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NEED TO KNOW Before Exams!!! > Cardio > Flashcards

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
Q

pleural aspirate analysis,
would typically be found in a patient with an empyema?

A

pH <7.2, ↑ LDH, ↓ glucose

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26
Q

Cystic fibrosis Gold Standard

A

Sweat test
Sodium chloride >60 mmol/L

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27
Q

Which of the following organisms, responsible for causing chronic pneumonia, is
most commonly found in patients with longstanding cystic fibrosis?

A

Pseudomonas aeruginosa

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28
Q

Long-term used medication causing pulmonary fibrosis

A

Amiodarone along with bleomycin,
bulsulfan, nitrofurantoin, methotrexate and sulfasalazine are drugs that
can cause pulmonary fibrosis with long-term use

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29
Q

Bibasal pneumonia

A

L. pneumophilia

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30
Q

Which of the drugs below would be the most appropriate to treat pulmonary Aspergillus spp. infection?

A

Amphotericin B

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31
Q

aspiration
pneumonia antibiotic regimen

A

Intravenous cefuroxime and metronidazole

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32
Q

Infective endocarditis:

A

Typically affects mitral valve (LS)
However in IVDU affects tricuspid valve

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33
Q

Head trauma

A

Subarachnoid: Surgery + Nimodipine
Subdural: Burr Hole + Craniotomy/IV mannitol
Extradural: IV mannitol

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34
Q

DEMENTIA

A
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35
Q

Cranial nerve lesions

A
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36
Q

Hypertension NICE

A

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)

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37
Q

Duke’s Criteria Infective Endocarditis

A
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38
Q

CHADSVASC

A
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39
Q

Heart Block

A
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40
Q

four stages of chronic limb ischaemia

A

Stage I: asymptomatic
Stage II: intermittent claudication
Stage III: rest pain/nocturnal pain
Stage IV: necrosis/gangrene

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41
Q

What is a consequence of regular blood transfusions and how do you treat this complication?

A

Iron overload
Iron chelation – deferoxamine/deferasirox

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42
Q

Medication used to stimulate Hbf production

A

Hydroxycarbamide

43
Q

First Line chemotherapy used for multiple myeloma

A

Bortezomid
Thalidomide
Dexamethasone

44
Q

Angina medication

A

1st GTN spray
2nd CCB/ Beta blocker (atenolol/veramapril)

45
Q

Signs for PAD

A

Hair loss , atrophic skin , brittle / slow-growing nails , ulcers,
numbness in feet, absent distal pulses, intermittent claudication.

46
Q

Ulcers Diff

A
47
Q

Where can you best hear aortic stenosis

A

2nd intercostal space (1), left sternal border (1).

48
Q

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?

A

G6PD deficiency
X-Linked recessive

49
Q

Pathophysiology of aortic stenosis

A

Narrowing of aortic valve 🡪 decreased stroke volume 🡪 increased afterload 🡪 increased left ventricular pressure 🡪 compensatory LVH 🡪 increased oxygen demand 🡪 ischaemia

50
Q

Pathophysiology of mitral regurgitation

A

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
Q

Pathophysiology of mitral stensosis

A

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
Q

Pathophysiology of aortic regurgitation

A

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
Q

Most common viral cause of pericardial effusion

A

Viral is the most common infectious cause → coxsackie 19 virus often

54
Q

What drugs are contraindicated in pregnanct women

A

ACEi and ARB should always be discontinued in pregnancy as they cause fetotoxicity

55
Q

Thyroiditis

A

-

56
Q

Management of Addisons crisis

A

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
Q

Top three cause sof SIADH

A

Post-operative
SSRIs
Small cell lung cancer

58
Q

Achalasia

A

Barium swallow: ‘bird’s beak’ sign
Manometry = GOLD
First line is upper GI endoscopy

59
Q

What hypersensitivity reaction is coeliac

A

Type 4

60
Q

Mnemonic for Absorption of Stuff in tummy

A

Dude Is Just Feeling Ill Bro = Duodenum (Iron), Jejunum (Folate), Ileum (B12)

61
Q

Pathophysiology for diverticular disease

A

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
Q

Pathophysiology of appendicits

A

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
Q

Causes of AKI

A
64
Q

Atherosclerosis formation

A

Endothelial dysfunction- NO is reduced in endothelial dysfunction
1. High LDL deposits in tunica intima. LDL becomes oxidised, activating endothelial cells

