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Y3 Medicine > 1 - ACS and Hypertension > Flashcards

1 - ACS and Hypertension Flashcards

1
Q

/What is ACS and what is the aetiology of this?

A

STEMI/NSTEMI/Unstable Angina

Due to either plaque rupture, thrombosis or inflammation

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2
Q

What are the signs and symptoms of ACS?

A

Signs: distress, anxiety, pallor, sweatiness, low grade fever, signs of heart failure (raised JVP, basal crepitations, 3rd heart sound)

Symptoms: acute central crushing chest pain lasting >20 minutes, nausea, sweating, dyspnoea, palpitations

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3
Q

What is a silent ACS and what patients does this occur in?

A

ACS without the chest pain. May have syncope, pulmonary oedema, epigastric pain, bomiting, post op hypotension, oliguria, diabetic hyperglycaemia

Seen in the elderly and diabetics often

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4
Q

What are some risk factors for ACS?

A

Non-Modifiable

  • Age
  • Male
  • FHx

Modifiable

  • Smoking
  • Hypertension
  • DM
  • Hyperlipidaemia
  • Obesity
  • Cocaine use
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5
Q

How are each of the three acute coronary syndromes diagnosed based on their investigation findings?

A

Triad of symptoms, ECG changes and hs-TnI levels

All will have cardiac sounding chest pain

STEMI:

  • ST elevation (>1mm in limb leads and 2mm in chest leads) or new LBBB
  • hs-TNI >100ng/L
  • CK often raised over 400

NSTEMI

  • ST depression, T-wave inversion or normal
  • hs-TnI>100ng/L

Unstable Angina

  • ST depression, T wave inversion or normal
  • hs-TnI is normal
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6
Q

What are the cardiac biomarkers used for a suspected MI and why?

A

- Trop I as high sensitivity as released from cardiomyocytes on necrosis.

  • Begins to rise 3-4 hours after myocardial damage and remains high for 2 weeks
  • Also check CK levels
  • Need to see if falling, static or rising so take Trop I on admission then again in 3 hours to assess trend. Only need one result if onset of symptoms >3hours before presentation
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7
Q

What can cause false positive elevation of hs-TnI, meaning the patient is not having an MI?

A

Common: advanced renal failure, PE, CPR, ablation therapy

Less common: severe congestive heart failure, myocarditis, prolonged tachyarrhythmia

Rare: aortic dissection, aortic stenosis, hypertrophic cardiomyopathy, malignancy, stroke, severe sepsis

ALWAYS TAKE SERIAL MEASUREMENTS AND LOOK AT THE TREND NOT THE VALUE OF TEST

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8
Q

What ECG leads correspond to each area of the heart e.g anterior, septal etc?

VERY IMPORTANT

A

- Lateral: circumflex artery

- Septal: LAD

- Inferior: right coronary artery

- Posterior (V7-V9): circumflex artery

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9
Q

What are the immediate ECG changes in a STEMI? (excluding a posterior STEMI)

A

- ST elevation in 2 or more leads from the same zone e.g II, III, aVF.

  • ST elevation >1mm in limb leads, >2mm in chest leads
  • Presence of LBBB
  • May have hyperacute tall T waves
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10
Q

What are the sequential ECG changes following an MI?

A

Within hours: ST elevation and hyperacute T waves or LBBB

24 hrs: T wave inversion, ST normal

Few days: pathological Q waves that persist

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11
Q

How does a posterior MI present on a 12 lead ECG, why is this and what should you do next?

IMPORTANT

A

- ST depression in leads V1-V4

  • Reciprocal changes (upside down) due to looking at ischaemic myocardium from the other side
  • Need to do 15 lead ECG (V7-V9 and RV4) in all STEMI patients, especially those with inferior STEMI or ST depression in V1-V4
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12
Q

What are the ECG changes in an NSTEMI or unstable angina?

A
  • ST depression or elevation
  • T wave inversion (reperfusion waves) or flattening
  • T wave pseudonormalisation
  • Previously established ECG changes e.g old MI, LV hypertrophy
  • Normal ECG
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13
Q

What is T wave pseudonormalisation?

A

NSTEMIs often have T wave inversion that represents reperfusion of the area

On repeat ECG T waves may appear back to normal after firstly being inverted but this just means the artery is reoccluded

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14
Q

Apart from an ECG and cardiac enzymes, what other investigations should you carry out for a patient who presents with cardiac chest pain ?MI?

