Med 1 LOs Flashcards
Understand and describe the physiology of common causes of chest pains
- Non Cardiac* (Pulmonary, pleuritic, PE, traumatic, musculoskeletal → e.g. Marfan’s syndrome in TALL individuals, arthritic, Upper GI, etc.) → if have autoimmune disease then INCREASE risk of coronary heart disease (as autoimmune)
- Aortic* (Aneurysm/dissection → when chest pain going from heart to BACK)
- Pericardial / Valvular*
- Pericarditis* → pain on INSPIRATION & EXPIRATION, LESS pain when sitting forward & WORSE when lying down(as MORE rubbing), HIGHER risk with diabetic nephropathy
- Cardiac* – Stable → knows when happens v Unstable → when have HYPOTENSION & wakes up at night
- Acute Coronary Syndromes* (STEMI, nonSTEMI, unstable angina, arrhythmia, sudden death)
Understand the presenting symptoms and signs for VTE disease and it’s risk factors and physiology
X
Understand the presenting symptoms and signs for aortic aneurysm and it’s risk factors and physiology - specifically here thoracic AA
Abnormal dilatation of Aorta (usually SLOW and PROGRESSIVE)
Location:
Thoracic / Abdominal
Causes : Degenerative, HIGH BP, Arteritis, Connective tissue diseases, Bicuspid AV, Family history
Usually asymptomatic incidental finding on CXR/CT
Severe sharp back/interscapular pain
Complications: Dissection, rupture, AV regurgitation
Surveillance, Repair, Replacement
Describe the physiology of atheroma & ischaemic heart disease (risk factors)
ADD PHYSIOLOGY
- Non-modifiable – Age, Gender, Family history, previous CHD event
- Modifiable – Lifestyle, BMI, Smoking, DM, BP, Lipids, Stress
- Often inter-related and additive
- Underlying Atherosclerosis
Understand the presenting symptoms and signs of heart
failure and it’s risk factors and physiology
X
Perform BLS and recognise simple rhythms e.g. VT, VF and asystole
X
Discuss the common causes of breathlessness
- Bronchiectasis - is chronic inflammation of the bronchioles causing clogging the airways, decreasing the SA and this DECREASING gas exchange
- Pleural effusion, pneumonia, lung cancer - are in the lungs when _shouldn’t_be there
- Acidosis - hyperventilate to get rid of CO2
- Pregnancy - push up on diaphragm
- Arrhythmias - affects how heart pumps
Manage oxygen therapy for SOB/hypoxic patient
- NASAL CANNULA: Connected to oxygen at the wall. Sit in the patients nostrils and curl around their ears to stay in place.
- VENTURI MASK: Coloured clip at the bottom of the mask controls how much additional air is entrained into the mask. It tells you how many litres of oxygen to deliver from the wall in order to deliver the correct percentage of oxygen with that clip. Can connect other devices such as nebuliser.
- SIMPLE MASK: Connect to any flow of oxygen from the wall. Uncertain amount of additional air breathed in by the patient. Can connect other devices such as nebuliser.
- NON-REBREATHE MASK: Has an oxygen reservoir bag at the bottom of the bag to maximise how much oxygen does into the patient.
Understand and describe the physiology of common causes of wheeze
X
Understand the causes, presentation, diagnosis, monitoring and management of acute and chronic asthma
X
Understand the likely pathogens, presenting features & treatment for Respiratory Tract Infection including community and healthcare associated pneumonia.
Symptoms:
- Fever (+/- Rigors)
- Breathlessness
- Cough (+ Sputum production → green/brown colour)
- Inspiratory Chest Pain → pleuritic chest pain
- CONFUSION (Elderly)
Signs:
- Reduced Chest Expansion
- Dull percussion
- Increased vocal resonance
- Coarse Crackles (improve on cough) → infective material on lung and when cough removed from alveolifor a short time
- Temperature
- Low Oxygen Saturations
MANAGEMENT
STEP 1
Oxygenation (e.g. nasal cannula)
NEXT
IV Fluids (dehydration)
PO/IV Antibiotics (guided by trust guidelines/CURB Score)
FOLLOW UP
CXR after 6 weeks to ensure resolution → takes 6 weeks heal (if frequent pneumonia possible lung cancer as cancer INCREASES risk of pneumonia)
Describe the presentation and understand the multisystem
nature of Chronic Obstructive Pulmonary Disease (COPD). Outline the management and prognosis of Chronic Obstructive Pulmonary Disease (COPD)
X
Understand the presenting symptoms, signs and risk factors for bronchiectasis and describe the management of this condition (& what is it?)
What is it?
Symptoms & signs
Risk factors
Management
Conservative: annual vaccinations, chest infections/pulmonary rehabilitation, community nurses
Medical: specialist respiratory input: prophylactic antibiotics, salbutamol inhaler, carbocysteine
Define subtypes of cardiomyopathy, list causes and describe presentation and management
X
Define cyanosis. Understand the causes of central and peripheral cyanosis
What is cyanosis?
Is the blue discolouration of the skin or mucous membranes due to the tissue near the skin surface having low oxygen saturation
Peripheral cyanosis
Peripheral Cyanosis: (only the extremities or fingers).
Causes:
- Reduced Cardiac Output (i.e. Poor Stroke Volume/Shock)
- Hypothermia (Peripheral blood vessel shut down)
- Arterial/Venous Obstruction
Central cyanosis
Central Cyanosis: (around the core, lips, and tongue) - is a BAD sign as is central → NOT peripheral
Central Cyanosis = Major causes of hypoxia/hypo-perfusion
Causes:
- Respiratory diseases (COPD, Pneumonia, PE)
- Cardiovascular (Heart Failure, Congenital Heart Disease - most common cause)
- CNS (Respiratory Depression) (ICH, Drug Overdose)
Interpret arterial blood gases and understand the causes of acid base disturbance
X
Understand the physiology of cough as a protective reflex and the pathophysiology as a symptom of disease. List causes of cough
X
Describe the risk factors, symptoms, investigations and management of thromboembolic disease
X
You should understand the physiology of ILD and how it affects lung function (investigations, management)
What is ILD?
Disease of the pulmonary interstitium:
- Area between the alveolar epithelium and capillary endothelium
- Effects of septal and bronchovascular tissues making up the fibrous framework of the lung
- Can involve airways, vasculature and alveolar spaces
Investigations
- Bloods
- CXR
- HRCT (high resolution CT)
- Full pulmonary function tests
- Spirometry
- Full lung function
- Gas exchange
- Transbronchial/opening lung biopsy
What is seen on full pulmonary function test?
- FEV1 → REDUCED
- FVC → REDUCED
- FEV1/FVC ration → NORMAL (>70%)
- Total lung capacity → REDUCE
- Residual volume → REDUCED
- TLCO → REDUCED
- KCO → REDUCED
What is seen on HRCT?
- Tram lines (enlarged airways)
- Honey-combe appearance
Management?
- Oxygen
- Treat connective tissue disease if present
- Remove causative agent
- Antifibrotics (medication)
- Anti-tussive → preventing coughing medication
- Pulmonary rehabilitation → breathing exercises
- Palliative care input
- Transplant → usually >65 age
Understand the common causes of interstitial lung diseases (ILD) and describe the presenting features and classical signs.
What is ILD?
Disease of the pulmonary interstitium:
- Area between the alveolar epithelium and capillary endothelium
- Effects of septal and bronchovascular tissues making up the fibrous framework of the lung
- Can involve airways, vasculature and alveolar spaces
Common causes?
- Idiopathic pulmonary fibrosis
- Connective tissue disease associated ILD
- Hypersensitive pneumonitis
- Sarcoidosis
- Drug induced ILD
- Cryptogenic organising pneumonia → unknown cause
- Infection → COVID
Signs
- Clubbing
- Fine inspiratory crackles
- Cyanosis
- Evidence of cor pulmonale
- Evidence of connective tissue disease
Symptoms
- Shortness of breath, especially with activity.
- Dry, hacking cough that does not produce phlegm.
- Extreme tiredness and weakness.
- No appetite.
- Unexplained weight loss.
- Mild pain in the chest.
- Labored breathing, which may be fast and shallow.
- Bleeding in the lungs
What is seen on HRCT?
- Tram lines (enlarged airways)
- Honey-combe appearance
Understand the genetics of Cystic fibrosis (CF) and its molecular biology and how this translates into a multisystem disease.
Describe the different types of presentation, how CF is diagnosed, and common complications of CF. Understand the management of CF and its implications for patients and relatives.
Genetics of CF
- Is an autosomal recessive genetic condition
- Mutations in the CFTR (cystic fibrosis transmembrane conductance regulator) protein results in production of thick mucus which lines the body e.g. bronchioles, pancreatic duct
Different types of presentations
- Recurrent exacerbations (chest infections) → difficult to treat
- At young age require a lot of medical intervention e.g. diabetes/failure to thrive/respiratory disease
- Likely to require lung transplants later in life
How is CF diagnosed
- In infancy using the Heel-Prick test and can be diagnosed with a sweat test
- Genetic counselling can be used with families with histories of CF
Complications of CF (systemic)
- Obstructive airway disease - can lead to bronchiectasis
- Diabetes - as thick mucus in the pancreatic ducts thus, prevents insulin release → blockage → inflammation → damages islets of Langerhans → prevents insulin release)
- Digestive problems - blockage of pancreatic duct prevents exocrine function by preventing
- Infertility - blockage of Fallopian tube/vas deferens
Management of CF
- Required a MDT approach
- Prophylactic antibiotics → to protect against recurrent chest infections
- Chest physiotherapy
- Annual diabetes screening
- Pancreatic enzyme replacement
Understand the histological types (complete) of lung cancer and differences in risk factors and prognoses
2018-2019
Histological types of lung cancer
Risk factors
- Smoking
- Ex-smoker
- Non-smoker → usually genetic
- Asbestos exposure
- Underlying interstitial lung disease
- COPD
Prognosis
Define sepsis and have an awareness of the “red flags” for sepsis recognition
This is the presence of SIRS with evidence of infection as the cause of inflammation (i.e. positive swabs/blood cultures, clinical signs of infection (e.g. CXR)).
RED FLAGS
RED FLAGS which raise suspicion are HR >130, RR >25, SBP <90, GCS > A (A for alert in AVPU → as worried about PERFUSION to brain), Needs O2 (to keep high O2 sats), non-blanching rash (meningococcal meningitis)/cyanotic, recent chemotherapy(immunocompromised → LOW WBC → HIGH risk of sepsis with NO other side effects (other than not looking well) as have littleimmune response, notpassed urine in 18hours (as kidneys NOT perfused adequately)
Recognize and interpret common symptoms and signs of inflammatory response
X
Understand the importance of early recognition of sepsis and
define early management
Think sepsis when: patient has a NEWS score of 5 or more OR a patient has a NEWS score of 3 or more in ONE parameter (RED box in red flag symptoms ticked)
qSOFA → do when patient LOW BP and HIGH risk of. SEPSIS
The presence of >2 factors suggests a likely poor outcome.
RR >22bpm,
SBP <100mmHg,
GCS <15.
Investigations
Bedside - Observations (NEWS score – detect sepsis)
Sputum Sample (send for MC&S to identify pathogen)
ECG (due to tachycardia/chest pain)
Tests -
FBC (WCC – assess for inflammatory response).
U&Es (Low BP and dehydration/sepsis may affect renal function).
CRP (assess for inflammatory response).
BLOOD CULTURES (due to pyrexia) → greatest chance in picking up bacteraemia
+/- LFTs, LACTATE (if severe), VBG/ABG
Imaging
CXR (history of chest pain and SOB).
Understand the mechanisms and spread of antimicrobial resistance
Mechanism
-
Bacterium destroys the antibiotic
- beta-lactamases
- aminoglycoside modifying enzymes
-
Bacterium modifies its target
- penicillin-binding proteins in PRP
- peptidoglycan structure in VRE
- ribosomal proteins in macrolide and tetracycline resistance
-
Bacterium shuts the door
- reduced permeability eg ertapenem resistance in Klebsiella
-
Bacterium pushes it out
- efflux pumps
Why does it happen?
- Pathogens are living things and evolve in response to selective pressure
- They become resistantto antibiotics!
- There are fewer and fewer new antibioticscoming to market
Describe the risk factors for UTI, likely pathogens and treatment options
PREGNANCY
increases UTI risk due to renal pelvis dilation in order to accommodate the additional volume of urine excreted (additional waste from foetus). This causes some urinary stagnation and increases risk of infection developing.
MENOPAUSE
increases UTI risk due to thinning of the urothelium secondary to reduction in oestrogen production. This makes the lining more vulnerable to damage and infection.
(chronic health conditions) -> Diabetes Mellitus is the main chronic health condition to significantly increase UTI risk. Excess glucose is excreted in urine and makes a favourable environment for bacterial growth.
Sexual activity
Easier for bacteria to migrate from one site to another. Encouraging patients to pass urine/void their bladder after intercourse can significantly reduce the risk of UTI.
Renal Stones/Bladder (tract blockages)
stones cause obstruction of the urinary tract. This causes urinary stagnation and increases infective proliferation. UTIs can also increase the future risk of stones (particularly Proteus infections)
Catheters
introduce a foreign body into a sterile urinary tract. Bacteria can colonise around the tubing and lead to infection.
Note:
- Higher risk of atypical bacterial infection.
- Catheter change with antibiotic cover (if infection suspected).
- Asymptomatic colonisation of catheter does not require treatment (do not routinely send Catheter urine specimens).
Common bacterial causes of UTI include:
E.COLI, PROTEUS (high relationship with renal stones), STAPH SAPROPHYTICUS.
Management:
Conservative: Fluids/Hydration.Medical: Antibiotics (see table).
Recognise features of septic arthritis and initial investigation and management
- Is the inflammation of the joint capsule
- May need joint replacement
- Usually localised joint pain (restriction in movement)
What is septic arthritis?
Septic arthritis refers to the infection of a joint. It requires a high index of suspicion and can affect both native and prosthetic joints.
Main causative organisms?
The main causative organisms that lead to septic arthritis are S. aureus (most common in adults) and Gonorrhoea (more common in sexually active patients).
Bacteria will ‘seed’ to the joint from a bacteraemia (e.g. recent cellulitis, UTI, chest infection), a direct inoculation, or spreading from adjacent osteomyelitis.
Septic arthritis can cause irreversible articular cartilage damage leading to severe osteoarthritis so must be identified EARLY.
Investigations
Bedside -Observations (fever, ?septic), JOINT ASPIRATION (joint fluid analysis) → done before IV antibiotics given
Blood tests - FBC, CRP, Urate Level (check for gout), Coag, Blood cultures (could be seeded infection).
Imaging - plain film X-ray
Management
Medical - long term IV antibiotics (4-6 weeks) (empirical and then specific after cultures come back)
Surgical - Infected native joints require surgical irrigation and debridement (‘washout’ → to get rid of as much bacteria as possible) to aid in source control. May require several washouts before clearance of infection.
Infected prosthetic joint, washout is still required, but revision surgery is typically needed also
