Cardiology Flashcards
(296 cards)
1
Q
How is an MI defined?
A
Rise and/or fall in troponin with at least one value greater than the 99th percentile of the the upper limit + cardiac chest pain OR ECG changes (new ST segment change or new LBBB)
2
Q
How is the of occlusion in an NSTEMI?
A
At least 70 percent of the luminal space
3
Q
If over 70 percent of the intraluminal space of the coronary artery is occluded what symptoms will result?
A
Unstable angina or non st elevation MI
4
Q
Which type of MI has less of the lumen included?
A
STEMI
5
Q
What is a type 1 MI and how does it happen?
A
Spontaneous MI due to plaque rupture
6
Q
What is a type 2 MI and how does it happen?
A
Ischaemic imbalance due to coronary spasm, embolism, dissection, hypotension etc
7
Q
What is a type 3 MI and how does it happen?
A
Cardiac death to due presumed MI
8
Q
What is a type 4a MI and how does it happen?
A
Related to PCI and shows > 5 times upper limit for troponin
9
Q
How does a type 4b MI occur and how is it confirmed?
A
Stent thrombosis and confirmed by angiography or autopsy
10
Q
What is type 5 MI and what is key diagnostic factor?
A
Related to CABG and over 10 times upper limit for troponin
11
Q
What percentage of those that die due to acute myocardial infarction die before they reach hospital?
A
33 percent
12
Q
What anatomical factors can determine infarct size?
A
Distribution of occluded artery
Proximity of coronary occlusion
Collateralised blood supply of site of occluded artery
13
Q
What is the first line treatment in a patient complaining of chest pain in A and E?
A
ECG followed by clinical assessment
14
Q
After ECG and clinical assessment what investigation should be done?
A
Bio markers such as troponin
15
Q
What is the emergency treatment for STEMI?
A
Primary PCI Aspirin plus ticagrelor GP IIb/IIIa inhibitor Unfractionated or low molecular weight heparin PPCI
16
Q
Give examples of P2Y12 receptor antagonists?
A
Clopidogrel - slow
Prasugrel - fast
Ticagrelor - fast
17
Q
Which P2Y12 receptor antagonists are given as pro drugs?
A
Clopidogrel and prasugrel
18
Q
Which P2Y12 have the greatest anti platelet activities?
A
Prasugrel
Ticagrelor
19
Q
Does a STEMI or NSTEMI give you a greater probability of dying?
A
NSTEMI
20
Q
What is the immediate treatment in suspected NSTEMI?
A
Aspirin 300mg, fondaparinux/ UFH, ticagrelor 300mg
+- tirofiban/eptifibatide for intermediate or high risk groups
21
Q
In low risk NSTEMI what is the second line treatment?
A
Conservative management
22
Q
How is a low risk NSTEMI defined?
A
Less than 3 percent
23
Q
How is an intermediate NSTEMI defined?
A
Between 3 and 6 percent
24
Q
How is a high risk NSTEMI defined?
A
Greater than 6 percent risk
25
What is the second line treatment in intermediate or high risk STEMI?
Coronary angiography within 96 hours and then decide PCI or CABG
26
What are the complications following MI?
Heart failure
Bradyarrhythmias
Tacharrhythmias
27
What type of Post MI bradyarrhymias may occur?
Intermittent AVN block (Mobitz I)
| Complete AVN block
28
How are Mobitz I heart block and complete AVN block treated post MI?
Atropine if rate is slow
Pacing rarely needed
Usually spontaneous recovery after 7 days with a good prognosis
29
How is heart failure post MI treated?
IV furosemide - give haemofiltration if diuretic resistant
RAAS inhibition either by ACEI/ARB and then give eplerenone
Ionotropes - noradrenaline and dobutamine
If needed give LV support device such as balloon pump or LVAD
30
How is intermittent block of both bundle branches (Mobitz II) or complete block of both bundle branches post MI treated?
Pacing needed
| No spontaneous recovery with a poor prognosis
31
How is post MI AF treated?
Rate control via beta blocker
DC cardio version if haemodynamically compromised
+\- cardio version
32
How is VT or VF post MI treated?
DC shock
33
When do VT or VF after MI occur?
In the first 24 hours - little effect on prognosis
34
How can late presenting VT/VF post MI complicate things?
Poor prognostic sign and predictive of sudden cardiac death within a year
35
How many people die from VF post MI pre hospital?
33 percent
36
How is VF pre hospital treated?
Defibrillator as soon as possible
37
What complication can a large MI cause?
Left ventricular failure - initiate reperfusion therapy ASAP
38
What two things usually cause late death post MI?
Recurrent ischaemic deaths - need to implement secondary prevention
Lethal arrhythmia- may need implantable defibrillator
39
What are the pharmacological agents for secondary prevention of MI?
```
Aspirin
Station
Beta blocker
ACE I
P2Y12 receptor antagonist (not given for life)
```
40
In what age groups in heart failure most diagnosed in?
Over 65s
41
What can cause systolic dysfunction of the heart muscle?
Ischaemic heart disease
Pressure or volume overload such as in AS or hypertension
Cardiomyopathy
42
What does diastolic dysfunction mean?
Inability of the heart muscle to relax and refill?
