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CV medicine Flashcards

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1
Q

technical name for a heart attack

A

myocardial infarction

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2
Q

ACS

A

angina (+PVD) - ischaemia

MI (+CVA) - infarction

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3
Q

diagnosis of ACS

A

history
ECG: STEMI, NSTEMI
biomarkers: troponin

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4
Q

atherosclerosis

A

build up of cholesterol/fats in artery walls
progressive
lose x8 in blood flow

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5
Q

what happens if an atherosclerotic plaque ruptures?

A

occlusion

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6
Q

stages of progression of atherosclerosis

A 
normal
fatty streak
plaque
increasing plaque
obstructive atherosclerotic plaque
plaque fissure erosion - thrombosis
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7
Q

why is CAD severe?

A

no anastomotic supply

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8
Q

angina definition

A

reversible heart muscle ischaemia

- coronary arteries narrow

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9
Q

classical angina

A 
no pain at rest 
pain with certain level of exertion (lactic acidosis) - worse with cold weather/emotion
pain relieved by rest
pt lives within levels of tolerance
gradual deterioration
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10
Q

signs of classical angina

A

often no signs

occ hyperdynamic circulation - anaemia, hyperthyroidism, hypovolaemia

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11
Q

unstable angina

A

symptoms at rest with no biomarkers

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12
Q

pain with angina

A

central crushing chest pain

  • radiation
  • same pain but varies between individuals
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13
Q

angina investigations

A

ECG - ST segment elevation/depression
angiography
echocardiography
isotope studies

eliminate other disease - thyroid, anaemia, valve

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14
Q

angina tx principles

A

reduce oxygen demands of heart

increase oxygen delivery to tissues

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15
Q

angina tx - reduce oxygen demands of heart

A

reduce after load and preload

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16
Q

afterload

A

bp

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17
Q

preload

A

venous pressure

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18
Q

effect of sitting up re angina

A

reduce venous return

reduce CO

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19
Q

angina tx - increase oxygen delivery to tissues

A

angioplasty - dilate
CABG - bypass

blocked/narrowed vessels

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20
Q

angina non-drug therapy

A

explain - live within limitations

modify risk factors

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21
Q

angina drug therapy

A

reduce MI risk - aspirin
hypertension - Ca channel blockers, diuretics, ACE inhibitors, B-blockers
reduce preload/dilate coronary vessels - nitrates
emergency - GTN spray/tab

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22
Q

angina surgery

A

CABG
angioplasty and stenting (PCI) - gold standard in HA

need anti platelets in both

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23
Q

CABG

A

bypass blockage in coronary artery that can’t be txed in any other way
can’t redo, mortality risk

