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Medicine > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

Outline lipid metabolism pathways.

A

EXOGENOUS:
fat ingestion –> triglycerides and cholesterol esters incorporated into chylomicrons –> lymphatics –> thoracic duct –> systemic circulation –> lipoprotein lipase on adipocytes takes FFAs into cells –> chylomicron remnants to liver.
ENDOGENOUS:
1. Liver releases VLDL –> lipoprotein lipase on adipocytes takes FFAs into cells –> produces IDL and then LDL –> LDL returns to liver, binds to LDL receptor on hepatocytes –> invaginates into the cell and fuses with lysosomes –> LDL receptor is recycled back to the surface of the hepatocyte (recycling inhibited by PCSK9).
2. Liver releases HDL –> takes up cholesterol via ABC-A1 –> returns to liver.

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2
Q

MOA of STATINS.

UE?

A

Statins inhibit HMG-CoA-reductase.
Decreased intrahepatic cholesterol synthesis –> upregulation of LDL receptor –> increased LDL uptake by hepatocytes –> decreased serum LDL.
UE:
MUSCLE: myalgia, myopathy, myositis, rhabdomyolysis.
HEPATIC: raised LFTs
GIT UPSET: diarrhoea, constipation, flatulence

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3
Q

MOA of FIBRATES
USE?
Unwanted Effects?

A

Fibrates –> activate PPAR-alpha –> increased activity of lipoprotein lipase.
Primary use is to decrease triglyceride level.
UE:
Myalgia
Raised LFTs
Cholelithiasis (contraindicated in gallbladder disease)

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4
Q

MOA of PCSK9 inhibitors e.g. evolocumab.

UE?

A

Monoclonal antibodies to PCSK9 –> increased recycling of LDL receptor to surface of hepatocyte –> increased LDL uptake into liver –> decreased serum LDL.
UE:
Myalgia

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5
Q

MOA of EZETIMIBE

UE

A 
Ezetimibe --> inhibition of cholesterol transporter in GIT
UE:
GIT UPSET: diarrhoea
Raised LFTs
Myalgia
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6
Q

MOA of CHOLESTYRAMINE

UE

A 
Cholestyramine --> binds to bile acids in intestine --> inhibition of enterohepatic circulation of bile acids --> increased bile acid excretion
UE:
GIT: nausea, bloating, abdominal pain
Myalgia
Raised LFTs
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7
Q

What is your approach to management of dyslipidemia?

A 
1. Calculate absolute cardiovascular risk in next 5 years. 
LOW RISK = < 10%. 
- provide healthy lifestyle advice
- repeat lipids every 5 years
MODERATE RISK = 10-15%
- provide healthy lifestyle advice
- consider pharmacotherapy if target not reached after 6 mo of lifestyle change. 
HIGH RISK = >15%
- provide healthy lifestyle advice
- pharmacotherapy: statin
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8
Q

What are your cholesterol target levels?

A

Total cholesterol < 4
LDL < 2
Triglycerides < 2
HDL > 1

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9
Q

How is STEMI diagnosed on ECG?

A

ST elevation in 2 contiguous leads or new LBBB.

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10
Q

What ECG leads correspond with:

  • Lateral MI?
  • Anterior MI?
  • Inferior MI?
A

Lateral: lead I, AVL, V5, V6
Anterior: V1, V2, V3
Inferior: II, III and AVF

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11
Q

Give contraindications to fibrinolysis for STEMI.

A 
ABSOLUTE:
Previous intracranial haemorrhage
Cerebral AVM
Ischemic stroke in last 3 months
Intracranial malignancy
Uncontrolled active bleeding
Bleeding diathesis
Suspected aortic dissection
Severe uncontrolled hypertension
RELATIVE:
Recent major surgery
Recent internal bleeding
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12
Q

Outline the options for reperfusion of STEMI.

A

For STEMI, PCI is preferred over fibrinolysis.
The goal is PCI within 90 minutes of arrival.
When PCI will be delayed by more than 120 min, fibrinolytic therapy should be given ASAP in the ED (unless contraindicated).
After fibrinolysis, the patient should be transferred to a PCI-capable hospital. PCI should be performed as early as feasible after fibrinolysis and is still beneficial.

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13
Q

How would you manage a STEMI?

