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CC2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define Thrombosis

A
  • Exaggeration of normal haemostatic mechanisms that lead to
  • formation of a solid mass within
  • the circulating vascular system during life
  • made from the blood constituents
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2
Q

Predisposing factors for thrombosis (3)

A

NB stasis -> turbulence

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3
Q

Mechanism of thrombus formation

A
  1. Stasis -> turbulence -> vessel wall damage
  2. Platelets recruited -> adhere, aggregate+ secrete factors to -> coagulation
  3. Vascular endothelium controls platelets + coagulation (protect blood)
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4
Q

Features of arterial/cardiac thrombi

A
  1. Mainly platelets = pale
  2. Mural or occlusive depending on vessel size
  3. Lines of Zahn
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5
Q

Features of venous thrombi

A
  1. Mainly blood clot = red
  2. Usually occlusive
  3. Lines of Zahn
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6
Q

Lines of Zahn

A

Light lamination layers - platelet + fibrin

Dark layers - blood

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7
Q

3 locations for cardiac thrombi and precipitating factors

A
  1. Atria - appendanges
    a) HF = stasis
    b) AF = stasis
  2. Valves -> vegetation
    a) Rheumatic fever
    b) Infective endocarditis
    c) Thrombotic endocarditis (Nonbac eg malignancy, SLE)
  3. Ventricles -> mural
    a) MI = stasis
    b) Cardiomyopathy = stasis
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8
Q

3 precipitating causes of ARTERIAL thrombi

A
  1. atherosclerosis -> ruptutre -> mural thrombus = wall
  2. aneurysms = stasis
  3. inflammation, vasculitis
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9
Q

Precipitating causes of VENOUS thrombosis

A
  1. trauma
  2. post op (muscle relax, breath pain)
  3. immobility
  4. MI
  5. HF
  6. pelvic mass inc pregnancy
  7. thrombophlebitis(rare)
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10
Q

Natural clot resolution sequence

A
  1. Resolution = fibrinolysis within clot
  2. Organisation = ingrowth of granulation tissue (fibroblasts->collagen, phagocytes, capillaries)
  3. Recanalisation = restore lumen, organised thrombus
  4. Fibrosis to reconstruct
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11
Q

Main complication of arterial thrombus

A

ischaemia/infarction

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12
Q

Main complication of venous thrombosis

A

Embolism

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13
Q

Define embolism

A
  • Passage of an insoluble mass
  • within the blood stream
    • impaction at a site distant from origin
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14
Q

Commonest places of emboli impaction and origin

A
  1. Pulmonary arteries when thrombus is R side of heart
  2. Systemic arteries when thrombus is from Lheart/aorta
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15
Q

Define ischaemia

A
  • reduced blood supply to tissue/organ
  • leading to harm effects due to hypoxia
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16
Q

3 mechanisms of ischaemia. think pipe

A
  1. Internal vessel disease
  2. Occlusion bc thrombus/emboli
  3. External compression of vessel
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17
Q

Define infarction

A
  • Tissue death due to ischaemia
  • usually caused by arterial occlusion
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18
Q

Clinical complications of PE

A
  1. Sudden death
  2. Pulmonary infarction
  3. Pulmonary hypertension
  4. Asmptomatic
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19
Q

Coronary artery network

A

LAD = apex, ant LV, ant IVS

LC = lat LV

RA = post inf LV, post IVS, RV

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20
Q

2 main types of MI

A

1.Transmural (majority)

  • full wall thickness infarct
  • usually bc main CA for that area occluded (atherosclerosis)
  • sometimes caused by vasopasm/emboli
  • see ST elevation + Q waves (STEMI)

2.Subendocondrial

  • involves diffuse infarction, least perfused region
  • usually due to critical stenosis, without plaque change event (eg triple vessle atheroma)
  • see ST depression (NSTEMI)
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21
Q

What is haemopericardium and when does it usually develop

A

Rupture of LV wall post MI

4-10 days

consider in MI pxs who are having HF symptoms

NB myocardial rupture on free wall -> tamponade

septum -> shunt

pap muscle -> acute severe MR

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22
Q

What is a late >3 month complication of MI due to fibrosis of wall

A

Cardiac aneurysm

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23
Q

Define Gangrene

A

Necrosis

w bacterial infection

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24
Q

Rare things that can be emboli

A
  1. Fat
  2. Air/gas
  3. Tumour
  4. Amniotic fluid
  5. Infective material
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25
Q

