Pre Long Case Flashcards

1
Q

What does COPDX stand for?

A

C - Confirm Diagnosis

O - Optimise Function

P - Prevent Deterioration

D - Develop a plan

X - Manage Exacerbations

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2
Q

Explain the management plan of COPDX?

A

C - Confirm diagnosis (Spirometry (Post-bronchodilator FEV1/FVC < 0.7))

O - Optimise Function (Pulm Rehab, Exercice, Stepwise - SABA, LAMA/LABA, LABA/LAMA/ICS)

P - Prevent Deterioration (Stop Smoking, Vaccinate - Pneumoccal/Influenza, Oxygen)

D - Develop a plan (Good multidisciplinary support)

X - Manage Exacerbations (Bronchodialators, Oxygen, Prednisone, Pulmonary Rehab, Antibiotics if symptoms of sputum change/fever)

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3
Q

What are the 5 A’s of smoking cessation?

A

Ask and identify smokers at every visit
Assess the motivation to quit
Advise about the risks of smoking and benefits of quitting
Assist cessation
Arrange follow-up within a week of the quit date and one month after

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4
Q

What are the acute risk factors for ACS?

A

Vasoconstrictive (Stimulation of a-adrenergic receptors)

Haemodynamic (increase in heart rate, ventricular contractility, vascular resistance and blood pressure)

Haemostatic forces (Increase in catecholamines enhances platelet aggregation -> thrombus formation)

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5
Q

What 4 classes of agents are commonly admistered to reduce ACS?

A

Lipid-lowering agents

Angiotensin-converting enzyme inhibitors

Beta-adrenergic blocking agents

Aspirin

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6
Q

Name 4 non-pharma management to prevent ACS?

A

Trigger reduction

Reduce stress

Meditation

Anger management

Reduce drug use

Reduce air pollution

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7
Q

What is the pharmacologic treatment for AS?

A

There is none - pharma is for prevention

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8
Q

What are the risk factors for AS?

A

Similar to CAD - Aging, Male sex, Hyperlipidaemia, Active inflammation, Obesity, Smoking…

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9
Q

How does AS affect the heart?

A

Initially, the LV generates increased pressure by concentric myocardial hypertrophy.
In the later stages, the left ventricle dilates, the wall thins, and the systolic function deteriorates

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10
Q

What is the 3 clinical manifestations of AS?

A

Heart failure (HF), syncope, and angina.

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11
Q

What three findings indicate severe AS on echo?

A

Maximum aortic jet velocity >4.0 m/s

Mean transvalvular pressure gradient >40 mm Hg

Valve area <1.0cm²

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12
Q

Complications of Mechanical Valves?

A

Will outlive the patient but require Warfarin -> risk of bleeding

Risk of Mechanical Haemolysis

Need replacement if endocarditis

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13
Q

Complications of Tissue valves?

A

Will only last 10-15 years

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14
Q

What is the no.1 cause of Aortic Regurgitation?

A

Longstanding Hypertension

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15
Q

Presentation of AR

A

Orthopnea, dyspnea, and palpitation

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16
Q

What is the severity at which AR is treated surgically?

A

LVEF <55%, Left ventricular end-systolic diameter (LVESD) > 55mm

17
Q

How do statins work?

A

HMG-CoA reductase inhibitors (inhibit cholesterol synthesis - decrease LDL)

Stabilise plaque

Slightly increase HDL

18
Q

How does ezetimibe work?

A

Prevents cholesterol for being absorbed in the intestine

19
Q

What are the targets for diabetes management? (HbA1c, Cholesterol, BP, BGL)

A

HbA1c: <7% (between 6.5-7.5)

Total cholesterol (mmol/L) <4.0

HDL-C (mmol/L) ≥1.0

LDL-C (mmol/L) <2.0

Triglycerides (mmol/L) <2.0

Blood pressure (mmHg) <130/80 (end organ)

Advise 6–8 mmol/L fasting and 8–10 mmol/L postprandia

20
Q

What is the ddx of crepitations?