43
What can cause diastolic dysfunction of the heart muscle?
Amyloid
Myocardial fibrosis
Constrictive pericarditis
44
What are the compensatory mechanisms the heart has to deal with heart failure.
Frank Starling - increased stretching leads to increased contraction
Hypertrophy with possible chamber dilatation
Activation of noradrenaline, RAAS, ANP
45
What type of hypertrophy does pressure overload lead to?
Concentric hypertrophy
46
Which type of heart remodelling does volume overload lead to?
Cavitary dilation that may be without thickening
47
How does hypertrophy affect the perfusion of the heart muscle?
Decreased capillaries leading to an increase in fibrotic tissue but there are already increased metabolic needs leading to worsening HF
48
How does pulmonary congestion and oedema occur in left sided heart failure?
Decreased peripheral pressure and damming of blood in pulmonary circulation causes the lungs to be congested, oedema to develop and accumulation of haemosiderin laden macrophages. These lead to dyspnoea, orthopnoea and PND
49
What is right sided heart failure usually secondary to?
Left ventricular failure
50
Which complications can arise from right sided heart failure?
Pulmonary hypertension that can cause the liver to become congested creating nutmeg liver. Portal vein pressure will also increase leading to splenomegaly and ascites.
51
What is nutmeg liver and how does it occur?
Blood backing up in the liver due to right sided heart failure causing pulmonary hypertension. This leads to centrilobular necrosis and fibrosis.
52
How is hypertension defined?
Diastolic > 90 or systolic > 140
53
What percentage of hypertension is primary?
95 percent
54
What percentage of hypertension is malignant?
5 percent
55
How is blood pressure worked out?
BP=COxPeriperal Resistance
56
What can affect cardiac output?
Blood volume
Heart rate
Contractility
57
What can alter blood volume?
Sodium
Mineralocorticoids
Atriopeptin
58
What can increase peripheral resistance?
Constrictors e.g. Angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin
Dilators e.g. Prostaglandins, kinins, NO
Local factors e.g. Autoregulation, pH, hypoxia
Neural factors, constrictors are alpha adrenergic and dilatory are beta adrenergic
59
What genetic influences may raise blood pressure?
```
Defects in renal homeostasis
Functional vasoconstriction (may lead to increased vascular reactivity)
Defects in vascular smooth muscle growth and structure
```
60
How does hypertension affect small vessels?
Hyaline ateriosclerosis (especially kidneys)
Hyper plastic ateriosclerosis (onion skinning)
Fibrinoid necrosis in accelerated disease
61
What is cor pulmonale?
Right ventricular hypertrophy with right atrial hypertrophy and dilation
62
What are clinical features of cor pulmonale?
Thickened right ventricle (normally greater than 0.5cm)
Possibly tricuspid regurgitation
Acute or chronic
63
What is vasculitis?
Inflammation of the vessel walls
64
Can vasculitis be caused by infection?
Yes
65
How is non infectious vasculitis mediated?
By immune complexes such as ANCA mediated, direct antibody mediated, cell mediated, paraneoplastic or idiopathic
66
What is common to all forms of vasculitis?
Vessel injury with mural necrosis and haemorrhage
67
How can vasculitis be classified?
```
On pathogenesis
Vessel size
Localised, systemic or organ restricted
Can be granulomatous
Secondary ischaemia of downstream tissue
```
68
What is the clinical picture of polyarteritis nordosa?
Systemic vasculitis
Small and medium sized arteries affected
Often spares lungs
Segmental necrosing inflammation of the GI tract/renal/cardiac arteries especially
Branching sites
Leads to aneurysms, infarcts and haemorrhage
Fibrinosis becomes nodular later on in the disease
Lesions of different ages
69
What is seen on histology with polyarteritis nodosa?
Transmural inflammation and fibrinoid necrosis
70
What is found in 30 percent of polyarteritis nodosa cases?
Hep B antigen positive
71
What further clues may point to a diagnosis of polyarteritis nodosa?
```
Young adults
Acute/subacute/chronic
Episodic
Gangrene
Vague aches and pains
Infarcts
Hep b or c
No haematuria
No glomerular involvement
```
72
How is polyarteritis nodosa treated?
Steroids and cyclophosphamide
73
What are the features of ANCA related vasculitis?
Systemic/renal limited/other
85 percent of cases ANCA positive
Flu like illness
Fever, athralgia, myalgia, purpura, peripheral neuropathy, GI involvement
Possibly provoked by drugs - propylthyrouracil, penicillamine, hydrasalazine)
74
Which drugs can trigger ANCA associated vasculitis?
Propylthyrouracil, penicillamine, hydrasalazine
75
What are the features of Wegeners granulomatous?
Upper and lower respiratory tract
Ocular/ ear involvement
Necrotising granulomas
Vasculitis
76
Which antibody is present in Wegners granulomatosis?
cANCA usually against proteinase 3 (PR3)
77
What are clinical signs and symptoms of Wegeners granulomatosis?
```
Sore joints
Destruction of the face
Trace of blood in the urine
Gangrene
Permanent kidney failure
Sore eyes and ears
Lung cavities and bleeds
```
78
Which test is positive in Wegeners granulomatosis?
