often interact with other drugs?

A

Combination therapy
Narrow therapeutic index
Enzyme inducers
Administer for all life

337
Q

Main way antiepileptic drugs interact with other drugs?

A

Enzyme induction- so may need to increase the dose of the other drug

338
Q

Example of an antiepileptic that causes enzyme inhibition?

A

Sodium valproate

339
Q

Common drug interactions that reduce levels of combined oral contraceptive pill?

A

Carbamazepine
Phenytoin
Primidone
Topiramate

340
Q

Example of a drug that has increased exposure when used alongside the combined oral contraceptive pill?

A

Lamotrigine

341
Q

Antiepileptic drugs with the lowest teratogenic potential?

A

Lamotrigine
Levetiracetam

342
Q

Examples of enzyme-inducing antiepileptic drugs?

A

Carbamazepine
Eslicarbazepine
Oxcarbazepine
Phenobarbital
Phenytoin
Primidone
Rufinamide
Topiramate
Perampanel

343
Q

How long after childbirth is emergency contraception needed?

A

21 days unless criteria for LAM

344
Q

How long after abortion, miscarriage or ectopic pregnancy before emergency contraception is needed?

A

5 days

345
Q

Effectiveness of emergency contraception?

A

CuIUD> ulipristal > levonorgestrel

346
Q

Main parts of the brain involved with ADHD?

A

Prefrontal cortex
Basal ganglia
Corpus callosum
Anterior cingulate

347
Q

What is the prefrontal cortex responsible for?

A

Planning actions, avoiding distraction, flexibility with change

348
Q

What is the basal ganglia responsible for?

A

Impulse control
Coordinates information coming from other regions of the brain to prevent automatic response to stimuli

349
Q

What is the corpus callosum responsible for?

A

Communication between the two hemispheres to ensure coordination

350
Q

What is the anterior cingulate responsible for?

A

Management of emotion

351
Q

What is an affective disorder?

A

illnesses that affect the way you think and feel

352
Q

What is mild major depression?

A

Symptoms cause distress, and the person may have some difficulty carrying out usual activities

353
Q

What is moderate major depression?

A

Several symptoms present to a marked degree and the person has considerable difficulty carry out usual tasks

354
Q

What is severe major depression?

A

Symptoms cause distress, agitation and psychomotor retardation. Person is unable to to continue usual activities beyond minimal extent. Somatic symptoms are prominent and suicide is a particular risk

355
Q

What is psychotic depression?

A

Rare form of severe major depression in which patients experience psychotic symptoms such as delusions, hallucinations or paranoia

356
Q

Are men or women more affected by depression?

A

Women

357
Q

Rule of halves in depression?

A

Half of people with depression do not seek help
- Half of those suffering with depression who seek help are not
correctly diagnosed
- Half of those correctly diagnosed receive treatment with an
antidepressant
- Half of those who receive an antidepressant do not complete an
adequate course

358
Q

Usual age of onset for depression?

A

Mid 20s

359
Q

Average peak of age of depression in women?

A

35-45

360
Q

Main aetiology of depression?

A

Genetics
Personality
Early environment
Precipitating factors
Biological
Drug causes

361
Q

Genetics and depression?

A

Risk increases in first-degree relatives
Greater concordance in identical twins
Gene coding for serotonin transporter may increase likelihood of depression following an adverse life event

362
Q

Personality and depression?

A

Anxious personality
Cyclothymic personality

363
Q

Early environment and depression?

A

Deprivation of maternal affection
Parental relationship
Maternal post-natal depression
Abuse/neglect

364
Q

Precipitating factors and depression?

A

Significant life events
Social vulnerability factors

365
Q

What is the monoamine hypothesis?

A

predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, and/or dopamine in the central nervous system

366
Q

Is suicide more common in men or women?

A

Men

367
Q

How to counsel the suicide risk of antidepressants?

A

Inform of the risk
Action plan to follow if thoughts occur
Regular reviews
Be hypervigilant

368
Q

Psychological symptoms of depression?

A

Hopelessness
Worthlessness
Guilt

369
Q

What is anhedonia?

A

Loss of pleasure in things you used to enjoy

370
Q

Physical symptoms of depression?

A

Insomnia
Poor appetite
Weight change
Feeling tired
GI upset
Pain

371
Q

Another name for physical symptoms of depression?

A

Somatic

372
Q

Cognitive symptoms of depression?

A

Poor concentration
Poor memory

373
Q

Behavioural symptoms of depression?

A

Agitation
Self-neglect
Psychomotor retardation

374
Q

How to diagnose depression using ICD-10?

A

Mild: 4 symptoms including 2 key
Moderate: >4 symptoms including 2 key
Severe: >7 symptoms
Must be present for at least two weeks

375
Q

Key symptoms of depression according to ICD-10? (3)

A

Low mood
Anhedonia
Reduced energy

376
Q

Ancillary symptoms of depression according to ICD-10? (7)

A

Reduced concentration and attention
Reduced self-esteem/confidence
Guilt and unworthiness
Pessimism
Ideas/acts of self-harm or suicide
Disturbed sleep
Diminished appetite

377
Q

How to diagnose depression using DSM-5?

A

Five or more symptoms must be present for at least two weeks, with change from previous functioning. Low mood or anhedonia must be present

378
Q

Symptoms of depression according to DSM-5? (9)

A

Depressed mood
Anhedonia
Weight/appetite change
Insomnia/hypersomnia
Psychomotor agitation/retardation
Fatigue/energy loss
Worthlessness or guilt
Diminished concentration or indecisiveness
Thoughts of death/suicide

379
Q

Depression differential diagnosis?

A

Anxiety
Bipolar
Hypothyroidism
Anaemia
Viral infection
Drug induced

380
Q

Average length of a depressive episode?