A

CXR: look for cardiomegaly, pleural effusion, widened mediastinum

Bloods: FBC, U+Es, random glucose, lipid profile, HbA1c, cardiac enzymes (2 tests 3 hours apart)

ECHO: regional wall abnormalities

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15
Q

What are some conditions that can mimic a STEMI on ECG?

A

- Early repolarisaition: usually leads V1 or V2, often in younger athletic patients and sometimes Afro-Caribbeans

- Pericarditis: widespread ST elevation

- Brugada Syndrome (sudden death): looks like anterior STEMI

- Takotsubo Cardiomyopathy: emotionial stress reaction in middle aged females that is temporary

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16
Q

What are some differential diagnoses for ACS?

A
  • Stable angina
  • Pericarditis
  • Myocarditis
  • Takotsubo cardiomyopathy
  • Pneumothorax
  • PE
  • Oesophageal spasm/reflux
  • MSK pain
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17
Q

What is the immediate management of an acute STEMI when a patient arrives at A+E?

A
  1. Brief history and exam with ECG (take bloods and CXR)
  2. Gain IV access
  3. Morphine with antiemetic e.g metoclopramide or cyclizine
  4. Aspirin 300mg if not already given
  5. Oxygen if hypoxic, keep >94%
  6. Anticoagulate (see next flashcard)
  7. Restore coronary perfusion if <12h since onset
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18
Q

Patients are given a loading dose of aspirin when they are having a STEMI. They also need to be further anticoagulated before reperfusion therapy, which drugs are used for this?

A

Prasugrel 60mg (inhibits ADP receptors)

If undergoing PPCI and are under 75 and weight more than 60kg and have not had prior TIA or stroke

Clopidogrel 600mg (inhibits ADP receptors)

If do not fufill criteria for prasugrel

Ticagrelor 180mg

If cannot have prasugrel or first line NSTEMI. Do not use if high bleeding risk

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19
Q

How do doctors choose which reperfusion therapy to offer to a patient with an acute STEMI?

A

PPCI

  • Used if <12h since onset and can be given PPCI within 120 minutes of first medical contact

Thrombolysis

  • Used if <12h since onset but cannot get PPCI within 120 minutes. Given infusion (e.g alteplase TPA) then transferred to PCI centre

No reperfusion

  • If presenting >12h, just given fondaparinux or enoxaparin
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20
Q

What are some contraindications for treating a STEMI with thrombolysis?

A
  • Previous intracranial haemorraghe
  • Ischaemic stroke <6months ago
  • Recent major head trauma/surgery
  • Known bleeding disorders
  • Liver biopsy or LP in past 24 hours
  • Pregnancy
  • GI bleeding
  • Cerebral malignancy
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21
Q

What blood tests are essential for a patient with a STEMI?

A
  • Cardiac enzymes (TropI)
  • FBC
  • Lipid profile
  • Random blood glucose
  • HbA1c
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22
Q

What medications are patients started on after an MI and for how long?

A

- Aspirin 75mg for life

- Ticagrelor (or another antiplatelet e.g Clopidogrel/Prasugrel) for 12 months

- ACEi or ARB for hypertension (checking renal function)

- Beta-blocker to lower heart rate (e.g Bisoprolol)

- Statin (e.g atorvastatin 80mg or rosuvastatin 5mg). Use ezetimibe if all statins have side effects

ATABS (also consider PPI for gastric protection with antiplatlets)

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23
Q

How much do you want LDL cholesterol to be lowered by with a statin?

A

40% reduction in non-HDL cholesterol. Total cholesterol should be below 4

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24
Q

After initial management of a STEMI and starting them on some cardioprotective medications, what are some other management principles you need to do for the patient?

A

CONTROL RISK FACTORS AND MANAGE ANY COMPLICATIONS

  • Smoking cessation
  • Control diabetes <7.5% Type 2 and <7% Type 1
  • Control hyoertension
  • Encourage daily exercise with cardiac rehabilitation programme
  • Advise diet low in saturated fats
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25
Q

If a patient is being anticoagulated for AF then has a STEMI and needs two more anticoagulants, what should you consider giving them?

A

Limit time on the drugs and give them a PPI

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26
Q

What are some complications of a STEMI and how are they managed?

A

- Heart failure: diuretics e.g Epleronone

- Cardiogenic shock: need inotropes and balloon pumps]

- Valve damage e.g Mitral Regurg: may present with pulmonary oedema, needs valve replacement

- Ventricular Septal Defect: pansystolic murmur that is diagnosed on ECHO and needs surgery

- Pericarditis: give NSAIDs

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27
Q

How long after an MI can a patient return to work and driving?

