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Year 3 Med 1 > Med 1 LO's > Flashcards

Med 1 LO's Flashcards

1
Q

list relevant conditions that can cause angina (chest pain)

A
  • Carcinoma in the bronchus
  • Pneumothorax- pleuritic chest pain
  • Pericardial disease
  • Respiratory tract infection (pneumonia, influenza, TB)
  • PE
  • Ischaemic heart disease
  • Pleurisy (sharp pain when breathing- inflamed pleural membranes)
  • Aortic dissection
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2
Q

what is VTE

what are the risk factors?

A

VTE- venous thromboembolism. Term for blood clots that form in the (typically deep) veins

Risk factors-

  • Vein wall damage
    • Fractures
    • Severe muscle injury
    • Major surgery
  • Slow blood flow
    • Confinement to a bed (hospitalisation)
    • Limited movement (e.g., cast)
    • Sitting for a long time
    • Paralysis
    • Dehydration
    • Varicose veins
  • Increased oestrogen
    • Birth control
    • Hormone replacement therapy, sometimes after menopause
    • Pregnancy
  • Certain chronic medical illnesses
    • Heart disease
    • Lung disease
    • Cancer and its treatment
    • Inflammatory bowel disease
  • Other factors include
    • Previous DVT or PE
    • Family history of DVT or PE
    • Age increasing
    • Obesity
    • Catheterisation of central vein
    • Inherited clotting disorders
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3
Q

symptoms of VTE

A

Many people have none at all.

Following are the most common in their affecting areas:

  • Swelling (may be unilateral)
  • Tenderness
  • Pain
  • Redness
  • Dilated veins
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4
Q

What is a pulmonary embolism

rfxs

A

Is when a blood clot in the pulmonary arterial vasculature develop, usually from an underlying DVT of the lower limbs.

Always suspect in someone <2 weeks post op

Rfxs:

  • Malignancy- myeloproliferative disorder like polycythaemia vera
  • Surgery - especially pelvic and lower limb
  • Immobility
  • Pregnancy, COC
  • Previous thromboembolism or thrombophilia disorder
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5
Q

Symptoms of PE

A
  • Sudden onset SOB, pleuritic chest pain and haemoptysis (may have these as a triad or individually)
  • Massive PE may present with syncope or shock
  • You can have these without any DVT symptoms
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6
Q

Signs of PE

A
  • Tachypnoea
  • Tachycardia
  • Hypoxia
  • Irregular heartbeat (gallop rhythm)
  • Signs of right sided heart strain (raised JVP, right ventricular heave and loud P2 sound)
  • Pleural rub
  • Cyanosis
  • AF
  • Severe hypotension
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7
Q

ECG findings in PE

A
  • Normal or sinus tachycardia
  • Evidence of right heart strain- right axis deviation, RBBB, non-specific T wave changes
  • Classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).
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8
Q

pathophysiology of PE

A

Caused by

  • damage to blood vessels
  • blood flow turbulence
  • hypercoagulability

Most common in the lower limb area below the knee in low-flow sites such as the soleal sinuses and behind venous valve pockets. Valves are a site for venous stasis and hypoxia. Hypoxia decreases antithrombotic proteins and increases the expression of procoagulants.

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9
Q

Blood tests in PE

A

ABG: will be normal or show a type 1 respiratory failure (hypoxia w/o hypercapnia) and/or respiratory alkalosis (hyperventilation secondary to hypoxia).

FBC: rule out anaemia, raised CRP, clotting (important in case patient is started on LMWH/ warfarin)

D-dimer- highly non-specific but a negative result means that 95% of the time you can rule out PE

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10
Q

imaging investigations in PE

A

CTPA- diagnostic test of choice for a PE and will show a defect in the pulmonary vasculature.

CXR- usually normal apart from a few specific signs

V/Q scan if the patient has renal impairment

Lower limb duplex: if DVT is thought to be the cause

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11
Q

Wells scoring system

criteria and meaning

A

3 points:

  • Clinical signs and symptoms of a DVT
  • If no alternative diagnosis is more likely than a PE

1.5 points:

  • Tachycardia (HR>100bpm)
  • Patient has been immobile for >3 days or has had major surgery in last month
  • Previous DVT or PE

1 point:

  • Presents with haemoptysis
  • Active malignancy

IF wells score is <4 then D-dimer should be measured. Low D-dimer excludes PE, high prompts diagnostic imaging by CTPA or V/1 scan

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12
Q

Management of PE

A
  • ABCDE approach
  • Thrombolysis- IV alteplase bolus for massive PE if in A and E
  • Antiplatelets like warfarin/ DOACs in general practice- rivaroxaban, dabigatran
  • LWMH for 5 days
  • Morphine 5mg/10mg IV if in pain or distress
  • Oxygen if hypoxaemic 10-15L/min
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13
Q

what is an aortic aneurysm

what is a psuudoaneurysm

A

aneurysm dilatation of diameter > 3.0cm or +50% of its original diameter. Involve all layers of the vessel wall.

only involves a collection of blood only in the adventitia (outer layer).

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14
Q

causes of an aortic aneurysm

common sites for an aneurysm

which group is invited for screening

A

causes

  • Atheroma
  • Trauma
  • Infection (mycotic aneurysm in endocarditis)
  • Connective tissue disorders (e.g., marfans)
  • Inflammatory

common sites of aneurysm

  • Aorta (infrarenal most common)
  • Iliac
  • Femoral
  • Popliteal arteries

invited for screening: all males aged 65 are invigted for screening

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15
Q

Signs and symptoms of AAA (unpopped)

A
  • ¾ asymptomatic (often incidental finding via X-ray, CT or MRI)
  • Pain in the abdomen, chest, lower back or groin. Can be severe or sudden.
  • Pulsing sensation in the abdomen
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16
Q

signs of ruptured AAA

A
  • Intermittent or continuous abdominal pain (radiates to back, iliac fossae or groin)
  • Expansile abdominal mass
  • Clammy, sweaty skin
  • Dizziness
  • Fainting
  • Tachycardia
  • Nausea and vomiting
  • SOB
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17
Q

rfx for developing AAA and Rfx for ruptured AAA

A

developing AAA

  • Tobacco use
  • Age increasing (typically 65 or over)
  • Being male
  • Being white
  • Family history
  • Other aneurysms
  • Atherosclerotic risk factors
  • Food and alcohol consumption

rfx for rupture

  • Baseline aortic diameter
  • Rapid expansion
  • Tobacco use
  • Hypertension
  • Etc.
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18
Q

pathophysiology of AAA

A
  • Thick wall with low elastin content, high wall tension and few vasa vasorum
  • Atherosclerosis
  • Damage to media (ischaemic)
  • Tunica media revascularisation causes influx of inflammatory cells
  • Inflammatory cells secrete proteases and degrade elastin and collagen
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19
Q

complications of AAA

A
  • rupture
  • thrombosis
  • embolism
  • fistulae
  • pressure on other structures
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20
Q

pathophysiology of atheroma

A

atheroma- physiological term for a build-up of materials that adhere to arteries

  • Hypercholesterolaemia
  • LDLs accumulate in the arterial intima where they may be modified by oxidation and aggregation.
  • Modified LDLs act as chronic stimulators of the innate and adaptive immune response.
  • Endothelial cells and smooth muscle cells to express adhesion molecules, chemoattractants, growth factors (e.g., macrophage colony stimulating factor) and interact with receptors on monocytes.
  • Monocytes are stimulate to home, migrate and differentiate into macrophages and dendritic cells.
  • Macrophages and dendritic cells are stimulated into differentiating into foamy cells.
  • Foam cells act as deposits for lipids.
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21
Q

How does atheroma ruptuere lead to an MI?

A

In ST elevated MI, the thrombus is typically occlusive and sustained.

In plaque rupture, a gap in the fibrous cap exposes the highly thrombogenic core to the blood. Therefore the plaque forms a new thrombus, causing further stenosis

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22
Q

heart failure definition

systolic vs diastolic

A

AKA CHF and congestive heart failure

when the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs. can be classified into that caused by: pump failure, arrhythmias, excess after-load or excess pre-load

pump failure can be further divided into systolic or diastolic dysfunction

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23
Q

causes of systolic and diastolic heart failure

A

causes of systolic heart failure

  • ischaemic heart disease
  • dilated cardiomyopathy
  • myocarditis
  • infiltration (e.g., haemochromatosis or sarcoidosis)

causes of diastolic heart failure

  • Hypertrophic obstructive cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
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24
Q

clinical features of left heart failure

symptoms

signs

A

causes pulmonary congestion and systemic hypoperfusion

symptoms:

  • SOB on exertion
  • orthopnea
  • paroxysmal noctural dyspnoea
  • nocturnal cough (pink, frothy, sputum)

signs:

  • tachypnoea
  • bibasal fine crackles on ausculatation of the lungs
  • cyanosis
  • prolonged CRT
  • hypotension
  • s3 gallop rhythm due to stiffened ventricle
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25
Q

clinical features of right sided heart failure

signs and symptoms

A

RSHF causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced r heart output)

symptoms

  • ankle swelling
  • weight gain
  • abdominal distension and discomfort

Signs

raised JVP

pitting oedema/ sacral oedema

tender smooth hepatomegaly

ascites

transudative pleural effusion

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26
Q

investigations in heart failure

A
  • ECG- underlying cause
  • NT-proBNP- released in response to myocardial stretch. has a high negative predictive value, so if BNP is low then theres a low chance that cardiac failure has occured. If raised over 400 refer for trans-thoracic echocardiogram. if >2,000 then 2 week referral for specialist and echo.
  • echocardiogram- helps measure the ejection fraction. <40%= heart failure with reduced ejection fraction. >40% but raised BNP =HF with REF
  • blood tests- U+E for renal function, LFTs for hepatic congestion, TFTs for hyperthyroidism, glucose and lipids for assessing CV rfs
  • CXR- ABCDEF (go into more detail in future)
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27
Q
  • lifestyle modification ofr heart failure
  • smoking cessation
  • salt and lfuid restriction
  • supervised cardiac rehabilitation
A
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28
Q

pharmacological management of HF

A
  1. ACEi and Bblocker (ARB if intolerant to ACEi)
  2. Loop diuretics (furosemide or bumetanide) for symptoms

if symptoms persist consider:

  • aldosterone antagonists like spironolactone or eplerenone
  • hydralazine or nitrate in afro-caribbeans
  • ivabradine if sinus rhythm but impaired EF
  • ARB
  • Digoxin- in those with AF, worsens mortality but improves morbidity
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29
Q

Surgical/ device management options for HF

A

surgical/ device management options for HF

cardiac resynchromisation therpy

ICDs are indicated if the following criteria are fulfilled

QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III

QRS interval 120-149ms without LBBB, NYHA class I-III

QRS interval 120-149ms with LBBB, NYHA class I

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30
Q

intial management of acute ehart failure

A
  1. Sit the patient up
  2. Oxygen therapy (aiming saturations >94% in normal circumstances)
  3. IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
  4. SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
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31
Q

advanced management of acute heart failure

A
  1. CPAP - reduces hypoxia and may help push fluid out of alveoli
  2. Intubation and ventilation
  3. Furosemide infusion - continuous IV furosemide given over 24 hours to maximise diuresis
  4. Dopamine infusion - Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility.
  5. Intra-aortic balloon pump - if the patient is in cardiogenic shock
  6. Ultrafiltration - If resistant to or contraindicated diuretics
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32
Q

adverse effects of HF medications

beta blockers

ACE inhibitors

spironolactone

furosemide

hydralazine/ nitrate

digoxin

A

beta blockers- bradycardia, hypotension, fatigue, dizziness

ACE inhibitors- hyperkalaemia, renal impairment, dry cough, light headedness, fatigue, GI disturbances, angioedema

spironolactone- hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/ hair growth in women, hyponatraemia

furosemide- hypotensio, hyponatraemia/kalaemia

hydralazine/ nitrate- headaceh, palpitation, flushing

digoxin- dizziness, blurred vision, GI disturbances

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33
Q

Atrial fibrillation

+causes

A
  • most commonly sustained rhythm
  • no p waves
  • absence of isoelectric baseline
  • cariable ventricular rate
  • QRS complexes > 120ms
  • fibrillatory waves may mimic P waves

causes of a fib

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34
Q

Wheeze

  • what is it
  • common causes
A
  • wheeze is a relatively high-pitched shound produced by movement of air through a narrowed or compressed SMALL LOWER airway (stridor = higher)
  • expiratory noise

Causes:

  • Asthma
  • COPD
  • Heart failure
  • Anaphylaxis
  • Taxic inhalation
  • Acute bronchitis
  • Bronchiolitis
  • Foreign body aspiration
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35
Q

what is pneumonia

A

Lower respiratory tract infection in which the alveoli and terminal bronchioles are infected

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36
Q

likley bacterial pathogens for pneumonia

A

Typicals- called so because of their rapid onset of symptoms, inc. high fever and productive cough;

  • Strep pneumoniae- 80% of acases (gram +ve coci)
  • Staph aureus
  • Haemophilius influenzae (gram -ve rod)

Atypicals- more gradual onset of symptoms, may be non-specific initially (fever, myalgia, dry cough)

  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Legionella pneumophila
  • Coxiella burnetti
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37
Q

viral causes of pneumonia

A

viral much less common

influenza A

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38
Q

symptoms of pneumonia

Signs of pneumonia

A

Symptoms

  • Cough
  • Sputum
  • Dyspnoea
  • Chest pain; may be pleuritic on inspiration
  • Fever
  • Rigors
  • Confusion (elderly)

Signs

  • systemic inflammatory response (fever, tachycardia, CRP)
  • reduced oxygen saturations
  • reduced chest expansion
  • dull percussion
  • ausculatation (reduced breathing sounds, bronchial breathing, inreased vocal resonance)
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39
Q

treatment for pneumonia

A

antibiotics if bacterial

non-severe: (CURB-65= 2)

  • 1st line- amoxicillin
  • alternative e.g., COPD use doxycycline

Severe; (CURB-65> 3)

co-amoxiclav+ consider clarithromycin in addition

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40
Q

What method is used for risk stratification when assessing pneumonia

A

CURB-65

  • Confusion
  • Urea> 7mmol/L
  • Respiratpry rate > 30/min
  • Blood pressure (systolic <90mmHg or diastolic <60 mmHg)
  • Age >65 years

score 1 point for each feature present

  • 0-1 low mortality 1.5% treat at home
  • 2 mortality intermediate 9.2% short stay inpatient
  • 3+ 22% mortality risk manage in hospital
  • 4/5 ICU
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41
Q
  • What is COPD
  • what is it usually caused by
A

COPD is an umbrella term encompassing the older terms:

  • Chronic bronchitis
  • Emphysema

Vast majority of cases is caused by smoking

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42
Q

Multisystem effects of COPD

A

Mutlisystem effects of COPD

  • Cardiovascular; heart failure, ischaemic heart disease, pulmonary hypertension, arrhythmias
  • Brain; depression, anxiety
  • Bone abnormalities: osteopenia and osteoporosis present in 89% of COPD cases
  • Skeletal muscle atrophy
  • Sleep: obstructive sleep apnoea
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43
Q

Features of COPD

A
  • dyspnoea
  • cough; often productive
  • wheeze
  • in severe cases: weight loss, fatigue, right sided heart failure

possible to have an infective exacerbation

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44
Q

typical history of COPD patient

A

Smoking history- are they still smoking

Occupational and industrial exposures

History of exacerbations

Presence of comorbidities

Impact on patient’s life

Typically >20 pack years

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45
Q

how to calculate packyears of smoking

A

(how many packs smoked per day) x (how many years smoked)

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46
Q

signs of COPD

A
  • Raised Resp rate
  • Hyperextended/ barrel chest
  • Prolonged expiratory time >5s with pursed lip breathing
  • Use of accessory muscles on respiration
  • Quiet breath sounds (especially in apices) +/- wheezing
  • Quiet heart sounds (due to overlapping hyperinflated lung)
  • Basal crepitations
  • Signs of cor pulmonale (Raised JVP, ankle odema, warm peripheries, bounding pulse)
  • CO2 retention flap
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47
Q

Investigations for COPD

A

post-bronchodilator spirometry to demonstrate airflow obstruction–> FEV/FCV ratio <70% is diagnostic

CXR: hyperinflated, bullae, flat hemidiaphragm

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48
Q

how do we grade severity (bar CURB-65)

A

looking at post-bronchodilator FEV1

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49
Q

What is the MRC scale

A

scale to measure severity of pneumonia

  • Grade 0= not troubled by breathlessness except on strenuous exercise
  • Grade 1= short of breath when hurrying or walking up a slight incline
  • Grade 2= Walks slower than contemporaries on ground level
  • Grade 3= Stops for breath every 100m
  • Grade 4= Too breathless to leave the house
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50
Q

pathological changes seen

A
  • Airflow limitation and gas trapping- chronic inflame and fibrosis of airways leads to air trapping in the small airways
  • Destruction of alveoli- permanent enlargement of airspaces
  • Mucous gland hyperplasia
  • Thickened pulmonary arteriolar wall and remodelling occur with hypoxia, leading to increased pulmonary vascular resistance, pulmonary hypertension and impaired gas exchange
  • Increased pul resistance–>more force needed for RV contraction–> dilation and hypertrophy –> loss of RV function –> backing up of blood into RA and subsequently systemic venous circulation
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51
Q

Non-pharmalogical management of stable COPD

A
  • Smoking cessation
  • Education
  • Pulmonary rehabilitation
  • Diet
  • Self-management therapy
  • Psychosocial support
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52
Q

pharmacological management of COPD

A

Stepwise approach (one is carried onto the next, higher step)

  1. Short acting beta2 antagonist (salbutamol) or short acting muscarinic antagonist (ipratropium)
  2. LABA (salmeterol) and LAMA (glycopyrronium)/ inasthmatics ICS
  3. LABA+LAMA+ICS
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53
Q

What is bronchiectasis

main organisms involved

A

Bronchiectasis is permanent dilation of the bronchi and bronchioles due to chronic infection.

