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Pharmacology > Blood disorders and pharmacological management > Flashcards

Blood disorders and pharmacological management Flashcards

1
Q

What is the composition of blood?

A

Plasma
- Water 91%
- Proteins 7-9%
- Electrolytes and other substances <2%

Formed elements
- Leukocytes (WBC)–> Immune response
- Thrombocyte. (platelets) –> blood clotting
- Erythrocytes (RBC) –> oxygen and nutrient transport

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2
Q

What is albumin and what does it do?

A

Family of proteins

  • transporter protein
  • carries nutrients and drugs around the body
  • help control fluid in the blood, and balance osmolarity and viscosity. Soaks up water
  • acts as a pH buffer
  • carries Na, K and some vitamins

Most abundant protein in plasma

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3
Q

What is Fibrinogen?

A

Clotting factor

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4
Q

What are the most abundant plasma proteins and what do they do?

A

Albumin
- regulates osmolarity and viscosity
- pH buffer
- transports lipids, hormones, nutrients, minerals

Globulins
- solute transport –> fat-soluble vitamins, hormones
- clotting (prothrombin)

Fibrinogen
- Soluble precursor of fibrin (major protein in blood clots)

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5
Q

How are blood clots formed?

A

When a blood vessel wall is damaged RBC leaves the vessel and platelets start to club together and travel to the damaged site to try and fix the damage.
Platelets are activated which causes them to move and clump together

Fibrin helps to bind the blot together

Clotting reaction depends on whether the damage is intrinsic (internal) or extrinsic (external).
Cascade of reactions occur
Each pathway comes together at factor X, where it is then moved to the common pathway.
Thrombin produced which then leads to fibrinogen being activated into Fibrin and stable Fibrin clot being formed.

Vitamin K involved in clotting. Factors 2, 4, 7, 9, and 10 rely on Vitamin K in order to become activated.
New born babies given an injection as they don’t have any stores.

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6
Q

What does Thrombin do in terms of clotting?

A

It converts fibrinogen into fibrin which then forms a mesh-like network at the site of vascular damage

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7
Q

What are the causes of abnormal bleeding

A

Platelet disorders –> thromboytopeania

Failure of production
- B12/folic acid deficiency
- Aplastic anaemia (cells not being produced)

Excessive platelet destruction
- Liver disease
- Drug-induced (heparin)

Von Willebrand disease (congenital)
- Low levels of VW factor - essential for clotting

Coagualtion defects
- Liver disease –> effecting vitamin K levels and recycling capacity
- Haemophilia A (factor 8 missing)
- Haemophilia B/ Christmas disease (factor 9 missing)

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8
Q

What is the treatment for coagulation defects?

A

Intravenous engineered clotting factors
- human clotting factors produced in lab and given via IV
- not oral as the proteins would be broken down in digestion by enzymes

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9
Q

What is required for a homeostatic balance in clotting?

A

Balance between procoagulant and anticoagulant

Procoagulant
- PAI1 - plasminogin activating factor
- Tissue factor
- Antiplasmin
- Clotting factors

Anticoagulant
- Prot. S
- Prot. C
- TFPI
- Fibrinolytic system

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10
Q

What is thrombosis?
What can cause it?

A

Blood clots within the blood vessels

  • Deep/ superficial vein thrombosis
  • Atherosclerosis (plaque build-up, could rupture and release contents in the vessel causing a clot to form over the top of the atherosclerotic plaque, stopping any blood moving around the body from that point, damaging for the rest of the limb)
  • Disseminated intravascular coagulation (DIC)
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11
Q

What is Disseminated Intravascular Coagulation?
Causes?
Treatment?

A

An acquired syndrome characterised by the intravascular activation of coagulation.
Not linked to atherosclerosis.

  • Suppression of anticoagulant pathways
  • Impaired fibrinolysis (breakdown of fibrin mesh, causing the mesh to remain)
    Process leads to rapid consumption of clotting factors and platelets

Caused by
- Infection, immune response
- Trauma
- Cardiac arrest
- Severe allergic/ toxic reaction

Treatment
- Underlying cause must be reserved or controlled –> cause must be identified urgently

Morbidity and mortality high

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12
Q

What are anticoagulants?

A

Agents that prevent or delay blood coagulation by inhibiting one or more clotting factors

Two main types of oral anticoagulants
- Vitamin K antagonists (VKAs) e.g. Warfarin
- Direct oral anticoagulants (DOACs) e.g. Apixaban or Dabigatran

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13
Q

What is Apixaban?

A

Direct oral anticoagulant

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14
Q

What is Warfarin?