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24
Q

PVD

A 
'angina' of the tissues - usually LL
atheroma in femoral/popliteal vessels
'claudication'
indicates 'arteriopath' - MI risk
limitation of fct
poor wound healing
men and smokers
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25
congestive heart failure
hypertrophy of myocyte but no increase in blood supply heart weight x2-3 of normal increased metabolic demands - ischaemia - apoptosis - HF oedema
26
cardiac tumours prevalence
rare
27
benign cardiac tumours
myxoma, lipoma
28
malignant cardiac tumours
angiosarcoma
29
what other sources of cardiac tumour?
local extension of tumours from the thoracic cavity e.g. bronchogenic carcinoma
30
calcific aortic stenosis
commonest valvular condition dystrophic calcium deposits due to tissue inflammation and hyperlipidaemia narrowing of valvular orifice
31
rheumatic heart disease
complication of RF host immune reaction against strep A antigens T2 and T4 hypersensitivity reactions fibrinoid necrosis thickening and fusion, calcification of valves risk for IE
32
why do L valves fail more commonly?
higher pressure
33
valve stenosis
narrowed opening
34
types of stenosis and importance
aortic stenosis can lead to heart failure | mitral stenosis not as important
35
valve incompetence
don't close properly - backflow
36
consequence of valvular disease
reduce efficiency of heart as pump - heart failure
37
symptoms of valvular disease
rarely any symptoms - undiagnosed
38
valvular issues
stenosis incompetence insufficiency vegetations
39
causes of valvular disease
``` common in elderly and Downs congenital MI - papillary muscle rupture RF dilatation of aortic root - syphilis, aneurysm formation ```
40
valvular disease investigation
Ultrasound
41
types of valve replacement
mechanical - metal | porcine
42
mechanical valve replacement
last longer anticoagulants middle age
43
porcine valve replacement
only last around 10yrs don't need anticoagulants v young - outgrow it, falls elderly
44
important principle when choosing valve replacement
few changes as possible - mortality risk
45
what is there a risk of after valve replacements?
IE
46
why are CHDs often undetected?
asymptomatic
47
cyanosis
central peripheral - cold env when 5g/dl or more deoxygenated Hb in blood
48
CHDs investigation
US
49
types of CHD
ASD (hypertrophy) VSD coarctation of aorta (narrowed) PDA (connects pulmonary artery to aorta)
50
potential risk of CHDs
IE risk?
51
IE
microbial infection of endocardium (usually valves)
52
what is the biggest risk factor for IE?
prev IE
53
pathogenesis of IE
``` surface abnormalities haemodynamic changes bacteraemia turbulence platelet/fibrin deposition vegetation microbial attachment and multiplication enlargement ```
54
is IE easy to recognise?
no
55
ABP drug regime
amoxicillin 3g 1hr before | clindamycin 1.5g (higher ADA risk - only use if penicillin allergic)
56
primary prevention
stop from getting disease
57
secondary prevention
detect early and prevent progression
58
aspects of secondary prevention
lifestyle changes control cholesterol - statin control hypertension anti-platelet drugs - aspirin
59
when should aspirin be used as secondary prevention?
when identified CV disease | when high risk with no identified disease
60
anticoagulants broad use
if in heart
61
antiplatelets broad use
if peripheral bvs
62
irreversible risk factors
- age - sex - FH
63
reversible risk factors
SMOKING obesity diet exercise
64
reversible genetic risk factors
hypertension hyperlipidaemia diabetes stress?
65
risk modification
info belief motivation behavioural change
66
ACE inhibitors - name
-pril
67
ACE inhibitors - mechanism of action
reduce excess water and salt retention reduce bp inhibit AT1 to AT2 (vasoconstrictor) so reduce aldosterone
68
ACE inhibitors - SEs
cough hypotension angio-oedema lichenoid reactions
69
AT2 blockers name
-artan
70
B-blockers - name
-olol
71
atenolol
selective (B1 only) | only on B-receptors in CV system
72
B-blockers - action
reduce heart muscle excitability stop arrhythmias reduce bp prevent increase in hr
73
negative effects of B blockers
postural hypotension make HF worse (reduce heart efficiency) non-selective can make asthma worse
74
diuretics indication
for heart failure
75
diuretics mechanism of action
reduce bp | increase salt and water loss - reduce plasma volume so reduce cardiac workload
76
types of diuretics
thiazide - bendroflumethiazide | loop - frusemide
77
side effects of diuretics
``` Na+/K+ imbalance if not monitored dry mouth (elderly) ```
78
types of nitrates
short-acting - GTN | long-acting - isosorbide mononitrate
79
GTN
short acting nitrate for emergency tx of angina
80
isosorbide mononitrate
long acting nitrate for prevention of angina
81
mechanism of action of nitrates
vasodilators - dilate veins so reduce preload - dilate resistance arteries so reduce afterload - dilate colateral coronary artery supply so reduce anginal pain
82
administration of nitrates
inactivated by FPM so sublingual, transdermal, IV | short-shelf life
83
side effect of nitrates
headache
84
Ca channel blockers mechanism of action
reduce bp | block Ca channels in smooth muscle
85
