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Phase 2 > CVS > Flashcards

CVS Flashcards

1
Q

Causes of primary hypertension

A

Unknown. Combination of environmental and genetics. (95%)

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2
Q

Causes of secondary hypertension

A

(5%)

1. Renal disease 2. Endocrine - Conn’s syndrome; Cushing’s 3. Drugs (NSAIDs etc) 4. Rare tumours (eg. adrenal)

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3
Q

Drugs that cause hypertension

A 
NSAIDs
Combined oral contraceptive
Coricosteroids
Ciclosporin
Cold cures e.g. phenylephedrine
SNRI antidepressants
Some recreational drugs such as cocaine and amphetamines
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4
Q

Lifestyle causes of hypertension

A 
In order of effectiveness to decrease BP:
Obesity (weight)
Salt in diet
Alcohol
Exercise
Stress
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5
Q

What is the main pathology of hypertension in white people

A

Changes in mechanisms that control total peripheral resistance. Eg. RAAS. Elevated Renin, Angiotensin II, Aldosterone.

May also be changes in CO, but this pathology is not as much of a driver as TPR changes, hence, treatment is more RAAS, rather than CO, targeted.

MAP = CO x TPR

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6
Q

What is the pathology of hypertension in black people

A

Increased TRP - but not driven by low renin profile.

Still target TPR over CO as first line, but not ACE inhibitors.

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7
Q

What is malignant hypertension and what are the complications

A

BP that is in the ~180-200/120-130 range.

Precipitates acute renal failure, heart failure and encephalopathy. Medical emergency.

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8
Q

What are the signs/ symptoms of malignant hypertension?

A

Rapid rise in BP.
Vascular damage - papillodema (although may not be present).
Headaches, visual disturbances.

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9
Q

What are signs of End organ damage in hypertension, how would you test for these to quantify risk

A
  1. Eyes - retinopathy - thick/ narrow arteries/ hemorrhage/ optic disc swelling (look at arteries in back of eye/ look for swelling)
  2. Cardiac - LVH - (ECG, echo, history of MI)
  3. Renal - protein in urine (Urine analysis)
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10
Q

Symptoms of hypertension

A

Usually asymptomatic. May be headache. Not v diagnostic.

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11
Q

How would you diagnose hypertension & stage it

A 
Ambulatory testing / home testing - 1 week.
<135/85 + no sign of EOD = no Rx
<135/85 + EOD = Rx
>135/85 + 20% Qrisk = Rx (Stage 1)
>150/95 = Rx (Stage 2)
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12
Q

Outline treatment options for white pt with hypertension

A

Step 1: ACE / ARB
Step 2: ACE / ARB + CCB
Step 3: ACE / ARB + CCB + Thiazide like diuretic
Step 4: All above + (BB, alpha agonist, centrally acting drugs -moxonidine etc…)

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13
Q

Outline treatment options for black pt with hypertension

A

CCB first line. rest is the same as Caucasian treatment steps.

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14
Q

What would you use to manage blood pressure in a pregnant pt?

A

Methyldopa

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15
Q

What hypertension meds are contraindicated in pregancy

A

All? definitely ACE inhibitors - teratogenic

Methyldopa only safe one

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16
Q

How does methyldopa work?

A

Decreases DA synthesis - required for NA synthesis = decrease NA = decrease sympathetic = decrease CO & vasoconstriction

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17
Q

Name a centrally acting anti-hypertension (4th line)

A

moxonidine

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18
Q

Symptoms of HF

A

SOB
Fatigue
Swelling/ odema

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19
Q

Signs of HF

A

3rd heart sound

Swelling/ odema

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20
Q

Types of HF

A

HFREF - EF ~40%, systolic problem
HFPEF - EF ~50%, diastolic problem

Acute HF - medical emergency

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21
Q

Causes of HF

A
  1. IHD
  2. Hypertension
  3. Alcohol
  4. Cardiomyopathy
  5. Values
  6. Dysrhythmias
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22
Q

Causes of acute HF

A
  1. Decompensated - from existing pathology

2. New onset - MI, etc

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23
Q

Treatment targets chronic HF

A 
Vasodilation:
ACE inhibitor (+BB - low dose)
Aldosterone inibitor

Symptomatic relief of congestion
Diuretic

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24
Q

Treatment targets for acute HF

A

Congestion - diuretics

NOT BB, or any vasodilators, unless already on these and require for another condition. b/c vasodilators will add to congestion, and BB could take EF into more dangerous level