A

The most commonly used VKA
Comes from Coumarin derivative
0.1mg/kg BW tolerable daily (Coumarin)
High cinnamon intake can have a similar effect
Some people more sensitive to toxic effect in the liver than others
Taken orally, once a day, with or without food
Acts by inhibiting Vitamin K-dependent clotting factors (II, VII, IX, X)
In addition to inhibiting anticoagulant proteins C and S

Long half-life (26-40 hours)
Narrow useful window of effect
Has a toxic upper limit, the amount taken needs to be controlled
Bind to Albumin then becomes inactive
Interacts with Aspirin, NSAIDs, and some antibiotics

Reduced relative Vitamin K levels increased therefore increasing clotting with green vegetables where VK is present. Needs to be taken in balance with VK. VK can act as an antidote to warfarin.
Also interacts with green tea (antioxidants), pomegranate juice, alcohol

Risk of bleeding

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15
Q

What does warfarin interact with?

A

Aspirin, NSAIDs, some antiobiotics
Green tea, pomegranate juice, alcohol
Vitamin K food sources

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16
Q

What are some alternatives to Warfarin?

A

Rivaroxaban, Dabigatron, Apixaban, Edoxaban

Apixaban, edoxaban, and rivaroxaban are direct and reversible inhibitors of factor Xa (inhibition of factor Xa prevents thrombin generation and thrombus develpoment0

Dabigatran is a reversible inhibitor of free thrombin fibrin-bound thrombin and thrombin-induced platelet aggregation

Tablet form, with food and water
Short acting, must be taken at the same time every day

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17
Q

What is low molecular weight heparin?

A

Naturally occurring in mammals
Binds to circulating protein antithrombin III and activates it
Prevents clotting cascade
Formation of prothrombin to thrombin and fibrin production halted (common pathwa)

Intravenous or subcutaenous injection
- 1-2 hour delay in effect

Used to treat and prevent DVT, pulmonary embolism
Immediately following myocardial infarction
Blood clots that are blocking peripheral artey acute ischaemia
Preventing blood from clotting during haemodialysis
Short half life, 30 minutes at low does

Can’t be used during surgery
No food interactions as not taken orally

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18
Q

Why does Heparin not interact with food

A

Not taken orally, as subcutaneous or intravenous injection

19
Q

What are fibrinolytics?

A

Thrombolytic agents - dissolve blood clots

Taken IV, no food interaction

Streptokinase, Alteplase, Eteplase, Tenecteplase and Urokinase

20
Q

What is Streptokinase?

A

A fibrinolytic
- Purified fibrinolytic bacterial protein
- Activates plasminogen to form plasmin which degrades fibrin and some breaks up thrombi
- Given in emergency situation
- DVT, acute myocardial infarction, PE

21
Q

Why is Aspirin a popular drug for helping with blood disorders?
Describe Aspirin

A

Antiplatelet drug and NSAID
- Reduces risk of myocardial infarction in patients with anigina
- Increases survival with acute MI
- Reduces risk of strokes

Taken with food, or just after food. Not on an empty stomach, due to NSAID complications

22
Q

How does Aspirin work as an antiplatelet drug?

A

Inhibits the production of Thromboxane A2 (which increases platelet stickiness)
- Inhibits platelet adhesion and aggregation for the entire lifespan of the platelet (8 days)
- Prevents platelet stickiness
- Dose vary with condition
- Normal platelet function returns 36 hours after last dose

Clopidogrel is similar to aspirin and can be taken in together for a limited period of time. Increased risk of bleeding in the gut.
With or without food

23
Q

What are anticoagulants prescribed for?
Give examples

A

Arterial and venous thrombosis

Warfarin
Low Molecular Weight Heparin
Direct Oral Anticoagulants e.g. Apixaban

24
Q

What are antiplatelets prescribed for?
Give examples

A

Arterial disease

Aspirin
Clopidogrel

25
Q

What are fibrinolytic prescribed for?
Give examples

A

Arterial and venous thrombosis

Streptokinase
Alteplase

26
Q

What is Normocytic anaemia?

A

Anaemia due to inflammation of chronic disease or acute blood loss

27
Q

What could cause small RBC?

A

Microcytic anaemia - may be caused by iron deficiency

28
Q

What could cause large RBC?

A

Macrocytic anaemia - may be due to B12 or folate deficiency, liver disease or toxicity

29
Q

What does Haematocrit (Hct) show?

A

% of blood made up by RBC

30
Q

What does a red cell count show?

A

Number of red blood cells present per unit of volume of blood

31
Q

What is a reticulocyte count?

A

A measure of newly formed, immature RBC. Indicates recent bone marrow function

32
Q

What is mean corpuscular haemolgobin?

A

The average mass of Hb per RBC

33
Q

What are the most common causes of anaemia?

A
  • Nutritional deficiencies (especially iron deficiency, folate and B12 and A - involved in RBC production)
  • Infectious diseases e.g. malaria, tuberculosis, HIV and parasitic infections
  • Haemoglobinpathies
  • Heavy blood loss
  • Excessive RBC destruction
  • Lack of new RBC being formed (e.g. from a bone marrow tumour)
  • Sickle cells anaemia
  • Bone marrow tumour or infection
34
Q

What are some common symptoms of anaemia?

