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Medicine year 4 CDM > Block 1: dyslipidaemia > Flashcards

Block 1: dyslipidaemia Flashcards

1
Q

Dyslipidaemia: overview

A
  • Relationship between total and LDL-C levels and CAD, CVD and peripheral vascular disease
  • 50% of the population, highly preventable
  • Majority of patients with atherosclerosis have dyslipidaemia
  • Asymptomatic
  • Too much cholesterol can build up in the arteries causing atherosclerosis
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2
Q

Progression of dyslipidaemia

A
  • Initially dyslipidaemia: no symptoms, reversible
  • Atherosclerosis: symptoms, reversible
  • Symptoms, non-reversible: can develop Ischaemic heart disease, CVD, Peripheral vascular disease
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3
Q

Dyslipidaemia bloods (lipid profile)

A
  • Total Cholesterol (Desirable <5 mmol / l)
  • Low density Lipoproteins (LDL) (Desirable <2.5 mmol / l): ‘Bad cholesterol’
  • High Density lipoproteins (HDL) (Desirable > 1.2 in women and > 1 in men): ‘Good cholesterol’
  • Triglycerides (Desirable < 2.5 mmol / l)
  • Total cholesterol/ HDL Ratio (Desirable < 4 )
  • Total cholesterol measures the combination of LDL, HDL, and VLDL. VLDL is a precursor of LDL, the bad cholesterol.
  • Others: Very low density lipoproteins (VLDL), Lipoprotein A, Apolipoproteins
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4
Q

LDL

A
  • Carries most of the cholesterol in the blood
  • Combines with other substances to clog arteries
  • Due to diet high in saturated and trans fats
  • Should be <2.5 but in heart disease should be lower
  • HDL helps remove LDL. Want high HDL
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5
Q

Triglycerides

A
  • The body converts excess calories, sugar and alcohol into triglycerides.
  • Type of fat that is carried in the blood and stored in fat cells
  • Increases risk of metabolic syndrome which is linked to heart disease and diabetes
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6
Q

Causes of dyslipidaemia

A
  • Primary: Genetic dyslipidaemia (Familial Hypercholesterolaemia)
  • Secondary: T2D, Nephrotic syndrome, Hypothyroidism, obesity, smoking, lifestyle

Familial hypercholesterolaemia: 3-4x risk of heart attack and stroke

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7
Q

Risk factors for high cholesterol

A
  • Diet high in saturated fats and cholesterol
  • Family history
  • Being overweight or obese
  • Age
  • Diabetes
  • Physical inactivity, smoking, alcohol
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8
Q

Ways to lower cholesterol: dietary modification

A
  • Saturated fats (animal fats and oils) raise LDL and trans fats increases LDL and reduces HDL
  • Reduce diet of baked goods, fried food and margarine
  • Unsaturated fats can lower LDL with other diet changes, they are in avocados, olive oil and peanut oil
  • Moderate alcohol intake, stop smoking
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9
Q

Other ways to lower cholesterol: lifestyle, medicine

A
  • Lifestyle: loose weight, stop smoking, increase physical activity
  • Statins: either lipid soluble (Atorvastatin) or water soluble (Rosuvastatin). Decrease LDL and TG, increase HDL
  • Fibrates, Ezetimibe, Omega 3 fatty acids
  • Bile acid sequestrants
  • PCSK 9 inhibitors, Inclisiron
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10
Q

Initial tests for dyslipidaemia

A
  • Full lipid profile
  • BMI: weight and hight
  • Blood pressure
  • Fasting glucose
  • Bloods: Hba1c, thyroid function tests, U&E, LFT
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11
Q

Signs of hyperlipidaemia

A
  • Tendon xanthomata: nodules that develop in the hands and Achilles tendon
  • Xanthelasma: nodules on the eyelids
  • Premature corneal arcus: bluish rims surrounding the iris
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12
Q

