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Disease Flashcards

1
Q

What is cardiogenic shock?

A

inadequate systemic perfusion as a result of cardiac dysfunction

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2
Q

What are some of the main differential diagnoses of chest pain?

A
  • GI tract
  • MSK
  • pericarditis
  • pleuritic pain
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3
Q

What are the main heart emergencies?

A
  • MI
  • PE
  • dissection of aorta
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4
Q

What are the pros of exercise testing?

A
  • cheap
  • reproducible
  • risk stratification
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5
Q

What are the cons of exercise testing?

A
  • poor diagnostic accuracy

- submaximal tests

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6
Q

What are the pros of perfusion imaging?

A
  • non-invasive
  • pharmacological stress in less mobile patients
  • more precise than exercise tests
  • risk stratification
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7
Q

What are the cons of perfusion imaging?

A
  • radiation

- false positives and negatives

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8
Q

What are the pros of CT angiography?

A
  • non-invasive

- anatomical data and risk stratification

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9
Q

What are the cons of CT angiography?

A
  • radiation
  • less precise than angiography, particularly when calcium is present
  • cost
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10
Q

What are the pros of angiography?

A
  • anatomical and risk stratification

- follow-on angioplasty

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11
Q

What are the cons of angiography?

A
  • risk of stroke
  • radiation
  • contrast: renal dysfunction, rash and nausea
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12
Q

What is the PCI technique?

A 
vascular access
anticoagulation
catheter to osmium of coronary
guide wire down vessel
balloons threaded over wire
stents implanted
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13
Q

What is the suitabilities for revascularisation?

A
  • multi-vessel disease
  • left main disease
  • diabetes
  • co-morbidities
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14
Q

What happens when infection gets into the compartments of the feet?

A

the infection gets trapped so there is a buildup of pus which builds pressure so there is cell death and necrosis

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15
Q

What are the systemic and local effects of diabetic foot sepsis?

A 
systemic-
pyrexia
tachycardia
tachypnoea
confusion
local-
swelling
tenderness
ulcer
erythema
necrosis
crepitus 
no pedal pulses
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16
Q

What is the management of diabetic foot sepsis?

A
  • emergency
  • debridement
  • removal of al infected tissue
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17
Q

What is stroke?

A

Acute onset of focal neurological symptoms and signs due to disruption of blood supply

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18
Q

What are the two types of stroke?

A

Haemorrhagic- bleeding occurs inside or around the brain tissue (raised blood pressure and weakened blood vessel walls due to inflammation or structural abnormalities)
Ischaemic- clot blocks blood flow to an area of the brain

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19
Q

What are the types of ischaemic stroke?

A

Thrombotic (clot blocking artery at the site of occlusion)
Embolic (clot blocking artery has moved and is blocking another area)
Hypoperfusion (reduced blood flow due to stenosed artery)

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20
Q

What is Virchow’s triad?

A

circulatory stasis, endothelial injury and hypercoagulable state

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21
Q

What are the risk factors for stroke?

A 
non-modifiable= age, family history, gender, race or previous stroke
modifiable= hypertension, hyperlipidaemia, smoking, AF, diabetes, exercise and alcohol
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22
Q

What is treatment of ischaemic stroke?

A

thrombolysis (dissolve clot) or thrombectomy (remove with stent)

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23
Q

How to tell is a stroke is caused by an atheroembolism or cardioembolism?

A

For atheroembolism carotid scanning or CT of aortic arch

For cardioembolism ECG , echo

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24
Q

How to test to see if stroke is haemorrhagic?

A

hypertension, look for aneurysm or other rare disease

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25
Q

How to treat stroke due to thrombus?

A

antiplatelet, statins, diabetes treatment, hypertension treatment and lifestyle

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26
Q

What are TIAs?

A

temporary neurological symptoms due to occlusion of artery stopping blood flow

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27
Q

What does clopidogrel bind to?

A

ADP on platelet to stop it causing activation of cascade

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28
Q

What does aspirin bind to?

A

stops thomboxane A2 being produced

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29
Q

What are the risks of thrombolysis?

