Clinical Flashcards
1
Q
WHO classification of diabetes mellitus?
A
Fasting glucose >7mmol/l
2 hours post-prandial >11.1mmol/l
2
Q
How many people in the UK have diabetes?
A
4.7 million
3
Q
Peak age of onset for type-1 diabetes?
A
12 years old
4
Q
What percentage of diabetes is type-1?
A
8%
5
Q
What percentage of diabetes is type-2?
A
90%
6
Q
Gestational diabetes is present in what percentage of pregnancies?
A
4-5%
7
Q
Rarer forms of diabetes mellitus?
A
Monogenic forms of diabetes
Endocrinopathies
8
Q
Other names for type-1 diabetes?
A
Autoimmune diabetes
Insulin-dependent diabetes Mellitus
Juvenile onset diabetes
9
Q
Main cause of type-1 diabetes mellitus?
A
T-cell mediated autoimmune destruction of the pancreatic beta-cells
10
Q
Clinical presentation of type-1 diabetes?
A
Hyperglycaemia
Glycosuria
Polyuria
Polydipsia
Weight loss
Pear drop breath
11
Q
What is glycosuria?
A
High levels of glucose in the urine
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
13
Q
How to test for glycosuria?
A
Clinical dipsticks
14
Q
What is polyuria?
A
Abnormally large quantities of urine
15
Q
Why is polyuria present in type-1 diabetes?
A
Exceeding renal threshold creates osmotic drag in the urine and increases diuresis
16
Q
What is polydipsia?
A
Increased thirst
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
18
Q
Why is weight loss present in type-1 diabetes?
A
Accelerated breakdown of fat and muscle in the absence of glucose uptake
19
Q
What causes diabetic ketoacidosis?
A
The liver produces ketone bodies from fat. These can be used as a temporary fuel source
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)
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
22
Q
Normal HbA1c level?
A
<42mmol/mol (6%)
23
Q
Pre-diabetic HbA1c level?
A
42-47mmol/mol (6-6.4%)
24
Q
Diabetic HbA1c level?
A
> 48mmol/mol (6.5%)
25
When was insulin discovered?
1921
26
Who discovered insulin?
Frederick Banting and Charles H Best
27
Insulin was discovered in the pancreatic extracts of what animal?
Dog
28
Who helped develop insulin for human use?
B Collip and JJR Macleod
29
Which pharmaceutical company first manufactured insulin?
Eli lilly
30
When was the first large-scale manufacture of insulin?
1923
31
When was the first biosynthetic insulin available?
1982
32
Which was the first biosynthetic human insulin?
Humulin
33
Management of type-1 diabetes?
Insulin
Transplantation
Dietary considerations
34
Types of transplantation for type-1 diabetes?
Pancreas transplantation
Islet transplantation
35
Dietary considerations in type-1 diabetes?
Glycaemic index
Increase complex carbohydrates
Reduced saturated fat intake
Decrease salt intake
36
What can cause hypoglycaemia?
Too much insulin
Not enough food
Too much exercise
Too much alcohol
37
Symptoms of hypoglycaemia?
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
38
Diagnosis of DKA?
Ketones in blood or urine with hyperglycaemia
39
Which ketone bodies are produced in DKA?
Beta-hydroxybutyrate and acetoacetate
40
DKA is most common in which type of diabetes?
1
41
Symptoms of DKA?
Pear drop smell on breath
Nausea and vomiting
Belly pain
Rapid breathing
Feeling sluggish
Trouble paying attention
Coma
Death
42
Treatment of DKA?
Fluid and electrolyte replacement
Insulin
43
Long-term microvascular complications of hyperglycaemia?
Retinopathy
Nephropathy
Neuropathy
Foot ulcers
Sexual dysfunction
44
Long-term macrovascular complications of hyperglycaemia?
Heart disease
Stroke
45
Common types of autoantibodies involved in type-1 diabetes?
Proinsulin (IAA)
Glutamic acid decarboxylase (GAD)
Insulinoma-associated (IA-2)
Zinc transporter (ZnT8A)
46
Environmental triggers of type-1 diabetes?
Viruses- coxsackie-B, rubella, mumps
Toxins- streptozotocin and alloxin
Diet- cows milk, smoked fish (nitrosamines)
Vitamins- low vitamin D
47
What are the four T’s of type-1 diabetes?
Toilet
Thirsty
Tired
Thinner
48
Why is HbA1c not essential for type-1 diabetes diagnosis?
Would not be raised in patients with classic acute onset as glucose will not have had time to bind to haemoglobin
49
Reasons to test for diabetic autoantibodies?
Not needed for diagnosis
But helpful if unclear clinical picture
For coding
For access to health technologies
50
C-peptide is most clinically useful to distinguish?
Between forms of diabetes in those on insulin
To identify misdiagnosis
51
What does low C-peptide, high glucose show?
Insulin deficient (type-1)
52
What does high C-peptide, high glucose show?
Insulin resistance (type-2/MODY)
53
What does low C-peptide, low glucose show?
Possible complex pathology (such as insulinoma)
54
Advantages of C-peptide test?
Cheap
Fast as can be done at local labs
55
Goals of type-1 diabetic therapy?
Glycaemic management
Prevention of microvascular and macrovascular complications
Management of cardiovascular risk factors
Minimising psychosocial burden
56
Types of very rapid-acting insulin?
Fiasp
Lyumjev
57
Type of rapid-acting insulin?
Humalog
Novorapid
Apidra
Trurapi
Admelog
58
Types of analogue biphasic insulin?
Novomix 30
Humalog mix 25
Humalog mix 50
59
Types of short-acting insulin?
Actrapid
Humulin S
Hypurin neutral
60
Types of isophane biphasic insulin?
Humulin M3
Hypurin 30/70 mix
61
Types of intermediate-acting insulin?
Insulatard
Humulin I
Hypurin isophane
62
Types of long-acting insulin?
Lantus
Levemir
63
Types of long-acting biosimilar insulin?
Absalagar
Semglee
64
Types of ultra-long-acting insulin?
Tresiba
Toujeo
65
When to take short-acting insulin?
10-30 minutes pre-meal
In secondary care for hyperglycaemic correction
66
Short-acting insulin action of onset?
30-60 minutes
67
Short-acting insulin peak of action?
1-3 hours
68
Short-acting insulin duration of action?
6-8 hours
69
When to take rapid-acting/very rapid-acting insulin?
Mealtimes and when required for sick day management or hyperglycaemic correction doses
70
Rapid-acting insulin onset of action?
10-20 minutes
71
Rapid-acting insulin peak of action?
1 hours
72
Rapid-acting insulin duration of action?
4 hours
73
Very rapid-acting insulin onset of action?
5-10 minutes
74
Very rapid-acting insulin peak of action?
1 hour
75
Very rapid-acting insulin duration of action?
3 hours
76
When to take intermediate-acting insulin?
Twice daily. Usually 30 minutes pre-meal or bedtime
77
Intermediate-acting insulin onset of action?
60-90 minutes
78
Intermediate-acting insulin peak of action?
4-6 hours
79
Intermediate-acting insulin duration of action?
12-20 hours
80
When to take analogue biphasic insulin?
Two or three times daily, always with meals
81
Analogue biphasic insulin onset of action?
10-20 minutes
82
Analogue biphasic insulin peak of action?
1 hour
83
Analogue biphasic insulin duration of action?
12-24 hours
84
When to take isophane biphasic insulin?
Twice daily, always with meals
85
Isophane biphasic insulin onset of action?
30-60 minutes
86
Isophane biphasic insulin peak of action?
1-4 hours
87
Isophane biphasic insulin duration of action?
12-24 hours
88
When to take long-acting insulin?
Once or twice daily
89
Long-acting insulin onset of action?
2-4 hours
90
Long-acting insulin peak of action?
Either no peak or 6-14 hours depending on brand
91
Long-acting insulin duration of action?
16-24 hours depending on brand
92
When to take ultra-long-acting insulin?
Once daily
93
Ultra-long-acting insulin onset of action?
30-90 minutes
94
Ultra-long-acting insulin peak of action?
No peak
95
Ultra-long-acting insulin duration of action?
24-42 hours
96
Safety standards for prescribing insulin?
Prescribe by brand
Beware of sound-alike drugs
Correct device
Correct dose
Do not abbreviate units
Correct time
Correct strength
97
Types of insulin regimens?
Basal bolus
Two or three times daily biphasic
5 minutes for insulin
98
What types of insulins are used for basal bolus regimens?
3 rapid-acting and 2 intermediate-acting OR 3 rapid-acting and 1 long-acting
99
Advantages of basal bolus regimens?
More flexibility with meal times
Tighter glycaemic control
Less chance of nocturnal hypoglycaemia
100
Disadvantages of basal bolus regimen?
