Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Management of hyperkalaemia

A

Stabilisation of the cardiac membrane
IV calcium gluconate
(does NOT lower serum potassium levels)

Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF) compartment
combined insulin/dextrose infusion
nebulised salbutamol

Removal of potassium from the body->
calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ECG changes in hyperkalaemia

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Three layers of the aorta

A

Intima
Media
adventitia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

With an aortic dissection blood enters which of the layers

A

blood enters between the intima and media layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Stanford system of classification of aortic dissections

A

Type A - affects ascending aorta before the brachiocephalic artery
Type B - affects descending aorta after left subclavian artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to diagnose an aortic dissection

A

CT angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of aortic dissection

A

surgical emergency
analgesia - morphine
BP and heart rate controlled (to reduce stress on aortic walls) - beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Strongest risk factor for IE

A

having a previous episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common cause of IE

A

Staphylococcus aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most common organism of IE in dental plaques

A

Streptococcus viridans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Non infective causes of IE

A

SLE
Malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Indications for surgery in IE

A
  • Severe valvular incompetence
  • Aortic abscess
  • infections resistant to antibiotics/fungal infections
  • cardiac failurerefractory to standard medical treatment
  • recurrent emboli after antibiotic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the DUKE criteria for

A

diagnosing IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Features of acute pericarditis

A

CP - may be pleuritic and relieved when leaning forward
Non productive cough, dyspnoea
pericardial rub
Tachypnoea
Tachycardia

— | — | — |

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of pericarditis

A

Viral infection - coxsackie
TB
Uraemia
trauma
post MI - dressler’s syndrome
connective tissue disease
Hypothyroidism
Malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations for pericarditis

A

ECG changes - often global and widespread changes; saddle shaped ST elevation; PR depression (most characteristic finding

All patients presenting with acute pericarditis should have a TTE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Difference between pericarditis and constrictive pericarditis

A

Constrictive has a positive Kussmual’s sign and calcification seen on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Secondary causes of hypertension

A

ROPE
R - renal disease
O- obesity
P - pregnancy/ pre-eclampsia
E - endocrine (Conn’s syndrome - hyperaldosteronism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How often does NICE recommend screening for hypertension

A

Every 5 years
Should be more for borderline patients and every year for patients with T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Stage 1 HTN

A

clinic reading >140/90
ambulatory reading >135/85

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Stage 2 HTN

A

> 160/100 clinic
150/95 ambulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Stage 3 HTN

A

> 180/120 clinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Investigations for end organ damage due to HTN

A

Urine albumin:creatinine ratio for proteinuria and dipstick for NVH
Bloods for HbA1c
Fundus examination - Hypertensive retinopathy
ECG - cardiac abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When would you medically manage HTN

A

All patients with stage 2 HTN
Patients <80 with stage 1 HTN and QRISK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

aged <55, non black patient htn first line management

A

A - ACE inhibitor (ramipril)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If HTN in diabetic patient what do you start as first line management

A

ACE or ARB regardless of age

27
Q

Signs and symptoms of malignant hypertension

A

Papilloedema
retinal bleeding
increased cranial pressure causing headache
CP - increased workload of the heart
Haematuria due to kidney failure
Epistaxis difficult to stop

28
Q

How to diagnose malignant hypertension

A

systolic >180 or diastolic >120
evidence of end organ damage

29
Q

Presentation of heart failure

A

SoB worsened on exertion
Cough - may produce frothy/white/pink sputum
Orthopnoea
PND
Peripheral oedema

30
Q

How to diagnose heart failure

A

Clinical presentation
BNP
Echocardiogram
ECG

31
Q

Causes of heart failure

A

IHD
Valvular heart disease - commonly aortic stenosis
Essential/secondary HTN
Arrhythmias

32
Q

Management of heart failure

A

Medical management
surgical treatment in aortic stenosis/mitral regurgitation
Yearly flu and pneumococcal vaccine
stop smoking

33
Q

First line treatment for heart failure

A

ABAL
A - ACE inhibitor (ramipril titrated up to 10mg a day) - avoid in patients with valvular heart disease
B - beta blockers (bisoprolol titrated up to 10mg a day)
A- aldosterone antagonist when symptoms not controlled by A+B (spirinolactone)
L - loop diuretics (furesomide 40mg once daily)

34
Q

What does the left coronary artery become

A

left circumflex and left anterior descending

35
Q

cardiac territories for RCA

A

I, III, and aVF
inferior

36
Q

LCx cardiac territories

A

I, V5 and V6
Lateral

37
Q

LAD cardiac territories

A

V1-V4
Anterior

38
Q

NSTEMI ECG changes

A

ST segment depression in a region
Deep T wave inversion
Pathological Q waves (suggesting a deep infarct - late sign)

39
Q

Causes of a raised troponin

A

MI
Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
PE

40
Q

Ix for MI

A

physical exam
ECG
FBC - anaemia
U&E - prior to ACEi and other meds
LFTs - prior to statins
Lipid profile
Thyroid function tests
HbA1c and fasting glucose
CXR
Echo
CT coronary angiogram

41
Q

Acute STEMI management - presenting within 12 hours of onset

A

Primary PCI if available within 2 hours of onset:

thrombolysis if PCI not available within 2 hours - streptokinase, alteplase, tenectplase

42
Q

Acute NSTEMI management

A

BATMAN
B - beta blocker unless CI
A - aspirin 300mg stat
T - ticagrelor 180mg stat
M - morphine analgesia
A - anticoagulant - fondaparinux
N - nitrates (GTN)

43
Q

GRACE score is for?

