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2226 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis

A

Pathological process that results in various ischemic syndromes

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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.

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3
Q

List 4 risk factors for atherosclerosis

A

Smoking
Hypertension
Elevated CRP
Insulin resistance

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4
Q

List 4 clinical manifestations of atherosclerosis

A

Chest pain
Nausea
Dysnpnea
Fatigue

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5
Q

4 diagnostic pathology test of atherosclerosis

A

U and e
FBE
Liver
Tropinin
\

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6
Q

Is systolic or diastolic hypertension more significant a risk for organ damage

A

Systolic

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7
Q

BP reading considered to be a hypertensive urgency

A

180/110

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8
Q

BP reading to be considered a hypertensive emergency

A
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9
Q

what is myocardial hypertrophy

A

increase in ventricular myocardial mass

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10
Q

what is angina

A

the pain caused by myocardial ischaemia

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11
Q

what causes the angina pain

A

lactic acid and abnormal stretching of nerve fibres

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12
Q

risk factors for angina pectoris

A

age
smoking
cholesterol
hypertension
diabetes

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13
Q

what is the purpose of nitrates in treating angina

A

they dilate BV

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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

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15
Q

describe CABG

A

redirects blood flow around a section of a blocked artery
health BV used to connect blocked artery

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16
Q

what is acute coronary syndrome

A

culmination of atheroscleoris and hypertension

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17
Q

risk factors for ACS

A

age
history
dyslipiademia
smoking

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18
Q

list 4 complications from ACS

A

electric dysfunction
mechanical dysfunction
thrombotic dysfunction
inflammatory dysfunction

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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
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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
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21
Q

list treatment options for a NSTEMI

A
  • acute intensive meds
  • glyceryl trinitrate
  • low molecular weight heparin
    clopidogel
  • glycoprotein inhibitors
  • coronary angiography
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22
Q

what is the purpose of LMWH

A

anticoagulant

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23
Q

purpose of clopidogel

A

reduces clot formation

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24
Q

purpose of glycoprotein inhibitors

A

prevents platelet aggregation

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25
Q

categories of lipid lowering agents

A

bile acid sequestration
HMG- CoA
Cholesterol absorption inhibitors
Fibrates and vitamin B

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26
Q

what class of drug is lipid lowering agents

A

HMG - CoA reductase inhibitors

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27
Q

list 4 generic names for lipid lowering agents

A

atovastatin
simvastatin
pravastatin
rouvastatin

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28
Q

MOA of lipid lowering agents

A

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

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29
Q

contraindications for LLA

A

liver disease
pregnancy and BF
renal impairment and altered endocrine

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30
Q

SE of LLA

A

cataracts
GI
hyperglycaemia
myopathy
CNS

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31
Q

NCC of LLA

A

avoid grapefruit juice and alchohol

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32
Q

explain how angiotensin converting enzyme inhibitors work

A

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

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33
Q

indications for ACE inhibitors

A

hypertension
heart failure
diabetic nephropathy
myocardial infarction

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34
Q

MOA of ACE inhibitors

A

prevents conversion of A1 to A2 by inhibiting ACE
results in reduced peripheral vascular resistance and decreased BP
decreases aldosterone production

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35
Q

SE of ACE inhib

A

cough, angiodema, hypotension, renal failure and hyperkalemia
dizziness, headache

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36
Q

what other class of drugs interact and diminish effects of ACE inhib

A

NSAIDs

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37
Q

how to anti anginal agents work

A

relieve angina pain by causing vasodilation

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38
Q

list 4 pharmacological agents of anti anginal meds

A

glyceryl trinitrate
isosorbide dinitrate
isosorbide mononitrate
calcium channel blockers

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39
Q

3 indications for anti anginal agents

A

manage acute pain and prevent further attacks
improve perfusion by reducing metabolic demand on heart
relaxes smooth muscle of coronary artery

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40
Q

describe the MOA of anti anginal agents

A

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
Q

SE of AAA

A

headache, hypotension, syncope, tachy, nausea

42
Q

how do calcium channel blockers work

A

prevent calcium ions from entering the cells, calcium ions have an effect on the heart and BC resulting in contraction and prevents vasodilation

43
Q

3 major family names for calcium channel blockers

A

dihydropyridines
phenylaikylamine
benzothiazepine

44
Q

indication for calcium channel blockers

A

hypertension, angina pectoris, cardiac dysthymias

45
Q

MOA of calcium channel blockers

A

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
Q

contraindications of calcium channel blockers

A

severe hypotension, sick sinus, 2nd or 3rd degree AV blocks

47
Q

SE of CCB

A

constipation, dizziness, headache, oedema, dry mouth, bradycardia, AV blocks

48
Q

Why should grapefruits be avoided during CCB treatment

A

Inhibits intestinal and hepatic metabolism of meds and leads to toxicity

49
Q

Indications of beta blockers

A

Angina pectoris
Hypertension
Cardiac dysthymia’s
Myocardial infarction
HF

50
Q

Describe the MOA of CCB

A

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
Q

SE of CCB

A

Bradycardia
Reduced CO
Hypotension
HF
AV heart block
Decreased libido
Fatigue
Bronchoconstriction and hypotension

52
Q

Contraindic of CCB

A

Asthma
COPD
Bronchoconstriction
Allergic disorder

53
Q

State the 3 classes of diuretics

A

Thiazide
Loop
Potassium sparing

54
Q

Indications for diuretics

A

HF
Oedema assoc with HF, cirrhosis and renal impairment, acute pulmonary oedema, hypertension

55
Q

MOA of thiazide diuretics

A

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
Q

MOA of loop diuretics

A

Lowers BP by reducing BV and promoting vasodilation. Inhibits reabsorption of sodium, potassium and chloride.