Multiple injections required
Can lead to more weight gain
Increased risk of hypoglycaemia
Requires patient compliance and responsibility
101
What does DAFNE stand for?
Dose adjustment for normal eating
102
What is DAFNE?
A course for ages 17 years and over to learn the necessary skills to count carbohydrates and inject the right amount if insulin
103
In an individual with the correct background and no resistance, how much insulin is needed for 10g of carbohydrates?
1 unit
104
Calculation for insulin needed?
ICR is usually 1 unit to 10g
ISF is sensitivity to insulin
IOB is insulin on board
105
What is insulin involved in two or three times daily insulin injection regimens?
2 or 3 analogue or isophane biphasic injections
106
Advantages of two or three times daily injections regimen?
Simple
Convenient
Can be provided by community nurses for those unable to administer their own insulin
107
Disadvantages of two or three times daily injections regimen?
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
108
What insulins are used in 5 minutes for insulin regimen?
1 true long-acting and 1 analogue biphasic
109
Advantages of 5 minutes for insulin regimen?
Increased patient compliance
No time spent thinking about diabetes
Keeps patient out of DKA/HHS
110
Disadvantages of 5 minutes for insulin regimen?
Facilitates disengaged behaviour
No glucose control other than keeping patients out of the danger zone
Usually progress towards diabetic-related complications
Reduced life expectancy
111
Does size matter for an insulin needle?
No
112
Why may a patient ask for a different size insulin needle?
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
113
Regular monitoring for type-1 diabetes?
HbA1c
Blood pressure
Cholesterol
Eye screening
Foot examination
Kidney function
Urinary albumin
BMI
Smoking review
114
NICE recommends diabetic patients should aim for a HbA1c of?
53mmol/mol but targets should be individualised for patients
115
Criteria for a continuous glucose monitor?
Formal diagnosis of type-1 diabetes
116
Disadvantages of HbA1c?
Not useful to diagnose type-1 diabetes
Only should average glucose levels, not necessarily time in range
117
Usual time in range target?
>70%
118
Time in range target for older people and those at risk of hypoglcaemia?
>50%
119
Time in range target for pregnant women?
>70%
120
What blood glucose level is defined as hypoglycaemia?
<4mmol/mol
121
Why is repeating glucagon administration not beneficial?
Glucagon causes release of glucose from the liver, this can only happen once
122
Driving and type-1 diabetes?
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
123
When may the DVLA revoke a license in a type-1 diabetic patient?
When they have more than 1 severe hypo, whilst awake, in a 12-month period. It can be reapplied for three months later
124
How long does a type-1 diabetic patients driving license last?
1-3 years
125
How can alcohol affect type-1 diabetes?
Effect on blood glucose
Hypoglycaemia may be mistaken for being drunk
Harder to manage
More likely to forget insulin
126
Threshold for offering blood pressure management in type-1 diabetic patients?
135/85mmHg
OR 130/80mmHg in the presence of albuminuria
127
First-line antihypertensive for all type-1 diabetic patients?
ACE inhibitor
128
Second-line antihypertensive for all type-1 diabetic patients?
Calcium channel blocker
129
Third-line antihypertensive for all type-1 diabetic patients?
Thiazide like diuretic
130
Target total cholesterol level for type-1 diabetics?
<4mmol/l
131
Target LDL level for type-1 diabetics?
<2mmol/l
132
What statin to recommend for the primary prevention of CVD?
Atorvastatin 20mg
133
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134
When should a statin be offered to type-1 diabetics?
>40 years old
Diabetic for >10 years
Established nephropathy
Other CVS risk factors
135
What statin should be recommended for secondary prevention of CVD in type-1 diabetics?
Atorvastatin 80mg
136
What causes peripheral vascular disease?
Atherosclerosis in arteries that feed the feet and legs
137
Therapy for peripheral vascular disease?
Statins
Clopidogrel
Naftidrofuryl
138
What causes neuropathic pain in type-1 diabetes?
High glucose levels destroy the small blood vessels that feed the peripheral nerves
139
Symptoms of diabetic neuropathic pain?
Initial pain: burning, stabbing, shooting, aching, electric shock-like
Later there is a complete loss of sensation
140
Treatment for diabetic neuropathic pain?
Amitriptyline, duloxetine, gabapentin, pregabalin, topical capsaicin
141
Types of diabetic retinopathy?
Nonproliferative
Proliferative
142
What causes diabetic retinopathy?
High blood glucose levels damage the retina
143
Treatment for diabetic retinopathy?
Laser treatment
Eye injections
Steroid eye implants
Eye surgery
144
Drugs used for diabetic retinopathy eye injections?
Ranibizumab
Aflibercept
145
Causes of diabetic nephropathy and kidney disease?
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
146
ACR stands for?
Urine albumin to creatinine ratio
147
Diagnosis of diabetic kidney disease?
ACR of >30mg/g
Creatine clearance <60ml/min
148
Types of diabetic emergencies?
Severe hypoglycaemia
Acute diabetic foot
Diabetic ketoacidosis
Hyperosmolar hyperglycaemic state
149
Features of DKA?
Hyperglycaemia
Ketonaemia
Metabolic acidosis
150
Ketone levels in DKA?
>3mmol/l in blood
>4mmol/l in urine OR ++ on standard urine stick
151
When may euglycaemic diabetic ketoacidosis occur?
In type-2 diabetes treated with SGLT2 inhibitors
152
DKA triggers?
New onset diabetes
Poor sick day management
Non-adherence to insulin
Infection
MI
Stroke
Illegal drugs
Pregnancy
Drugs
Acute stresses
153
What should be checked before starting insulin in DKA?
Potassium levels
154
Brand names of biphasic insulin aspart?
Novomix 30
155
Brand names of biphasic insulin lispro?
Humalog mix 25
Humalog mix 50
156
Brand names of biphasic isophane insulin?
Humulin M3
Insuman comb 25
Hypurin Porcine 30/70
157
Brand names of insulin soluble?
Actrapid
Humulin S
Hypurin Porcine Neutral
Insuman Rapid
158
Brand names of insulin aspart?
Novorapid
Fiasp
Trurapi
159
Brand names of insulin degludec?
Tresiba
160
Brand names of insulin detemir?
Levemir
161
Brand names of insulin glargine?
Toujeo
Lantus
Semglee
Abasaglar
162
Brand names of insulin glulisine?
Apidra
163
Brand names of insulin lispro?
Humalog
Admelog
Lyumjev
164
Brand names of insulin isophane?
Humulin I
Insulatard
Insuman Basal
Hypurin Porcine Isophane
165
What does the thyroid gland secrete?
Thyroid hormones
Calcitonin
166
What does the parathyroid secrete?
Parathyroid hormone
167
What does parathyroid hormone do?
Maintenance of serum calcium and phosphate levels
168
Outline thyroid hormone synthesis?
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
169
What is thyroglobulin?
A large protein rich in tyrosine
170
Important element in regards to the thyroid?
Iodine
171
What enzyme makes iodide reactive?
Thyroid peroxidase
172
How does iodide bind to thyroglobulin?
On the benzene ring of tyrosine residues
173
What does MIT stand for?
Monoiodotyrosine
174
What does DIT stand for?
Diiodotyrosine
175
What is produced when MIT and DIT couple?
T3
176
What is produced when DIT and DIT couple?
T4
177
Which thyroid hormone is produced more?
T4
178
Cardiac symptoms of hypothyroidism?
Bradycardia
Diastolic hypertension
Pericardial effusion
179
Gastrointestinal symptoms of hypothyroidism?
Weight gain
Decreased appetite
Abdominal distension
Constipation
180
Neuromuscular symptoms of hypothyroidism?
Fatigue
Increased sensitivity to cold
Low mood
Impaired cognition
Paraesthesia
Peripheral neuropathy
Muscle weakness or pain
Joint pain
Delayed relation of deep tendon reflexes
181
Reproductive symptoms of hypothyroidism?
Irregular menstrual cycle
Menorrhagia
Infertility
182
Appearance symptoms of hypothyroidism?
Hoarse voice
Dry, flaking, thickened skin
Goitre
Reduced sweating
Yellow complexion
Facial swelling (particularly eyelids)
Brittle nails
Thin hair
Hair and eyebrow loss
183
Causes of hypothyroidism?
Autoimmune thyroiditis
Iodine deficiency
Post thyroidectomy
Post-radioactive iodine treatment
Drug-induced
Peripheral resistance to thyroid hormone
Congenital disease
184
How to diagnose hypothyroidism?
Symptoms
Biochemical test: TSH and free T4
185
What does high TSH and low free T4 show?
Overt primary hypothyroidism
186
What does slightly raised FSH and normal free T4 show?
Subclinical primary hypothyroidism
187
What does low TSH and low free T4 show?
Secondary hypothyroidism (hypothalamic or pituitary dysfunction)
188
What can rT3 testing be used for?
