Block 31 Week 2 Flashcards
1
Q
what is angina?
A
- Angina refers to thecentral pressing, squeezing, or constricting chest discomfortthat is experienced when there is a reduction in blood flow through the coronary arteries
- There may be typical radiation to the arm, jaw or neck and it is bought on by physical or emotional exertion and relieved by rest.
2
Q
angina typically lasts?
A
less than 10 minutes
3
Q
People with angina secondary to CAD are at risk of a major cardiac event:
A
- MI
- cardiac arrest
- death
4
Q
stable angina?
A
- pain with physical or emotional exertion
- that lasts less than 10 mins
- should be relived within minutes of rest or with the use of medication (e.g. GTN spray).
5
Q
UA?
A
- sudden new onset angina
- or sig or abrupt deterioration in angina that has been stable
- This typically relates to pain that increases with frequency and severity or pain that is experienced at rest
- urgent admission required for ACS exclusion
6
Q
Aetiology of angina?
A
- most commonly due to CAD - atheroscleortic plaques in coronary vessels
7
Q
angina RF?
A
- High cholesterol
- Hypertension
- Smoking
- Diabetes
- Obesity
8
Q
Non mod RF for angina?
A
- age
- FHx
- male sex
- premature menopause
9
Q
other causes of angina - prinzmetal?
A
- Coronary artery spasm(Prinzmetal angina)
10
Q
other causes of angina - microvascular?
A
- Microvascular angina(diffuse vascular disease within the microvasculature of the coronary circulation)
11
Q
Other causes of angina - vasculitis?
A
(e.g. Kawasaki disease, polyarteritis nodosa)
12
Q
other causes of angina - mismatch?
A
(oxygen supply/demand mismatch)
13
Q
other causes of angina - severe?
A
- Severe left ventricular hypertrophy(reduced subendocardial blood flow and increased susceptibility to ischaemia)
- Severe aortic stenosis(increases myocardial oxygen demand)
14
Q
Chronic CS
A
- results from atherosclerotic obstruction of coronary vessels
- may present in different ways: ACS or CCS
- symptomatic CAD without ACS
15
Q
CFs of angina - 3 classical?
A
- Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw
- Precipitated by physical exertion
- Relieved by rest or GTN within 5 minutes
16
Q
non anginal chest pain?
A
≤1 of the above features
17
Q
grading angina?
A
18
Q
Factors that make the chest pain more likely to be non-anginal?
A
- Continuous or very prolonged pain, and/or
- Unrelated to activity, and/or
- Bought on by breathing, and/or
- Associated with dizziness, palpitations, paraesthesia
19
Q
A
20
Q
other features of angina?
A
- dyspnoea
- palpitations
- syncope
21
Q
dysponea?
A
may be the only presenting feature of CAD in the absence of chest pain - consider CAD if made worse by exertion and improved on rest
22
Q
palpitations?
A
- Palpitations - angina may be precipitated by tachyarrhythmias (e.g. atrial fibrillation).
- These increase the oxygen supply/demand mismatch and reduce the filling time of the coronary vessels during diastole.
23
Q
syncope with angina?
A
- syncope - may be suggestive of dangerous valvular or cardiac muscle disease causing angina, particularly if it occurs on exertion.
24
Q
Chest pain suggestive of ACS?
A
- Chest pain lasts > 10 minutes
- Chest pain not relieved by two doses of GTN taken 5 minutes apart
- Significant worsening/deterioration in angina(e.g. increased frequency, severity or occurring at rest)
25
how is angina graded?
* Canadian Cardiovascular Society
26
Diagnostic work-up of angina?
* required for patients w suspected angina or recent onset chest pain
* excludes posibility of ACS
* basic investigations - blood tests, ECG, echo, +/- chest X ray
* CAD probaibility
27
rapid access chest pain clinic?
* new onset angina
* aims to identify new CAD and prevent a major cardiac event by offering earlier intervention.
28
basic Ix of angina - CAD?
* determining if patients have evidence of CAD or major risk factors for CAD (e.g diabetes mellitus).
29
Ix of angina - blood tests?
* blood tests - FBC, U&Es, Lipid profile, blood glucose, HbA1c (TFTs if concern re. thyroid disease)
30
Angina ECG?
* resting ECG - look for indirect signs of CAD (e.g. pathological q waves, conduction abnormalities, ST-T wave changes).
31
Echo for angina?
* echo - assess LV function, valvular pathology and any motion abnormalities (sign of ischaemic disease
32
CXR of angina?
may be needed if atypical symptoms, features of heart failure or suspicion of pulmonary disease.
33
diagnostic testing for angina?
* CT coronary angiography
* if low likelihood of CAD
* no history of CAD
34
stress echo for angina?
* high likelihood of CAD
* revascularisation therapy
* established CAD
35
invasive coronary angiography for angina?
* high likelihood of CAD and symptoms unresponsive to therapy
* Typical angina at low activity level and high risk of cardiac event
* LV dysfunction on ECHO suspected secondary to CAD
36
anatomical testing for angina?
