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Cardiovascular conditions Flashcards

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1
Q

What is cardiovascular disease (CVD)?

A

a class of diseases that involve the heart or blood vessels

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2
Q

List eight conditions that cause CVD.

A 
coronary artery disease
angina
peripheral arterial disease
myocardial infarction
hypertensive heart diseases
cerebral vascular disease (stroke)
heart failure
atrial fibrillation
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3
Q

List six behavioural risk factors of CVD that can be modified.

A 
smoking
high cholesterol
high blood pressure
poor diet
harmful drinking
physical inactivity
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4
Q

List five environmental and social risk factors of CVD.

A 
family history
financial inequalities
employment
housing
air pollution
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5
Q

What genetic condition can lead to CVD?

A 
familial hypercholesterolaemia (FH)
affects 1 in 250-500 people in the UK
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6
Q

What is the main risk factor for CVD?

A

cholesterol (7.1% of deaths)

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7
Q

What is an atheroma?

A

reversible accumulation of cholesterol and degenerative tissue in the tunica intima of the arterial wall
include (1) lipids (intracellular and extracellular) (2) fibrous connective tissue (3) cells (macrophages and smooth muscle)

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8
Q

What happens if cholesterol and degenerative tissue continue to accumulate?

A

macrophages enter the tunica intima to digest the lipids leading to foam cells
this coincides with growth factors and the infiltration/proliferation of smooth muscle with connective tissue forming a thin fibrous cap on the surface

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9
Q

What are the five stages of atherosclerosis?

A

(1) endothelial dysfunction
(2) formation of lipid layer within the intima
(3) migration of leukocytes and smooth muscle cells into the vessel wall
(4) foam cell formation
(5) degradation of extracellular matrix

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10
Q

What is the QRISK assessment tool?

A

calculates a person’s risk of developing a heart attack or stroke over the next 10 years
used in primary care
focuses on the primary prevention of CVD in people aged up to 84

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11
Q

Who does not benefit from the QRISK tool?

A

people with a diagnosis of CVD (e.g. peripheral arterial disease, CVA, TIA)
people at high risk of CVD due to FH
people aged 85+ years (considered high risk due to age, higher if they smoke or have hypertension)

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12
Q

What is the prevalence of coronary heart disease in the UK?

A

7.4 million

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13
Q

What is the prevalence of angina in England?

A

2 million

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14
Q

What is the prevalence of peripheral arterial disease in the UK?

A

1 in 5 >60 years

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15
Q

What is the prevalence of myocardial infarction in the UK?

A

750-1250 per million

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16
Q

What is the prevalence of hypertension in England?

A

1 in 4 adults

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17
Q

What is the prevalence of CVA in the UK?

A

150,000 per year

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18
Q

What is the prevalence of heart failure in the UK?

A

920,000

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19
Q

What is the prevalence of atrial fibrillation in the UK?

A

1.4 million

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20
Q

What is the third biggest risk factor for premature death and disability in England after smoking and poor diet (PHE, 2017)?

A

hypertension

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21
Q

People from the most deprived areas in England are how much more likely to have hypertension compared to people from the least deprived areas (PHE, 2017)?

A

30%

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22
Q

What percentage of all heart attacks and strokes are associated with hypertension (PHE, 2017)?

A

at least 50%

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23
Q

Hypertension is a major risk factor for which other conditions (PHE, 2017)?

A

chronic kidney disease, heart failure, dementia

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24
Q

What percentage of GP appointments are related to hypertension and its complications?

A

12%

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25
Q

What is the estimated cost of hypertension to the NHS per year?

A

£2 billion

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26
Q

What is the renin-angiotensin system (RAS)?

A

a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance

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27
Q

The development of hypertension can be broken down into which two parts?

A

primary and secondary

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28
Q

What factors are involved in the primary development of hypertension?

A 
family history
race
stress
obesity
diet high in fat or sodium
smoking
sedentary lifestyle
ageing
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29
Q

What factors are involved in the secondary development of hypertension?

A

the presence of other conditions (e.g. diabetes mellitus, neurological disorders, pregnancy, renovascular disorders)

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30
Q

What is stage 1 hypertension?

