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1

4 phases of pharmacokinetics:

Absorption
Distribution
Metabolism
Excretion

2

Absorption:

Process by which an unchanged drug moves from the site of administration to the blood.

3

Metabolism:

Chemical modification of the drug by enzymes.
It is important to consider the first pass effect, genetics and the 2 phases: Functionalisation and conjugation.

4

Distribution:

Irreversible transfer of the drug from one location to another.

5

First pass effect:

Orally delivered drugs circulate through liver before reaching systemic circulation.
The effect of liver metabolism determines the amount of drug reaching the circulation.

6

Excretion:

Irreversible loss of the drug from sites of measurement.
Lipid soluble drug metabolites in filtrate return to plasma.

7

Enterohepatic cycling:

Drug and drug metabolites present in bile that enter duodenum become available for reabsorption. They are returned to the liver via hectic portal vein.

8

Adipose tissue in regards to drug:

Acts as a stable reservoir. Holds a high affinity for lipid soluble drugs so the drug can stay in the tissue and not make its way back to the liver for metabolism.

9

Lipid soluble drugs:

Can diffuse across the phospholipid cell membrane. Need plasma protein for binding.

10

Un-ionised drugs:

Are lipid soluble and can cross the phospholipid cell membrane.

11

Ionised drugs:

Are a charged polar form. Is water soluble which means it can not pass the phospholipid cell membrane.

12

Half-life:

The amount of time it takes for the concentration of the drug to reduce by half.

13

Functionalisation metabolism:

Add a chemical group to produce more water soluble products to be excreted. Involves P450 enzymes.

14

Conjugation metabolism:

Adds a chemical group to a molecule that is polar. This increases water solubility which enhances renal excretion. Involves a wide range of enzymes.

15

What implications might renal failure have on half-life and what effect will it have?

The kidneys are responsible for excreting drugs in urine, so if they are failing then the drugs will be reabsorbed back into the blood and will continue circulating. Therefore if another dose is given it increases the risk for toxicity and overdose.

16

Agonist drug:

Produces a functional response such as opening ion channels and activating receptors. It is determined by the role of the receptor. Partial agonist = Produces less than maximal effect.

17

Antagonist drug:

Blocks a response. Binds but produces no functional response, eg. deactivate enzymes.
Competitive antagonist = Competes for binding site. Will not have a permanent effect.
Competitive irreversible antagonist = Receptor becomes permanently blocked.

18

Prophylaxis:

Prophylaxis is a preventative strategy. It is an agent given to prevent onset of a disease process eg. antimalarial drugs given prior entry to a malaria carrying mosquito region.

19

What characteristics make up a useful drug:

- High efficacy.
- It is specific to its target.
- Has to be efficient.
- Has to be potent enough to do its job.
- It is selective.

20

Necrosis:

- Uncontrolled cell death.
- Lack of supply of oxygen or glucose - cannot maintain ATP - cannot drive sodium potassium pump - cells swell - cells burst.
- Uncontrolled release of cytoplasmic contents initiates the inflammatory response.

21

Apoptosis:

- Programmed cell death.
- Condensation of chromatin - memrane blebs - cellular fragmentation - phagocytosis of cells and fragments.

22

Atrophy:

Decrease in cell SIZE, eg. muscle wastage, neuro wasting in alzheimers disease.

23

Hypertrophy:

Increase in cell size eg. building muscle, hypertension 0 cardiac hypertrophy.

24

Hyperplasia:

Increase in number of cells eg. wound healing

25

Dysplasia

Deranged growth e.g.. epithelial dysplasia of the cervix

26

Metaplasia:

Change from one cell type to another eg. cell changes from smoking

27

Anaplasia:

Change from mature cell to immature cell type e.g. neoplastic cells

28

What is gene mutation? How might the environment lead to mutation?

Gene mutation is the alteration of DNA. The mutations are only important if they change the protein of that gene.

29

Clinical manifestations of cancer and how they occur:

Pain:
Increased risk of infection:
Anaemia:
Thrombocytopenia:

30

Pain causes in cancer:

Caused by the tumour causing pressure, obstruction, tissue destruction and inflammation.

31

Anaemia causes in cancer:

Caused by chronic bleeding resulting in iron deficiency, severe malnutrition, medical therapies

32

Increased risk of infection in cancer:

Caused by leucopenia, due to direct tumour invasion of the bone marrow.