Positive anti neutrophil cytoplasm test (cANCA)
79
How is Wegeners granulomatosis treated?
Aggressive immunosuppression with cyclophosphamide and steroids.
80
What is cardiomyopathy?
Cardiac disease resulting from a primary intrinsic myocardial abnormality - other causes, such as ischaemia, need to be excluded
81
What types of cardiomyopathy are there?
Idiopathic or secondary to a known cause
Dilated - ventricles enlarge
Hypertrophic - ventricles thicken and become stiff
Restrictive - walls of the ventricle become stiff but do not thicken
82
What are features of dilated cardiomyopathy?
Progressive cardiac dilatation and contractile dysfunction
Large heart with four chamber dilation
Valves are arteries are not significantly abnormal
Micro myocardial hypertrophy/fibrosis
May be thrombi
83
What are the causes of dilated cardiomyopathy?
```
Idiopathic
30 percent genetic
Past myocarditis
Alcohol or other drug toxicity e.g. Doxorubicin
Pregnancy associated
Haemochromatosis
Sarcoidosis
```
84
What are the clinical signs of dilated cardiomyopathy?
Occurs at any age but especially 20-50
Progressive congestive cardiac failure
Signs of LVF and RVF
Death from heart failure or sudden cardiac death via arrhythmia
85
What is the treatment for dilated cardiomyopathy?
Heart transplant
86
What are the features of hypertrophic cardiomyopathy?
Poor diastolic filling
Often outflow obstruction
Little to no dilation
Classical disproportionate thickening of septa, especially sub aortic
Micro hypertrophy p, disarray and fibrosis
87
What is the aetiology of hypertrophic cardiomyopathy?
Mutation of muscle protein especially beta myosin heavy chain, this leads to poor compliance and reduced left ventricular chamber size with possible outflow obstruction
Mostly familial
Many different mutations found
88
What do people die from in dilated or hypertrophic cardiomyopathy?
Heart failure
Stroke
Atrial fibrillation
Sudden death from arrhythmia
89
What are the features of restrictive cardiomyopathy?
Primary decrease in vascular compliance
Idiopathic
Firm normal sized ventricles with dilated atria
Secondary to irradiation fibrosis, amyloid, sarcoidosis, tumour metastasis (cause found with LM)
90
What is myocarditis?
Inflammation causing myocardial injury
91
Which viruses can cause myocarditis?
Cocksackie
Enteroviruses
HIV
92
Which bacteria typically cause myocarditis?
Chlamidya
| Rickettsiae
93
Other than viruses and bacteria, which pathogens may cause myocarditis?
Fungi
Protozoa
Helminths
94
What are the immunological causes of myocarditis?
```
Post viral infection
SLE
Drug reactions
Transplant reaction
Sarcoidosis and giant cell myocarditis (more rare)
```
95
What is the aetiology of myocarditis?
Direct damage or T cell mediated injury to antigens on myocyte surface causing inflammation and myocyte necrosis
96
How might myocarditis present clinically?
May mimic acute infarct clinically
May lead to dilated cardiomyopathy
Arrhythmia, sudden death, fatigue, fever, chest discomfort, heart failure
97
What is the aetiology of ischaemic heart disease?
95 percent of cases are coronary artery atheroma
Coronary artery vasculitis
Coronary artery vasospasm
98
What is the aetiology of ischaemic heart disease due to thrombus?
Encrustation (rokitansky) - platelets thrombi over injured endothelium
Imbibition (Virchow) - low grade inflammation leads to increased plasma filtration
Reaction to injury (Ross and glomset) - endothelial injury with increased permeability and macrophage and smooth muscle accumulation
Monoclonal hypothesis - smooth muscle cells
99
What are the complications of ischaemic heart disease?
```
Ulceration
Fissuring
Haemorrhage
Thrombosis
Aneurysm
```
100
What are the throw types of acute myocardial infarct?
Transmural and subendocardial
101
What is a transmutation infarct?
Involves whole of the ventricular wall
| The underlying lesion is an atheromatous plaque that undergone fissuring and occlusive thrombosis
102
What is a subendocardial infarct?
Confined to the inner third or half of the myocardium and results from generalised under perfusion of the myocardium
103
If the main left coronary artery is occluded, where would the sit of the MI be?
Massive anterolateral MI
104
If there was an occlusion in the left anterior descending artery where would the MI be?
Anteroseptal MI
105
If there was an occlusion in the left circumflex artery, where the MI be?
Lateral MI
106
If there was an occlusion in the right coronary artery where would the MI be?
Posterior inferior MI
107
How does a MI appear macroscopically and on histology if it has lasted 0-12 hours?
No changes
108
How does an MI appear visually aft 12-24 hours?
Pale with blotchy discolouration
109
How does the histology appear with a MI that has lasted 12-24 hours?
Bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis
Intracellular oedema
110
How does a MI appear macroscopically if it has lasted 24-72hr?
Soft, pale and yellow
111
What is the histological appearance of an infarct lasting 24-72 hours?
Coagulation necrosis with loss of nuclei and strait ions, beginning of acute inflammatory response with neutrophil infiltrate
112
How does an MI macroscopically after 3-10 days
Soft, yellow - brown border with hyperaemic border
113
How does an MI appear histologically after 3-10 days?