Genetic dysipidaemia

A
  • Familial combined hyperlipidaemia: increased LDL, triglycerides or both
  • Heterozygous familial Hypercholesterolaemia: increased LDL
  • Polygenic Hypercholesterolaemia
  • Familial Hypertriglyceridemia
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13
Q

Familial Hypercholesterolaemia

A
  • Family history of early cardiac event
  • High LDL cholesterol, above 190 in adults and 160 in children
  • Autosomal dominant inheritance, if you have it children have 50% chance of getting it
  • 1:200
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14
Q

When to suspect FH

A
  • High LDL >5
  • Early cardiovascular event: in themselves or close relatives
  • Strong family history
  • Stigmata: Tendon xanthoma, Arcus Lipidalis
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15
Q

Testing for FH

A
  • Risk calculated using Dutch lipid scoring system. If >8 definite FH, 6-8 probable FH, 3-5 possible FH, <3 unlikely FH
  • Confirmatory test: gene sequencing, once confirmed family members are screened (family cascading)
  • Simon Broom criteria: helps confirm FH
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16
Q

Management of FH

A
  • Life style modification: better diet and increase exercise
  • Family cascading: test rest of the family
  • Statins
  • Ezetimibe
  • PCSK-9 inhibitors: Alirocumab, Evolucumab. Work on LDL receptors to destroy more LDL in the liver
  • Inclisiron: reduces production of PCSK-9
  • Medication aim: bring LDL as low as possible <2.5
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17
Q

Diabetic neuropathy

A
  • When it causes damage to your nerves
  • 4 types: peripheral neuropathy, sensory neuropathy, autonomic neuropathy, motor neuropathy
  • Treatment: monotherapy with antidepressant drugs inclusing tricyclics (amitriptyline, hydrochloride), duloxetine, Can use antiepileptics (pregabalin and gabapentin)
  • For diarrhoea use tetracycline or codein phosphate. In gastroparesis use erythromycin
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18
Q

Symptoms of diabetic neuropathy

A
  • Peripheral: pain in hands or feet
    -Sensory: tingling, numbness, inability to feel pain/temperature, shooting pain, loss of coordination
  • Autonomic: gastroparesis (bloating, constipation, diarrhoea), loss of bladder control, irregular heart beats, impotence
  • Motor: muscle weakness
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19
Q

Hyperosmolar hyperglycaemia

A

Life threatening complication of T2D: severe hyperglycaemia, extreme dehydration, hyperosmolar state and altered consciousness

Often due to concurrent illness
Treatment- IV saline and insulin
Complications: coma, seizure, death
Symptoms: urination, thirst, nausea, dry skin
No ketones in blood

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20
Q

Types of thinking

A
  • Type 1: fast paced intuitive, unconscious. Processes information quickly. Influenced by emotions, experiences and memories
  • Type 2: deliberate effort, concentrated thought. Processes information slowly. Is influenced by facts, logic and evidence
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21
Q

Types of reasoning: 1

A
  • Deductive reasoning: start with a general rule to reach a conclusion, only valid if premise is correct
  • Hypothetico-deductive reasoning Eg. In disease X, the finding Y occurs. Patient A does not have Y, therefore disease X is not the diagnosis.Find a hypothesis and then try and prove/disprove it. But this process only rules out some possibilities.
  • Inductive reasoning– based upon general conclusions. Wegather evidence, seek patterns and form a hypothesis.The conclusions are probable not certain.
  • Abductive reasoning–working backwards from signs and tests to the cause.Eg. Moving from the effect to cause – “What is the best explanation?”Conclusions are probable not certain.
22
Q

