Cardio Flashcards

1
Q

Name the 3 ‘cardinal signs’ of heart failure

A

Ankle swelling
Dyspnoea
Fatigue

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2
Q

Signs of infective endocarditis

A

Roth spots
Osler nodes
Janeway lesions
Splinter haemorrhages
Petechiae
Splenomegaly
Features of heart failure (raised JVP, bilateral crackles)
Note: Fever and a new murmur are also two common signs of infective
endocarditis but they were already stated in the context of the question.

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3
Q

Pericardial rubg: ECG

A

Saddle-shaped ST elevation
PR depression

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4
Q

The patient presents with fever and neutropenic sepsis – what treatment would you give (inc. class, drug and route of administration)?

A

IV (1) beta lactam (1) piperacillin + tazobactam (1) is the Tx for febrile neutropenia.

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5
Q

Fe2+ iron deficiency anaemia tests

A

Ferritin
Iron Studies

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6
Q

PAD

A

Pain in Buttocks = lower aorta or iliac
Pain in Thigh = iliac or common femoral
Pain in Upper 2/3 of calf = Superficial femoral
Pain in Lower 1/3 = popliteal
Pain in Foot = tibial or peroneal artery

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7
Q

When can you best hear mitral regurgitation

A

left lateral position

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8
Q

What should patients on atrial fibrillations be started on?

A

antihypertensives, a beta blocker
and a statin

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9
Q

Barlow syndrome

A

mid systolic click followed by a late systolic
murmur is heard at the apex.

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10
Q

A 57-year-old male is admitted complaining of headaches and blurring of vision.
His blood pressure is found to be 240/150 mmHg and he has bilateral papilloedema,
but is fully orientated and coherent. He had been known to be hypertensive for
about five years and his blood pressure control had been good on three drugs.
However, he had decided to stop all medication two months before this event.
Which of the following would be your preferred parenteral medication at this
point?

A

Sodium Nitroprusside

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11
Q

Complication of ventral septal defect

A

Endocarditis

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12
Q

A 49-year-old woman presents with increasing shortness of breath on exertion
developing over the past three months. She has no chest pain or cough, and has
noticed no ankle swelling. On examination, blood pressure is 158/61 mmHg, pulse
is regular at 88 beats per minute and there are crackles at both lung bases. There is
a decrescendo diastolic murmur at the left sternal edge. What is the most likely
diagnosis?

A

Aortic regurgitation

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13
Q

Hypertrophic Cardiomyopathy Treatment

A

1st Beta blocker
2nd Followed by CCB

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14
Q

A 71-year-old man is being treated for congestive heart failure with a combination
of drugs. He complains of nausea and anorexia, and has been puzzled by observing
yellow rings around lights. His pulse rate is 53/minute and irregular and blood
pressure is 128/61 mmHg. Which of the following medications is likely to be
responsible for these symptoms?

A

These symptoms are characteristic of digoxin (cardiac glycosides). The
yellow-tinged vision (xanthopsia) is particular to these drugs. The slow
pulse, with probable ectopics, together with the subjective symptoms,
suggests toxicity and plasma digoxin should be measured, with lowering
of the dosage or withdrawal of the drug, which is not considered first-line
therapy in any case in the management of congestive heart failure.

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15
Q

most common cause of
apparent resistance to hypertensive therapy

A

Poor adherence to therapy

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16
Q

CAP pneumonia

A

H. influenzae and S. pneumoniae
are organisms which are usually responsible for community-acquired
pneumonia.

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17
Q

HAP pneumonia

A

S. aureus and Pseudomonas spp

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18
Q

Atypical pneumonia

A

L. pneumophilia along
with Chlamydia spp. and Mycoplasma pneumoniae

A urinary antigen test is routinely used for
the detection of Legionella spp. Serological tests can be used for the
detection of Mycoplasma and Chlamydia spp. and also Legionella spp

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19
Q

ECG findings on pulmonary embolism

A

Deep S-wave in lead I, pathological Q-wave in lead III and inverted
T-waves in lead III

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20
Q

What is bronchiectasis

A

Bronchiectasis is defined as chronic infection of the bronchi and bronchioles
leading to permanent dilatation of these airways.