33

Thrombocytopenia in cancer:

Caused by malignancy in blood-forming organs, suppression of the bone marrow by disease or treatment

34

Weight loss in cancer:

Anorexia, early satiety, taste alterations, and altered metabolism.

35

Different types of pain:

Nociceptive pain: External damage or Internal damage that is detected by noiceoceptors
Visceral pain: Walls of the visceral organs. Deep, aching pain.
Somatic pain: Originates in the skin, external facing environment. Burning, throbbing pain.
Acute pain: Usually sudden
Chronic pain: Defined as pain that lasts that exists for longer than 3 months
Neuropathic: Nerve pain. No physical damage, apart from the nerve itself. Burning, tingling pain.

36

Right sided heart failure:

Blood in right ventricle is not going to be squeezed out into the pulmonary artery to the lungs = decreased amount of blood making it to the lungs and back up of blood through the right atrium.
Jugular vein distention is seen.
Symptoms:
SOB
Frequent urination
Weakness

37

Left sided heart failure:

Left ventricle is not squeezing blood out through aorta effectively, this leads to a decreased amount of blood going to the body. The blood that is coming from the left atrium will back up to the lungs.
Symptoms:
Dyspnoea
Fatigue
Orthopnoea

38

Cytotoxic drugs slow or stop the effects of neoplastic cellular changes?

Anti-metabolites – Inserts a false building block in metabolic pathway. Site of action is DNA synthesis.
Alkylating agents - Cross link strands of DNA preventing replication. Site of action is DNA synthesis.
Anti-tumour antibiotics – Block DNA to RNA transcription.
Mitotic inhibitors – Block metaphase. Site of action is Metaphase.
Draw diagram.

39

What happens when there is too much calcium in the blood? What happens when there is too little calcium in the blood?

Too much:
Increased thirst and urination
Stomach pain
Bone pain
Nausea
Too little:
Muscle cramps
Confusion
Tingling in lips and fingers

40

How do the symptoms of hypercalcaemia arise?

Hypercalcaemia can arise from Hyperparathyroidism. This means overactivity in the parathyroid glands. Other causes of hypercalcemia include Vitamin D pathway failure.

41

How do the symptoms of hypocalcemia arise?

Usually due to hypoparathyroidism. This regulates calcium and phosphorus. Hypoparathyroidism is the state of decreased secretion or activity of parathyroid hormone.

42

What is anaphylaxis? What is anaphylactic shock?

Anaphylaxis is an allergic reaction to an antigen to which the body has become hypersensitive. Anaphylactic shock is the result of widespread hypersensitivity reaction. The onset is sudden and progress rapidly to death. Treatment includes adrenaline which reverses vasodilation & bronchial constriction, fluids which reverse relative hypovolaemia and antihistamines which stop the inflammatory reaction.

43

Asthma physiology:

1. Antigen/allergy enters the airway.
2. Mast cell degranulates and releases histamine.
3. Histamine causes brochoconstriction which narrows the airway.
Goblet cells increases mucus secretion.
Increase of vascular fluid causes airway oedema.
Inflammatory cells damage airway epithelium reducing cilia.
4. These all increase airway resistance.
5. Which causes air to become trapped which leads to impaired gas exchange.

44

Manifestations of asthma:

Wheeze on exhalation due to air pushing past mucus obstruction.
Increased use of accessory muscles.
Cracking noises from fluid build up in lungs.
Cough attempting to open airway by excreting excess mucous.

45

Bacterial pnemonia:

Much quicker and less severe. Failure of first-line defence mechanisms to contain microbe which initiates inflammatory response. This causes damage to mucous and capillary membrane, causes an increase in mucous and exudate in the alveoli. Can overflow to other alveoli and spread the infection.

46

Viral pnemonia:

Viruses invade goblet cells causing mucous hypersecretion.
Viruses can also damage ciliated epithelial cells leading to a secondary bacterial infection as mucous is not moving up and out.

47

Cardinal signs of inflammation and how do they manifest:

Redness: Due to increased blood flow to the area
Heat: Due to increased blood flow to the area
Swelling: Due to accumulation of fluid
Loss of function: Combination of these factors
Pain: Due to release of chemicals that stimulate nerve endings