A

Six months

381
Q

Aims of depression treatment?

A

Restore normal function
Increase resilience
Reduce mortality (suicide)
Preventing relapse

382
Q

Lifestyle actions to treat depression?

A

Sleep management
Exercise
Diet
Address negative habits

383
Q

Sleep hygiene principles?

A

Regular sleep and wake times
Avoid excessive eating, smoking or drinking alcohol before bed
Create a good environment for sleep: noise, temperature, comfort
Relax before bed
Regular physical exercise

384
Q

Non-pharmacological treatment for depression?

A

Lifestyle changes
Psychosocial interventions such as mindfulness
Psychological/talking therapies such as CBT
Physical therapy such as ECT

385
Q

How long should an antidepressant be taken for, for the first episode?

A

Six months post recovery

386
Q

How long should an antidepressant be taken for, for the second episode?

A

1-3 years

387
Q

How long should an antidepressant be taken for, for the third episode?

A

> 5 years

388
Q

How long should an antidepressant be taken for, for the fourth episode?

A

Lifelong unless good reason to stop

389
Q

What does TCA stand for?

A

Tricyclic antidepressant

390
Q

What does SSRI stand for?

A

Selective serotonin reuptake inhibitor

391
Q

What does SNRI stand for?

A

Selective serotonin and noradrenaline reuptake inhibitor

392
Q

What does MAOI stand for?

A

Monoamine oxidase inhibitor

393
Q

What does RIMA stand for?

A

Reversible inhibitor of MOA-A

394
Q

What does NARI stand for?

A

Noradrenaline reuptake inhibitor

395
Q

What does NASSA stand for?

A

Noradrenaline and specific serotonin antidepressant

396
Q

Symptoms of discontinuation syndrome with antidepressants?

A

Flu-like
Paraesthesia
Electric shock sensation
Insomnia
Headache
Excessive dreaming
Agitation

397
Q

Specialist resources for pharmacotherapy in depression?

A

Maudsley prescribing guidelines
Psychotropic drug directory

398
Q

What to consider when choosing an antidepressant?

A

Efficacy
Tolerability
Cost-effectiveness
Guidelines
Patient factors

399
Q

Examples of SSRIs?

A

Citalopram
Escitalopram
Fluoxetine
Fluvoxamine
Paroxetine
Sertraline

400
Q

Common side effects of SSRIs?

A

feeling agitated, shaky or anxious
feeling or being sick
dizziness
blurred vision
low sex drive
difficulty achieving orgasm during sex or masturbation
in men, difficulty obtaining or maintaining an erection (erectile dysfunction

401
Q

Caution specific to citalopram/escitalopram?

A

QT prolongation

402
Q

Most appropriate SSRI for use in pregnancy?

A

Sertraline

403
Q

SSRI to avoid in pregnancy?

A

Paroxetine

404
Q

SSRI to avoid in breastfeeding?

A

Fluoxetine

405
Q

SSRIs that can cause hepatic enzyme inhibition?

A

Fluoxetine
Fluvoxamine
Paroxetine

406
Q

Examples of SNRIs?

A

Duloxetine
Venlafaxine
Bupropion

407
Q

Monitoring with venlafaxine?

A

Blood pressure

408
Q

Side effecs of mirtazapine?

A

Blood dyscrasia
Sedation
Weight gain

409
Q

Monitoring for mianserin?

A

Regular FBC

410
Q

Examples of tricyclic antidepressants?

A

Clomipramine
Amitriptyline
Dosulepin
Doxepin
Imipramine
Lofepramine
Nortriptyline
Trimipramine

411
Q

Why can SSRIs cause nausea?

A

Increased 5-HT in gut and area postrema

412
Q

Why can SSRIs cause akathisia?

A

Increased 5-HT leads to dopamine inhibition in striatum

413
Q

How can SSRIs cause bleeding?

A

Reduction of platelet aggregation due to reduced uptake of serotonin into platelets

414
Q

SSRI with the longest half-life?

A

Fluoxetine

415
Q

SSRI with the shortest half-life?

A

Paroxetine

416
Q

SSRI most likely to cause weight gain?

A

Paroxetine

417
Q

SSRI most likely to cause sexual dysfunction?

A

Paroxetine

418
Q

SSRI most likely to cause diarrhoea?

A

Sertraline

419
Q

Type of antidepressants most likely to cause hyponatremia?

A

SSRIs and SNRIs

420
Q

Type of antidepressant most likely to cause osteopenia?

A

SSRIs

421
Q

Anti-depressant of choice in cardiac patients?

A

Sertraline

422
Q

Risk factors for bleeding with an SSRI?

A

> 65 years old
Alcohol misuse
Smoking
Hypertension
Peptic ulcer
Previous GI bleed
Concomitant use of NSAIDs, anticoagulants, aspirin

423
Q

What plant is St Johns wort from?

A

Hypericum perforatum

424
Q

SSRIs that may cause sedation?

A

Paroxetine
Fluvoxamine

425
Q

Preferred SSRIs in generalised anxiety?

A

Fluoxetine
Sertraline

426
Q

Class of antidepressants most likely to cause anticholinergic side effects?

A

TCAs

427
Q

How do TCAs work?

A

block the reuptake of serotonin and norepinephrine, as well as
another neurotransmitter known as acetylcholine

428
Q

Drugs recommended in post-stroke depression?

A

SSRIs- possible paroxetine first choice
Notriptyline

429
Q

Newest TCA?

A

Lofepramine

430
Q

Discontinuation symptoms are most likely with which TCAs?

A

Amitriptyline
Imipramine

431
Q

Class of antidepressants most likely to cause arrhythmia?

A

TCAs apart from lofepramine

432
Q

Classes of antidepressants to avoid in diabetics?