A
  • Fatigue
  • Lack of energy
  • Breathlessness
  • Headaches
  • Fainting/ lightheadedness
  • Palpitations
  • Pale skin

Iron deficiency anaemia
- Koilonychia -> spoon-shaped tongue
- Smooth tongue, Angular Chelitis
- Dysphagia - Cricoid web, an abnormal extension of oesophageal tissue

35
Q

What are the different types of RBC cause anaemia?

A

Microcytic - e.g. iron deficiency
Macrocytic - e.g. vitamin B12 deficiency
Depleted - e.g. aplastic anaemia
Deformed - e.g sickle cell anaemia

36
Q

What forms does iron come in in the diet?

A

Ferrous iron –> in meat, readily absorbed
Ferric iron 00> in vegetables, inefficiently absorbed. Ascorbic acid helps convert to ferrous iron for absorption

Tea can prevent iron absorption

37
Q

How is anaemia treated?

A

Look at diet, cells under a microscope, blood loss.
FInd cause and treat cause.
Advise adequate iron intake
Consider dietetic referral
Supplementation for 3 months, side effects such as constipation may occur. Taken with food

38
Q

What is Anaemia of chronic disease?

A

Anaemia prevalent in patients with diseases that cause prolonged immune activation, including infection, autoimmune diseases, cancer, CKD, congestive heart failure, CPD and obesity.

Inflammation inducible cytokines and the master regulator of iron homeostasis, hepcidin, block intestinal iron absorption and cause iron retention in reticuloendothelial cells, resulting in iron-restricted eryhtopoesis

39
Q

How is anemia of chronic disease treated?

A

Treatment of the disease underlying the anaemia
Combination of iron therapy and eryhtropoiesis-stimulating agents
- iron supplementation (oral/IV)
- blood transfusion
Use of anti-inflammatory food supplements: fatty acids and vitamin D
Future treatment targeting at the genes coding inflammatory cytokines

The clinician needs to consider the contribution of anaemia to patient morbidity and the impact of anaemia treatment on the patient’s prognosis.

40
Q

Describe Macrocytic Anaemia
Causes?

A

B12 and folic acid deficiency
Otherwise known as Megaloblastic anaemia

Anaemia characterised by
- Megaloblasts in bone marrow
- Lave oval macrocytic erythrocytes

B12 and folic acid essential for normal bone marrow function.
B12 essential for normal function of cells in nervous system

  1. Malabsorption
    Pernicious anaemia
    - an autoimmune disorder
    - strong familial tendency
    Gastrectomy –> cells removed that produce intrinsic factor
    Ileum diseases
    - not absorbing B12
  2. Inadequate intake of food containing B12
    - Animal products
    - Marmite
    - Fortified foods
41
Q

What are the signs and symptoms of Pernicious Anaemia?

A

Commonly found in middle aged-elderly, usually women
Slow onset over several years
Lemon complexion - excess bilirubin as fragile erythrocyte disintegrate
- Sore mouth

Neurological problems
- Demyelination of neural axons
- Sensations altered (peripheral neuropathy)
- Memory problems
- Leg pains
- Ataxia and weakness

42
Q

How is Pernicious Anaemia diagnosed and treated?

A

Diagnosis
- FBC - macrocytic cells, low serum B12, folate deficiency

Treatment (without nerve problems)
- Vitamin B12 supplements, usually injection
- Initial treatment with hydroxocobalamin 1mg intramuscularly three times a week for 2 weeks
- Maintenance treatment with hydroxocobalamin 1mg intramuscularly every 3 months for life - when B12 deficiency is not thought to be diet related
- Maintenance treatment with oral cyanocobalamin tablets or twice yearly 1mg injection - where vitamin B12 is thought to be diet related.

Treatment (with nerve problems)
Seek urgent specialist hematologist advice
- Initial treatment - Hydroxocobalamin 1mg intramuscularly on alternate days until there is not further improvement, then every 2 months
Treatments may be needed throughout life

Cautions:
- Some medicines such as metformin can affect B12 absorption
- Long-term use of medicines that effect stomach acid production e.g. PPI can worsen B12 deficiency

43
Q

What are some plant-based sources of B12

A

Fortified…
- Milk alternatives
- Soya yoghurt alternatives
- Yeast extract e.g. marmite
- Breakfast cereals

44
Q

How does intrinsic work with B12?

A

When foods are eaten with B12, its needs to be protected until where its absorbed in the ileum, the stomach coats it with intrinsic factor - produced by parietal cells of gastric muscosa.

B12 binds with IF as protection from digestion by

in the ileum it is bind to mucosal receptors and transported across the musocsa into bloodstream and freed of IF and bound to plasma globulins, transcobalamin I, II and II.
Then goes to bone marrow or stored in liver.

Pharmacology (8 decks)

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