A

haemorrhage, hypersensitivity and failure to re-perfuse

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30
Q

What is the treatment for STEMI?

A 
analgesia (diamorphine)
anti-emetic (IV)
aspirin 
GTN (if BP us over 90mmHg)
oxygen (if hypoxic)
primary angioplasty
thrombolysis (if angioplasty not available in 120 minutes)
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31
Q

What are the main complications of STEMI?

A

death
arrhythmic complications- ventricular fibrillation
structural complications- cardiac rupture, ventricular septal defect and mitral valve regurgitation, left ventricular aneurysm formation, mural thrombus, inflammation and acute pericarditis
functional complications- acute ventricular failure, chronic cardiac failure and cardiogenic shock

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32
Q

What other conditions can have elevated troponin?

A 
CCF
hypertension
renal failure
sepsis
PE
stroke
pericarditis
post-arrhythmia
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33
Q

What is a type 2 MI?

A

due to imbalance of oxygen supply from coronary spasm etc, anything that increases myocardial oxygen demand or reduces myocardial blood flow

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34
Q

What does interstitial fluid act as?

A

the go-between blood and body cells

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35
Q

How much of the body water is extra-cellular?

A

1/3rd

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36
Q

What do the terminal arterioles do?

A

regulate regional blood flow to the capillary bed

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37
Q

Why is blood flow through the capillary bed slow?

A

to allow for adequate exchange

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38
Q

What do pre-capillary sphincters do and what is an example of where they are found?

A

regulate blood flow eg in mesentery

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39
Q

What is trans-capillary fluid flow passively driven by?

A

pressure gradients across capillary wall

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40
Q

What is net filtration pressure proportional to?

A

forced favouring filtration minus forces opposing filtration

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41
Q

What is the filtration coefficient representative of?

A

how permeable the capillaries are to fluid

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42
Q

What are the forces favouring filtration?

A

capillary hydrostatic pressure and interstitial fluid osmotic pressure

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43
Q

What are the forces opposing filtration?

A

capillary osmotic pressure and interstitial fluid hydrostatic pressure

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44
Q

What do Starling forces favour?

A

filtration at the arteriolar end and reabsorption and the venular end

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45
Q

What forces change from arteriole to venule end?

A

osmotic doesn’t change

hydrostatic pressure decreases

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46
Q

What is oedema?

A

is an accumulation of fluid in the interstitial space

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47
Q

What is different about the lung circulation?

A

pulmonary resistance is much lower so hydrostatic pressure is lower in the lungs but osmotic pressure is normal

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48
Q

What happens to diffusion and gas exchange in pulmonary oedema?

A

increased diffusion distance

compromised gas exchange

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49
Q

What is pulmonary oedema?

A

pulmonary oedema is accumulation of fluid in the interstitial and intra-alveolar lung spaces

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50
Q

What is clinically seen in pulmonary oedema?

A

SOB seen and crepitations in lung bases, haziness in perihilar region of CXR

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51
Q

What are the factors causing oedema?

A
  • Raised capillary pressure: arteriolar dilation, raised venous pressure (LVF so pulmonary oedema as fluid can’t come back from the lungs and RVF so peripheral oedema)
  • Reduced plasma osmotic pressure: malnutrition, protein malabsorption, excessive renal excretion of protein and hepatic failure
  • Lymphatic insufficiency: lymph node damage and filariasis
  • Changes in capillary permeability: inflammation and histamine increases leakage of protein
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52
Q

What does heart failure do to the Frank-Starling curve?

A

shifts to the right so the curve appears to have dropped in height

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53
Q

What type of MI causes bradycardia?

A

inferior

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54
Q

What are the complications of MI?

A
  • arrhythmias
  • ventricular septal perforation
  • mitral regurgitation
  • ventricular free wall rupture
  • systemic embolism
  • ventricular aneurysm
  • pericarditis
  • cardiogenic shock
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55
Q

How do you treat a polymorphic VT?

A

DCCV, Cath lab, electrolyte correction, amiodarone (w/glucose not saline), beta-blocker

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56
Q

When should you not give nitrates?

