Cardiovascular Disorders Flashcards

Haemodynamic, Vascular, Heart Disorders

1
Q

Oedema: Aetiology and Pathophysiology

A

Oedema results from changes in capillary pressures.
the selectively permeable capillary walls balance hydrostatic and osmotic pressure
-Hydrostatic pressure: pushes fluid into the tissues
Osmotic pressure: pushes fluid back into capillaries

Chemical mediators in injuries can increase capillary permeability
High blood pressure or venous blockages can raise Hydrostatic Pressure -> oedema
Lymphatic system obstructions post surgery -> lymphoedema
if there isn’t enough proteins in the capillary bed and if the kidneys excrete the proteins into the urine, it can decrease osmotic pressure –> oedema

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2
Q

Oedema: Epidemiology and Clinical Manifestations

A

Epidemiology:
exact prevalence (commonness and frequency) of Oedema is unknown
influenced by factors such as pregnancy, heart failure, kidney, or liver diseases, deep vein thrombosis, and certain medications
Clinical Manifestations:
weight gain, swelling, or puffiness
can be localised or systemic
Severe Oedema may threaten life, particularly in vital organs

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3
Q

Oedema: Diagnosis and Management

A

Diagnosis:
medical history, physical exams, tests e.g. X-rays and blood analysis
Management:
depends on Oedema location
e.g. leg elevations, compressions stockings, albumin, and diuretics are effective for limb oedema
e.g. specific management protocols for abdominal, brain and lung oedema

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4
Q

Hypertension: Background

A

is high blood pressure - a major cause CV Disease and stroke
Normal BP: 120/80 mmHg
Hypertension: 140/90 mmHg or higher
Young people: higher diastolic pressure
Older people: higher systolic pressure
often Asymptomatic, leading to underdiagnosis, known as the ‘silent killer’

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5
Q

Hypertension: Causes and Pathophysiology

A

Essential Hypertension: no known causes
Secondary Hypertension: from other conditions
Pregnancy can instigate Hypertension
involves vessel inflammation and muscle hypertrophy
Some theories include SNS imbalance, RAAS overactivity, metabolic syndrome (especially insulin resistance)

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6
Q

Hypertension: Epidemiology, risk factors and Management

A

Epidemiology and Risk Factors:
Higher prevalence in males and older individuals
influenced by obesity, diet, alcohol use, and nicotine
Management:
Regular monitoring for diagnosis
Lifestyle modifications (diet, exercise, stress reduction) and medications like diuretics and beta blockers

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7
Q

Circulatory Shock

A

Acute condition with significant hemodynamic alterations
leads to poor tissue perfusion and impaired cellular metabolism

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8
Q

Types of Circulatory Shock

A

cardiogenic (heart cannot pump enough blood to meet the body’s needs)
neurogenic (HR, BP and temp become unstable due to nervous system damage after a spinal cord injury)
anaphylactic (results from severe allergic reaction)
hypovolemic (when fluid or blood volume is lost drastically)
septic (when your blood pressure drops to a dangerously low level after an infection)

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9
Q

Circulatory Shock: Pathophysiology and phases of shock

A

due to Inadequate tissue perfusion and oxygen delivery
contains compensated (body can fix poor tissue perfusion) and non-compensated (body can no longer fix poor tissue perfusion) phases

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10
Q

Circulatory Shock: Clinical manifestations, diagnosis and management

A

symptoms include changes in BP, HR and consciousness
Treatment varies by type, often focusing on oxygenation and underlying causes

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11
Q

Peripheral Arterial Disease: Causes and Pathophysiology

A

reduced blood flow to limbs causing ischemia (reduced blood flow) and necrosis
imbalance in vasoconstriction and vasodilation regulation

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12
Q

Peripheral Arterial Disease: Clinical manifestations, diagnosis and management

A

Key symptom is claudication (muscle pain caused by little or lack of blood flow) and atherosclerosis (gradual) and embolism (sudden)
Diagnosis: doppler studies, angiography, or venography,
Management: aims to maintain or improve circulation, using surgical techniques and medications (e.g. aspirin - NSAID and clopidogrel - anti-platelet medication - to prevent blood clots)

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13
Q

Aneurysms: Causes and pathophysiology

A

changes in blood vessel walls leading to potential rupture due to abnormal bulging/dilation
often linked to atherosclerosis (thickening or hardening of arteries)
Types include:
True - vessel breaks
Dissecting - tear in vessel
False aneurysm - vessel leaks

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14
Q

Aneurysms: Clinical manifestations, diagnosis and management

A

is asymptomatic until rupture
Management: through surgery to prevent growth or rupture

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15
Q

Deep Vein Thrombosis (Thrombophlebitis and phlebothrombosis): causes and pathophysiology

A

Deep Vein Thrombosis is clot formation in deep veins
conditions related to inappropriate blood clot formation
Thrombophlebitis involves clot formation with venous wall inflammation
Phlebothrombosis involves blood clot formation but no inflammation

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16
Q

Deep Vein Thrombosis (Thrombophlebitis and phlebothrombosis): Management

A

with exercise, hydration, support stockings, and medications

17
Q

Varicose Veins: Causes and pathophysiology

A

abnormally twisted, lengthened, and dilated leg veins
caused by venous valve insufficiency (veins cannot effectively bring blood back up to the heart) and vessel wall dilation
can lead to chronic venous insufficiency

18
Q

Varicose Veins: Clinical manifestations, diagnosis and management

A

symptoms include aching pain, burning, throbbing, swelling in the legs
diagnosed through observation, endoscopy, or ultrasound
Management: with lifestyle changes and surgical interventions

19
Q

Coronary Heart Disease: Causes and pathophysiology

A

primarily caused by atherosclerosis
involves stages like fatty streak and plaque formation

20
Q

Coronary Heart Disease: Clinical manifestations, diagnosis and management

A

symptoms can include ‘silent’ angina
management: by addressing risk factors, lifestyle changes, and medications

21
Q

Acute coronary Syndrome: Causes and pathophysiology

A

conditions affecting myocardial blood flow
includes stable, unstable and variant angina

22
Q

Acute coronary Syndrome: Clinical manifestations, diagnosis and management

A

Symptoms: includes increased HR, chest pain, and sometimes nausea
Diagnosis: through clinical findings, ECG, and angiograms
Management: focuses on life support, pain reduction, and addressing complications

23
Q

Myocardial Infarction

A

otherwise known as Heart Attack, is a blockage of blood flow to the heart’s muscle

24
Q

Heart Failure: Causes and Pathophysiology

A

a syndrome where the heart cannot meet the body’s commands
characterised by systolic and diastolic dysfunction
Risk factors include ischemic heart disease and HT

25
Q

Heart Failure: Clinical manifestations, diagnosis and management

A

Symptoms includes fatigue, and shortness of breath.
complications include atrial fibrillation and kidney failure
Diagnosis: ECG
Management: lifestyle changes, and a range of medications

26
Q

Valve Defects: Causes and Pathophysiology

A

can be congenital (from birth) or accquired, leading to regurgitation or stenosis (backbone becomes too small)
Symptoms include dyspnoea, oedema, and chest pain

27
Q

Valve Defects: Clinical manifestations, diagnosis and management

A

Diagnosis: ECG
Management: with surgical repair or replacement

28
Q

Cardiomyopathies: Causes and Pathophysiology

A

range of heart muscle disorders, including dilated, hypertrophic and restrictive types

29
Q

Cardiomyopathies: Clinical manifestations, diagnosis and management

A

symptoms include dyspnea, chest pain, palpitations, oedema
Diagnosis: echocardiography, chest X-rays, and ECG
Management: similar to Heart Failure