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WEEK 1 Flashcards

1
Q

Aetiology :

A

Study of causation or origination

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2
Q

Pathogenesis :

A

Development of disease

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3
Q

Aetiology

A 
Inherited or familial
Congenital
Toxic
Infectious
Traumatic
Degenerative
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4
Q

Pharmacodynamics
vs
Pharmacokinetics

A 
Drug-receptor interaction
Patient’s functional state
Placebo effects
vs
Absorption
Distribution
Metabolism
Excretion
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5
Q

Healthcare professional Responsibilities

A

1.Pre-administration assessment
Baseline data
Stratification of risk

2.Planning and Implementation: Dosage and Administration
Understand the correct dosing range
Appropriate safety measures

3.Evaluating and Promoting Therapeutic Effect
Evaluating Therapeutic Response
Promoting compliance/adherence
Implementing non-drug measures
Minimize Adverse Effects
Minimize Adverse Interactions
Managing Toxicity
Patient education
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6
Q

Approval of Drugs: Drug Legislation?

A

1906: A drug must be what it says it is
1938: Drugs must be tested for safety and approved by FDA
1962: Drugs must be effective for what they claim: testing procedures
1970: Controlled Substances Act
1992: Relaxed procedures for Cancer and AIDS drugs
1997: FDA Modernizing Act
Fast track for AIDS, cancer, and other life threatening conditions
Manufacturers must give 6 month notice before discontinuing a drug
FDA can require testing in children
Clinical trial database
Drug companies can provide physicians with articles on “off-label” uses

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7
Q

Drug Approval: Process

A 
1.Preclinical testing
Toxicity
Pharmacokinetics
Possible Useful Effects
2.Clinical Testing (in Humans)
Phase I: Normal subjects; metabolism and side effects
Phase II: Patients, therapeutic utility and dosage range
Phase III: Patients; safety and effectiveness
Conditional Approval
Phase IV: Posmarketing Surveillance
3.Limitations of Process
Women and children
Failure to detect all adverse effects
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8
Q

P450 cytochrome system

A

hepatic microsomal enzyme system

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9
Q

metabloism Considerations

A

Inductions of P450 system
Competition between drugs
First Pass Effect
Nutritional status

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10
Q

Renal Drug Excretion

A

Glomerular Filtration
Passive Tubular Reabsorption
Active Tubular Secretion

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11
Q

Pharmacodynamics

A 
1.Dose – Response Relationships
Maximal Efficacy
Potency
2.Drug – Receptor Interactions
Receptor-Types
Selectivity
Theories
Mode of Action
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12
Q

Mode of Action

A

Agonists
Antagonists
Partial Agonists
Regulation of Sensitivity

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13
Q

Drug Interactions

A 
1.Drug-Drug Interactions
Intensification: Effect and/or Adverse Effects
Reduction
2.Food-Drug Interaction
Absorption
Metabolism
Toxicity
Action
3.Food-Herb Interactions
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14
Q

Idiosyncratic:

A

also known as type B reactions, are drug reactions that occur rarely and unpredictably amongst the population

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15
Q

Iatrogenic (i·at·ro·gen·ic) :

A

refers to being caused by the action of doctors and/or surgeons

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16
Q

Physical Dependence:

A

state resulting from chronic use of a drug that has produced tolerance and where negative physical symptoms of withdrawal

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17
Q

Carcinogenic:

A

capable of causing cancer

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18
Q

Teratogenic:

A

an agent, which can cause a birth defect

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19
Q

What Is a cell?

A

Basic functional unit of the body

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20
Q

eukaryotic cells and the three major componests

A

(cells with a true nucleus)
1/ plasma membrane
2, nucleus
3. cytoplasm

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21
Q

ribosomes

A

syn proteins and other materials for cell function

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22
Q

the nucleus

A

Contains DNA, RNA, nuclear proteins
Nuclear membrane
Chromatin (during mitosis becomes chromosomes)
Nucleolus

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23
Q

Lysosomes

A
  1. Originate from enzymes in Golgi apparatus walls
  2. Give rise to residual bodies (lipofusion)
  3. digestion of the cell
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24
Q

Lipofusion

A

Brown pigment composed of oxidized lipids
Also known as “brown fat of aging”
“Undigested complex lipids”
Accumulates in aging tissues