To ascertain peripheral T4 to T3 conversion. Low levels can show peripheral hypothyroidism
189
Which thyroid antibodies can be tested for?
Thyroid peroxide antibodies (TPOAb)
Thyroglobulin antibodies (TgAb)
Thyroid stimulating hormone receptor antibodies (TSHRAb/TRAb)
190
First line treatment of hypothyroidism?
Levothyroxine
191
Usual starting dose of levothyroxine?
1.6mcg/kg rounded to nearest 25mcg
192
When to use a reduced levothyroxine starting dose?
>65 years old
Pre-existing CVD
193
What deficiency should be corrected before starting levothyroxine?
Glucocorticoid
194
Congenital hypothyroidism dose?
10-15mcg/kg for three months of life and then adjust according to TSH
195
How often to monitor TFTs?
Every three months until stable and then annually
196
Levothyroxine counselling?
Life-long compliance
30-60 minutes before food
Interactions: milk, calcium, PPIs etc
Monitoring requirements
197
side effects of levothyroxine?
Flushing
Restlessness
Palpitations
Insomnia
Angina
Thyroid crisis
198
What is liothyronine?
Synthetic form of T3
199
What is liothyronine used for?
Rarely used due to lack of clinical evidence apart from myxoedema coma
200
How to manage hypothyroidism in pregnancy?
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
201
Can levothyroxine be used in pregnancy?
Yes- increased monitoring
202
Can levothyroxine be used when breastfeeding?
Yes
203
Normal TSH levels?
0.38-5.33mU/l
204
Normal free T4 levels?
7.9-14.4pmol/l
205
Target TSH in first trimester of pregnancy?
<2.5mU/l
206
Target TSH in third trimester of pregnancy?
<3mU/l
207
Common levothyroxine drug interactions?
Amiodarone
Lithium
Antacids
Colestyramine
Warfarin
Beta-blockers
Ferrous sulphate
208
What is myxoedema crisis?
a rare life-threatening clinical condition in patients with longstanding severe untreated hypothyroidism
209
Symptoms of myxoedema crisis?
Hypothyroidism symptoms and:
Hypothermia
Macroglossia (swollen tongue)
Ptosis (upper eyelid droop)
Periorbital swelling
Puffy face
210
What can precipitate myxoedema crisis?
Stress
Infection
Trauma
Possible drugs
211
In hyperthyroidism what does a symmetrical enlargement of the thyroid gland suggest?
Graves disease
212
In hyperthyroidism what does a unilateral enlargement of the thyroid gland suggest?
Nodular disease
213
Cardiac/respiratory symptoms of hyperthyroidism?
Tachycardia
Shortness of breath
Reduced exercise tolerance
Palpitation
AF
Decline in pre-existing cardiac disease
214
Gastrointestinal symptoms of hyperthyroidism?
Weight loss
Increased appetite
Diarrhoea
215
Neuromuscular symptoms of hyperthyroidism?
Insomnia
Restlessness
Iritability
Mood swings
Muscle weakness
Fine motor tremor
Rapid deep tendon reflexes
Psychosis
216
Reproductive symptoms of hyperthyroidism?
Reduced fertility
Reduced libido
Reduction/loss of periods
Gynaecomastia in males
217
Skin symptoms of hyperthyroidism?
Wet skin
Thin hair
Hair loss
Increased sweating and heat sensitivity
218
How do the eyes look in graves disease?
Eyelids retract
Bulging eyes
Eye redness
219
Most common cause of hyperthyroidism?
Graves disease
220
What causes graves disease?
Autoimmune condition where the thyroid is attacked leading it to become overactive
221
What can cause hyperthyroidism?
Graves disease
Nodular disease
Thyroiditis
Pituitary disease
222
Risk factors for graves disease?
Young and middle-aged women
Can run in families
Smoking
223
What are thyroid nodules?
Lumps develop on thyroid. They are usually non-cancerous but can contain thyroid tissue resulting in excess production of thyroid hormones
224
Age group most likely to be affected by thyroid nodules?
>60 years old
225
Why can amiodarone cause hyperthyroidism?
It contains iodine
226
How to diagnose hyperthyroidism?
Symptoms
Biochemical tests: TSH, free T3 and T4, TSH receptor antibodies
227
What does low TSH but high FT3 and FT4 suggest?
Hyperthyroidism of thyroidal origin (possibly thyroiditis)
228
What does high TSH and high FT3 and FT4 suggest?
Hyperthyroidism of extrathyroidal origin (hypothalamic or pituitary disease)
229
What does this thyroid likely show?
Graves’ disease
230
What does this thyroid likely show?
Normal thyroid
231
What does this thyroid likely show?
Thyroiditis
232
What does this thyroid likely show?
Single nodular (overactive)
233
What does this thyroid likely show?
Single nodular (under active)
234
What does this thyroid likely show?
Toxic multi nodular
235
Treatments for hyperthyroidism?
Anti thyroid drugs
Radioactive iodine
Thyroidectomy
236
When to use anti-thyroid drugs first line in graves disease?
When remission is likely
237
When to use radioactive iodine first line for graves disease?
When remission is unlikely
238
When to use thyroidectomy first line in graves disease?
Concerns regarding compression or malignancy
239
Can radioactive iodine be given in pregnancy?
No
240
What does GREAT stand for? (Thyroid)
Graves recurrent events after therapy
241
What does the GREAT score take into account?
Age
Sex
Smoking
Genetics
Goitre size
Biochemical tests
Pathology
Extrathyroidal involvement
242
How to grade a goitre?
Using the WHO goitre grading system
243
First-line anti-thyroid drug?
Carbimazole
244
First-line anti-thyroid drug in pregnancy?
Propylthiouracil
245
How long does it take to show benefit with anti-thyroid drugs?
6-8 weeks
246
Types of anti-thyroid regimens?
Titration
Block and replace
247
Carbimazole mechanism of action?
Inhibition of the organification of iodide and thyroglobulin and the coupling of iodothyronine residues which in turn suppress the synthesis of thyroid hormones
248
Initial dose of carbimazole?
20-60mg daily in divided doses
249
Titration carbimazole regimen?
Initial dose and then:
5-15mg daily
Regular TFT checks and dose adjusted according to response
250
Block and replace carbimazole regimen?
Continue high starting dose to completely block production
Levothyroxine started alongside which is titrated until TSH, T3 and T4 are in range
251
Carbimazole side effects?
Macropapular rash
Bone marrow suppression
252
What to counsel patients on when starting carbimazole?
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
253
Monitoring requirements for carbimazole?
FBCs every six months
TFTs
254
Carbimazole/propylthiouracil contraindications?
Severe hepatic impairment
Pre-existing blood disorders
History of pancreatitis
255
Why can carbimazole not be used in severe hepatic impairment?
Carbimazole is a pro-drug so the liver needs to be able to metabolise it into the active form, methimazole
256
Carbimazole drug interactions?
Warfarin
Digoxin
Trimethoprim
Drugs that cause myelosuppression
257
Propylthiouracil mechanism of action?
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
258
Propylthiouracil inhibits what enzyme?
Peroxidase
259
What does propylthiouracil take 4 weeks to take effect?
All the pre-formed hormones need to be used up before circulatory concentrations fall
260
Initial dose of propylthiouracil?
200-400mg once daily
261
Titration dose regimen for propylthiouracil?
Once levels in range then give 50-150mg daily. Regular TFT tests and adjust dose according to response
262
Block and replace regimen dose for propylthiouracil?
Continue high starting dose to completely block production
Levothyroxine started alongside which is titrated until TSH, T3 and T4 are in range
263
1mg of carbimazole is roughly equivalent to how much propylthiouracil?
10mg
264
Side effects of propylthiouracil?
Macropapular rash
Severe hepatic reactions
Bone marrow suppression
265
Counselling for propylthiouracil?
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
266
Aim of radioactive iodine treatment?
Resolve hyperthyroidism without post-ablation hypothyroidism
267
Advice for patients after radioactive iodine treatment?
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
268
How long does radioactive iodine treatment take to have effect?
2-3 months
269
What is thyroid crisis (thyrotoxic storm)?
A rare, extreme manifestation of thyrotoxicosis due to over production of thyroid hormones
270
What can precipitate thyroid crisis?
Infection
Trauma
Medications e.g. Amiodarone
Radioactive iodine treatment
Sudden cessation of anti-thyroid drugs
Some anaesthetics
Surgery
271
Symptoms of thyroid crisis?
Hyperthyroidism symptoms with:
Hyperthermia
Tachycardia
Atrial arrhythmias
Hypotension
Swearing
Nausea
Vomiting
Diarrhoea
Jaundice
Abdominal pain
Confusion
Seizures
272
How to diagnose thyroid storm?
Using the scoring system
>45 indicates storm
273
Drugs used for thyroid storm?