The main organisms include:

Haemophilius Influenzae, Pseudomonas aeruginosa, Streptococcus Pneumoniae, Staphylococcus aureus

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54
Q

causes of bronchiectasis

A

Post-Infection: Tuberculosis; HIV; Measles; Pertussis; Pneumonia

  • Bronchial Pathology: Obstruction by foreign body or tumour
  • Allergic Bronchopulmonary aspergillosis (ABPA)
  • Congenital: Cystic fibrosis; Kartagener’s syndrome; Primary ciliary dyskinesia; Young syndrome
  • Hypogammaglobulinaemia
  • Idiopathic
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55
Q

presenting symptoms of bronchiectasis

A

Begin insidiously and gradually get worse with periods of exacerbation

  • (Most common) Chronic cough that produces thick, tenacious, often purulent sputum
  • Dyspnoea
  • Wheezing
  • Hypoxia
  • Haemoptysis (can be massive)
  • Fever and constitutional symptoms
  • Exacerbations are common and often triggered by new infection
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56
Q

signs of bronchiectasis

A

Abnormal breath sounds (crackles, rhonchi, wheezing)

Digital clubbing

Pulmonary hypertension

Nasal polyps

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57
Q

risk factors for bronchiectasis

A
  • Previous childhood respiratory infections due to viruses
  • Previous infections by TB or severe bacteria pneumonia
  • Immunodeficiency
  • CF
  • Alpha-1-antitrypsin deficiency- also causes COPD and emphysema
  • Aspiration or inhalation injury
  • CT disorders- rheumatoid arthritis
  • IBD
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58
Q

management of bronchiectasis

A

conservative

  • Patient Education
  • Support Group
  • Chest Physiotherapy – Postural drainage at least twice daily to aid mucous drainage
  • Smoking Cessation

Medical

  • Antibiotics – recurrent exacerbations may require long term antibiotic treatment
  • Bronchodilators – Including salbutamol can be given to patients with symptoms of dyspneoa and wheeze such as COPD, ABPA, asthma
  • Corticosteroid - Prednisolone is used in ABPA treatment
  • Carbocysteine - Mucolytic which reduces the viscosity of sputum

surgical

  • Surgical excision of localized area of disease or cessation of haemoptysis.
  • Lung transplant may be indicated in certain patients
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59
Q
  • aortic dissection
  • what is it
  • most common site
A
  • Blood splits the arotic media with sudden tearing chest pain (with or without radiation to back) . Surging of blood through a tear I the intima. Forms a false lumen (channel) through which blood can flow.
  • Hypertension is an important contributor.
  • Most common site is the proximal ascending aorta- within 5cm of the aortic valve
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60
Q

what are the 2 classification systems for aortic dissections

A

deBakey-

  • type 1- 50%- ascending aorta through to aortic arch and below
  • type 2- start in and are confined to ascending aorta
  • type 3- dissections start in the descending aorta

Stanford

Type A: Involves the ascending aorta, arch of the aorta

Type B: Involves the descending aorta.

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61
Q

Rfxs for AAA

A
  • Hypertension
  • Connective tissue disease e.g. Marfan’s syndrome
  • Valvular heart disease
  • Cocaine/amphetamine use
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62
Q

Symptoms of AAA

A

Usually presents in men over the age of 50

  • Sudden onset ‘tearing’ chest pain or interscapular pain radiating to the back.
  • It can also present with (depending on how far the dissection extends):
  • Bowel/limb ischaemia
  • Renal failure
  • Syncope
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63
Q

Signs of AAA

A
  • Unequal arm pulses
  • Acute limb iscahemia
  • Paraplegia if spinal arteries affected
  • Anuria if renal arteries affected
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64
Q

diagnosis

A
  • Transoesophageal echocardiography
  • CT angiography
  • MRA (Magnetic Resonance Angiography)
  • ECG and CXR
  • Bloods- troponin, D-dimer
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65
Q

intial management

definitive management

A
  • reuscitation
  • Cardiac monitoring
  • Strict blood pressure control (e.g. IV metoprolol infusion)

definitive treatment

  • Type A: Usually requires surgical management (e.g. aortic graft)
  • Type B: Normally managed conservatively with blood pressure control. If there is evidence of end organ damage then endovascular/open repair may be performed.
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66
Q

what are cardiomyopathies?

broad classifications

A

heterogenous group of diseases of the myocardium, characterised by mechanical and/ or electrical dysfunction that typically results in inappropriate ventricular hypertrophy or dilatation due to multiple causes (usually genetic).

classifications

  • Primary cardiomyopathies- predominantly confined to the heart
  • Secondary cardiomyopathies- typically part of generalised multisystem diseases
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67
Q

divided also into 3 other groups:

A
  1. dilated
  2. hypertrophic
  3. restrictive
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68
Q

dilated cardiomyopathy

causes

A

Myocardial dysfunction causing heart failure in which dilation causes systolic dysfunction predominate. Most common form

causes

  • Ischaemic changes can over time particularly post-myocardial infarction
  • Hypertensive
  • Genetic and congenital
  • Toxin-related - excessive alcohol consumption Cocaine is also associated with ischaemia and DCM.Clozapine
  • Infiltrative - haemochromatosis, amyloidosis and sarcoidosis are known to cause DCM
  • Peripartum -
  • Thyrotoxicosis
  • Infectious - DCM can occur secondary to myocarditis, or as a direct result of infection from HIV, Lyme disease and Chagas disease
  • Stress induced cardiomyopathy (Takotsubo cardiomyopathy) refers to transient left ventricular ballooning precipitated by intense psychologic stress. Almost all patients recover completely
  • Idiopathic - when other potential causes have been ruled out

presentation

  • Mostly gradual onset
  • Fatigue
  • Acute pulmonary oedema
  • Progressive symptoms of heart failure:
    • Nocturnal dyspnoea
    • Orthopnea
    • Paroxysmal nocturnal dyspnoea
    • Swelling

management

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69
Q

dailated cardiomyopathy

signs and symptoms

A

symptoms

  • Exertional dyspnoea
  • Orthopnoea
  • Proxysmal nocturnal dyspnoea
  • Peripheral oedema

Signs

  • displaced apex beat
  • S3 gallop rhythm (rapid ventricular filling)
  • Murmur of mitral regurgitation (due to displacement of the valve leaflets)
  • Signs of heart failure (such as oedema, hepatomegaly, ascites, raised JVP).
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70
Q

treatment for dilated cardiomyopathy

A

(Standard treatment for heart failure with reduced ejection fraction)

  • Diuretics
  • ACE inhibitors
  • Angiotensin II receptor inhibitors
  • B-blockers
  • Spironolactone
  • Digoxin
  • Nitrates
  • Aldosterone antagonists
  • Antiarrhythmic agents
  • Device therapy
  • Cardiac resynchronisation

+anticoagulants when AF present

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71
Q

hypertrophic cardiomyopathy

patho

A

Hypertrophic cardiomyopathy (HCM) is a genetic condition characterised by left ventricular hypertrophy of varying degrees.

a mutation in one of several myocyte sarcomere genes such as myosin and troponin. ratio of vessels to tissue is low so widespread low grade ischaemia, leads to fibrosis

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72
Q

hypertrophic cardiomyopathy

presentation

A
  • Found alongside acromegaly, pheochromocytoma, neurofibromatosis
  • Symptoms appear between 20 and 40 and are exertional but symptoms may be highly variable
  • Dyspnoea
  • Chest pain (resembling typical angina)
  • Palpitations
  • Syncope
  • (ejection fraction is preserved so fatigue isn’t often felt- abnormal diastolic function responsible for symptoms)
  • Mitral regurgitation sound heard at the apex
  • Bifid carotid pulse
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73
Q

management of hypertrophic cardiomyoapthy

A

Symptoms

B-blockers- mainstay for angina, dyspnoea, giddiness and syncope treatment

Calcium channel antagonists- verapamil and diltiazem

Arrythmias

B blockers

Amiodarone (both for SVTs)

Radiofrequency ablation

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74
Q

restrictive cardiomyopathy

causes

A
  • Characterised by non-compliant ventricular walls that resist diastolic filling
  • One (most commonly the left) ventricle is usually involved
  • Least prevalent form of cardiomyopathy
  • Genetic abnormality
    • Fabry disease
    • Gaucher disease
    • Haemachromatosis
  • CT disorders
    • Amyloidosis
  • Other
    • Carcinoid tumours
    • Radiation
    • Sarcoidosis
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75
Q

presentation of restrictive cardiomyopathy

A
  • Exertional dyspnoea
  • Orthopnea
  • Peripheral oedema
  • AF and ventricular arrhythmia
  • Fatigue
  • LV +/- RV failure
  • Functional AV valve regurgitation
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76
Q

what is takatsubo cardiomyopathy

symptoms

diagnosis

treatment

A

“stress induced cardiomyopathy”

  • Weakening of the left ventricle because of severe emotional or physical stress such as sudden illness or the loss of a loved one.
  • Left ventricle changes shape, having a narrow neck and a round bottom.
  • Typically affects more women than men,

Symptoms: mimics MI- sudden intense angina and SOB

Diagnosis; ECG, echocardiogram, MRI, angiogram

Treatment; diuretics, B blockers and ACEi, anti-coagulation

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77
Q

infective endocarditis

rfx and comorbid disease

A

Infection of endovascular structures causes infective endocarditis- think valves

rfx:

  • Age > 60 years
  • Male sex
  • Intravenous drug use - predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis
  • Poor dentition and dental infections

co-morbid conditions:

  • Valvular disease
  • Congenital heart diseases
  • Prosthetic valves
  • Intravascular devices
  • Haemodialysis
  • HIV infection
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78
Q

common infective organisms of infective endocarditis

symptoms of endocarditis

A
  • Staph. aureus
  • Strep. viridans**** (most common)
  • Enterococci
  • Coagulase negative staphylococci e.g. Staph. epidermidis
  • Strep. bovis - often in patients with colonic lesions, e.g. IBD or carcinoma
  • Fungi
  • HACEK organisms - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

Symptoms

  • Fever (most common)
  • Anorexia
  • Weight loss
  • Headache
  • Myalgia
  • Night sweats
  • Cough
  • Pain made worse by leaning forwardss??
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79
Q

signs of infective endocarditis

complications

A

signs of infective endocarditis

  • Murmurs are common
  • Janeway lesions- nontender macules on plasms and soles
  • Osler nodes- tender subcutaneous nodules on finger pads and toes
  • Roth spots- exudative haemorrhagic retinal lesions with pale centres
  • Microscopic haematuria and glomerulonephritis
  • Splinter haemorrhages
  • PR prolongation or complete av block

complications

  • May often be the presenting complaint
  • Valvular insuffiency causing heart failure
  • Neurological complications
  • Embolic complications causing infarction of kidneys, spleen or lung
  • Infection e.g., osteomyelitis
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80
Q

Investigations for infective endocarditis

which criteria is used to help diagnose infective endocarditis

A
  • ECG
  • CXR
  • Blood tests: FBC, UE, LFT, CRP
  • 3 sets of cultures
  • Transthoracic echocardiogram
  • Transoesophageal echocardiogram

duke’s criteria

  • Blood positive for IE
  • Imaging positive for IE
    • 1 minor point (predisposing condition, fever, vascular phenomena, immunological phenomena, microbiological evidence)
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81
Q

which score is used to calculate your chance of having a DVT and therefore of having a PE?