Types of reasoning 2

A
  • Deterministic reasoning– rule based and categorical. Eg. Urinary frequencyand dysuria in woman = infection. This is very experience dependent.
  • Probabilistic– classifies the likelihood of hypotheses. Probabilities used are based on clinician experience and context.
  • Causal– using knowledge of physiology to help diagnosis. Eg. In the presence of a low thyroid hormone (T4), a high thyroid stimulating hormone (TSH) will confirm hypothyroidism. Its absence may suggest alternatives such as “sick euthyroid syndrome”. This is very context specific.
  • Heuristics ‘devices’ for helping interpret and organise information i.e. mnemonics or CURB-65
23
Q

Types of error

A
  • No fault: unusual presentation, missing information
  • System error: technical i.e. unavailable tests. Organisational i.e. workload
  • Cognitive: faulty data gathering, poor reasoning
24
Q

Types of bias

A
  • Availability bias: when you pick a diagnosis because its at the forefront of your mind from reading/learning
  • Anchoring: relying too heavily on the first bit of information obtained
  • Overconfidence bias: tendency to believe we know more than we actually do linked particularly to:
  • Authority bias – the natural tendency to defer to age/ experience/ seniority and reluctance to challenge opinions
  • Cognitive overload: thinking is hard and our brains are lazy so we revert to Type 1 thinking.
25
Q

Sensitivity vs specificity

A
  • Sensitivity: the likelihood a disease is present with a positive test
  • Specificity: the likelihood a disease is absent with a negative test
  • Positive Predictive Value (PPV): if the test is positive what is the probability that the disease is absent
  • Negative Predictive Value (NPV): if the test is negative what is the probability that the disease is absent
  • Likelihood ratio = Probability of finding in person with disease/ Probability of finding in person without disease. Only works when there’s a diagnostic test.
  • Evidence based medicine is only useful when there is a diagnostic test
26
Q

Factors that influence the decision to investigate

A
  • Seriousness of disorder
  • Urgency of disorder and management
  • Cost of investigation
  • Invasiveness of investigation
  • Patient and clinician factors
  • Does the investigation perform well?- can it differentiate between disease and normal
27
Q

Can the investigation perform well?

A
  • Mean value can often mean well. Normal can be 1/2 standard deviation around the mean
  • When distribution is skewed to one side the median might be a better test of normality as well as percentile i.e. 5% to 95% of values
  • Instead of using a ‘normal’ value we can use a desirable value by looking at risk factors i.e. better serum cholesterol is lower
  • There are overlap in values between the healthy and diseased population meaning tests can never be 100% specific or sensitive so a compromise is made
28
Q

What laboratory diagnostic tests are available

A
  • Haematology:investigating blood and its components, including coagulation pathways
  • Biochemistry/Chemical Pathology:investigating chemicals within the bodily fluids
  • Microbiology and Virology:culturing, isolation and identification of micro-organisms as well as identifying sensitivity to treatments
  • Immunology:investigating abnormalities in the immune system
  • Cellular pathology:investigating cellular based specimens
  • Histopathology:investigating tissues
29
Q

x-ray

A
  • Benefits: fast, accessible and cheap
  • Downsides: avoid in pregnancy, hard to differentiate between densities, only a 2D image
  • Must remove any metalwork, if its a CXR you should take a deep breath in
30
Q

CT

A
  • Takes a series of x-rays that are combines to create a 3D image. Useful for bony structures
  • Contrast (Iodine) is used to differentiate the densities easier, causes blood vessels to light up.
  • The most common non-contrast scans are CT head and CT KUB (kidney, ureter, bladder)
  • Benefits: creates 3D image, faster and cheaper then MRI
  • Negatives: lots of radiation, not appropriate in pregnancy, contrast can damage kidneys,
  • Practical information: patient needs large bore canula for contrast, patient needs to sit still
31
Q

MRI

A
  • Useful for soft tissue, preferred in brain and musculoskeletal. Contrast is gadolinium and enhances vascular structures
  • T1:water is dark, this is better to see the anatomy and soft tissues
  • T2:water is bright, this is better to see pathology e.g. inflammation or oedema.
  • Benefits: no ionising radiation, can see soft tissue
  • Negatives: no magnetising metalwork is allowed i.e. aneurysm clips, cardiac stents and pacemakers, can take be up to 60 minutes of sitting still, less available, contraindicated in first trimester, expensive
32
Q

