Cardiology Flashcards
1
Q
What is atherosclerosis
A
Pathological process that results in various ischemic syndromes
2
Q
Compare atherosclerosis and arteriosclerosis
A
Arteriosclerosis is the narrowing of the wall due to hardening and thickening.
Atherosclerosis is a form of arteriosclerosis that occurs when intra arterial fat and fibrin along vessel walls harder.
3
Q
List 4 risk factors for atherosclerosis
A
Smoking
Hypertension
Elevated CRP
Insulin resistance
4
Q
List 4 clinical manifestations of atherosclerosis
A
Chest pain
Nausea
Dysnpnea
Fatigue
5
Q
4 diagnostic pathology test of atherosclerosis
A
U and e
FBE
Liver
Tropinin
\
6
Q
Is systolic or diastolic hypertension more significant a risk for organ damage
A
Systolic
7
Q
BP reading considered to be a hypertensive urgency
A
180/110
8
Q
BP reading to be considered a hypertensive emergency
A
9
Q
what is myocardial hypertrophy
A
increase in ventricular myocardial mass
10
Q
what is angina
A
the pain caused by myocardial ischaemia
11
Q
what causes the angina pain
A
lactic acid and abnormal stretching of nerve fibres
12
Q
risk factors for angina pectoris
A
age
smoking
cholesterol
hypertension
diabetes
13
Q
what is the purpose of nitrates in treating angina
A
they dilate BV
14
Q
Describe how a stent works
A
catheter inserted into blocked or narrowed CA
wire with deflated balloon passed through
balloon inflates compressing the plaque
stent inserted to keep artery open
15
Q
describe CABG
A
redirects blood flow around a section of a blocked artery
health BV used to connect blocked artery
16
Q
what is acute coronary syndrome
A
culmination of atheroscleoris and hypertension
17
Q
risk factors for ACS
A
age
history
dyslipiademia
smoking
18
Q
list 4 complications from ACS
A
electric dysfunction
mechanical dysfunction
thrombotic dysfunction
inflammatory dysfunction
19
Q
explain the pathophysiology of ACS
A
- ECG detects abnormality after 1 minute of hypoxia
- anaerobic metabolism
- glycolysis
- hydrogen + lactic acid build up
- electrolyte imbalance
- decrease in myocardial contract
- caecholamine release and hyperglycaemia
- vasoconstriction
- fluid retention
- ventricular remodelling
20
Q
pathophysiology of AMI
A
- cellular injury and death
- cardiac cells withstand hypoxia for 20 mins
- changes detected in 10s
- anaerobic metabolism and lactic acid build up
- electrolyte disturbances. loss of potassium, calcium, and magnesium
- effects contractability
- catecholamine released: coronary artery spasm, peripheral vasoconstriction, fluid retention, hyperglycaemia
- cellular death occurs: intracellular enzyme release of creatine and troponin
21
Q
list treatment options for a NSTEMI
A
- acute intensive meds
- glyceryl trinitrate
- low molecular weight heparin
clopidogel - glycoprotein inhibitors
- coronary angiography
22
Q
what is the purpose of LMWH
A
anticoagulant
23
Q
purpose of clopidogel
A
reduces clot formation
24
Q
purpose of glycoprotein inhibitors
A
prevents platelet aggregation
25
categories of lipid lowering agents
bile acid sequestration
HMG- CoA
Cholesterol absorption inhibitors
Fibrates and vitamin B
26
what class of drug is lipid lowering agents
HMG - CoA reductase inhibitors
27
list 4 generic names for lipid lowering agents
atovastatin
simvastatin
pravastatin
rouvastatin
28
MOA of lipid lowering agents
reversibly inhibit HMG -CoA reductase which reduces cholesterol synthesis and increases the number of liver LDL receptors reducing LDL.