A

Well’s score

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82
Q

what is central cyanosis

common causes in neonates and adults

A
  • Caused by diseases of the heart, lungs, or abnormal haemoglobin
  • Seen in the tongue, lips and is due to desaturation of central arterial blood resulting from cardiac and respiratory disorders associated w shunting of deoxy venous blood into systemic circulation
  • Often peripherally cyanosed also

common causes: neonates

  • Transposition of great arteries
  • Fallots tetralogy
  • Stenosis of pulmonary valve
  • Tricuspid valve
  • Truncus arteriosus

In adults

  • Birth injury
  • Haemorrhage
  • Pulmonary oedema
  • Pleural effusion
  • Pulmonary oedema
  • PE
  • Severe pneumonia
  • COPD
83
Q

peripheral cyanosis

causes

A
  • Caused by decreased local circulation and increased extraction of oxygen in peripheral tissues
  • Isolated peripheral cyanosis occurs in conditions with peripheral vasoconstriction and stasis of blood in the extremities- e.g., congestive heart failure, circulatory shock, exposure to cold temperatures and abnormalities of the peripheral circulation
  • Bluish tinge to affected area

all the same causes as central +

  • Peripheral arterial disease- e.g., thrombosis, atheroma or embolism
  • Vasoconstriction
  • Cold exposure
  • Raynauds
  • Beta blocker drugs
  • Venous obstruction
84
Q

what info is included in an ABG?

A
  • Blood pH (normal range 7.35 - 7.45) - high indicates alkalosis; low indicates acidosis.
  • Blood carbon dioxide level (PaCO2 level; normal range 4.7 - 6.5 KPa) - this may indicate a breathing problem.
  • Bicarbonate level (represents levels of alkali; normal range 22-26 mEq/L).
  • Blood oxygen levels (PO2 level; normal range 10.5 - 13.5 KPa) - if the PO2 level is low, it indicates an abnormally low concentration of blood oxygen (hypoxaemia).
85
Q

When would you see metabolic acidosis and metabolic alkalosis

respiratory acidosis and alkalosis

A

metabolic acidosis

  • Build-up of lactic acid; seen in shock, infection, hypoxia
  • Acute or chronic kidney injury
  • Build up of ketones; diabetes mellitus, alcohol poisoning
  • Severe diarrhoea

metabolic alkalosis

  • Vomiting
  • Hypokalaemia
  • Excessive amounts of alkali-containing medication
  • Burns

respiratory acidosis

  • depression of central resp centre by stroke
  • inability to ventilate properly- myasthenia gravis, muscular dystrophy
  • acute asthma exacerbation of COPD

resp alkalosis

  • hyperventailtion- anxiety, stroke, meningitis, altitude, pregnancy
86
Q

Cough reflex

A

afferent pathway-

  • cough receptors activated, receptor potential to afferent nerves, info reaches vagus nerve and is passed to medulla oblangata

central pathway-

  • sensory info to nucleus tractus solitarius of the medulla
  • vagus nerve passes info to effector muscles

motor efferent pathway-

  • diapragm, laryngeal muscles, rectus abdominus
87
Q

causes of cough

A
  • smoking
  • heartburn (acid reflux)
  • allergies – for example, hay fever
  • infections like bronchitis
  • mucus dripping down the throat from the back of the nose
  • cancer
  • ACEi
88
Q

What are interstitial lung diseases?

symptoms

signs

A

This is a generic term used to describe a number of conditions that primarily affect the lung parenchyma in a diffuse manner. Characterised by chronic inflammation and/ or progressive interstitial fibrosis.

symptoms

  • paroxysmal (sudden attack of) dry hacking cough
  • SOB at rest or aggravated by exertion
  • reduced exercise tolerance

Signs

  • Alveolar septal thickening
  • Fibroblast hyperproliferation
  • Collagen deposition
  • Pulmonary fibrosis
  • Abnormal breath sounds
89
Q

common causes of interstitial ling diseases

A
  • CT disorders: ankylosing spondylitis, SLE
  • Drugs: carbamazapine, nitrofurantoin, dexamethasone
  • Occupational/ environmental: aluminium, asbestos, bird fanciers lung, charcoal
  • Infections: pneumonia, TB
  • Vasculitis: eosinophilic granulomatosis
  • Sarcoidosis
  • pulmonary lymphoma
90
Q

effect of ILD on lung function

A

restrictive ventilatory effect due to decreased distensibility of lung parenchyma

  • FEV1 normal or decreased
  • Decreased FVC
  • Normal or decreased FEV1/FVC

reduced total lung capacity

reduced diffusing capacity

91
Q

what is pulmonary hypertension

A

Pulmonary hypertension- type of high blood pressure that affects the arteries in the lungs and the right side of the heart

92
Q

groups of pulmonary hypertension (5)

A
  1. pulmonary arterial hypertension- mutations, CHD, HIV
  2. due to left sided heart disease- valvular disease
  3. hypoxia+/- COPD- pul fibrosis, obstructive sleep apnoea
  4. chronic thromboembolic pulmonary hypertension - PE, clotting disorder
  5. unclear or multifactorail aetiologies- sarcoidosis, kidney disease
93
Q

management of pulmonary hypertension

A
  • Calcium channel blockers- amlodipine
  • Anticoagulants- apixaban, dabigatran, rivaroxaban, warfarin
  • Diuretics
  • Oxygen treatment
94
Q

Give examples of anti-coagulants and their drug class

A

Antiplatelets

Cox inhibitors- aspirin, NSAIDs (nurofen)

P2Y12 inhibitors- clopidogrel, ticagrelor

Anticoagulants

Direct thrombin inhibitors- dabigatran

Indirect thrombin inhibitors- dalteparin, fondaparinux

Direct factor X inhibitors- apixaban, rivaroxaban

Thrombolytics- plasminogen activators, alteplase, streptokinase

95
Q

What is a penumothorax

rfxs

A

A pneumothorax is defined as air within the pleural space.

Rfxs

  • Previous PTX
  • COPD
  • Alpha-1 antitrypsin deficiency
  • Underlying lung disease
  • Smoker
  • Valvular heart disease
  • Tall and thin
  • Marfan’s syndrome
96
Q

causes of pneumothroax

A

spontaneous

  1. primary- (no underlying lung pathology - typically tall thin young men)
  2. secondary- (underlying lung pathology) CT disorders (Marfan’s syndrome), obstructive lung disease (such as asthma and COPD), infective lung disease (such as TB and pneumonia), fibrotic lung disease (such as cystic fibrosis and idiopathic pulmonary fibrosis), and neoplastic disease (such as bronchial carcinoma

Traumatic causes

  1. iatrogenic causes (such as insertion of a central line or positive pressure ventilation)
  2. Non-iatrogenic causes (either a penetrating trauma or blunt trauma with rib fracture).
97
Q

Symptoms of pneumothorax

Signs of pneumothorax

A
  • sudden-onset SOB
  • Pleuritic chest pain
  • Important to note in the history whether there are any risk factors for a spontaneous primary pneumothorax (tall and thin young male, smoker), spontaneous secondary pneumothorax (COPD, asthma, Marfan’s syndrome), or traumatic pneumothorax (recent chest trauma, recent invasive medical procedure).

signs:

  • tachypnoeac
  • respiratory distress
  • reduced chest expansion
  • hyper resonant percussion note
  • reduced or absent breath sounds

Additional signs in a tension pneumothorax include: signs of haemodynamic compromise (tachycardia and hypotension) and tracheal deviation to the contralateral side.

98
Q

investigations for pneumothorax

what is a pleural aspiration

A
  • History and exam
  • Bloods
    • U+E, LFT, FC, CRP
    • ESR, autoantibodies
    • Amylase
  • CXR- should not be ordered in tension pneumothorax as it will delay immediate treatment , otherwise look for area devoid of lung markings at the periphery of lungs
  • Pleural ultrasound
  • Consider CT chest
  • Pleural aspiration

pleural aspiration

  • Ultrasound guided
  • Pass needle into pleural fluid
  • Aspirate sample
  • Investigations
    • Colour, viscosity, smell
    • Biochemistry: protein, LDH, glucose
    • Fluid pH
    • Microbiology
    • Cytology
99
Q

management of pneumothorax

A
  • Observation- if rim of air >2cm on CXR then…
  • Aspiration if not successful then…
    • Chest drain
  • Pleural vent

Chronic management

  • reoccurance at 3 years is 50%
  • main treatment is surgical where blebs are stapled
100
Q

what is a tension pneumothorax

signs

treatment

A

what is a tension pneumothorax

  • Air drawn into the pleural space w every inspiration and has no route of escape. Mediastinum gets pushed over to the contralateral hemithorax, kinking and compressing the great veins. Unless air is removed, cardiorespiratory distress will occur.

signs

  • resp distress, tachycardia, hypotension, distended neck veins, deviated trachea

treatment

  • To remove air, large bore caneedle with syringe, partially filled with 0.9% saline intp 2nd intercostal space in the midclavivular line on the side of the suspected pneumothorax
  • Remove plunger to allow air to bubble through the syringe until a chets tube can be placed
101
Q

pulmoanry effusion

what is the pleural space

A

pleural space- potential space between the visceral and parietal pleura which naturally contains 10-20ml of fluid. the aim is the lubrication of the pleura to maintain apposition of the membranes

pleural effusion

increased accumulation of pleural fluid in the pleural space

102
Q

factors causing increased fluid accumulation

increased entry:

  • Increased permeability – inflammation, infection, malignancy.
  • Increased microvascular pressure – CCF, mitral stenosis.
  • Decrease pleural pressure – atelectasis/collapse of lung.
  • Decrease oncotic pressure – Hypolbuminaemia (Nephrotic syndrome, liver cirrhosis)

Decreased exit (affecting the lymphatics):

  • Hypothyroidism
  • Yellow nail syndrome
  • Radiation injury
A
103
Q

classifications of pleural effusions (2) is done via which critera?

review this and google

A

done via Light’s criteria

transudative effusions- caused by increase in hydrostatic pressure and decreased plasma oncotic. Can be treated without extensive investigations.

