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Sam Pharm Cards > Exam Prep > Flashcards

Exam Prep Flashcards

1
Q

What is a receptor agonist?

A

An agonists is a drug that activates a receptor and takes the place of the endogenous ligand.

100% efficacy

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2
Q

What is a receptor antagonist?

A

An antagonist is a drug that binds to a receptor to limit its activity by blocking the binding site of the endogenous ligand to the receptor.

Zero efficacy

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3
Q

Define efficacy

A

The ability of a drug to produce its biological response

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4
Q

Define potency

A

How much of the drug is required to produce a response.

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5
Q

PK Antagonism is

A

Where the antagonist effectively reduces the concentration of the active drug at its site of action by affecting its PK.

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6
Q

PK Agonism is

A

Where the PK of Drug A is affecting PK of Drug B leading to an increase in activity of Drug B

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7
Q

What are the 2 types of Competitive Antagonism and give a brief description of each.

A

Reversible competitive antagonism - is when the antagonist competes with the agonist for the same binding site. Maximal response to the agonist can still be achieved but requires higher dosage.

Irreversible competitive antagonism - is when the antagonist dissociates very slowly or not at all from the receptor.

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8
Q

What is Non competitive antagonism?

A

This refers to antagonist and agonist binding to different receptor at different sites, or one drug inhibits the activity of the other drug by altering cell signalling down stream of the receptor.

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9
Q

What are the different types of drug targets?

A

Receptors
Enzymes
Ion channels
Transporters

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10
Q

What are the types of receptor proteins?

A

Ligand gated ion channels
G-protein coupled receptors
Kinase-linked receptors
Nuclear proteins

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11
Q

Factors that influence the passage of drugs across barriers are:

A

Molecule size

Lipid solubility

Ionisation (if ionised won’t be able to cross membrane due to having low lipid insolubility however, it will be highly water soluble)

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12
Q

How are drugs mostly excreted from the body?

A

Most commonly in the urine and to a lesser extent in the faeces. Some are exhaled.

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13
Q

What is first-pass metabolism?

A

The hepatic and intestinal degradation or alteration of a drug taken ORALLY, after absorption, removing some of its active substance from the blood before it enters general circulation.

Drugs that undergo first-pass metabolism will have reduced bio-availability.

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14
Q

List the common modes of drug administration.

A 
Oral
Intravenous injections & infusions 
Intramuscular injections 
Subcutaneous injections
Inhalation 
Sublingual
Application 
Rectal
Other specialised routes eg. joints or spine
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15
Q

Where are drugs most commonly metabolised and what are the consequences?

A

Liver (if you don’t get that fuuuuck me)

Inactivation of a drug
An increase or change in drug action
Activation of a prodrug
Alteration of drug toxicity

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16
Q

Disorder:

A

This describes an abnormality of function

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17
Q

Syndrome:

A

A set of clinical manisfestations that occur together in a condition in which the cause is unknown.

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18
Q

Disease:

A

Has a well-defined cause, clinical manifestations and a corresponding set of diagnostic and treatment strategies.

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19
Q

Acute:

A

Describes a condition that develops and resolved quickly.

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20
Q

Chronic:

A

Describes a condition that develops more gradually and lasts longer.

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21
Q

Aetiology:

A

Describes the underlying cause.

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22
Q

Epidemiology:

A

The study of factors that affect the health populations.

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23
Q

Incidence:

A

The number of new cases diagnosed per unit of time.

24
Q

Prevalence:

A

The total number of people who are affected by a disease at a particular time, regardless of either they have been diagnosed for a short or long time.

25
Q

Morbidity:

A

Describes the proportion of the population with the disease.

26
Q

Comorbidity:

A

Describes the presence of another disease/condition in the same patient.

27
Q

Mortality rate:

A

Describes the death rate from a disease, disorder or syndrome.

28
Q

List the 5 types of necrosis:

A 
Coagulative necrosis
Liquefactive necrosis 
Caseous necrosis 
Fat necrosis 
Gangrenous necrosis
29
Q

What is necrosis and what are the two phases?