A

Driving: 1 week after successful angioplasty or 4 weeks after unsuccessfil angioplasty

Work: depends on clinical progress and nature of work. Should be encourage to modify work activities

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28
Q

How is an NSTEMI/Unstable angina managed immediately?

A
  1. Pain relief with morphine
  2. Aspirin 300mg
  3. Start LMWH (Enoxaparin for 48h based on weight and creatinine)
  4. Repeat ECG
  5. Calculate if low or high risk with GRACE score
  6. If high risk >3% give Ticagrelor and offer angiography
  7. Consider antianginals whilst waiting for angiography e.g nitrates, ranolazine, CCBs
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29
Q

What is the GRACE score?

A

Score that risk stratifies a patients 6 month mortality with ACS. If >3% then high risk

Looks at age, heart rate, systolic BP, creatinine, abnormal cardiac enzymes, ST segment abnormalities

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30
Q

What medications should patients be placed on after an NSTEMI?

A

Same as with a STEMI, ATABS!!!!!

  • Dual antiplatelet
  • ACEi
  • Beta blocker
  • Statin

Make sure you address modifiable risk factors e.g hyperlipidaemia, diabetes, ACEi, statin

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31
Q

What is angina and how does it present?

A

Symptomatic reversible myocardial ischaemia causing chest discomfort

  1. Constricting/heavy discomfort to chest, jaw, shoulders or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5 mins of rest or with GTN
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32
Q

What are some associated symptoms with angina if it is severe, and what symptoms make the diagnosis of angina less likely?

A

Associated symptoms: fear, sweating, nausea, dyspnea

Less likely to be angina: pain that is continuous, pleuritic or worse with swallowing, palpitations, dizziness, tingling

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33
Q

Angina can be difficult to distinguish from other differentials e.g GORD, MSK pain, pulmonary disease. What makes a diagnosis of angina more likely?

A

Two or more risk factors for coronary artery disease means the chest pain is more likely to be due to angina:

  • Smoking
  • Hypertension
  • Valvular heart disease
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34
Q

Apart from exercise, what are some other things that can precipitate angina?

A
  • Emotion
  • Cold weather
  • Heavy meals
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35
Q

Angina is usually due to atheromas in the coronary arteries (coronary artery disease). What are some other conditions that can cause symptoms of angina in the absence of coronary artery disease?

A
  • Aortic syenois
  • Hypertensive heart disease
  • Hypertrophic cardiomyopathy
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36
Q

What is decubitus angina and variant (Prinzmetal) angina?

A

Decubitus: precipitated by laying flat

Variant: caused by coronary artery spasm, occurs at rest

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37
Q

What questions are important to answer in the history of a patient with suspected stable angina?

A
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38
Q

What are some things you should look at on examination of a patient with suspected angina?

A
  • Height and weight for BMI
  • Blood pressure
  • Presences of murmurs (particularly aortic stenosis)
  • Evidence of hyperlipidaemia
  • Evidence of peripheral vascular diease or carotid bruits
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39
Q

What are some tests you should do as standard for all patients with suspected angina

A
  • FBC, U+Es, TFTs HbA1c, Gluocose
  • Full lipid profile
  • Resting 12 lead ECG
  • Consider ECHO and CXR
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40
Q

Patients who have angina like pain are scored based on their estimated likelihood of CAD. What investigations should you offer for different likelihood scores?

A

- 61-90%: Invasive coronary angiography

- 30-60%: Functional imaging e.g stress MRI, echo or myoview

- 10-29%: CT calcium scoring. If zero likelihood is minimal. If 1-400 consider CTCA or stress perfusion imaging. If >400 CTCA

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41
Q

What is the likelihood score for coronary artery disease in males and females over 70 presenting with angina symptoms?

A

Male >70: >90%

Women >70: 61-90% unless women at high risk and typical symptoms then risk of >90%

42
Q

When should you not use an exercise ECG to diagnose or exclude stable angina?

A

People without known CAD

43
Q

What are the principles of management in angina?

A
  1. Address exacerbating symptoms e.g anaemia
  2. Secondary prevention of CVD
  3. PRN symptom relief
  4. Antianginal medication
  5. Revascularisation if all above fails
44
Q

What medications are all patients with angina started on for secondary prevention of CVD?