A

clinic reading is 140/90 mmHg or higher
subsequent ambulatory BP monitoring (ABPM) daytime average or home BP monitoring (HBPM) average BP is 135/85 mmHg or higher

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31
Q

What is stage 2 hypertension?

A

clinic reading is 160/100 mmHg or higher

subsequent ABPM daytime average or HBPM average BP is 150/95 mmHg or higher

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32
Q

What is severe hypertension?

A

clinic systolic BP is 180 mmHg or higher, OR

clinic diastolic BP is 110 mmHg or higher

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33
Q

What are the main complications of persistent hypertension?

A

brain - CVA, hypertensive encephalopathy (confusion, headache, convulsion)
retina of eye - hypertensive retinopathy
heart - MI, hypertensive cardiomyopathy (heart failure)
blood - elevated glucose levels
kidneys - hypertensive nephropathy (chronic renal failure)

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34
Q

What are the signs and symptoms of hypertension?

A

signs - elevated BP, nosebleed, shortness of breath
symptoms - persistent headache, dizziness, vision problems
many people have no signs and symptoms as part of the 5.5 million people with undetected hypertension

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35
Q

What is usually the first-line approach for treating hypertension?

A

altering lifestyle choices (e.g. diet, weight loss, smoking, exercise)
can be combined with pharmacological interventions

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36
Q

Why should adults of black African or Afro-Caribbean origin be considered for an angiotensin II receptor blocker (ARB) or calcium channel blocker (CCB)?

A

angiotensin-converting enzyme (ACE) inhibitors have limited benefit in managing hypertension in this patient group

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37
Q

What is the pharmacological treatment pathway for patients under 55 years?

A

target < 80 years 140/90 mmHg
first-line - ACE/ARB
second-line - ACE and ARB
third-line - ACE and ARB and thiazide-like diuretic

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38
Q

What is the pharmacological treatment pathway for patients over 55 years?

A

target > 80 years 150/90 mmHg
first-line - CCB
second-line - CCB and ACE/ARBs
third-line - CCB and ACE/ARB and diuretic

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39
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - actions

A

vascular dilatation lowers blood pressure
amlodipine and nifedipine dilate arterial resistance vessels
(verapamil acts mainly on the heart, slowing the rate)

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40
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - MOA

A

block voltage-gated calcium channels in vascular smooth muscle which inhibits calcium influx and thus contraction

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41
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - abs/distrib/elim

A

given orally
amlodipine half-life 35h
nifedipine half-life 2h
verapamil undergoes first-pass metabolism, half-life ~4h

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42
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - clinical use

A

hypertension
chronic stable angina pectoris
Prinzmetal’s angina

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43
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - adverse effects

A

nifedipine and amlodipine: reflex tachycardia, hypotension and headache due to vasodilatation
ankle swelling
constipation

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44
Q

CALCIUM CHANNEL BLOCKERS

Amlodipine, nifedipine, verapamil, diltiazem - special points

A

grapefruit juice increases the effects

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45
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - actions

A

lowers blood pressure by decreasing vasoconstrictor tone

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46
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - MOA

A

blocks the action of angiotensin II on the angiotensin II (AT1 subtype) receptor

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47
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - abs/distrib/elim

A

given orally
half-life 1-2h
half-life of metabolite 3-4h

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48
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - clinical use

A

hypertension
congestive heart failure
nephropathy

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49
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - adverse effects

A

hypotension, dizziness

hyperkalaemia can occur

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50
Q

ANGIOTENSIN ANTAGONISTS

Losartan, valsartan, candesartan, irbesartan - special points

A

does not cause the dry cough or angioedema seen with the ACE inhibitors

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51
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - actions

A

lowers blood pressure by decreasing vasoconstrictor tone and reducing cardiac load

52
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - MOA

A

inhibits angiotensin-converting enzyme (ACE) which reduces synthesis of vasoconstrictor angiotensin II
this decreases aldosterone secretion, which increases salt and water excretion, indirectly decreasing plasma volume and cardiac load

53
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - abs/distrib/elim

A

all are given orally
captopril half-life ~2h
lisinopril half-life 12h
enalapril is a prodrug converted to an active moiety by liver enzymes