A

hypotension and if headaches are too bad (1 in 10)

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57
Q

What is cardiac arrest?

A

effective cessation of the heart so there is no circulation and no oxygen delivered

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58
Q

What are the four parts of the chain of survival?

A
  • early recognition and call for help
  • early CPR
  • early defibrillation
  • post resuscitation care
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59
Q

How to treat excess or reduced afterload?

A

vasodilators for excess afterload
vasoconstrictors for reduced
afterload

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60
Q

How do you assess oxygen delivery factors in an ABC scenario?

A
  • SaO2: clinical, pulse oximetry and ABG

- [Hb]: clinical, part of FBC and bedside

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61
Q

What can the airway be obstructed by?

A
  • CNS depression so tongue
  • Blocked lumen
  • Swelling
  • Muscle
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62
Q

What are some primary causes of circulatory problems?

A
  • acute coronary syndromes
  • dysrhythmias
  • hypertensive heart disease
  • valve disease
  • drugs
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63
Q

What are some secondary causes of circulatory problems?

A
  • asphyxia
  • hypoxaemia
  • blood loss
  • hypothermia
  • septic shock
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64
Q

What things do you test in D of ABCDE?

A

AVPU
GCS
Pupils
Glucose

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65
Q

What are the features of VF?

A
  • shockable
  • bizarre irregular waveform
  • random frequency and amplitude
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66
Q

What are the features of VT?

A
  • shockable if pulseless
  • monomorphic has broad complex rhythm, rapid rate and constant QRS morphology
  • polymorphic is torsades de pointes
67
Q

How often do you defibrillate between rounds of CPR?

A

every 2 minutes

68
Q

How often do you administer adrenaline in CPR?

A

after 3rd shock then after every alternate shock

69
Q

What are the features of asystole?

A
  • non-shockable
  • absent QRS
  • P waves may persist
  • adrenaline as soon as possible then every 3-5 minutes
70
Q

What are the features of PEA?

A

Pulseless electrical activity

  • non-shockable
  • ECG with an output
  • treat reversible causes
  • give adrenaline asap then every 3-5 minutes after
71
Q

What are the two drugs in advanced life support?

A
  • adrenaline 1mg every 3-5 minutes which is an alpha vasoconstrictor and is beta inotropic
  • amiodarone 300mg
72
Q

What are the reversible causes of cardiac arrest (4Hs and 4Ts)?

A
  • hypoxia
  • hypovolaemia
  • hypo-/hyperkalaemia
  • hypothermia
  • thrombosis
  • tension pneumothorax
  • tamponade
  • toxins
73
Q

What are exertion symptoms characteristic of?

A

valvular heart disease

74
Q

What will be the signs of right heart failure?

A

raised JVP (4cm or above is not normal)
pitting oedema
hepatic congestion

75
Q

What is a tapping apex a sign of?

A

mitral stenosis

76
Q

What does a displaced and diffuse apex beat suggest?

A

LV dilation so volume overload

77
Q

What does a displaced and heaving apex beat suggest?

A

LVH and pressure overload

78
Q

What is the sign associated with right ventricular overload?

A

left parasternal heave

79
Q

What are the main categories for describing murmurs?

A
  • systole or diastole
  • type (eg pansystolic)
  • where it is loudest
  • radiation
  • grade (1-6 with 4+5 including addition of a thrill)
  • changes with respiration
80
Q

What is the condition associated with a continuous murmur?

A

patent ductus arteriosus

81
Q

What is an innocent murmur?

A

soft, position dependent and is often early systolic (if diastolic it is almost always pathological)

82
Q

What are the features of aortic stenosis?

A
  • Degeneration with age
  • Congenital (aortic valve is bicuspid)
  • Rheumatic §
83
Q

What are the symptoms and signs of aortic stenosis?

A

SOB, chest pain, dizziness, syncope
low volume pulse, forceful displaced apex, ejection systolic murmur radiating to the carotids, pressure gradient across the valve indicates aortic stenosis

84
Q

What is seen on an ECG with aortic stenosis?

A

LVH

85
Q

What is the treatment for aortic stenosis?