A

- Aspirin 75mg (clopidogrel if cannot tolerate)

- Statin

  • ACEi if diabetic
  • Always address risk factors like smoking, hypertension, diabetic control
45
Q

What medication are patients with angina given for symptomatic relief?

A
  • Sublingual GTN spray
  • Take dose every 5 mins then after 15 mins call ambulance if not improved
  • Can cause headaches and hypotension
46
Q

Rate limitation is the goal in patients with angina.

What antianginal medications are patients with angina started on?

A

1st Line

B-Blockers: Atenolol or bisoprolol

or

NDHP CCB if above Cx: Diltiazem or Verapamil

2nd Line

- BB + CCB

  • If one of the above is Cx give one with long acting nitrate isosorbibe mononitrate, nicorandil or ranolazine
47
Q

How do the following drugs act as anti-anginal medicine and when are they used?

  • Nicorandil
  • Ivabradine
  • Ranolazine
A

Used 1st line as monotherapy if CCB and BB contraindicated or used in conjunction with one of them as 2nd line

Nicorandil: K+ channel activator. Can’t use in pulomary oedema or hypotension

Ivabradine: Reduces HR without lowering BP by blocking sinus node. Do not give if HR<70 or not in sinus rhythm, and do not coprescribe with CCB

Ranolazine: Inhibits late Na current. Caution in heary failure, elderly, <60kg, eGFR<30

48
Q

Why do you need to be careful when prescribing long acting nitrates for angina?

A

Want to avoid nitrate tolerance. No point adding a nitrate if patient already established on nicorandil for example

49
Q

What medicines are given to patients with angina?

A
  • Aspirin
  • Statin
  • ACEi if diabetic
  • BB +/ CCB
  • Long acting nitrate, Ivabradine, Nicorandil, Ranolazine
50
Q

When are patients with angina considered for revascularisation and what are the options for this?

A

When medical therapy is not providing symptomatic relief

Percutaneous Coronary Intervention: Balloon inflated in the vessel opening the lumen. Stent placed in. Dual antiplatelet therapy (aspirin and clopidogrel) for 12 months to reduce risk of in stent thrombosis

CABG: Less likely to need revascularisation but needs open heart surgery so slower recovery

51
Q

When is a CABG carried out and what are the complications with this?

A
  • Angina unresponsive to drugs
  • Unstable angina
  • Unsuccessful angioplasty

PCI is preferred as shorter recovery time and similar 5 year survival rates

52
Q

What vessel is harvested for a CABG?

A

- Saphenous vein

OR

- Internal mammary artery (last longer but risk of chest wall numbness)

53
Q

What are some non-cardiac causes of chest pain?

A
  • Costochondritis
  • Gastro-oesophageal
  • Pneumonia
  • PE
  • Pleural effusion
  • Pneumothorax
  • Psychogenic

Often sharp localised pain, worse on inspiration

54
Q

How do you take a cardiac history for an OSCE?

A

HPC: socrates, palpitations, dyspnoea, dizziness, blackouts, claudication

PMHx: ask about angina, any heart attacks/stroke, diabetes, hypertension, hypercholesterolaemia, past tests

DHx and Allergies: aspirin, GTN, statins, anticoagulants, ACEi

FHx: 1st degree relatives with cardio events especially <60

Social history: alcohol, smoking, exercise

Systems review and ICE

55
Q

What are some ischaemic heart disease risk factors?

A
56
Q

How do you do a cardiovascular exam for an OSCE?

A

https://geekymedics.com/wp-content/uploads/2020/10/OSCE-Checklist-Cardiovascular-Examination-2.pdf

  1. Wash hands, introduce, confirm identity, gain consent
  2. Expose to waist then poisition at 45 degrees
  3. General inspection
  4. Hands
  5. Pulses and Blood prssure
  6. Neck JVP and carotids
  7. Face
  8. Inspect, Palpate, Auscultate
  9. Look for sacral or peripheral oedema
  10. Auscultate lung bases
  11. Complete with . peripheral vascular examination, 12- lead ECG, urine dipstick, capillary blood glucose, fundoscopy, O2 sats, temp
57
Q

How long is the treatment for PE?

A
  • Cause known 3months
  • Cause unknown 6months-1year
58
Q

What are the signs on cardiovascular examination that would distinguish between right and left heart failure?

A

Right: raised JVP

Left: bibasal crepitations

59
Q

When should BB and CCB not be used in the acute setting?

A

BB: acute pulmonary oedema or heart failure

CCB: as negative inotrope in acute setting

60
Q

What are the different stages of hypertension?