A

TCAs and MOAIs

433
Q

Sexual dysfunction is most likely with which TCAs?

A

Clomipramine
Amitriptyline

434
Q

TCAs least likely to cause sedation?

A

Nortriptyline
Lofepramine

435
Q

Examples of MAOIs?

A

Isocarboxazid
Phenelzine
Tranylcypromine
Selegiline

436
Q

How do MAOIs work?

A

Prevent monoamine oxidase from breaking down serotonin, noradrenaline and dopamine

437
Q

Class of antidepressants that can cause hypertension?

A

SNRIs

438
Q

Dietary considerations when taking MAOIs?

A

Avoid food rich in tyramine as it can cause dangerously high blood pressure

439
Q

Food/drink rich in tyramine?

A

Cheeses
Cured meats
Certain sauces
Beer
Dried fruit
Red wine

440
Q

Classes of antidepressants most likely to cause postural hypotension?

A

TCAs
MAOIs

441
Q

Symptoms of serotonin syndrome?

A

Tremor
Hyperreflexia
Clonus
Myoclonus
Rigidity
Tachycardia
Blood pressure changes
Hyperthermia
Diaphoresis
Shivering
Diarrhoea
Agitation
Confusion
Mania

442
Q

TCA more selective for serotonergic transmission?

A

Clomipramine

443
Q

TCA more selective for noradrenergic transmission?

A

Imipramine

444
Q

MAOIs most likely to cause hepatotoxicty?

A

Isocarboxazid
Phenelzine

445
Q

How does bupropion work?

A

Inhibits the reuptake of noradrenaline and dopamine

446
Q

Other uses of bupropion?

A

Smoking cessation

447
Q

Risks to consider with bupropion?

A

Lowers seizure threshold
Monitor blood pressure

448
Q

How does mirtazapine work?

A

Antagonist a1 receptors leading to enhanced noradrenaline and serotonin activity
Antagonist 5-HT2/3 indirectly increasing 5-HT1 transmission

449
Q

What is anxiety?

A

A natural emotion. It includes activation of the sympathetic nervous system, feeling frightened or an urge to escape. It becomes a disorder when it interferes with normal functioning

450
Q

Risk factors for anxiety disorders?

A

Family history
Life events
Childhood adversity
Being female
Being unmarried
Social isolation
Unemployment
Poverty
Comorbid medical conditions

451
Q

Examples of drugs that may cause anxiety symptoms?

A

CNS stimulants
CNS depressant withdrawal
Antipsychotics
Anticonvulsants
Antidepressants
Bronchodilators
Corticosteroids

452
Q

How to diagnose anxiety?

A

Clinical interview
Can use DSM-5 and validated questionnaires
Consider severity
Exclude other causes

453
Q

Common symptoms of anxiety?

A

Sensitivity to noise
Palpitations
Restlessness
Breathlessness
Irritable
Fearful
Nausea
Insomnia
GI symptoms

454
Q

What part of the brain mediates fear response?

A

Amygdala

455
Q

Common types of anxiety disorders?

A

GAD
OCD
PTSD
Panic disorder
Phobic disorder
Social anxiety disorder

456
Q

What is generalised anxiety disorder?

A

Excessive worry and anxiety about multiple life circumstances

457
Q

How to diagnose GAD?

A

Excessive anxiety and worry about multiple things and three or more of the other symptoms
- occurring more days than not
- for at least six months

458
Q

Ancillary symptoms of GAD?

A

Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating
Irritability
Muscle tension
Sleep disturbance

459
Q

How many ancillary symptoms needed to diagnose GAD?

A

3

460
Q

First line therapy for GAD?

A

CBT

461
Q

GAD treatment options?

A

CBT
Anxiety management therapy
Pharmacotherapy

462
Q

First-line pharmacotherapy for GAD?

A

SSRI

463
Q

Pharmacotherapy options for GAD?

A

SSRI
SNRI
Pregabalin

464
Q

How long to continue drug treatment in GAD for a patients who respond?

A

Up to 18 more months

465
Q

Main symptoms of OCD?

A

Obsessions
Compulsions

466
Q

Pathology of OCD?

A

Assumed to be primarily 5-HT dysfunction as improvement seen with SSRIs

467
Q

DSM-5 criteria for OCD diagnosis?

A

Symptoms must:
- create marked distress
- consume >1 hour per day
- affect normal function
- cannot be related to medication, drugs or other conditions

468
Q

Recommended treatment for OCD?

A

Combination of CBT and pharmacotherapy

469
Q

Which condition requires high drug doses, depression or OCD?

A

OCD

470
Q

How long to use drug therapy for in OCD?

A

6-12 months in first instance
Some may need indefinitely

471
Q

What is panic disorder?

A

Recurrent, unexpected panic attacks associated with:
Intense cardiac and nervous symptoms, fear of losing control, fear of dying and feelings of unreality

472
Q

Criteria for panic disorder diagnosis?

A

2 or more panic attacks

473
Q

Main neurotransmitters involved in panic disorder?

A

GABA
Cholecystokinin

474
Q

First line treatment for panic disorder?

A

Psychological interventions

475
Q

First line pharmacotherapy for panic disorder?

A

SSRI
Venlafaxine

476
Q

Second line pharmacotherapy for panic disorder?

A

TCA
MAOIs

477
Q

When are benzodiazepines used in panic disorder?

A

Only for those who do not respond to/tolerate SSRIs or TCAs

478
Q

When do PTSD symptoms usually occur?

A

1-6 months after exposure to event and persist for more than one month after exposure

479
Q

The three symptom clusters of PTSD?

A

Intrusive phenomena
Hyperarousal phenomena
Avoidance of reminders/emotional numbing

480
Q

First line PTSD management?