A

valve replacement, Trans catheter aortic valve replacement (TAVI is not an open heart procedure) and balloon aortic valvotomy (BAV)

86
Q

What are the choices of prosthetic valves for aortic stenosis?

A

mechanical lasts longer and need warfarin so younger patients, bio-prosthetic only lasts 10 years and no warfarin so older patients

87
Q

What are the features of mitral regurgitation?

A
  • Leaflets can be affected by prolapse, rheumatic, myxomatous or endocarditis
  • Chordae rupture can prolapse
  • Papillary muscle rupture
  • Annular dilation
88
Q

What are the signs and symptoms of mitral regurgitation?

A

SOB, peripheral oedema, fatigue

Displaced apex and pansystolic murmur radiating to axilla

89
Q

What is seen on a CXR for mitral regurgitation?

A

cardiomegaly

90
Q

What is the treatment for mitral regurgitation?

A

medication (diuretics and heart failure), surgical (repair prolapse or replace degenerative) and percutaneous

91
Q

What is the main feature of mitral stenosis?

A

rheumatic

92
Q

What are the main symptoms and signs of mitral stenosis?

A

SOB, fatigue, palpitations so AF

Malar flush, tapping apex beat and mid diastolic rumbling localised to apex

93
Q

What is seen on a CXR in mitral stenosis?

A

cardiomegaly and straight left heart border for enlarged left atrium

94
Q

What is the treatment for mitral stenosis?

A

medication (diuretics and treat AF), surgery (valve replacement) and balloon valvuloplasty

95
Q

What are the features of aortic regurgitation?

A

Leaflets so endocarditis, connective tissue disease or rheumatic
Annulus so Marfans or aortic dissection

96
Q

What are the signs and symptoms of aortic regurgitation?

A

SOB

Collapsing pulse, wide pulse pressure, displaced apex and early diastolic murmur at left sternal edge

97
Q

What is seen on a CXR for aortic regurgitation?

A

cardiomegaly

98
Q

What is the treatment for aortic regurgitation?

A

medications so ACEI and surgery

99
Q

What is congenital heart disease?

A

an abnormality of the structure of the heart which is present at birth

100
Q

What is the spectrum of severity for congenital heart disease?

A

Mild- asymptomatic that can resolve or progress
Moderate- requires intervention from a specialist and monitoring from a cardiac centre
Severe- will present very ill and will be an extreme problem if not dealt with

101
Q

How can congenital heart disease present?

A
  • antenatal screening
  • well baby with clinical signs
  • unwell baby with cyanosis, shock or cardiac failure
102
Q

How are newborns tested for congenital heart disease?

A

clinical examination
femoral pulses
murmurs
pre and post ductal sats

103
Q

What are the differentials of mixing oxygenated and deoxygenate blood causing cyanosis?

A
  • cardiac disease (undistressed)
  • respiratory disease (grunting, respiratory stress and CXR changes)
  • PPHN (very unwell babies, septic, acidotic with large pre to post ductal differences)
104
Q

What are the differentials of a collapsed baby at time of duct closure?

A

sepsis
congenital heart disease
metabolic condition

105
Q

How will a collapsed baby present?

A
  • very severe cyanosis, pallor, tachypnoea, distress, rapid deterioration to death
  • poor pulses, hepatomegaly, creps, increased work of breathing and acidosis
106
Q

What does a left to right shunt cause in cardiac failure?

A

increased pulmonary blood flow and increased ventricular load

107
Q

How does cardiac failure present in a baby?

A

failure to thrive, breathless when feeding, no more weight increase

108
Q

What is the treatment for congenital heart disease?

A

surgery (repair or palliation), developmental problems in later life (hypoxia and bypass time), further surgery and emotional issues

109
Q

What are the differences between fetal and adult circulation?

A
  • placenta has a role in gas exchange, waste excretion, acid base balance, hormone production, IgG transport, nutrition
  • baby has unexpanded fluid-filled lungs
  • liver does not have a large role in nutrition or waste management
  • gut is not used
110
Q

What is the placenta’s role in fetal circulation?