The main organisms
involved in this condition are H. influenzae, S. pneumoniae, S. aureus and
P. aeruginosa.

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21
Q

Causes of bronchiectasis

A

Congenital: cystic fibrosis, Young’s
syndrome, primary ciliary dyskinesia, Kartagner’s syndrome; and (2)
Acquired: Post-infection with measles, pertussis, bronchiolitis, pneumonia,
TB and HIV

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22
Q

Most common lung cancer in non-smokers

A

Adenocarcinoma

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23
Q

What word is used to describe pleural effusion

A

‘Stony dullness’

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24
Q

pulmonary embolism first line treatment

A

Treatment dose subcutaneous low molecular weight heparin
+ loading with warfarin and aim for INR between 2 and 3

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25
pleural aspirate analysis, would typically be found in a patient with an empyema?
pH <7.2, ↑ LDH, ↓ glucose
26
Cystic fibrosis Gold Standard
Sweat test Sodium chloride >60 mmol/L
27
Which of the following organisms, responsible for causing chronic pneumonia, is most commonly found in patients with longstanding cystic fibrosis?
Pseudomonas aeruginosa
28
Long-term used medication causing pulmonary fibrosis
Amiodarone along with bleomycin, bulsulfan, nitrofurantoin, methotrexate and sulfasalazine are drugs that can cause pulmonary fibrosis with long-term use
29
Bibasal pneumonia
L. pneumophilia
30
Which of the drugs below would be the most appropriate to treat pulmonary Aspergillus spp. infection?
Amphotericin B
31
aspiration pneumonia antibiotic regimen
Intravenous cefuroxime and metronidazole
32
Infective endocarditis:
Typically affects mitral valve (LS) However in IVDU affects tricuspid valve
33
Head trauma
Subarachnoid: Surgery + Nimodipine Subdural: Burr Hole + Craniotomy/IV mannitol Extradural: IV mannitol
34
DEMENTIA
35
Cranial nerve lesions
36
Hypertension NICE
A – ACE inhibitor (e.g., ramipril) B – Beta blocker (e.g., bisoprolol) C – Calcium channel blocker (e.g., amlodipine) D – Thiazide-like diuretic (e.g., indapamide) ARB – Angiotensin II receptor blocker (e.g., candesartan) Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C. Step 2: A + C. Alternatively, A + D or C + D. Step 3: A + C + D Step 4: A + C + D + fourth agent (see below)
37
Duke's Criteria Infective Endocarditis
38
CHADSVASC
39
Heart Block
40
four stages of chronic limb ischaemia
Stage I: asymptomatic Stage II: intermittent claudication Stage III: rest pain/nocturnal pain Stage IV: necrosis/gangrene
41
What is a consequence of regular blood transfusions and how do you treat this complication?
Iron overload Iron chelation – deferoxamine/deferasirox
42
Medication used to stimulate Hbf production
Hydroxycarbamide
43
First Line chemotherapy used for multiple myeloma
Bortezomid Thalidomide Dexamethasone
44
Angina medication
1st GTN spray 2nd CCB/ Beta blocker (atenolol/veramapril)
45
Signs for PAD
Hair loss , atrophic skin , brittle / slow-growing nails , ulcers, numbness in feet, absent distal pulses, intermittent claudication.
46
Ulcers Diff
47
Where can you best hear aortic stenosis
2nd intercostal space (1), left sternal border (1).
48
A 9 year old boy presents to the hospital after an acute onset of anaemia, jaundice, diarrhoea, and dark urine. After taking a history from his parents, it is revealed he has just been to a restaurant and eaten a dish with Fava beans. What is the inheritance pattern of the most likely underlying condition?
G6PD deficiency X-Linked recessive
49
Pathophysiology of aortic stenosis
Narrowing of aortic valve 🡪 decreased stroke volume 🡪 increased afterload 🡪 increased left ventricular pressure 🡪 compensatory LVH 🡪 increased oxygen demand 🡪 ischaemia
50
Pathophysiology of mitral regurgitation
Regurgitation into the left atrium 🡪 left atrial dilatation 🡪 left atrial enlargement 🡪 LVH (since ventricle needs to put in more effort to pump less blood) 🡪 pulmonary hypertension 🡪 right ventricular dysfunction