Layers of arterial wall

A

Intima - thin, where atherosclerotic plaque lesions occur

Media- full of smooth muscle or elastic

Adventitia - blood supply to artery itself

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26
Q

Constituents of atherosclerotic plaque

A

Fibrous cap

Lipid core

CT, ECM

smooth muscle and inflamm cells

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27
Q

clinical consequences of atherosclerosis

A
  1. stroke
  2. Mi, CHD, sudden death
  3. AAA
  4. Gut ischaemia
  5. Gangrene of leg
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28
Q

Modifiable and non modifiable RF for atherosclerosis

A

Non modifiable:

  1. Age
  2. male
  3. FH
  4. Genetics

Modifiable:

  1. Hyperlipidaemia
  2. Hypertension
  3. Smoking
  4. Diabetes

NOT exercise

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29
Q

Response to injury hypothesis

A

Continuous endothelial damage -> inflammation -> plaque formation

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30
Q

Precipitating factors of ischaemic heart disease

A
  1. Atherosclerosis (majority)
  2. Hypertrophy, inc demand
  3. Inc HR, inc demand
  4. Hypotension, dec supply
  5. Hypoxoemia
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31
Q

MI vs Angina

A

Angina = episodic ischaemia -> pain

MI = prolonged ischaemia -> myocyte necrosis

= raised CrK, Trop

both rise within 4-8 hours of MI

Crk stays for 3 days

trop 10

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32
Q

Define critical stensosis

A

Atleast 75% cross sectional area of vessel occluded

compensatory vasodilation is insufficient to meet demand

NB less than this w unstable plaque, don’t produce angina but dangerous bc no pre-conditioning

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33
Q

Explain the terms:

  1. Reperfusion Injury
  2. Stunned myocardium
  3. Pre-conditioning

in the context of MI

A
  1. Ischaemic tissue gets ox for 1st time = free radical release = 2nd hit
  2. Saved ischaemic myocytes takes days to recover function
  3. Rep’d ischaemic hits may prepare tissue to protect from infarction eg via bv formation
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34
Q

Complications post-MI

A
  1. Cardiogenic shock (pump failure)
  2. Arrhythmias -> sudden death
  3. Late heart failure

4. post infarct unstable angina

  1. Cardiac rupture (MR, tamponade)
  2. Pericarditis
  3. Mural thrombus over scarred infarct
  4. Ventricular aneurysm
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35
Q

Body’s natural compensatory mechanisms for HF

A
  1. Hypertrophy SIZE.
  2. Dilation to inc preload
  3. Fluid retention -> inc BP + HR -> CO

NB hypertensive hypertrophy -> AF bc inc stiffness -> atrial load inc

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36
Q

LHF

A
  1. organ ischaemia
  2. pulmonary oedema
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37
Q

RHF

A
  1. Peripheral oedema
  2. congestion of organs
  3. ascites/ PE

usually secondary to LHF

Cor pulmonale is RHF due to pulmonary hypertension

Cor pulmonale can be acute - straight dilation eg due to PE (LHF cant)

or chronic = hypertrophy -> dilation

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38
Q

Define Valve Stenosis

A

Failure of valve to open comletely

impedes forward blood flow

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39
Q

Define Valve Regurg/Incompetence + functional regurg

A

Failure of valve to close completely

due to valve OR environmental abnormality

leads to backward flow

functional regurg - due to ventricle dilation

can be acute OR chronic

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40
Q

Which valve is normally bicuspid

A

Mitral

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41
Q

Causes and consequences of mitral stenosis

A
  1. RHEUMATIC FEVER (99%)

minority congenital

Consequences:

  1. Inc atrial pressure -> dilatation -> AF -> thromboemboli
  2. inc atrial pressure -> pul hypertension -> oedema
  3. Pul hypertension -> RH dilation + failure
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42
Q

What is rheumatic fever and relevance in cardio

A

Systemic inflammatory disease caused by group A strep infection

usually few weeks after throat infection

multiple infections = cumulative damage = chronic rheumatic heart disease :

  • Mitral stenosis (fish mouth, button hole sten)
  • Pancarditis
    *
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43
Q

symptoms of mitral stenosis

A
  • Exertional dyspnoea
  • Fatigue
  • Haemoptysis
  • Emboli - stroke, PE, cyanosed face
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44
Q

Signs of mitral stenosis

A

AF

Raised JVP

Malar flush (low CO)

Others - palpable + loud S1 (snap)