Ca channel blockers in peripheral bv's
relaxation and vasodilation | -pine
86
Ca channel blockers in heart muscle
slow conduction of pacing impulses | Verapamil
87
side effect of Ca blockers
gingival hyperplasia
88
Warfarin mechanism of action
coumarin inhibits synthesis of vitK dependent CFs - 2,7,9,10 (slow) - protein C and S (quick) ACs
89
why do you need to use heparin when starting warfarin?
because you get initial hypercoagulation | as warfarin quickly inhibits proteins C and S which are anticoagulants
90
what should INR on warfarin be?
2-4
91
why should you monitor pt on warfarin closely?
food and drug interaction | unpredictable bioavailability
92
Warfarin and IDBs
avoid if can but not contraindicated
93
mechanism of action of statins
lipid lowering HMG coA reductase inhibitors inhibit cholesterol synthesis in liver
94
side effects of statins
myositis with interaction with antifungals | muscle pain - reduce dose or take before bed
95
statins and antifungals
fluconazole | omit statin - fine as makes difference over years not days
96
antiplatelets
``` aspirin clopidogrel dipyridamole Prasugrel Ticagrelor ```
97
aspirin mechanism of action
inhibits platelet aggregation - alters TA2 and prostacyclin balance irreversible for life of platelet
98
clopidogrel mechanism of action
inhibits ADP induced platelet aggregation
99
dipyridamole mechanism of action
inhibits platelet phosphodiesterase
100
new antiplatelets
Prasugrel, Ticagrelor | only prescribe in conjunction with aspirin
101
advantage of antiplatelets
can have more atherosclerosis without the severe consequences - platelets don't stick on platelets as much
102
NOACs
rivaroxaban apixaban dabigatran
103
rivaroxaban mechanism of action
inhibit FXa
104
apixaban mechanism of action
inhibit FXa
105
dabigatran mechanism of action
direct thrombin inhibitor
106
NOACs pros and cons
short 1/2 life fewer interactions £ less testing
107
what should you avoid on NOACs?
NSAIDs, erythromycin, clarithromycin
108
atherosclerosis
fat deposits in walls of mostly large and medium blood vessels multifactorial
109
atherosclerosis risk factors
``` HYPERLIPIDAEMIA age gender genes: familial hypercholesterolaemia (mutation of LDL receptor gene) diabetes/hypertension lifestyle ```
110
atheroma formation
chronic endothelial cell injury - hypertension etc permeability increases. lipid deposited in initial layers macrophages in - foam cells, fatty streaks, may regress smooth muscle proliferation healing phase - fibrous tissue over lipid. Plaque
111
effects of atherosclerosis
``` ischaemia infarction thrombosis embolism CV effects - angina, MI, CVA ```
112
thick atherosclerotic plaques
stable
113
thin atherosclerotic plaques
platelets can hit against endothelium - thrombosis
114
what stage of atherosclerosis is reversible?
fatty streaks
115
aneurysms
abnormal dilatation | may be fatal
116
causes of aneurysms
developmental degenerative traumatic
117
most common aneurysms
AAAs - atherosclerosis
118
factors influencing hypertension
gene | env
119
hypertension boundaries
systolic >140mmHg - >160 in isolated systolic hypertension diastolic >90mmHg
120
diastolic bp
resting arterial pressure | important one - spend more time in this pressure
121
diagnosing hypertension
3 separate measurements, sitting | - diff days, a week apart
122
hypertension risk factors
``` FH drugs - OCP, NSAIDs, steroids age obesity pregnancy etc ```
123
outcome of hypertension
accelerated atherosclerosis | renal failure
124
mechanism of hypertension
``` none usually found essential hypertension: no obvious cause, probably related to control mechanism within arterial walls rare triggers - renal artery stenosis - endocrine tumours ```
125
S and S of hypertension
usually none headaches TIAs
126
hypertension indications for further investigations
young pt resistant accelerated 'unusual' history
127
hypertension investigations
``` urinalysis serum biochemistry serum lipids ECG renal US ```
128
hypertension tx
modify risk factors | drugs
129
heart failure
pump failure | tissue hypoxia - failure of circulation
130
high output heart failure
system works but can't provide enough as demand has increased rare anaemia, thyrotoxicosis
131
low output heart failure
more common = pump failure
132
causes of low output heart failure
heart muscle disease - MI, myocarditis pressure overload - hypertension, aortic stenosis vol overload - mitral/aortic incompetence prolonged low level ischaemia arrhythmias - AF, heart block drugs - B-blockers, CS, anticancer drugs
133
left side failure S and S
``` dyspnoea pulmonary oedema frothy cough tachycardia low bp low vol pulse hypo perfusion - systemic ```
134
right side failure S and S
ascites, ankle oedema - systemic venous hypertension raised JVP tender enlarged liver pulmonary hypoperfusion
135
general heart failure symptoms
SOB swelling of feet and legs chronic lack of energy cough - frothy sputum
136
acute heart failure tx
hospital | O2, morphine, frusemide
137
chromic heart failure tx
``` community based improve fct reduce compensation effects e.g. reduce bp, fix valves, reduce compensatory increase in fluid where possible tx the cause - high bp - AF - valve disease - anaemia - thyroid disease ```