* CTA - visualisation of coronary artery lumens
* low risk patients, excludes CAD
37
functional testing for angina?
* used to diagnose obstructive CAD by detection of myocardial I
* high likelihood of CAD
38
what are the functional tests for angina?
* Dobutamine stress echocardiography
* Stress or contrast cardiac MRI
* Perfusion changes by single-photon emission CT (SPECT)
39
the invasive investigations for angina?
* diagnose and treat obstructive CAD
* first line for:
* High clinical likelihood of CAD and symptoms unresponsive to medical therapy
* Typical angina at low activity level and high risk of cardiac event
* LV dysfunction on ECHO suspected secondary to CAD
40
management of angina?
* lifestyle: diet, alcohol, smoking, excerise, weight reduction
* Tx of comorbidities - hypertension, hypercholesterolaemia, diabetes mellitus
* aspirin and statin prescribed
41
which drugs are those w angina put on?
aspirin and statins
42
Angina: GTN?
* GTN - causes vascular SM relaxation and improves coronary BF
43
Side effects of GTN?
headache and dizziness due to low BP
44
How should GTN be used?
* Patients should be advised to spray 1 to 2 doses under the tongue for an attack of angina.
* If pain has not subsided in 5 minutes they should repeat the dose.
* If the pain is ongoing after 10 minutes they should call for an ambulance.
45
Pharm management of angina?
1) BB or CCB
2) OR long acting nitrate, ivababraine, nicrorandil, ranolazine
46
Which CCB is commonly used for angina?
amlodepine
47
which CCBs are contra-indicated in angina?
* Non-dihydropyridine calcium channel blockers, such as verapamil or diltiazem, are contraindicated with beta-blockers due to the risk of atrioventricular block (i.e. heart block).
48
BB + usually amlodepine for angina -
* Occasionally they may be used in angina treatment as monotherapy. They should be avoided in heart failure.
49
2) if patients can't take BBs or CCBs then monotherapy with:
| Angina
- long acting nitrate
- ivabradine
- nicorandil
- ranolazine
50
long acting nitrate?
(e.g. isosorbide mononitrate): relaxation of vascular smooth muscle and increases coronary blood flow
51
ivabradine?
lowers heart rate through inhibition of cardiac ‘funny channels’
52
Nicorandil?
potassium channel agonist, which inhibits voltage-gated calcium channels leading to muscle relaxation
53
Ranolazine?
inhibition of late inward sodium channel, which reduces calcium overload in cardiomyocytes.
54
invasive management of angina?
* revascularisation therapy in high risk patients
* in combination with pharm therapy
55
revascularisation - the 2 options are?
PCI or CABG
56
PCI for angina?
* Stent inserted into CA to improve coronary blood flow
* Following a stent insertion for ‘stable’ angina, dual anti-platelet therapy should be offered for a minimum of 6 months (e.g. aspirin and clopidogrel).
57
CABG?
* Coronary artery bypass grafting is a cardiothoracic surgical procedure that aims to restore flow within a coronary vessel through bypass of the obstructed segment.
* This usually involves using vein grafts or redirecting flow from the internal mammary artery.
58
risk stratification for MI?
* risk stratification to determine need for revascularisation therapy
* High risk: >3% annual risk of cardiac mortality
* Low risk: <1% annual risk of cardiac mortality
* may be based on CAD or SCORE scores
59
revasularisation for stable angina?
revascularisation for those who's symptoms aren't being controlled well
60
STEMI revasc?
* STEMI: reperfusion therapy delivered ASAP
* coronary angiohgraphy w follow on PCI if indicated is preferred of the person peresents within 12 hours of onset of symptoms
61
unstable angina and NSTEMI revasc?
* unstable angina and NSTEMI: coronary angiography
* for those w intermediate ot higher risk of advserse CV events
* performed ASAP for those clinically unstable or at high ischaemic risk
62
periprocedural risks of PCI?
* for PCI, there's an increased risk of platelet aggregation and thrombus formation which can lead to periprocedural ischaemic events like MI or stent thrombosis
63
Anti-thrombotics after PCI?
* antithrombotis: aspirin and either clopidogrel, prasugrel, or ticagrelor
64
Which drugs are preferred over clopidoregl in UA/ NSTEMI?
* prasugrel or ticagrelor are perferred over clopirogrel in unstable ngina/ NSTEMI or STEMI who are undergoing PCI as they're faster acting
65
Benefits of revasc?
* Decrease in risk of major cardiac events
* reduced mortality
66
cardiac rehab involves?
* Helps u recover and get back to as full a life as possible after a heart attack, heart surgery or following a diagnosis such as heart failure
* individualised exercise, education and support programme built around your personal circumstances and needs.
67
Cardiac rehab - resources?
* cardiac rehab - video calls, websites, telephone support
68
cardiac rehab -RF?
* risk factors - eating healthy, stopping smoking, building exercise
* exercise sessions - tailored to need and ability
69
Cardiac rehab - info and support?
