Brainscape's Knowledge GenomeTM

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


See full index

ΩΩ 3a Bateman - Neuro + Cardio > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

What are some examples of some common ECG abnormalities?

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

What is the defintion of an aneurysm?

A

Dilation >150% of original diameter

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

What is the difference between a true aneurysm and a false aneurysm?

A

True = abnormal dilation of vessel

False = collection of blood around a blood vessel that communicates with the lumen

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

HOW CAN ISCHAEMIA OF HEART MUSCLE OCCUR?

A
  1. Reduced blood flow to the heart muscle (clot or atheroma)
  2. Increased distal resistance (LV hypertrophy)
  3. Reduced O2 carrying capacity (anaemia) or availability (hypoxia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some risk factors for IHD?

Modifaible and non-modifiable?

A

MODIFIABLE

  1. Smoking.
  2. Diabetes
  3. Hypertension.
  4. Hypercholesterolaemia.
  5. Sedentary lifestyle

Non-modifiable

  1. Gender.
  2. Family history.
  3. Personal history.
  4. Age.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

WHAT IS ANGINA?

A

Chest pain brought on either:

By exertion which resloves with rest

Or at rest

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

What are the different types of angina?

A
  1. Stable angina
  2. Unstable angina
  3. Decubitus angina (precipitated by lying flat)
  4. Variant (Prinzmetal’s) angina: caused by coronary artery spasm.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of angina?

A
  1. Atheroma
  2. Anaemia
  3. Spasm
  4. Tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the symptoms of angina?

A
  1. Chest pain/discomfort.
  2. Heavy, central, tight, radiation to arms, jaw, neck.
  3. Precipitated by exertion.
  4. Relieved by rest or GTN within 5 mins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the tests for stable angina?

A
  1. CT Angiogram
    • Gold standard, shows luminal narrowing
  2. ECG
    • Pathological Q waves in particular, LBBB, and ST-segment and T wave abnormalities (for example, flattening or inversion).
  3. Bloods
    • May show anaemia
  4. CXR
    • May show increased heart size and pulmonary vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the management options for stable angina pectoralis?

A
  1. Drugs
    • Aspirin to prevent clots
    • Statin to lower cholesterol
    • Glyceryl Trinitrate (SL) (GTN Spray)
    • BB (atenolol) (best in heart failure patients too)/CCB OR (verapamil/diltiazem) - FIRST LINE
      • If adding drug to beta blocker then nifedipine is drug of choice, if not tolerate then ivabradine
      • NEVER PUT BETA BLOCKER AND VERAPAMIL/DILTIAZEM TOGETHER
  2. If patient can’t tolerate beta blocker or calcium channel blocker then a long acting nitrate can be used
    • Ivabradine
    • Nicorandil - can cause ulcers
  3. Percutaneous Intervention (PCI)
  4. Coronary Artery Bypass Graft (CABG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHAT IS ACUTE CORONARY SYNDROME PATHOLOGY?

A

Plaque rupture, thrombosis, and inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the different acute coronary syndomes?

A
  1. Unstable angina
  2. (NSTEMI) Non-Q wave infarction, ST depression and T wave inversion
  3. (STEMI) Q wave infarction, ST elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the different ECG changes for ACS?

A

STEMI
ST elevation and tall T waves, may be a new LBBB in larger MIs (STEMI)

NSTEMI
A retrospective diagnosis, will see ST depression

Ischaemia
ST depression and T wave flattening

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

What are the poor prognostic factors for ACS?

A
  1. Age
  2. Development (or history) of heart failure
  3. Peripheral vascular disease
  4. Reduced systolic blood pressure
  5. EVIDENCE OF CARDIOGENIC SHOCK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

WHAT IS UNSTABLE ANGINA?

A

An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage

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

What is the clinical classification of unstable angina?

A
  1. Cardiac chest pain at rest.
  2. Cardiac chest pain with crescendo pattern.
  3. New onset angina.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the test for unstable angina?

A
  1. FBC
    • Anaemia aggravates it
  2. Cardiac enzymes
    • Excludes infarction
  3. ECG
    • When in pain shows ST depression
  4. Coronary angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment for unstable angina?

A
  1. M - Morphine
  2. O - Oxygen (if sats <94%)
  3. N - Nitrates
  4. A - Aspirin

If STEMI then a second anitplatlet should be added (e.g. clopidogrel, ticagrelor)

Then patinets go for PCI

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

WHAT IS A MYOCARDINAL INFARCTION?

A

Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial cell death and inflammation.

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

What are the symptoms of a myocardial infarction?

How long does it need to last to be an MI?

A
  1. Acute central chest pain radiating to jaw or shoulder
  2. Nausea
  3. SOB
  4. Palpitations

Lasting >20 mins

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

What are the signs of a myocardial infarction?

A
  1. Clammy and pale
  2. 4th heart sound
  3. Pansystolic murmur
  4. May later develop peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the tests for a MI?

A
  1. ECG
    • ​​Classically, hyperacute (tall) T waves, ST elevation or new LBBB occur within hours of transmural infarction.
    • T wave inversion and development of pathological Q waves follow over hours to days.
  2. CXR:
    • Cardiomegaly, pulmonary oedema, or a widened mediastinum
  3. Cardiac enzymes
    • Troponin
    • Creatine kinase MB - If MI’s occur close together is better for for 4-5 days
    • Myoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the initial management for a MI?

A
  1. M - Morphine
  2. O - Oxygen (if sats <94%)
  3. N - Nitrates
  4. A - Aspirin

If from cocaine overdose then benzodiazepine should be added

If STEMI then a second anitplatlet should be added (e.g. clopidogrel, ticagrelor)

Then patinets go for PCI within 2 HOURS

IF NOT WITHIN 2 HOURS THEN FIBRINOLYSIS WITHIN 12 HOURS

Recheck ECG within 60-90 minutes to see if ST elevation gone - urgent PCI if not

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

What is the further management after an MI?

A

Drug Treatment:

  1. Dual antiplatelet therapy (aspirin plus a second antiplatelet agent)
  2. ACE inhibitor
  3. Beta-blocker
  4. Statin
  5. Diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish
  6. Exercise: advise 20-30 mins a day until patients are ‘slightly breathless’
  7. Sexual activity may resume 4 weeks after an uncomplicated MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the complications of MI?

A
  1. Cardiac arrest; cardiogenic shock; LVF.
  2. Unstable angina
  3. Bradycardias or heart block.
  4. Tachyarrhythmias
  5. Pericarditis
  6. DVT & PE
  7. Systemic embolism
  8. Cardiac tamponade
  9. Mitral regurgitation
  10. Ventricular septal defec
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Dressler’s syndrome?

A
  1. Recurrent pericarditis
  2. Pleural effusions
  3. Fever
  4. Anaemia and ESR increase

1–3 wks post-MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the signs of a posterior MI?

A

Tall R waves in V1-V2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the contraindications to thrombolysis?

A
  1. Active internal bleeding
  2. Recent haemorrhage, trauma or surgery (including dental extraction)
  3. Coagulation and bleeding disorders
  4. Intracranial neoplasm
  5. Stroke < 3 months
  6. Aortic dissection
  7. Recent head injury
  8. Severe hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the symptoms of left ventricular free wall rupture?

A
  1. This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards.
  2. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).
  3. Urgent pericardiocentesis and thoracotomy are required.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the symptoms of acute mitral regurgitation?

A
  1. More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.
  2. Acute hypotension and pulmonary oedema may occur.
  3. An early-to-mid systolic murmur is typically heard.
  4. Patients are treated with vasodilator therapy but often require emergency surgical repair.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

WHAT IS SHOCK?

A

Circulatory failure resulting in inadequate organ perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is shock defined as?

A
  1. Low BP
  2. Evidence of tissue hypoperfusion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does a patient in shock look like?

A

Skin is pale, cold, sweaty and vasoconstricted

Pulse is weak and rapid

Pulse pressure reduced, MAP may be maintained

Urine output reduced

Confusion, weakness, collapse, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the main cause of injury from shock?