138
drug therapy in chronic heart failure
diuretics ACE inhibitors nitrates digoxin stop negative inotropes - B blockers
139
digoxin
inotrope increase force of contraction RS HF - reduce symptoms but not problem
140
shockable arrhythmias
VF and pVT
141
non-shockable arrhythmias
asystole and PEA
142
tachy
AF | V tachycardia
143
brady
``` heart block drug induced (B-blocker, digoxin) ```
144
cardiac pacemakers
treat bradyarrhythmias keep hr at minimum level theoretical risk of electrical interference
145
sinus rhythm stages
P - atrial depolarisation QRS - ventricular depolarisation T - ventricular repolarisation
146
regular hr
60-100 bpm
147
VF
disorganised, v irregular, 300-600bpm unstable heart electrical activity no CO - death defibrillate
148
asystole appearance
slight waves as still some electrical activity in body
149
AF
common in IHD irregular rhythm P wave fibrillatory (fine to course)
150
infarction
thrombosis on atheroma plaque | may detach and travel to block vessels
151
limb infarction
blocked femoral and popliteal arteries | thrombolysis, salvage surgery
152
heart infarction
MI | coronary artery atheroma
153
brain infarction
``` carotid arteries 'stroke' - usually embolism from atheroma - occ a cerebral bleed - rarely vessel thrombosis (good collateral blood supply`) loss of fct ```
154
TIAs
platelets removed naturally so fct returns | risk of a big stroke
155
types of MI
``` spontaneous - primary coronary event - plaque fissure/rupture MI secondary to ischaemia sudden death with symptoms of ischaemia and evidence of ST elevation or thrombus (PCI/autopsy) MI from PCI MI from CABG ```
156
MI strategies
reduce tissue loss from necrosis | prevent further episode
157
MI strategies - reduce tissue loss from necrosis
oedema blocks other tissues open blood flow to ischaemic tissue - thrombolysis, angioplasty bypass obstruction - CABG, fem/popliteal bypass
158
MI strategies - prevent further episode
risk factor management | aspirin
159
MI S+S
pain, nausea, pale, sweaty 'going to die' silent MIs
160
effect of MI
death around 50% | fct limitation
161
complications of MI
``` death arrhythmias HF ventricular hypofct and thrombosis - papillary muscle rupture - valve disease DVT and pulmonary embolism complications of thrombolysis ```
162
MI investigations
``` ECG - ST segment elevation/T wave abnormalities - may be normal - Q waves only indicate old MI cardiac enzymes - troponin - creatinine kinase - LDH and AST increase - not specific ```
163
MI tx primary care
get to hospital analgesia, aspirin, reassurance (BLS)
164
MI tx hospital
``` primary PCI thrombolysis if indicated drug tx to reduce tissue damage prevent recurrence/complications aspirin - secondary prevention ```
165
thrombolysis
can do up to 6hrs - if can't get to PCI centre in time | inject streptokinase, TPA
166
contraindications to thrombolysis
injury/surgery/IM injections severe hypertension, active PUD diabetic eye disease, liver disease, pregnancy
167
medical management of MI
prevent next MI - risk modification and aspirin - B-blocker, ACE inhibitor tx complications: HF, arrhythmias, psychological distress
168
haemangioma
hamartoma of blood vessels without CT capsule rapid growth first few weeks, usually regress over 1st 10yrs 60% H+N
169
vascular malformations
present at birth and persist may become more noticeable in elderly - epithelium thinner, calcium deposits can get intraosseous malformations types - cavernous, capillary, Sturge Weber syndrome can develop them IO and inside bone tx pts in hospital if bleeding risk can also get in meninges of brain - may have epilepsy
170
kaposi sarcoma
HHV-8 multi-focal low grade sarcoma of lymphatics and bv's HIV immune deficiency - role in carcinogenesis
171
angiosarcoma
develops in cells of blood or lymph glands rare, aggressive malignant, surgery
172
drugs to prevent further disease
antiplatelets statins B-blockers anticoagulants
173
drugs to reduce symptoms of current disease
``` diuretics B-blockers nitrates Ca channel blockers ACE inhibitors ```
174
advice about reducing IE risk
attendance for oral care rapid management infection max OH and prevention avoiding risk activity - piercings
175
CV pathology
``` 2 processes 1 - blood vessel narrowing - inadequate O2 delivery for tissue needs - 'cramp' in affected tissue/muscle - no residual deficit at first 2 - blood vessel occlusion - no O2 delivery - tissue death - more severe pain - loss of fct of tissue ``` both processes result in loss of heart muscle 1 - long-term 2 - short-term
176
when can you get VF?
heart attack electrocution long QT syndrome Wolf-Parkinson-White syndrome
177
coagulation necrosis
cells retain outline, can be identified cytoplasm darker remains of nuclei - small and dark staining or break up and disappear striations disappear always inflammation - neutrophils first then macrophages
178
granulation tissue
don't get replacement of myocardium by myocardium leaves scar will affect fct of heart
179
STEMI
classic heart attack
180
NSTEMI
may be unstable angina
181
if had MI how long should you avoid complex tx for?
at least 6m

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