A

Pulmonary fibrosis / interstitial lung disease (fine crepitations)

Bronchiectasis (coarse crepitations)

Pulmonary congestion / pulmonary oedema (may associate with wheezing)

Atelectasis (basal).

21
Q

Investigations that should be requested in a patient with hypertension are:

A

Electrolyte profile and renal function indices—looking for evidence of renal failure. Abnormal renal function indices should prompt further investigations to rule out parenchymal renal disease.

Electrocardiogram (ECG)—looking for left ventricular hypertrophy by voltage as well as strain criteria and evidence of ischaemic heart disease

Chest X-ray—to exclude cardiomegaly, left ventricular hypertrophy and congestive cardiac failure

Echocardiogram—to assess left ventricular wall thickness and chamber size and any evidence of diastolic dysfunction

Urine analysis—looking for proteinuria. A positive urine analysis for proteinuria should be followed up with a 24-hour urine collection to quantify the proteinuria and to assess creatinine clearance. Proteinuria of more than 2 g per day is much more likely to reflect primary renal disease and usually indicates a need for renal biopsy. Calculate the albumin-to-creatinine ratio (ACR), which is an important cardiovascular risk marker.

Fasting blood sugar levels and lipid profile—to assess the presence of other significant cardiovascular risk factors.

22
Q

What end organ damage results from hypertension?

A

Myocardial infarction

Left ventricular hypertrophy

Cardiac failure

Stroke

Hypertensive nephropathy

Hypertensive retinopathy

Arteriosclerosis

23
Q

Adverse effects of thiazide diuretics?

A

Hypercholesterolaemia, hyperglycaemia, thrombocytopenia and gout

24
Q

Adverse effects of beta blockers?

A

Bradycardia, postural hypotension, depression and cold peripheries

25
Q

Adverse effects of ACE Inhibitors?

A

Angio-oedema, cough, postural hypotension, hyperkalaemia, progression of renal failure and first-dose hypotension

26
Q

What is the initial management of a non stemi?

A

In a non-STEMI, the patient should be managed initially with anticoagulation and antiplatelet therapy

27
Q

What is follow-up for a ACS?

A

ECHO

Coronary Angio if angina persists

Stress test

Post MI rehab

28
Q

Why do patients who have CHF complain of anorexia?

A

Due to hepatic congestion

29
Q

Investigations in heart failure?

A

Full blood count—looking for anaemia

Electrolyte profile and renal function indices—hyponatraemia is common in severe congestive cardiac failure.

Plasma B-type natriuretic peptide (BNP) levels

Levels of serum markers of cardiac damage—Troponin I or T and the MB fraction of the enzyme creatinine kinase (CKMB)

Urine analysis—looking for protein, blood, white cells and organisms

Arterial blood gases—to assess the level of oxygenation and the acid–base status, particularly in the severely dyspnoeic and those in pulmonary oedema

Electrocardiogram—looking for evidence of acute ischaemia, previous ischaemic cardiac damage, arrhythmias and left ventricular hypertrophy.

Chest X-ray—looking for cardiomegaly as well as pulmonary congestion

Transthoracic echocardiogram—looking for wall motion abnormalities and valvular lesions. The echocardiogram will quantify the ejection fraction and the dynamic ventricular chamber and wall dimensions.

Thyroid function tests—hyperthyroidism can lead to high-output cardiac failure. Hypothyroidism causes low-output cardiac failure as well as diastolic cardiac failure due to pericardial effusion.

Serum vitamin B1 levels in potentially malnourished patients—to exclude beriberi (remember: this is very rare in our society!)

Renal arterial Doppler study—to exclude renal artery stenosis in the patient who suffers from recurrent episodes of unexplained pulmonary oedema (flash pulmonary oedema).

30
Q

What are the complications of chronic renal failure?

A

A—anaemia, arthritis, acidosis, anorexia

B—blood pressure, bleeding, bone disease

C—cholesterol elevation, cardiac failure, constipation

D—planning dialysis

E—endocrine problems, entrapment neuropathy

P—pruritus, peripheral neuropathy, pancreatitis, peptic ulcer disease, platelet dysfunction.