57
Q

MOA of potassium sparing diuretics

A

Mild diuretic and anti hypertensive effect. Conserves potassium.

58
Q

contraindications of using thiazide diuretic

A

increases serum levels of lithium and risks toxicity
increases risk of hypotension with ACE inhibitors
anura, oliguria, kidney or liver failure, preeclampsia

59
Q

contraindications of using loop diuretics

A

hypotension
increases serum levels of theophyline
lithium or NSAIDs
renal impairment

60
Q

contraindications of potassium diuretics

A

hyperkalemia adverse event
lithium or NSAIDs

61
Q

SE of diuretics

A

hypotension
hypokalemia
dehydration
hypovalemia
hyperglycaemia
hyperuricemia

62
Q

list 4 generic names of angiotension 2 receptor antagonists

A

irbesartan
candesartan
losartan
valsartan

63
Q

indications for A2 receptor antagonists

A

hypertension

64
Q

describe the MOA of A2 receptor antagonists

A

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
Q

SE of A2 receptor antagonists

A

hypotension, chest pain, tachy, hypertriglyderidaemia

66
Q

what is digoxin used for

A

heart failure, atrial fib, paroxymal atrial tachy

67
Q

MOA of digoxin

A

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
Q

list 3 classes of anticoagulants

A

unfractioned heparin
low molecular weight heparin - enoxaparin
fonaparinux

69
Q

indication for anticoagulants

A

prevent DVTs., PE and thrombophlebitis

70
Q

MOA for anticoagulants

A

supresses coagulation by helping antithombin inactivate clotting factors suppressing formation of fibrin
inhibits activation of fibrin stabilising factor to prevent stable clot formation.

71
Q

SE of anticoagulants

A

haemorrhage
thrombocytopenia
local irritation, erythema, haematoma, ulceration with cub cut inj

72
Q

indications for warfrin

A

prophylaxis of thrombis
prevention of thrombosis in patients with atrial fib
prevention of thromboembeloism in patients with prosthetic heart valves.

73
Q

MOA warfrin

A

suppresses coagulation by decreasing production of clotting factors

74
Q

contraindications of warfrin

A

severe thrombocytopenia
lumbar puncture
high risk of GI bleeds
vit k deficiency
preg and bf

75
Q

Indications for asprin

A

ischaemic stroke
TIAs
chronic stable angina
unstable angina
coronary stent
AMI
non visceral pain
inflammatory assoc pain

76
Q

MOA for aspririn

A

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
Q

contraindications for aspirin

A

decreased blood platelets
anemia
heamophillia
GI ulcer
preg, lact, bf

78
Q

NCC for admin of aspirin

A

elderly at greater risk
may increase blood levels of sodium valporate, sulphomides, and methotrexate

79
Q

explain the 6 step method of ECG interpretation

A

identify and examine P waves
Measure PR interval
Measure QRS complex
identify rhythm
HR
interperet strip

80
Q

location of V1

A

right sternal border in 4th IS

81
Q

Location of V2

A

left sternal border in 4th IS

82
Q

Location of V3

A

between v2 and v4

83
Q

location of V4

A

5th IS in midclavicular line

84
Q

location of V5

A

ant axillary line on the same plane as V4

85
Q

location of V6

A

mid axillary line in same HP as 5

86
Q

Where does the sinus rhythm originate in the heart

A

sinus node

87
Q

list the pathway of a sinus rhythm through the heart

A

AV, BOH and then down to purkinje fibres

88
Q

Sinus
P wave:
PR interval :
QRS complex:
BPM:
T wave:
mechanical contraction: p or a

A

Present and upright
0.12 to 0.2s
proceeded by a normal p wave <0.12s
60-100
present and upright
present

89
Q

Sinus tachy
P wave
PR interval
QRS
T wave
Mechanical contraction

A

present and upright
0.12 to 0.2s
proceeded by normal p wave
present and upright
present

90
Q

what causes a fib

A

abnormal electrical pathways in the atria

91
Q

list 3 examples of clinical manifestation that can cause A fib

A

myocardial ischemia
HF
thyroid disfunction

92
Q

name 3 types of A fib

A

paroxysmal
persistant
permanent

93
Q

list 3 caises of A fib

A

excess catecholamines, atrial enlargement and an abnormality in the conducting system

94
Q

list 3 complications from A fib

A

loss of atrial kick
atrial thrombus
heart failure

95
Q

what lead best analyses a fib

A

2

96
Q

describe the pathophys of A fib

A
  • 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
Q

CM of a fib

A

altered conscious state
irregular pulse
palipitations
chest pain

98
Q

treatment of a A fib

A

anti arrhythmic agents
beta blockets, CCB and or digoxin
anticoagulation meds
electrical cardio version
catherter ablation

2226 (2 decks)

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