A
  • foetal heart pumps blood to the placenta via the umbilical arteries
  • blood from the placenta returns to the foetus via the umbilical vein
111
Q

What does the ductus venous do?

A

connects the umbilical vein to the inferior vena cava next to the liver and carries the majority of the placental blood

112
Q

What is the foramen ovale?

A

connection between the RA and LA and is an opening in the mitral septum so allows oxygenated blood into the left atria to go into the aorta

113
Q

What does the ductus arteriosus do?

A

connects pulmonary bifurcation to the descending aorta

114
Q

How is the patency of the ductus arteriosus maintained?

A

circulating prostaglandin E2 made by the placenta that relaxes the smooth muscle in the walls

115
Q

What are the main changes that occur at birth?

A
  • lungs open, arterioles have more space to expand so they unfold and the oxygen levels go up so pulmonary vascular resistance drops
  • systemic resistance rises as cardiac output to the lungs increases
  • foramen ovale closes
  • ductus arteriosus closes as it constricts due to oxygen, less blood it flowing and less prostaglandin is holding it open, it then becomes ligament arteriosum
116
Q

How to treat ductus arteriosus that has failed to close?

A

wait
ibuprofen
surgery

117
Q

When does pulmonary resistance drop to normal levels in a baby?

A

2-3 months

118
Q

What is PPHN?

A

Persistent pulmonary hypertension of the newborn is when the resistance to flow in the lungs fails to drop
Pressure in the right heart > left side of the heart so right to left shunt at foramen ovale and ductus arteriosus

119
Q

What is seen clinically in PPHN?

A

difference between pre and post ductal o2 sats so hands and feet

120
Q

How is PPHN treated?

A
  • lowering PVR so oxygen, ventilation, sedation, thermoregulation, sepsis treatment, acidosis correction and inhaled NO
  • increasing systemic vascular resistance so high blood pressure and inotropes
121
Q

What can cause failure to thrive in babies?

A
  • sepsis
  • hypoxic ischaemic insult
  • meconium aspiration syndrome
  • cold stress
  • prematurity
122
Q

What ECG feature supports the diagnosis of ischaemic heart disease?

A

ST depression while exercising

123
Q

What are the main anti-anginal drugs?

A 
potassium channel activators eg Nicorandil
nitrates
beta-blockers
calcium channel blockers
ivabradine
124
Q

What diseases have raised endothelin?

A 
MI
heart failure
ARF
asthma
primary pulmonary hypertension
125
Q

What does infective endocarditis increase the risk of?

A

stroke/ systemic emboli

126
Q

What is bacteraemia?

A

bacteraemia is bacteria in the bloodstream which is life-threatening and can cause septic shock

127
Q

What is the coagulase test used for in infective endocarditis?

A

coagulase test distinguishes S.aureus from coagulase-negative staph

128
Q

What are the most common skin organisms?

A

S. aureus

S. epidermidis Corynebacterium sp. Propionibacterium acnes

129
Q

What are the risk factors for having an infected implantable cardiac device?

A

are lack of prophylaxis, number of interventions, fever within 24 hours, heart or renal failure

130
Q

What are the symptoms of ICD infections?

A

fevers, chills, night sweats, malaise and anorexia

131
Q

What is the criteria used to assist diagnosis of infective endocarditis?

A

Duke’s criteria

132
Q

What is infective endocarditis?

A

an infection of the endothelium of the heart valves and can be acute or subacute

133
Q

What are the risk factors for infective endocarditis?

A

heart valve abnormalities, prosthetic heart valves, IV drug users

134
Q

What is the pathogenesis of infective endocarditis?

A
  • damages heart valve
  • turbulent flow
  • platelets deposited
  • bacteraemia and organisms settle and form a microbial vegetation
  • vegetations are fixable and break off
  • these cause abscess or haemorrhage
135
Q

What are the most common organisms for infective endocarditis?

A
  • S.aureus and viridans streptococci are the most common
  • can be by enterococcus sp or staph epidermidis
  • Q-fever so coxiella burnetii is atypical
  • HACEK is a group of organisms that are Gram-negatives
136
Q

What is the presentation of acute infective endocardiits?