Ultrasound

A
  • Used to visualise soft tissue. Used to evaluate masses, examine the biliary and urological tracts and in gynaecology, used to visualise gallstones
  • Works by sending out high frequency sound waves and analysing the echoes
  • Advantages: no radiation, few contra-indication, non invasive, cheap, safe in pregnancy
  • Downsides: operator dependent, cant see well through bone/air/ dep layers of fat
  • Practical information= a full bladder for bladder/pelvic US, fasting for 6 hours prior to an abdominal US.
33
Q

Nuclear imaging

A
  • Used to track certain molecules in the body like water or glucose, a radioactive substance is attached to them which the scanner can detected. The substance is then excreted
  • PET scan: detect and monitor cancer, a tracer of glucose is tracked
34
Q

Type 1 Myocardial infarction

A
  • Underlying pathology is plaque rupture/erosion
  • Development of pathological Q waves
  • Raised troponin or ischaemic changes
  • Imaging may show loss of myocardium
  • Angiography may show a plaque
  • STEMI and NSTEMI
35
Q

ACS: types of plaques

A
  • Ruptured plaque: thin fibrous cap. Large lipid core, many macrophages. Fibrin rich thrombus. When rupture expose highly thrombotic material to the blood. Red thrombus its prognostically worse and more likely to occur in young men.
  • Eroded plaque: Proteoglycan, Glycosaminoglycan rich. Little or no lipid core. Neutrophils and NETS, many smooth muscle cells. Platelet rich thrombus. More fibrous, destruction of endothelium lining exposing the matrix to blood causing platelet aggregation. White thrombus
36
Q

Type 2 MI

A
  • Ischaemic myocardial injury due to mismatch between oxygen supply and demand
  • Will have +ve cardiac biomarkers, symptoms and/or ischaemic ECG changes
  • Extent of injury depend on extent of physiological stressor i.e. sepsis, sustained tachycardia, extent of underlying CAD, patients co-morbidities and frailty
  • Causes: atherosclerosis, vasospasm
37
Q

Other types of MI

A
  • Type 3 myocardial infarction – Cardiac death in patients with suspected myocardial ischaemia prior to any cardiac biomarker sampling
  • Type 4 myocardial infarction: Percutaneous Coronary Intervention related
  • Type 5 myocardial infarction: Coronary Artery Bypass Graft surgery related
38
Q

The three main types of MI

A
  • ST elevation myocardial infarction (STEMI): ST segment elevation + elevated biomarkers of myocardial damage
  • non-ST elevation myocardial infarction (NSTEMI): ECG changes but no ST segment elevation + elevated biomarkers of myocardial damage
  • unstable angina: normal troponin, rapid deterioration of existing angina. Chest pain at rest, new onset severe angina, treatment resistant
39
Q

Risk factors of MI

A

Age, male gender, family history, smoking, diabetes, hypertension, hypercholesterolaemia, obesity

40
Q

Clinical features of MI

A
  • Chest pain: left sided. Characterised by pressure, tightness or crushing sensation. May radiate to left arm or neck. Might not be present in elderly or diabetic
  • Dyspnoea
  • Nausea and vomiting: due to vagal activation and gastric distension
  • Sweating: poor prognostic indicator, accompanies chest pain
  • Palpitations
  • Epigastric pain: seen in diabetics, elderly and women
  • Fatigue: can be sole symptom, especially in elderly
  • Syncope/pre-syncope: can indicate arrhythmias or severe ischaemia affecting cardiac output
41
Q