* information and education sessions - eating healthy, abt medications, smokingc cessation etc
* peer support - meet people in the same situation
* emotional support and wellbeing
70
what can cardiac rehab help w?
* recovering from surgery, procedure or heart attack
* reducing risk of further heart probs
* improving MH
* making lifestyle changes
71
women w CHD have ? outcomes?
* women w CHD have worse outcomes than males
* Women tend to present with coronary artery disease later in life
72
how do women w CHD present?
* Women experience longer delays in access to hospital care and are less likely than men to have invasive diagnostic procedures
* fewer women present with classical symptoms of chest pain
73
why are women's symptoms often not recognised?
* The historic limited interpretation of women’s symptoms based on the traditional approaches such as the Diamond and Forrester risk model results from under-recognition of the sex-specific presentation of IHD and contributes to misdiagnosis and delayed recognition of ischemia
74
women w IHD use more?
* women with IHD use more cardiac resources and incur greater healthcare costs bc of greater symptom burdern and hospitalization
75
subgroups of women who experience worse outcomes?
* Subgroups of women who experience worse outcomes for IHD include younger women (aged <55 years) and those of Black, Latino, and South Asian descent
76
south asian MI risk?
upto 30% more likely
77
black people MI risk?
* Black people were at 51% lower risk of myocardial infarction
78
mortality from IHD in both SA men and women?
* mortality from IHD in both South Asian men and women is 1.5 times that of the general population
79
which conditions do you tend to get increased TLC in?
asthma and COPD due to hyperinflation and less air being exhaled
80
when is the prev of HTN higher in women?
before 60, equal after this point
81
what is HTN a RF for?
* major risk factor for myocardial infarction (MI), stroke and chronic kidney disease (CKD).
82
primary causes of hypertension?
* 95%
* no identifiable cause
* essential or idiopathic HTN
83
secondary causes of HTN - endocrine?
* primary aldosteronism
* phaechromocytoma
* cushings syndrome
* acromegaly
84
secondary causes of HTN - renal?
* Renovascular disease (e.g. atheromatous, fibromuscular dysplasia)
* Intrinsic renal disease (e.g. CKD, AKI, glomerulonephritis)
85
drugs causing HTN?
* Glucocorticoids
* Oral contraceptives
* SSRIs
* NSAIDs
* EPO
86
Causes of HTN to consider in younger patients?
* Coarctation of the aorta (consider in children / young adults with hypertension).
87
CFs of HTN?
* typically asymptomatic
* signs and symptoms may reflect end organ damage or a potential secondary cause
88
Symptoms of HTN?
* palpitations
* angina
* headaches
* blurred vision
* new neurology (e.g. limb weakness, paraesthesia)
89
Signs of HTN?
* New neurology (e.g. limb weakness, paraesthesia)
* Retinopathy
* Cardiomegaly
* Arrhythmias
* Proteinuria
90
How is hypertensive retinopathy graded?
* Keith-Wagener Barker (KWB) grades
91
In the following HTN patients underlying causes should be thoroughly excluded:
* Age < 40 years
* Reduced eGFR (suggestive of renal disease)
* Proteinuria or haematuria (suggestive of renal disease)
* Hypokalaemia and hypernatraemia (suggestive of Conn’s syndrome)
* Hypertension that is sudden onset, variable or worsening.
92
Bloods to do for HTN?
* FBC
* U&Es
* Fasting glucose
* Cholesterol (CVS risk)
* HbA1c
93
Tests for HTN?
* BP
* urinanalysis
* uPCR
* ECG
* opthalmoscopy
94
special tests for HTN?
* Ambulatory BP monitoring (ABPM or HBPM)
* Renal USS
* Endocrine tests
95
Diagnosis of HTN?
* ABPM measurements for the diagnosis of stage 1& 2 HTN
* If clinic BP is 140/90 mmHg or higher, ABPM is used to confirm the diagnosis (except in Stage 3 hypertension, in which immediate treatment is initiated).
96
ABPM?
* With ABPM, at least two measurements an hour are taken during the patient's usual waking hours (e.g. 8 am - 10 pm).
* The average value of these measurements is used to confirm the diagnosis.
97
HBPM?
* This involves taking two measurements a day (morning & evening) over a period of at least 4 days, ideally 7.
* At each recording, two consecutive measurements should be taken at least 1 minute apart when the person is seated.
* The readings on the first day are discarded and the average of the following readings are used to confirm a diagnosis of hypertension.
98
white coat hypertension?
* ABPM monitoring prior to diagnosis of hypertension unless BP is dangerously evelated - i.e. stage 3
99
stage 1 hypertension?
- ABPM > 135/85
- Or clinic >140/90
100
stage 2 HTN?
- ABPM >150/95
- Clinic > 160/100
101
stage 3 HTN?
> 180/120
102
HTN staging
103
Mx of HTN - modifiable RFs?