A 
Admit the patient. 
Continuous monitoring. 
Bedrest. 
NBM until stable. 
Serial troponins. 
IV access. 
Oxygen as needed to maintain sat > 90%.
Analgesia - morphine, GTN
Definitive treatment: reperfusion - PCI preferred if available within 90 min; otherwise fibrinolysis and transfer to PCI-capable facility for fibrinolysis ASAP (as long as not contraindicated). 
Begin medications:
IMMEDIATELY:
Dual antiplatelet:
Aspirin PO 325mg immediately, then 100 mg daily. 
P2Y12 inhibitor - ticagrelor or clopidogrel
IV heparin.
Metoprolol (if not contraindicated)
BEFORE DISCHARGE:
Statin
ACE-Inhibitor
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14
Q

How would you manage a NSTEMI?

A

When DX is made, perform risk assessment - e.g. using TIMI score
If high risk - manage as per STEMI
If low risk - may manage conservatively: as per STEMI with delayed or w/o revascularisation.

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15
Q

How would you manage stable angina?

A 
LIFESTYLE:
- Exercise
- Healthy diet
- Weight loss: BMI < 25
- Cease smoking
- Healthy alcohol intake
CONTROL RISK FACTORS:
- Statin
- ACE-Inhibitor if HTN
- DM: ensure good control
CONTROL SYMPTOM:
- GTN or B-blocker (use cardioselective: atenolol or metoprolol)
PREVENT ACS:
- Low dose aspirin PO 100-150 mg daily
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16
Q

What are the features of rheumatic fever?

A 
Sydenham chorea
Migratory polyarthritis
Subcutaneous nodules
Erythema marginatum
Carditis
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17
Q

How would you treat strep throat?

A
  1. Confirm it is a GAS infection.
    - Serology (antistreptolysin O or antistreptococcal DNAse B titers increased) OR throat swab + culture OR rapid antigen detection test.
    - Assess for complications: ECG and echo
  2. Prompt treatment of pharyngitis - penicillin
  3. Secondary prevention if rheumatic heart disease:
    IM penicillin G every 4 weeks for 10 years or until 21 years (whichever is longer).
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18
Q

How would you manage AF?

A

For persistent AF, you need to:
CONTROL SYMPTOMS - using RATE control or RHYTHM control.
CONTROL VTE RISK - using anticoagulant.

Usually the preference is:
Symptomatic from AF, heart failure or younger pt –> rhythm control.
Asymptomatic, older pt –> rate control.

RHYTHM CONTROL:
- Pharmacological or electrical cardioversion.
Pharmacological cardioversion use: (1) FLECAINIDE if no structural heart disease or IHD; (2) amiodarone if structural heart disease or IHD present. Likely continue the drug used long term to prevent recurrence of AF.
For safe cardioversion, consider length of time pt has been in AF:
If < 48 hours –> may cardiovert immediately. If 48+ hours –> anticoagulate for 4 weeks before cardioversion attempt.
RATE CONTROL:
Can use: (1) B blocker - atenolol or metoprolol, or (2) ca channel blocker - verapamil or diltiazem.

ANTICOAGULATION:
For VALVULAR AF –> warfarin
For NONVALVULAR AF –> calculate risk of stroke using CHADs VASC - use NOAC if score 2+ in men and 3+ in women.

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19
Q

How would you treat AV node re-entrant or AV re-entrant tachycardias?

A

If STABLE –>
- Vagal manoeuvre: carotid sinus massage, Valsalva
- Adenosine
Both of these (1) decrease rate of SA depolarisation; (2) decrease rate of conduction esp through AV node.
If UNSTABLE or above does not work –>
- Electrical DC cardioversion

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20
Q

Explain Wolff-Parkinson-White syndrome.
Why does it occur?
What does it look like on ECG?

A

WPW is a type of AV reentrant tachycardia.
It is caused by an accessory pathway between the atria and ventricle.
On ECG:
- Slurred upstroke of QRS known as delta wave
- Short PR interval
- Wide QRS

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21
Q

What are the 4 classes of antiarrhythmics?

Give examples of each class.

A

Class 1 = Na channel blockers: flecainide
Class 2 = B blockers:
CARDIOSELECTIVE = atenolol, bisoprolol, metoprolol, nebivolol
NON-SELECTIVE = propranolol, labetalol
Class 3 = K channel blockers: amiodarone, sotalol
Class 4 = Ca channel blockers
DIHYDROPYRIDINE = amlodipine
NON-DIHYDROPYRIDINE = diltiazem (intermediate), verapamil (most cardio-selective).