Endothelial function, inflammatory response, modify thrombus formation, stabilises atherosclerotic plaques and increases fibrolytic action
29
contraindications for LLA
liver disease
pregnancy and BF
renal impairment and altered endocrine
30
SE of LLA
cataracts
GI
hyperglycaemia
myopathy
CNS
31
NCC of LLA
avoid grapefruit juice and alchohol
32
explain how angiotensin converting enzyme inhibitors work
A2 raises BP through vasoconstriction and renal retention of water and sodium. By inhibiting ACE levels of A2 are reduced resulting in dilated BC resulting in BC reduction. Positive effect on ventricular remodelling
33
indications for ACE inhibitors
hypertension
heart failure
diabetic nephropathy
myocardial infarction
34
MOA of ACE inhibitors
prevents conversion of A1 to A2 by inhibiting ACE
results in reduced peripheral vascular resistance and decreased BP
decreases aldosterone production
35
SE of ACE inhib
cough, angiodema, hypotension, renal failure and hyperkalemia
dizziness, headache
36
what other class of drugs interact and diminish effects of ACE inhib
NSAIDs
37
how to anti anginal agents work
relieve angina pain by causing vasodilation
38
list 4 pharmacological agents of anti anginal meds
glyceryl trinitrate
isosorbide dinitrate
isosorbide mononitrate
calcium channel blockers
39
3 indications for anti anginal agents
manage acute pain and prevent further attacks
improve perfusion by reducing metabolic demand on heart
relaxes smooth muscle of coronary artery
40
describe the MOA of anti anginal agents
relaxes smooth muscles causing peripheral arteries and veins to dilate decreasing arterial pressure and CO
results in decreased myocardial oxygen demand
dilates coronary vessels increasing myocardial perfusion and oxygen delivery
41
SE of AAA
headache, hypotension, syncope, tachy, nausea
42
how do calcium channel blockers work
prevent calcium ions from entering the cells, calcium ions have an effect on the heart and BC resulting in contraction and prevents vasodilation
43
3 major family names for calcium channel blockers
dihydropyridines
phenylaikylamine
benzothiazepine
44
indication for calcium channel blockers
hypertension, angina pectoris, cardiac dysthymias
45
MOA of calcium channel blockers
impedes influx of calcium ions through slow channels of cell membranes during depolarisation of cardiac and vascular smooth muscle.
Dilates coronary arteries reducing peripheral vascular resistance and BP
improves myocardial oxygen supply, reduces myocardial work by reducing afterload which improves cardiac output.
46
contraindications of calcium channel blockers
severe hypotension, sick sinus, 2nd or 3rd degree AV blocks
47
SE of CCB
constipation, dizziness, headache, oedema, dry mouth, bradycardia, AV blocks
48
Why should grapefruits be avoided during CCB treatment
Inhibits intestinal and hepatic metabolism of meds and leads to toxicity
49
Indications of beta blockers
Angina pectoris
Hypertension
Cardiac dysthymia’s
Myocardial infarction
HF
50
Describe the MOA of CCB
Inhibits beta adrenoreceptors which reduces some response to adrenaline, noradrenaline and isoprenaline
Blocking of beta 1 receptors in heart results in reduced HR, FOC and reduced velocity of impulse conduction through the AVnode leading to reduced CO and myocardial and oxygen demand. Inhibits release of renin from kidneys.
51
SE of CCB
Bradycardia
Reduced CO
Hypotension
HF
AV heart block
Decreased libido
Fatigue
Bronchoconstriction and hypotension
52
Contraindic of CCB
Asthma
COPD
Bronchoconstriction
Allergic disorder
53
State the 3 classes of diuretics
Thiazide
Loop
Potassium sparing
54
Indications for diuretics
HF
Oedema assoc with HF, cirrhosis and renal impairment, acute pulmonary oedema, hypertension
55
MOA of thiazide diuretics
Reduce blood volume and reduce arterial resistance with some vasodilator activity. Increases excretion of sodium and chloride ions and water in the proximal segment of the distal tubule
56
MOA of loop diuretics
Lowers BP by reducing BV and promoting vasodilation. Inhibits reabsorption of sodium, potassium and chloride.
57
MOA of potassium sparing diuretics
Mild diuretic and anti hypertensive effect. Conserves potassium.
58
contraindications of using thiazide diuretic
increases serum levels of lithium and risks toxicity
increases risk of hypotension with ACE inhibitors
anura, oliguria, kidney or liver failure, preeclampsia
59
contraindications of using loop diuretics
hypotension
increases serum levels of theophyline
lithium or NSAIDs
renal impairment
60
contraindications of potassium diuretics
hyperkalemia adverse event
lithium or NSAIDs
61
SE of diuretics
hypotension
hypokalemia
dehydration
hypovalemia
hyperglycaemia
hyperuricemia
62
list 4 generic names of angiotension 2 receptor antagonists
irbesartan
candesartan
losartan
valsartan
63
indications for A2 receptor antagonists
hypertension
64
describe the MOA of A2 receptor antagonists
block angiotensin 2 receptors on the vascular smooth muscle and adrenal cortex
A2 responsible for vasoconstriction, stim aldosterone, regulation of salt and water homeostasis.