A

Stage 1: 140/90 or 135/85 HBPM/ABPM

Stage 2: 160/100 or 150/95 HBPM/ABPM

Severe/Stage 3: Sys>180 or Dia>120

61
Q

How is hypertension diagnosed?

A

If >140/90 then offer ambulatory BP or home BP to check it is true before treating

If severe treat immediately with no ABPM/HBPM

62
Q

What is malignant hypertension?

A

Rapid rise in blood pressure to over 200/130, leading to vascular and organ damage

Can causes bilateral retinal haemorrhages, headache, visual disturbances

Needs urgent treatment (BB or CCB)

63
Q

Hypertension can be primary (90%) or secondary (10%). What are some secondary causes of hypertension?

A
  • Renal disease: renal artery stenosis, polycystic kidneys
  • Cushing’s
  • Phaeochromocytoma
  • Pregnancy
  • Drugs
  • COCP
  • Cocaine
64
Q

What are some symptoms of hypertension?

A
  • Usually asymptomatic
  • Sweating, headache, palpitations and anxiety if phaeochromocytoma
  • Muscle weakness or tetany in hyperaldosteronism
65
Q

What are some signs on examination of a patient with hypertension?

A
  • Retinopathy
  • Palpable kidneys/renal bruits
  • Radiofemoral delay in coarctation
  • Signs of Cushing’s
66
Q

What other tests apart from BP are performed when a patient is newly diagnosed with hypertension?

A
  • Urine dip
  • Bloods
  • Retinopathy
  • ECG
  • ECHO

- Q Risk score

67
Q

How do you test for end organ damage in hypertension?

A
  • Check for proteinuria or haematuria
  • Check for retinopathy
  • Do ECHO for LV hypertrophy
68
Q

When should hypertension be pharmacologically managed?

A

Stage 1: if under 80 and end organ damage

Stage 2 and above: everyone should be offered

69
Q

What are target blood pressures to bear in mind when treating hypertension?

A
  • Low-moderate risk: <140/90

- Diabetic/Previous Stroke: <130/80 (keep below 85)

- Elderly >80: <150/90

Reduce slowly, can be fatal if lower too rapidly!

70
Q

How is hypertension treated non-pharmacologically?

A
  • Weight loss
  • Stop smoking
  • Reduce alcohol
  • Reduce salt intake
  • Aerobic exercise
71
Q

How is hypertension treated pharmacologically?

A

ACD rule!

72
Q

What are some side effects of the following antihypertensive drugs?

  • Thiazides
  • CCBs
  • ACEi
  • ARB
  • BB
A

Thiazides: impotence, hypoK, hypoNa, cannot use in gout

CCB: ankle oedema, flushing, gum hyperplasia

ACEi: cough, hyper K, renal failure, angio-oedma

ARB: vertigo, urticaria, be careful in valve disease

BB: bronchospasm, cold peripheries, impotence

73
Q

Why should you drop hypertension slowly?

A

Any sudden drops in BP increases stroke risk as cerebral autoregulation is poor

74
Q

What is the definition of a hypertensive emergency?

A

Increase in BP which if sustained over the next few hours will cause irreversible end organ damage (encephalopathy, LV failure, aortic dissection, unstable angina, renal failure)

75
Q

What is the difference between a hypertensive emergency and urgency?

A

Emergency - High BP with critical illness (AKI,MI, Encephalopathy). Will cause damage over hours

Urgency - High BP without critical illness at the moment, often accompanied by retinal damage. Will cause damage over days

76
Q

How is a hypertensive emergency managed?

A

Aim to reduce diastolic BP to 110 in 3-12 hours (if emergency) or 24 hours (if urgency)

77
Q

How is hypertensive urgency managed?

A

Reduce diastolic gradually to <100 over 48-72 hours using PO drugs

Usually a combination of ACEi and CCB or Nifedipine AND Amlodipine for 3 days and then continue Amlodipine alone

  • Amlodopine
  • Diltiazem
  • Lisinopril
78
Q

What is the classic triad of symptoms for patients with a phaeochromocytoma?

A
  • Episodic headache
  • Sweating
  • Tachycardia

with sustained/paroxysmal hypertension

79
Q

How is phaeochromoctyoma diagnosed?

A

24h urine collection: measure urinary and plasma metanephrines and catecholamines

Can do MRI or CT abdo/pelvis to detect adrenal tumours

80
Q

How is a phaeochromocytoma managed after diagnosis?

