Cardiovascular Conditions 3 Flashcards

1
Q

What causes anaemia?

A

All anaemias are a clinical manifestation of the blood having less capacity to carry oxygen – why?

The protein haemoglobin is a component of erythrocytes (red blood cells) and is critical for carrying oxygen The haem- part of haemoglobin is the iron component in the blood, and also the component to which oxygen binds. If there is not enough (or not structurally correct) haemoglobin, the blood capacity to carry oxygen is reduced.

Overarching causes of anaemia
* Lack of iron, vitamin B12 or folate
* Hypoplasia - not enough cells being made
* Haemolysis - cells being destroyed
* Blood loss
In other words lack of input, excessive turnover or excessive loss

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2
Q

What are the risk factors for anaemias?

A
  • Previous infections
  • Diet- eg lack of nutrient, malabsorption
  • Toxin input e.g. alcohol, chemical exposure
  • Menstruation - excessive blood loss
  • Pregnancy - creates a big demand for iron
  • Family history
  • Chronic Disorders - demands on the body or impariment to absorption
  • Gastrointestinal disease
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3
Q

What are the signs and symptoms of anaemias?

A

A wide range of signs and symptoms are associated with anaemia – all associated with reduced oxygen-carrying capacity.

  • Signs: Pallor, Tachycardia (racing heart), Oedema, Systolic flow murmur
  • Symptoms: Fatigue, Tinnitus, Paraesthesia (numbness and tingling in fingers and toes), Headache, Palpatations, Breathlessness on exertion
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4
Q

What causes anaemias?

A

Iron deficiency Aetiology: (most common type) Loss from bleeding, poor dietary intake, malabsorption due to gastrointestinal disease or antagonistic dietary factors
Megaloblastic Aetiology: Deficiency of intake of vitamin B12, dietary deficiency of folate, malabsorption of vitamin B12 due to disease of the ileum or intrinsic factor deficiency
Haemolytic Aetiology: Erythrocyte abnormalities shorten RBC lifespan, and causes may be congenital e.g. thalassaemia, or acquired e.g. infection with malaria
Aplastic Aetiology: Primary – failure of stem cells, possibly autoimmune though not conclusive. Secondary (acquired) – drugs, chemicals, radiation, viral hepatitis, pregnancy.
Anaemia of chronic disease Aetiology: Significant Chronic infection, Chronic inflammation, Neoplasia or Cancer Treatment

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5
Q

What tests might be carried out for anaemias?

A

Key diagnostic methods:
* Blood tests
* Urinalysis
* Endoscopy, colonoscopy
* Stool sample
Consider why gastrointestinal investigations might be used?

Key diagnostic methods for aplastic and anaemia of chronic disease:
* Blood tests
* Bone marrow aspiration

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6
Q

What is the pathophysiology of anaemias?

A
  • Iron deficiency Pathophysiology: Lack of iron causes production of abnormally small RBCs which contain a low level of haemoglobin
  • Megaloblastic Pathophysiology: Lack of B12 or folate causes impairment of DNA synthesis of RBCs leading to the presence of megaloblasts (abnormally big cells) within bone marrow
  • Haemolytic Pathophysiology: Haemolysis may occur intra- or extra-vascularly, or within bone marrow, bilirubin and urobilinogen levels in blood rise from excessive RBC destruction occurring
  • Aplastic Pathophysiology: Dysfunction of the immune system leading to T cell autoreactivity against haematopoietic stem cells in an individual who is genetically susceptible (look for bleeding and bruising during physical examination)
  • Anaemia of chronic disease Pathophysiology: Immune system reacts to autoantigens/tumour antigens/microbial infection which suppresses RBC production and shortens life of RBCs
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7
Q

What traditional treatments are used for anaemias?

A

Treatment is Dependent on type of anaemia
* Iron deficiency – supplementation with iron and treatment of underlying GIT disease
* Megaloblastic – injections of B12 in the form of hydroxocobalamin, potential dietary supplementation
* Haemolytic – transfusion and chelation therapy (pulls excess out of the blood), stem cell or bone marrow transplant - this is the most invasive
* Aplastic – again, blood transfusion, and possible bone marrow transplant
* Anaemia of chronic disease – treatment directed at underlying disease causing the anaemia, transfusion and erythropoietin (usually made by the kidney) injections for severe symptoms

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8
Q

What are the potential complications of anaemia?

A

The potential impact of anaemia on a patient’s future wellbeing depends of course on the type of anaemia:

  • Iron deficiency – with dietary changes and treatment of any underlying gastrointestinal disorder, impacts on future wellbeing tend to be minimal and often positive (better diet and awareness of own health)
  • Megaloblastic– requirement to have injections at regular intervals long term or for life may present a challenge for a patient and require both administrative and emotional support
  • Haemolytic – impacts of this kind of anaemia are the most severe, both with possible complications and the invasive nature of regular blood transfusions :(
  • Aplastic – requirement for blood transfusion and possible transplantation are highly challenging for patients to contend with, with possible concerns around all areas of their future wellbeing
  • Anaemia of chronic disease – the complexity and severity of developing anaemia alongside chronic illness creates a significant impact on the life of the patient, with need for extensive support to navigate the progress of the disease.