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25
Q

Drug treatment chronic HF

A

Triple therapy + diuretic

ACE inhibitor + BB + aldosterone inhibitor

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26
Q

Lifestyle changes HF

A

Stop smoking
Low salt
Optimse weight & diet

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27
Q

Investigations HF

A

Bloods - BNP
ECG - hypertophy (long QRS), tall R wave, dysrhythmias
Echo - valve, EF
CXR - eliminate SOB differentials, infection , PE etc

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28
Q

Important diagnostic markets for HF

A
  1. BNP >100 ng/L
  2. Paroxysmal nocturnal dyspnea (only see this in HF or mital valve disease)
  3. 3rd heart sound
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29
Q

How do you diagnose HF

A

Eliminate other causes
BNP
PND
3rd heart sound - all good diagnostic indicators

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30
Q

Where is atherosclerosis most likely to form and what are the 3 main consequences

A

Medium - large arteries: peripheral or coronary arteries.
Coronary = heart attack
Carotids = stroke
Peripheral = gangrene/ limb ischemia

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31
Q

Risk factors for atherosclerosis

A
  • Age (exponential increase in plaques over 55 years)
  • Tobacco Smoking (tobacco - endothelial irritant)
  • High Serum Cholesterol
  • Obesity (increased fat around the heart)
  • Diabetes (high blood sugar, damages endothelium)
  • Hypertension (sheer forces)
  • Family History
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32
Q

Where are plaques most likely to form

A

Where there is a change in blood flow.

Bends, bifurcation etc.

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33
Q

Describe the mechanism of athersclerosis

A

Inflammatory mechanism.
1.Stimulus (irritant) gets into endothelial (intima layer) and oxidises. This triggers an injury response by the endothelium.
2.Chemokines (maybe IL-1) released by endothelium to attract neutrophils.
3.Adhesion & migration of neutrophils into intima.
4. Neutrophils then attract more WBCs including macrophage. AT THIS POINT = FATTY STREAK, only inflammatory cells, macrophage & lipidsATTY
5.Macrophage engulfs LDL/ stimulant.
Over time, macrophage dies & get fat spill = necrotic fatty core.
Smooth muscle migrates to intima layer to form a fibrous cap. NOW INTERMEDIATE LESION W CAP FORMING.
6.This either stabalises (inflammation stops) or continues to be resorbed/ deposited & at risk of rupture (if inflammatory reponse continues). FIBROUS CAP/ ADVANCED ATHEROMA - this is the stage you will see patients - prone to rupture stage.

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34
Q

How is a plaque most likely to rupture

A

Deposition (bc of inflammatory response being continuously triggered) or hemorrhage

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35
Q

Summarise the stages of atherosclerosis

A 
Fatty streak (think layer of inflammatory cells, macrophage &amp; fat in intima)
Intermediate lesion (some smooth muscle recruited to intima)
Advanced atheroma (prone to rupture) - large necrotic core with fiberous cap - stage where you see patients
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36
Q

Outline the treatment for atherosclerotic plaques

A

SECONDARY PREVETION
Surgical: If detected at advanced stage & caused an acute coronary event, stroke or peripheral vascular disease = PIC (percutaneous coronary intervention) +/- stent, with anti-thombus drug on stent.
Pharmacological = statin
PRIMARY PREVENTION
Patient at risk, eg over 55 years, QRISK score 20% heart disease in next 10 years = statin.

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37
Q

What blood pressure is indicative of hypertension

A

140/90 - clinic

135/85 - home

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38
Q

What is the normal length of an R wave on ECG - at what length would you interpret hypertrophy on an ECG

A

Under 11-13 mm
In exceeds this - hypertrophy
(or hyperkalemia?)

