Substances affecting blood Flashcards

1
Q

Blood accounts for approx. what % of body weight?

A

Blood accounts for 4-8 % of the body weight.

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2
Q

The lifespan of cellular elements of blood is short: how many days?

A

110 to 120 days for erythrocytes and a couple of days for leukocytes and thrombocytes.

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3
Q

Blood loss of what% = hypovolemic shock.

A

Blood loss of 25 to 40% – hypovolemic shock.

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4
Q

What are some causes of Hemolytic anemia?

A

blood parasites (babesiosis),
bacterial pathogens (Leptospira, Clostridium),
medicinal products (Phenothiazines),
toxins (snake venom),
metabolic illnesses,
severe training exercises (in horses),
stress

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5
Q

Define Hypoplastic (aplastic) anemia

A

Inhibition of bone marrow function, the reduction of synthesis of various types of blood cells.

bone marrow is either empty (aplastic) or contains few blood cells (hypoplastic)

Hypoplastic anaemia, aplastic anaemia – red blood cells synthesis disorder.

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6
Q

Pancytopenia =

A

a decrease in the synthesis of all types of blood cells.

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7
Q

Define Agranulocytosis.

A

an acute condition involving a severe and dangerous lowered white blood cell count (leukopenia, most commonly of neutrophils)

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8
Q

Causes of Hypoplastic (aplastic) anemia.

A

Among medicinal products, the causes are chloramphenicol, to a lesser extent sulfonamides, NSAIDs, organophosphorus substances.

may also be exposure to radiation, chemicals and chronic infections.

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9
Q

Stimulation of erythropoiesis

A

A decrease in the amount of oxygen that reaches tissues stimulates an increase in the production of erythrocytes by bone marrow.

Specialized cells in the kidneys, called interstitial fibroblasts, sense the low oxygen levels in the blood passing through them.

In response to hypoxia, these interstitial fibroblasts release erythropoietin (EPO) into the bloodstream. EPO binds to receptors on the surface of hematopoietic stem cells (HSCs).

Chronic heart failure and lung disease is accompanied by cellular hypoxia and the production of erythrocytes increases.

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10
Q

Describe Alimentary anemia .

A

Anemia related to nutrition, frequently described as an iron deficiency anemia.

The cause is the insufficient absorption, excessive breakdown, accelerated expulsion of nutrients, minerals and vitamins, or an increased iron requirement (bleeding, gestation).

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11
Q

Normoblastic anemia

A

the bone marrow produces red blood cells (RBCs) that are of normal size (normocytic) and contain a normal amount of hemoglobin, but there is a decrease in the overall number of RBCs.

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12
Q

Hemoglobin contains 75% of the entire organism’s iron content in the two storage forms of iron:

A

ferritin and hemosiderin.

0.1% is contained in respiratory enzymes (cytochrome, cytochrome oxidase, catalase).

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13
Q

3-7% of an organims’s total iron content is contained in muscle in the form of

A

myoglobin.

0.1% is contained in respiratory enzymes (cytochrome, cytochrome oxidase, catalase).

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14
Q

hypochromic, normoblastic anaemia is also called

A

Iron deficiency anaemia

A reduced number of mature erythrocytes with a low haemoglobin content.

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15
Q

Iron deficiency anaemia is rare in

A

adult animals. An iron deficiency in adults is associated with chronic bleeding.

It is typically experienced by newborns whose iron levels are still low after birth and who also receive little iron in the milk.

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16
Q

Iron deficiency anaemia typically occurs in

A

piglets, infrequently in calves.

Piglets require 300 mg of iron in their first 3 weeks of life. They obtain 1 mg per day from milk and up to 100 mg from the environment. They additionally need at least 200 mg.

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17
Q

Piglets require how mg of iron n their first 3 weeks of life?

A

300 mg of iron in their first 3 weeks of life.

They obtain 1 mg per day from milk and up to 100 mg from the environment. They need additionally at least 200 mg.

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18
Q

Signs of anemia in piglets:

A

growth disturbance,
wrinkled pale-blue toned skin,
pale mucous membranes,
drooping ears and tail,
mortality.

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19
Q

Name 3 forms of Iron supplements.

A

Reduced iron, iron dextran, iron lactate.

Administered through the oral route, or into muscle.

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20
Q

Describe the path of iron in a biological organism.

A

Trivalent iron in the gut is reduced to a divalent form through the effect of hydrochloric acid and is absorbed from the small intestine.

It becomes trivalent once again in the intestinal mucous membrane.