UNCLASSIFIED:
Adenosine - K channel activation –> decrease rate of SA depolarization and decrease rate of conduction through AV node.

22
Q

DIGOXIN
MOA
Use
UE

A

MOA:

  1. Inhibition of Na-K-ATPase in cardiac myocytes –> altered Na and Ca exchange –> increased intracellular calcium stores and release of calcium on depolarization –> increased force of contraction
  2. Increases parasympathetic tone and decreases sympathetic tone –> slows HR

USE: CHF (increased force of cardiac contraction), AF and A flutter (rate control)

UE:
GIT: N&V, anorexia
CARDIO: arrhythmia, bradycardia
NEURO: drowsy, dizzy, blurred vision

23
Q 
ASPIRIN
MOA
USES
UE
CI
A

Aspirin is an irreversible COX-1 inhibitor –> inhibits production of thromboxane A2 synthesis in platelets –> decreased platelet aggregation –> antithrombotic effect.
USES: Used in angina, MI and stroke prevention
UE:
- PUD
- Coagulopathy, bleeding
- AKI
- Hypersensitivity reactions, anaphylaxis
CI:
Febrile illness in paediatric patients –> causes Reye syndrome (hepatic encephalopathy when aspirin used to tx viral illness in paediatric patients)

24
Q

P2Y12 Inhibitors

  • Name 2 P2Y12 inhibitors
  • MOA
  • Uses
  • UE
A

Clopidogrel, ticagrelor, prasugrel
Inhibition of the ADP receptor on platelets –> inhibition of platelet aggregation
Used in dual antiplatelet therapy with aspirin, or if aspiring CI/not tolerated.
Prevent MI, stroke
UE:
Haemorrhage, allergic reaction

25
Q

Glycoprotein 2B/3A inhibitors.

  • Name 1 drug of this class
  • MOA
  • Use
A

Abciximab, tirofiban
MOA: block the glycoprotein 2B/3A receptor on the surface of activated platelets –> prevent platelets binding to fibrinogen –> inhibition of platelet aggregation and thrombus formation.
Use: in unstable angina/ NSTEMI when PCI planned for within 24 hours.

26
Q 
HEPARIN
Types of heparin
For each type: MOA, route, CI
Uses
UE
Monitoring
A

LMWH = enoxaparin
Has anti-factor X activity
SC only
CANNOT be used in ESRD.

UFH
Has both anti-factor X and anti-thrombin activity.
SC or IV
Used in ESRD.

USES:

  • DVT prophylaxis (low dose)
  • Treatment of DVT & PE (high dose)
  • Treatment of MI (high dose)

UE:
Allergic reaction/ hypersensitivity
Heparin-induced thrombocytopenia

Monitoring: APTT
Antidote: protamine

27
Q

WARFARIN
MOA?
Monitoring?
Uses?

A

MOA: inhibition of hepatic vit K epoxide reductase enzyme –> decreased active vitamin K –> decreased gamma-carboxylation of glutamate on clotting factors 2, 7, 9, 10, protein C and protein S.

Requires regular monitoring of INR (PT).
Requires bridging anticoagulation.

Use:
Prophylaxis against VTE in:
- Valvular AF
- Some DVT and PE

28
Q

List the 3 features of Virchow’s triad.

A

Stasis
Endothelial damage
Hypercoagulability

29
Q

Define the types of AV block.

How would you treat them?

A

1st DEGREE
Prolonged PR interval, > 5 small square (200ms)
Every P wave followed by QRS.

2nd DEGREE
Mobitz type I (aka Wenckebach) - progressive lengthening of PR until a beat is dropped –> regularly irregular
Mobitz type II - intermittent dropping of QRS after P wave with constant PR interval - typically follows a regular pattern –> regularly irregular

3rd DEGREE
AV dissociation - no relationship between P waves and QRS complexes

TREATMENT
STABLE:
1st degree and Mobitz I --> monitor
Mobitz II and 3rd degree --> continuous monitoring, admit for temporary pacing and arrange permanent pacemaker for irreversible blocks
UNSTABLE:
DRSABCD, ALSD
30
Q

Explain advanced life support.

A
31
Q

Explain the treatment of chronic CHF.

A

Treat underlying cause, risk factors and comorbidities.

  • Manage htn, dyslipidaemia, DM, obesity, smoking cessation, limit alcohol
  • Avoid medications that worsen CHF - NSAIDs, beware antiarrhythmics, chemotherapy

Treat heart failure.

  • -> relieve symptoms
  • -> improve QOL
  • -> prevent hospitalisation
  • -> prevent progressive cardiac remodelling/ disease progression
  • -> improve mortality

DRSABCD
Consider need for admission.
Call cardiology.

LIFESTYLE:

  • Salt and fluid restriction, DASH diet
  • Healthy weight/ weight loss
  • Smoking cessation
  • Healthy alcohol intake
  • Exercise - refer for cardiac rehabilitation program
  • Patient to monitor weight –> education to see GP if weight rises above certain kg
PHARMACOLOGIC
All patients -->
- ACE-Inhibitor
- B blocker (don't start in acute decompensation, start low and go slow)
- Spironolactone
  • Digoxin (symptom relief only, no survival benefit)
  • Frusemide if fluid overloaded
  • Consider ARB/Neprilysin inhibitor

DEVICE THERAPY
Devices that might be beneficial:
- Implantable cardioverter-defibrillator
- Biventricular pacemaker - cardiac resynchronisation therapy

32
Q

What is your approach to the acute management of decompensated/acute heart failure?

A 
LMNOP
L - loop diuretic
M - morphine
N - nitrates
O - oxygen
P - position (sitting up) and PEEP (CPAP, BIPAP)
33
Q

SYSTOLIC MURMURS
What are the systolic murmurs?
How would you distinguish between them?

A

AORTIC STENOSIS

  • Systolic ejection murmur, crescendo-decrescendo
  • Aortic area
  • Radiates to carotids
  • Slow rising pulse

MITRAL REGURGITATION

  • Pansystolic
  • Mitral area
  • Radiates to left axilla

TRICUSPID REGURGITATION

  • Pansystolic
  • Tricuspid area - lower left sternal edge
  • Pulsatile liver
34
Q

AORTIC STENOSIS

  • characteristics of murmur?
  • aetiology?
  • other clinical features?
A

MURMUR
Loudest in aortic area –> radiates to carotid.
Systolic ejection murmur, crescendo-decrescendo
Loudest sitting up in full expiration
AETIOLOGY
Degenerative calcific AS
Rheumatic heart disease
CLINICAL FEATURES:
Symptoms - exertional symptoms: (1) chest pain, (2) SOB and (3) syncope on exertion.
Signs -
Pulse: plateau, slow rising
Apex beat: forceful/ hyperdynamic
Systolic thrill
S2: narrowly split or reversed (delayed L ventricular ejection)

35
Q

AORTIC REGURGITATION

  • Characteristics of murmur?
  • Aetiology?
  • Other clinical features?
A

MURMUR
- Diastolic, early, decrescendo
AETIOLOGY
- Rheumatic heart disease
- Congenital defect of aortic valve (e.g. bicuspid valve)
- Ankylosing spondylitis
- Aortic root dilation assoc with Marfan syndrome, aortitis, aortic dissection
CLINCIAL FX
Pulse: water hammer aka collapsing (i.e. falls quickly), wide pulse pressure, carotid pulse can be seen pulsating strongly (Corrigan’s sign)
Soft A2

36
Q

What are the reversible causes of cardiac arrest?

A 
4H and 4T
Hypovolemia
Hypoxia
Hypo/hyperkalaemia
Hypo/hyperthermia

Thrombosis (MI or PE)
Tension pneumothorax
Tamponade
Toxins

37
Q

Define an aneurysm.

A

Dilatation of a vascular structure
to at least 1.5x normal diameter
true = contains all three layers of vessel wall

38
Q

Abdominal Aortic Aneurysm

  • Definition?
  • Aetiopathogenesis?
  • Risk factors: for development of AAA, for rupture of AAA?
A

AAA is 3.0cm or > in diameter (at least 1.5x the normal 2cm diameter)

Main cause is inflammation - especially smoking –> increased ROS –> inflammation –> (1) apoptosis of vascular smooth muscle cells + (2) production of MMPs that degrade the ECM –> combined = weakened vessel wall –> dilatation

Risk factors:
For AAA Development –
Older age (>60)
Male
Family history, personal hx of other large vessel aneurysm e.g. popliteal
Atherosclerosis risk factors esp smoking
Connective tissue disease: Marfan, Ehlers-Danlos

For AAA Rupture --
Larger diameter: >5.5cm
Rapid increase in size: 5+mm in 6 months
Symptomatic aneurysm
Continued smoking
39
Q

What are the clinical features of AAA -
Non-ruptured?
Ruptured?

