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YR 3 - Illness and Wellbeing > Blood Disorders > Flashcards

Blood Disorders Flashcards

1
Q

what is the composition of blood?

A

55% plasma - water and proteins

45% other
- 99% erythrocytes
- leukocytes
- platelets

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2
Q

define haematocrit aka packed cell volume

A

the percentage of red blood cells

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3
Q

what is the function of blood? (4)

A

Transport
- gases - oyxgen and co2
- hormones
- enzymes

Combat Infection
- w/ antibody and leukocytes

Homeostasis
- regulate temperature, pH and volume

Haemostasis
- stops bleeding from a blood vessel

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4
Q

define anaemia

A

when the haemoglobin and red blood cells count falls below a certain range

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5
Q

why may there be apparent changes in haemoglobin concentration during dehydration or pregnancy, but not actually?

A

dehydrated
- the plasma vol decrease
- hb conc apparently increases

pregnancy
- the plasma vol increase
- hb conc apparently decreases

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6
Q

two ways in which anaemia is classified.

A

by red blood cell size
by their underlying aetiology

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7
Q

how do you work out the RBC size?

A

MCV
- mean corpuscular volume

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8
Q

what are the 3 classifications of anaemia?

A

small cells MCV = <80 = Microcytic Anaemia

MCV = 80-96 = Normocytic Anaemia/Haemolytic Anaemia

large cells MCV = >96 = Macrocytic Anaemia

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9
Q

what are the underlying mechanisms of anaemia?

A
  • increased blood loss
  • increased destruction = haemolytic anaemias
  • impaired production of red cells
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10
Q

give an example of microcytic anaemia, MCV <80

A

iron deficient anaemia

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11
Q

what is iron deficiency anaemia?

A

when the level of iron in the blood is too low, causing a reduction in red blood cells

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12
Q

describe 4 causes of iron deficiency anaemia

A
  • blood loss
  • an increased demand
  • decreased absorption of iron
  • poor dietary intake

= microcytic and hypochromic
- RBC are smaller and paler

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13
Q

how can iron deficiency anaemia be investigated for diagnosis?

A
  • do a blood count, microcytic (<80) and hypochromic (<27)
  • do a blood film
  • poikilocytosis - varies in shape
  • anisocytosis - varies in size
  • blood test for levels of iron
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14
Q

what is the MCH?

A

mean corpuscular haemoglobin
- average count of Hb in RBC

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15
Q

how does iron deficiency affect the MCV?

A

becomes microcytic
below 80

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16
Q

how can iron deficiency anaemia be treated?

A

iron tablets
iron-rich foods

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17
Q

what is the most common cause of microcytic anaemia?

A

iron deficiency anaemia

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18
Q

what are other causes of microcytic anaemia, apart from iron deficient?

A
  • anaemia chronic disease
  • thallasaemia
  • sideroblastic anaemia
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19
Q

what is an example of macrocytic anaemia? MCV>96

A

Pernicious Anaemia

20
Q

what is B12 deficiency/pernicous anaemia?

A

an autoimmune condition causing destruction of cells that produce intrinsic factor, leading to a decrease in B12 absorption and B12 deficiency

21
Q

what are the causes of B12 deficiency? (6)

A

most common = autoimmune

  • dietary
  • surgery
  • parasites
  • drugs
  • ileal disease - disease limited to the lower third of small bowel
22
Q

describe the pathogenesis of B12 deficiency/pernicous anaemia.

A
  • B12 from food passes into GIT
  • binds to protein = Haptocorrin
  • B12-HC complex move to stomach
  • in stomach, B12-HC splits
  • gastric parietal cells in stomach secrete intrinsic factor
  • IF binds with B12
  • both absorb in the small bowel
  • if anything interferes with process = B12 deficiency
23
Q

how is B12 deficiency/pernicous anaemia investigated?

A
  • blood count
  • MCV >96
  • look at blood film
  • oval macrocytes
  • hypersegmented polymorphs
  • if severe = leukopenia and thrombocytopenia
  • look at bone marrow
  • more megaloblasts = immature red-cells
24
Q

what is the treatment for B12 deficiency/pernicous anaemia?

A

B12 injections

25
Q

with B12 deficiency, there may be an increase of megaloblasts. what is this called?