A

Mainly non-drug therapy

481
Q

Only class of drug recommended for PTSD?

A

SSRIs as effective against all symptom clusters

482
Q

What is a phobic disorder?

A

Excessive or unrealistic fears that are unreasonable. Leads to avoidance behaviour in an attempt to minimise anxiety

483
Q

Treatment for phobic disorder?

A

CBT
Pharmacotherapy not recommended

484
Q

When can pharmacotherapy be used in phobic disorder?

A

For specific circumstances e.g.
-benzodiazepines before MRI
- propranolol before public speaking

485
Q

What is social anxiety disorder?

A

Marked and persistent fear and avoidance of social situations in which embarrassment or humiliation may occur

486
Q

Treatment for social anxiety disorder?

A

CBT
SSRI/Venlafaxine

487
Q

How long to use drug therapy for in social anxiety?

A

6-12 months with aim to titrate off therapy

488
Q

What are anxiolytics?

A

Drugs that reduce anxiety

489
Q

What are hypnotics?

A

Drugs that produce drowsiness and facilitates the onset of sleep

490
Q

How do benzodiazepines work?

A

Promote GABA binding to GABA(a) receptors. They have allosteric action.

491
Q

Pharmacological effects of benzodiazepines?

A

Anxiety reduction
Aggression reduction
Induction of sleep
Reduction of muscle tone
Anticonvulsant
Amnesia

492
Q

Which is the most lipophilic benzodiazepine?

A

Diazepam

493
Q

Long-acting benzodiazepines?

A

Diazepam

494
Q

Short-acting benzodiazepines?

A

Temazepam
Oxazepam
Lorazepam

495
Q

Short-acting benzodiazepines with intermediate-acting metabolites?

A

Alprazolam
Midazolam

496
Q

Side effects of benzodiazepines?

A

Sedation
Cognitive impairment
Paradoxical effects
Respiratory depression
Dependence
Driving ability
Falls

497
Q

Can benzodiazepines be used in pregnancy?

A

Yes but avoid in third trimester

498
Q

Contraindications for benzodiazepines?

A

Respiratory depression
Myasthenia gravis
Severe hepatic impairment

499
Q

Most common way to discontinue benzodiazepines?

A

Calculate the equivalent daily dose of benzodiazepine to diazepam
Give diazepam in 3/4 divided doses
Reduce dose by 10/20% each week

500
Q

How do Z drugs work?

A

GABA(a) agonists

501
Q

Half-life of Z drugs?

A

2.5-5 hours

502
Q

What type of benzodiazepine to use for anxiety?

A

Long acting

503
Q

What type of benzodiazepine to use for insomnia?

A

Short acting

504
Q

Zolpidem side effects?

A

Common: diarrhoea, dizziness
Rare: hallucination, acute rage, agitation

505
Q

Zolpidem contraindications?

A

Myasthenia Gravis
Alcohol use
Acute/severe pulmonary insufficiency

506
Q

Zopiclone side effects?

A

Common: bitter taste, dry mouth, drowsiness
Rare: nightmares, hallucinations, dyspepsia, angioedema

507
Q

Zopiclone contraindications?

A

Alcohol intake

508
Q

Difference between bipolar type I and II?

A

Type I experiences at least one full manic episode whereas type II experience hypomania

509
Q

Signs of a manic episode?

A

Elevated mood
Increased motor activity
Accelerate thought or speech
Irritability
Decreased sleep
Change in appetite
Distractibility
Grandiose ideas
Change in dress
Delusions or hallucinations

510
Q

Common drug options in bipolar?

A

Lithium
Valproate
Carbamazepine
Gabapentin
Lamotrigine
Topiramate
Quetiapine

511
Q

How is lithium thought to work?

A

Inhibits dopamine release
Enhances 5HT release
Decreases intracellular messenger formation

512
Q

Half life of lithium?

A

18-24 hours

513
Q

How is lithium excreted?

A

Unchanged in the urine
Competes with sodium to be reabsorbed in proximal convoluted tubule

514
Q

Blood levels for lithium?

A

Mania: 0.6-1mmol/l
Prophylaxis: 0.6-0.8mmol/l

515
Q

Toxic level of lithium?

A

> 1.2 associated with signs of toxicity
2.0 associated with severe toxicity

516
Q

What type of level is uses for lithium?

A

Trough

517
Q

When to take a sample for a lithium trough level?

A

12 hours post-dose

518
Q

How often to monitor lithium levels?

A

Every 3-6 months

519
Q

Signs of acute lithium toxicity?

A

Nausea
Vomiting
Diarrhoea
ECG changes
Arrhythmias
Prolonged QT

520
Q

Signs of chronic lithium toxicity?

A

Ataxia
Confusion
Tremor
Cardiac symptoms
Renal impairment

521
Q

Common causes of lithium toxicity?

A

Drug interactions
Renal impairment
Dehydration
Overdose

522
Q

Drug classes that can reduce lithium clearance?

A

Thiazides
NSAIDs
ACEi
CCBs

523
Q

How to manage lithium toxicity?

A

Stop lithium
Use levels to guide therapy
<3mmol/l use NaCl infusion
If severe renal dialysis may be used

524
Q

Benefit of SR lithium?

A

Side effects usefully related to peak plasma levels so SR preparations avoid this

525
Q

Approximate conversion from lithium citrate to carbonate?

A

Lithium citrate 520 mg is equivalent to lithium carbonate 204 mg.

526
Q

Does related side effects of lithium?

A

Metallic taste
Nausea
Diarrhoea
Polydipsia
Cognitive impairment
Tremor

527
Q

Non-dose-related side effects of lithium?

A

Diabetes
Hypothyroidism
Hypercalcaemia
Weight gain
Maculopapular rash

528
Q

Precautions for lithium?