Replacement of infarct end area with granulation tissue
114
How does an MI appear after weeks to months?
White fibrous scar
115
How does an MI appear histologically after weeks to months?
Collagenous scar tissue
116
What are the long term complications of MI?
Intractable heart failure
Ventricular aneurysm
Dressler's syndrome
Recurrent MI
117
What factors may influence the severity of a PE?
Size of occluded vessel
No. Emboli
Adequacy of bronchial blood supply
118
What is a saddle emboli?
Embolus in the pulmonary trunk leading to circulatory collapse
119
Why is a small to medium sized PE not life threatening?
Dual blood supply protects lungs from effects of pulmonary artery obstruction
120
What is angina?
Clinical syndrome characterised by discomfort in the chest, jaw, shoulder, back or arm. Typically aggravated by exertion or emotional stress and relieved by GTN. Angina normally occurs in patients with coronary artery disease involving at least epicardium artery.
121
What is unstable angina?
Angina that is either severe new onset, worsening or occurring at rest
122
How is unstable angina treated?
Combination antiplatelet therapy
| PCI or CABG carries prognostic benefit
123
How is stable angina treated?
Medically with PCI or CABG for symptom releif
124
Why does chest pain occur on exertion in angina?
Increased myocardial oxygen demand that cannot be met as coronary blood flow cannot increase
125
What can cause decreased oxygen supply to the heart?
Coronary artery disease
Anaemia
Hypoxia
126
What can cause increase oxygen demand in ischaemic heart disease?
Left ventricular hypertrophy
| Thyrotoxicosis
127
What are modifiable risk factors relevant to angina?
Smoking
Blood pressure target of 130/80 or less
Hypercholesterolaemia - give statins anyway
Diabetes - importance for good glycemic control
128
What clinical sign indicates hypercholesterolaemia and may point to ischaemic heart disease?
Xanthalasma - fatty deposits around the eyes
129
How should angina be investigated?
Taking the clinical history and ECG into account
If estimated coronary artery disease is 61-90 percent offer invasive coronary angiograph
If estimated coronary artery disease is 30-60 percent off nuclear perfusion scan
If estimated coronary artery disease is 10-29 percent off CT calcium scoring as first line diagnostic investigation
DO NOT USE EXERCISE ECG TO DIAGNOSE OR EXCLUDE STABLE ANGINA FOR PEOPLE WITHOUT KNOWN CORONARY ARTERY DISEASE
130
How should stable angina be treated?
Improve symptoms with sublingual GTN and beta blocker
Improve prognosis with addressing lifestyle, aspirin, statins and ACEI
IF they cannot tolerate beta blocker due to wheeze give second line therapy of CCB/nitrate/potassium channel opener/ IF channel blocker (ivabradine)
131
What treatment should be considered in stable angina persists?
PCI or CABG after angiogram
132
How is a coronary artery stent designed?
Metallic lattice structure
| Balloon mounted scaffold
133
What are physiological role of lipids?
```
Important part of cell membranes
Helps to absorb fat soluble vitamins
Maintains membrane fluidity
Acts as a thermal insulator and cellular metabolic regulator
Hormone synthesis
Organ padding
```
134
What are the sizes of cholesterol containing particles from largest to smallest?
Chylomicron
VLDL
LDL
HDL
135
What is the role of chylomicrons?
To transport fats from the intestinal mucosa to the liver. In the liver the chylomicrons release triglycerides and some cholesterol becomes LDLs and free cholesterol
136
What is the role of LDLs?
To carry fat into the body's cells
137
What is the role of HDLs?
HDLs carry fat and cholesterol back to the liver for excretion
HDLs can remove cholesterol from an atheroma
138
What happens when oxidised LDLs get too high?
Atheromatous formation
139
Which transport molecules are atherogenic?
VLDL, LDL and IDL
140
Is primary or secondary hyperlidaemia more common?
Secondary
141
What is familial hypercholesterolaemia?
Autosomal dominant genetic condition caused by gene mutations in the pathway that clears LDL from the bloodstream, present from birth and may lead to early atherosclerosis and coronary artery disease. Mutation is in LDL receptor.
142
What is the epidemiology around familial hypercholesterolaemia?
Occurs in 1 in 500 individuals
Mortality from CHD is 10x the normal population
High risk premature CHD
143
What is dysbetalipoproteinaemia?
Results in apoE2, a binding defect form of apoE (this is normally vital in catabolism of chylomicrons and VLDLs)
Increased risk of atherosclerosis and peripheral vascular disease
144
How many people does dysbetalipoproteinaemia affect?
1 in 10,000
145
What signs can be seen in dysbetalipoproteinaemia?
Tuberous xanthomas and striae palmaris
146
What cholesterol level is usually present in those with FH?
Greater than 7.5mmol/l
147
What clinical signs are present in many patients with FH?
Tendon xanthomas
Tuberous xanthomas
Xanthaelasma of the eyes
148
How is definite FH diagnosed with the Simon Boome criteria?
Definite FH with total cholesterol above 7.5mmol/l and LDL-C over 4.9 Plus tendon xanthoma in first or second degree relative OR identified genetic mutation for FH
149
How is possible FH diagnosed with the Simon Boome criteria?
