Blood Flashcards

1
Q

What are the different blood types?

A

A - a antigens
B - b antigens
AB - a and b antigens
O - no antigens

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2
Q

What is Rh factor?

A

A red blood cell antigen (named after rhesus monkey)
Most people have Rh factor, however some do not. SO you are either Rh +ve or Rh -ve

A person who is Rh -ve (dd) needs to be sensitized before they can produce Rh antibodies. (by having an Rh+ blood transfusion - produces anti-Rh positive antibodies) If she is exposed to Rh+ve blood type again the antibodies will attack the transfused blood)
If she ever became pregnant with a Rh +ve child this will become a problem because her body may reject the child.
This is known as Mother-fetus incompatibility.

A first time mother will develop Rh antibodies if her child is Rh+, during birth Placental ruptures occur so that some fetal blood gets into the mother’s system, stimulating the development of antibodies to Rh+ blood antigens. This means that there is a risk for any further pregnancies.

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3
Q

What is Mother-fetus incompatibility?

A

When a mother is Rh -ve (dd) and her child is Rh -ve (Dd). If the mother has been exposed to Rh+ve blood (wrong blood transfusion or previous pregnancy )before her body will contain anti-Rh antibodies, Maternal antibodies can cross the placenta and destroy fetal red blood cells.

As a result, the newborn baby may have a life-threatening anemia, and may be jaundiced, fevered, quite swollen, and has an enlarged liver and spleen. This condition is called erythroblastosis fetalis
The standard treatment in severe cases is immediate massive transfusions of Rh- blood into the baby with the simultaneous draining of the existing blood to flush out Rh+ antibodies from the mother. This is usually done immediately following birth, but it can be done to a fetus prior to birth.
Because the baby’s own Rh+ red blood cells have been replaced with Rh- ones, the mother’s anti-Rh+ antibodies don’t agglutinate any additional red cells. Later, the Rh- blood will be replaced naturally as the baby gradually produces its own Rh+ blood. Any residual anti-Rh+ antibodies from the mother will leave gradually as well because the baby does not produce them.

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4
Q

How can Erythroblastosis fetalis be prevented?

A

Erythroblastosis fetalis can be prevented for women at high risk (i.e., Rh- women with Rh+ mates or mates whose blood type is unknown) by administering a serum Rho-gram

This contains anti-Rh+ antibodies - they are injected into the mother around the 28th week of pregnancy and again within 72 hours after the delivery of an Rh+ baby.
The injected antibodies quickly agglutinate any fetal red cells as they enter the mother’s blood, thereby preventing her from forming her own antibodies. The serum provides only a passive form of immunization and will shortly leave her blood stream. Therefore, she does not produce any long-lasting antibodies.

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5
Q

What is autologous blood transfusion

A

A blood transfusion using your own blood, ythis can be:

preop - donated blood which is then stored until the surgery

recycled - Blood lost during surgery is filtered, and put back into your body during surgery. (cannot be used when there is cancer or an infection)

Post-operative autologous transfusion: recycling your blood after surgery. Blood lost after surgery is collected, filtered and returned to your body

Hemodilution: donating your own blood during surgery. Immediately before surgery, some of your blood is taken and replaced with IV fluids. After surgery, your blood is filtered and returned to you. This is done only for elective surgeries. This process dilutes your own blood so you lose less concentrated blood during surgery. It has the advantage of eliminating or minimizing the need for someone else’s blood during surgery.

Apheresis: donating your own platelets and plasma. Before surgery, your platelets and plasma, which help stop bleeding, are withdrawn, filtered and returned to you when you need it later.

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6
Q

What are two sources of donor blood?

A

Volunteer blood: blood collected from the community blood supply (blood banks). This has the advantage of being readily available, and can be life-saving when your own blood is not available. The disadvantage is that there is a risk of disease transmission, such as hepatitis, and allergic reactions.

Designated donor blood: blood is collected from the donors you select. You can select people with your own blood type who you feel are safe donors. Like volunteer blood, there is still a risk of disease transmission, such as hepatitis and AIDS, and allergic reactions. This process usually requires several days for advanced donation. It may not necessarily be safer than volunteer donor blood.

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7
Q

What is anaemia?

A

When a person has low hemoglobin often due to a lack of iron
symptoms: tired, reduced exercise tolerance, shortness of breath, agina and claudication
signs: paler, pale mucus membranes and palmar creases, , glossitis
underlying causes: iron deficiency, B12/folate deficiency, hemolysis, bone marrow failure/infiltration

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8
Q

Where is folate/B12 found and what can cause a deficiency?

A
  • Found in veg, fruit and supplemented foods
  • Deficiency can be due to malabsorption, low dietary intake, or an increased need for b12
  • Needed for DNA synthesis
  • Deficiency causes pancyyopenia, (when there are less WBC, RBC and platelets)
  • The deficiency affects are dividing cells but manifests as anaemia because these cells are more active/form at a higher rate (in bonemarrow)
  • A lack of gastric parietal cells = less absorption from terminal ileum where B12 is absorbed = B12 deficiency
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9
Q

What is macrocytic anaemia?