In the blood it joins with transferrin, is transferred into tissue, is incorporated into apoferritin, is used for the synthesis of hemoglobin and enzymes, is stored in the liver, spleen and bone marrow in the form of ferritin and hemosiderin.

The excess is excreted through kidneys.

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21
Q

Signs of iron overdose are (4)

A

constipation,
black stool,
tachycardia and
shortness of breath.

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22
Q

The absorption of iron is enhanced by

A

sugars, amino acids, ascorbic acid, lactic acid, citric acid and hydrochloric acid.

The absorption of iron is inhibited by phosphates, oxalates and sodium carbonate solution (alkali).

23
Q

Iron salts become inactive when administered together with

A

tetracyclines, forming chelates, neither of them has any effect.

24
Q

Megaloblastic anaemia

A

Hyperchromic anaemia – Large-sized megaloblasts with increased haemoglobin content that replace normal erythrocytes.

abnormally large and immature red blood cells called megaloblasts. These cells are unable to divide properly, leading to fewer and larger red blood cells being released into the bloodstream.

25
Q

The primary cause of megaloblastic anemia is

A

a deficiency in vitamin B12 (cobalamin) or folate (folic acid), both of which are essential for DNA synthesis and red blood cell production.

26
Q

Where do ruminants, cats and dogs get B12 from?

A

Rumen microbes synthesize vitamin B12 in ruminants and intestinal bacteria synthesize vitamin B12 in non-ruminants.

Is also Found in dairy and meat, eggs.

27
Q

The reason for B12 deficiency is typically

A

absorption disorders, also intestinal parasites.

28
Q

in case of absorption disorders in the gastrointestinal tract, B12 is administered…

A

through the parenteral route.

Distributed quickly and evenly across the whole organism. Stored in the liver, inventories may last for 2-3 years.

29
Q

Why is vitamin B12 deficiency seen most quickly in the decrease of erythrocytes ie. anemia?

A

Because B12 is a key factor in the formation of DNA, necessary for the development of cell nuclei and cell proliferation. A deficiency will lead to an overall cell development and tissue growth disorder.

Erythrocyte-producing bone marrow is the tissue that grows and develops at the fastest rate, reflecting any vitamin B12 deficiency the fastest.

30
Q

Ruminants require what element for B12 synthesis?

A

Ruminants require cobalt for B12 synthesis.
A cobalt deficiency will disrupt vitamin B12 synthesis.

Grasses that have grown in boggy or sandy soil contain a lower than normal level of cobalt (hypocobalaminemia is also referred to as cobalt deficiency).

31
Q

Signs of cobalt deficiency disease are:

A

low hemoglobin content of blood,
pale-blue toned mucous membranes (anemia),
weight loss,
appetite disorder,
“frosted” fur.

Cobalt supplements are used for treatment, only through the oral route of administration.

32
Q

Treatment of anemia due to blood loss.

A

A blood transfusion is not always necessary (if the bleeding is under control) because the organism produces an increased quantity of erythrocytes due to a lack of oxygen.

Intake of fluids must be increased in order to restore blood volume.
Crystalloid solutions, colloid solutions.

If the blood loss endures, there will not be sufficient erythrocytes for oxygen transport, hemoglobin needs to be replaced (for instance a blood transfusion).

33
Q

Physiological hemostasis: Vascular and platelet phases.

A

After trauma, the vascular cell (vessel) contracts and platelets start adhering to the injury.

Vasoconstriction lasts 20-30 min.

34
Q

Substances enhancing blood coagulation, hemostatic drugs (name 4).

A

Thrombin
Fibrinogen
Calcium compounds
Vitamin K

35
Q

Describe Thrombin preparation for blood coagulation.

A

The medicinal product replaces the natural enzyme, induces the transformation of the fibrinogen contained in the blood into fibrin and blood coagulation can occur.

Only used locally in case of bleeding of parenchymal organs, in laryngeal and nasal surgery.

Thrombin must not be injected or otherwise allowed to enter large blood vessels.

Systemic administration will lead to thrombus formation and infarctions in vital organs.

36
Q

Describe fibrinogen preparation for blood coagulation.

A

Globulin as a medicinal product replaces the natural blood plasma fibrinogen.

It enhances blood coagulation and transforms into fibrin through the effect of thrombin and calcium ions.

It is administered systemically.

37
Q

Describe calcium preparations for blood coagulation.

A

Calcium chloride, calcium gluconate.

Blood coagulation factor. Activates the thromboplastin, enhances the transformation of prothrombin into thrombin and fibrinogen polymerization into fibrin.

Participates in the contraction of blood vessels, reduces bleeding and enhances blood coagulation.