Total cholesterol above 7.5 and LDL-C above 4.9 and at least one of
Family history of premature CHD MI under 60 in first degree relative or under 50 in second degree relative
OR
family history of raised cholesterol in first or second degree relative (above 7.5 in an adult, above 6.7 in a child)
150
Which drugs can cause hyperlidaemia?
Thiazides
Beta blockers
Antriretrovirals
Anti depressants
151
What are the clinical categories of hyperlipidaemia?
Predominant hypercholesterolaemia
Predominant hypertriglyceridaemia
Mixed hyperlipidaemia
152
Describe how fat can accumulate in subcutaneous tissue
Eruptive xanthoma - small itchy nodules that are VLDL and chylomicron associated (reversible)
Tuberous xanthomata - yellow plaques over elbows and knees - IDL induced
Xanthalasma- periorbital skin deposits - LDL associated
153
What clinical sign in the eye is indicative of hyperlipidaemia?
Cornea arcus (seen in under 40s with FH)
154
Where do tendon xanthomata tend to occur?
Extensor tendons
| Achilles tendon
155
What is the pathology of familial combined hyperlidaemia?
Over production of VLDL and apo B100
156
Give the features of familial combined hyperlipidaemia?
Raised LDL and triglyceride
Reduced HDL
Autosomal dominant
No clinical features until premature coronary heart disease
157
What are the features of polygenic hypercholesterolaemia?
Modest LDL increase due to impaired LDL clearance
Heterogenous multigene disorder
Continuous cholesterol distribution seen
158
What drug can be given to lower triglycerides?
Omega 3 fatty acids (Omacor)
159
What are symptoms of hypertension?
Generally asymptomatic
Nosebleeds
Headaches
Signs of end organ damage
160
What are the stages of hypertension?
Stage 1: 140/90 and ABPM 135/85
Stage 2: 160/100 and ABPM 150/95
Stage 3: systolic above 180 or diastolic above 110
Malignant: stage 3 with signs of papilloedema and retinal haemorrhage
161
How is postural hypotension diagnosed?
Measure BP supine or seated and stand patient for 1min, the BP should not drop by more than 20mm
162
How does ABPM work?
Checks BP 3 times per hour in the day and 1 times per hour in the night
Done for 24 hours
163
What are the stages of hypertension treatment?
1. ACE inhibitor or ARB (give both in Afro Carribeans) if under 55
2. Add CCB if Afro Carribean or over 55
3. Diuretics
164
What is the target for BP?
Under 80 = 140/90
Over 80 = 150/90
If end organ damage, diabetes or renal disease = 130/80
165
Which blood pressure drug should be considered in pregnancy?
Labetolol
166
What is the treatment for acute left ventricular failure?
Nitrate infusion
IV loop diuretics
IV diamorphine
Oxygen
167
How does a nitrous infusion work?
Causes venous dilation so reduces preload
| Does this by being metabolised and releasing nitric oxide which increase cGMP that activates protein kinase G
168
Give examples of lop diuretics
Bumetanide
| Furosemide
169
How do loop diuretics work?
Inhibit transport of NaCl from ascending loop of Henle into interstitial fluid by acting on the Cl binding site
Causes wanted sodium loss but unwanted potassium and magnesium loss
170
What other effects can loop diuretics be useful for?
Reno dilator effect when given IV
| Calcium loss may be useful in hypercalcaemia
171
What can decrease the absorption of loop diuretics?
Gut oedema and ascites
172
Give examples of potassium sparing diuretics?
Amiloride
| Triameterine
173
Give examples of aldosterone antagonists?
Spironolactone
| Eplerenone
174
Which drug inhibits angiotensin 1?
ACE inhibitors
175
Which drugs act on angiotensin II?
ARBs
176
Give examples of ACE inhibitors
Ramipril
Perindopril
Lisinopril
177
Do ACE inhibitors improve mortality?
Yes
178
What are the side effects of ACE inhibitors?
```
Angioedema
First dose hypotension
High potassium
Improves prognosis
Dry cough
```
179
How do ARBs work?
Blocks the A2 angiotensin receptor
180
Do ARBs improve mortality?
Yes
181
Give examples of ARBS
Losartan
Irbesartan
Valsartan
182
What are the side effects of ARBs?
High potassium
| First does hypotension
183
How does spironolactone work?
Aldosterone antagonist
184
Does spironolactone improve mortality?
Yes
185
What are the side effects of spironolactone?
Gyaecomastia due to oestrogen receptor effects
High potassium
Eplerenone has less side effects
186
Do beta blockers improve mortality?
Yes
187
When should beta blockers be used?
Only if patient is stable as can cause acute left ventricular failure
188
What is the mechanism of action of beta blockers?
Blocks actions of catecholamines
| Improves diastolic function
189
What treatment should be given in ischaemic heart disease?
Statin
Aspirin
Clopidogrel
190
When is digoxin used?
Antiarrhymic in AF and atrial flutter
191
What is the mechanism of digoxin?
Inhibits Na/K+ pump
192
How is digoxin excreted?
Renally - watch out if patient is renally impaired
193
What are the side effects of digoxin?