54
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - clinical use

A

hypertension
heart failure
ventricular dysfunction following myocardial infarction
diabetic nephropathy
chronic renal insufficiency to prevent progression

55
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - adverse effects

A

hypotension
dry cough
angioedema
renal failure can occur

56
Q

ACE INHIBITORS

Captopril, enalapril, lisinopril - special points

A

hyperkalaemia can occur if given with potassium-sparing diuretics
the dry cough and angioedema are due to the drugs producing bradykinin by stimulating the kallikrein-kinin system

57
Q

α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - actions

A

vasodilatation and thus ↓BP
↑heart rate (a reflex β-receptor response to the ↓BP)
↓bladder sphincter tone
inhibition of hypertrophy of smooth muscle of bladder neck and prostate capsule

58
Q

α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - MOA

A

blocks the action of endogenous and exogenous agonists on α1 receptors
tamsulosin is an α1A-receptor antagonist that is “uro-selective”
phenoxybenzamine is a non-selective, irreversible inhibitor

59
Q

α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - abs/distrib/elim

A

selective agents are absorbed orally and metabolized by liver
prazosin has a shorter half-life of 3-4h, whilst the other ones are longer acting

60
Q

α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - clinical use

A

for severe hypertension: prazosin, doxazosin (in combination with other agents)
for benign prostatic hypertrophy: tamsulosin, doxazosin
for phaechromocytoma: phenoxybenzamine

61
Q

α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - adverse effects

A 
orthostatic hypotension, dizziness
hypersensitivity reactions
insomnia
sometimes priapism
tamsulosin can also cause abnormal ejaculation and back pain
62
Q

What is heart failure?

A

a complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired

63
Q

What causes heart failure?

A

structural or functional abnormalities of the heart

64
Q

How many people in the UK have a diagnosis of heart failure?

A

around 920,000

65
Q

What is the relationship between heart failure and age?

A

incidence and prevalence increase steeply with age

the average age at diagnosis is 77

66
Q

Why is the prevalence of heart failure increasing despite improvements in care and treatment?

A

population ageing and increasing rates of obesity

67
Q

What is systolic heart failure (HFrEF)?

A

the left ventricle loses its ability to contract normally
the heart cannot contract with sufficient force to push enough blood into circulation
more common in people with ischaemic heart disease (IHD)

68
Q

What is diastolic heart failure (HFpEF)?

A

the left ventricle loses its ability to relax normally (the muscle has become stiff)
the heart cannot properly fill with blood during diastole
more common in people with hypertension and valve disease

69
Q

What percentage of patients with heart failure have a diagnosis of systolic ventricular failure?

A

66%

70
Q

What are the main causes of heart failure?

A

myocardial infarction
hypertension
cardiomyopathy (disease of the heart muscle either inherited or caused by other factors, e.g. viral infections)

71
Q

List some of the other causes of heart failure.

A 
damaged or diseased heart valves
arrhythmias
congenital heart conditions 
viral infection affecting the heart muscle
some cancer treatments (e.g. chemotherapy) 
excessive alcohol consumption 
anaemia 
thyroid disease
72
Q

How many people with heart failure have associated medical conditions?

A

diabetes - over one third
COPD - 20%
asthma - 8-9%

73
Q

What are the signs and symptoms of left ventricular failure?

A

dyspnoea, orthopnoea
large amounts of pink frothy sputum
bubbly chest
tachycardia
cold and clammy
anxious/frightened
palpitations/chest pain (due to increased HR)
confusion (due to decreased oxygen to the brain)
fatigue (lack of sleep, increased work of breathing)

74
Q

What are the signs and symptoms of right ventricular failure?

A 
peripheral oedema
weight gain
enlarged liver
ascites
distended neck veins
nausea
nocturia
weakness/lethargy
75
Q

What is the N-terminal pro-B-type natriuretic peptide (NT‑proBNP) test?

A

used to determine a diagnosis in people with suspected heart failure

76
Q

What does an NT‑proBNP level above 2,000 ng/litre (236 pmol/litre) indicate?

A

require urgent specialist assessment and transthoracic echocardiography within 2 weeks

77
Q

What does an NT‑proBNP level between 400 and 2,000 ng/litre (47 to 236 pmol/litre) indicate?