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39
Q

What is the mechanism of Digoxin

A

Na+/K+ pump inhibitor
= Increase Na+ in cell
Na+/Ca2+ pump becomes inactive (bc no gradient driving Na+ into cell)
=Increase in Ca2+ in cell
This, = more ions in cell = more binding of troponin C = force of contraction

T/F digoxin is Positive Inotrope, bc contractility increased
Also increased parasympathic to heart - Ach - so negative chronotrope

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40
Q

What is heart conditions is Digoxin indicated for

A 
Heart failure - bc decreases heart rate and increases contractility 
Arrhythmias - ↓ AV nodal conduction
(parasympathomimetic effect)
↓ ventricular rate in atrial flutter
and fibrillation
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41
Q

What type of calcium channels do CCB inhibit

A

L type - long Ca2+ voltage dependent channels - the ones that control Ca2+ sustaining contraction

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42
Q

What should verapamil not be used for and why

A

Heart failure

Because it is a negative inotrop - decreases contractility so may make HF worse

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43
Q

How do amlodipine and verapamil differe pharmacologically

A

Both target L type Ca2+ channels
Amlodipine targets them at rest = tonic vasodilation - smooth muscle
Verapamil targets during contraction = negative inotrope (contractility) - decreases work of the myocardium - acts on heart muscle more than smooth muscle

44
Q

What additional property of propranolol means it is used to treat arrhythmia after heart attack

A

Sodium channel block

45
Q

What transporter does furosemide block in the LoH to treat HF

A

NKCC2

Na+/K+/ 2Cl transporter

46
Q

What is the mechanism of nitrates in treating angina

A

venodilation - reduce preload

47
Q

What is the mechanism of CCB in treating angina

A

arteriodilator - reduce afterload of heart

48
Q

List two second line anti-anginals and their mechanisms

A

Nicorandil - mixed venous and artery dilation

Ivabridine - block F type Na+ to lower HR (pacemaker currents) -ve chronotrope

49
Q

What is the action of atenolol

A

Peripheral beta blocker

50
Q

What is the action of doxazosin

A

Alpha-1 adrenoreceptor blocker - blood vessels
Indicated in hypertension
Can be used during pregnancy

51
Q

Which antihypertensive is most likely to cause postural hypotension

A

CCBs

52
Q

Which anginal drug causes tolerance

A

Nitrates

53
Q

What is the mechanism of action for BB in HF

A

Blocking reflex sympathetic (NA) input to heart

54
Q

What are the complications of IHD (atherosclerosis)

A

Angina, Myocardial Infarction, Heart failure

55
Q

Cardiac causes of syncope

A 
Ventricular tachycardia (very fast HR)
Complete heart block (very slow HR)
Both = unable to maintain cardiac output

Disruption to ventricular outflow
Aortic stenosis
Hypertropic cardiomyopathy

56
Q

Symptoms of HF

A

Tiredness, lethargy - due to poor perfusion
SOB
Odema
PND - paroxysmal nocturnal dyspnoea

57
Q

Signs of heart failure on an x ray

A 
A - alveolar odema 
B - Kerley B line
C - cardiomegaly 
D - distension of pulmonary vessels
E - pleural effusion
58
Q

How do you calculate HR off an ECG

A

Count the number of ‘big’ square (5mm = 0.2 sec) between the R waves and divide the number by 300

59
Q

How can you identify normal, right and left heart axis

A

Normal:
I R wave positive
II R wave positive
III R wave 1/2 and 1/2

Right:
I R wave negative
II R wave positive
III R wave positive

Left:
I R wave positive
II R wave negative
III R wave negative

60
Q

Signs of arrhythmia

A

Chest pain
Hypotension
Impaired consciousness
Pulmonary oedema

61
Q

What is sinus bradycardia

A

Low HR - below 60 beats per minute

62
Q

List the different types of sinus bradycardia and the causes

A
  1. Athletes
  2. Drugs - beta blocks, digoxin, antiarrhythmic drugs
  3. Intrinsic problems of the heart: MI/ infarction to the SA-node; fibrosis of the SA node
  4. Sinus sick syndrome - when your heart intermittently drops one or two beats (2s). On ECG, see bradycardia, that intermittently drops out. P waves lost for 2s = 10 big squares)
63
Q

What are the complications of sinus node dysfunction

A

Thromboembolism - blood flow slows down - clot forms and travels into systemic circulation

64
Q

What are neural causes of sinus bradycardia

A

Vasovagal - fainting and bradycardia

Carotid sinus syndrome

65
Q

What is the immediate and longer term treatment for sinus arrthymias

A

Atropine (adrenaline) IV from 500 micrograms to 3mg - contraindicated in myasthenia gravis
Pace maker