Does not control exercise induced tachycardia
Narrow therapeutic window
Log half life so may need loading dose
Toxicity increased by low potassium leading to arrhythmias, nausea and vomiting
194
What is amiodarone used for?
Ventricular and atrial arrhythmias
195
What are the side effects of amiodarone?
```
Can cause bradycardia
Very long half life of 6 weeks due to protein binding
Must give loading dose
Contained iodine so hypothyroid and hyperthyroid is a risk
Pulmonary fibrosis
Hepatitis,
Photosensitive skin rashes
Corneal deposits
```
196
Give examples of dihyropyridine CCBs
Amlodipine
| Rifedipine
197
Give examples of anti arrhythmic CCBs
Dilatizem
| Verapamil
198
How do CCBs work?
Block calcium channels (3 different sites) for anti anginal and anti hypertensive therapy
199
What are the side effects of calcium channel blockers?
```
Beta blockers
CCBs
Nitrates
Nicorandil (potassium channel activator)
Ivradibine - acts on sinus node to cause bradycardia
Aspirin
Statins
```
200
Is flecanide use for rhythm control?
Yes
201
In which conditions is flecanide used for?
Paroxysmal AF
Paroxysmal SVT
Paroxysmal VT
202
What changes occur in a stenotic mitral valve?
Thickening of cusps
| Fusion of chordae
203
What can cause mitral stenosis?
Rheumatic fever (most common)
Degenerative
Congenital
204
What can cause mitral regurgitation?
```
Rheumatic fever
Infective endocarditis
Ischaemic heart disease
Functional
Mitral valve prolapse
Congenital
```
205
What is the time line of right ventricular failure from mitral stenosis?
Mitral stenosis leading to raised left atrial pressure so the left atrium enlarges. Cephalisation occurs leading to pulmonary arterial hypertension causing increased pulmonary vessel resisitance so the right ventricle enlarges causing pulmonic regurgitation. This causes the tricuspid annulus to dilate causing tricuspid insufficiency and right ventricular failure.
206
What are the symptoms of mitral valve disease?
```
Dyspnoea on exertion and rest
Palpitations - predisposed to AF
systemic emboli
Fatigue
Chest pain
Recurrent chest infections
Haemoptysis from bronchial vein rupture, alveolar capillary rupture, PE)
Dysphasia - hoarse voice (dilated left atrium - Ortners syndrome)
Infective endocarditis
```
207
How should mitral valve disease be assessed?
ECG
CXR
Transthoracic or transoesphageal echo
208
What are the characteristics on auscultation of mitral stenosis?
```
Mid diastolic murmur
Loud S1
Length of murmur indicates severity
Opening snap after S1
Best heard with patient lying on left side
```
209
What are the characteristics on auscultation of mitral regurgitation?
Holosystolic from s1 to s2
| Heard best at the apex and radiates to the axilla
210
What may be seen on chest X-ray with tricuspid regurgitation?
Right atrial enlargement
211
What might be seen on chest X-ray with mitral stenosis?
Enlarged left atrial enlargement
212
How is mitral valve disease graded with echo?
```
On valve size
Normal 4-6cm
Mild 2-2.5cm
Moderate 1-2cm
Severe is less than 1com
```
213
What can cause acute mitral regurgitation?
Chord rupture and papillary rupture (+\-) acute left ventricle failure
214
What interventions can be done for mitral regurgitation?
Percutaneous balloon mitral valvotomy for mitral stenosis
Mitral clip for vertical types of mitral regurgitation
Surgical - valve replacement or repair
215
What can cause aortic stenosis?
Degenerative
Biscuspid aortic valve
Rheumatic fever
Congenital
216
What can cause aortic regurgitation?
```
Rheumatic fever
Bicuspid aortic valve
Infective endocarditis
Syphillis aortis
Ankylosing spondylitis
Rheumatoid arthritis
```
217
What are the symptoms of aortic valve disease?
```
Shortness of breath due to HF
Chest pain similar to angina
Presyncope or syncope
Palpitation or conduction disease
Infective endocarditis
Sudden death
```
218
What are the characteristics on auscultation with aortic stenosis?
Systolic
Harsh
Crescendo-descrescendo
Character of s2
219
What are the characteristics on auscultation with aortic regurgitation?
Early diastolic murmur
Best heard when patient is sitting forward on full expiration
3rd or 4th intercostal space left sterna, edge or 2nd intercostal space on right edge of sternum
220
What intervention can be done in aortic valve disease?
Percutaneous balloon valvotomy in aortic stenosis
Percutaneous transcatheter aortic valve implantation
Surgical valve replacement
221
What is the most common form of tricuspid valve disease?
Functional tricuspid regurgitation secondary to left heart disease (infective endocarditis, rheumatic fever, carcinoid, congenital)
222
What are the symptoms of tricuspid regurgitation?
```
Right heart failure (mimics liver disease)
Raised JVP
Hepatic tenderness
Ascites
Pedal oedema
```
223
What are the characteristics on auscultation with tricuspid regurgitation?
Soft inspiratory pansystolic murmur at the left eternal edge
224
How is tricuspid regurgitation managed?