A

Acute hyponatremia
Psoriasis
Serotonin enhancing drugs
Renal impairment
Surgery
Elderly

529
Q

Contraindications for lithium?

A

Severe renal impairment

530
Q

Can Lithium be used whilst breastfeeding?

A

No

531
Q

Can lithium be used in pregnancy?

A

Ideally should be avoided but can be used in second and third trimesters if essential

532
Q

Why should lithium never be used in the first trimester?

A

Causes malformation of heart and large vessels which develop during weeks 3-9 of pregnancy

533
Q

Monitor for lithium?

A

TDM
ECG if cardiac risk
Renal function
Thyroid function

534
Q

Patient counselling for lithium?

A

Do not stop taking suddenly
May take 6-10 days to take effect
Maintain sodium and fluids
Avoid sodium bicarbonate
Educate on signs of toxicity

535
Q

Most effective medication for rapid-cycling in bipolar?

A

Valproate
Carbamazepine

536
Q

When would valproate/carbamazepine be used in bipolar?

A

If Lithium failed or contraindicated

537
Q

Wound definition?

A

A break in the structure of an organ of tissue caused by an external agent

538
Q

Examples of wounds?

A

Bruises
Grazes
Tears
Cuts
Punctures
Burns

539
Q

Medical term for a bruise?

A

Contusion

540
Q

What can cause burns?

A

Heat
Chemicals
Electricity
Sunlight
Nuclear radiation

541
Q

What is a first degree burn?

A

Only affects epidermis

542
Q

What is a second degree burn?

A

Affects epidermis and dermis

543
Q

What is a third degree burn?

A

Damage to full skin depth and tissues below

544
Q

Are burns painful?

A

First degree is painful
Second degree is very painful
Third degree is not painful due to nerve damage

545
Q

What are ulcers?

A

Breaks in the skin that extend to all layers and fail to heal. Associated with inflammation

546
Q

Average time for a skin ulcer to heal?

A

26 weeks

547
Q

What scale was originally used to predict pressure ulcer risk?

A

Waterlow score

548
Q

Medications that can increase the risk of pressure ulcers?

A

Steroids
Anti-inflammatories
Cytotoxics

549
Q

How can tissue damage be restored?

A

Regeneration if cells can regrow
Healing by repair if cells cannot regrow

550
Q

What does healing by repair lead to?

A

Scarring and loss of specialised function

551
Q

Four steps of the wound healing process?

A

Rapid haemostasis
Appropriate inflammation
Proliferation
Remodelling

552
Q

What happens during the haemostasis stage of wound repair?

A

Immediately after wound occurs
Local vascular constriction
Fibrin clot formation
Proinflammatory cytokines and growth factors released
Clotting cascade

553
Q

Extra steps at haemostasis in wound repair if a blood vessel is damaged?

A

Kinin system
Coagulation system
Both help for a physical barrier to prevent infection spread

554
Q

What is the kinin system?

A

Enzymatic cascade if plasma proteins
Produce proinflammatory cytokines
Such as bradykinin which increases vascular permeability promoting plasma proteins at injury site and causes pain

555
Q

Purpose of the acute inflammation stage of wound repair?

A

Clear away dead tissue
Protect against local infection
Allows access for immune system to damaged area

556
Q

What do neutrophils do during the inflammation stage of wound repair?

A

Act from wound edge
Clear away invading microbes and cellular debris
Produce proteases and reactive oxygen species which cause collateral damage

557
Q

What do macrophages do during the inflammation stage of wound repair?

A

Enter wound area
Release cytokine to activate leukocytes
Induce apoptosis
Stimulate keratinocytes, fibroblasts and angiogenesis to promote tissue regeneration

558
Q

What do T-lymphocyes do during the inflammation stage of wound repair?

A

Last immune cell to enter wound
Role not completely understood but wound healing impaired if they are reduced

559
Q

At what stage of wound repair do T-lymphocytes peak?

A

Late proliferation and early remodelling stages

560
Q

What kind of T-cells have a positive impact on wound repair?

A

CD4+ (T-helper cells)

561
Q

What kind of T-cells have a negative impact on wound repair?

A

CD8+ (T-suppressor-cytotoxic cells)

562
Q

What happens during the proliferation stage of wound repair?

A

Re-epithelization to close the external surface: epithelial-mesenchymal stem cells migrate over provisional clot
Repair the dermis: fibroblasts and endothelial cell support angiogenesis, collage formation and formation of granulation tissue
In wound bed: fibroblasts produce collagen, glycosaminoglycans and proteoglycans to generate extracellular matrix to hold cells together

563
Q

What happens during the remodelling stage of wound repair?

A

Physical contraction of wound by myofibroblasts
Regression of newly formed capillaries to reduce vascular density back to normal
Extracellular matrix remodelling to look how it did before

564
Q

What is a scar made up of?

A

Fibrocollagenous tissue from endothelial cells, fibroblasts and myofibroblasts

565
Q

Common types of scars?

A

Hypertrophic
Keloid

566
Q

What are keloid scars?

A

Large
Do not fade
Overproduction of fibroblasts even after wound has closed

567
Q

Local factors that can affect wound healing?

A

Oxygenation
Wound colonisation

568
Q

Why is oxygen critical for wound healing?

A

Prevents infection
Induces angiogenesis
Helps re-epithelialisation
Enhances fibroblast proliferation
Enhances collagen synthesis
Promotes wound contraction

569
Q

Systemic factors that affect wound healing?

A

Age
Sex hormones in older people
Obesity
Smoking
Alcohol consumption
Nutrition
Stress
Diabetes
Medication

570
Q

Why do older men have delayed healing of wounds?