RV heave + loud P2 bc pul hypertension

rumbling diastolic

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45
Q
A

Malar Flush

Indicitave of mitral stenosis because of Co2 retention

NB more commonly because of rosacea, SLE, COPD

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46
Q
A

Mitral Stenosis

Mid diastolic murmur

Rumbling

slight click after s2 (opening) before wooshing sound

NB can have presystolic murmur if sinus rhythm

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47
Q
A

Mitral Stenosis

Descending, ascending

Mid diastolic murmur, rumbling

loud S1, open snap

ACCENTUATE IT

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48
Q

Causes of Mitral Regurg (4,4)

A

PRIMARY (degen) : 1. Valve prolapse ( may be congenital)

  1. Rheumatic heart disease
  2. Infective endocarditis
  3. Collagen diseases

SECONDARY(func): IHD or cardiomyopathy

  1. Papillary/chordae rupture
  2. Papillary muscle dysfunction (post MI)
  3. functional = LV dilation due to HF
  4. Dilated cardiomyopathy
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49
Q

ACUTE MR presentation

A

No time for LV dilation to compensate so LA pressure inc -> pulmonary hypertension + oedema

SOB

Fatigue

RHF signs

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50
Q

CHRONIC MR presentation

A

Same as acute (SOB, fatigue)

+ palpitatons (dilation)

LHF

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51
Q

http://www.3m.com/healthcare/littmann/sn124.html

A

MR

Pan systolic

soft S1

Loudest at apex, radiates to axilla

accentuate by expiration, NOT move

may hear S3 w bell, lower pitch than S2

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52
Q

Signs of MR

A

Displaced apex beat, thrusting

if get LVF -> S3 sound

if get pul hypertension -> RV heave and loud S2

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53
Q

INV for MR

A

Transthoracic echo

ECG

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54
Q

Medical + surgical management of MR

A

IF LVF -> diuretics and ACEI

IF AF -> anti-coag + digoxin

treat any systemic hypertension and prophylaxis for infective endocarditis. Observe

Surgical

  • valve replacement prosthetic or bioprosthesis (donate or animal)
  • valve repair/ring
  • mitraclip
  • issue: emboli (anticoag), deterioration, infective endocarditis
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55
Q

Causes of AS

A
  1. Calcification (most common, elderly > 70)
  2. Calcification of congenital bicuspid valve (middle age)
  3. Rheumatic heart disease
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56
Q

Presentation of AS

A
  1. Angina
  2. Breathlessness/HF (LVH on ecg)
  3. Collapse/syncope
  4. Death

ABCD

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57
Q

Signs of AS

A
  1. Slow rising carotid pulse
  2. Thrusting apex beat
  3. Soft/absent S2
  4. May have LVF (S3), LVHeave
  5. PP small
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58
Q
A

AS

Ejection Systolic murmur

loud S1

soft/absent S2

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59
Q
A

Early AS
Ejection systolic

soft S2

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60
Q

Causes of aortic regurgitation

A

ACUTE:

  1. Infective endocarditis
  2. Aortic dissection (usually due to aortic root dilation)

CHRONIC:

  1. Rheumatic fever
  2. Congenital bicuspid aortic valve
  3. Other eg syphylis, hypertension, CT disorder (lead to dilation of aortic root)
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61
Q

Presentation of AR

A
  1. SOB (sudden if acute cause)
  2. LVF signs
  3. Fatigue, chronic
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62
Q

http://www.3m.com/healthcare/littmann/sn124.html

A

AR

End diastolic murmur

flat woosh after S2

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63
Q

Signs of AR

A

Collapsing pulse

Wide PP

displaced apex

Quinke

Head nodding (de mussets)

Visible carotid pulsation (corrigan’s)

64
Q

Layers of heart

A
65
Q

Define infective endocarditis and complications

A

Usually bacterial infection of endocardium of heart

can be acutem (on normal valve) or chronic (on congenital or acquired valve defect)

Usually -> bulky, friable, mitral/aortic valve (L sided) -> L sided thromboemboli, kidney

IF IV drug user -> tricuspid (R sided-> PE

emboli may be septic

can lead to myocardial abscess

valve rupture

circulating immune complexes -> golemrular nephritis

66
Q

Risk factors for infective endocarditis

A
  1. Abnormal valve
  2. IV drug abuse
  3. Immunosuppresion
  4. DM
  5. Alcohol
67
Q

Symptoms and signs of infective endocarditis

A
  1. Systemic features of infection: fever, sweats, acheetc
  2. Murmurs and heart failure signs
  3. Immune complex deposits -> vasculitis:

Skin petechial haemorrhages

Oslers nodes (finger tender)

Janeway lesions (painless palm)

Splinter haemorrhages (nails)

68
Q

Organisms and their virulence for infective endocarditis

A
69
Q

Non- bacterial thrombotic endocarditis define, clinical relevance and risk

A

deposition of small sterile, fibrin/platelet thrombi on any normal heart valve

does NOT destroy the heart valve but can -> emboli

WHY: hypercoaguable state:

  • pregnancy
  • cancer
  • DIC
70
Q

Define Myocarditis and causes

A

inflammatory process of myocardium -> cardiac myocyte injury

usually caused by viral infection

can be caused by immune response:

  • post infection
  • rheumatic
  • SLE
  • drug sensitivity
  • transplant

OR unknown cause : sarcoidosis

71
Q

Complications of myocarditis

A
  1. Asymptomatic -> dilated cardiomyopathy later
  2. Arrythmias
  3. Acute HF (present w this + fever)
  4. sudden death
72
Q

Define pericarditis and causes

A

inflammation of pericardium typically post viral infection or MI

other causes:

cardiac, thoracic, systemic, mets

73
Q

Pericarditis symptoms and signs

A
  1. sharp, pleuritic chest pain, relieved when sit forward

NB pain can mimic MI in being dull and radiating to shoulder and back

also get ST elevation but its in ALL leads

  1. May have fever

SIGNS:

  1. pericardial rub because fibrosed layers
74
Q

Pericardial rub

A
75
Q

What is Erb’s point

A

3rd ICS MCL

loudest S2

76
Q

What is cardiomyopathy and the 3 types

A

Cardiomyopathyis heart disease resulting from primary abnormality in myocardial tissue.

  1. dilated (90%)

2. hypertrophic

3. restrictive

77
Q

Dilated cardiomyopathy characteristics

A
  1. Hypertrophy
  2. Dilation
  3. Cardiac dysfunction -> (arrythmias + thromboembolism + HF)
78
Q

Causes of dilated cardiomyopathy

A
  1. Idiopathic mostly ( can be in young people)
  2. alcohol
  3. peripartum - pregnancy reveals it about 5 months before
  4. Genetic
  5. Myocarditis
  6. Haemochromotosis
  7. chronic anaemia
  8. drugs - doxorubicin, adriamycin
  9. Sarcoidosis
79
Q

Characteristics of hypertrophic cardiomyopathy

A
  1. Hypertrophed myocardium (may inc septum) -> angina, AF, HF
  2. Impaired ventricle filling
  3. Obstruction to outflow

NB there is NO ventricle dilation

can lead to ventricular arrhythmia -> sudden death

80
Q

Causes of hypertrophic cardiomyopathy

A
  1. Genetic (50%)

4 contraction genes can have many mutate (aut dominant):

  • cardiac troponin T
  • B myosin heavy chain
  • A tropo-myosin
  • Myosin binding C protein
  1. Sporadic (50%)
81
Q

What is restrictive cardiomyopathy

A

Primary impairment of ventricular compliance -> impaired ventricular filling

so have normal sized atria and ventricles, both atria dilated but actual myocardium is firm

82
Q

Causes of restrictive cardiomyopathy

A
  1. Idiopathic
  2. Fibrosis secondary to radiotherapy (cancer)
  3. Tumour mets
  4. Amyloidosis (deposition of protein)
  5. Sarcoidosis
  6. Endomyocardial fibrosis and fibroelasticosis (tropical, young)
  7. Congenital
83
Q

Most common type of heart tumour + location

A
  1. L atrial myxoma -> mitral valve damage

most common primary heart tumour, but still rare

84
Q

3 main categories of congenital heart disease

A
  1. L->R shunt (abnormal connection, flow from high -> low P)
  2. R-> L shunt
  3. Obstructive
85
Q

CONGENITAL : R-> L shunts = T’s

A

= de-ox blood in systemic circulation -> CYANOTIC CONGENITAL HEART DISEASE

  1. Tetralogy of fallot
  2. Transposition of great arteries
  3. Persistent truncus arteriosus
  4. Tricuspid atresia
  5. Total anomalous pulmonary venous connection
86
Q

L->R = D’s

A

systemic -> pulm = inc flow -> pul hypertension

TYPES:

  1. ASD
  2. VSD = congenital, most common
  3. PDA (patent ductus arteriosus)
  4. AV septal defect

over time the pul P> systemic = reversal of flow = R-> L shunt

Eisenmenghers syndrome = late cyanosis

87
Q

CONGENITAL : Obstructive

A

Abnormal narrowing of chambers, valves or vessels

usually congenital coarctation of aorta

88
Q

Define hypertension

Stages of hypertension + limits

A

Persistently raised arterial BP

Stage 1- 140/90

Stage 2- 160/100

Stage 3- 180/110

89
Q

BP drugs

A

Under 55: ACEi/ARB

55+ or Afro-carribean: CCB or D

stage 2 treatment: A+C

stage 3 : A+C+D

stage 4 (resistant): ACD + D + alpha/beta blocker

NB may need to give statins, antiplatelts etc to reduce CV risk if high

90
Q

How ACEi work and why not useful in afro/carrib

A
  1. Inhibits conversion of angiotensin 1->2
  2. Black ppl have low plasma renin
91
Q

ACEi indication, examples, SE, contraindications

A
  1. First line antihypertensive in non black under 55. ALSO in CKD, HF, post MI
  2. -pril eg ramipril, preinidopril, lisinopril, enalapril
  3. SE
  • dry cough (ACE mediated break down of bradykinin in lungs is inhibited)
  • hypotension with first dose
  • AKI reversible
  • hyperkalaemia
  • normal cr release
  • angiodema - lip and airway

CONTRAINDICATION: pregnancy, breastfeeding, bilateral RAS

92
Q

ARBs mechanism, indication, example, SE, contraindication

A

Inhibit the receptor of angiotensin 2 (AT1)

Indication: Alternative 1st line antihypertensive non black, CKD, HF, post MI

Example: - sartan, candesartan ,losartan, valsartan, irbesartan

SE: similar to ACEi other than cough ( rare)

CI: same as ACEi

NB dont use with ACEi = > risk of AKI

93
Q

CCB two types

A
  1. Dihydropyridines = preferential action on vascular smooth muscle
    - dipine
  2. Non-dihydropyridines = act on heart and vascularture (rate limiting)
94
Q

CCB: Dihydropyridine indication, mechanism, examples, SE, contraindications

A

Indications: First line antihypertensive in obver 55/afrocar. ALSO raynauds, angina

Mechanism: block L type calcium channels to block vasoconstriction, vasoselective so not rate limit

Examples: amlodipine, filodipine, nifedipine (short acting)

SE: ankle swelling, acid reflux, flushing, gingival hyperplasia

95
Q

CCB: Non-dihydropyridines mechanism, indication, example, SE, contraindication

A

Rate limiting CCB (heart and vasculature Ca2+ block)

Indication: can use in hypertension but also: tachy’s, angina, migraine + cluster headaches

Example: Verapamil(cardioselective), Diltiazem (heart + bv)

SE: worsens HF, cause bradychardia, heart block

verapamil = constipation

dont use in HF or px on beta blockers

96
Q

Thiazide like diuretics mechanism, examples + SE

A

Block Na/Cl channel on DCT -> Na + water loss

Examples: indapimide, chlortalidone. og thiazides -> dm

SE: gout, erectile dysfunction,electrolyte disturbance,impaired glucose tolerance, hypercalcaemia (dont give in px with hyperparathyroidism)

97
Q

Loop diuretics mechanism of action, examples, se

A

Block Na+K+CL- channel on ascending limb of LoH = block water and na reabsorption

indication: hypertension but longer diuretic than antihypertensive

other indications: pulmonary oedema,HF,nephrotic syndrome, ascites

Examples: furosemide, bumetanide

SE: elecrolyte disturbance, polyuria, dehydration

98
Q

Potassium sparing diuretics AA mechanism, examples, SE, other indications

A

Aldosterone antagonists - block aldosterone mediated Na absoprtion and K+ excretion in CD eg spironolactone

eplerenone - primary aldosteronism or post MI

low dose in hypertension

SE: gynaecomastea, erectile dysfunction, hyperkalaemia

Other indications: HF, ascites

99
Q

Potassium sparing diuretics NOT AA mechanism, examples, Se

A

Blocks epithelial Na+ channels and K+ excretion in CD, not via aldosterone

Eg. amiloride , triamterene

Indication: in combo with stronger diuretic eg furosemide

SE: hyperkalaemia

100
Q

Alpha blockers mechanism of action, indications, examples, side effects

A

blocks alpha adrenoreceptor mediated vasoconstriction -> vasodilation

Indication: men w BPH (tamsulosin), add on to other treatments

End in -zosin eg doxazosin, terazosin, prazosin

101
Q

Beta blockers mechanism and selectivity examples

A

B1 = HR inc + force

B2 = smooth muscle dilation (vaso, broncho, muscle)