Fluid balance
Diuretics
Limited response to surgery
225
What is the leading microorganism for infective endocarditis?
Staphylococcus aureus followed by Strep
226
What are predisposing factors to infective endocarditis?
Valve prosthesis
Degenerative valve sclerosis
IV drug abuse
Invasive procedures
227
What causes infective endocarditis with a positive blood culture (85 percent of cases)?
Mostly staph
Strep
Enterococci
228
What causes infective endocarditis with negative blood culture due to previous antibiotics?
Oral strep or coagulate negative staph
229
What causes an infective endocarditis that is frequently associated with a negative blood culture?
Usually fastidious organisms such as nutritionally variant strep, fastidious gram negative bacilli of the HACEK group
230
What causes infective endocarditis with an always negative blood culture
Intracellular bacteria such as Coxiella burnetti, Bartunella, Chlamidya, Trophyerma whippelei (Whipples disease)
231
What percentage of infective carditis cases always present with a negative blood culture?
5 percent
232
What is the pathophysiology of infective endocarditis?
Normal valve resistant to colonisation
Predisposing factors such as endothelial damage cause turbulent blood flow, electrodes, catheters, inflammation (rheumatic carditis) and degeneration in the elderly also cause it.
233
What is transient tacteraemia?
In infective endocarditis a consequence of invasive procedures, chewing and tooth brushing (usually causes low grade disease though)
234
What are major criteria in the Dukes criteria for diagnosing infective endocarditis?
1. Blood culture positive - typical microorganisms consistent with infective endocarditis from two separate blood cultures (Viridians, strep, staph, HACEK, strep bovis, enterococci)
2. Microorganisms consistent with infective endocarditis from persistently positive blood cultures either greater than 12 or less than 4 hours apart
3. Single culture for Coxiella burnetti or phase 1 IgG antibody titre
4. Echo showing vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation
235
What are minor Dukes criteria for diagnosing infective endocarditis?
```
Predisposition
Fever over 38 degrees
Vascular phenomenon
Immunological phenomenon
Microbiological evidence that doesn't fit a major criteria
```
236
How can the Dukes criteria be used to make a diagnosis of infective endocarditis?
1. Pathological diagnosis with microorganisms in the tissue
| 2. Clinical diagnosis of 2 major/ 1 major +3 minor/5 minor criteria
237
What are the clinical signs of infective endocarditis?
Splinter haemorrhages
Oslers nodes - immune complex deposition
Clubbling
Roths spots - retinal haemorrhages with white/pale centre
238
What is a small vegetation?
Less than 2mm
239
Is TTE or TOE more sensitive in diagnosing infective endocarditis?
TOE (sensitivity 90-100 percent vs 40-63 percent with TTE)
240
What is the role of a cardiac CT in diagnosing infective endocarditis?
Look a perivalvular extent of abscess and pseudoaneurysms
241
How should infective endocarditis be treated?
Antibiotics
Surgical intervention if haemodynamically compromised, embolisation, large vegetation, prosthetic valve
Surgery in HF, uncontrolled infection or presenting with aneurysm
242
What prophylaxis is recommended for high risk patients regarding infective endocarditis?
Dental antibiotics for procedures requiring manipulation of the gingival or peri apical region of the teeth or perforation of the oral mucosa NOTHING ELSE!!!
243
How is uncomplicated flu treated?
Send the patient home with supportive advice
244
How is complicated flu treated?
If complicated or immunosupressed give oseltamivir (PO or NG) first line or zanamivir second line
Should be given within 48 hours of the onset of symptoms
245
What is pharyngitis?
Sore throat
246
How does pharyngitis present?
Sore throat, fever, feeling ill, tonsillar exudate, tender cervical lymph nodes
Absence of cough may point to group A strep
Tonsillar exudate and tender cervical lymph nodes may point to group A strep but 20 percent chance
247
Which viruses commonly cause upper respiratory tract infection?
```
EBV
CMV
HSV
measles
HIV
```
248
Which bacteria commonly cause upper respiratory tract infection?
Group A/B/C strep
Mycoplasma pneumoniae
Nisseria gonorrhoea
Cornyebacterium diptheriae
249
How is pharyngitis treated?
Empirically with penicillin V (clarithromycin if allergic)
250
How is group A strep treated?
All are pencillin sensitive or erythromycin in those that are allergic
251
What complication is seen when amoxicillin is given to those with EBV infection?
Rash
252
How does acute otitis media normally present?
Child with unilateral painful ear
253
Which viruses normally cause otitis media?
The ones normally indicated in upper respiratory tract infection
254
Which bacteria normally cause otitis media?
```
Strep pneumoniae
Haemophilus influenza
Moraxella catarrhalis
Mycoplasma pneumoniae
Strep pyogenes
```
255
How should otitis media be treated?
No antibiotics unless under 2 years
Give amoxicillin/ coamoxiclav or clarithromycin if symptoms last more than 48 hours, high fevers, bilateral disease, otorrhoea
256
What are the complications of otitis media?
Decreased hearing
Mastoiditis
Brain abscess
257
What is the pathophysiology of sinusitis?
Obstruction from tissue swelling leading to mucus and pressure build up in the sinus cavity
258
Which bacteria commonly cause sinusitis?