Carbimazole or propylthiouracil
Iodine/lugols/lithium (very rarely)
Beta-blocker (usually propranolol)
Glucocorticoids
Can also use cholestyramine to bind free thyroid hormone
274
What is infertility?
A failure to conceive after a year of regular intercourse without contraception
275
What is virility?
The quality of having strength, energy and a strong sex drive
276
What is primary infertility?
One who has never conceived a child
277
What is secondary infertility?
One who has had a child before
278
Questions to ask patients trying to conceive?
Previous pregnancies/children
Trial timeframe
Sex life
Contraception
Medical history
Current medications
Lifestyle
279
Physical examination for females trying to conceive?
Weight
Pelvic examination: PID, fibroids, lumps, tenderness
280
Physical examination for males trying to conceive?
Weight
Penial/testicular examination for abnormalities
281
Five test to diagnose infertility?
Sperm test
Blood test to check ovulation
Chlamydia test
X-ray of Fallopian tubes
Trans-vaginal ultrasound scan
282
What is a normal sperm count?
15-150 million/ml AS LONG AS the total ejaculate sperm count is over 22 million
283
What is oligozoospermia?
Low sperm count
<15 million/ml
284
What is azoospermia?
No sperm count
285
What can cause azoospermia?
Problems with production
Blockage so cannot reach ejaculate
286
What factors can damage sperm production?
Untreated STIs
Excess heat
Alcohol
Smoking
Recreation drugs
287
What is a fallopian tube X-ray called?
Hysterosalpingogram (HSG)
288
Process of fallopian tube x-ray?
Opaque dye injected through the cervix. Dye helps to see if there are any blockages
289
Treatment options for infertility?
Drug therapy
Surgery
Assisted conception
290
Common drugs prescribed to women with infertility?
Clomifene
Tamoxifen
Metformin
Gonadotrophins
Dopamine agonists (bromocriptine, cabergoline)
291
How does metformin work for infertility?
Stimulates ovulation
Encourages monthly periods
Reduced risk of miscarriage
292
How do gonadotrophins help male infertility?
Improve sperm production
293
Why is folic acid important for pregnancy?
Reduces the risk of neural tube defects such as spina bifida and anencephaly
294
What dose of folic acid is recommended during pregnancy?
400mcg daily or 5mg daily if increased risk, for the first 12 week whilst the baby’s spine is developing
295
Risk factor for neural tube defects in pregnancy?
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
Dietary sources of folic acid?
Green, leafy vegetables
Brown rice
Granary bread
Fortified cereals
297
Why is liver not safe to eat in pregnancy?
High in vitamin A
298
Types of combined hormonal contraceptives?
Pill
Patch
Ring
299
How do combined hormonal contraceptives work?
Act on hypothalamopituitary-ovarian axis to suppress LH and FSH to inhibit ovulation
300
Types of progesterone only contraceptives?
Pill
Patch
Ring
Implant
301
How do progesterone only contraceptives work?
Inhibit ovulation and thicken cervical mucus
302
Combined oral contraceptives are generally not recommended after what age?
50 years old
303
Risks of combined hormonal contraception?
VTE
MI
Stroke
Breast cancer
Cervical cancer
304
Health benefits of combined hormonal contraception?
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
How to assess if suitable for combined hormonal contraception?
Medical history
Current medication
BMI
Blood pressure
306
What BMI is combined hormonal contraception not recommended for?
>35
307
Symptoms that should prompt urgent medical attention when using combined hormonal contraception?
Calf pain, swelling or tenderness
Chest pain
Breathlessness
Hemoptysis
Loss of motor or sensory function
308
Symptoms that should prompt medical review when using combined hormonal contraception?
Breast changes
Unilateral nipple discharge
New onset sensory/motor symptoms one-hour preceding onset of migraine
Persistent unscheduled vaginal bleeding
309
Types of combined hormonal contraception regimens?
Standard or tailored
310
What is standard combined hormonal contraception regimen?
Using the contraception for 21 days and then having a seven-day break to induce a bleed
311
What is a tailored combined hormonal contraception regimen?
Reducing or completely stopping having a break in contraception so a bleed is not induced
312
Negative of tailored combined hormonal contraception regimen?
Not licensed but it is supported by the Faculty of Sexual and Reproductive Health (FSRH)
313
Negatives of standard combined hormonal contraception regimen?
Withdrawal bleed
Symptoms such as headache and nodo changes
Potential risk of pregnancy
314
Should combined oral contraceptives be stopped before surgery?
Yes prior to major elective surgery, surgery to legs and surgery that involved prolonged immobilisation of lower limbs
315
How long should combined oral contraceptives be stopped for before surgery?
4 weeks
316
When can combined oral contraceptives be restarted after surgery?
At least two weeks after full mobilisation
317
What happens if the combined oral contraceptive is not stopped before surgery?
Thromboprophylaxis required
318
When may combined oral contraception be contraindicated?
High VTE risk
Heavy smokers
BP above 160/95
Valvular heart disease
Diabetes with complications
Migraine with aura
319
Progestogen-only contraceptive mechanism of action?
Alter cervical mucus to prevent sperm entry and may inhibit ovulation
320
What is the pregnancy prevention programme?
Helps to stop women exposed to teratogenic drugs from becoming pregnancy
321
Drugs with high teratogenic potential?
Isotretinoin
Sodium valproate
322
Which drugs can lower the efficacy of hormonal contraception?
Most antiepileptics (metabolic enzyme-inducing drugs)
Carbamazepine
Phenytoin
Phenobarbital
323
Recommended contraception for women taking enzyme-inducing antiepileptics?
Long-acting reversible contraceptives such as depot injections, IUD and IUS
324
What is defined as a missed contraceptive pill?
Combined: >24 hours
Progestogen-only: 3 hours
Deogesterel: 12 hours
325
Common hormonal contraception drug interactions?
Carbamazepine
Phenytoin
Nevirapine
Ritonavir
St John’s wort
Rifampicin
326
How long to use barrier contraception after taking ulipristal?
Combined and parenteral progestogen only: 14 days
Progestogen-only pill: 9 days
Qlaira: 16 days
327
What happens if you miss a progestogen-only pill and have had unprotected intercourse in the last 5 days?
Emergency contraception recommended
Take pill next day as normal
Barrier contraception for 48 hours
328
What happens if you miss a progestogen-only pill and have NOT had unprotected intercourse in the last 5 days?
Take one pill as soon as possible then continue at that time daily
Use barrier methods for 48 hours
329
How long to use barrier methods for is combined pill is missed?
7 days
330
What to do if vomiting occurs within two hours of taking the contraceptive pill?
Take another
331
What if a patient has vomiting or diarrhoea for more than 24 hours whilst taking the contraceptive pill?
Class it as a missed pill
Use barrier methods for 7 days
332
What does LAM stand for?
Lactational amenorrhea method
333
What is the Lactational amenorrhea method?
Avoids pregnancy through the natural reduction in gonadotrophins caused by breastfeeding
334
How effective is Lactational amenorrhea method?
98% if all criteria fulfilled
335
Criteria for Lactational amenorrhea method?
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
Why does anti-epileptics often interact with other drugs?
Combination therapy
Narrow therapeutic index
Enzyme inducers
Administer for all life
337
Main way antiepileptic drugs interact with other drugs?
Enzyme induction- so may need to increase the dose of the other drug
338
Example of an antiepileptic that causes enzyme inhibition?
Sodium valproate
339
Common drug interactions that reduce levels of combined oral contraceptive pill?
Carbamazepine
Phenytoin
Primidone
Topiramate
340
Example of a drug that has increased exposure when used alongside the combined oral contraceptive pill?
Lamotrigine
341
Antiepileptic drugs with the lowest teratogenic potential?
Lamotrigine
Levetiracetam
342
Examples of enzyme-inducing antiepileptic drugs?
Carbamazepine
Eslicarbazepine
Oxcarbazepine
Phenobarbital
Phenytoin
Primidone
Rufinamide
Topiramate
Perampanel
343
How long after childbirth is emergency contraception needed?
21 days unless criteria for LAM
344
How long after abortion, miscarriage or ectopic pregnancy before emergency contraception is needed?
5 days
345
Effectiveness of emergency contraception?
CuIUD> ulipristal > levonorgestrel
346
Main parts of the brain involved with ADHD?
Prefrontal cortex
Basal ganglia
Corpus callosum
Anterior cingulate
347
What is the prefrontal cortex responsible for?
Planning actions, avoiding distraction, flexibility with change
348
What is the basal ganglia responsible for?
Impulse control
Coordinates information coming from other regions of the brain to prevent automatic response to stimuli
349
What is the corpus callosum responsible for?
Communication between the two hemispheres to ensure coordination
350
What is the anterior cingulate responsible for?
Management of emotion
351
What is an affective disorder?
illnesses that affect the way you think and feel
352
What is mild major depression?