A

Oestrogen can help age-related impairment in healing whereas androgens negatively affect wound healing

571
Q

What is the difference between a dressing and a bandage?

A

Dressings are in direct contact with the wound whereas bandages hold dressings in place

572
Q

Possible purposes of dressings?

A

Reduce infection risk
Stop bleeding and start clotting
Absorb excess blood, plasma and other fluids
Wound debridement
Begin healing process

573
Q

Main types of dressings?

A

Haemostatic
Occlusive

574
Q

Types of occlusive dressings?

A

Absorbent/foam/hydrocolloid
Antimicrobial
Film
Hydrogel
Negative pressure/vacuum
Synthetic skin

575
Q

Lifetime prevalence of schizophrenia?

A

1%

576
Q

Three symptoms clusters of schizophrenia?

A

Positive
Negative
Cognitive

577
Q

Is an earlier onset of schizophrenia more common in men or women?

A

Men

578
Q

What are positive symptoms of schizophrenia?

A

changes in thoughts and feelings that are “added on” to a person’s experiences
PSYCHOTIC

579
Q

Examples of positive symptoms of schizophrenia?

A

Though process disturbance
Delusions
Hallucinations
Erratic or extreme emotion
Very slow or fast movement
Behavioural changes

580
Q

What are negative symptoms in schizophrenia?

A

things that are “taken away” or reduced

581
Q

Examples of negative symptoms in schizophrenia?

A

Anhedonia
Low energy or motivation
Blank facial expression
Inability to make or keep friends
Difficulty initiating activities
Social isolation
Flat affect

582
Q

Examples of cognitive symptoms of schizophrenia?

A

Poor concentration
Memory disturbance
Inability to plan
Difficulty executing tasks
Impaired decision making

583
Q

What type of schizophrenia symptoms are usually more responsive to treatment?

A

Positive

584
Q

What are delusions?

A

Flash beliefs that are firmly and consistently held despite disconfirming evidence or logic

585
Q

Types of delusions?

A

Grandeur
Control
Thought broadcasting
Thought withdrawal
Reference
Persecution

586
Q

What are delusions of grandeur?

A

Belief that one is a famous or powerful person from past or present

587
Q

What are delusions of control?

A

Belief that an external force is trying to take control of one’s thoughts, body or behaviour

588
Q

What is thought broadcasting?

A

Belief that one’s thoughts are being broadcasted or transmitted to others

589
Q

What is thought withdrawal?

A

Belief that one’s thoughts are being removed from the mind

590
Q

What are delusions of reference?

A

Belief that all happening things revolve around oneself

591
Q

What are delusions of persecution?

A

Belief that one is the target of others’ evil plots

592
Q

What are hallucinations?

A

Sensory experiences in the absence of any stimulation from the environment. Any sense can be involved.

593
Q

Most common type of hallucination?

A

Auditory

594
Q

Examples of disorganised speech?

A

Loose associations
Neologisms

595
Q

What are loose associations in schizophrenia?

A

Continual shifting from topic to topic without any apparent or logical connection between thoughts

596
Q

What are neologisms?

A

New, seemingly meaningless words are formed by combining words

597
Q

What is avolition?

A

Inability or lack of energy to engage in routine

598
Q

What is alogia?

A

Lack of meaningful speech

599
Q

Main neurotransmitter involved in schizophrenia?

A

Dopamine

600
Q

Evidence for the dopamine hypothesis in schizophrenia?

A

Phenothiazines reduce dopamine activity and psychotic symptoms are reduced
Levodopa and amphetamines increase dopamine activity and can produce psychotic symptoms

601
Q

How many subtypes of dopamine?

A

5

602
Q

Most important subtype of dopamine in regards to schizophrenia?

A

D2

603
Q

The four main dopamine pathways?

A

Nigrostriatal
Mesolimbic
Mesocortical
Tubero-infundibular

604
Q

How is the mesocortical dopamine pathway related to schizophrenia?

A

Low levels of dopamine can cause negative symptoms
Therefore treatment that lowers dopamine levels can increase negative symptoms

605
Q

How is the mesolimbic dopamine pathway related to schizophrenia?

A

High levels of dopamine can cause positive symptoms. Therefore D2 antagonist can reduce positive symptoms

606
Q

How is the nigrostriatal dopamine pathway related to schizophrenia?

A

Dopamine blockade in this pathway can lead to EPS side effects and tardive dyskinesia. This is why these are side effects of some antipsychotics

607
Q

How is the tuberoinfundibular dopamine pathway related to schizophrenia?

A

Blockade of dopamine in this pathway can lead to increase prolactin, this can lactation, gynecomastia, infertility and sexual dysfunction as side effects of some antipsychotics

608
Q

What causes EPSE?

A

D2 blockade in nigrostriatal pathway
Blockade of dopamine receptors also increases activity of acetylcholine

609
Q

What happens to acetylcholine activity when dopamine activity is reduced?

A

Acetylcholine activity increases

610
Q

How may glutamate be involved in schizophrenia?

A

NMDA antagonists e.g. Ketamine can induce psychotic symptoms in non-schizophrenics
Increased NMDA receptors have been seen in post-mortem schizophrenic brains

611
Q

DSM-V criteria for schizophrenia?

A

A) characteristic symptoms
B) social/occupational dysfunction
C) duration of six months
D) schizoaffective and mood disorder exclusion
E) substance/medical exclusion
F) relationship to pervasive developmental disorder

612
Q

What cluster of symptoms do typical antipsychotics treat?

A

Only positive

613
Q

What cluster of symptoms do atypical antipsychotics treat?

A

Positive and sometimes negative

614
Q

What is the most effective drug for schizophrenia?

A

Clozapine

615
Q

What type of antipsychotics have a lower rate of EPSE?