Strep pneumoniae
Haemophilus influenzae (unencapsulated)
Moraxella catarrhalis
259
What treatment is advised in sinusitis?
Not usually needed but consider coamoxiclav or clarithromycin
260
How should legionella pneumonia be treated?
Quinolones>macrolides>tetracyclines (+rifampicin in severe disease)
261
How should mild CAP be treated?
Oral amoxicillin
262
How should moderate CAP be treated?
IV benzylpenicillin + clarithromycin
263
How should severe CAP be treated?
IV coamoxiclav + clarithromycin
264
How should CAP be treated in a traveller?
Ceftriaxone + clarithromycin
265
How is mild to moderate HAP treated?
Doxycycline
266
How is severe HAP treated?
Piperacillin- tazobactam
267
What are the symptoms of an exacerbation of COPD?
Shortness of breath
Cough
Sputum
268
What can trigger an exacerbation of COPD?
```
CCF
VTE
Aspiration
Pollution
Bacteria
Viruses
```
269
Which bacteria commonly cause an infective exacerbation of COPD?
```
H.influenzae
Moraxella catarrhalis
Strep pneumoniae
Pseudomonas oeurginosa
Chlamidya pneumoniae
```
270
What viruses can cause IECOPD?
```
Rhinovirus
Influenza
Parainfluenza
Adenovirus
RSV
Metapneumovirus
Corona virus
```
271
When are antibiotics effective in treated IECOPD?
If two of increased dyspnoea, increased sputum purulence, increased sputum amount
272
What is the empirical treatment for an infective exacerbation of COPD?
Doxycycline or clarithromycin for 5 days
| If relapse within 3 months treat with alternative
273
What is empyema (complicated parapneumonic effusion)?
Effusion into the pleural space adjacent to bacterial pneumonia, bacteria also invade pleural space and empyema develops
274
How is empyema treated?
Parapneumonic effusion usually resolves with treatment of pneumonia
If not drainage and give antibiotics for 2-4 weeks
275
Which pathogens normally cause the infection of a normal heart valve?
Staph aureus
Strep pneumoniae
(Usually iatrogenic)
276
Can phagocytes penetrate vegetations?
No
277
What is the empirical treatment of endocarditis?
Vancomycin plus gentamicin BUT vancomycin plus meropenem if risk of gram negative sepsis
If prosthetic valve give vancomycin plus gentamycin plus rifampicin (to stop biofilm developing)
278
What directed therapy is given in infective endocarditis with staph?
Fluxocillin 4 hourly
279
What directed therapy is given in infective endocarditis with MRSA?
Vancomycin
280
What directed therapy is given in infective endocarditis with step?
Benzylpenicillin 4 hourly
| If resistant give vancomycin plus gentamicin
281
What directed therapy is given in infective endocarditis with enterococci?
Amoxicillin 4hourly plus gentamicin
282
What can cause high output heart failure?
Anaemia, thyrotoxicosis, pregnancy, thiamine deficiency (beriberi), Paget's disease, AVM
283
What is heart failure with preserved ejection fraction?
Objective evidence of normal systole LV function but usually evidence of diastolic dysfunction causing reduction in heart compliance resulting in compromised ventricular filling and ejection
No evidence that treatment works in the long term
284
Does preload and after load decrease in CCF?
Yes
285
Which nutritional deficiencies can lead to heart failure?
Selenium
| Thiamine (beriberi)
286
What are the signs and symptoms of left heart failure?
Pulmonary congestion - tachypnoea, fine basal inspiratory crackles, wheeze
Systemic hypoperfusion - cold clammy peripheries, feeble pulses, tachycardia, pulsus alternans
Hypotension and shock
Faint first heart sound and 3rd and 4th heart sounds
287
What are the signs and symptoms of right heart failure?
Systemic congestion - peripheral pitting oedema, raised JVP, ascites, liver congestion, pleural effusion
Pulmonary hypoperfusion
288
What is the target saturation in managing acute heart failure?
Above 95 percent (88-92 in chronic lung disease)
289
What are the role of ionotropes in heart failure?
Increased force of contraction - indicated in cardiogenic shock
290
Give examples of ionotropes used in heart failure?
Dobutamine - non selective beta 1 and 2 adrenergic receptor agonist
Milrinone/enoximone - phosphodiesterase type III inhibitor
Levosimendan - calcium channel sensitiser
Dopamine/dopexamine- DA1 receptor agonist
291
What are the side effects of furosemide?
Low potassium/ magnesium/ calcium
Gout
Impaired glucose tolerance
Tinnitus with fast IV bolus
292
What are the side effects of thiazides?
Low potassium (especially with metolazone), low magnesium, low sodium
High calcium
Gout
Impaired glucose tolerance
293
What are side effects of ACE inhibitors?
```
High potassium
First dose postural hypotension
AKI with flash bilateral pulmonary oedema
Cough
Angioedema
```
294
What are the side effects of spironolactone?
High potassium
| Gynaecomastia
295
Which medications can be used instead of spironolactone in patients with gynaecomastia as a side effect?
Eplerenone
| Amigo ride
296
What are the side effects of beta blockers?
Nightmares
| Cold peripheries