Symptoms cause distress, and the person may have some difficulty carrying out usual activities
353
What is moderate major depression?
Several symptoms present to a marked degree and the person has considerable difficulty carry out usual tasks
354
What is severe major depression?
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
What is psychotic depression?
Rare form of severe major depression in which patients experience psychotic symptoms such as delusions, hallucinations or paranoia
356
Are men or women more affected by depression?
Women
357
Rule of halves in depression?
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
Usual age of onset for depression?
Mid 20s
359
Average peak of age of depression in women?
35-45
360
Main aetiology of depression?
Genetics
Personality
Early environment
Precipitating factors
Biological
Drug causes
361
Genetics and depression?
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
Personality and depression?
Anxious personality
Cyclothymic personality
363
Early environment and depression?
Deprivation of maternal affection
Parental relationship
Maternal post-natal depression
Abuse/neglect
364
Precipitating factors and depression?
Significant life events
Social vulnerability factors
365
What is the monoamine hypothesis?
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
Is suicide more common in men or women?
Men
367
How to counsel the suicide risk of antidepressants?
Inform of the risk
Action plan to follow if thoughts occur
Regular reviews
Be hypervigilant
368
Psychological symptoms of depression?
Hopelessness
Worthlessness
Guilt
369
What is anhedonia?
Loss of pleasure in things you used to enjoy
370
Physical symptoms of depression?
Insomnia
Poor appetite
Weight change
Feeling tired
GI upset
Pain
371
Another name for physical symptoms of depression?
Somatic
372
Cognitive symptoms of depression?
Poor concentration
Poor memory
373
Behavioural symptoms of depression?
Agitation
Self-neglect
Psychomotor retardation
374
How to diagnose depression using ICD-10?
Mild: 4 symptoms including 2 key
Moderate: >4 symptoms including 2 key
Severe: >7 symptoms
Must be present for at least two weeks
375
Key symptoms of depression according to ICD-10? (3)
Low mood
Anhedonia
Reduced energy
376
Ancillary symptoms of depression according to ICD-10? (7)
Reduced concentration and attention
Reduced self-esteem/confidence
Guilt and unworthiness
Pessimism
Ideas/acts of self-harm or suicide
Disturbed sleep
Diminished appetite
377
How to diagnose depression using DSM-5?
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
Symptoms of depression according to DSM-5? (9)
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
Depression differential diagnosis?
Anxiety
Bipolar
Hypothyroidism
Anaemia
Viral infection
Drug induced
380
Average length of a depressive episode?
Six months
381
Aims of depression treatment?
Restore normal function
Increase resilience
Reduce mortality (suicide)
Preventing relapse
382
Lifestyle actions to treat depression?
Sleep management
Exercise
Diet
Address negative habits
383
Sleep hygiene principles?
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
Non-pharmacological treatment for depression?
Lifestyle changes
Psychosocial interventions such as mindfulness
Psychological/talking therapies such as CBT
Physical therapy such as ECT
385
How long should an antidepressant be taken for, for the first episode?
Six months post recovery
386
How long should an antidepressant be taken for, for the second episode?
1-3 years
387
How long should an antidepressant be taken for, for the third episode?
>5 years
388
How long should an antidepressant be taken for, for the fourth episode?
Lifelong unless good reason to stop
389
What does TCA stand for?
Tricyclic antidepressant
390
What does SSRI stand for?
Selective serotonin reuptake inhibitor
391
What does SNRI stand for?
Selective serotonin and noradrenaline reuptake inhibitor
392
What does MAOI stand for?
Monoamine oxidase inhibitor
393
What does RIMA stand for?
Reversible inhibitor of MOA-A
394
What does NARI stand for?
Noradrenaline reuptake inhibitor
395
What does NASSA stand for?
Noradrenaline and specific serotonin antidepressant
396
Symptoms of discontinuation syndrome with antidepressants?
Flu-like
Paraesthesia
Electric shock sensation
Insomnia
Headache
Excessive dreaming
Agitation
397
Specialist resources for pharmacotherapy in depression?
Maudsley prescribing guidelines
Psychotropic drug directory
398
What to consider when choosing an antidepressant?
Efficacy
Tolerability
Cost-effectiveness
Guidelines
Patient factors
399
Examples of SSRIs?
Citalopram
Escitalopram
Fluoxetine
Fluvoxamine
Paroxetine
Sertraline
400
Common side effects of SSRIs?
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
Caution specific to citalopram/escitalopram?
QT prolongation
402
Most appropriate SSRI for use in pregnancy?
Sertraline
403
SSRI to avoid in pregnancy?
Paroxetine
404
SSRI to avoid in breastfeeding?
Fluoxetine
405
SSRIs that can cause hepatic enzyme inhibition?
Fluoxetine
Fluvoxamine
Paroxetine
406
Examples of SNRIs?
Duloxetine
Venlafaxine
Bupropion
407
Monitoring with venlafaxine?
Blood pressure
408
Side effecs of mirtazapine?
Blood dyscrasia
Sedation
Weight gain
409
Monitoring for mianserin?
Regular FBC
410
Examples of tricyclic antidepressants?
Clomipramine
Amitriptyline
Dosulepin
Doxepin
Imipramine
Lofepramine
Nortriptyline
Trimipramine
411
Why can SSRIs cause nausea?
Increased 5-HT in gut and area postrema
412
Why can SSRIs cause akathisia?
Increased 5-HT leads to dopamine inhibition in striatum
413
How can SSRIs cause bleeding?
Reduction of platelet aggregation due to reduced uptake of serotonin into platelets
414
SSRI with the longest half-life?
Fluoxetine
415
SSRI with the shortest half-life?
Paroxetine
416
SSRI most likely to cause weight gain?
Paroxetine
417
SSRI most likely to cause sexual dysfunction?
Paroxetine
418
SSRI most likely to cause diarrhoea?
Sertraline
419
Type of antidepressants most likely to cause hyponatremia?
SSRIs and SNRIs
420
Type of antidepressant most likely to cause osteopenia?
SSRIs
421
Anti-depressant of choice in cardiac patients?
Sertraline
422
Risk factors for bleeding with an SSRI?
>65 years old
Alcohol misuse
Smoking
Hypertension
Peptic ulcer
Previous GI bleed
Concomitant use of NSAIDs, anticoagulants, aspirin
423
What plant is St Johns wort from?
Hypericum perforatum
424
SSRIs that may cause sedation?
Paroxetine
Fluvoxamine
425
Preferred SSRIs in generalised anxiety?
Fluoxetine
Sertraline
426
Class of antidepressants most likely to cause anticholinergic side effects?
TCAs
427
How do TCAs work?
block the reuptake of serotonin and norepinephrine, as well as
another neurotransmitter known as acetylcholine
428
Drugs recommended in post-stroke depression?
SSRIs- possible paroxetine first choice
Notriptyline
429
Newest TCA?
Lofepramine
430
Discontinuation symptoms are most likely with which TCAs?
Amitriptyline
Imipramine
431
Class of antidepressants most likely to cause arrhythmia?
TCAs apart from lofepramine
432
Classes of antidepressants to avoid in diabetics?
TCAs and MOAIs
433
Sexual dysfunction is most likely with which TCAs?
Clomipramine
Amitriptyline
434
TCAs least likely to cause sedation?
Nortriptyline
Lofepramine
435
Examples of MAOIs?
Isocarboxazid
Phenelzine
Tranylcypromine
Selegiline
436
How do MAOIs work?
Prevent monoamine oxidase from breaking down serotonin, noradrenaline and dopamine
437
Class of antidepressants that can cause hypertension?
SNRIs
438
Dietary considerations when taking MAOIs?
Avoid food rich in tyramine as it can cause dangerously high blood pressure
439
Food/drink rich in tyramine?
Cheeses
Cured meats
Certain sauces
Beer
Dried fruit
Red wine
440
Classes of antidepressants most likely to cause postural hypotension?
TCAs
MAOIs
441
Symptoms of serotonin syndrome?
Tremor
Hyperreflexia
Clonus
Myoclonus
Rigidity
Tachycardia
Blood pressure changes
Hyperthermia
Diaphoresis
Shivering
Diarrhoea
Agitation
Confusion
Mania
442
TCA more selective for serotonergic transmission?
Clomipramine
443
TCA more selective for noradrenergic transmission?
Imipramine
444
MAOIs most likely to cause hepatotoxicty?
Isocarboxazid
Phenelzine
445
How does bupropion work?
Inhibits the reuptake of noradrenaline and dopamine
446
Other uses of bupropion?
Smoking cessation
447
Risks to consider with bupropion?
Lowers seizure threshold
Monitor blood pressure
448
How does mirtazapine work?
Antagonist a1 receptors leading to enhanced noradrenaline and serotonin activity
Antagonist 5-HT2/3 indirectly increasing 5-HT1 transmission
449
What is anxiety?