  1. Plural fluid protein/serum protein >0.5
  2. Pleural fluid LDH/serum LDH > 0.6
  3. Pleural fluid LDH > 2/3 upper limit of lab normal value for serum LDH

exudative effusions- caused by local changes to capillary wall permeability.

  • High fluid protein- fluid: serum >0.5
  • High LDH- fluid: serum LDH >0.6
  • Haemothorax- blood in pleural space
104
Q

causes of transudates and exudates

A

transudate causes

  • Fluid leaks in to pleural space from elsewhere
  • Too much fluid in the body
    • Heart failure or pericarditis
    • Renal failure
    • Liver cirrhosis
  • Fluid leaking from elsewhere
    • Hypoalbuminaemia
    • Ascites/ peritoneal dialysis
  • Other stuff
    • Infections e.g., pneumonia
    • TB
    • PE
    • Swelling of the pancreas

exudate causes

  • Too much fluid produced/ failure of reabsorption due to damage to pleural surface
  • Pleural malignancy
  • Pneumonia
  • Empyema- infection in pleural space
  • Connective tissue disease
  • Benign asbestos pleuritis
  • Pancreatitis
  • Drug induced
105
Q

rfx

signs and symptoms of pleural effusion

A

rfx pleural effusion

  • Chest injury
  • Radiation therapy
  • Surgery (especially to the: heart, lungs, belly, organ transplants)

symptoms

  • Dyspnoea
  • Tachypnoea
  • Pleuritic chest pain
  • Stomach pain
  • Cough
  • Haemoptysis
  • Weight loss
  • Fever or chills

signs

  • Absent tactile fremitus
  • Dullness on percussion
  • Reduced chest wall movements
  • Decreased breath sounds on the affected side
  • Rapid and shallow breaths in big effusions
  • Pericardial rub
106
Q
  • tests
  • initial management
  • chronic management of pleural effusion
A

tests

  • CXR
  • LFTs, U&Es, FBC, CRP, LDH
  • Thoracentesis (procedure to remove fluid or air from around the lungs) looking at: LDH and protein, cytology, pH, ADA, AFB and TB culture, amylase, haematocrit and glucose

management

  • Pleural aspiration (thoracentesis)- Treat underlying cause e.g., pneumonia or heart failure
  • Consider contrast enhanced CT thorax
  • Pleural biopsy (radiologically guided VATS)
  • NSAID’s for pain

chronic management

  • Pleurodesis- artificially obliterating pleural space
  • Intermittent drainage with indwelling catheter
107
Q
  • What is cystic fibrosis?
  • Which systems are affected by it?
  • When are babies screened for it?
A

Cystic fibrosis- inherited disease of the exocrine glands affecting primarily the GI and respiratory systems.

Leads to chronic lung disease, exocrine pancreatic insufficiency, hepatobiliary disease and abnormally high sweat electroytes.

All babies screened at birth

108
Q

Explain the genetics of Cystic fibrosis

A
  • autosomal recessive inheritance
  • responsible gene found on the long arm of chromosome 7
  • this genes ecnodes for thr DF transmembrane conductance regulator (CFTR)
  • CFTR is a cAMP-regulated chloride channel, regulating chloride and sodium transport across epithelial membranes

multisystem disease as the CFTR gene is found within multiple organ systems

109
Q

pathopshyiology of CF

A

Nearly all exocrine glands are affected in varying distribution and severity. Increased sodium absorption and abnormal chloride secretion. This leads to thicker mucous that impairs the function of cilia.

Glands may be:

  • Obstructed by viscid or solid eosinophilic material in the lumen (pancreas, gall bladder etc.)
  • Produce excessive secretions (tracheobronchial and Brunner glands)
  • Secrete excessive sodium and chloride (sweat, parotid and salivary glands)
110
Q

Effect of cystic fibrosis on lungs and GI system

A

Lungs- comes on as child

  • Mucous plugging
  • Chronic lower resp bacterial infection
  • Damage to airways- eventual bronchiectasis
  • Nasal Polyps
  • Symptoms including cough, wheeze, haemoptysis
  • Pneumothorax
  • Cor pulmonale

GI-

  • Pancreatic insufficiency resulting in diabetes mellitus and steatorrhea
  • Cirrhosis
  • Portal hypertension
  • Gallstones

Male infertility

  • Duodenal- viscous and lacks bicarbonate
111
Q

neonatal features of cystic fibrosis

A
  • Failure to thrive
  • Meconium Ileus
  • Rectal prolapse
112
Q

Diagnosis of cystic fibrosis

conservative management of CF

A
  • Neonatal heel prick day between day 5 and day 9
  • Sweat test: sweat sodium and chloride >60mmol/L
  • Faecal elastase: this can provide evidence for abnormal pancreatic exocrine function.
  • Genetic screening: This can identify CF mutations

Conservative management

  • Education about the condition
  • Fertility and genetic counselling
  • Dietician
  • Psychosocial counselling
  • Chest physiotherapy: postural drainage and active cycle breathing techniques
  • Screening for complications of Cystic Fibrosis such as osteoporosis
113
Q

Medical treatment of CF

surgical treatment of CF

A

infective exacerbations: antibiotics, nebulised mucolytics, bronchodilators

pancreatic insufficiency: insulin replacement regime, exocrine enzymatic replacement, vitmains A,D,E,K

Liver: ursodeoxycholic acid

Worsening progressive lung disease: oxygen, non-invasive ventilation, diuretics if signs of cor pulmonale

Surgical treatment of CF

cirrhosis eventual liver tranplant, lung transplant

114
Q

Causes of hyperventilation

A
  • Anxiety
  • Haemorrhage
  • Drug overdose (aspirin for example)
  • Severe pain
  • Pregnancy
  • Lung infection
  • Lung diseases- COPD, asthma
  • Diabetic ketoacidosis
115
Q

What is the most common form of lung cancer?

A

non-small cell carcinoma

116
Q

symptoms of lung cancer

A
  • Cough
  • Haemoptysis
  • Chest pain
  • Weight loss
  • SOB
  • Hoarse voice and other features of direct intrathoracic invasion
  • Hoarseness (left recurrent laryngeal)
  • SVC obstruction from tumour or thrombosis
  • Dysphagia from oesophageal compression
  • Elevated diaphragm
  • Pericardial involvement
  • Recurrent or slowly resolving pneumonia
117
Q

SOE of lung cancer:

A
  • Fixed monophasic wheeze
  • Cachexia
  • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  • Finger clubbing
  • Pleural effusion
  • Tracheal deviation (lobar collapse/ whole lung collapse)
  • Osetoarthropy
  • Confusion
  • Fits falls
118
Q

Lung cancer is largely grouped into 2:

A

small cell lung cancer (SCLC)- about 15%

non-small cell lung cancer (NSCLC)- 85%

119
Q

Info on small cell lung cancer

A
  • highly aggressive
  • almost always occurs in smokers
  • starts from endocrine cells (Klutchisky cells) so often secrete polypeptide hormones resulting in paraneoplastic syndromes
  • rapidly growing and disseminating
  • 80% have evidence of metastasis at diagnosis
  • not amenable to surgery
  • often very chemosensitive/ radiotherapy
120
Q

what are the 4 groups within non-small cell lung cancer?

which features do they share?

A
  • squamous 30%
  • adenocarcinoma 27%
  • large cell 10%
  • adenocarcinoma in situ (rare) 1%

Shared features:

  • early stage is curable by surgery
  • radiotherapy and cehmotherapy can help symptoms
  • immunotherapy pr biological egnts possible
121
Q

in paraneoplastic syndrome of small cell lung cancer which hormones are often screted

A

based on the secretion of;

  • antidiuretic hormone (ADH) resulting in hyponatremia
  • secretion of adrenocorticotropic hormone (ACTH) or rarely corticotropin-releasing hormone (CRH) resulting in Cushing syndrome
  • secretion of growth hormone-releasing hormone
122
Q

risk factors for lung cancer

A
  • Smoking (tobacco and cannabis)
  • Passive smoking
  • Occupation exposure (asbestos, silica, welding fumes, coal)
  • HIV
  • Organ transplantation
  • Radiation exposure (X-ray, gamma rays).
  • Beta-carotene supplements in smokers.
123
Q

common metastatic destinations of lung cancer

A

brain, breast, adrenals and bone.