38
Q

Describe vitamin K preparations for blood coagulation.

A

Fat-soluble vitamin.

Part of the coenzyme that participates in the synthesis of prothrombin (coagulation factor II) and proconvertin (coagulation factor VII) in the liver.

K1 – in plants
K2 – produced by microorganisms
K3 – synthetic derivative

The therapeutic agent of choice is K1.

A deficiency of vit K may occur after trauma and blood loss or due to poor absorption of vitamin.

Vitamin K is also administered in the event of anticoagulant poisoning (e.g. rodenticides containing coumarin, warfarin).

39
Q

Describe the Hemostatic agent - Etamsylate.

A

Antihemorrhagic, blood vessel protecting agent.

Increases resistance in the endothelium of capillaries.

Promotes platelet adhesion.

Inhibits biosynthesis and action of those prostaglandins which cause platelet disaggregation, vasodilation and increased capillary permeability.

Does not influence fibrinolysis, nor the amount of thrombocytes.

40
Q

Describe substances inhibiting blood coagulation, anticoagulants in general.

A

Direct acting anticoagulants are substances that reduce the activity of thrombin.

Indirect acting anticoagulants are substances that inhibit the formation of prothrombin.

Substances enhancing fibrinolysis.

Substances that bind calcium ions, i.e. blood stabilizers.

41
Q

Direct acting anticoagulants are substances that

A

reduce the activity of thrombin.

42
Q

Indirect acting anticoagulants are substances that

A

inhibit the formation of prothrombin.

43
Q

Give an example of a Direct-acting anticoagulant.

A

Heparin

44
Q

Describe heparin.

A

Heparin is an acidic mucopolysaccharide substance that prevents the formation of the prothrombin activator thromboplastin.

It also enhances fibrinolysis. In large doses, it inhibits the aggregation of thrombocytes and improves coronary blood circulation.

It is synthesized in Ehrlich’s mast cells when present naturally in an organism.

Medicinal heparin has both antithrombotic and anticoagulatory effects.

IV, SC and local administration.

45
Q

Indications for the use of heparin drug preparation.

A

Use of heparin (human med):
- Treatment and prophylaxis of thromboembolism.
- Treatment of myocardial infarction.
- Thrombophlebitis of extremities (heparin ointment).

In veterinary medicine:
- Arterial thrombi in cats
- Management of disseminated intravascular coagulation.
- Potentially hypercoagulable states (cardiomyopathy, nephrotic syndrome etc.).

46
Q

Why is Heparin unsuitable for the treatment of cerebral thrombosis?

A

it does not penetrate the blood-brain barrier.

Side effect is haemorrhage.

47
Q

What drugs reduce the effect of heparin? (4)

A

The following reduce the effect of heparin: aspirin, digitalis medications, antihistamines, tetracyclines.

48
Q

Give examples of Indirect-acting anticoagulants.

A

Vitamin K antagonists:
dicumarin,
neodicoumarin,
warfarin,
fenylin.

49
Q

Describe Indirect-acting anticoagulants.

A

Vitamin K antagonists such as warfarin.

The onset of the effect is 8 to 12 hours after administration and lasts for days until treatment is ended.

Used for the prophylaxis of thrombus formation, in case of thrombophlebitis, and in case of infarctions.

Contraindicated in the case of hemophilia, ulcers in the stomach and the duodenum, malignant tumors and after giving birth.

50
Q

Give an example of an antiplatelet drug.

A

Aspirin

51
Q

Describe asprin.

A

The only NSAID that in low doses irreversibly inhibits the cyclooxygenase that impacts thrombocytes.

After administration it causes quick and irreversible anticoagulation - thrombocytes reduce the production of enzymes necessary for aggregation.

The ability to coagulate will be restored with the creation of new thrombocytes.

52
Q

Example of a Blood stabilizer.

A

They are used for the stabilization of blood preserves.

E.g. Sodium citrate.

It is easily dissociated in the blood. The acid anion binds the Ca contained in the blood plasma into a poorly dissociable compound, therefore the concentration of Ca in the blood is reduced, formation of thromboplastin does not occur and prothrombin is not activated into thrombin and the coagulation of blood becomes slower.

53
Q

What is oxyglobin?

A

Oxyglobin, a hemoglobin-based oxygen-carrying fluid, is indicated in the treatment of anemia in dogs and may be life saving if compatible red blood cells are not available for transfusion.

Enhances the transport of oxygen in dogs by alleviating the clinical signs caused by anemia for up to a 24-hour period regardless of condition.

Not to be used in animals previously treated with oxyglobin as it is intended for single administration only.