A

Necrosis describes the sum of cellular changes after after local cell death and the process of cellular auto digestion.

Karyolysis is where there is nuclear dissolution and chromatin lysis.

Pyknosis is characterised by clumping of the nucleus.

30
Q

What is cyclosporin?

Include it’s MOA and effect.

A

Blocks IL-2 synthesis and down regulates the proliferation of T cells (less T helper and cytotoxic T cells). This reduces cell mediated immunity and B cell activation.

Unwanted effects include nephrotoxicity.

31
Q

What is Azathioprine?

Include MOA and effect.

A

Inhibits DNA synthesis leading to an inhibition of all cell proliferation including both T & B cells. (Suppresses both arms of adaptive immunity)

Due to DNA synthesis being inhibited it’s is also cytotoxic to all dividing cells not just T & B lymphocytes.

Depression of bone marrow is a major unwanted effect.

32
Q

Glucocorticoids

A

Blocks cytokines synthesis, inhibits not cell mediated and adaptive immunity. Also inhibits inflammation by inhibiting inflammatory cell mediators and promoting synthesis and release of endogenous anti-inflammatory proteins.

33
Q

What are monoclonal antibodies?

List some advantages and disadvantages.

A

Uses own body response to fight cancer by stopping growth of blood vessels to a tumour, or by stimulating own immune system to attack and lyse tumour cells (NK cells)

A disadvantage is the response is very narrowly targeted, therefore the specific antigen must be present on the cancer cells for it to work.

34
Q

Systemic Lupus Erythematosus - Effects

A

Causes destruction of multiple tissues

Auto-antibodies & immune complexes cause destruction of multiple tissues (eg. musculoskeletal, skin, CV, lung, kidney and CNS tissues)

Auto-antibodies target components found in the cell nuclei (eg. DNA, RNA & Nuclear proteins)

RBC & Plasma proteins are also affected

35
Q

Systemic Lupus Erythematosus - Causes/RF and Symptoms

A

Causes + RFS:
Genetic predisposition (HLA types)
Environmental triggers - exposure to UV, chemicals, some food, infectious agents

Symptoms (depends on tissue affected):
Joint pain 
Butterfly rash, hair loss and sun sensitivity 
CNS effects
Proteinuria & oedema 
Pericarditis & hypertension
36
Q

COX1

A

Plays a major role in house keeping roles including protection of gastric mucosa, platelet aggregation and renal blood flow.

37
Q

COX2

A

Expressed mainly in inflammatory cells when activated leading to the production of inflammatory mediators.

38
Q

DMARD

A 
Slow onset
Delays progression of disease
Reduces number of swollen joints 
Decrease pain
Increase QOL
Decrease progression of bone & joint damage
39
Q

Polyuria and glycosuria (DM)

A

Polyuria: Excessive urination

Occurs due to high levels of glucose in the filtrate (water isn’t able to be reabsorbed due to high solute concentration) - insufficient number of glucose transporters.
Excessive glucose in the urine leads to glycosuria.

40
Q

Polydipsia and Polyphasia (DM)

A

Polydipsia is due to the effect of polyuria decreasing BV and increasing the solute concentration with in the blood - this stimulate thirst sensation (polydipsia).

Polyphagia (T1DM) occurs because glucose is not being taken up into the cells and there is erratic carbohydrate, protein and lipid metabolism. The satiety centre in hypothalamus is also involved.

41
Q

Ketoacidosis

A

Type 1 DM

Unopposed action of glucagon > Lipolysis

Fatty acid breakdown generates ketone bodies which are acidic and can lead to metabolic acidosis. This can be triggered by stress which causes an increase in adrenaline and cortisol. pH decreases and this can lead to stupor and coma.

Rapid deep breathing to increase ventilation and to compensate for low pH

42
Q

Hyperosmolar coma

A

Occurs in Type 2 DM

Hyperglycaemia causes a hyperosmolar state. This leads to diuresis, hypovolaemia and water movement out of cells into the blood. This can result in severe dehydration leading to stupor and coma.