A

megaloblastic anaemia

26
Q

with pernicous anaemia, why do you actually get an increase in megaloblastic cells?

A
  • with decreased B12
    = DNA synthesis is impaired
  • impaired division and replication
  • get more megaloblasts not maturing
27
Q

What is Haemolytic Anaemia?

A

when RBC have short lifespan and break down quicker than usual

28
Q

what is Normocytic Anaemia and most common cause?

A

MCV = 80-96, so RBC are normocytic and normochromic

most common cause = haemolytic anaemia

29
Q

describe both ways in which you can develop normocytic anaemia. hereditary or acquired.

A

hereditary
- abnormal Hb synthesis = sickle cell
- RBC membrane defect
- metabolic pathway defect
= all of above lead to haemolytic anaemia

acquired
- immune mediated
- non-immune mediated

30
Q

what is sickle cell anaemia?

A

a inherited single gene mutation, distorting the red blood cells

31
Q

describe the cause of sickle cell anaemia.

A
  • single gene mutation on the 6th codon of beta-globing chain
  • valine gets substited for glutamic acid
    = HbS
  • when O2 drops
  • HbS molecules polymerise
    = sickle-shaped cells
32
Q

describe the results of sickle-cell anaemia

A

polymerisation
obstructs the small vessels - tissue infarction

33
Q

how is sickle cell anaemia investigated?

A
  • usually asymptomatic
  • only symptomatic with VOC
    = vaso-occlusive crisis
  • infection, dehydration, cold, acidosis, hypoxia
  • very painful for the patient
  • 30% acute chest syndrome
  • vaso-occlusion can cause necrosis of tissues
  • blood count = normal
  • blood film = sickled cells
34
Q

how is sickle cell anaemia treated?

A
  • hospital
  • iv fluids
  • analgesia
35
Q

what can be the oral manifestations resulting from anaemia?

A
  • angular chelitis
  • atrophic glossitis
  • recurrent aphthous stomatitis - recurrent ulcers, commonly B12 def.
  • dry, cracked mouth
  • fat tongue
  • mucous ulcers
36
Q

what is haemostasis

A

the process of which blood clots form at sites of vascular injury

37
Q

describe the process of haemostasis (4)

A
  1. vasoconstriction
  2. primary haemostasis - platelet plug formation
  3. secondary haemostasis - fibrin meshwork
  4. clot stabilisation
38
Q

describe what happens during vasoconstriction.

A

blood flow is reduced
- endothelin is secreted
- tightens the blood vessel

= a temporary fix

39
Q

describe primary haemostasis (5)

A
  1. endothelial disruption
  2. exposed collagen from the blood binds to von willebrand factor in the endothelial cells
  3. platelets adhere and activate
  4. platelets change shape = spiky
  5. aggregation
    = platelet plug
40
Q

describe secondary haemostasis.

A
  • tissue factors are exposed from the endothelial
  • coagulation cascade activates
  • thrombin cleaves fibrinogen into fibrin
    = meshwork
  • activate more platelets and traps RBC
41
Q

3 ways in which why you may have defects in blood clotting.

A
  • vessel wall is abnormal
  • platelet deficiency/dysfunction
  • abnormal coagulation
42
Q

Describe VW Disease and Haemophilia A - bleeding disorders due to abnormalities in haemostasis?

A

Von Willebrand Disease
- autosomal inherited disorder

  • Type 1
  • 80% of people have
  • decreased VWF
  • Type 2
  • 20% of people have
  • dysfunction

Type 3
- rare/severe
- no VWF at all

Haemophilia A
- X linked recessive (males)
- Factor 8 mutation = impaired coagulation
- easy bruising/haemorrhage

43
Q

How is Von Willebrand Disease treated?

A

with desmopressin or plasma infusions

44
Q

how is Haemophilia A treated?

A

infusion of F8

45
Q

define pathophysiology

A

physiological processes which are disordered due to association with disease or injury

46
Q

what is the pathophysiology of disseminated intravascular coagulation?

A

manifestations of abnormalities in bleeding and clotting

  • lots of tissue factor is released

= lot of thrombosis
need to break it down
= break down thrombus
= widespread bleeding
= vascular occlusions
= ischaemic tissue damage

YR 3 - Illness and Wellbeing (31 decks)

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