A

Atypical

616
Q

How do typical antipsychotics work?

A

by blocking dopamine D2 receptors in the brain

617
Q

How do atypical antipsychotics work?

A

modulate serotonin (5-HT), norepinephrine, and/or histamine neurotransmission as well as dopamine blockade

618
Q

Types of typical antipsychotics?

A

Phenothiazines
Butyrophenones
Thioxanthenes
Other heterocyclics

619
Q

Examples of phenothiazines?

A

Chlorpromazine
Prochlorperazine
Fluphenazine
Pericyazine
Pipothiazine
Trifluoperazine

620
Q

Examples of butyrophenones?

A

Haloperidol
Penfluridol
Droperidol

621
Q

Examples of atypical antipsychotics?

A

Clozapine
Olanzapine
Risperidone
Aripiprazole
Ziprasidone

622
Q

What is parkinsonism?

A

Tremors, rigidity, slowness of movement, temporary paralysis

623
Q

What is dystonia?

A

Involuntary muscle contractions

624
Q

What is Akathisia?

A

Inability to resist the urge to move

625
Q

What is tardive dyskinesia?

A

Involuntary movements of the mouth, lips and tongue

626
Q

Examples of EPSE?

A

Parkinsonism
Dystonia
Akathisia
Tardive dyskinesia

627
Q

Example of an antipsychotic with no anticholinergic effect?

A

Haloperidol

628
Q

Why are atypical antipsychotics the less likely to cause EPSE?

A

their rapid dissociation from the dopamine D2 receptor

629
Q

What is the extrapyramidal system?

A

a neural network located in the brain that is part of the motor system involved in the coordination of movement

630
Q

What is neurolepsis?

A

Psychomotor slowing
Emotional quieting
Effective indifference

631
Q

Brain changes present in schizohrenia?

A

Cerebral atrophy
Enlargement of ventricles

632
Q

Types of dopamine receptors?

A

D1
D2
D3
D4
D5

633
Q

Types of glutamate receptors?

A

NMDA
AMPA
Kainate
Metabotropic

634
Q

Types of serotonin receptors?

A

5-HT1A
5-HT2A
5-HT2C
5-HT3
5-HT6
5-HT7

635
Q

Types of GABA receptors?

A

GABAa
GABAb
GABAc

636
Q

Function of the nigro-straital pathway?

A

Movement

637
Q

Function of the mesocortical pathway?

A

Motivation, pleasure, reward, desire and socialisation

638
Q

Function of the mesolimbic pathway?

A

Speech
Perception of reality

639
Q

Function of the tuberoinfundibular pathway?

A

Regulation of prolactin

640
Q

What happens in the dopamine mesocortical pathway when 5HT2 receptors are activated?

A

Inhibits firing of mesocortical dopaminergic neurons

641
Q

Limitations of the dopamine hypothesis in schizophrenia?

A

Does not explain cognitive deficits
Psychotomimetic effects of activations of other pathways not included e.g. D-lysergic acid

642
Q

Clinical efficacy of antipsychotics correlated closely to?

A

The relative ability to block D2 receptors in the mesolimbic pathway

643
Q

What happens during the prodromal phase of schizophrenia?

A

Negative symptoms dominate
Can last days to months

644
Q

Examples of treatment for mental health before medication was available?

A

Isolation/restraint
Shock therapy using insulin-induced seizures or electrical current
Surgery e.g. Prefrontal lobotomy

645
Q

What does D2 receptor activation do to cAPM?

A

Decreases it

646
Q

How does the 5HT2A/D2 theory of a-typicality explain the low risk of extrapyramidal symptoms?

A

5HT2A antagonism can increase dopaminergic neurotransmission in the nigrostriatal pathway, reducing the risk of extrapyramidal symptoms

647
Q

Example of a partial dopamine agonist?

A

Aripiprazole

648
Q

What do all typical antipsychotic drug structures have in common?

A

Phenothiazine nucleus

649
Q

What is a phenothiazine nucleus?

A
650
Q

What is this?

A

Haloperidol

651
Q

What is this?

A

Chlorpromazine

652
Q

What is this?

A

Aripiprazole

653
Q

What is this?

A

Clozapine

654
Q

What is this?

A

Prochlorperazine

655
Q

What is this?

A

Quetiapine

656
Q

What is this?

A

Promethazine

657
Q

Main area of the brain affected in ADHD?

A

Prefrontal cortex
Cortical-striatal-thalamic-cortical circuit

658
Q

ADHD DSM-V definition?

A

Age-inappropriate persistent and impairing symptoms with the presence of hyperactive-impulsive or inattentive symptoms that causes impairment that were present before aged seven years. Must cause significant impairment and be present in two or more settings

659
Q

Types of ADHD?

A

Inattentive
Hyperactive-impulsive
Combined

660
Q

Aims of ADHD drug treatment?

A

Reduce symptoms
Improve academic performance
Improve quality of life

661
Q

Inattentive type ADHD symptoms?

A

Lack of attention to detail
Lack of sustained attention
Poor listener
Failure to follow through on tasks
Poor organisation
Avoids tasks requiring sustained mental effort
Loses things
Easily distracted
Forgetful

662
Q

Hyperactive-impulse type ADHD symptoms?

A

Fidgeting
Leaving seat
Inappropriate running or climbing
Difficulty with quiet activities
Always on the go
Excessive talking
Blurting answers
Can’t wait turns

663
Q

What is the most common type of ADHD?

A

Combined

664
Q

Co-morbidities associated with ADHD?

A

Sleep disorder
Anxiety disorder
Mood disorder
Conduct disorder
Autism
Oppositional defiant disorder

665
Q

Differential diagnoses of ADHD?