124
Q

important features of squamous cell carcinoma

A

squamous cell carcinoma

tends to cause early symptoms

usually begins in the bronchial tubes

  • 2nd most common type of lung cancer in the UK
  • presents as obstructive lesions of the bronchus leading to an infection
  • most likely lung cancer to cavitate
  • hypercalcaemia- bone degradation or PTH
125
Q

imprtant features of adenocarcinoma

A

imprtant features of adenocarcinoma

most common type in the UK

Usually starts in the outer border of the lungs

  • arises from the mucous cells in the bronchial epithelium
  • commonly invades mediastinal lymph nodes and the pleura, and soreads to the brain and bones
  • does not cavitate
  • most likely to cause pleural effusion
126
Q

important features of large cell carcinoma

A

important features of large cell carcinoma

  • tends to grow rapdily and cause late symptoms
  • usually begins in the outer edges of the lungs
127
Q

how would you investigate for lung cancer?

A
  • CXR
  • Urgent referral to clinic
  • CT or combined PET-CT- also used to guide biopsy
  • Pleural tap-cytopathology examination of pleural fluid or sputum
  • Usually bronchoscopy-guided biopsy and core biopsy
  • Sometimes open lung biopsy
  • PET scan if curative treatment feasible
128
Q

complications of lung cancer

A
  • Pancoast syndrome
  • Recurrent laryngeal nerve palsy
  • Phrenic nerve palsy
  • Rib erosion
  • Pericarditis
  • AF
129
Q

what is pancoast syndrome?

A

Occurs when apical tumours, usually NSCLC invade the branchial plexus, pleura or ribs causing shoulder and upper-extremity pain and weakness or atrophy of the ipsilateral hand. May also include Horner’s syndrome.

130
Q

what is Horner’s syndrome

A

Horner’s syndrome is characterised by ptosis, meiosis with or without anhydrosis. It is due to an interruption of the sympathetic nerve supply to the eye

  • *Ptosis**- drooping of the upper eyelid (due to oculomotor palsy levator palpebri superioris
  • *Miosis**- pupil constriction

Anhidrosis

131
Q

when light levels drop what happens to the pupil?

what is the name for this?

which muscles contract?

and if light shines into the eye?

A

pupil dilates

mydriosis

radial muscles contract

pupil constricts

miosis

sphincter muscle innervated by parasympathtic fibres constricts

132
Q

what is mesothelioma

what causes it

A

Only known pleural cancer

Caused by asbestos exposure- asbestos was heavily used historically in the shipbuilding and construction industries due to its fire resistant qualities.

133
Q
  • signs and symptoms of mesothelioma
  • diagnosis
  • treatment
A

Signs and symptoms

  • Dyspnoea
  • Non-pleuritic chest pain
  • Constitutional symptoms are uncommon
  • Pain
  • Hoarseness
  • Dysphagia
  • Horner syndrome
  • Brachial plexopathy
  • Ascites

Diagnosis

  • CXR
  • Pleural fluid cytology// pleural biopsy
  • Staging via- CT chest, mediastinoscopy, MRI

Treatment

  • Supportive care
  • Pleurectomy
  • Analgesia with opioid’s
  • Chemotherapy
134
Q

Systemic inflammatory response syndrome (SIRS) definition

sepsis diagnosis

severe sepsis

septic shock

A

SIRS ≥ 2 of:

  • > 38°C or < 36°C
  • Heart rate > 90
  • Respiratory rate > 20
  • WBC > 12,000/mm³ or < 4,000/mm³

Sepsis- SIRS+ suspected or confirmed infection

Severe sepsis- Sepsis plus evidence of organ dysfunction: confusion, hypoxia, oliguria, metabolic acidosis

Septic shock- severe sepsis with hypotension, despite adequate fluid resuscitation, or lactic acidosis (lactate > 4mmol/L)

135
Q

“sick person” bloods

lactate

bicarb

CRP

LFTs

coag

platelets

A

lactate >2

bicarb <18

CRP raised

LFTs off

coag deranged (PT>20)

platelets low

136
Q

red flags for sepsis

  • responds to
  • mental state
  • systolic bp
  • HR
  • RR
  • Sp02
  • rash
  • urine
  • lactate
  • recent chemotherapy
A
  • responds to voice/ pain/ unresponsive
  • mental state- acute confusional state
  • systolic bp- 90mmHg or drop of >40% of normal
  • HR- >130
  • RR- >25/min
  • Sp02- oxygen needed to maintain above 92%
  • rash- non-blanching, cyanotic, mottled
  • urine- not passed urine in the last 18 hrs
  • lactate- >2 mmol.L
  • recent chemotherapy
137
Q

what is the sepsis 6?

A

3 in

  • administer oxygen, aim to keep sats >94%
  • administer broad spectrum antibiotics
  • give IV fluid

3 out

  • take blood cultures
  • measure serum lactate (via ABG)
  • measure accurate hourly urine output
138
Q

additional tests for diagnosing sepsis

A

Imaging e.g chest xray, echocardiogram, abdominal ultrasound

Viral PCR for e.g. influenza

Urinalysis +/- culture

Lumbar puncture

139
Q

symptoms and signs of sepsis

A

symptoms

  • Fever, sweats or chills
  • Breathlessness
  • Headache
  • Nausea and vomiting
  • Diarrhoea

signs

  • Tachycardia
  • Hypotension
  • Pyrexia
  • Peripherally vasodilated
  • Hypoxia
  • Tachypnoea
140
Q

Which score is used to calculate someones sequential risk of sepsis related organ failure

A

qSOFA and SOFA

  • O2
  • platelets
  • bilirubin
  • cardiovascular
  • GCS
  • creatinine
  • urine output

Score of more than 3 in any parameter then think sepsis

141
Q

normal values for ABG

  • pH
  • paCO2
  • HCO3-
  • PaO2
A
  • pH 7.35-7.45
  • paCO2 35-45
  • HCO3- 21-28
  • PaO2 80-110
142
Q

Pathology of inflammation in sepsis

A
  • Antigen pro-inflammatory stimulus is found in the intravascular compartment.
  • Innate immune system is activated— pro-inflammatory response and coagulative cascade produces microemboli
  • Initial hypotension in response to arteriole dilation, cardiac output increases for a time “warm shock”
  • Eventually hypotension increases further due to dilatation and increased permeability of vessels
  • Distributive shock as oxygenated blood is shunted away from capillary beds and tissues become hypoxic
  • Micro-emboli also block capillary beds
143
Q

Common sites of infection

A
  • Mouth and throat
  • Skin
  • Lungs
  • Kidneys and bladder, especially if you have a catheter to drain urine
  • Cannula sites
  • Wounds or where wound
144
Q

identify sources of common infection

A
  • Person to person contact
  • Person to animal contact (e.g., bites)
  • Contaminated surfaces
  • Contaminated food
  • Environment into open wounds
  • Hospital setting
145
Q

name 3 ways that antibiotics can be used

what is empiric therapy

A

targeted- when you know the exact causative organism

empirical- when you don’t the precise organism but you have a good idea of what it will be and its sensitivities

Prophylactic- use before the fact in anticipation of infection

146
Q

how can we manage antimicrobial resistance

A

infection prevention and control

  • prevent spread- vaccines, antiseptic technique

antimicrobial stewardship

  • reduce broad spectrum use
  • reduce treatment regime
  • reduce antibiotic use when no infection present
147
Q

5 forms of acquired resistance

A
  • Efflux pumps- remove the active substance
  • Limiting uptake of drug-
  • Modification of target- make it so antibiotic cant bind
  • Inactivation of a drug
  • Bypassing the targeted process- e.g., metabolism routes
148
Q

What is HIV?

how is it transmitted?

A

HIV is a retrovirus which infects and replicates within human lymphocytes (CD4+ T cells) and macrophages. This leads to progressive immune system dysfunction, opportunistic infections and malignancy –> AIDS (acquired immunodeficiency syndrome).

Transmission is via? –> blood, sexual fluids and breast milk

  • Sexual
  • Perinatal
  • Blood transfusion
  • Sharing needles
149
Q

what are the 2 kinds of HIV? which is more common in the UK?

Pathophysiology of HIV?

if hIV is a retrovirus, what is the key enzyme?

A
  • HIV-1 (global epidemic)
  • HIV-2: less common, mostly in West Africa, less transmissible

Pathophysiology

HIV binds, via its GP120 envelope glycoprotein, to CD4 receptors on helper T cells, monocytes and macrophages. These infected cells migrate to lymphoid tissue where the virus replicates producing millions of virions. They are released as they burst out of the cell, in turn infecting more CD4+ cells, leading to ↓ immune function.

key enzyme? reverse transcriptase

150
Q

presentation of HIV

in which stage is HIV most infectious?

A

early/ primary infection-

asymptomatic in 80%

coryzal symptoms: fever, rash, myalgia, pharyngitis, lymphadenopathy, headache

most infectious in primary infection

151
Q

what are the 3 stages of HIV infection?