  1. Adhesion of blood leukocytes to activated endothelium move to tunica intima
  2. Macrophages take in oxidised LDLs, becoming foam cells
  3. Foam cells promote the migration of smooth muscle cells from tunica media to the intima and smooth muscle cell proliferation
  4. Increased smooth muscle cell proliferation and heightened synthesis of collagen
  5. Foam cells die, causing lipid content released
  6. Thrombosis plaque ruptures lead to blood coagulation and thrombus impeding blood flow.
65
Q

Useful drugs in treating CAD

A

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
Q

Second line treatment options for angina

A

Ivabradine, ranolazine and nicorandil

1st: Amlodopine

67
Q

Pericarditis
CARDIAC RIND

A

Collagen Vascular Disease
* Aortic aneurysm
* Radiation
* Drugs
* Infections
* Acute Renal Failure
* Cardiac infarction
* Rheumatic Fever
* Injury
* Neoplasms
* Dressler’s syndrome

68
Q

Pericarditis 1st line treatment

A

NSAID/aspirin

69
Q

Acute pericardits triad of symptoms

A

chest pain, friction rub and ECG changes

70
Q

Signs of Cardiac tamponade other than becks triad

A

Absent Y wave in the JVP

71
Q

Stanford system for aortic dissection

A

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

72
Q

X ray findings for aortic dissection

A

D:Dilated aortic arch
W: Widened mediastinum
E: Effusion (pleural)
E: Effusion (pericardial)
B: Blurring of aortic contour
S: Separation of intimal calcification

73
Q

G.S for infective endocarditis

A

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
Q

Modified Duks’s Croteria

A

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
Q

Management for infective endocarditis

A

Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin)

76
Q

Budd-Chiari Syndrome

A
77
Q

Respiratory finding in pumonary embolism

A

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
Q

Major risk factor for tetralogy of fallot

A

RUBELLA

79
Q

Tet spells options

A

Seen in tetralogy of fallot
Beta blockers
O2

80
Q

Murmur seen in ventricular septal defect

A

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
Q

What is Eisenmenger syndrome

A

pulmonary pressure is greater than the systemic pressure

82
Q

Atrial septal defects and stroke

A

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
Q

Murmur for patent ductus arteriosus

A

continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear.

84
Q

Heart Block

A

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
Q

Ventricular ectopics

A
86
Q

Mnemonics for tachycardias

A
87
Q

Acute management of supraventricular tachycardia

A

Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion

88
Q

ECG changes in Wolff-Parkinson-White syndrome are

A

Short PR interval, less than 0.12 seconds
Wide QRS complex, greater than 0.12 seconds
Delta wave

89
Q

Right-Sided Heart Failure Manifestations: “AW HEAD”

A

A: Anorexia and nausea
W: Weight gain

H: Hepatomegaly
E: oEdema (Bipedal)
A: Ascites
D: Distended neck vein

90
Q

Left-Sided Heart Failure Manifestations: “DO CHAP”

A

D: Dyspnea
O: Orthopnea

C: Cough
H: Haemoptysis
A: Adventitious breath sounds
P: Pulmonary congestion (crackles/rales)

91
Q

What does establishing a diagnosis for heart failure involve

A

Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
ECG
Echocardiogram

92
Q

Rheumatic fever

A

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
Q

Tumour lysis syndrome

A

high potassium and high phosphate level in the presence of a low calcium

94
Q

Features of haemolytic anaemia

A

Anaemia
Jaundice
Splenomegaly

95
Q

autoimmune haemolytic anaemia G.S

A

Direct Coombs test

96
Q

What triggers G6PD deficiency

A

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
Q

Haemolytic anaemia how are they carried on

A

Spherocytosis: autosomal dominant
Elliptocytosis: autosomal dominant
G6PD: X-linked recessive
Warm: Idiopathic
Cold: Cold allutination disease

98
Q

Lifecycle malaria

A

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
Q

What to look out for infectious mononucleosis

A

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
Q

Heterophile antibody tests

A

Monospot test
Paul-Bunnell test

101
Q

There are some key bits of information that you should learn to be able to spot which leukaemia is in the exam:

A

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
Q

ITP is worth remembering as it is a key differential diagnosis of a

A

non-blanching rash

103
Q

What are petechiae

A

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.

NEED TO KNOW Before Exams!!! (13 decks)

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