51
Pathophysiology of mitral stensosis
Thickening and immobility of valve 🡪 obstruction of blood flow from right atrium to right ventricle 🡪 left atrial pressure increases 🡪 LAH 🡪 pulmonary venous, arterial and right heart pressures increase 🡪 pulmonary oedema 🡪 pulmonary HTN 🡪 RVH 🡪 tricuspid regurgitation
52
Pathophysiology of aortic regurgitation
To maintain cardiac output more blood needs to be pumped out of the left ventricle to compensate for the backflow 🡪 LVH 🡪 heart failure Decreased coronary artery supply
53
Most common viral cause of pericardial effusion
Viral is the most common infectious cause → coxsackie 19 virus often
54
What drugs are contraindicated in pregnanct women
ACEi and ARB should always be discontinued in pregnancy as they cause fetotoxicity
55
Thyroiditis
-
56
Management of Addisons crisis
Intensive monitoring if they are acutely unwell Parenteral steroids (i.e. IV hydrocortisone) IV fluid resuscitation Correct hypoglycaemia Careful monitoring of electrolytes and fluid balance
57
Top three cause sof SIADH
Post-operative SSRIs Small cell lung cancer
58
Achalasia
Barium swallow: ‘bird’s beak’ sign Manometry = GOLD First line is upper GI endoscopy
59
What hypersensitivity reaction is coeliac
Type 4
60
Mnemonic for Absorption of Stuff in tummy
Dude Is Just Feeling Ill Bro = Duodenum (Iron), Jejunum (Folate), Ileum (B12)
61
Pathophysiology for diverticular disease
The wall of the large intestine contains a layer of muscle called the circular muscle. The points where this muscle layer is penetrated by blood vessels are areas of weakness. Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle. These gaps allow the mucosa to herniate through the muscle layer and pouches to form (diverticula). Diverticula do not form in the rectum, because it has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum, adding extra support. In the rest of the colon, there are three longitudinal muscles that run along the colon, forming strips or ribbons called teniae coli. The teniae coli do not surround the entire diameter of the colon, and the areas that are not covered by teniae coli are vulnerable to the development of diverticula.
62
Pathophysiology of appendicits
The appendix is a small, thin tube arising from the caecum. It is located at the point where the three teniae coli meet (the teniae coli are longitudinal muscles that run the length of the large intestine). There is a single opening to the appendix that connects it to the bowel, and it leads to a dead end. Pathogens can get trapped due to obstruction at the point where the appendix meets the bowel. Trapping of pathogens leads to infection and inflammation. The inflammation may proceed to gangrene and rupture. When the appendix ruptures, faecal contents and infective material are released into the peritoneal cavity. This leads to peritonitis, which is inflammation of the peritoneal lining.
63
Causes of AKI
64
Atherosclerosis formation
*Endothelial dysfunction*- NO is reduced in endothelial dysfunction 1. High LDL deposits in tunica intima. LDL becomes oxidised, activating endothelial cells 2. Adhesion of blood leukocytes to activated endothelium move to tunica intima 3. Macrophages take in oxidised LDLs, becoming foam cells 4. Foam cells promote the migration of smooth muscle cells from tunica media to the intima and smooth muscle cell proliferation 5. Increased smooth muscle cell proliferation and heightened synthesis of collagen 6. Foam cells die, causing lipid content released 7. Thrombosis plaque ruptures lead to blood coagulation and thrombus impeding blood flow.
65
Useful drugs in treating CAD
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase Clopidogrel/ ticagrelor – inhibits of the P2Y12 ADP receptor on platelets Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
66
Second line treatment options for angina
Ivabradine, ranolazine and nicorandil 1st: Amlodopine
67
Pericarditis CARDIAC RIND
Collagen Vascular Disease * Aortic aneurysm * Radiation * Drugs * Infections * Acute Renal Failure * Cardiac infarction * Rheumatic Fever * Injury * Neoplasms * Dressler’s syndrome
68
Pericarditis 1st line treatment
NSAID/aspirin
69
Acute pericardits triad of symptoms
chest pain, friction rub and ECG changes
70
Signs of Cardiac tamponade other than becks triad
Absent Y wave in the JVP
71
Stanford system for aortic dissection
Type A – affects the ascending aorta, before the brachiocephalic artery Type B – affects the descending aorta, after the left subclavian artery
72
X ray findings for aortic dissection
D:Dilated aortic arch W: Widened mediastinum E: Effusion (pleural) E: Effusion (pericardial) B: Blurring of aortic contour S: Separation of intimal calcification
73
G.S for infective endocarditis
Transoesophageal echocardiography (TOE) is more sensitive and specific than transthoracic echocardiography. Vegetations (an abnormal mass or collection) may be seen on the valves. Special imaging investigations may be used in patients with prosthetic heart valves, where it can be more challenging to determine whether an infection is present in the prosthesis: 18F-FDG PET/CT SPECT-CT
74
Modified Duks's Croteria
Modified Duke Criteria The Modified Duke criteria can be used to diagnose infective endocarditis. A diagnosis requires either: One major plus three minor criteria Five minor criteria Major criteria are: Persistently positive blood cultures (typical bacteria on multiple cultures) Specific imaging findings (e.g., a vegetation seen on the echocardiogram) Minor criteria are: Predisposition (e.g., IV drug use or heart valve pathology) Fever above 38°C Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions) Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis) Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
75
Management for infective endocarditis
Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin)
76
Budd-Chiari Syndrome
77
Respiratory finding in pumonary embolism
Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic. It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.
78
Major risk factor for tetralogy of fallot
RUBELLA
79
Tet spells options
Seen in tetralogy of fallot Beta blockers O2
80
Murmur seen in ventricular septal defect
When you hear a pan-systolic murmur it is worth giving your top differential but also mention the other causes of this type of murmur. The causes of a pan-systolic murmur are ventricular septal defect, mitral regurgitation and tricuspid regurgitation. -Left lower sternal border in the 3rd and 4th intercostal space
81
What is Eisenmenger syndrome
pulmonary pressure is greater than the systemic pressure
82
Atrial septal defects and stroke
It is worth remembering atrial septal defects as a cause of stroke in patients with a DVT. Normally when patients have a DVT and this becomes an embolus, the clot travels to the right side of the heart, enters the lungs and becomes a pulmonary embolism. In patients with an ASD the clot is able to travel from the right atrium to the left atrium across the ASD. This means the clot can travel to the left ventricle, aorta and up to the brain, causing a large stroke. An exam question may feature a patient with a DVT that develops a large stroke and the challenge is to identify that they have had a lifelong asymptomatic ASD.
83
Murmur for patent ductus arteriosus
continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear.
84
Heart Block
First: Electrical Impulses are delayed. This results in a longer P wave but the P wave is followed by QRS complex Second degree 1: Wenckenback 2:
85
Ventricular ectopics
86
Mnemonics for tachycardias
87
Acute management of supraventricular tachycardia
Step 1: Vagal manoeuvres Step 2: Adenosine Step 3: Verapamil or a beta blocker Step 4: Synchronised DC cardioversion
88
ECG changes in Wolff-Parkinson-White syndrome are
Short PR interval, less than 0.12 seconds Wide QRS complex, greater than 0.12 seconds Delta wave
89
Right-Sided Heart Failure Manifestations: “AW HEAD”
A: Anorexia and nausea W: Weight gain H: Hepatomegaly E: oEdema (Bipedal) A: Ascites D: Distended neck vein
90
Left-Sided Heart Failure Manifestations: “DO CHAP”
D: Dyspnea O: Orthopnea C: Cough H: Haemoptysis A: Adventitious breath sounds P: Pulmonary congestion (crackles/rales)
91
What does establishing a diagnosis for heart failure involve
Clinical assessment (history and examination) N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test ECG Echocardiogram
92
Rheumatic fever
Rheumatic fever is caused by group A beta-haemolytic streptococcal, typically streptococcus pyogenes causing tonsillitis. This results in a type 2 hypersensitivity reaction, Throat swab for bacterial culture ASO antibody titres Echocardiogram, ECG and chest xray can assess the heart involvement A diagnosis of rheumatic fever is made using the Jones criteria Can cause mitral stenosis
93
Tumour lysis syndrome
high potassium and high phosphate level in the presence of a low calcium
94
Features of haemolytic anaemia
Anaemia Jaundice Splenomegaly
95
autoimmune haemolytic anaemia G.S
Direct Coombs test
96
What triggers G6PD deficiency
The key piece of knowledge for G6PD deficiency relates to triggers. In your exam look out for a patient that turns jaundice and becomes anaemic after eating broad beans, developing an infection or being treated with antimalarials. The underlying diagnosis might be G6PD deficiency.
97
Haemolytic anaemia how are they carried on
Spherocytosis: autosomal dominant Elliptocytosis: autosomal dominant G6PD: X-linked recessive Warm: Idiopathic Cold: Cold allutination disease
98
Lifecycle malaria
Malaria is spread by female Anopheles mosquitoes, most commonly at night time. Infected blood is sucked up by feeding mosquito. The malaria in the blood reproduces in the gut of the mosquito producing thousands of sporozoites (malaria spores). When that mosquito bites another human or animal the sporozoites are injected by the mosquito. These sporozoites travel to the liver of the newly infected person. They can lie dormant as hypnozoites for several years in P. vivax and P. ovale. They mature in the liver into merozoites which enter the blood and infect red blood cells. In red blood cells the merozoites reproduce over 48 hours, after which the red blood cells rupture releasing loads more merozoites into the blood and causing a haemolytic anaemia. This is why people infected with malaria have high fever spikes every 48 hours.
99
What to look out for infectious mononucleosis
Look out for the exam question that describes an adolescent with a sore throat, who develops an itchy rash after taking amoxicillin. Mononucleosis causes an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.
100
Heterophile antibody tests
Monospot test Paul-Bunnell test
101
There are some key bits of information that you should learn to be able to spot which leukaemia is in the exam:
Acute lymphoblastic leukaemia: Most common leukaemia in children. Associated with Down syndrome. Chronic lymphocytic leukaemia: Most common leukaemia in adults overall. Associated with warm haemolytic anaemia, Richter’s transformation into lymphoma and smudge / smear cells. Chronic myeloid leukaemia: Has three phases including a 5 year “asymptomatic chronic phase”. Associated with the Philadelphia chromosome. Acute myeloid leukaemia: Most common acute adult leukaemia. It can be the result of a transformation from a myeloproliferative disorder. Associated with Auer rods.
102
ITP is worth remembering as it is a key differential diagnosis of a
non-blanching rash
103
What are petechiae
pin-prick spots (around 1mm) of bleeding under the skin. Purpura are larger (3 – 10mm) spots of bleeding under the skin. When a large area of blood is collected (more than 10 mm), this is called ecchymoses. These are all non-blanching lesions.