Beta blockers refer to beta 1

MOA: reduce HR and renin release

-olol

Cardioselective BAMN: bisoprolol, atenolol, metoprolol, nebivolol

Non selective : propranolol for anxiety etc

102
Q

Beta blockers indications, adverse effects, CI

A

Indications: HF, IHD, arrhythmias, anxiety, migraine, oesophageal varices, glaucoma, thyrotoxicosis, essential tremor

SE: Bradycardia, tiredness, bronchoconstriction, cold extremities, depression, hypoglycaemia(may be masked) + depression

CI: absolute in asthma

relative in acute HF, peripheral arterial disease

103
Q

Direct renin inhibitor MOA, Eg, SE

A

Renin secreted by juxtaglomerular cells to convert angiotensin 1->2

eg Aliskiren but limited clinical use

SE: diorrhoea, AKI

104
Q

Postural hypotension - define and causes

A

Drop in SBP of >=20, diastolic >=10 from sitting to standing

Causes:

  • drugs (doxazosin/a blockers)
  • adrenal insufficiency
  • DM
  • alcohol
  • PD
105
Q

Management of postural hypotension

A
  1. fludrocortisone
  2. Midrodine (alpha agonist, opp of doxazosine)
  3. droxydopa

nb can -> hypertension

106
Q

Define HF and 2 types

A

CO inadequate to perfuse organs

  1. HF w reduced LVEF: systolic HF
  2. HF w preserved LVEF: diastolic HF
107
Q

Management of systolic heart failure

A
  • ACEi or ARB (pril or sartan to reduce preload/afterload = work, slow disease progression)
  • NB can combine with neprylisin inhibition = natriuresis -> diuresis. sacubitril-valsartan
  • Aldosterone antagonist (spironolactone, epleronone to reduce mortality)
  • B blocker (olol, reduce HR/work = long term survival)
  • Diuretic (thiazide or loop=reduce preload, doesn’t reduce mortality)
  • Digoxin (if HF caused by AF, inc force of contraction)
  • Ivabridine (if B blocker not tolerated)
  • Hydralazine w nitrate = dilate
108
Q

Diastolic HF

A

Usually cuased by hypertension so control bp

symptomatic treatment

no evidence of systolic treatment reducing mortality here

109
Q

Sinus bradycardia define, causes + treat

A

Regular heart beat, reduced rate.

ECG normal P-P increased

Causes:

  • Young healthy, athletes (physiological)
  • Increased vagal tone (psymp = slows)
  • Hypoxia, hypothermia
  • Drugs - beta blockers, calcium channel blockers
  • post Mi ISCHAEMIA
  • Sick sinus syndrome

Treat symptomatic: Atropine, block vagal tone

110
Q

Heart Block define, types and describe ECG

A

Impaired A->V conduction

  1. First degree - dont treat

heart rate consistent (P-P), P-QRS delay (>0.2)

2. Second degree

  • Mobitz type 1 - P-P gets bigger until QRS drops
  • Mobitz type 2- P-P stays same, random QRS drop

3. Complete heart block - AV node sets pace

30-55bpm

111
Q

RBBB

A
112
Q

LBBB

A
113
Q

Atrial tachy

A
114
Q

Atrial flutter

A
115
Q

Atrial fibrillation

A
116
Q

Ventricular tachy

A
117
Q

Ventricular fibrilation

A
118
Q

Secondary hypertension causes

A

NB only 5% of hypertension is secondary

  1. Primary hyperaldosteronism (and other endocrine disorders)
  2. Renal disease
  3. Vascular disorders like aortic coarctation
  4. Drugs like alcohol and cocaine
119
Q

Hypertension increases your risk of:

A
  1. Stroke, haemorrhage
  2. Retinopathy
  3. CHD, LVH, HF
  4. Aortic dissection/aneurysm
  5. CKD, renal failure
  6. peripheral vascular disease

(causes atherosclerosis)

120
Q

Direct vasodilators for hypertensive emergencies

A
  1. Nitrates
  2. Hydralazine
  3. Minoxidil
  4. Sdium Nitroprusside
121
Q

Centrally acting antihypertensives

A
  1. Methyldopa
  2. Moxonidine
  3. Clonidine
122
Q

Causes of angina

A
  1. Narrowing or occlusion of major CA
  2. AS, hypertrophic cardiomyopathy, severe anaemia = angina without CAD
  3. CAD w anaemia, tachy, uncontrolled hypertension, hyperthyroidism
123
Q

Diagnosis and treatment of stable angina

A

Present: chest pain on exertion/stress, relieved onr est/by GTN, lasting a few minutes

INV: resting ECG (normal or with ST dep or Q waves), FBC (anaemia) HbA1c (DM, silent), lipid profile

Manage: lifestyle, GTN, Bblock or CCB 1st line anti-angina, prevent CV event: aspirin (antiplatelet), statins (lipid), ACEi (bp, dm)

MAY decide to revasculate

124
Q

Diagnosis and treatment of ACS (Unstable, NSTEMI, STEMI)

A

PRES: chest pain >20min at rest/new onset/inc freq/severity, radiating to jaw/neck/arm, dyspnoea

INV: ECG (normal or ST depression), Trop, CrK, FBC (anaemia precipitate), U+E (baseline), Hba1c, lipid profile, INR (baseline), CXR (rule out DDs), coronary angiography (CAD)

Manage: MONAC - morphine, oxygen, nitrates, aspirin, clopidogrel + statin + betablocker

may have reperfusion therapy

NOTE distinguish from NSTEMI by troponin- only raised with infarction not ischaemia. ie normal troponin in unstable angina.

125
Q

Treatment of STEMI

A
  1. Reperfusion - PCI may have thrombolysis (fondaparinux)
  2. MONAC
  3. Long term:
  • Beta blocker (reduce ox demand, inc diastole)
  • ACEi
  • Clopidogrel (12m) + Aspirin for life
  • Statin
  • BP control
  • Lifestyle
  • GTN prn
126
Q

What is ACS

A

Unstable angina, NSTEMI + STEMI going from ischaemia -> necrosis

Mostly caused by atherosclerosis but can have normal CA with other problems (See causes of agina flashcard)

127
Q

Reperfusion therapy for ACS

A
  1. PCI- requires angiography then angioplasty done where stent is inserted, balloon inflated
  2. CABG- where there is anatomical indication
128
Q

What is shock?

A

Clinical syndrome categorised by drop in mean arterial bp -> tissue hypoperfusion and hypoxia

BP = CO X R

CO = SV X HR

SV = EDV-ESV

129
Q

4 types of shock and eg

A
  1. Cardiogenic - pump failure eg MI
  2. Hypovolemic - reduced vol eg bleed,burn,diorrhoea
  3. Obstructive - filling or after failure eg tamponade, PE
  4. Distributive - widespread vasodilation eg sepsis, anaphylaxis

CHOD

All ead to tissue death

130
Q

Physiological compensation for shock

A
  1. Inc CO - symp stim = inc HR (SV) + vasoconstrict (R)
  2. Inc Ox - symp stim = bronchodilate, inc resp
  3. Redistribute to vital organs - vasoconstriction, ADH, renin (reduce urine)
  4. Cortisol
  5. Glucagon
  6. Complement + inflamm cascade
131
Q

Clinical signs of shock

A
  1. tachy, hypotensive
  2. inc resp rate
  3. cold, mottled skin unless septic
  4. reduced urine output
  5. reduced consciousness

Other depending on cause: fever, SOB, chest pain etc

132
Q

Management of shock

A
  • A- stabilise airway even if GCS <8
  • B- oxygen (15L non-rebreathe), position
  • C- 2 large bore (OG) cannulas, control haemorrhage, Cross match, fluid (crystalloid or colloid), Catheter
  • D- manage blood sugar, monitor GCS
  • Treat cause
  • Analgesia
133
Q

Crystalloid vs Colloid fluids and examples

A

Crystalloid = replace, maintain

  • Dextrose, Saline, Hartmanns

Colloid = haemorrhage

  • Gelofusine, hydroxyethyl starch
134
Q

Types of blood product

A
  1. Packed RBC = RBC + SAGM
  2. FFP
  3. Cryoprecipitate
  4. Platelets
135
Q

Universal blood donor and recipient

A

donor: O negative, no antigens, RHD-

recipient: AB (no antibodies)

136
Q

4 classifications of haemorrhagic blood loss

A
  1. <15%(750ml) HR may inc, no change BP
  2. 15-30%(750-1.5L), HR inc, no change bp
  3. 30-40% (1.5-2L) HR inc, BP dec
  4. 40+% (>2L) HR inc, BP inc
137
Q