A

Prolonged hypotension can lead to life threatening organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the different types of shock?

A

Hypovolaemic shock

Cardiogenic shock

Distributive shock
Septic shock
Analphylactic shock
Neurogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

WHAT IS HYPOVALEMIC SHOCK?

A

Low circulating blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What can cause hypovalemic shock?

A

Loss of blood

  1. Acute GI bleeding
  2. Trauma
  3. Ruptured AA

Loss of fluid

  1. Dehydration
  2. Burns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do you treat hypovalaemic shock?

A
  1. Identify and treat underlying cause.
  2. Raise the legs.
  3. Give fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

WHAT IS CARDIOGENIC SHOCK?

When can it occur?

A

Cardiogenic shock is a state of inadequate tissue perfusion primarily due to cardiac dysfunction.

—May occur suddenly or after progressively worsening heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are some causes of cardiogenic shock?

A
  1. MI
  2. Arrhythmias
  3. PE
  4. Tension pneumothorax
  5. Cardiac tamponade
  6. Myocarditis
  7. Endocarditis
  8. Aortic dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the symptoms for cardiogenic shock?

A
  1. Low BP
  2. High HR
  3. High RR
  4. Confusion
  5. Pallor
  6. Clammy
  7. Pale peripheries
  8. Reduced urine output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the investigations for cardiogenic shock?

A
  1. ECG
    • Tachycardic
  2. Blood pressure
    • Low
  3. JVP pressure
    • RAISED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the management of cardiogenic shock?

What do you need to monitor?

A
  1. Treat the cause
  2. Oxygen
  3. Diamorphine IV for pain and anxiety
  4. Correct arrhythmias, U&E abnormalities or acid–base disturbance

—Monitor CVP, BP, ABG, ECG, urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

WHAT IS SEPSIS?

A

Sepsis exists when a systemic inflammatory response is associated with an infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is septic shock?

A

Septic shock exists when sepsis is complicated by persistent hypotension unresponsive to fluid resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the risk factors for septic shock?

A
  1. Age
  2. Diabetes mellituis (DM)
  3. Immunocompromised
  4. Alcoholics
  5. Burns
  6. IVDU
  7. Pregnancy
  8. Catheter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the symptoms for septic shock?

A
  1. Low BP
  2. High HR
  3. Low sats (O2)
  4. High resp rate (RR)
  5. Lactate >2
  6. Unresponsive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the investigations for septic shock?

A

Cultures (2 peripheral blood, plus urine/sputum/CSF)

LACTATE

ABG and BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the treatment for septic shock?

A

OXYGEN

FLUIDS (check BP and ABG)

IV ANTIBIOTICS
(Tacozin and gentamicin, and vancomycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

WHAT IS ANAPHYLATIC SHOCK?

A

Intense allergic reaction.

Massive release of histamine and other vasoactive mediators causing haemodynamic collapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What type of hypersensitivity is anaphylatic shock?

A

Type-I IgE-mediated hypersensitivity reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are some causes of anaphylatic shock?

A
  1. Drugs, eg penicillin, and contrast media in radiology
  2. Latex
  3. Stings, eggs, fish, peanuts, strawberries, semen (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the signs and symptoms of anaphylatic shock?

A
  1. Itching
  2. Sweating
  3. Diarrhoea and vomiting
  4. Erythem
  5. Urticaria
  6. Oedema
  7. Wheeze
  8. Laryngeal obstruction
  9. Cyanosis
  10. Tachycardia
  11. Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the management of anaphylatic shock?

A
  1. Oxygen
  2. Remove the cause
  3. Adrenaline IM - 500 micrograms - 1 in 1000
    Repeated every 5 minutes if necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

WHAT IS NEUROGENIC SHOCK?

A

Distributive

Disruption of the autonomic pathways within the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What can cause neurogenic shock?

A
  1. Spinal cord injury
  2. Epidural
  3. Spinal anaesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the treatment options for neurogenic shock?

A
  1. Dopamine and vasopressin (ADH).
  2. Atropine is administered for slowed heart rate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What organs are at risk of shock?

A
  1. Kidneys - Acute tubular necrosis
  2. Lung – Acute Respiratory Distress Syndrome (ARDS) (or “shock lung”)
  3. Heart – myocardial ischaemia and infarction
  4. Brain – confusion, irritability, coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

WHAT IS ACUTE RESPIRATORY DISTRESS SYNDROME?

A
  1. Increase in alveolar permeability
  2. Fluid accumilation in the alveoli
  3. Not associated with cardiac causes
  4. Impaired oxygenation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are some causes of ARDS?

A
  1. Infection: sepsis, pneumonia
  2. Massive blood transfusion
  3. Trauma
  4. Smoke inhalation
  5. Acute pancreatitis
  6. Cardio-pulmonary bypass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the clinical features of ARDS?

A
  1. Dyspnoea
  2. Elevated respiratory rate
  3. Bilateral lung crackles
  4. Low oxygen saturations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the investigations for ARDS?

A
  1. Chest x-ray
  2. ABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the management for ARDS?

A
  1. ITU - Oxygenation/ventilation to treat the hypoxaemia
  2. General organ support e.g. vasopressors as needed
  3. Treatment of the underlying cause e.g. antibiotics for sepsis
  4. Certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

WHAT DOES CARDIOMYOPATHY REFER TO?

A

Primary heart muscle disease – often genetic.

Three types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

WHAT IS HYPERTROPHIC CARDIOMYOPATHY?

https://www.youtube.com/watch?v=8RnkKB8xvwA

A

Heart muscle becomes thick, heavy and hypercontactile.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is Hypertrophic cardiomyopathy (HCM) caused by?

What inheritance is it?

A

Sarcomeric protein gene mutations.

Autosomal dominant inheritance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the epidemology of HCM?

A

Leading cause of death in the young

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the pathology of heart walls in HCM?

A
  1. Asymmetric septal hypertrophy
  2. Intervenricular septum more than free wall takes up more room so less filling
  3. More stiff and less compliant
  4. Stroke volume goes down
  5. LV outflow tract (LVOT) obstruction which pulls mitral valve towards it
    • Venturi effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What type of heart failure if HCM?

A

Diastolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What kind of heart sound is heard in HCM? Where is it also seen?

A

Crescendo-decrescendo murmur

Aortic valve stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the symptoms of HCM?

A
  1. Sudden death
  2. Fast arrythmias
  3. Palpitations
  4. Dyspnoea
  5. Dizzy spells or syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the signs of HCM?

A
  1. —Jerky pulse
  2. Double apex beat
  3. Systolic thrill at lower left sternal edge
  4. Harsh ejection systolic murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the tests for HCM?

A

Echo
Asymmetrical septal hypertrophy; small LV cavity with hypercontractile posterior wall; midsystolic closure of aortic valve

ECG
LVH; progressive T wave inversion; deep Q waves, AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the treatment for HCM?

A
  1. Beta-blockers or verapamil for angina + SOB.
  2. Amiodarone for arrhythmias (AF, VT)
  3. DIGOXIN IS CONTRAINDICATED
  4. Anticoagulate for paroxysmal AF or systemic emboli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What drug is contraindicated in HCM?

A

Digoxin

Increase contraction force, increase obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How is sudden cardiac death caused in HCM?

A

Ventricular arrythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

WHAT IS DILATED CARDIOMYOPATHY (DCM)?

A

Causes all four chambers of the heart to enlarge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Dilated Cardiomyopathy (DCM) often caused by?

A
  1. Alcohol
  2. Increased BP
  3. Haemochromatosis
  4. Viral infection
  5. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What happens in Dilated cardiomyopathy (DCM)?

What type of heart failure is it?

A
  1. Large space, thin walls
  2. Weak contraction
  3. Less blood pumped out in each beat
  4. Biventicular congestive heart failure
  5. Systolic heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What type of heart sound is heard in Dilated Cardiomyopathy (DCM)?

A
  1. Holosystolic murmur
  2. S3 sounds also present, blood slamming into wall in diastole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the symptoms of Dilated Cardiomyopathy (DCM)?

A
  1. Fatigue
  2. Dyspnoea
  3. Pulmonary oedema
  4. Right ventricular failure
  5. Emboli
  6. Atrial fibrillation
  7. Ventricular tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the signs of Dilated Cardiomyopathy (DCM)?

A
  1. —Increased pulse
  2. Decreased blood pressure
  3. Increased JVP
  4. Pleural effusion
  5. Oedema
  6. Jaundice, hepatomegaly, ascites
  7. —Displaced diffuse apex beat, S3 gallop
  8. —Mitral or tricuspid regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the tests for Dilated Cardiomyopathy (DCM)?

A
  1. Blood:
    • Plasma BNP is sensitive and specific in diagnosing heart failure.
  2. CXR:
    • Cardiomegaly, pulmonary oedema.
  3. ECG:
    • Tachycardia, non-specific T wave changes, poor R wave progression.
  4. Echo:
    • Globally dilated hypokinetic heart and low ejection fraction. Look for MR, TR, LV mural thrombus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the treatment for Dilated Cardiomyopathy (DCM)?

A
  1. Stop drinking
  2. Treatment of cardiac failure
    • ACE inhibitors
    • Beta Blockers
    • Diuretics + Digoxin
  3. Anti-arrythmic drugs
    • Amiodarone
  4. Cardiac transplantation and cardiomyoplasty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

WHAT IS RESTRICTIVE CARDIOPATHY?

A

Heart muscle becomes stiff and less compliant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the causes of RCM?

A
  1. Amyloidosis
  2. Sarcoidosis
    • Collection of immune cells
  3. Radiation
  4. Loffler endomcarditis
    • Eosinophils in lung tissue and heart tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What happens in amyloidosis?

A

Proteins that have been misfolded and become insoluble

Deposit in tissue in organs making them become less compliant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the pathology of RCM?

A
  1. Heart muscle stays same size
  2. When blood comes in heart doesn’t stretch
  3. Less blood
  4. Less pumped out
  5. = Heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What type of heart failure is RCM?

A

Diastolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the signs of RCM?

A
  1. These are mainly of right heart failure with increase JVP
  2. Kussmaul’s sign (JVP rising paradoxically with inspiration)
  3. Quiet heart sounds
  4. S3
  5. Diastolic pericardial knock, hepatosplenomegaly, ascites, and oedema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the investigations for RCM?

A

ECG
Low amplitude QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the treatment for RCM?

A
  1. Treat underlying cause
  2. Heart transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What do all cardiomyopathies carry?

A

An arrhythmic risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

WHAT IS INHERITED ARRHYTHMIA (CHANNELOPATHY) CAUSED BY?

A

Ion channel protein gene mutations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Which ions are involved with channelopathy?

A
  1. Potassium
  2. Sodium
  3. Calcium channel.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What do channelopathies include?

A
  1. Long QT
  2. short QT
  3. Brugada
  4. CPVT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What do channelopathies normally present with and what do they have that is normal?

A

Recurrent syncope and have a structurally normal heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is sudden cardiac death in young people normally due to?

What disease is it most likely to be?

A
  1. An inherited condition.
  2. Cardiomyopathy or ion channelpathy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What does sudden arrhythmic death syndrome (SADS) usually refer to?

A

Normal heart/arrhythmia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

WHAT IS AN ANEURYSM?

https://www.youtube.com/watch?v=pEOqffiwE7k

A

Abnormal buldge in vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the risk factors for aneurysms?

A
  1. Male
  2. Over 60
  3. Hypertension
  4. Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the typical causes of an anneurysm

A
  1. Atheroma
  2. Trauma
  3. Infection
  4. Connective tissue disorders
  5. Inflammations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the pathology of an aneurysm?

A

Weakness in vessel wall

Ballooning outwards of vessel wall due to pressure

Laplace’s law causes positive feedback loop

Gives bigger aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

When is an aneurysm official labelled an aneurysm?

A

When the diameter exceeds 1.5 times the normal size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the common sites for anneurysms

What are the complications?

A

Common sites Aorta (infrarenal most common), iliac, femoral and popliteal arteries.

Complications Rupture; thrombosis; embolism; fistulae; pressure on other structures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are the different types of aneurysms?

A
  1. True aneurysms
    • Abnormal dilatations that involve all layers of the arterial wall.
    • THEN EITHER
    • Fusiform
    • OR
    • saccular (Berry aneurysms)
  2. False aneurysms (pseudoaneurysms)
    • Blood in the outer layer only (adventitia) which communicates with the lumen (eg after trauma).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What happens when an aneurysm explodes?

A

Blood spurts out of the hole

Less blood goes downstream

Ischaemia of downstream cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the features of an abdominal aortic aneurysm?

A
  1. Severe, central abdominal pain radiating to the back
  2. Pulsatile, expansile mass in the abdomen
  3. Patients may be shocked (hypotension, tachycardic) or may have collapsed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the options for a unruptured anneurysm?

A
  1. Elective surgery
  2. Stenting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

WHAT ARE THE CAUSES OF A AAA?

A
  1. Several different groups of patients suffer from aneurysmal disease.
  2. The commonest group is those who suffer from standard arterial disease, i.e. Those who are hypertensive, have diabetes and have been or are smokers.
  3. Other patients such as those suffering from connective tissue diseases such as Marfan’s may also develop aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a change in the balance of collagen and elastic fibres.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

When is a AAA referred for surgery?

A

>5.5cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are the different follow up times for each anneurysm size?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are the treatments for a AAA?

A
  1. Open surgery - needed if iliac arteru is too tortous
  2. Endovascular aneurysm repair (EVAR) - longer follow-up, reintervention rate, not suitable for every type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is a common complication of AAA repair?

What is this caused by?

A
  1. Trash foot
    • Disloged emboli travels around the body and lodges in distal vessels, causing ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

WHAT IS AORTIC DISSECTION?

https://www.youtube.com/watch?v=AZElPJtyxck

A

Tear in tunica intima, causes blood to pool between intima and media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What can cause aortic dissection?

A
  1. Chronic hypetension
  2. Increase blood volume
  3. Coarctation
  4. Weakened aortic wall
  5. Marfan’s
  6. Ehlers-Danlos syndrome
  7. Aneurysms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Where does aortic dissection normally occur?

A

Within the first 10cm of aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What can a aortic dissection cause?

A
  1. Blood back up into pericardial space causing
    • Pericardial temponade
  2. Blood goes out intima and comes back into blood vessel through and hole
  3. Blood flows does the aorta inbetween the layers and puts compression on other arteries
    • Renal artery
    • Subclavian artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What are the different types of aortic dissection?

A

Type A (70%) dissections involve the ascending aorta, irrespective of site of the tear,

Whilst if the ascending aorta is not involved it is called type B (30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are the symptoms of aortic dissection?

A
  1. Sharp chest pain radiating to back
  2. Hypotension
  3. Shock

Type A

  1. Weak pulses
  2. Aortic regurgitation
  3. Weak pulse in downstream artery
  4. Difference in BP between left and right arms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are the investigations for aortic dissection?

A
  1. CXR
    • Widend mediastinum
  2. CT Angiogram chest, abdo, pelvis
    • ​​Suitable for stable patients and planning surgery
  3. Transoesophageal echo
    • True lumen and flase aorta
123
Q

What is the management of aortic dissection?

A
  1. Type A
    • IV labetalol AND
    • Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
  2. Type B*
    • Conservative management
    • Bed rest
    • Reduce blood pressure IV labetalol to prevent progression
124
Q

HOW MANY LAYERS IS THE PERICARDIUM?

WHAT IS THE STRUCTURE?

A

Two.

Visceral single cell layer adherent to epicardium

Fibrous parietal layer

2mm thick

Acellular collagen and elastin fibres

50ml of serous fluid.

125
Q

Why is the pericardium important?

What is important about the small reserve volume?

A
  1. Restrains the filling volume of the heart.
  2. If the volume is exceeded the pressure is translated to the cardiac chambers.
126
Q

WHAT IS CARDIAC TAMPONADE?

A

Fluid builds up in the pericardium and results in compression of the heart.

127
Q

What is the cause of cardiac tamponade?

A
  1. Any pericarditis
  2. Aortic dissection
  3. MI
  4. Trauma
  5. Trans-septal puncture at cardiac catheterization
  6. Cancer
128
Q

What are the signs of cardiac tamponade?

A
  1. Pulse increase
  2. BP decerease
  3. Pulsus paradoxus
    • An abnormally large drop in BP during inspiration
  4. JVP increase
  5. Kussmaul’s sign
  6. Muffled S1 and S2.
129
Q

What is Beck’s triad?

A

Symptoms of cardiac tamponade:

  1. Falling BP
  2. Rising JVP
  3. Muffled heart sounds.
130
Q

What are the investigations for cardiac tamponade?

A
  1. Beck’s triad
    • Falling BP; rising JVP; muffled heart sounds.
  2. CXR
    • Big globular heart (if >250mL fluid).
  3. ECG
    • Low voltage QRS ± electrical alternans
  4. Echo is diagnostic
    • Echo-free zone around the heart ± diastolic collapse of right atrium and right ventricle.
131
Q

What is the management of cardiac tamponade?

A

The pericardial effusion needs urgent drainage

132
Q

What does chronic pericardial effusion have that is unique?

A

Pericardium slowly adapts to the increasing fluid and therefore reduces the effect on diastolic filling of the chambers.

133
Q

WHAT IS PERICARDIAL EFFUSION?

A

Accumulation of fluid in the pericardial sac.

134
Q

What are the causes of pericardial effusion?

A

Any cause of pericarditis

  1. Idiopathic.
  2. Viral
    • Coxsackie B virus
    • Enteroviruses
    • Herpesviruses (EBV, CMV, HHV-6),
  3. Dresseler’s syndrome
    • Happens after heart attack
    • When an MI happens lots of necrosis
    • This also affects the pericardium
  4. Autoimmune
    • Rheumatoid arthritis
    • Scleraderma
    • SLE
135
Q

What are the symptoms of pericardial effusion?

A
  1. Dyspnoea
  2. Raised JVP
  3. Bronchial breathing at left base
  4. Look for signs of cardiac tamponade
136
Q

What are the investigations for pericardial effusion?

A
  1. CXR
    • Enlarged, globular heart.
  2. ECG
    • Low-voltage QRS complexes and alternating QRS morphologies (electrical alternans).
  3. Echo
    • Shows an echo-free zone surrounding the heart.
137
Q

What are the management options for pericardial effusion?

A
  1. Treat the cause.
  2. Pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or therapeutic (cardiac tamponade).
138
Q

WHAT IS ACUTE PERICARDITIS?

https://www.youtube.com/watch?v=jqClJsqnFFA

A

Inflammatory pericardial syndrome with or without effusion.

139
Q

What are the causes of pericarditis?

A
  1. Idiopathic.
  2. Viral
    • Coxsackie B virus
    • Enteroviruses
    • Herpesviruses (EBV, CMV, HHV-6),
  3. Dresseler’s syndrome
    • Happens after heart attack
    • When an MI happens lots of necrosis
    • This also affects the pericardium
  4. Autoimmune
    • Rheumatoid arthritis
    • Scleraderma
    • SLE
140
Q

What is the patholgy of pericarditis?

A

Fluid and immune cells move from tiny blood cells into the fibrous pericardium

141
Q

What is the clinical presentation of somebody with pericarditis?

A
  1. Fever
  2. Chest pain
    • Worse with heavy breathing
    • Better with sitting up and leaning forward
142
Q

What can a clinical diagnosis of acute pericarditis be diagnosed from?

A

2 of 4 of:

  1. Chest pain.
  2. Friction rub.
  3. ECG changes.
  4. Pericardial effusion.
143
Q

What tests can you do to check if somebody has pericarditis?

A
  1. ECG changes
    • The changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
    • ‘Saddle-shaped’ ST elevation
    • PR depression: most specific ECG marker for pericarditis
  2. All patients with suspected acute pericarditis should have transthoracic echocardiography TOE
144
Q

What does an ECG look like with a patient who has pericarditis?

A

First few weeks
Diffuse saddle shaped ST segment elevation
Decrease PR

After that
T waves flattened

After that
ECG returns back to normal

145
Q

What is the management of pericarditis?

A
  1. Treat underlying cause
  2. NSAID
    • Ibuprofen PO or Aspirin PO
  3. Colchicine
146
Q

WHAT IS HEART FAILURE?

A

A symptomatic condition where breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output

A state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues

147
Q

How do you calculate cardiac output?

A

CO = HR x SV

148
Q

What is the most common cause of heart failure?

What does this usually result from?

What are some other causes?

A
  1. Myocardial dysfunction.
    • Result of IHD.
  2. Hypertension.
  3. Alcohol excess.
  4. Cardiomyopathy.
  5. Valvular.
  6. Endocardial.
  7. Pericardial causes.
149
Q

What is systolic heart failure?

A

Inability of the ventricle to contract normally, resulting in decreaed cardiac output.

Ejection fraction (EF) is <40%

150
Q

What are the causes of systolic heart failure?

A
  1. IHD
  2. MI
  3. Cardiomyopathy.
151
Q

What is diastolic heart failure?

A

Inability of the ventricle to relax and fill normally

Causing increased filling pressures.

EF is >50%.

152
Q

What are the causes of diastolic heart failure?

A
  1. Constrictive pericarditis
  2. Tamponade
  3. Restrictive cardiomyopathy
  4. Hypertension
153
Q

How may left and right sided heart failure occur?

A

Left ventricular failure (LVF) and right ventricular failure (RVF) may occur independently, or together as congestive cardiac failure (CCF).

154
Q

What are some causes of left sided heart failure?

A

Hypertension

155
Q

What are the symptoms of left sided heart failure?

A
  1. Dyspnoea,
  2. Poor exercise tolerance
  3. Fatigue
  4. Orthopnoea
  5. Paroxysmal nocturnal dyspnoea (PND)
  6. Nocturnal cough (±pink frothy sputum)
156
Q

What are some causes of right ventricular failure?

A
  1. LVF,
  2. Pulmonary stenosis
  3. Lung disease.
157
Q

What are the symptoms of right ventricular heart failure?

A
  1. Peripheral oedema (up to thighs, sacrum, abdominal wall),
  2. Ascites
  3. Nausea
  4. Anorexia
  5. Facial engorgement
  6. Pulsation in neck and face (tricuspid regurgitation)
  7. Epistaxis.
158
Q

What tests can you do for heart failure?

A
  1. Blood Tests - FIRST LINE
    • BNP
  2. LFTS, FBC, U&Es, BNP, TFTs
  3. Cardiac enzymes
    • Creatinine kinase, troponin I, troponin T
  4. CXR
  5. ECG
  6. Echocardiography
159
Q

What would you see on a chest XR for heart failure?

A

ABCDE

  1. Alveolar oedema
  2. Kerley B lines
  3. Cardiomegaly
  4. Dilated prominant upper lobe vessels
  5. Pleural Effusion
160
Q

What are the systems involved with protection and survival of the heart?

A

The sympathetic system
Increases afterload by causing peripheral vasoconstriction

The renin-angiotensin-aldosterone axis
Salt and water retention
Increases afterload and preload (^ volume and vasoconstriction)

Cardiac changes
Ventricular dilatation
Myocytehypertrophy

161
Q

What does an increase in cardiac norepinephrine produce?

What happens in the long term?

A

Increased adrenergic activation

Direct toxicity to myocytes

Increased HR and contractility causing extra strain on heart

Increased vasocontriction, increased afterload, more strain on heart

162
Q

What does angiotensin 2 produce?

A

Increase salt and water retention

Increased preload, extra strain on heart

163
Q

What is the ACUTE treatment for chronic heart failure?

A
  1. Recommended treatments for all patients
    • IV loop diuretics
    • e.g. furosemide or bumetanide
  2. Possible additional treatments
  3. Oxygen
    • this should be given in line with British Thoracic Society guidelines, i.e. keep oxygen saturations at 94-98%
  4. Vasodilators
    • Nitrates should not be routinely given to all patients
    • They may, however, have a role if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease
    • The major side-effect/contraindication is hypotension
  5. Patients with respiratory failure
    • CPAP
  6. Patients with hypotension (e.g. < 85 mmHg)/cardiogenic shock
  7. inotropic agents
    • e.g. dobutamine
    • should be considered for patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock
  8. Vasopressor agents
    • e.g. norepinephrine
    • normally only used if insufficient response to inotropes and evidence of end-organ hypoperfusion
  9. Mechanical circulatory assistance
    • e.g. intra-aortic balloon counterpulsation or ventricular assist devices
164
Q

What is the treatment for chronic heart failure?

A
  1. First-line treatment
    • ACE-inhibitor and a beta-blocker
  2. Second-line treatment
    • Aldosterone antagonist - e.g. spironolactone
  3. Third-line treatment
    • ​​Ivabradine - if heart rate above 75
    • Sucubitil-valsartan if EF <35%
    • Digoxin
    • Hydralazine and nitrate
    • Spironolactone

Loop diuretics DO NOT help

165
Q

WHAT IS TETRALOGY OF FALLOT?

A
  1. Pulmonary stenosis
  2. RV hypertrophy
  3. Overriding aorta
  4. VSD
166
Q

What are the physiology of Tetralogy of Fallot?

A
  1. The stenosis of the RV outflow leads to the RV being at higher pressure than the left
  2. Therefore blue blood passes from the RV to the LV
  3. The patients are BLUE
  4. Toddlers may squat
167
Q

What is the presentation of infants in tetralogy of Fallot and why?

A
  1. Infants may be acyanotic at birth
  2. Pulmonary stenosis murmur as the only initial finding.
  3. Cyanotic due to decreasing flow of blood to the lungs as well as right-to-left shunt across the VSD.
  4. Toddlers may squat
  5. Typical of TOF, as it increases peripheral vascular resistance and decreases the degree of right to left shunt.
  6. Adult patients are often asymptomatic
168
Q

What are the tests for tetrology of Fallot?

A
  1. ECG
    • RV hypertrophy with a right bundle-branch block.
  2. CXR
    • Boot-shaped heart
  3. Echocardiography
    • Can show the anatomy as well as the degree of stenosis.
169
Q

What is the management of tetrology of Fallot?

A
  1. Surgical repair is often undertaken in two parts
  2. Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm
170
Q

WHAT IS A VENTRICULAR SEPTAL DEFECT?

A

Hole in the connecting venticles

171
Q

What are the different pressures in the ventricles and what is the result in VSD?

A
  1. High pressure LV
  2. Low pressure RV
  3. Blood flows from high pressure chamber to low pressure chamber
  4. Therefore NOT blue
  5. Increased blood flow through the lungs
172
Q

What are the causes of VSD?

A

Congenital

  1. Down’s syndrome
  2. Edward’s syndrome
  3. Patau syndrome
  4. cri-du-chat syndrome

Acquired (post-MI).

173
Q

What are the ventricular septal defects clinical signs?

A

Large

  1. Pan-systloic murmur varies in intensity
  2. Small breathless skinny baby
  3. Increased respiratory rate
  4. Tachycardia
  5. Big heart on chest X ray

Small

  1. Loud systolic murmur
  2. Thrill (buzzing sensation)
  3. Well grown
  4. Normal heart rate
  5. Normal heart size
174
Q

What is the treatment for VSD?

A
  1. Large
    • Require fixing in infancy (PA band, complete repair)
  2. Small
    • Endocarditis risk
    • Need no intervention
175
Q

What may VSD lead to?

A

May lead to Eisenmengers syndrome

  1. High pressure pulmonary blood flow
  2. Damages to delicate pulmonary vasculature
  3. The resistance to blood flow through the lungs increases
  4. The RV pressure increases
  5. The shunt direction reverses
  6. The patient becomes BLUE.
176
Q

WHAT IS ATRIAL SEPTAL DEFECT?

A
  1. Abnormal connection between the two atria (primum, secundum, sinus venosus)
  2. Common
  3. Often present in adulthood.
177
Q

What are the two types of ASD?

A
  1. Primum: present earlier, may involve AV valves
  2. Secundum: may be asymptomatic until adulthood
178
Q

What is the physiology of atrial septal defects i.e blood flow direction?

A
  1. Slightly higher pressure in the LA than the RA
  2. Shunt is left to right
  3. Therefore NOT blue
  4. Increased flow into right heart and lungs
179
Q

What is the physiology between large and small atrial septal defects?

A

Large

  1. Significant increased flow through the right heart and lungs in childhood
  2. Right heart dilatation
  3. SOBOE
  4. Increased chest infections
  5. If any stretch on the right heart should be closed

Small

  1. Small increase in flow
  2. No right heart dilatation
  3. No symptoms
  4. Leave alone
  5. NB. The shunt on small to moderate sized defects increases with age
180
Q

What are some complications of ASD?

A
  1. Reversal of left-to-right shunt, ie Eisenmenger’s complex
  2. Paradoxical emboli (vein to artery via ASD; rare)
  3. EMBOLI
181
Q

What are the clinical signs of atrial septal defects?

A
  1. Pulmonary flow murmur
  2. Fixed split second heart sound (delayed closure of PV because more blood has to get out)
  3. Big pulmonary arteries on CXR
  4. Big heart on chest X ray
182
Q

What is the treatment of ASD?

A
  1. In children closure is recommended before age 10yrs.
  2. In adults, transcatheter closure is now more common than surgical.
183
Q

WHAT CAN ATRIA-VENTRICULAR SEPTAL DEFECTS INVOLVE?

A

Hole in the centre. Can involve the ventricular septum, the atrial septum, the mitral and tricuspid valves.

184
Q

What is the symptoms of atria-ventricular septal defect? For a partial and complete defect?

A

Complete defect

  1. Breathless as neonate
  2. Poor weight gain
  3. Poor feeding
  4. Torrential pulmonary blood flow
  5. Needs repair or PA band in infancy
  6. Repair is surgically challenging

Partial defect

  1. Can present in late adulthood
  2. Presents like a small VSD / ASD
  3. May be left alone if there is no right heart dilatation
185
Q

WHAT IS PATENT DUCTUS ARTERIOSUS?

A

Failure of ductus arterioles to close.

186
Q

What are the clinical signs of ductus arteriosis?

A
  1. Continuous ‘machinery’ murmur
  2. If large, big heart, breathless
  3. Heaving apex beat
  4. Wide pulse volume
  5. Large volume, bounding, collapsing pulse
  6. Eisenmenger’s syndrome
    • Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)
187
Q

What is the physiology of patent ductus arterioles with a large and a small?

A

Large

  1. Torrential flow from the aorta to the pulmonary arteries in infancy
  2. Breathless, poor feeding, failure to thrive
  3. More common in prem babies –Need to be closed (surgically)

Small

  1. Little flow from the aorta to Pas
  2. Usually asymptomatic
  3. Murmur found incidentally
  4. Endocarditis risk
188
Q

How do you close the ductus arteriosus?

A
  1. Indomethacin or Ibuprofen
    • Given to the neonate
    • Inhibits prostaglandin synthesis
    • Closes the connection in the majority of cases
  2. If associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
189
Q

WHAT IS COARCTATION OF THE AORTA?

A

Narrowing of the aorta at the site of insertion of the ductus arterioles.

190
Q

What is the physiology for coarctation of the aorta?

A

Severe
Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair

Mild
Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term

191
Q

What are the clinical signs of coarctation of the aorta?

A
  1. Infancy: heart failure
  2. Adult: hypertension
  3. Radio-femoral delay
  4. Mid systolic murmur, maximal over back
  5. Apical click from the aortic valve
  6. Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
192
Q

What are the long term problems of coarctation of the aorta?

A
  1. Hypertension
  2. Early coronary artery disease
  3. Early strokes
  4. Sub arachnoid haemorrhage
  5. Re-coarctation requiring repeat intervention
  6. Aneurysm formation at the site of repair
193
Q

What is the treatment of coarctation of the aorta?

A
  1. IV prostaglandins are used in neonates to maintain a patent ductus arteriosus to allow adequate circulation until it is possible to attempt corrective surgery.
  2. Surgery, or balloon dilatation ± stenting.
194
Q

WHAT ARE THE PROBLEMS ASSOCIATED WITH BISCUSPID AORTIC VALVES?

A
  1. Can be severely stenotic in infancy or childhood
  2. Degenerate quicker than normal valves
  3. Become regurgitant earlier than normal valves
  4. Are associated with coarctation and dilatation of the ascending aorta
195
Q

How can you treat bicuspid aortic valve?

A

Surgery

196
Q

WHAT IS PULMONARY STENOSIS?

A

Narrowing of the outflow of the right ventricle

197
Q

What is the treatment for pulmonary stenosis?

A
  1. Balloon valvuloplasty
  2. Open valvotomy
  3. Open trans-annular patch
  4. Shunt (to bypass the blockage)
198
Q

WHAT IS HYPERTENSION?

A

Over 140/90

199
Q

What are the two types of hypertension?

A

Essential hypertension (primary, cause unknown). ~95% of cases.

Secondary hypertension ~5% of cases.

200
Q

What are some causes of secondary hypertension?

A
  1. Renal
    • CKD
  2. Endocrine disease
    • Conn’s syndrome
  3. Others
    • Coarctation, pregnancy
201
Q

What are the tests for hypertension?

A
  1. 24hr ambulatory BP monitor
  2. Multiple home BP monitoring
  3. Fundoscopy–in severe HTN
    • Bilateral retinal haemorrhages
    • Papilloedema
  4. Overall CVD risk
    • Fasting glucose
    • Cholesterol
  5. End Organ Damage
    • 12 lead ECG –past MI, LV hypertrophy
    • Urine analysis –protein, blood
202
Q

What are some lifestyle to lower blood pressure?

A
  1. Stop smoking
  2. Low-fat diet
  3. Reduce alcohol and salt intake
  4. Increase exercise
  5. Reduce weight if obese
203
Q

What is the pharmocological management of hypertension?

A

Step 1
<55 years old and not afro-carribean - ACEi or ARB E.g. Ramirpil or losartan
>55 years old or afro-carribean - CCB - Amlodipine

Step 2
Add the other from step 1 OR thiazide-like duirectic

Step 3
ACEi or ARB + CCB + thiazide-like diuretic (Indapamide)

Step 4
Low-dose spironolactone if K+ <4.5 mmol/l
Alpha-blocker (doxazosin) or beta blocker if K+ >4.5 mmol/l

204
Q

How can renal artery stenosis cause hypertension?

A
  1. Less blood flow to kidneys
  2. Secretes Renin
  3. More water and salt retention
  4. Higher BP
205
Q

What is a pheochromocytoma? How does it cause hypertension?

A

Tumour on adrenal glands

Constantly produce catecholamines (e.g. adrenaline)

Increase heart rate and peripheral vascular resistance

Increase BP

206
Q

How does cushing’s cuase hypertension?

A
  1. Enhances adrenalines effect on blood vessels to constrict them
  2. Also can act as a mineralacorticoid (aldosterone)
  3. Increase BP
207
Q

How does Conn’s syndrome cause hypertension?

A
  1. High aldosterone
  2. Increased sodium and water retention
  3. Increased BP
208
Q

Over what value should an ACE inhibitor be stopped for potassium?

A

>6 mmol/L

209
Q

What is the first antihypertensive for diabetics?

A

Ace inhibitor

210
Q

What is malignant hypertension?

A

Severe hypertension and bilateral retinal hemorrhages and exudates

211
Q

WHAT IS RHEUMATIC FEVER?

A

Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection

212
Q

What are the features of rheumatic fever?

A

Major criteria

  1. Erythema marginatum
  2. Sydenham’s chorea: this is often a late feature
  3. Polyarthritis
  4. Carditis and valvulitis (eg, pancarditis)
  5. The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur)
  6. Subcutaneous nodules

Minor criteria

  1. raised ESR or CRP
  2. pyrexia
  3. arthralgia (not if arthritis a major criteria)
  4. prolonged PR interval
213
Q

What is the management of rheumatic fever?

A
  1. Antibiotics: oral penicillin V
  2. Anti-inflammatories: NSAIDs are first-line
  3. Treatment of any complications that develop e.g. heart failure
214
Q

What is rheumatic heart disease?

A

Fusion of cusps.

215
Q

WHAT ARE THE CAUSES OF AORTIC STENOSIS?

A
  1. Congenital bicuspid valve
  2. Degenerative calcification
  3. William’s syndrome
  4. Rheumatic Heart disease
216
Q

How does a person with aortic stenosis present?

A
  1. Syncope
  2. Angina
  3. Dyspnoea
  4. Sudden death
217
Q

What physical signs would you hear on aortic stenosis?

A
  1. Narrow pulse pressure
    • ​​Slow rising carotid pulse (pulsus tardus)
    • & decreased pulse amplitude (pulsus parvus)
  2. Heart sounds
    • ​​Soft or absent S2, S4 gallop due to LVH.
  3. Ejection systolic murmur
    • Crescendo-decrescendo character.
218
Q

What tests would you do for someone with aortic stenosis?

A
  1. Echocardiography
    * *Two measurements obtained are:**
    • Left ventricular size and function: LVH, Dilation, and EF
    • Doppler derived gradient and valve area (AVA).
  2. ECG
  3. CXR
    • LVH, calcified aortic valve
219
Q

What is the management for aortic stenosis?

A
  1. General:
    • Fastidious dental hygiene / care
    • Consider IE prophylaxis in dental procedures
  2. Medical - limited role since AS is a mechanical problem.
    • Vasodilators are relatively contraindicated in severe AS
  3. Surgical Replacement
    • Definitive treatment
  4. TAVI
    • Transcatheter Aortic Valve Implantation - IF SYMPTOMATIC
220
Q

What is the difference between aortic stenosis and aortic sclerosis?

A

Aortic sclerosis doesn’t radiate to carotids

221
Q

WHAT IS THE CAUSE OF MITRAL VALVE REGURGITATION?

A
  1. Myxomatous degeneration (MVP)
  2. Ischemic MR
  3. Rheumatic heart disease
  4. Infective Endocarditis.
222
Q

What is the pathophysiology of mitral valve regurgitation?

A
  1. Pure Volume Overload
  2. Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
  3. Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
  4. Progressive left ventricular volume overload leads to dilatation
223
Q

What are the symptoms of mitral valve regurgitation?

A
  1. Mainly asymptomatic
  2. Exertion dyspnoea –exercise intolerance
  3. Palpitations
  4. Fatigue
224
Q

What are the signs of mitral valve regurgitation?

A
  1. Pansystolic murmur at apex radiating to axilla
  2. Soft S1
  3. Displaced hyperdynamic apex
225
Q

What are the investigations for mitral regurgitation?

A
  1. ECG
    • May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
  2. CXR
    • LA enlargement, central pulmonary artery enlargement.
  3. ECHO
    • Estimation of LA, LV size and function. Valve structure assessment TOE v helpful
226
Q

What are the management for MR?

A
  1. Medical management in acute cases involves
    • Nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
  2. If patients are in heart failure
    • ACE inhibitors may be considered along with beta-blockers and spironolactone
  3. In acute, severe regurgitation
    • Surgery is indicated
227
Q

What are the indications for surgery of severe MR?

A
  1. ANY symptoms at rest or exercise with (repair if feasible)
  2. IF asymptomatic:
    • If EF <60%, LVESD >45mm
    • If new onset atrial fibrillation/raised PAP.
228
Q

WHAT IS THE CAUSE OF AORTIC REGURGITATION?

A
  1. Bicuspid aortic valve
  2. Rheumatic fever
  3. Infective endocarditis
229
Q

What is the pathophysiology of aortic regurgitation?

A
  1. Combined pressure AND volume overload
  2. Compensatory Mechanisms: LV dilation, LVH
  3. Progressive dilation leads to heart failure
230
Q

What are the symptoms of aortic valve regurgitation?

A
  1. Exertional dyspnoea
  2. Orthopnoea
  3. Paroxysmal nocturnal dyspnoea
231
Q

What are the signs of aortic regurgitation?

A
  1. Collapsing (water hammer) pulse
  2. Wide pulse pressure
  3. Displaced hyperdynamic apex beat
  4. Early diastolic murmur

Notable eponyms

  1. Corrigans sign (ear movements)
  2. De Musset’s sign (head movements)
  3. Duroziez’s sign (Femoral artery murmur)
  4. Austin flint murmur (cardiac apex murmur)
  5. Traube’s sign (pistol shot over femoral)
232
Q

What would cardiac tests show you for aortic regurgitation?

A
  1. CXR
    • Cardiomegaly
  2. ECHO
    • LV dilation and hypertrophy
233
Q

What is the management for aortic regurgitation?

A
  1. Vasdilators
    • ACEi only if symptomatic or HTN
  2. Surgical
    • Replace valve before LV dysfunction
234
Q

WHAT IS MITRAL VALVE STENOSIS?

A

Obstruction of LV inflow that prevents proper filling during diastole

235
Q

What are causes of mitral valve stenosis?

A
  1. Rheumatic heart disease
  2. Infective endocarditis
  3. Mitral annular calcification.
236
Q

What is mitral valve stenosis pathophysiology?

A
  1. LA dilation incerease pulmonary congestion (reduced emptying)
  2. Increased Transmitral Pressures
    • Leads to left atrial enlargement and atrial fibrillation.
  3. Right heart failure symptoms: due to Pulmonary venous HTN
237
Q

What are the symptoms of mitral valve stenosis?

A
  1. Dyspnoea
  2. Fatigue
  3. Palpitations
  4. Chest pain
238
Q

What are the signs in mitral valve stenosis?

A
  1. Malar flush on cheeks
  2. Low volume pulse
  3. Tapping, non displaced apex beat
  4. Rumbling mid-diastolic murmur
  5. Loud opening S1
  6. P mitrale/bifid p wave
239
Q

What tests can you do on mitral valve stenosis and what will they show?

A

MV ECHO
The GOLD STANDARD for diagnosis
Asses mitral valve mobility, gradient and mitral valve area

ECG
May show atrial fibrillation and LA enlargement

CXR
LA enlargement and pulmonary congestion
Occasionally calcified

240
Q

How would you manage a patient with mitral valve stenosis?

A
  1. Patients with associated atrial fibrillation require anticoagulation
    • Currently warfarin is still recommended
  2. Asymptomatic patients
    • Monitored with regular echocardiograms
    • Percutaneous/surgical management is generally not recommended
  3. Symptomatic patients
    • Percutaneous mitral balloon valvotomy
    • Mitral valve surgery (commissurotomy, or valve replacement)
241
Q

WHAT IS INFECTIVE ENDOCARDITIS?

A

Infection of heart valve/s or other endocardial lined structures within the heart.

242
Q

What is the criteria used for defining infective endocarditis?

A

Duke criteria

243
Q

What is the major and minor criteria for infective endocarditis?

A
  1. Major criteria
    • Positive blood cultures
      • two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
      • persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
      • positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
      • positive molecular assays for specific gene targets
    • Evidence of endocardial involvement
      • positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
      • new valvular regurgitation
  2. Minor criteria
    • predisposing heart condition or intravenous drug use
    • microbiological evidence does not meet major criteria
    • fever > 38ºC
    • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
    • immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
244
Q

What is the most causative organism in infective endocarditis?

A
  1. Staph aureus - MOST COMMON and in IVDU or prosthetic valves
  2. Strep viridans
  3. Staph epidermis - prosthetic valves if < 2 months post valve surgery
245
Q

Who is infective endocarditis most likely to affect?

A
  1. The elderly (in an ageing population)
  2. The young i.v. drug abusers
  3. The young with congenital heart disease.
  4. Anyone with prosthetic heart valves.
246
Q

What is the clinical presentation of infective endocarditis?

A
  1. Persistent fever
  2. Emboli
  3. New or changing murmurs
247
Q

What are some peripheral signs of infective endocarditis?

A
  1. Microscopic heamaturia
  2. Petechiae 10 to 15%
  3. Splinter hemorrhages
  4. Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
  5. Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
  6. Roth spots (boat shaped haemorrhages) on fundoscopy.
248
Q

What test can you do for infective endocarditis?

A
  1. Blood cultures - FIRST LINE
    • ​​Three sets, taken from 3 different places, 3 times
  2. Echocardiography, cardiac doppler, transoesophageal doppler
  3. Urine
    • Microscopic haematuria and proteinuria are common
  4. Blood
    • Coomb’s test
249
Q

How can you treat infective endocarditis?

A

Native valve endocarditis (NVE):

  1. IV amoxicillin + consider low dose gentamicin
  2. If penicillin allergic: IV vancomycin

Staph

  1. Flucloxacillin

Prosthetic valve endocarditis:

  1. IV vancomycin, gentamicin + rifampacin

Surgery if needed

  1. e.g. causing congestive cardiac failure
250
Q

What prophylaxtic treatment is given for dental procedures in prosthetic valve replacement patients?

A

Good oral hygiene

251
Q

WHAT IS PERIPHERAL VASCULAR DISEASE?

https://www.youtube.com/watch?v=rTbIazck7rk&t=229s

A

Blood vessels outside of your heart and brain to narrow, block, or spasm.

252
Q

What are the three patterns of disease seen in PVD?

A
  1. Intermittent cludication
  2. Critical limb ischaemia
  3. Acute limb-threatening ischaemia
253
Q

What is the classification of PVD called?

What do the numbers mean?

A

—Fontaine

—1 Asymptomatic

—2 Intermittent claudication

—3 Ischaemic rest pain

—4 Ulceration/gangrene (critical ischaemia)

254
Q

What is claudication?

A

Intermittent claudication is a cramp-like, muscular pain in the calf, brought on by exercise and relieved only by rest.

255
Q

What are the symptoms of claudication?

A
  1. Intermittent claudication: aching or burning in the leg muscles following walking
  2. Patients can typically walk for a predictable distance before the symptoms start
  3. Usually relieved within minutes of stopping
  4. Not present at rest
256
Q

What are the investigations for claudication?

A

ABPI
Normal is 1-1.2; PAD is 0.5-0.9 gangene<0.5

Colour Duplex USS
Quick and non-invasive, can show vessels and blood flow within them

MR/CT angiography
Identify stenosesand quality of vessels.

Blood tests
Raised CK-MM, shows muscle damage

257
Q

What is the management for claudication?

A

Medications
1st line - Clopidogrel

Risk factor modification
Quit smoking, treat HTN, lower cholesterol, improve DM control, lower fat diet.

Exercise programmes
Reduce claudication by improving blood flow.

PTA or surgery if severely stenosed

258
Q

WHAT IS CRITICAL LIMB ISCAHEMIA?

A

Critical limb ischaemia results from severe peripheral arterial disease

259
Q

What are the causes of critical limb ischaemia?

A
260
Q

What are the symptoms of critical limb ischaemia?

A
  1. Pale
  2. Pulseless
  3. Painful
  4. Paralysed
  5. Paraesthetic
  6. ‘Perishing with cold’
261
Q

What are the investigations for ctitical limb ischaemia?

A

Handheld arterial Doppler examination.

If Doppler signals are present, an ankle-brachial pressure index (ABI) should also be obtained.

262
Q

What is the management for critical limb ischaemia?

How quick must this be done?

A

Initial management

  • ABC approach
  • Analgesia: IV opioids are often used
  • IV unfractionated heparin is usually given to prevent thrombus propagation
  • Vascular review

Under 6 hours to salvage tissue

Definitive management:

  • Intra-arterial thrombolysis
  • Surgical embolectomy
  • Angioplasty
  • Bypass surgery
  • Amputation: for patients with irreversible ischaemia
263
Q

What is critical limb ischaemia due to?

A

May be due to a thrombosis (in ‘vasculopaths’), emboli, graft occlusion or trauma

264
Q

What drugs cuase prolongation of QT interval?

A
  1. Amiodarone
  2. Tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
  3. Methadone
  4. Erythromycin
  5. Haloperidol
  6. Ondanestron
265
Q

What are the normal S heart sounds?

A
  1. S1
    • closure of mitral and tricuspid valves
    • soft if long PR or mitral regurgitation
    • loud in mitral stenosis
  2. S2
    • closure of aortic and pulmonary valves
    • soft in aortic stenosis
    • loud in pulmonary hypertension
    • splitting during inspiration is normal
266
Q

What are the pathological S heart sounds?

A
  1. S3 (third heart sound)
    • Caused by diastolic filling of the ventricle
    • Considered normal if < 30 years old (may persist in women up to 50 years old)
    • Heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
  2. S4 (fourth heart sound)
    • May be heard in aortic stenosis, HOCM, hypertension
    • Caused by atrial contraction against a stiff ventricle
    • therefore coincides with the P wave on ECG
    • in HOCM a double apical impulse may be felt as a result of a palpable S4
267
Q

WHAT IS ATRIAL FIBRILATION?

A

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia.

268
Q

What are the different types of atrial fibrillation?

A
  1. First detected episode (irrespective of whether it is symptomatic or self-terminating)
  2. Recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days
  3. In permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rated control and anticoagulation if appropriate
269
Q

What are the features of atrial fibrillation?

A
  1. Symptoms
    • palpitations
    • dyspnoea
    • chest pain
  2. Signs
    • an irregularly irregular pulse
270
Q

What is the investigation for atrial fibrillation?

A

An ECG is essential to make the diagnosis as other conditions can give an irregular pulse, such as ventricular ectopics or sinus arrhythmia.

271
Q

What is the management of AF?

A
  1. Rate/rhythm control
    • Normall rate control unless have heart failure, new onset AF or reversible cause​
      • ​A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem/verapamil) is used first-line to control the rate in AF
      • Can also use:
      • Digoxin
    • Only rhythm control if had for less than 48 hours for new onset
  2. Reducing stroke risk
  3. Catheter ablation
    • ​​Still need to continue DOAC
272
Q

What is cardioverson for atrial fibrillation?

A

Onset < 48 hours

  1. If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised.
  2. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either:
    • Electrical - ‘DC cardioversion’ - uses R waves
    • Pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease
    • Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary

Onset > 48 hours

  1. If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion
  2. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus.
  3. If excluded patients may be heparinised and cardioverted immediately.
273
Q

What is used for atrial fibrilation post stoke?

A
  1. Aspirin 300mg OD for 2 weeks THEN
  2. Following a stroke or TIA - Warfarin or direct thrombin or factor Xa inhibitor should be gien
  3. Anticoagulation should be given after 2 weeks
274
Q

What drugs can be used in atrial fibrilation to cardiovert a patient into normal rhythm?

A
  1. amiodarone
  2. flecainide (if no structural heart disease)
275
Q

HOW DO THROMBOLYSIS DRUGS WORK?

A
  1. Thrombolytic drugs activate plasminogen to form plasmin
  2. This in turn degrades fibrin and help breaks up thrombi
  3. They in primarily used in patients who present with a ST elevation myocardial infarction
276
Q

What are some examples of thrombolysis drugs?

A
  1. Alteplase
  2. Tenecteplase
  3. Streptokinase
  4. Fondaparinux
277
Q

What are some contraindications to thrombolysis drugs?

A
  1. active internal bleeding
  2. recent haemorrhage, trauma or surgery (including dental extraction)
  3. coagulation and bleeding disorders
  4. intracranial neoplasm
  5. stroke < 3 months
  6. aortic dissection
  7. recent head injury
  8. severe hypertension
278
Q

What are the side effects of thrombolysis drugs?

A
  1. haemorrhage
  2. hypotension - more common with streptokinase
  3. allergic reactions may occur with streptokinase
279
Q

WHAT IS TAKAYASU’S ARTERITIS?

A
  1. Takayasu’s arteritis is a large vessel vasculitis.
  2. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse.
  3. It is more common in younger females (e.g. 10-40 years) and Asian people.
280
Q

What are the features of takayasu’s arteritis?

A
  1. systemic features of a vasculitis e.g. malaise, headache
  2. unequal blood pressure in the upper limbs
  3. carotid bruit and tenderness
  4. absent or weak peripheral pulses
  5. upper and lower limb claudication on exertion
  6. aortic regurgitation (around 20%)
281
Q

What is the association with takayasu’s arteritis?

A

Renal artery stenosis

282
Q

What is the management of takayasu’s arteritis?

A

Steroids

283
Q

WHAT IS THE ANTIHYPERTENSIVE OF CHOICE FOR DIABETIC PATIENTS?

A

ACE inhibitors/ARBs

ARBs in black/afrocarribean patients

284
Q

HOW TO STATINS WORK?

A

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

285
Q

What range should statins stay within?

A

three times the reference range for transferase

286
Q

What statin should be started with a high QIRSK?

A

Atorvastatin

287
Q

WHAT IS THE DEFINTION OF POSTURAL HYPOTENSION?

A

Postural hypotension may be defined as a fall of systolic blood pressure > 20 mmHg on standing

288
Q

What are the causes of postural hypotension?

A
  1. Hypovolaemia
  2. Autonomic dysfunction: diabetes, Parkinson’s
  3. Drugs: diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives
  4. Alcohol
289
Q

WHAT IS THE TARGET INR FOR A PATIENT WHO SUFFERS FROM RECURRENT PE’S?

A

3-4

290
Q

HOW CAN YOU CAPTURE A EPISODIC CARDIAC ARRHYTHMIA?

A

The most common investigation is Holter monitoring

  1. Portable battery operated device
  2. Continuously records ECG from 2-3 leads
  3. Usually done for 24 hours but may be used for longer if symptoms are less than daily
  4. Patients are asked to keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptoms
  5. At the end of the monitoring a report is generated summarising a number of parameters including heart rate, arrhythmias and changes in ECG waveform
291
Q

WHAT ARE THE SIDE EFFECTS OF THIAZIDE DIURECTS?

A
  1. dehydration
  2. postural hypotension
  3. hyponatraemia, hypokalaemia, hypercalcaemia*
  4. gout
  5. impaired glucose tolerance
  6. impotence
292
Q

WHAT IS THE ANTICOAGULAT OF CHOICE WITH A MECHANICAL HEART VALVE?

A

Warfarin

293
Q

What are the results of pulmonary artery occlusion monitoring?

A
294
Q

HOW DOES FONDAPARINUX WORK?

A

Activates antithrombin III

295
Q

WHAT IS THE MANAGEMENT OF WARFARIN WITH A MAJOR BLEED?

A
  1. Stop warfarin
  2. Give intravenous vitamin K 5mg
  3. Prothrombin complex concentrate - if not available then FFP*
296
Q

What is the management of warfarin with different INRs and bleeding?

A
297
Q

When should warfarin be stopped before surgery?

A

5 days before, and once the INR is less than 1.5 the surgery can go ahead

298
Q

WHAT ON AN ECG IS ALWAYS CONCERNING?

A

Left bundle branch block (LBBB)

299
Q

Which conditions is associated with mitral valve prolapse?

A

Polycystic Kidney Disease

300
Q

WHICH ARTERY SUPPLIES THE AV NODE?

A

Right coronary artery

301
Q

What are the investigations for capturing episodic arrhythmias?

A
  1. Holter monitor - FIRST LINE
  2. External loop recorder
  3. Implantabe loop recorder
302
Q

What are the signs of hypercholesterolaemia on examination?

A
  1. Xanthelasma
  2. Corneal arcus
  3. Tendon xantoma
303
Q

What are normal variants for ECG?

A
  1. Sinus bradycardia
  2. Junctional rhythm
  3. First degree heart block
  4. Mobitz type 1 (Wenckebach phenomenon)

ΩΩ 3a Bateman - Neuro + Cardio (2 decks)

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