* discourage excessive caffeiene and alcohol
* smoking cessation
* consider need for anti-platelets or statins
104
who to treat for HTB
* If clinic BP < 140/90 mmHg or ABPM < 135/85 mmHg, check BP at least every 5 years or more often if clinic BP close to 140/90 mmHg.
105
Features of accelerated HTN?
* New onset confusion
* Chest pain
* Signs of heart failure (e.g. shortness of breath, fluid overload)
* Acute kidney injury
* Papilloedema
* Retinal haemorrhage
106
Tx of HTN patients with T2DM or under 55?
* 1) ACEi/ ARB
* 2) add CCB or thiazide
* 3) A + CCB + thiazide
107
first line for white patients under 55?
ACEi
108
first line for white patients over 55?
CCB
109
first line for caribbean patients?
CCBs
110
Tx for HTN - Age over 55 or black or caribbean origin?
* 1) CCB
* 2) add ARB/ ACEi/ thiazide
* 3 A + CCB + thiazide
111
What can be used instead of an ACEi?
f patients do not tolerate an ACE-inhibitor (e.g. dry cough), offer an ARB. A combination of ACE-inhibitor and ARB should NOT be used to manage hypertension.
112
113
114
115
malignant/ accelerated HTN?
A BP >180/120 with signs of papilloedema and/or retinal haemorrhage.
116
117
Tx of malignant HTN aims to?
* Tx attempts to reduce BP over 24-48hrs to prevent hypoperfusion
* rapid reduction in blood pressure, even to normal levels, may result in profound organ hypoperfusion as changes may have occured to mechanisms of BP control
118
tx options for hypertensive emergencies?
- IV nitroprusside, labetalol, and GTN
- phentolamine
119
phenotolamine?
(alpha-adrenergic antagonist) also used in phaeochromocytoma crisis.
120
renal artery stenosis?
* fibromuscular dysplasia of the renal artery is one of the most common causes of secondary hypertension and should be excluded by imaging (screening with duplex ultrasound, confirmation by angiography)
* If fibromuscular dysplasia is detected, other vascular beds (i.e. cerebrovascular) should be screened
121
what can HTN lead to?
* TIA, stroke, dementia
* heart failure, left ventricular hypertrophy
* angina, myocardial infarct
* peripheral vascular disease
* fundal haemorrhages or exudate
* renal impairment, proteinuria
122
Assessing for end organ damage?
* Test for haematuria.
* Arrange measurement of:
* Urine albumin:creatinine ratio (to test for the presence of protein in the urine).
* HbA1C (to test for diabetes).
* Electrolytes, creatinine, and estimated glomerular filtration rate (to test for chronic kidney disease).
123
other tests for end organ damage?
* Examine the fundi (for the presence of hypertensive retinopathy).
* 12 lead ECG (to assess cardiac function and detect left ventricular hypertrophy).
124
screening for secondary causes of HTN
125
Secondary causes of HTN that are screened for?
- primary hyperaldosteronism/ Conns syndrome
- phaechromocytoma
- cushings syndrome
126
Primary hyperaldosteronism/ Conn's syndrome?
* cause of up to 25% of drug resistant HTN
* Aldosterone:renin ratio (ARR) is the first line test for the diagnosis of primary hyperaldosteronism
* discontinuation of aldosterone antagonist (spironolactone and epleronone) and diuretics for 4 weeks prior to the test
127
Phaeochromocytoma?
* Rare cause
* the diagnosis is more likely if the patient also has symptoms such as sweating, palpitations or frequent sweating.
* check levels of plasma metanephrines
128
cushings syndrome?
- v rare cause
- central weight gain
- easy bruising
- buffalo hump
- round puffy face
- proximal muscle weakness
- abd striae
129
cushings tests?
* urine free cortisol - urine passed in 24 hours collected
* late night salivary collection
* overnight dexamethasone suppression test
130
thyroid disease?
* Hypo- and hyperthyroidism can both rarely cause secondary hypertension,
131
symptoms of hypothyroidism:
- tiredness
- cold intolerance
- weight gain
- constipation
- muscle weakness
132
symptoms of hyperthyroidisim?
- weight loss,
- mood swings,
- difficulty sleeping,
- heat sensitivity,
-palpitations
-neck swelling
133
lifestyle advice in HTN Mx?
* lifestyle advice
* ask about diet and exercise
* discourage excessive consumption of coffee and other caffiene rich products
* sodium intake low
* inform patients of local incentives
* advise ppl w hypertension who choose to self monitor BP to use HBPM
134
BP target for those Under 80 with or without T2D, CKD, T1D with A:C ratio of less than 70?
* below 140/90
135
BP target for those with T1D plus A:C of >70mg/mmol or CKD plus A:C of >70?
below 130/80
136
BP target for over 80s with or without diabetes?
150/90
137
BP target for over 80s with CKD and an AC of under 70?
CKD plus A:C under 70
- below 140/90
CKD plus A:C of 70 or more
- below 130/80
138
overall BP targets?
* <80 reduce BP to under 140/90
* > 80 reduce BP to below 150/90
139
ACEi mechanism?
* angiotensin 2 is a vasoconstrictor that causes aldosterone release
* aldosterone causes renal sodium and fluid retention
* downreg sympathetic adrenergic activitity by blocking the effects of A2 on sympathetic nerves
* ACEi also increase bradykinin production which makes BVs dilate
140
ACEi indications?
* hypertension
* HF
* post MI
141
side effects of ACEi?
* dry cough
* hypotension - especially in HF patients
* hyperkalaemia - reduced aldosterone
142
side effect of ACEi which is 2-4x higher in african americans?
angioedema
143
when are ACEi contra-indicated?
pregnancy
144
how do diuretics work?
* inhibit sodium chloride transporter in DCT
* increases potassium loss -> risk of hypokalemia
145
when are aldosterone blocking diuretics used for HTN?
* Potassium-sparing, aldosterone-blocking diuretics (e.g., spironolactone or eplerenone) are used in secondary hypertension caused by primary hyperaldosteronism
146
Side effects of diuretics?
* hypokalemia
* metabolic alkalosis
* dehydration (hypovolemia)
* hyponatremia
* hyperglycaemia in diabetics
147
BBs mechanism in HTN?
* decreased arterial BP by reducing CO
148
side effects of BBs?
* bradycardia
* reduced exercise capacity
* heart failure
* hypotension
* atrioventricular (AV) nodal conduction block.
* from the excessive blockage of normal sympathetic influences
149
what can BBs NOT be prescribed with?
* can't prescribe it with cardiac selective CCBs e.g. verpamil
150
contra-indications of BBs?
* CI with asthma due to bronchoconstriction
151
how do CCBs work?
* by causing vascular SM relaxation they decrease systemic vascular resistance which lowers arterial BP
* some also reduce heart rate and contractility
152
indications of CCBs?
* hypertension
* angina
* arrhythmias
153
cardio-selective nondihydropyridine CCBs?
- verapamil and diltiazem
- can cause excessive bradycardia, constipation, impaired electrical conduction (e.g., atrioventricular nodal block), and depressed cardiac contractility.
154
CCBs espec non-dihydropyridines should not be administered to?
- ppts w HF caused by systolic dysfunction
- ppts on BBs as BBs also depress cardiac electrical activity
155
Drug interactions: Beta blockers and verpamail and dilitiazem ->
bradycardia and AV block
156
Verapamil and diliitizem with digoxin ->
digoxin toxicity mainly with verapamil
157
Diuretics with digoxin ->
increased digoxin toxicity due to hypokalemia
158
ACEi/ ARBs with diuretics ->
addiitive hypotensive action
159
potassium sparing diuretics ->
hyperkalemia when used together
160
compliance of anti-hypertensive meds?
* poor compliance
* reminders/ phone apps to measure BP
* promote self care and education
* awareness of risks
161
metabolic syndrome?
hypertension, diabetes, obesity and hypercholesterolemia
162
Sx of MS
* large weight circumference
* symptoms of diabetes - inc thirst and urination
* fatigue
* blurred vision
163
164
Causes of MS?
* overweight/ obesity
* insulin resistance syndrome
165
RF for metabolic syndrome?
* FHx
* poor diet
* inadequate exercise
166
pathophys of MS?
* insulin resistance
* pancreatic beta cell dysfunction
* Chronic inflammation
* Suppression of insulin receptor substrate-1 and 2 (IRS1/IRS2) gene expression and function
167
what is primary prevention?
- population strategy
- targeted strategy
168
population strategy?
modifying RF for whole population through diet and lifestyle advice on basis that a small reduction in smoking, cholesterole etc will produce worthwhile benefits
169
targeted strategy?
- identify high risk individuals using scoring systems and treat RF by medication
170
secondary prevention?
- people who alr have evidence of athermatous vascular disease and @ high risk of futyre CV events
- should all be given a statin and BP target 140/85
171
groups that CVD risk tools might underestimate risk for:
* people treated for HIV
* people who have recently stopped smoking
* people who are already taking meds to treat CVD
* ppl w severe mental illness
172
choice of anti-hypertensive
- add spironolactone 4th line if K <4,5
- add alpha blocker otherwise
173
CVD risk - explore the person's?
beliefs about what determines future health (this may affect their attitude to changing risk)
174
CVD risk - assess?
* assess their readiness to make changes to their lifestyle (diet, physical activity, smoking and alcohol consumption), to undergo investigations and to take long-term medication
* assess their confidence to make changes to their lifestyle, undergo investigations and take medication
175
CVD risk - inform them of?
potential future management options based on current evidence and best practice
176
asthma =
* chronic - lM lung condition leading to variable and recurring symptoms
* characterised by intermittent obst and hyperresponsiveness of the airways - affects large and small airways
causes
177
what causes asthma?
* meds: beta blockers
178
triggers for asthma?
- grass
- pollen
- house dust mites
- pets
179
what happens in asthma?
* T2h cell driven
* IgE: early onset asthma, allergic asthma
* eospinophilic asthma tends to occur in middle aged patients - IL 4, IL5, IL13
180
who does neutrophilic asthma tend to affect?
female, smoker, obese patietns
181
usual asthma symptoms?
- intermittent dry cough sometimes productive
- intermittent wheezing nocturnal symptoms
- SOB
182
Bedside measurement for asthma?
- peak flow
* asthmatics will show variation - morning will be low and will be better during the day
183
Other tests for asthma in adults
* CXR rules out pneumonia and PE
* FeNO- shows if there's eosnophilic inflammation
184
when there is both COPD and asthma =
overlap syndrome
185
management of acute asthma in adults - assessment of severity
186
near fatal asthma =
when CO2 becomes raised
187
management of asthma
oxygen
1) steroids
2) beta agonists and AM for bronchodilation
3) magnesium sulfate injected
4) ipatropium
188
acute asthma in pregnancy?
- give drug therapy as for the non pregnant patient
- continuous fetal monitoring recommended for severe acute asthma
189
why predict CV risk?
* to allow weighing up costs and benefits of treatment
190
Number needed to treat =
- is the number of patients you need to treat to prevent one additional bad outcome (death, stroke, etc.).
- For example, if a drug has an NNT of 5, it means you have to treat 5 people with the drug to prevent one additional bad outcome.
191
population attributable risk?
* population attributable risk: represents the proportion of all the disease risk in a population that may be caused by a factor.
* it illustrates how much of the risk in the population would be removed if that risk factor was not present (or was successfully treated).
192
CVD risk prediction charts?
* joint british socities 10 year CVD risk prediction charts
- underestimates when there's impaired glucose regulation and when the ppt is * Indian, Pakistani, Bangladesh or Sri Lankan
193
focusing interventions based on the risk level of the patient means?
* By focusing interventions on those at highest risk we focusing the possible benefits on those with most at stake.
* Some interventions such as drugs carry harms of their own. By focusing their use on individuals at high risk of disease we ensure that the risk of harm:benefit remains low.
194
Other methods of risk prediction?
* SCORE
* ASSIGN - takes into acount SES
* QRISK - derived from the experience of UK patients identified and followed in GP record systems
195
% of HTN cases caused by secondary HTN?
* 95% of HTN cases caused by essential HTN
* 5-10% of cases caused by secondary HTN
196
BBs in the Tx of HTN?
* added late in the Tx of HTN
* consider them for younger people especially women of childbearing age or people with intolerance/ CI to ACEi/ARBs
197
When should ACEi not be used?
* renovascular disease
198
alpha blockers indications?
* benign prostatic hypertrophy/ HTN
199
contra-indications of alpha blockers?
urinary incontienence
200
signs of aortic coarctation?
radio-femoral delay or weak femoral pulses
201
benefits of smoking cessation?
* smokers who quit at 25 to 34 years had survival curves nearly identical to those who never smoked, with a ten-year survival gain compared to current smoker
* lowered risk of stroke, TIA, cardiovascular diseases, lung cancer
* improved mortality
202
smoking cessation: lower risk of?
* less cancer risk: liver, stomach, pancreatic, kidney, cervix etc - linked to over 12 types of cancer
203
Primary prevention of CV disease?
* aims to keep an individual at risk of cardiac events from having them
* usually aimed at people who have aleady developed CV risk factors such as hypertension
* focuses on controlling RF by making healthy lifestyle changes e.g.
* statins if lifestyle change is ineffective/ inappropriate
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Secondary prevention of CV disease?
* after someone has a cardiac event or undergoes angioplasty or bypass surgery, or develops some other form of heart disease
* medications like aspirin/ statins
* smoking cessation and weight loss
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what is the point of secondary prevention of CV disease?
* prevention of further cardiac events, halts progression of heart disease, prevention of early death
* start statin treatment and consider lifestyle changes
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Preventative measures?
* behaviour changes
* healthy eating - eat well guide
* cardiprotective diet - reducing saturated fats and salt intake
* physical activity - aerobic and muscle strengthening activities
* weight management
* reducing alcohol consumption and smoking cessation
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Aspirn?
* irreversibly inhibits COX-1 and COX-2
* Inhibition of COX-1 results in the inhibition of platelet aggregation for 7-10 days
* inhibition of COX-1 also reduces production of prostaglandins which stops the conversion of arachidonic acid to thromboxane A2 which is a platelet aggregator
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statins mechanism?
* inhibition of HMG-CoA reductase
209
ezetimibe?
* inhibitor of cholesterol absorption
* targets NPC1L1 protein which is expressed on eneterocytes
210
Epidemiology of CV disease?
* In developed countries heart disease and stroke are the first and second leading cause of death among adult men and women.
* Twice as many deaths from CVD occur in developing countries as in developed countries
* main cause of death in the UK
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Outline a strategy to reduce cardiovascular disease in the local community?
* Encouraging smoking cessation
* education on the impacta of smoking and beenfits of smoking cessation
* NHS Smokefree website and referral to smoking cessation clinics
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arryhthmia =
abnormal heart rate or rhythm
213
Symptoms of arrythmias?
* asymptomatic
* palpitations
* decompensated failure
* syncope
* sudden death
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types of arrythmias?
brady-arrythmias and tachy-arrythmias
215
bradyarrythmias?
sinus arrythmia or sinus arrest, or AV block
216
SA/ sinus arrest?
sinus pauses or sick sinus syndrome - episodes of brady and tachy A - e.g. AF
217
first degree AV block?
* conduction within the AV node is slowed
* benign condition, doesn't require Tx
218
what are the types of second degree HB?
* Mobitz type 1: sometimes requires pacemaker
* Mobitz type 2: always requires a pacemaker
219
Third degree AV block?
* always requires a pacemaker
* complete HB - no signal transmitted through AVN
220
A patient who is in permanent AF who has a rhythm that suddenly becomes regular/ slow =
equiv to complete hB
221
tachy-arrhythmia can be classified depending on whether they're ?
* narrow complex
* broad complex
222
narrow complex ARS means
< 120ms
223
a narrow complex QRS and irregular rhythm is usually
AF
224
Narrow QRS + regular R?
sinus tachycardia, atrial flutter, AVRT/ AVNRT
225
Broad complex tachycardia with a regular rhythm can be:
* ventricular tachycardia - it's this unless ECG shows otherwise
* SVT + BBB
* sinus tachy + BBB
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broad complex tachycardia with irregular rhythm?
* EXCLUDE V FIB
* could be A fib w BBB
227
what to look for on an ECG for arrythmias?
* rate
* rhythm - regular, irregular, irregularly irregular - broad/ narrow complexes
228
first degree AV block?
* Conduction slowed at the AVN
* gives a prolonged PR interval
* > 200ms PR interval
229
second degree AV block - type 1/ wenchebach?
* P-R interval progressively prolongs each beat then beat (QRS) drops
-type 2: normal PR then beat drops
230
what can second degree AV block be due to?
BBs or a high vagal tone
231
Type 2, 2:1 AV block?
* every second beat goes through the AV node
* usually due to structural AV node disease
232
How serious is 2:1 AV block?
* always progresses to complete heart block, requires a pacemaker
233
Second degree AV block Type 1 ECG
234
How does 2:1 AV block look
P QRS P then P QRS
235
2nd degree 3:1 AV block?
* 3 P waves for every QRS
236
3rd degree AV block (complete heart block)
* complete blockage at the AV node so no impulses get through from the SAN - no P waves conducted through
* ventricles start pacing themselves but ventricular pacemaker cells are at a lower rate so usually slow
* much more unstable pathway -> if untreated usually leads to death within 6 weeks
237
how serious is complete heart block?
* much more unstable pathway -> if untreated usually leads to death within 6 weeks
238
when is an immediate ppm required for 3rd degree AV block?
* immediate ppm if syncope or HR <35bpm
239
Complete HB ECG?
* can see P waves and QRS on ECG but no consistent pattern to them
* P waves at regular intervals
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LBBB?
* Signal travels down the right branch
* has to move over the left from the right branch in order for the left bundle to depolarise
* depolarisation takes longer so broad QRS
241
LBBB ECG?
242
RBB?
* SAN -> AV -> LBBB then moves across to RBB slowly
* broad QRS
243
RBBB ECG?
* RSR in V1 and V2/ V3
* wide S wave in lateral leads
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What are the narrow complex (regular) tachycarrythmias?
- sinus tachy
- atrial flutter
- AVRT/ AVNRT
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Atrial flutter?
* regular re-enterance circuit going around RA
* normal QRS
246
AV node re-entrant tachycardia?
* repeating loop at the AV node which passes on a rapid rate to ventricles
* no P waves bc its not the SAN thats activating
* narrow normal QRS complexes
* same ECG as AVRT
247
AVNRT ECG
248
AV re-rentrant tachycardia?
* additional conductive pathway occurs elsewhere between the atria and ventricle
* e.g. wolf parkinson white syndrome
249
AVRT ECG?
* impulses being trabsmitted through to the ventricles at a fast rate
* no P waves
* narrow complex unless additional block
* regular
* might get delta waves which make the QRS complex more broad
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Narrow complex irregular tachycardia?
AF
251
What happens in AF?
* chaotic activity within atria
* intermittently randomly passes through AVN
* narrow complex QRS
252
ECG of AF?
* no P waves
* narrow complex
* irregular tachycardia
253
Broad complex regular tachycardias?
- ventricular tachycardia
- ventricular fibrillation
254
what happens in ventricular tachycardia?
* abn tissue within ventricle (often related to scar after a heart attack) can form a re-enterant loop that runs around the ventricle
* abn conduction within ventricle means QRS is broad and re-enterant loop is rapid so fast re-enterant tachy
255
Ventricular tachycardia ECG?
* no P waves
* broad complex of single morphology
256
V fib ECG?