A
  • Surgical resection

- Whilst awaiting surgery hypertension control: combined alpha and beta blockade. Start alpha blocker first (phenoxybenzamine) then add beta blocker when alpha blockade achieved. Never BB first

81
Q

How do you diagnose Cushing’s syndrome as the underlying cause of hypertension?

A
  • Physical appearance
  • Hyperglycaemia
  • Elevated 24h urine cortisol

- Diagnosis: low dose dexamethasone suppression test

  • Need to do adrenal CT
82
Q

When should you suspect primary hyperaldosteronism as the cause of hypertension and how do you diagnose this?

A

Suspect:

  • Low K+ and high/normal Na+
  • FHx of premature hypertension
  • Resistant hypertension

Diagnose:

  • Aldosterone:renin ratio measured in the morning. Will be very high
  • Adrenal CT
83
Q

How does the RAAS system work?

A
84
Q

What are some causes of postural hypotension?

A
  • Hypovolemia
  • Drugs e.g diuretics, nitrates, antipsychotics
  • Autonimic neuropathy
  • Hypopituatirism
85
Q

How do you treat postural hypotension?

A
86
Q

What are some signs of hyperlipidaemia?

A
  • Xanthoma
  • Xanthelasma
  • Corneal arcus
87
Q

What are the causes of the following pulses:

  • Bounding pulse
  • Collapsing waterhammer pulse
  • Slow rising anacrotic pulse
  • Jerky pulse
  • Pulsus paradoxus
A

Bounding: sepsis, CO2 retention, liver failure

Collapsing pulse: aortic regurgitation, AV malformation, PDA

Slow rising: aortic stenosis

Jerky pulse: HCM

Pulsus paradoxus: severe asthma, pericardial constriction, cardiac tamponade

88
Q

What does each part of the JVP wave form represent?

A
89
Q

S1 is the closure of the mitral and tricuspid valve. S2 is closure of the pulmonary and aortic valve. What makes a loud S1, soft S1, loud A2 and loud P2?

A

Loud S1: Mitral stenosis

Soft S1: Mitral regurg

Loud A2: tachycardia, hypertension

Loud P2: pulmonary hypertension

90
Q

When do you hear an opening snap?

A

Mid diastolic murmur of mitral stenosis usually due to calcification

91
Q

What do the following murmurs indicate:

  • Ejection-systolic
  • Pansystolic
  • Early diastolic
  • Mid diastolic
A

Ejection Systolic: (Crescendo-Decresendo) aortic stenosis, pulmonary stenosis

Pansystolic: mitral regurgitation, tricuspid regurgitation

Early diastolic: aortic regurgitation

Mid diastolic: mitral stenosis, rheumatic fever, Carey Coombs

92
Q

Which murmurs radiate and to where?

A

Aortic stenosis: carotids

Mitral regurgitation: axilla

93
Q

Which murmurs can be heard best when leaning forward, left lateral positioned, expiring?

A

- Leaning forward: aortic regurg

- Left lateral: mitral stenosis

- Expiring: left sided murmurs as expiring increases blood follow to left side of heart

94
Q

What are the following signs:

  • De Mussets
  • Corrigan’s
  • Muller’s
  • Quincke’s
  • Traubes’
A

All signs of aortic regurgitation

95
Q

Why are transoesophageal echos better than transthoracic and what are they used for?

A

Closer to the heart so more sensitive

  • Cardiac emboli
  • Aortic dissections
  • Assessing prosthetic valves
96
Q

What is cardiac catheterisation used for and what are some complications of this procedure?

A
  • Angioplasty
  • Valvuloplasty
  • Intravascular ultrasound or ECHO
97
Q

What is used second line to treat hypertension for an Afro-Carribbean patient?

A

ARB e.g Valsartan

98
Q

Which valve is the most commonly affected in infective endocarditis?

A

Mitral valve

99
Q

What medication do you need to give a patient before PCI?

A

Dual antiplatelet therapy with aspirin and a P2Y12 antagonist

PLUS

Unfractionated Heparin

100
Q

What is the difference between a STEMI and an NSTEMI?

A

STEMI is complete occlusion of the coronary artery but NSTEMI is only partial

Both result in tissue necrosis

101
Q

How is hypertensive retinopathy graded?

A

1 - Tortuous arterterues with thick shiny walls

2 - AV nipping where arteries cross veins

3 - Flame haemorraghes and cotton wool spots

4 - Papilloedema

102
Q

How should cocaine induced MI be managed?

A

Benzodiazepine plus GTN

Y3 Medicine (24 decks)

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