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
Risk factors for anxiety disorders?
Family history
Life events
Childhood adversity
Being female
Being unmarried
Social isolation
Unemployment
Poverty
Comorbid medical conditions
451
Examples of drugs that may cause anxiety symptoms?
CNS stimulants
CNS depressant withdrawal
Antipsychotics
Anticonvulsants
Antidepressants
Bronchodilators
Corticosteroids
452
How to diagnose anxiety?
Clinical interview
Can use DSM-5 and validated questionnaires
Consider severity
Exclude other causes
453
Common symptoms of anxiety?
Sensitivity to noise
Palpitations
Restlessness
Breathlessness
Irritable
Fearful
Nausea
Insomnia
GI symptoms
454
What part of the brain mediates fear response?
Amygdala
455
Common types of anxiety disorders?
GAD
OCD
PTSD
Panic disorder
Phobic disorder
Social anxiety disorder
456
What is generalised anxiety disorder?
Excessive worry and anxiety about multiple life circumstances
457
How to diagnose GAD?
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
Ancillary symptoms of GAD?
Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating
Irritability
Muscle tension
Sleep disturbance
459
How many ancillary symptoms needed to diagnose GAD?
3
460
First line therapy for GAD?
CBT
461
GAD treatment options?
CBT
Anxiety management therapy
Pharmacotherapy
462
First-line pharmacotherapy for GAD?
SSRI
463
Pharmacotherapy options for GAD?
SSRI
SNRI
Pregabalin
464
How long to continue drug treatment in GAD for a patients who respond?
Up to 18 more months
465
Main symptoms of OCD?
Obsessions
Compulsions
466
Pathology of OCD?
Assumed to be primarily 5-HT dysfunction as improvement seen with SSRIs
467
DSM-5 criteria for OCD diagnosis?
Symptoms must:
- create marked distress
- consume >1 hour per day
- affect normal function
- cannot be related to medication, drugs or other conditions
468
Recommended treatment for OCD?
Combination of CBT and pharmacotherapy
469
Which condition requires high drug doses, depression or OCD?
OCD
470
How long to use drug therapy for in OCD?
6-12 months in first instance
Some may need indefinitely
471
What is panic disorder?
Recurrent, unexpected panic attacks associated with:
Intense cardiac and nervous symptoms, fear of losing control, fear of dying and feelings of unreality
472
Criteria for panic disorder diagnosis?
2 or more panic attacks
473
Main neurotransmitters involved in panic disorder?
GABA
Cholecystokinin
474
First line treatment for panic disorder?
Psychological interventions
475
First line pharmacotherapy for panic disorder?
SSRI
Venlafaxine
476
Second line pharmacotherapy for panic disorder?
TCA
MAOIs
477
When are benzodiazepines used in panic disorder?
Only for those who do not respond to/tolerate SSRIs or TCAs
478
When do PTSD symptoms usually occur?
1-6 months after exposure to event and persist for more than one month after exposure
479
The three symptom clusters of PTSD?
Intrusive phenomena
Hyperarousal phenomena
Avoidance of reminders/emotional numbing
480
First line PTSD management?
Mainly non-drug therapy
481
Only class of drug recommended for PTSD?
SSRIs as effective against all symptom clusters
482
What is a phobic disorder?
Excessive or unrealistic fears that are unreasonable. Leads to avoidance behaviour in an attempt to minimise anxiety
483
Treatment for phobic disorder?
CBT
Pharmacotherapy not recommended
484
When can pharmacotherapy be used in phobic disorder?
For specific circumstances e.g.
-benzodiazepines before MRI
- propranolol before public speaking
485
What is social anxiety disorder?
Marked and persistent fear and avoidance of social situations in which embarrassment or humiliation may occur
486
Treatment for social anxiety disorder?
CBT
SSRI/Venlafaxine
487
How long to use drug therapy for in social anxiety?
6-12 months with aim to titrate off therapy
488
What are anxiolytics?
Drugs that reduce anxiety
489
What are hypnotics?
Drugs that produce drowsiness and facilitates the onset of sleep
490
How do benzodiazepines work?
Promote GABA binding to GABA(a) receptors. They have allosteric action.
491
Pharmacological effects of benzodiazepines?
Anxiety reduction
Aggression reduction
Induction of sleep
Reduction of muscle tone
Anticonvulsant
Amnesia
492
Which is the most lipophilic benzodiazepine?
Diazepam
493
Long-acting benzodiazepines?
Diazepam
494
Short-acting benzodiazepines?
Temazepam
Oxazepam
Lorazepam
495
Short-acting benzodiazepines with intermediate-acting metabolites?
Alprazolam
Midazolam
496
Side effects of benzodiazepines?
Sedation
Cognitive impairment
Paradoxical effects
Respiratory depression
Dependence
Driving ability
Falls
497
Can benzodiazepines be used in pregnancy?
Yes but avoid in third trimester
498
Contraindications for benzodiazepines?
Respiratory depression
Myasthenia gravis
Severe hepatic impairment
499
Most common way to discontinue benzodiazepines?
Calculate the equivalent daily dose of benzodiazepine to diazepam
Give diazepam in 3/4 divided doses
Reduce dose by 10/20% each week
500
How do Z drugs work?
GABA(a) agonists
501
Half-life of Z drugs?
2.5-5 hours
502
What type of benzodiazepine to use for anxiety?
Long acting
503
What type of benzodiazepine to use for insomnia?
Short acting
504
Zolpidem side effects?
Common: diarrhoea, dizziness
Rare: hallucination, acute rage, agitation
505
Zolpidem contraindications?
Myasthenia Gravis
Alcohol use
Acute/severe pulmonary insufficiency
506
Zopiclone side effects?
Common: bitter taste, dry mouth, drowsiness
Rare: nightmares, hallucinations, dyspepsia, angioedema
507
Zopiclone contraindications?
Alcohol intake
508
Difference between bipolar type I and II?
Type I experiences at least one full manic episode whereas type II experience hypomania
509
Signs of a manic episode?
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
Common drug options in bipolar?
Lithium
Valproate
Carbamazepine
Gabapentin
Lamotrigine
Topiramate
Quetiapine
511
How is lithium thought to work?
Inhibits dopamine release
Enhances 5HT release
Decreases intracellular messenger formation
512
Half life of lithium?
18-24 hours
513
How is lithium excreted?
Unchanged in the urine
Competes with sodium to be reabsorbed in proximal convoluted tubule
514
Blood levels for lithium?
Mania: 0.6-1mmol/l
Prophylaxis: 0.6-0.8mmol/l
515
Toxic level of lithium?
>1.2 associated with signs of toxicity
>2.0 associated with severe toxicity
516
What type of level is uses for lithium?
Trough
517
When to take a sample for a lithium trough level?
12 hours post-dose
518
How often to monitor lithium levels?
Every 3-6 months
519
Signs of acute lithium toxicity?
Nausea
Vomiting
Diarrhoea
ECG changes
Arrhythmias
Prolonged QT
520
Signs of chronic lithium toxicity?
Ataxia
Confusion
Tremor
Cardiac symptoms
Renal impairment
521
Common causes of lithium toxicity?
Drug interactions
Renal impairment
Dehydration
Overdose
522
Drug classes that can reduce lithium clearance?
Thiazides
NSAIDs
ACEi
CCBs
523
How to manage lithium toxicity?
Stop lithium
Use levels to guide therapy
<3mmol/l use NaCl infusion
If severe renal dialysis may be used
524
Benefit of SR lithium?
Side effects usefully related to peak plasma levels so SR preparations avoid this
525
Approximate conversion from lithium citrate to carbonate?
Lithium citrate 520 mg is equivalent to lithium carbonate 204 mg.
526
Does related side effects of lithium?
Metallic taste
Nausea
Diarrhoea
Polydipsia
Cognitive impairment
Tremor
527
Non-dose-related side effects of lithium?
Diabetes
Hypothyroidism
Hypercalcaemia
Weight gain
Maculopapular rash
528
Precautions for lithium?
Acute hyponatremia
Psoriasis
Serotonin enhancing drugs
Renal impairment
Surgery
Elderly
529
Contraindications for lithium?
Severe renal impairment
530
Can Lithium be used whilst breastfeeding?
No
531
Can lithium be used in pregnancy?
Ideally should be avoided but can be used in second and third trimesters if essential
532
Why should lithium never be used in the first trimester?
Causes malformation of heart and large vessels which develop during weeks 3-9 of pregnancy
533
Monitor for lithium?
TDM
ECG if cardiac risk
Renal function
Thyroid function
534
Patient counselling for lithium?
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
Most effective medication for rapid-cycling in bipolar?
Valproate
Carbamazepine
536
When would valproate/carbamazepine be used in bipolar?