* no P waves
* broad complex irregular tachycardia - looks like a child's scribbles
257
assessment of arrythmias - ABCDE?
* monitor O2 and give oxygen if hypoxic
* ECG, BP and 12 lead ECG
* obtain IV access
* identify and treat reversible causes i.e. electrolytes paticularly potassium
258
Adverse features of arrythmias?
* shock
* syncope
* if yes and the patient has a tachyarrythmia we need to cardiovert the patient, 3 attempts of this
* if this doesn't work try chemical cardioversion with amiodarone, repeat shock, give more amiodarone
259
Tx of AVNRT or flutter?
- vagal manouvers
- adenosine
- continous ECG monitoring
260
adenosine?
* adenosine blocks AV node which will stop an AVNRT or pause activity through AV node allowing flutter waves to be seen
* continous monitoring through this
261
Atrial fibrillation Tx?
- rate control - BBs, digoxin, amiodarone
- anticoag
- consider DCCV if no thromboembolic risk
262
Broad QRS - reg vs irregular rhythm?
* irregular rhytm -> seek expert help
* rule out V fib
* reg R - rule out ventricular tachycardia (serious arrythmia)
* both may need immediate cardioversion
263
Broad QRS
264
breathlessness from pulm oedema?
Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night)
265
PO chest XR findings?
- Chest X-ray will show fluid in the alveolar walls,
- Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern,
- upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions.
266
IPF most common clinical features?
- age over 50 years,
- exertional dyspnea,
- inspiratory bibasilar “velcro-like” crackles on auscultation, clubbing of the digits,
- abnormal pulmonary function test results, with evidence of restriction (low FVC with normal FEV1/FVC ratio)
267
drug which causes dry mouth and urinary retention?
- tiotropium
- anticholingeric effects of muscarnic antagonist
268
What is the most common mode of presentation of mesothelioma?
Breathlessness from pleural effusion
269
feature of LVF?
A left ventricular 3rd heart sound
270
Treatable causes of HTN?
- Hypokalaemia
- Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium.
- These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands, e.g., Conn's syndrome
- Cushings synfrome
271
analine dyes may cause?
lung cancer
272
coal mining leads to?
fibrosis
273
occupations most linked to asthma?
- spray painting
- food processing
- nurses
- chemical workers
- those who work with animals
- welders
- hairdressers
- timber workers
274
# Production of what
role of eosinophils in asthma?
leukotriene production
275
characteristid pathophys of an acute asthma exacerbation?
bronchial mucus plugging
276
high protein and LDH pleural effusion cause?
The high protein and LDH suggest an exudate, commonly secondary to malignancy or infection
277
doasge of LMWH?
based on body weight
278
pleuritic chest pain?
- originates from parietal pleura (VP has no sensory innervation)
- associated with a frction rub
279
drug which does not interact w warfarin?
furosemide
280
warfarin and alcohol?
Excessive use of alcohol is also known to affect the metabolism of warfarin and can elevate the INR
281
IPAH?
- Is associated with chest pain, dyspnoea and syncope, ESPEC in adolescence
- Is secondary to inc foetal pulm HTN
- more common in females
282
Pulmonary Hypertension is most severe in which untreated valvular disease?
- mitral stenosis
283
signs and symptoms of IE?
FROM JANE
- Fever
- Roth's spots
- Osler's nodes
- Murmur
- Janeway lesions
- Anemia
- Nail hemorrhage (splinter hemorrhages)
- Emboli
284
what does not cause pleural effusion?
IPF
285
Amiodarone toxicity?
- interstitial pneumonitis secondary to amiodarone causing fibrosis and a restrictive pattern on pulmonary function testing
- One characteristic finding in all patients exposed to amiodarone is the presence of numerous foamy macrophages in the air spaces.
286
Which oral rate limiting medication will produce the quickest effect in AF?
Metoprolol - rapid onset
287
ankle swelling from amlodepine mechanism?
- The peripheral oedema associated with calcium channel blockers is related to redistribution of fluid from the vascular space into the interstitium.
- `increased calcium channel blocker-mediated vasodilation leads to increased pressure and subsequent permeability in the capillary circulation.
288
which drugs when combined risk hyperkalaemia?
- multiple inhibitors of the RAAS system
- ACE inhibitors, angiotensin receptor blockers and aldosterone antagonists all cause a rise in serum potassium which can be additive when combined
289
clarithromycin strongly interacts with?
statins
290
Angina Ix?
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography
2nd line: Non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: Invasive coronary angiography
291
Examples of non-invasive functional imaging:
- Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
- Stress echocardiography or
- First-pass contrast-enhanced magnetic resonance (MR) perfusion or
MR imaging for stress-induced wall motion abnormalities
292
muscle weakness, tetatany, cramps or arrythmias ->
primary hyperaldostosteronism
293
rapid onset acute PO ->
renal artery stenosis
294
sweating, palpitations, freq headaches ->
phaechromocytoma
295
snoring or daytime sleepiness ->
OSA