25
Cytoskeleton
Cell shape | External pressure, cell movement
26
cytoskeleton Consist of three types of filaments:
Microtubules (22 nm): composed of tubulin Microfilaments (5 nm): composed of actin and myosin Intermediate filaments (10 nm): composed of cell-specific proteins
27
Plasma Membrane composd of
proteins, lipids, carbohydrates
28
DNA is imporant because
it provides info nesscary for for the synthesis of the various proteins that the cell must produce to stay alive and genetic info
29
er
tubular communication system through which substances can be transported from one part of the cell to another and protin synthesis
30
golgi app
modifies syn shit from the ER and then packs them into granules for transport
31
mitochondria
have their own dna
32
autocrine secretion
has its own chemical messenger/ receptrs on the one cell
33
paracrine secretion
one cell has chemical messenger to many receptors on other cells
34
endorine secretion
chemical messengers sent through capillaries to receptors in another tissue
35
Imbalance in homeostasis can cause:
Cell injury | Cell death
36
Reversible cell injury VS | Irreversible cell injury
Cellular swelling vs Cell death
37
necrosis
Necrosis: localized death of cells or tissues in living organisms
38
apoptosis
-programmed death of single cells within living organisms
39
Necessities for the Movement of Substances across the Plasma Membrane
To transport nutrients into the cell For gases exchange To excrete metabolic waste To maintain the pH value and ionic concentration of the cell
40
Causes of Cell Injury
``` Hypoxia Anoxia* Microbes Inflammation Immune reactions Genetic & metabolic disorders ```
41
Hypoxia
Hypoxia refers to low oxygen, usually less than 2 mg/L of dissolved oxygen (DO) in aquatic ecosystems,
42
anoxia
means a complete absence or total lack of oxygen.
43
Cell Hypoxia
Cellular swelling (which is associated with hypertrophy) is due to cellular hypoxia, which damages the sodium-potassium membrane pump. This in turn changes the intracellular electrolyte balance with an influx of fluids into the cell, causing it to swell.
44
Toxic Cell Injury
Direct toxin: heavy metals (i.e., mercury) disrupt S-S bonds – DNA damage Indirect toxin: carbon tetrachloride metabolized in liver to form carbon trichloride, which is more toxic Transient or reversible if stress removed May present diminished cellular or tissue capacity
45
peremanment cell damage
neurons skeletal and cardiac muscle
46
Viruses:
“exploit and control or kill cells from within”
47
Cell Adaptations
Occur as result of prolonged exposure to adverse or exaggerated normal stimuli ``` Main forms of adaptation: Atrophy Hypertrophy Hyperplasia Metaplasia Intracellular accumulation ``` Plasia: development (number) Dys: abnormal Trophy: growth (size)
48
Atrophy
Decrease in size of cell, tissue, organ, or entire body: Physiologic & predictable: atrophy caused by aging Pathologic: lack of nutrition, chronic ischemia, denervation, inactivity
49
Intracellular Accumulations
``` Exogenous materials Coal particles (anthracosis) ``` Endogenous metabolites Hemosiderin (in iron overload condition) Lipids
50
Types of Necrosis
Coagulative necrosis: most common form Liquefactive necrosis: in brain Caseous necrosis: tuberculosis Enzymatic fat necrosis: acute pancreatitis
51
Coagulative Necrosis
Its morphological pattern is primarily a consequence of protein degradation frequently caused by ischemia where lack of oxygen causes cell death in a localized area.
52
Liquefactive Necrosis
Liquefactive necrosis is a pattern of necrosis which occurs as a consequence of enzymatic degradation. This is in contrast to coagulative necrosis which occurs as a result of protein degradation.
53
Caseous Necrosis
Caseous necrosis is a form of necrosis characteristic of mycobaterial infections and is most commonly observed in tuberculosis lesions. The term ‘caseous’ (meaning cheese-like) arises from the gross morphology of the necrotic tissue, described to resemble crumbly yellow-white cottage cheese.
54
Enzymatic Fat necrosis
As the name suggests, fat necrosis occurs in tissues with a high lipid content and is primarily characterised by focal areas of fat destruction. It is usually caused by acute pancreatitis (inflammation of the pancreas) or by direct physical trauma to fat (for example as a result of surgery).
55
GANGRENE
Dry gangrene is ischemic coagulative necrosis (usually a limb) Wet gangrene is gangrene and an infection with a liquifactive component
56
Treatment of Necrosis
The underlying cause of the necrosis must be treated before the dead tissue itself can be dealt with. The standard therapy of necrosis (wounds, bedsores, burns, etc.) is surgical removal of necrotic tissue. Depending on the severity of the necrosis, this may range from removal of small patches of skin, to complete amputation of affected limbs or organs. Chemical removal, via an enzymatic debriding agent, is another option.
57
ATP is formed through what three cell metabolism pathways
``` (anaerobic metabloism) 1. glycolytic pathway (aerobic metabloism) 2. critic acid cycle 3. electron transport chain ```
58
signal transduction
chemical messangers between cells
59
four basic tissue types
epithelial (lines an covers body surfaces) , connective (forms bones and skeletal- fibroblasts are the most abundant) , muscle (skeletal, cardiac , and smooth. , and nervous.

PNP (7 decks)

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