If Lithium failed or contraindicated
537
Wound definition?
A break in the structure of an organ of tissue caused by an external agent
538
Examples of wounds?
Bruises
Grazes
Tears
Cuts
Punctures
Burns
539
Medical term for a bruise?
Contusion
540
What can cause burns?
Heat
Chemicals
Electricity
Sunlight
Nuclear radiation
541
What is a first degree burn?
Only affects epidermis
542
What is a second degree burn?
Affects epidermis and dermis
543
What is a third degree burn?
Damage to full skin depth and tissues below
544
Are burns painful?
First degree is painful
Second degree is very painful
Third degree is not painful due to nerve damage
545
What are ulcers?
Breaks in the skin that extend to all layers and fail to heal. Associated with inflammation
546
Average time for a skin ulcer to heal?
26 weeks
547
What scale was originally used to predict pressure ulcer risk?
Waterlow score
548
Medications that can increase the risk of pressure ulcers?
Steroids
Anti-inflammatories
Cytotoxics
549
How can tissue damage be restored?
Regeneration if cells can regrow
Healing by repair if cells cannot regrow
550
What does healing by repair lead to?
Scarring and loss of specialised function
551
Four steps of the wound healing process?
Rapid haemostasis
Appropriate inflammation
Proliferation
Remodelling
552
What happens during the haemostasis stage of wound repair?
Immediately after wound occurs
Local vascular constriction
Fibrin clot formation
Proinflammatory cytokines and growth factors released
Clotting cascade
553
Extra steps at haemostasis in wound repair if a blood vessel is damaged?
Kinin system
Coagulation system
Both help for a physical barrier to prevent infection spread
554
What is the kinin system?
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
Purpose of the acute inflammation stage of wound repair?
Clear away dead tissue
Protect against local infection
Allows access for immune system to damaged area
556
What do neutrophils do during the inflammation stage of wound repair?
Act from wound edge
Clear away invading microbes and cellular debris
Produce proteases and reactive oxygen species which cause collateral damage
557
What do macrophages do during the inflammation stage of wound repair?
Enter wound area
Release cytokine to activate leukocytes
Induce apoptosis
Stimulate keratinocytes, fibroblasts and angiogenesis to promote tissue regeneration
558
What do T-lymphocyes do during the inflammation stage of wound repair?
Last immune cell to enter wound
Role not completely understood but wound healing impaired if they are reduced
559
At what stage of wound repair do T-lymphocytes peak?
Late proliferation and early remodelling stages
560
What kind of T-cells have a positive impact on wound repair?
CD4+ (T-helper cells)
561
What kind of T-cells have a negative impact on wound repair?
CD8+ (T-suppressor-cytotoxic cells)
562
What happens during the proliferation stage of wound repair?
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
What happens during the remodelling stage of wound repair?
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
What is a scar made up of?
Fibrocollagenous tissue from endothelial cells, fibroblasts and myofibroblasts
565
Common types of scars?
Hypertrophic
Keloid
566
What are keloid scars?
Large
Do not fade
Overproduction of fibroblasts even after wound has closed
567
Local factors that can affect wound healing?
Oxygenation
Wound colonisation
568
Why is oxygen critical for wound healing?
Prevents infection
Induces angiogenesis
Helps re-epithelialisation
Enhances fibroblast proliferation
Enhances collagen synthesis
Promotes wound contraction
569
Systemic factors that affect wound healing?
Age
Sex hormones in older people
Obesity
Smoking
Alcohol consumption
Nutrition
Stress
Diabetes
Medication
570
Why do older men have delayed healing of wounds?
Oestrogen can help age-related impairment in healing whereas androgens negatively affect wound healing
571
What is the difference between a dressing and a bandage?
Dressings are in direct contact with the wound whereas bandages hold dressings in place
572
Possible purposes of dressings?
Reduce infection risk
Stop bleeding and start clotting
Absorb excess blood, plasma and other fluids
Wound debridement
Begin healing process
573
Main types of dressings?
Haemostatic
Occlusive
574
Types of occlusive dressings?
Absorbent/foam/hydrocolloid
Antimicrobial
Film
Hydrogel
Negative pressure/vacuum
Synthetic skin
575
Lifetime prevalence of schizophrenia?
1%
576
Three symptoms clusters of schizophrenia?
Positive
Negative
Cognitive
577
Is an earlier onset of schizophrenia more common in men or women?
Men
578
What are positive symptoms of schizophrenia?
changes in thoughts and feelings that are “added on” to a person's experiences
PSYCHOTIC
579
Examples of positive symptoms of schizophrenia?
Though process disturbance
Delusions
Hallucinations
Erratic or extreme emotion
Very slow or fast movement
Behavioural changes
580
What are negative symptoms in schizophrenia?
things that are “taken away” or reduced
581
Examples of negative symptoms in schizophrenia?
Anhedonia
Low energy or motivation
Blank facial expression
Inability to make or keep friends
Difficulty initiating activities
Social isolation
Flat affect
582
Examples of cognitive symptoms of schizophrenia?
Poor concentration
Memory disturbance
Inability to plan
Difficulty executing tasks
Impaired decision making
583
What type of schizophrenia symptoms are usually more responsive to treatment?
Positive
584
What are delusions?
Flash beliefs that are firmly and consistently held despite disconfirming evidence or logic
585
Types of delusions?
Grandeur
Control
Thought broadcasting
Thought withdrawal
Reference
Persecution
586
What are delusions of grandeur?
Belief that one is a famous or powerful person from past or present
587
What are delusions of control?
Belief that an external force is trying to take control of one's thoughts, body or behaviour
588
What is thought broadcasting?
Belief that one's thoughts are being broadcasted or transmitted to others
589
What is thought withdrawal?
Belief that one's thoughts are being removed from the mind
590
What are delusions of reference?
Belief that all happening things revolve around oneself
591
What are delusions of persecution?
Belief that one is the target of others' evil plots
592
What are hallucinations?
Sensory experiences in the absence of any stimulation from the environment. Any sense can be involved.
593
Most common type of hallucination?
Auditory
594
Examples of disorganised speech?
Loose associations
Neologisms
595
What are loose associations in schizophrenia?
Continual shifting from topic to topic without any apparent or logical connection between thoughts
596
What are neologisms?
New, seemingly meaningless words are formed by combining words
597
What is avolition?
Inability or lack of energy to engage in routine
598
What is alogia?
Lack of meaningful speech
599
Main neurotransmitter involved in schizophrenia?
Dopamine
600
Evidence for the dopamine hypothesis in schizophrenia?
Phenothiazines reduce dopamine activity and psychotic symptoms are reduced
Levodopa and amphetamines increase dopamine activity and can produce psychotic symptoms
601
How many subtypes of dopamine?
5
602
Most important subtype of dopamine in regards to schizophrenia?
D2
603
The four main dopamine pathways?
Nigrostriatal
Mesolimbic
Mesocortical
Tubero-infundibular
604
How is the mesocortical dopamine pathway related to schizophrenia?
Low levels of dopamine can cause negative symptoms
Therefore treatment that lowers dopamine levels can increase negative symptoms
605
How is the mesolimbic dopamine pathway related to schizophrenia?
High levels of dopamine can cause positive symptoms. Therefore D2 antagonist can reduce positive symptoms
606
How is the nigrostriatal dopamine pathway related to schizophrenia?
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
How is the tuberoinfundibular dopamine pathway related to schizophrenia?
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
What causes EPSE?
D2 blockade in nigrostriatal pathway
Blockade of dopamine receptors also increases activity of acetylcholine
609
What happens to acetylcholine activity when dopamine activity is reduced?
Acetylcholine activity increases
610
How may glutamate be involved in schizophrenia?
NMDA antagonists e.g. Ketamine can induce psychotic symptoms in non-schizophrenics
Increased NMDA receptors have been seen in post-mortem schizophrenic brains
611
DSM-V criteria for schizophrenia?
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
What cluster of symptoms do typical antipsychotics treat?
Only positive
613
What cluster of symptoms do atypical antipsychotics treat?
Positive and sometimes negative
614
What is the most effective drug for schizophrenia?
Clozapine
615
What type of antipsychotics have a lower rate of EPSE?
Atypical
616
How do typical antipsychotics work?
by blocking dopamine D2 receptors in the brain
617
How do atypical antipsychotics work?
modulate serotonin (5-HT), norepinephrine, and/or histamine neurotransmission as well as dopamine blockade
618
Types of typical antipsychotics?
Phenothiazines
Butyrophenones
Thioxanthenes
Other heterocyclics
619
Examples of phenothiazines?
Chlorpromazine
Prochlorperazine
Fluphenazine
Pericyazine
Pipothiazine
Trifluoperazine
620
Examples of butyrophenones?
Haloperidol
Penfluridol
Droperidol
621
Examples of atypical antipsychotics?