A
  • Acute HIV infection- 0-12 weeks
  • Chronic HIV infection- clinical latency
  • Acquired immunodeficiency (AIDS)- constitutional symptoms and opportunistic infections

each stage gets worse

152
Q

stage 1 of HIV infection- acute/ primary stage

A
  • Generally, develops within 2-4 weeks after infection with HIV.
  • Flu-like symptoms: headache, rash, fever, sore throat
  • As infection slowly weakens the immune system,
    • Swollen lymph nodes
    • Weight loss
    • Diarrhoea
    • cough
  • HIV multiplies rapidly and spreads throughout body
  • Virus invades, replicated within and destroys CD4+ cells
  • HIV levels in blood (viral load) very high- very infectious
  • Start RT here to experience health benefits
153
Q

Stage 2 of HIV infection- AKA asymptomatic or clinical latency

A
  • HIV continues to divide but at a much lower rate
  • May not have any HIV symptoms it will present with deranged lab results- e.g., anaemia, neutropenia, lymphopenia, thrombocytopaenia, diffuse hypergammaglobulinaemia
  • Possible to stay in this stage for 10+years if on ARTs
  • If well medicated- very small chance of passing on disease via sex
154
Q

AIDS- acquired immunodeficiency syndrome

A
  • Cannot fight off opportunistic infections- PCP, CMV, MAI, non-Hodgkins lymphoma
  • High viral load and very infectious
  • 3 year survival rate if unmedicated
  • Constitutional symptoms may present like: night sweats, malaise, fatigue, diarrhoea, weight loss of more than 10kg
155
Q

common opportunistic infections with HIV

A
  • Karposi’s sarcoma- herpes virus 8
  • Oral hairy leukolakia- caused by EBV
  • Oesophageal candiasis- white plaques on the buccal and pharyngeal mucosa
156
Q
  • What is a UTI
  • what is cystitis
  • symptoms
A

UTI- infection of the urinary tract (anywhere from the kidney to the urethra)

Cystitis- infection from UTI that affects urinary bladder

Symptoms

  • dysuria- pain on urination
  • frequency- increased fequency of urination
  • urgency- abrupt, strong overwhleming need to urinate
  • haematuria in older patients
157
Q

rfx for UTIs in women

likley pathogens

A

Rfxs

  • Sexual intercourse
  • Diaphragm and spermicide use
  • Antibiotic use
  • New sex partner within the past year
  • History of UTIs within 1st degree female relatives
  • History of recurrent UTIs
  • First UTI at early age
  • Catheter insertion

Likely pathogens

abx use can kill off native flora and allow commensal E.coli to overgrow

staph saprophycitcus

likely pathogens for cystis:

enteric gram negative (enterobacteria, klebsiella, pseudomonas auruginosa)

158
Q

investigations for UTI

A

NEWS monitoring

  • Urine dip (check for presence of leukocytes or nitrate positive
  • Urine cultures (to confirm epirical treatment)
  • consider bloods if unwell

treatment options for UTI

159
Q

how would you treat a woman with a UTI without haematuria, who is not pregnant or catheterised?

A

advice on self care- paracetamol, intake of fluids to avoid dehydration, don’t encourage cranberry products

immediate abxs take into account local guidelines:

  • Nitrofurantoin 100mg modified-release twice a day for 3 days
  • Trimethoprim 200mg twice a day for 3 days
160
Q

how would you treat a woman who gets recurrent uncomplicated UTIs?

A
  • discuss behavioural and personal hygiene advice
  • in post menopasual women consider prescribing vaginal oestrogen
  • abx prophylaxis: trimethoprim or amoxicillin
161
Q

how would you treat a pregnant woman with a UTI?

A

pain relief

AVOID nitrofurantoin at term (39 weeks?)

use amoxicillin or cefalexin

162
Q

cryptosporidium

A

Protozoan infection

Acquired through ingestion of contaminated water or food

Self-limiting in immunocompetent people, but causes

  • chronic diarrhoea
  • abdominal cramps and weight loss in people with HIV
  • diagnosed on stool microscopy or PCR
163
Q

toxoplasmosis

A

Protozoan parasite, commonest cause of brain lesion in people with HIV

Usually due to reactivation of previous infection, causes focal neurological symptoms, fever , seizures

Can also cause chorioretinitis

164
Q

Shingles

A

caused by herpes zoster infection

painful vesicular lesions that occur in a dermatomal distribution

complications:

post-herpetic neuralgia, blindness, meningitis

165
Q

Pneumocystis jiroveci pneumonia

A

Commonest cause of infection in patients with HIV

Presents with

  • Progressive dyspnoea
  • Fever
  • Malaise
  • Desaturation on exertion, CXR shows diffuse alveolar infiltrates
  • Diagnosis is by PCR of induced sputum or BAL or histology
166
Q

Progressive multifocal leukocephalopathy

A

Rare brain and spinal cord disease caused by JC virus, seen almost exclusively in people with HIV

Symptoms include:

  • Loss of muscle control
  • Paralysis
  • Blindness
  • Speech problems
  • Altered mental state

Progresses rapidly and can be fatal

167
Q

CMV

A

Herpes virus

Viral infection that can cause pneumonia, colitis, encephalitis and retinitis

Can cause blindness if not treated promptly

168
Q

Cryptococcus neoformans

A

Common cause of meningitis in HIV

Presents with insidious onset:

  • Fever
  • Headache
  • Visual change
  • Neck stiffness
  • Seizures
169
Q

Features of septic arthritis

initial investigtions

A
  • Singular acute, painful, swollen joint
    • Restricted movement in 80% of patients
      • Pain on active and passive movemnts
      • Examination findings: warm to touch/ fluctuant
  • Fever- present in the majority of patients
  • Unable to weight bear
  • Symptoms more obvious and florid in native joint infection

initial investigations for septic arthritis

  • Synovial fluid sampling- look for white cells and bacteria -> send for gram stain
  • Done prior to administration of antibiotics ideally
  • Blood cultures
  • FBC + CRP+ ESR+ urate levels
  • Plain radiograph- nothing in early disease, capsule and soft tissue swelling, fat pad shift or joint space widening in later disease
  • CT or MRI in specific joints- e.g., sternoclavicular joint
170
Q

pathophysiology of septic arthritis

causative agents

A

usually bacterial

Due to either:

  • Hematogenous spread (most common)
  • Direct inoculation.

Staphylococcus aureus (including MRSA) - 50% of cases

Streptococci - (group A, B, C or G) 2nd

Neisseria gonorrhoeae - particularly in young, sexually active patients

Pseudomonas aeurginosa - usually healthcare associated

Salmonella - those with sickle cell anaemia particularly at risk.

171
Q

risk factors for septic arthritis:

A
  • IV drug users
  • Diabetes Mellitus
  • Older age
  • Underlying joint injury
  • Underlying joint disease (e.g. osteoarthritis, rheumatoid arthritis)
  • Prosthetic joint
  • Immunosuppression (due to medications or disease e.g. HIV)
  • Unprotected sex (gonococcal arthritis)
  • Peripheral vascular disease
  • Alcoholism
172
Q

ibvestigations for septic arthritis

A
  • Synovial fluid sampling- look for white cells and bacteria  send for gram stain
  • Done prior to administration of antibiotics ideally
  • Blood cultures
  • FBC + CRP+ ESR+ urate levels
  • Plain radiograph- nothing in early disease, capsule and soft tissue swelling, fat pad shift or joint space widening in later disease
  • CT or MRI in specific joints- e.g., sternoclavicular joint
173
Q
  • May need aspiration for small joints or arthroscopy and arthrotomy for large joints. Artificial joints replaced

Empirical antibiotics:

  • Gram-positive cocci (staph and strep):
  • Vancomycin
  • Alternatives: clindamycin, cephalosporin

Gram-negative infection:

  • ceftriaxone (or other 3rd generation cephalosporins)
  • Alternative: ciprofloxacin (give gentamicin if associated with sepsis)

Confirmed organism:

  • Staph aureus/strep: flucloxacillin (or clindamycin)
  • MRSA: Vancomycin
A
174
Q

Understand and list causes of immunodeficiency and how they relate to
host defence mechanisms.

A

Primary immunodeficiencies- genetically determined and may appear alone or as part of a syndrome. Usually present during childhood. Defined by which part of the immune system they interact with.

Secondary immunodeficiencies- occur in older or sick patients

  • Endocrine- diabetes mellitus
  • GI- hepatic insufficiency
  • Haematologic- aplastic anaemia, multiple myeloma
  • Iatrogenic- certain drugs such as chemotherapeutics, immunosuppressants
  • Infectious- HIV, EBV, measles
  • Nutritional- alcoholism, undernutrition
  • Physiologic- physiological immunodeficiency
  • Renal- nephrotic syndrome
  • Rheumatologic- SLE
175
Q

what kind of bacterium is TB?

how are they distinguished in the lab?

where in the lung do they like to grow?

A

mycobacteria- slow growing aeorbic bacilli

Distinguished by a complex, lipid rich cell envelope responsible for characterisation as acid-fast (i.e. resistant to decolourisation by acid after staining) and their relative resistance to gram stain. STAINS BRIGHT RED

aerobic so like to grow in the apices

176
Q

risk factors for TB

spread

A

Have to be in contact for a while cramped conditions and residents

  • Tight living quarters
  • Below or at the poverty line
  • Refugees or immigrants
  • Immune system issues (HIV, immunosuppressants)
  • Substance abusers
  • Kids< age of 5

via droplets that can survive in their environment for a long time

177
Q

Natural history of TB

A

Primary and secondary infection:

  • Infection- In 90% the immune system contains the infection, through macrophages that engulf bacteria and localize them to the hilar lymph nodes. Here, they are eliminated or may be encapsulated by a barrier of granulation tissue (considered to be in a dormant state).
  • A small proportion progress to active TB, with an increased risk in those who are immunosuppressed (e.g. HIV). This is known as Secondary TB and usually occurs in the apex of the lungs. From here it can spread locally or to distant sites.
  • Some patients are not able to contain the primary infection, and it disseminates widely via the bloodstream. This is known as miliary TB (due to the characteristic pattern on Chest X-ray like ‘millet-seeds’ when re-infection of lungs occurs after passing through circulation).
  • When immune system is weak you see secondary infection of TB
178
Q
A
179
Q

general presentation of TB

A
  • Subacute to chronic in onset
  • Symptoms depend on the main site of infection, but are usually accompanied by;
  • night sweats
  • fever
  • weight loss
  • other systemic symptoms
180
Q

respiratory presentation of TB

Cns Presentation

Additional presentation

A
  • Most common
  • Chronic cough productive of purulent sputum +/- hemoptysis.
  • Can get bronchiectasis, pneumonia and pleural effusions.