A

Sleep apnea/poor sleep
Mood and anxiety disorders
Sensory impairment
Learning disabilities
Absence seizures
Iron deficiency anaemia
Inappropriate school placement

666
Q

What is the biochemical hypothesis of ADHD?

A

Can be treated with stimulants which increase noradrenaline and dopamine. Therefore these neurotransmitter are implicated in ADHD

667
Q

Neurotransmitters involved in ADHD?

A

Noradrenaline
Dopamine

668
Q

How do stimulants work?

A

Increase dopamine outside nerve cells

669
Q

How does methylphenidate work?

A

Slows the reuptake of dopamine and noradrenaline
Significantly amplifies extracellular dopamine in the basal ganglia

670
Q

How do amphetamines work?

A

Increasing production/release of dopamine and noradrenaline

671
Q

How does atomoxetine work?

A

Decreases noradrenaline reuptake

672
Q

What is DAT1?

A

Dopamine transport protein

673
Q

Function of DAT1?

A

Reuptake of dopamine

674
Q

What is MAO-A?

A

Monoamine oxidase A

675
Q

Function of MAO-A and COMT?

A

Catabolism of dopamine

676
Q

What is COMT?

A

Catechol-o-methyl-transferase

677
Q

How is noradrenaline related to ADHD?

A

Increases the signal
Enhances executive operations
Increases inhibitor
Increases firing to neurons of relevant input

678
Q

In regards to ADHD where in the brain does noradrenaline act?

A

The prefrontal cortex

679
Q

Possible brain abnormality in ADHD?

A

Abnormalities in the right prefrontal cortex

680
Q

Key noradrenaline receptor in ADHD?

A

Alpha2a

681
Q

Key dopamine receptor in ADHD?

A

D1

682
Q

What does activation of alpha2a receptors by noradrenaline do? (ADHD)

A

Enhances the strength of relevant sensory input (increases the signal)

683
Q

What does activation of D1 receptors by dopamine do? (ADHD)

A

Weakens irrelevant sensory input (decreases noise)
Also modulates motivation so can illicit interest in tasks

684
Q

When should drug therapy be used in ADHD?

A

Reserved for those with severe symptoms and impairment or those with moderate impairment who have not responded to non-drug interventions

685
Q

First-time drug treatment for ADHD?

A

Stimulants such as methylphenidate

686
Q

How does guanfacine/clonidine work for ADHD?

A

They are alpha2a agonists

687
Q

Which drug has greater selectivity for alpha-2a adrenoreceptors, clonidine or guanfacine?

A

Guanfacine

688
Q

Common side effects of methylphenidate?

A

Dry mouth
Appetite and weight loss
Slower growth
Sleep disturbance

689
Q

When may methylphenidate be contraindicated?

A

In situations where it may induce or worsen psychosis

690
Q

Benefits of modified-release methylphenidate preparations?

A

Convenience
Improving adherence
Reduces stigma
No need to store or administer controlled drugs in schools

691
Q

Benefits of immediate-release methylphenidate preparations?

A

Flexible dosing regimens
During titration
Cheaper

692
Q

Why are modified-release methylphenidate preparations not equivalent?

A

contain an immediate-release component and a modified-release component. The biphasic-release profiles of different preparations contain different proportions of immediate-release and modified-release components

693
Q

Brand of methylphenidate that is 30% immediate release and 70% modified release?

A

Equasym

694
Q

Equasym biphasic pharmacokinetic profile?

A

30% immediate release
70% modified release

695
Q

Brand of methylphenidate that is 50% immediate release and 50% modified release?

A

Medikinet XL

696
Q

Medikinet XL biphasic pharmacokinetic profile?

A

50% immediate release
50% modified release

697
Q

Brand of methylphenidate that is 22% immediate release and 78% modified release?

A

Concerta XL
Xenidate XL
Matoride XL

698
Q

Concerta XL biphasic pharmacokinetic profile?

A

22% immediate release
78% modified release

699
Q

Concerns with atomoxetine?

A

Suicidal thinking
Liver damage

700
Q

What is the cortical-striatal-thalamic-cortical circuit?

A

chain of neurons in the brain that connects the prefrontal cortex, the basal ganglia, and the thalamus in one continuous loop

701
Q

Functions of the cortical-striatal-thalamic cortical circuit?

A

Emotions and attention
Executive function
Motor activity
Impulsivity

702
Q

What is the difference between a seizure and epilepsy?

A

Seizure is a one-off occurrence

703
Q

What is epileptogenesis?

A

Development and extension of tissue capable of generating spontaneous seizure
The sequence of events that turns a normal neuronal network into a hyperexcitable one

704
Q

Epilepsy definition?

A

A transient occurrence of symptoms due to abnormal excessive or synchronous neuronal activity of the brain
Two or more seizures must occur

705
Q

How to diagnose epilepsy?

A

Symptoms
Medical history
EEG
Neuroimaging

706
Q

What is a generalised seizure?

A

Begins spontaneously in both hemispheres

707
Q

What is a focal seizure?

A

Starts in localised region of the brain

708
Q

What is focal seizure with secondary generalisation?

A

Starts locally but spreads across both hemispheres

709
Q

Types of focal seizures?

A

Simple
Complex

710
Q

What is a simple focal seizure?

A

No loss of consciousness

711
Q

What is a complex focal seizure?

A

Includes impairment of consciousness

712
Q

Types of generalised seizures?

A

Absence
Tonic
Clonic
Tonic-clonic
Atonic
Myoclonic

713
Q

Causes of epilepsy?

A

Trauma
Infection
Fevers
Alcohol and other drugs
Medication
Brain tumour
Stroke
Genetics

714
Q

Why can domoic acid poisoning cause seizures?

A

Domoic acid is structurally similar to the excitatory neurotransmitter glutamate.

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