Clozapine
Olanzapine
Risperidone
Aripiprazole
Ziprasidone
622
What is parkinsonism?
Tremors, rigidity, slowness of movement, temporary paralysis
623
What is dystonia?
Involuntary muscle contractions
624
What is Akathisia?
Inability to resist the urge to move
625
What is tardive dyskinesia?
Involuntary movements of the mouth, lips and tongue
626
Examples of EPSE?
Parkinsonism
Dystonia
Akathisia
Tardive dyskinesia
627
Example of an antipsychotic with no anticholinergic effect?
Haloperidol
628
Why are atypical antipsychotics the less likely to cause EPSE?
their rapid dissociation from the dopamine D2 receptor
629
What is the extrapyramidal system?
a neural network located in the brain that is part of the motor system involved in the coordination of movement
630
What is neurolepsis?
Psychomotor slowing
Emotional quieting
Effective indifference
631
Brain changes present in schizohrenia?
Cerebral atrophy
Enlargement of ventricles
632
Types of dopamine receptors?
D1
D2
D3
D4
D5
633
Types of glutamate receptors?
NMDA
AMPA
Kainate
Metabotropic
634
Types of serotonin receptors?
5-HT1A
5-HT2A
5-HT2C
5-HT3
5-HT6
5-HT7
635
Types of GABA receptors?
GABAa
GABAb
GABAc
636
Function of the nigro-straital pathway?
Movement
637
Function of the mesocortical pathway?
Motivation, pleasure, reward, desire and socialisation
638
Function of the mesolimbic pathway?
Speech
Perception of reality
639
Function of the tuberoinfundibular pathway?
Regulation of prolactin
640
What happens in the dopamine mesocortical pathway when 5HT2 receptors are activated?
Inhibits firing of mesocortical dopaminergic neurons
641
Limitations of the dopamine hypothesis in schizophrenia?
Does not explain cognitive deficits
Psychotomimetic effects of activations of other pathways not included e.g. D-lysergic acid
642
Clinical efficacy of antipsychotics correlated closely to?
The relative ability to block D2 receptors in the mesolimbic pathway
643
What happens during the prodromal phase of schizophrenia?
Negative symptoms dominate
Can last days to months
644
Examples of treatment for mental health before medication was available?
Isolation/restraint
Shock therapy using insulin-induced seizures or electrical current
Surgery e.g. Prefrontal lobotomy
645
What does D2 receptor activation do to cAPM?
Decreases it
646
How does the 5HT2A/D2 theory of a-typicality explain the low risk of extrapyramidal symptoms?
5HT2A antagonism can increase dopaminergic neurotransmission in the nigrostriatal pathway, reducing the risk of extrapyramidal symptoms
647
Example of a partial dopamine agonist?
Aripiprazole
648
What do all typical antipsychotic drug structures have in common?
Phenothiazine nucleus
649
What is a phenothiazine nucleus?
650
What is this?
Haloperidol
651
What is this?
Chlorpromazine
652
What is this?
Aripiprazole
653
What is this?
Clozapine
654
What is this?
Prochlorperazine
655
What is this?
Quetiapine
656
What is this?
Promethazine
657
Main area of the brain affected in ADHD?
Prefrontal cortex
Cortical-striatal-thalamic-cortical circuit
658
ADHD DSM-V definition?
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
Types of ADHD?
Inattentive
Hyperactive-impulsive
Combined
660
Aims of ADHD drug treatment?
Reduce symptoms
Improve academic performance
Improve quality of life
661
Inattentive type ADHD symptoms?
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
Hyperactive-impulse type ADHD symptoms?
Fidgeting
Leaving seat
Inappropriate running or climbing
Difficulty with quiet activities
Always on the go
Excessive talking
Blurting answers
Can't wait turns
663
What is the most common type of ADHD?
Combined
664
Co-morbidities associated with ADHD?
Sleep disorder
Anxiety disorder
Mood disorder
Conduct disorder
Autism
Oppositional defiant disorder
665
Differential diagnoses of ADHD?
Sleep apnea/poor sleep
Mood and anxiety disorders
Sensory impairment
Learning disabilities
Absence seizures
Iron deficiency anaemia
Inappropriate school placement
666
What is the biochemical hypothesis of ADHD?
Can be treated with stimulants which increase noradrenaline and dopamine. Therefore these neurotransmitter are implicated in ADHD
667
Neurotransmitters involved in ADHD?
Noradrenaline
Dopamine
668
How do stimulants work?
Increase dopamine outside nerve cells
669
How does methylphenidate work?
Slows the reuptake of dopamine and noradrenaline
Significantly amplifies extracellular dopamine in the basal ganglia
670
How do amphetamines work?
Increasing production/release of dopamine and noradrenaline
671
How does atomoxetine work?
Decreases noradrenaline reuptake
672
What is DAT1?
Dopamine transport protein
673
Function of DAT1?
Reuptake of dopamine
674
What is MAO-A?
Monoamine oxidase A
675
Function of MAO-A and COMT?
Catabolism of dopamine
676
What is COMT?
Catechol-o-methyl-transferase
677
How is noradrenaline related to ADHD?
Increases the signal
Enhances executive operations
Increases inhibitor
Increases firing to neurons of relevant input
678
In regards to ADHD where in the brain does noradrenaline act?
The prefrontal cortex
679
Possible brain abnormality in ADHD?
Abnormalities in the right prefrontal cortex
680
Key noradrenaline receptor in ADHD?
Alpha2a
681
Key dopamine receptor in ADHD?
D1
682
What does activation of alpha2a receptors by noradrenaline do? (ADHD)
Enhances the strength of relevant sensory input (increases the signal)
683
What does activation of D1 receptors by dopamine do? (ADHD)
Weakens irrelevant sensory input (decreases noise)
Also modulates motivation so can illicit interest in tasks
684
When should drug therapy be used in ADHD?
Reserved for those with severe symptoms and impairment or those with moderate impairment who have not responded to non-drug interventions
685
First-time drug treatment for ADHD?
Stimulants such as methylphenidate
686
How does guanfacine/clonidine work for ADHD?
They are alpha2a agonists
687
Which drug has greater selectivity for alpha-2a adrenoreceptors, clonidine or guanfacine?
Guanfacine
688
Common side effects of methylphenidate?
Dry mouth
Appetite and weight loss
Slower growth
Sleep disturbance
689
When may methylphenidate be contraindicated?
In situations where it may induce or worsen psychosis
690
Benefits of modified-release methylphenidate preparations?
Convenience
Improving adherence
Reduces stigma
No need to store or administer controlled drugs in schools
691
Benefits of immediate-release methylphenidate preparations?
Flexible dosing regimens
During titration
Cheaper
692
Why are modified-release methylphenidate preparations not equivalent?
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
Brand of methylphenidate that is 30% immediate release and 70% modified release?
Equasym
694
Equasym biphasic pharmacokinetic profile?
30% immediate release
70% modified release
695
Brand of methylphenidate that is 50% immediate release and 50% modified release?
Medikinet XL
696
Medikinet XL biphasic pharmacokinetic profile?
50% immediate release
50% modified release
697
Brand of methylphenidate that is 22% immediate release and 78% modified release?
Concerta XL
Xenidate XL
Matoride XL
698
Concerta XL biphasic pharmacokinetic profile?
22% immediate release
78% modified release
699
Concerns with atomoxetine?
Suicidal thinking
Liver damage
700
What is the cortical-striatal-thalamic-cortical circuit?
chain of neurons in the brain that connects the prefrontal cortex, the basal ganglia, and the thalamus in one continuous loop
701
Functions of the cortical-striatal-thalamic cortical circuit?
Emotions and attention
Executive function
Motor activity
Impulsivity
702
What is the difference between a seizure and epilepsy?
Seizure is a one-off occurrence
703
What is epileptogenesis?
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
Epilepsy definition?
A transient occurrence of symptoms due to abnormal excessive or synchronous neuronal activity of the brain
Two or more seizures must occur
705
How to diagnose epilepsy?
Symptoms
Medical history
EEG
Neuroimaging
706
What is a generalised seizure?
Begins spontaneously in both hemispheres
707
What is a focal seizure?
Starts in localised region of the brain
708
What is focal seizure with secondary generalisation?
Starts locally but spreads across both hemispheres
709
Types of focal seizures?
Simple
Complex
710
What is a simple focal seizure?
No loss of consciousness
711
What is a complex focal seizure?
Includes impairment of consciousness
712
Types of generalised seizures?
Absence
Tonic
Clonic
Tonic-clonic
Atonic
Myoclonic
713
Causes of epilepsy?
Trauma
Infection
Fevers
Alcohol and other drugs
Medication
Brain tumour
Stroke
Genetics
714
Why can domoic acid poisoning cause seizures?
Domoic acid is structurally similar to the excitatory neurotransmitter glutamate.