increases renal blood flow and maintain GFR whilst decreasing renal vascular resistance. does not inhiit ACE therefor bradykinins is not affected and less likely to have adverse effects
65
SE of A2 receptor antagonists
hypotension, chest pain, tachy, hypertriglyderidaemia
66
what is digoxin used for
heart failure, atrial fib, paroxymal atrial tachy
67
MOA of digoxin
positive inotropic action which increases myocardial contractile force and increases CO by inhibiting sodium potassium pump exchange.
alters electrical activity of the heart by slowing conduction rate through AV mode.
68
list 3 classes of anticoagulants
unfractioned heparin
low molecular weight heparin - enoxaparin
fonaparinux
69
indication for anticoagulants
prevent DVTs., PE and thrombophlebitis
70
MOA for anticoagulants
supresses coagulation by helping antithombin inactivate clotting factors suppressing formation of fibrin
inhibits activation of fibrin stabilising factor to prevent stable clot formation.
71
SE of anticoagulants
haemorrhage
thrombocytopenia
local irritation, erythema, haematoma, ulceration with cub cut inj
72
indications for warfrin
prophylaxis of thrombis
prevention of thrombosis in patients with atrial fib
prevention of thromboembeloism in patients with prosthetic heart valves.
73
MOA warfrin
suppresses coagulation by decreasing production of clotting factors
74
contraindications of warfrin
severe thrombocytopenia
lumbar puncture
high risk of GI bleeds
vit k deficiency
preg and bf
75
Indications for asprin
ischaemic stroke
TIAs
chronic stable angina
unstable angina
coronary stent
AMI
non visceral pain
inflammatory assoc pain
76
MOA for aspririn
supresses platelet aggregation by causing irreversible inhibition of cycloxegnease enzye required by platelets to synthesis TXA2
TXA2 acts on vascular smooth muscle to cause vasoconatriction, reduce risk of arterial thrombosis.
77
contraindications for aspirin
decreased blood platelets
anemia
heamophillia
GI ulcer
preg, lact, bf
78
NCC for admin of aspirin
elderly at greater risk
may increase blood levels of sodium valporate, sulphomides, and methotrexate
79
explain the 6 step method of ECG interpretation
identify and examine P waves
Measure PR interval
Measure QRS complex
identify rhythm
HR
interperet strip
80
location of V1
right sternal border in 4th IS
81
Location of V2
left sternal border in 4th IS
82
Location of V3
between v2 and v4
83
location of V4
5th IS in midclavicular line
84
location of V5
ant axillary line on the same plane as V4
85
location of V6
mid axillary line in same HP as 5
86
Where does the sinus rhythm originate in the heart
sinus node
87
list the pathway of a sinus rhythm through the heart
AV, BOH and then down to purkinje fibres
88
Sinus
P wave:
PR interval :
QRS complex:
BPM:
T wave:
mechanical contraction: p or a
Present and upright
0.12 to 0.2s
proceeded by a normal p wave <0.12s
60-100
present and upright
present
89
Sinus tachy
P wave
PR interval
QRS
T wave
Mechanical contraction
present and upright
0.12 to 0.2s
proceeded by normal p wave
present and upright
present
90
what causes a fib
abnormal electrical pathways in the atria
91
list 3 examples of clinical manifestation that can cause A fib
myocardial ischemia
HF
thyroid disfunction
92
name 3 types of A fib
paroxysmal
persistant
permanent
93
list 3 caises of A fib
excess catecholamines, atrial enlargement and an abnormality in the conducting system
94
list 3 complications from A fib
loss of atrial kick
atrial thrombus
heart failure
95
what lead best analyses a fib
2
96
describe the pathophys of A fib
- electrical activity is irregular and no discernible p wave
- abnormal erratic and disorganised rhythm creating a quivering of atria
- multiple re entry circuits developing in atria
- SA node no longer pacemaker
- AV node bombarded by rapid atrial impulses resulting in irregular response
- sudden onset or chronic
97
CM of a fib
altered conscious state
irregular pulse
palipitations
chest pain
98
treatment of a A fib
anti arrhythmic agents
beta blockets, CCB and or digoxin
anticoagulation meds
electrical cardio version
catherter ablation