43
Q

Microvascular (Long-term complication of DM)

A

Thickening of the basement membrane and endothelial hyperplasia. This leads to ischemia, neuropathy, nephropathy and retinopathy.

44
Q

Macrovascular (Long-term complication of DM)

A

Damage to medium and large arteries resulting in atherosclerosis and thrombosis. Leads to CAD, stroke, gangrene and cardiomyopathy.

45
Q

Why does increased infections happen in DM?

A

Occurs due to poor wound healing. This results from poor circulation (hypoxia) and hyperglycaemia. This increased glucose provides an energy source for pathogens and the reduced circulation means there is poor delivery of WBCs and chemical mediators. There is also reduced sensation due to glucose damaging nerves.

46
Q

Why does insulin need to be administered and through what mode?

A
  1. They no longer produce or produce very little endogenous insulin.
  2. Subcutaneously due to insulin being a protein and would be digested by pepsin in the stomach if administered orally.
47
Q

Causes of cellular injury (6)

A

Hypoxia
Nutritional imbalances
Chemical agents (altered cellular permeability)
Physical agents (temperature, sunlight & trauma)
Infectious agents (toxins)
Genetic causes

48
Q

Free Radicals, Reactive Oxygen Species & Altered Calcium Homeostasis

A

FRs and ORS are an electrically uncharged atom or group of atoms having an un-paired electron that causes damage via: lipid peroxidation, alteration of protein, alteration of DNA or mitochondrial oxidative stress.

Alteration to calcium homeostasis leads to damage to mitochondria and reduced capacity to produce ATP. It also causes the activation of destructive enzymes which will cause inappropriate protein digestion and nuclear damage. Thirdly, it causes the breakdown of cell membranes and cytoskeleton leading to altered permeability.

49
Q

3 main functions of NSAIDS

A
  1. Decrease fever by inhibiting IL-1 stimulated prostaglandin pyretic activity.
  2. Decrease pain by decreasing nocioceptor activity sensitivity to inflammatory mediators like bradykinin and decreasing neural transmission to spinal cord.
  3. Decrease vasodilation which will reduce blood flow, oedema and possible headache
    This is achieved through the inhibition of prostaglandin synthesis.
50
Q

Biguanides (OH)

A

MOA:
• Increase glucose uptake and utilisation in skeletal muscle
• Reduces gluconeogenesis
• Reduces LDL and VLDL
• Increases insulin sensitivity (^ receptors & affinity)
• Unlikely to cause hypoglycaemia
• Contraindicated in patients at greater risk of lactic acidosis

51
Q

Sulfonylureas (OH)

A

MOA:
• Stimulate insulin secretion (by depolarising beta cells)
• Increase insulin sensitivity
• Decrease glycogenolysis & gluconeogenesis
• Decrease BGL
• Always taken with food to avoid hypoglycaemia
• Bind strongly to albumin
• Most common adverse effect is hypoglycaemia
• Others include weight gain, rashes, GIT disturbances

52
Q

Repaglinide (OH)

A
  • Stimulates beta cells of pancreas to produce insulin
  • Improves insulin secretion in response to glucose load
  • similar mode of action to sulfonylurea (acts on ATP potassium channels)
  • Adverse effects include hypoglycaemia and GIT disturbances
53
Q

Glitazones (OH)

A
  • Enhances sensitivity of peripheral tissues and liver to insulin
  • Reduces insulin resistance
  • Alters gene expression to alter glucose & lipid metabolism
  • Increases glucose uptake
  • Effect on insulin occurs after a few weeks
  • Adverse effects include anaemia, peripheral oedema, weight gain and increased risk of heart failure
54
Q

Incretin enhancers

A
  • Mimic effects of incretins (released in response to food and signal pancreas to release insulin)
  • Slow gastric emptying
  • Reduce appetite
  • Can reduces glucagon secretion
55
Q

Alpha-glucosidase inhibitor

A
  • Delays digestion and absorption of carbohydrates
  • Leads to smaller increase in BGL after meals
  • Common adverse effects include flatulence, loose stools and abdominal pain

Sam Pharm Cards (1 decks)

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