Treatment of AR

A
  1. Valve repair
  2. Replace w tissue valve
    xenograft: pig
    autograft: ross kids
    homograft: autopsy
  3. TAVI
  4. Mechanical valce:

bileaflet

138
Q

Causes of AF

A

PIRATES

  1. PE
  2. IHD
  3. Resp problems
  4. Anaemia
  5. Thyroid disease
  6. Ethanol
  7. Sepsis
139
Q

Management of AF

A
  1. Haem unstable -> DC cardioversion
  2. Rate control = beta blockers, CCB diltiazem, verapamil
  3. Rhythm control - flecainide, procainamide pill in pocket or DC
  4. Anticoagulation - assess risk of stroke w AF via CHA2DS2VAS score and risk of bleeding via HAS BLED score . start on lifelong warfarin or doac
140
Q

What is CHA2DS2VAScore stand for

A

CHF
Hypertension

Age

Diabetic

Stroke history

Vascular disease

Age

Sex (female)

141
Q

ACEi

SE’s

CI

A

SE:

First dose hypotension

Dry cough

RAS (reversible AKI)

Angiodema

CI:

Bilateral RAS

Pregnancy/breastfeeding

142
Q

Can an ARB be used with ACEi

A

No, risk of severe AKI

143
Q

CCB - dihydropyridines

A

Uses: 1st line antiHTN for black + over 55. Also in raynauds, angina

preferential for vascular smooth muscle, not rate limiting

SE: ankle swelling,flushing, gingival hyperplasia, acid reflux

144
Q

CCB : non dihydropyridines

A

verapamil, diltiazem (AF) because rate controlling

SE- verapamil = constipation

SE: slow HR in HF, brady pxs = bad

145
Q

Name 2 diuretics that work in PCT , descending LoH respectively

A

PCT - acetazolamide (CA inhibitor, glaucoma)

descending LoH - mannitol (osmotic diuretic, ICP reduction)

146
Q

MoA of loop diuretics, SE, examples

A

Loop = ascending LoH block NaKCl

SE- polyuria, dehydration, hypoelectrolytes inc calcium

Eg: furosemide, bumetanide

147
Q

Thiazide diuretics + Thiazide like

A

Thiazide : bendroflumethiazide
Thiazide LIKE: indapamide

MoA block NaCL channels in DCT

SE - diabetes, gout, erectile dysfunction, electrolyte disturbed (hyponatraemia, hypercalcaemia)

148
Q

Name some K sparing diuretics and moa

A

spironolactone - AA

amiloride, triamterene- block ep NaK channels in CD

149
Q

MoA and SE of spironolactone

A

competitive antagonist for aldosterone in collecting ducts

SE - gynaecomastia, erectile dysfunction, hyperkalaemia

150
Q

What is tamsulosin

A

alpha blocker used in BPH

SE - orthostatic hypotension

Alpha blockers can be used as last resort in hypertension but don’t reduce mortality

151
Q

SVT management

A

Narrow complex, regular rhythm tachy

Manage with:

1) vagal manouvers (syringe, carotid sinus massage)
2) Adenosine

If sinus rhythm does not return ?atrial flutter and start rate control = beta blocker

152
Q

How does adenosine work (drug for SVTs) + SE

what drugs do the opposite

A

Works on receptors in AVN to cause K efflux, hyperpolarise cells, reduce HR

SE - impending doom transiently, flushing

Opp - theophylline, caffeine

153
Q

Side effects of digoxin and how to treat OD

A

rate controller

can cause hypokalaemia in a px on a diuretic already

toxicity (OD) can cause hyperkalaemia, arrhythmias, NVDiorrhoea, yellow tingue to vision, fatigue, confusion

OD digoxin = atropine (blocks vagal tone to heart)

154
Q

Name a few things that increase INR

A

interact with p450 - slows warfarin metabolism

INC: cranberry juice, ciprofloxacin, clarithromycin, metranidazole

155
Q

Name a few things that decrease INR

A

Dietary vitamin K

Rifampicin

Carbamezapine

St Johns Wort

156
Q

2 types of DOACs and examples

A
  1. Direct thrombin inhibitors - dabigatran
  2. Factor Xa inhibitors - apixaban, rivaroxaban
157
Q

Name ways to support a px with smoking cessation

A
  1. Behavioural
  2. Nicotine replacement therapy - patches, lozynges, vape
  3. Nicotine receptor partial agonist- Varenicline
  4. Buproprion - helps with withdrawal symptoms

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