A

Most are asymptomatic- discovered incidentally on abdominal examination or imaging.

Symptomatic, non-ruptured –>

  • Pain: abdomen, back, flank, groin
  • Acute lower limb ischemia

Ruptured –>
SYMPTOMS:
- Pain: severe abdominal pain, radiates to back
- Syncope

SIGNS:

  • Vitals: hypotension, tachycardia, shock
  • Abdomen - pulsatile mass, bruit, bleeding signs (Grey-Turner = flank; Cullen’s = periumbilical)
  • Vessels - acute lower limb ischemia
40
Q

How would you diagnose/ work-up a (1) non-ruptured AAA, (2) ruptured AAA?

A

Non-Ruptured:
— Imaging: CT angiography imaging of choice

Ruptured:
— Imaging: USS if unstable; CTA if stable

41
Q

How would you manage a non-ruptured AAA?

A
  • Observation and monitoring
    — Frequency depends on size:
    3-3.9cm –> every 3 years
    4-4.9cm –> every 1 year
    5-5.4cm –> every 6 months
  • Smoking cessation!!!
  • Plus management of all other cardiovascular risk factors
  • Select appropriate patients for surgical intervention:
    — Indicated for:
    (1) diameter >5.5cm in men or >5.0cm in women
    (2) symptomatic (high risk of rupture regardless of diameter)
    (3) rapid expansion >5mm in 6 months
    — Procedure:
    Endovascular AAA repair - femoral artery is cannulated and a stent placed inside the aneurysm - blood flows through the graft instead of the aorta
42
Q

How would you manage a ruptured AAA?

A

DRSABCD
Prepare for surgery ASAP
Immediate surgical repair -
open or endovascular aneurysm repair (EVAR)

43
Q

What are the grades of hypertension?

A

Normal
Systolic < 140
Diastolic < 90

Grade 1
Systolic 140-159
Diastolic 90-99

Grade 2
Systolic 160-179
Diastolic 100-109

Grade 3
Systolic 180+
Diastolic 110+

44
Q

What investigations would you order in a patient with newly diagnosed HTN?

A

Urinalysis and urine ACR
Bloods: FBC, EUC, fasting lipids, fasting BGL
12 lead ECG

45
Q

What is your approach to the management of hypertension?

A

Calculate the risk of a cardiovascular event in the next 5 years.

LOW RISK < 10%
if Grade 1 HTN –> lifestyle measures and recheck in 2 months
if Grade 2 or 3 HTN –> lifestyle measures and start medication

MODERATE RISK 10-15% or HIGH RISK >15%
if HTN –> lifestyle measures and start medication

Start 1st line medication at low dose –>
wait 3 months
If target not achieved –> start 2nd 1st line drug at low dose –>
wait 3 months
If target not achieved –> increases dose of drugs to maximum tolerated –>
wait 3 months
If target not achieved –> start 3rd antihypertensive –>
wait 3 months
If target not achieved –> seek specialist advice

46
Q

List the first line antihypertensives.

A

ACE-I
ARB
Thiazide
Ca channel blocker

47
Q

What antihypertensives are used in pregnancy?

A

Mums Love Healthy Newborns

M = methyldopa
L = labetalol
H = hydralazine
N = nifedipine
48
Q

What are the complications of hypertension?

A 
CARDIAC
LV hypertrophy --> CHF
LA hypertrophy --> arrhythmia
Atherosclerosis --> MI
Increased risk of AAA rupture, dissection

NEUROLOGICAL
SAH

KIDNEYS
Hypertensive nephropathy –> CKD

EYES
Hypertensive retinopathy

49
Q

What are the features of hypertensive retinopathy seen on fundoscopy?

A 
AV nicking
Copper wiring
Cotton wool spots
Retinal haemorrhages
Microaneurysms
Papilloedema
50
Q

Outline your approach to smoking cessation.

A 
5As framework:
Ask (do you smoke?)
Assess (level of nicotine dependence, motivation to quit)
Advise to quit
Assist with quitting
Arrange F/U

Pharmacology
1. NRT
combination patch plus oral preferred
caution with recent MI

2. Varenicline: 
nicotinic ACH partial agonist
risk of suicidal thoughts
most effective single agent
often used in combination with NRT
  1. Bupropion:
    inhibits reuptake of dopamine and NA
    risk of seizure
    useful in pregnancy

Medicine (13 decks)

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