66
Q

What are the common causes of heart block

A

Coronary artery disease
Cardiomyopathy (elderly)
Fibrosis of conducting system (elderly)

AV or BoH –> Atrioventricular block
Lower than BoH –> Bundle branch block

67
Q

What are the different types of AV block

A

1st - long PR interval - AV node conduction is slow
2nd - i) increasing PR interval, p wave drops out, cycle starts again - AV node problem
ii) PR interval normal - p waves drop out 2:1 P to QRS - think BoH level
3rd - complete heart block. p and QRS independent. Thin QRS = problem in BoH, Wide = purkinje

68
Q

Type of Bundle branch block

A

RBBB - MaRRoW V2 - V6
LBBB - WiLLiaM V2 - V6

Decribe the patter as ‘deep slurred S waves’ on ECG in eg V5, V6 leads

69
Q

How would you identify AV block from an ECG

A

Look at relationship between p and QRS - does P always come before QRS, if so, is it prolonged, changing/ constant?
Do QRS drop out?
Are they completely separate?

70
Q

What is the most common arrhythmia

A

Atrial fibrillation

71
Q

How long does Atrial fibrillation last

A

No more than 7 days

72
Q

What are the complications of atrial fibrillation

A

Stroke - thromboembolus clot (or MI, or PVD)

Acute heart failure - bc of inadequate cardiac output from ventricles

73
Q

What are the symptoms of atrial fibrillation

A 
May be asymptomatic
Palpitations
Fatigue - if cardiac output is affected
Acute HF signs if progressed to this
SOB
74
Q

How does atrial fibrillation look on ECG

A

Regularly irregular - no clear p waves

75
Q

Describe the pathology of atrial fibrillation

A

Damage to the atrial myocardium = generation of ectopic beats, happens through:
Change in ion channels (eg post MI; or ischemia)
Change in Ca2+ regulation (as above)
Structural change (eg hypertrophy - hypertension, CAD ischemia etc)
Neural dysregulation - eg fibrosis of conducting tissue - age, hypertension, ischemia, hypertrophy

76
Q

List some of the causes of structural remodelling of the heart

A

Aging, hypertension, valve disease, heart failure, myocardial infarction, obesity, smoking, diabetes mellitus, thyroid dysfunction, and endurance exercise training all cause structural remodeling

77
Q

When would digoxin be indicated as rate control over a beta blocker

A

Patient with asthma

Patient that is sedentary

78
Q

What is the mechanism of action of amioderone - how does it act as a rate control medication

A

Its a K+ channel inhibitor
Slows down the movement of K+ out of the cell as a part of repolarisation of membrane potential
Takes longer for cell to repolarise

79
Q

Outline the treatment of Atrial fibrillation

A
  1. are they haemodynamically stable? If no - start heparin
  2. If stable:
    - Rate control - BB
    - Rhythm control - convert to sinus rhythm by electrical CD cardioconversion then rate control

Can do add on rate control with CCB, K+ inhibitors, depending on underlying heart condition

80
Q

In which cardiac condition should negative inotropes not be used

A

Heart failure

BB are - but this is bc of their negative chronotrope effects

81
Q

What assessment should always be done on a patient who had atrial fibrillation

A

Assessment for anticoagulation

82
Q

How is atrial flutter treated

A

Most cases can be treated with radiofrequency catheter ablation of the re-entry circuit
+ Rate control with BB

83
Q

Summarise cardiac medicine - what are the general groups

A
  1. Those that target the HEART:
    Chronotropes - rate (BB, Digoxin)
    Inotropes - contractility (CCB, Amioderone, Digoxin, Na+ blockers)
    2.Those that target TOTAL PERIPHERAL RESISTANCE
    ACE inhibitors
    CCBs
    Diuretics
84
Q

Causes of infective endocarditis

A

abnormal valve
regurgitant or prosthetic valves are most likely to get infected.
Introduction of infectious material into the blood stream or directly onto the heart during surgery
Have had IE previously

85
Q

IE presents with what 3 things

A

Fever + additional infection signs
Murmur - new, or worse
Emboli signs - splinter haemorrhages, Janeway’s lesions etc

86
Q

What imaging would you do for IE

A 
Transthoracic echo
Transoesophageal echo (better sensitivity than first but unpleasant for patient)
87
Q

Peripheral signs of IE - but remember not that common

A

Petechiae 10 to 15%,
Splinter hemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
Roth spots on fundoscopy.