MI: physical examination and obs

A
  • General appearance: may appear anxious, restless or diaphoretic due to sympathetic activation. Cyanosis in severe cases indicating hypoxia
  • Blood Pressure:[Hypotension] may indicate cardiogenic shock, whereas hypertension may reflect a stress response.
  • Heart Rate: Tachycardia is common but can worsen ischemia; bradycardia may be present in inferior myocardial infarction due to vagal activation.
  • Respiratory Rate: Tachypnoea may be indicative of heart failure or anxiety.
  • Oxygen Saturation: Hypoxia may be present depending on the degree of cardiac dysfunction and should be addressed promptly.
42
Q

ECG changes in an acute MI

A
  • hyperacute T waves are often the first sign of MI but often only persists for a few minutes
  • ST elevation may then develop
  • the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
  • pathological Q waves develop after several hours to days. This change usually persists indefinitely
  • NSTEMI: ST segment depression and T wave inversion
43
Q

STEMI criteria

A

Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads measured at the J point (the transition between the QRS and ST segment) of:

  • V2-V3= 2.5 mm (i.e ≥ 2.5 small squares) ST elevation inmen <40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in men over 40 years
  • 1.5 mm ST elevation in V2-3 in women
  • 1 mm ST elevation in other leads
  • new LBBB (LBBB should be considered new unless there is evidence otherwise
44
Q

Correlation between ECG changes and coronary territories

A
  • Anteroseptal: V1-V4: Left anterior descending coronary artery
  • Inferior: II, III, aVF: Right coronary artery
  • Anterolateral: V4-6, I, aVL: Left anterior descending or left circumflex coronary artery
  • Lateral: I, aVL +/- V5-6: Left circumflex coronary artery
  • Posterior: Tall R waves V1-2: Usually left circumflex, also right coronary artery
45
Q

Common management for all patients with ACS

A
  • Dual antiplatelet therapy: Asprin 300mg and a P2Y12 inhibitor (Clopidogrel, Prasugrel) usually for 12 months ([PPI for GI protection)]
  • Secondary prevention: statin, ACEi, beta blocker, ACEi/ARB
  • Oxygen should be given to patients with oxygen sats <94%
  • Morphine in severe pain but not routinely
  • Nitrates: either sublingually or intravenously. Useful if chest pain or hypertension. Used in caution if hypotensive
  • Anticoagulation: Fondaparineux or LMWH leading up to the procedure
46
Q

Conservative management ACS

A
  • Risk factor modification: BP and glycaemic control optimisation
  • Cardiac rehabilitation i.e. diet, exercise, weight loss and smoking cessation
  • Management of complication i.e. heart failure, mechanical complications and arrhythmias
47
Q

Management of STEMI

A
  • Primary coronary intervention: If within 12 hours of symptom onset and PCI can be delivered within 120 minutes of the time thrombolysis could be given i.e. consider thrombolysis if significant delay. Can be given after 12 hours if ongoing ischaemia. Stent is inserted, radial artery access is preferred. Must have persistent ST segment elevation
  • Thrombolysis: Given within 12 hours of symptoms if PCI will take 120 minutes longer then thrombolysis
48
Q

PCI for STEMI medications given before

A
  • Antiplatelet treatment prior to PCI: dual antiplatelet therapy (aspirin and another drug). If taking oral anticoagulant its Clopidogrel otherwise Prasugrel
  • During PCI: If radial access- unfractionated heparin with bailout glycoprotein IIb/IIa inhibitor (GPI). If femoral access- bivalirudin with bailout GPI
  • Other procedures: thrombus aspiration should be considered. Complete revascularisation can be considered for multivessel coronary artery disease without cardiogenic shock
49
Q

Thrombolysis for STEMI

A
  • Should be given antithrombin drug
  • If patients have persistent myocardial ischaemia after thrombolysis then PCI can be considered
50
Q

Management of NSTEMI/unstable angina

A
  • Antithrombin treatment: Fondaparinux should be offered if not high risk of bleeding and aren’t having angiography immediately
  • If immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

Medicine year 4 CDM (44 decks)

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