CNS

  • TB meningitis or tuberculoma
  • Headache
  • Meningism
  • Focal neurological signs
  • Decreased consciousness

Additional presentation

  • May get palpable tender, firm superficial lymphadenopathy.
  • Causes ‘sterile’ pyuria, kidney pathology, abscesses, salpingitis and infertility, epididymo-orchitis.
181
Q

comparison of active and latent TB

contagious?

signs and symptoms?

CXR?

Sputum sample positive?

Result of mantoux test?

Purpose of treatment?

A

Latent TB

Active TB

Not contagious

Contagious

No signs and symptoms

Signs and symptoms

Normal CXR

Abnormal CXR

Negative sputum

Positive sputum for mycobacterium

Mantoux + blood test positive

Mantoux + blood test positive

Still needs Tx to prevent active status

Can spread via lymphatic system to other organs

182
Q

tests for TB

A
  • CXR- look for multinodular infiltrate behind the clavicle. Calcified hilar nodes.
  • Acid-fast stain and culture from sputum culture- use ZE stain. Drug susceptibility tests.
  • Mantoux test- indell will appear if you are positive for infection. This doesn’t specify whether active, latent or from inoculation. 6-15mm is a positive test
  • Bronchoscopy
  • IGRA- blood test. Interferon Gamma Release Assay-
  • PCR- quick and easy + helps detect sensitivity to rifampicin
183
Q

Treatment for TB

which TB medication makes your urine red?

A

RIPE

  • Rifampicin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol

rifampicin makes your urine red

184
Q

what is osteomyelitis

presentations

A
  • inflammation and destruction of bone,caused by bacteria, mycobacteria and fungi

presentations

Peripheral bones

  • Weight loss
  • Fatigue
  • Fever
  • Localised warmth
  • Swelling
  • Erythema
  • Tenderness

Vertebral osteomyelitis

Localised back pain

Tenderness with paravertebral muscle spasm

185
Q

likley pathogens for osteomyelitis

investigations

A

Staphylococcus bacteria in most cases

Staph. Aureus

Staph. Epidermidis

investigations

  • Definitive diagnosis - need a bone biopsy for pathology and culture.

Supportive diagnostic tests:

  • Blood inflammatory markers

Imaging:

  • X-ray - may be negative early on as periosteal reaction cannot be seen until about 7 days and bone necrosis after 10 days. It is useful in the diagnosis of chronic osteomyelitis.
  • MRI - good for viewing bone and soft tissue. Imaging modality of choice.
  • CT - good for identifying necrotic bone and for guiding needle for biopsy.

Other tests;

  • Blood cultures, and culture of any expressed pus (but note that samples from sinus tracts are unreliable)
186
Q

measles description

A
  • Unvaccinated child
  • Fever >40
  • Cough
  • Coryza
  • Conjunctivitis
  • White spots in the mouth (koplik spots)
  • MEASLES- erythematous maculopapular rash across head, neck, torso and limbs
187
Q

roseola infantum

A

3-5 day high fever

Followed by a maculopapular rash

Caused by human herpes virus 6

188
Q

henoch schonlein purpura

A

Child 2-10 years

Triad of:

  1. Purpura over extensor surfaces of the lower limb
  2. Abdominal pain
  3. Arthritis

Urinalysis and blood pressure to check renal involvement

189
Q

malaria

  1. which species
  2. spread by
  3. which cells are destroyed
  4. particularly dangerous for
A
  • An infection caused by a few Plasmodium species
  • Caused by single celled parasites that are spread by mosquito
  • Once plasmodium enters the blood stream it infects and destroys mainly liver and red blood cells.

Particularly dangerous for:

  • Young children under 5
  • Pregnant women
  • Patient with other conditions like HIV/ AIDS
  • Travellers with no prior exposure to malaria
190
Q

malaria is prevalent in which part of the world?

multiple infections leads to

most common plasmodium that infects humans?

A

tropical areas

premunition- tolerance

plasmodium vivax

191
Q

life cycle of the mosquito (9)

A
  1. Plasmodium infected female anopheles mosquito hunts for a blood meal in the evening- night. Mosquitos are drawn to CO2.
  2. Plasmodium is in a stage of development called a sporozoite in the mosquito’s salivary gland.
  3. When mosquito pierces skin, worm like sporozoites enter our bloodstream.
  4. Reach liver and go dormant for months/ years before engaging in asexual reproduction (reason for gap in infection  symptoms)
  5. Merozoites are released into blood where each one enters a RBC (young RBCs)
  6. Undergoes asexual reproduction and changes form.
  7. Gametocytes released within RBC.
  8. Infected RBC collected by a different mosquito taking a blood meal.
  9. Gametocytes reach the mosquitos gut where they fuse into a mature zygote.
  10. Zygote matures into oocyst and ruptures releasing sporozoites into the mosquito gut
  11. Migration into salivary gland to repeat cycle.
192
Q

Symptoms of malaria infection

A

incubation period for months asymptomatic

then

  • haemolytic anaemia- extreme fatigue, headaches, jaundice, splenomegaly
  • tertian fever every 48 hours
  • rigors
  • muscle pains
  • chills
  • ischaemic damage from RBC clumping together
    *
193
Q

diagnosis of malaria

A
  • Thick blood smear- locates parasites sitting in RBCs
  • Thin blood smear- directly identifies plasmodium species
  • FBC
    • Important to know percentage of RBCs affected
    • Thrombocytopaenia
    • Normochromic + normocytic anaemia (few RBC but normal in size and colour)
194
Q

treatment divided by stage of infection (4)

which medication for non-severe infections

A

1) Suppressive treatment or chemoprophylaxis

Kills sporozoites before they infect hepatocytes

Given to travellers before they go

2) Therapeutic treatment

Aimed at eliminating merozoites in the erythrocytic phase (while replicating in RBCs)

Given during active infection

3) Gametocidal treatment

Aimed at killing gametocytes

Prevents spread of disease and creation of resistant forms of the parasite

4) Radical treatments

Aimed at killing hypnozoites in the liver

for non-severe–> Chloroquinone, doxycycline, quinine

195
Q

what is valvular heart disease

what does stenosis mean

what does regurgitation mean

what does insufficiency mean

A

Valvular heart disease- one or more of the valves in your heart doesn’t work properly

stenosis- narrowing or constriction of valve

regurgitation- when blood travels back through a valve when it shouldn’t

insufficiency - when a valve doesn’t close properly

196
Q
  • Where is the tricupsid valve found?
  • pulmonary?
  • mitral?
  • aortic?
A

Tricuspid valve- located between the right atrium and right ventricle.

Pulmonary valve- located between the right ventricle and the pulmonary artery

Mitral valve- located between the left atrium and the left ventricle

Aortic valve- located between the left ventricle and aorta

197
Q

what is the management of vlavular disease?

A

options:

Valvuloplasty- balloon valvuloplasty is a procedure done to open a stenosed heart valve.

Valve replacement- annuloplasty or valvuloplasty. Important procedure as it can preserve heart function.

valve replacement

treatment of secondary heart failure to manage symptoms

198
Q

causes of valvular disease

A
  • Changes in heart valve structure due to aging
  • Coronary heart disease and heart attack
  • Heart valve infection
  • Birth defect
  • Rheumatic disease- happens after infections from bacteria that cause strep throat. Causes valvular scarring
  • Endocarditis- disease in the blood leads to endocarditis. Therefore IV use can cause it.
  • Heart failure
  • Hypertension
  • MI
  • Autoimmune diseases- lupus
  • Marfan syndrome- disease of connective tissue
  • Syphilis (a sexually transmitted infection)
199
Q

Symptoms of valvular disease

A
  • Angina
  • Palpitations caused by irregular heartbeats (atrial flutter or fib)
  • Fatigue
  • Exertional syncope
  • Dizziness
  • Low or high blood pressure
  • SOB
  • Abdo pain (hepatomegaly if tricuspid failure)
  • Leg swelling
  • Orthopnea
  • Heart murmur
  • Heart failure symptoms essentially
200
Q

possible causes of angina/ chest pain

A
  • Carcinoma in the bronchus
  • Pneumothorax- pleuritic chest pain
  • Pericardial disease
  • Respiratory tract infection (pneumonia, influenza, TB)
  • PE
  • Ischaemic heart disease
  • Pleurisy (sharp pain when breathing- inflamed pleural membranes)
  • Aortic dissection
201
Q

possible causes of pyrexia of unknown origin

A
  • Lymphoproliferative disease- lymphadenopathy
  • Malaria
  • Myeloproliferative disorders- problems with bone marrow e.g., polycythemia vera
  • Thromboembolic disease
  • TB
  • Endocarditis
202
Q
  • which 1st line antihypertensive would you give to someone <55 years old?
  • which 1st line antihypertensive would you give to someone >55 years old or originates from an afro-caribbean heritage?

what would you do if you’ve already maxed out this dose?

what would you do if this doesn’t work?

A
  • ramipril- ACE inhinitor
  • Nefedipine- DHP-Calcium Channel Blocker
  • Combine CCB and ACE-I/ARB
  • Add a thiazide like diuretic (Indapamide)
203
Q

what is a delta wave?

what is it indicative of?

A

slurred upstroke of the QRS complex

Wolff parkinson syndrome

204
Q

What is the indication of adenosine?

A

it is an AVN blocking drug used in SVTs

Year 3 Med 1 (10 decks)

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