A

require specialist assessment and transthoracic echocardiography within 6 weeks

78
Q

What does an NT‑proBNP level less than 400 ng/litre (47 pmol/litre) indicate?

A

makes a diagnosis of heart failure less likely in an untreated person
NT-proBNP levels do not alter in this with either reduced or preserved ejection fraction

79
Q

What groups of people can have reduced NT‑proBNP levels?

A

classed obese
Black African or Afro-Caribbean family origin
treated with diuretics, ACE inhibitors, beta-blockers, ACE II receptor blockers (ARBs) or mineralocorticoid receptor antagonists

80
Q

What are some of the other causes of high serum natriuretic peptide levels?

A

age over 70 years
left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload
hypoxaemia including pulmonary embolism
renal dysfunction (eGFR <60 ml/minute/1.73 m2)
sepsis, COPD, diabetes, liver cirrhosis

81
Q

What is the purpose of a transthoracic echocardiography?

A

to exclude valve disease, assess the systolic and diastolic function of the left ventricle and detect intracardiac shunts

82
Q

What alternative methods of imaging the heart should be considered if a poor image is produced by transthoracic echocardiography?

A

radionuclide angiography multigated acquisition scanning
cardiac MRI
transoesophageal echocardiography

83
Q

What is the ejection fraction?

A 
a measurement of the percentage of blood the left ventricle pumps out of the heart with each contraction 
high function >70%
normal function 55-70%
low function 40-55%
possible heart failure <40%
84
Q

What findings from a cardiac or other relevant history indicate a possible diagnosis of heart failure?

A 
previous MI
angina
hypertension
valvular disease
metabolic or autoimmune disease
85
Q

What findings from observations and clinical examination indicate a possible diagnosis of heart failure?

A 
tachycardia
tachypnoea (RR >18/min)
oxygen saturation <94% on room air
raised jugular venous pressure
displaced apex beat
third heart sound
murmur
pulmonary crackles
peripheral oedema
86
Q

What blood tests can be taken to indicate a possible diagnosis of heart failure?

A 
BNP or NT-proBNP 
full blood count
renal function
liver function
thyroid function
87
Q

What heart imaging and electrical activity tests can be taken to indicate a possible diagnosis of heart failure?

A

electrocardiogram
chest X-ray
transthoracic echocardiogram

88
Q

What treatments can be used to manage heart failure?

A

diuretics (furosemide IV)
ACE inhibitors (ramipril)
beta blockers (atenolol)
mineralocorticoid receptor antagonists (spironolactone)
oxygen
IV diamorphine (relieves anxiety and causes peripheral vasodilation)
fluid restriction

89
Q

Why are diuretics used in the management of heart failure?

A

routinely used for people with preserved or reduced ejection fraction and are titrated (up and down) accordingly
people with preserved ejection fraction are offered a low to medium dose of loop diuretics (e.g. less than 80 mg furosemide per day)

90
Q

Why are anticoagulants used in the management of heart failure?

A

patients with heart failure and atrial fibrillation have additional NICE guidelines in this area
in people with heart failure in sinus rhythm, anticoagulation should be considered for those with a history of thromboembolism, left ventricular aneurysm or intracardiac thrombus

91
Q

What is the first-line treatment for patients with systolic heart failure?

A

ACE inhibitor and beta-blocker at the lowest dose and titrate accordingly for those licensed for heart failure, unless there is clinical suspicion of haemodynamically significant valve disease.
ARB licensed for heart failure if ACE inhibitors are not tolerated

92
Q

What is the second-line treatment for patients with systolic heart failure?

A

mineralocorticoid receptor antagonists offered in addition to an ACE inhibitor or ARB and beta-blocker if symptoms persist

93
Q

What is the lifestyle advice given to people with heart failure?

A

salt and fluid restriction is not routinely advised in patients with heart failure unless there is dilutional hyponatraemia (dilution of electrolytes), or high levels of salt and/or fluid consumption

94
Q

How are the effects of ACE inhibitors, ARBs and beta-blockers monitored in patients with heart failure?