A

overwhelming sepsis and cardiac failure

137
Q

How does subacute infective endocarditis present?

A

fever, malaise, weight loss, tiredness and breathlessness with clubbing, splinter haemorrhage, splenomegaly, janeway lesions and osler nodes

138
Q

What are the ways in which streptococci can be named?

A

oxygen requirement, lancefield groups, haemolysis on agar

139
Q

What are the features of viridian’s strep?

A

alpha haemolytic and cause subacute endocarditis

140
Q

What is the treatment for prosthetic valve infections?

A

vancomycin and gentamicin IV then add in rifampicin PO delayed 3-5 days

141
Q

What is the treatment for native vale infection?

A

amoxicillin and gentamicin IV

142
Q

What is the treatment for IV drug abusers with valve endocarditis?

A

flucloxacillin IV

143
Q

How long are antibiotics given for infective endocarditis?

A

4-6 weeks

144
Q

What is mortality for infective endocarditis?

A

15-30%

145
Q

What is the presentation of myocarditis?

A
  • more common in young people and sudden death, - - presents with chest pain, fever, SOB and palpitations, with arrhythmia and cardiac failure
  • diagnosed with viral PCR
146
Q

What is the presentation of pericarditis?

A
  • often occurs with myocarditis
  • chest pain
  • supportive treatment for mostly viral causes
147
Q

What is seen on a CXR with heart failure?

A

Pulmonary oedema/congestion: A-Alveolar oedema
Septal/Kerley B lines: B-B lines
Cardiomegaly: C-Cardiomegaly
Upper zone vessel enlargement: D-Diversion of vessels
Pleural effusion: E-Effusion

148
Q

What are the ECG signs with PE?

A

Sinus tachycardia (the most common)
Signs of right heart strain (not left)
T wave inversion in the anterior leads

149
Q

What are channelopathies?

A

mutations in the genes that encode the cardiac ion channels

150
Q

What are the features of channelopathies?

A
  • repolarisation is affected
  • abnormalities on the ECG
  • normal cardiac structure and function
  • atrial and ventricular arrhythmias can arise
151
Q

What does congenital long QT present with?

A

usually asymptomatic but can present with sudden cardiac death, palpitations and syncope

152
Q

What are the common associated arrhythmias with clQT?

A

polymorphic VT (Torsades de Pointes with spiral and axis change), lone AF or heart block

153
Q

What are triggers for clQT?

A
  • exercise
  • sudden auditory stimuli
  • sleep
  • QT prolonging states so medication or hypokalemia
154
Q

What is the basic mechanism of clQT?

A

less K+ out and more Na+ and Ca2+ in

155
Q

What is the treatment for clQT?

A

beta blockers (nadolol) and avoidance of triggers and QT prolonging drugs

156
Q

What does Brugada present with?

A

asymptomatic or palpitations and syncope

157
Q

What is seen on an ECG for Brugada?

A

ST elevation with right bundle branch block in leads V1-V3

158
Q

What is the treatment for Brugada?

A

Insert an ICD, avoid some drugs and screen family members

159
Q

What are the associated arrhythmias with Brugada?

A

AF is common and there is a risk of polymorphic VT and VF (triggered by sleep, fever, large meals and alcohol)

160
Q

What is the treatment for HCM?

A

beta-blocker, if there is outflow tract obstruction then drugs, septal ablation or surgery

161
Q

What is the presentation of arrhythmogenic right ventricular cardiomyopathy?

A

ventricular arrhythmia, cardiac failure and sudden cardiac death

162
Q

What happens to the heart in ARVC?

A

fibro-fatty replacement of cardiomyocytes in the right ventricle and sometimes there is left ventricular involvement

163
Q

What heart failure medications are only for symptoms?

A

vasodilators (nitrates and hydralazine)
loop diuretics
digoxin

164
Q

What heart failure medications are to increase prognosis?

A

selective beta blockers
ACEIs
angiotensin II antagonist
spironolactone (potassium-sparring diuretic)

My Cardiovascular (13 decks)

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