A

When RBCs are large.
normal size - 82-96fl
macrocytosis - >100fl
Can be due to liver disease

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10
Q

What is pernicious anaemia?

A

-An autoimmune disease
-body’s anitbodies act against gastric parietal cells and intrinsic factor
-This leads to achlorhydria
-And therefore malabsorption
(most people have 4 years b12 stores)

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11
Q

What is haemolysis?

A
  • Increased RBC destruction
  • RBC life span is decrease to less than 30 days
  • This leads to jaundice and anaemia
  • There is an increase of young RBCs called reticulocytes

If it is due to immune antibodies destroying RBCs there will be a +ve coombs test

CAUSES;

  • Membrane, heriditary spherocytosis
  • Enzymes, rare pyruvate kinase
  • Haemoglobin, sickle cell thalassemia
  • Acquired, immune
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12
Q

What are the two types of lymphocytes?

A

-B Lymph
differentiate into plasma cells and produce immunoglobins when exposed to foreign antigens
-T Lymph
some are helper cells CD4
some are cytotoxic cells CD8
*and B cells in antibody generation and are also responsible for cellular and cell mediated immunity

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13
Q

What is acute leukaemia? What 3 conditions can it lead to?

A

Proliferation (rapid increase in) precursor cells usually found in bone marrow. (Proliferation without differentiation)

-These cells replace normal bone marrow cells and leads to
ANAEMIA - tired & lethargic
NEUTROPENIA - infections due to low numbers of neutrophils
THROMBOCYTOPENIA - increased bleeding due to lack of platelets

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14
Q

What is acute myeloblasmic leukaemia?

A

Acute myeloblasmic leukaemia - maligant proliferation of the precursor myeloblasts in bone marrow
-treatment with chemo and possible bone marrow transplant
(myeloblasts differentiate into granulocytes)

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15
Q

What is acute lymphocytic leukaemia?

A

Acute lymphocytic leukaemia - maligant proliferation of precursor lymphoblast cells in the bone marrow
-Causing damage and death by inhibiting the production of normal cells
-Chemo, this is the primarily childhood leukaemia
-CNS specific
(lymphoblasts differentiate into B&T Lymph, and natural killer cells)

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16
Q

What is high grade lymphoma?

A

High grade lymphoma - can be Hodgkin’s (contains Reed-Sternberg cells which are mature B cells that have become maligant) or Non-Hodkins

  • cancerous tumours of the lymph nodes
  • Spreads to liver, spleen, bone marrow, blood
  • Agressive chemo/localized radiotherapy
Symptoms:
Swelling of lymph nodes
Fever
Night sweats
Weight loss
17
Q

What are baroreceptors? Where are they located?

A

They sense pressure
Primary (arterial) - carotid sinus & aortic arch
Secondary (veins) - myocardium, pulmonary vessels

18
Q

Name two vasodilators

A

Epinephrine
Atrial Natriuretic peptide

(Epinephrine acts on alpha receptors causing vasoconstriction and on beta receptors causing vasodilation.)

19
Q

Name three vasoconstrictors

A

Epinephrine
Angiotensin II
Vasopressin

(Epinephrine acts on alpha receptors causing vasoconstriction and on beta receptors causing vasodilation.)

20
Q

How does Nitroglycerin (GNT) work?

A

GNT i denitrated to produce the active metabolite nitric oxide (NO)

21
Q

How do we treat hypovolemic shock?

A
  • ECF volume loss eg blood
  • Direct pressure should be applied to external bleeding vessels to prevent further blood loss.
  • IV fluids
  • Have the person lie flat with the feet lifted about 12 inches to increase circulation.
  • Keep warm and confortable

-Medicines such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output).
(Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.

22
Q

What complications can hypovolemic shock lead to>?

A
Kidney damage
Brain damage
Gangrene of arms or legs, sometimes leading to amputation
Heart attack
Other organ damage
Death
23
Q

What symptoms are associated with hypovolemic shock?

A
Anxiety or agitation
Cool, clammy skin
Confusion
Decreased or no urine output
General weakness
Pale skin color (pallor)
Rapid breathing
Sweating, moist skin
Unconsciousness

(Low blood pressure
Low body temperature
Rapid pulse, often weak and thready)

24
Q

What are lymphatic capillaries?

A

Single layer of endothelial cells on a basement membrane.

They are large water filled chambers that are permeable to all interstitial fluid including protein.

25
Q

Where are lymph nodes located?

A

Neck, armpits, groin, around intestine

26
Q

What are 2 main veins that the lymph drains into

A

-drains into veins near the junction of the jugular and subclavian veins in the upper chest

27
Q

What condition occurs due to lymph flo occlusion?

A

elephantiasis

-surgical removal of nodes due to breast cancer can also result in fluid pooling in affected tissues

28
Q

How does lymph travel along the lymphatics? What are they innervated by?

A

Smooth muscle in the lymphatics produces rhythmic contractions that propel the lymph along

  • ve feedback which prevents edema (increased lymph = increased contractions, decreased lymph=decreased contractions)
  • Innervated by sympathetic neurons