A

measure serum sodium and potassium - includes assessing renal function, before and 1 to 2 weeks after starting ACE inhibitor, and after each dose increment
measure BP - before and after each dose increment
once the target/maximum tolerated dose of ACE inhibitor is reached, monitor treatment monthly for 3 months and then at least every 6 months, and at any time the person becomes acutely unwell

95
Q

LOOP DIURETICS

Furosemide, bumetanide - actions

A

cause copious urine production by inhibiting NaCl reabsorption in the thick ascending loop
increase excretion of Ca2+ and Mg2+
decrease excretion of uric acid

96
Q

LOOP DIURETICS

Furosemide, bumetanide - MOA

A

inhibit the Na+/K+/2Cl− co-transporter in the luminal membrane by combining with the chloride binding site

97
Q

LOOP DIURETICS

Furosemide, bumetanide - abs/distrib/elim

A

given orally (can be given IV in severe cases)
well absorbed
reaches site of action by being secreted into the proximal tubule
half-life 90 min

98
Q

LOOP DIURETICS

Furosemide, bumetanide - clinical use

A

pulmonary oedema
chronic heart failure
ascites due to liver cirrhosis
hypercalcaemia

99
Q

LOOP DIURETICS

Furosemide, bumetanide - adverse effects

A

hypokalaemic alkalosis
hyperuricaemia (can precipitate gout)
hypovolaemia and hypotension in elderly patients
nephro- and ototoxicity

100
Q

THIAZIDE-LIKE DIURETICS

Indapamide - actions

A

cause moderate degree of diuresis by inhibiting NaCl reabsorption in the distal tubule
increase excretion of K+, Na2+ and Mg2+
decrease excretion of Ca2+ and uric acid
some vasodilator action

101
Q

THIAZIDE-LIKE DIURETICS

Indapamide - MOA

A

inhibit the Na+/Cl− co-transporter in the luminal membrane of the distal convoluted tubule

102
Q

THIAZIDE-LIKE DIURETICS

Indapamide - abs/distrib/elim

A

given orally
extensive metabolism in liver
elimination half-life 13.9-18 hrs

103
Q

THIAZIDE-LIKE DIURETICS

Indapamide - clinical use

A

hypertension

congestive heart failure

104
Q

THIAZIDE-LIKE DIURETICS

Indapamide - adverse effects

A 
electrolyte imbalance
hypochloraemic alkalosis
hyperuricaemia (can precipitate gout)
postural hypotension
hypersensitivity 
hyperglycaemia
erectile dysfunction
105
Q

THIAZIDE DIURETICS

Hydrochlorothiazide, bendroflumethiazide, chlortalidone - actions

A

cause moderate degree of diuresis by inhibiting NaCl reabsorption in the distal tubule
increase excretion of K+, H+ and Mg2+
decrease excretion of Ca2+ and uric acid
some vasodilator action

106
Q

THIAZIDE DIURETICS

Hydrochlorothiazide, bendroflumethiazide, chlortalidone - MOA

A

inhibit the Na+/Cl− co-transporter in the luminal membrane of the distal convoluted tubule

107
Q

THIAZIDE DIURETICS

Hydrochlorothiazide, bendroflumethiazide, chlortalidone - abs/distrib/elim

A

given orally
reaches site of action by being secreted into the proximal tubule
half-life 90 min

108
Q

THIAZIDE DIURETICS

Hydrochlorothiazide, bendroflumethiazide, chlortalidone - clinical use

A

hypertension
mild heart failure
nephrogenic diabetes insipidus
kidney stones

109
Q

THIAZIDE DIURETICS

Hydrochlorothiazide, bendroflumethiazide, chlortalidone - adverse effects

A 
potassium loss
metabolic alkalosis
hyperuricaemia (can precipitate gout)
hypotension
mild hypercalcaemia
insulin resistance
erectile dysfunction
110
Q

MINERALOCORTICOID RECEPTOR ANTAGONISTS

Spironolactone, eplerenone - actions

A

inhibits Na+ reabsorption in the distal nephron
has limited diuretic efficacy
reduces K+ excretion

111
Q

MINERALOCORTICOID RECEPTOR ANTAGONISTS

Spironolactone, eplerenone - MOA

A

spironolactone is a competitive antagonist of aldosterone
causes diuresis by preventing the production of the aldosterone mediator that normally causes influx of sodium by activating the sodium channel in the luminal membrane of the collecting tubule