A

6 month risk of death or repeat MI after having NSTEMI:
PCI in NSTEMI if medium or high risk

44
Q

Complications of MI

A

DREAD
D - death
R - rupture of heart septum or papillary muscles
E - Edema (HF)
A - arrhythmia and aneurysm
D - Dressler’s syndrome

45
Q

What is Dressler’s syndrome

A

usually 2-3 weeks post MI
Caused by localised immune response and causes pericarditis

presents with pleuritic CP, low grade fever and pericardial rub

Diagnosis made with ECG (global ST elevation and T wave inversion), echo (pericardial effusion) and raised inflammatory markers (CRP and ESR)

Management with NSAIDs (aspirin and ibuprofen) and in severe cases steroids (prednisolone) ; may need pericardiocentesis to remove fluid around heart

46
Q

Secondary prevention medical management of MI

A

6As
Aspirin 75mg once daily

Another antiplatelet e.g. clopidogrel or ticagrelor for up to 12 months

Atorvastatin 80mg once daily

ACE inhibitor (ramipril titrated as tolerated up to 10mg OD)

Atenolol (or another beta blocker)

Aldosterone antagonist for those with clinical heart failure (eplerenone titrated to 50mg once daily

47
Q

What is AF

A

Atrial fibrillation
- Contraction of the atria is uncoordinated, rapid and irregular
- Due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node

48
Q

AF presentation

A

Palpitations
SoB
Syncope
Symptoms of associated conditions (stroke, sepsis, or thyrotoxicosis)

49
Q

Valvular AF

A
  • Moderate or severe mitral stenosis or a mechanical heart valve
    • Assumption is valvular pathology itself has lead to AF
50
Q

Non valvular AF

A

AF without valvular pathology such as mitral regurgitation or aortic stenosis

51
Q

Causes of AF

A

AF affects mrs SMITH
S - sepsis
M - mitral valve pathology
I - IHD
T - thyrotoxicosis
H - HTN

52
Q

Treatment for AF

A

Rate or rhythm control
- Anticoagulation to prevent stroke
- The following DOACs are recommended by NICE for reducing stroke risk in AF:
- apixaban
- dabigatran
- edoxaban
- rivaroxaban
- Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated

53
Q

Who doesnt have rate control as first line management in AF

A
  • Reversible cause of AF
  • AF is of new onset (within last 48hrs)
  • AF is causing HF
  • Remain symptomatic despite being effectively rate controlled
54
Q

Options for rate control in AF

A
  • Beta blocker → first line (atenolol 50-100mg OD)
  • Calcium channel blocker → diltiazem (not preferable in HF)
  • Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
55
Q

Rhythm control for AF

A
  • Pharmacological cardioversion:
    • Flecanide
    • Amiodarone (drug of choice in patients with structural heart disease)
  • Electrical cardioversion
    • Rapidly shock heart back into sinus rhythm
    • involves sedation or a GA and using a cardiac defibrillator machine to deliver controlled shocks in attempt to restore sinus rhythm
  • Long term rhythm control
    • Beta blockers
    • Dronedarone→ second line for maintaining normal rhythm where patients have had successful cardioversion
    • Amiodarone → useful in patients with HF or left ventricular dysfunction
56
Q

Paroxysmal AF

A

Where AF comes and goes in episodes
usually doesnt last longer than 48hrs
should be anticoagulated based on CHADVASc score

pill in pocket method - flecanide (have to have frequent episodes without underlying structural changes

57
Q

What is rheumatic fever

A

Autoimmune condition triggered by streptococcus bacteria. Caused by antibodies created against the Streptococcus bacteria that also target tissues in the body.

58
Q

Pathophysiology of rheumatic fever

A
  • Caused by group A beta-haemolytic streptococcus
    • Typically streptococcus pyogenes causing tonsillitis
  • Immune system creates antibodies to fight the infection
    • Antibodies do not just target bacteria but also the antigens of the body, such as the myocardium of the heart
  • Results in type II hypersensitivity reaction
    • Where immune system attacks cells throughout the body
      • Process is delayed by 2-4weeks after the infection
59
Q

Presentation of rheumatic fever

A

presents 2-4 weeks after a strep infection such as tonsillitis

Fever
joint pain
rash
SoB
Chorea
Nodules

60
Q

Skin involvement in rheumatic fever

A
  • Subcutaneous nodules
    • Occur over extensor surfaces such as the joints
  • Erythema marginatum rash
    • pink rings of varying sizes affecting the torso and proximal limbs
61
Q

What antibodies would you send for if youre suspecting rheumatic fever

A

Antistreptococcal antibodies titre

  • Rise over 2-4 weeks
  • Peak around 3-6 weeks
  • Gradually falls over 3-12 months
  • ASO levels are usually repeated over 2 weeks to:
    • Confirm a negative test
    • Assess whether levels are rising or falling
62
Q

What criteria do you use to diagnose rheumatic fever

A

Jones criteria
need two major or one major plus two minor

JONES - FEAR

major criteria
J - J → joint arthritis

O → organ inflammation, such as carditis

N → Nodules

E → Erythema marginatum rash

S → Syndenham chorea

Minor criteria:

F→ Fever

E→ ECG changes (prolonged PR interval) without carditis

A → Arthralgia without arthritis

R → Raised inflammatory markers (CRP and ESR)

63
Q

Difference between a thrombus and an embolus

A

A thrombus is a blood clot that forms within a blood vessel. If a thrombus breaks free and travels through the bloodstream, it has become an embolus.

Year 3 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions