Med 1 LO's Flashcards
list relevant conditions that can cause angina (chest pain)
- 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
what is VTE
what are the risk factors?
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
symptoms of VTE
Many people have none at all.
Following are the most common in their affecting areas:
- Swelling (may be unilateral)
- Tenderness
- Pain
- Redness
- Dilated veins
What is a pulmonary embolism
rfxs
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
Symptoms of PE
- 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
Signs of PE
- 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
ECG findings in PE
- 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).
pathophysiology of PE
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.
Blood tests in PE
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
imaging investigations in PE
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
Wells scoring system
criteria and meaning
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
Management of PE
- 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
what is an aortic aneurysm
what is a psuudoaneurysm
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).
causes of an aortic aneurysm
common sites for an aneurysm
which group is invited for screening
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
Signs and symptoms of AAA (unpopped)
- 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
signs of ruptured AAA
- 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
rfx for developing AAA and Rfx for ruptured AAA
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.
pathophysiology of AAA
- 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
complications of AAA
- rupture
- thrombosis
- embolism
- fistulae
- pressure on other structures
pathophysiology of atheroma
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.
How does atheroma ruptuere lead to an MI?
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
heart failure definition
systolic vs diastolic
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
causes of systolic and diastolic heart failure
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
clinical features of left heart failure
symptoms
signs
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