112
Q

MINERALOCORTICOID RECEPTOR ANTAGONISTS

Spironolactone, eplerenone - abs/distrib/elim

A

given orally
spironolactone half-life 10 min, but its active metabolite canrenone has a plasma half-life of 16h
eplerenone has a shorter elimination half-life and has no active metabolites

113
Q

MINERALOCORTICOID RECEPTOR ANTAGONISTS

Spironolactone, eplerenone - clinical use

A

given with K+-losing diuretics (thiazides, loop diuretics) to limit K+ loss
spironolactone or eplerenone are used in heart failure, primary hyperaldosteronism, resistant essential hypertension, secondary hyperaldosteronism caused by hepatic cirrhosis complicated by ascites

114
Q

MINERALOCORTICOID RECEPTOR ANTAGONISTS

Spironolactone, eplerenone - adverse effects

A

hyperkalaemia, may cause acidosis

spironolactone can cause gynaecomastia

115
Q

What is coronary artery bypass grafting (CABG)?

A

the process of taking a blood vessel from somewhere in the patient’s body and attaching it to the coronary artery in order to bypass a clogged or narrowed part

116
Q

Approximately how many CABG operations are performed annually (National Institute for Cardiovascular Outcomes Research, 2018)?

A

15,000

117
Q

What is aortic valve replacement?

A

the process of removing faulty valves and replacing with a synthetic or animal valve

118
Q

Approximately how many aortic valve replacements are performed annually (National Institute for Cardiovascular Outcomes Research, 2018)?

A

5,000

119
Q

What is a pacemaker?

A

a permanent implantable device used to maintain a sufficient heart rate

120
Q

What is coronary stenting?

A

this is performed to maximise blood flow to the heart that is reduced by a blockage
less invasive than CABG

121
Q

Approximately how many coronary stenting operations are performed annually (National Audit of Percutaneous Coronary Interventions, 2015)?

A

97,376

122
Q

What is the Lester Tool?

A

a summary poster to guide health workers to assess the cardiometabolic health of people experiencing psychosis and schizophrenia
it enables staff to deliver safe and effective care to improve the physical health of mentally ill people

123
Q

Besides iatrogenic harm caused by prescribed medication, list two other factors that increase the risk of CVD in people with SMI (Royal College of Psychiatrists, 2016).

A

smoking - more than twice as common in people with SMI than the general population
obesity - a common comorbidity of SMI

124
Q

What assessments should be undertaken before a patient is commenced on antipsychotic medication (NICE, 2014)?

A

multidisciplinary assessment - psychiatric history; medical history and physical examination; physical health and wellbeing; psychological and psychosocial; development; social; occupational and educational; quality of life; economic status
assess for PTSD as this is common with patients with psychosis or schizophrenia
monitor for comorbidities, including depression, anxiety, and substance misuse

125
Q

What baseline investigations should be taken when a patient is prescribed antipsychotic medication (NICE, 2014)?

A

weight (plotted on a chart)
waist circumference
pulse and blood pressure
fasting blood glucose, glycosylated haemoglobin (HbA1c), blood lipid profile, and prolactin levels
assessment of any movement disorders
assessment of nutritional status, diet, and level of physical activity

126
Q

Under what circumstances should an ECG be offered to a patient who is prescribed antipsychotic medication (NICE, 2014)?

A

if specified in the summary of product characteristics (SPC)
if a physical examination has identified specific cardiovascular risk
if personal history of CVD
if the service user is admitted as an inpatient

127
Q

What should health professionals monitor when a patient is prescribed antipsychotic medication (NICE, 2014)?

A

response to treatment
side effects of treatment
the emergence of movement disorders
weight, weekly for the first 6 weeks, then at 12 weeks, at 1 year and then annually (plotted on a chart)
waist circumference annually (plotted on a chart)
pulse and blood pressure at 12 weeks, at 1 year and then annually
fasting blood glucose, HbA1c and blood lipid levels at 12 weeks, at 1 year and then annually
adherence
overall physical health

Therapeutic Nursing (16 decks)

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