Complications from the first three:
* Tachycardia
* Arrhythmia
* Heart failure
* Nerve damage and subsequent neurological dysfunction

  • Aplastic anaemia - first three above, but also bleeding and blood disorders e.g. leukaemia
  • Anaemia of chronic disease – first three above, but also specific complications associated with the underlying condition
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9
Q

What is Antiphospholipid syndrome?

A

It is an uncommon autoimmune hypercoagulability disorder. May occur in isolation with genetic predisposition implicated, or secondary to an underlying autoimmune disorder

Pathophysiology
Antibodies react to the proteins binding phospholipids within plasma membranes, and to the thrombin precursor prothrombin – both of these promote increased coagulation causing several signs and symptoms

Signs and symptoms
* Deep vein thrombosis
* Stroke
* Transient Ischaemic Attack (TIA)
* Lacey-type Rash
* Repeated miscarriage
* Cardiovascular disease
* Bleeding from nose and gums
* Neurological symptoms associated with blocked vessels

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10
Q

What is Haemophilia?

A
  • A hypocoagulability disorder associated with reduced ability to clot and so increased bleed time from injuries
  • Primary congenital haemophilia is caused by inherited or acquired genetic mutation, the latter rare and usually autoimmune in origin

Pathophysiology
Clotting factor VIII is the key factor affected by mutation of its parent gene – resultant dysfunction or deficiency of this factor prevents the appropriate activation of the coagulation cascade

Signs and symptoms
* Generalised weakness
* Pain, warmth, stiffness and tingling in knees, elbows, ankles
* Abnormally protracted bleeding from injuries and injections
* Nosebleed (epistaxis), coughing blood (haemoptysis)
* Numerous large, deep bruises

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11
Q

What are the signs and symptoms of Stroke and Transient Ischaemic Attack?

A

Linking back to atherosclerosis and clotting, STROKE is caused by interruption (clot) or reduction (narrowed vessels) of blood supply to the brain – ISCHAEMIC STROKE, or by bleeding in the brain from vessel rupture – HAEMORRHAGIC STROKE

Transient ischaemic attack (TIA) is a temporary pattern of symptoms like those of stroke, resulting from temporary interruption of blood supply to the brain. Risk factors mirror those for heart disease, as the incidence of stroke is intrinsically linked to cardiovascular disease.

Signs and symptoms:
* Slurring of words, struggling to understand speech
* Numbness or paralysis in face, arm or leg
* Sudden difficulty walking, loss of balance and coordination
* Visual disturbance
* Sudden severe headache with vomiting and alteration of consciousness

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12
Q

What is the pathophysiology of Stroke and TIA?

A
  • The most common presentation involves ischaemic occlusion (atherosclerotic narrowing of vessels or decrease in blood flow to the brain) leading to clotting, reduction of perfusion of brain tissue and necrosis.
  • Subsequent to necrosis there is loss of neuronal function, giving rise to the neurological picture observed in stroke
  • Less commonly blood vessels in the brain rupture as a result of a number of factors (e.g.
    uncontrolled hypertension, weak points in vessel walls, use of anticoagulant therapy) – this similarly disrupts neuronal function giving rise to the clinical presentation of stroke.
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13
Q

What is the treatment for Stroke and TIA?

A

Diagnosis
* CT scan
* MRI
* Blood tests
* Carotid ultrasound - in neck
* Echocardiogram - size and image of the heart

Treatment
* Thrombolysis - dissolve clot
* Thrombectomy - remove clot
* Aspirin
* Anticoagulants

Rehabilitation plans will usually include physiotherapy, psychological therapy and speech and language therapy to assist in restoration of physical and cognitive functions, and to provide support for emotional challenges presented by living with the consequences of stroke.

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14
Q

What is vascular dementia?

A
  • A diffuse condition second in prevalence to Alzheimer’s as a form of dementia
  • Not one single mechanism but relates to several vascular mechanisms
  • Damage to the blood vessels of the brain (e.g. by stroke) underpins a lack of
    oxygen and nutrients thus impairing cognitive function

Pathophysiology:
Thrombotic or embolic vascular occlusions cause a focal form of cerebrovascular disease, while hypertension initiates a diffuse presentation. White matter of the cerebral hemispheres and the deep
grey nuclei are commonly affected by focal disease. Co-occurrence of focal and diffuse presentations is common. Multiple infarcts in the cortex, a single infarct in an area causing maximum damage and small vessel disease are the most common vascular mechanisms in this form of dementia

Signs and symptoms
* Mood and behaviour changes (depression and psychosis may be present)
* Confusion and restlessness/agitation
* Unsteady gait
* Urinary frequency or incontinence

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