88
Q

What ECG changes might you see with IE

A

Prolonged PR interval
AV block

bc of anatomical relation of aorta abscess to AV node.

89
Q

What is the best imagine test for confirming IE

A

TOE

90
Q

Treatment of fungal IE

A

Amphotericin

91
Q

Antibiotics for IE

A

Think - gentamicin
Prosthetic valcue - gentamicin + rifampicin, + either vancomycin or flucloxicillin (if staph confirmed)

Native valve - gentimicin, fluclox, ampicillin, or when confirmed for stap - just fluclox

92
Q

Diagnosis for IE

A

2 Major
1 major + 3 minor
5 minor

93
Q

Describe the diagnostic criteria for IE

A

MAJOR

  • 2 positive cultures of typical pathogen
  • 3 or 4 positive cultures of atypical pathogen >12 hours
  • Single positive for coxiella burnetti

MINOR

  • Prosthetic valve
  • > 38
  • Vascular signs - haemorrhages, janeway’s lesions etc
  • Immunological signs - olser’s nodes, glomerulonephritis
  • +ve blood cultures that dont meet criteria above
94
Q

Investigations for IE

A 
Blood cultures: 3 sets (6 bottles), from different sites at different times
FBC - normocytic anaemia
neutophillia
CRP/ ESR
Rheumatoid factor
Serology - viruses

Urinalysis - haematuria

ECHO - TOE, or TTE if can’t tolerate but may not be able to see anything is smaller than 2 mm
Can do CT if needed

CXR

Regular ECG

95
Q

Signs and symptoms of IE

A

Infection signs - fever, malaise, rigor, weight loss etc
Cardiac signs - murmur, breathless, chest pain
Emboli signs - vasculature, micro haematuria
Immunological signs - osler’s nodes

96
Q

Risk factors for IE

A

Prosthetic valve - strep viridens
Prolapsed valve - strep viridens
IV drug user - R side of heart - risk of septic PE - staph a
Hickmen line/ long time - anyone in hospital - fungal
Catheters - enterococci

97
Q

What is a bifid p wave - what pathology does it show

A

‘m’ shaped p wave - shows left atrial hypertrophy P mitrale
Peaked p wave - right atrial hypertrophy - P pulmonale
biphasic is where it goes up and down - also sign of left atrial pressure/ hypertropy

98
Q

Changes to the PR interval indicate what conditions/ pathology

A

WPW syndrome - short PR, delta wave

Long = AV block - 1st?

99
Q

What differentiates between type I and II 2nd degree heart block

A

PR interval
Type I = prolonging PR until resets
Type II = no change in PR

100
Q

What are the signs of left ventricular hypertrophy on ECG

A

VI - S
V5,6 - R

If >35 mm = hypertrophy

101
Q

How would you differentiate between supraventricular and ventricular tachycardia from an ECG

A

Supra - QRS usually normal (unless causing BBB)

Ventricular - wide based QRS

102
Q

Inherited LV hypertrophy

A 
Hypertrophic cardiomyopathy (HCM - SARCOMERE PROTEIN
1 in 500
103
Q

Symptoms of HCM

A

HCM may cause angina, dyspnoea, palpitations, dizzy spells or syncope

104
Q

Dilated cardiomyopathy

A 
Dilated cardiomyopathy (DCM) – often caused by cytoskeletal gene 
*Presents with HF
DCM  - LV/RV or 4 chamber dilatation and dysfunction
105
Q

Arrhythmogenic

A

Arrhythmogenic cardiomyopathy (ARVC/ALVC) – desmosome gene mutations

106
Q

Inherited channelopathies

A 
Inherited arrhythmia (channelopathy) caused by ion channel protein gene mutations
These usually relate to potassium, sodium or calcium channels
Channelopathies include long QT, short QT, Brugada and CPVT
*Have structurally normal heart*

Present with syncope

107
Q

Inheritance pattern of ICCs

A

Dominant

Phase 2 (12 decks)

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