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Week1 Flashcards

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1
Q

Weak acid

A

Ampicillin/aspirin
Stomach absorption
Uncharged permeable

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2
Q

Weak base

A

Amiodarone

Intestine absorption

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3
Q

Bioavailability

A

Efficiency of delivery to systemic circulation
Fraction of dose in systemic circulation in unchanged form
Affected by metabolism & excretion

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4
Q

First pass effect

A

Amt of drug eliminated by metabolism before systemic circulation
Determines bioavailability

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5
Q

Enteral administration

A

Oral
Rectal
Sublingual
Buccal

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6
Q

Parenteral administration

A 
Intravenous
Subcutaneous
Intramuscular
Topical/transdermal 
Pulmonary 
Intrathecal
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7
Q

IV bioavailability

A

100%

Most rapid onset

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8
Q

Phase I reactions

A

Parent drug to polar metabolite
(-OH, -NH2, -SH)
Inc water solubility
Reduction in activity

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9
Q

Phase II reactions

A

Polar substances conjugated to endogenous polar substances (glucuronic acid, sulfuric acid, acetic acid, glycine)
Highly polar
Highly water soluble
Completely inactive

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10
Q

Enzyme Induction

A

Repeated substrate administration —> inc isoform metabolite compound —> inc metabolism of isoform substrates

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11
Q

CYP2D6 polymorphism

A

Debrisoquin/4-hydroxydebrisoquin ratio
(P-450 substrate)
Low ratio gene duplication (ultrarapid)
High ratio null mutation (poor)

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12
Q

Slow acetylators

A

Ar

Slow acetylation of anti-Tb drug isoniazid

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13
Q

CYP2C9

A

Lower affinity for warfarin substrate

Bleeding risk

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14
Q

TPMT*3

A

TPMTL phenotype
Test for allele before starting leukaemia treatment
Use reduced dose in treatment

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15
Q

Leukocytes

A

Granulocytes:
Neutrophils
Eosinophils
Basophils

Agranulocytes/mononuclear cells:
Lymphocytes
Monocytes

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16
Q

Azurophilic granules

A 
Primary
Produced first in cell differentiation 
Present in all leukocytes
Contents:
Myeloperoxidase 
Cationic proteins
BPI (damages G- bacteria) 
Lysozyme (G+) 
Defensins 
Elastase
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17
Q

Specific granules

A 
Secondary
Made later in differentiation
In granulocytes
Contents: 
Lysozyme 
Lactoferrin (competes w bacteria for Fe/Cu) 
Collagenase
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18
Q

TLRs

A

Toll-like receptors (PRRs)

Bind to PAMPs on pathogens (direct binding)

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19
Q

Fc-are

A 
For IgG (opsonin) —> binds to bacteria
Indirect : neutrophil bonds to Fc portion of IgG Ab post-opsonisation
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20
Q

Sterilization

A

All forms of microbial life killed (incl spores)

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21
Q

Disinfection

A

Kill most infections agents on inanimate surfaces

Fail to kill spores, mycobacterium, Hep Virus

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22
Q

Sanitation

A

Lower # of bacteria to safe levels

Food industry

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23
Q

Antiseptics

A

Prevent microorganism growth on living tissue

Temporary: recolonisation from pores & ducts

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24
Q

Pasteurization

A

Heat (62C/30mins or 74C/3-5mins) to kill pathogenic bacteria often found in milk (salmonella, mycobacterium, listeria, streptococcus, brucella, campylobacter)
Doesn’t kill spores
Reduce bacterial content by 97-99%

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25
Germicide
``` Kills microorganisms (bacteriocide) Sporicides: kill spores Viricide: viruses Fungicide: fungi Tuberculocide: mycobacteria ```
26
Pyrogens
Microbe-derived contaminants that cause fever Via dead bacteria (LPS) Low MW, survive filtration and autoclaving Pyrogen free= never any microbial growth
27
Transformation
Free donor DNA (fragment or plasmid) taken you by competent recipient From later cells, occurs naturally
28
Transfection
Donor DNA is bacteriophage | Transformation + infection
29
Transduction
Donor DNA carried to recipient in phage capsid | Generalised vs. Specific
30
Conjugation
Transfer via conjugation F/R Plasmid Tra gene Donor keeps copy (rolling circle replication)
31
Coagulative Necrosis
Dead tissue architecture Enzyme denaturation—> eosinophilic cells no nuclei WBC phagocytosis Infarct
32
Liquefactive Necrosis
Focal bacterial/fungal infection Neutrophils and macrophages degrade CNS hypoxic injury Pus (dead WBCs/debris)
33
Gangrenous necrosis
Loss of blood supply: coagulative necrosis (dry) | + bacterial infection: liquefactive necrosis (wet)
34
Caseous Necrosis
Cheeselike central granuloma Tuberculosis & infections Pink, amorphous, granular
35
Fat necrosis
``` Pancreatic lipase release Breast trauma Fat + calcium = soap (dystrophic calcification) Chalky-white Normal serum Ca2+ ```
36
Mitochondrial Damage
1. Permeability pore: ox phos fail—> dec ATP 2. ROS formation 3. Proteins released (cytochrome c): activate caspases
37
Free radical effects
Lipid peroxidation Oxidative protein modification DNA lesions
38
Point of no return
Inability to reverse mitochondrial dysfunction No ox phos and dec ATP Membrane function disturbances
39
Metabolic Derangement Pathways
1. Inadequate removal via packing/transport deficit 2. Abnormal endogenous substance 3. Storage diseases 4. Abnormal exogenous substance
40
Granulocytes
Specific granules Azurophilic granules Lobulated nucleus
41
Agranulocytes
Mononuclear leukocytes Azurophilic granules No specific granules Non-lobulated nucleus
42
Neutrophils in acute inflammation
Leukocytosis | Shift to the left
43
Cross-linked IgE basophil activation
1. Degranulation (histamine, heparin sulfate, ECF, NCF) 2. Cytokines synthesis (IL-4, IL-3) 3. Membrane phospholipid cleavage (arachadonic acid pathway)
44
Type I Hypersensitivity Response
Hay fever Asthma Hives Anaphylaxis
45
Small Lymphocytes
6-8 microns 90% of lymphocytes in blood, 70% T cells Nucleus: RBC size, kidney/round shape, heterochromatic Sky blue cytoplasm rim
46
Large lymphocytes
``` Via Blast transformation 30 microns Dichromatic nucleus Smudged chromatin More cytoplasm ```
47
PAMPs
``` LPS (G-) Peptidoglycan/lipotechoic acid (G+) Unmethylated CpG (bacterial DNA) dsRNA (viruses) Glycolipids/lipoprotein (bac, fungi, paras) ```
48
DAMPs
``` Intracellular: HSP HMGB1 S100 Hyaluronan ``` ``` Non-protein: ATP Uric acid Heparin sulfate DNA ```
49
PRRs
``` Innate immune system R for PAMPs/DAMPs Germ line encoded Limited repertoire On all cells of same lineage Cell associated & soluble ```
50
Resident macrophage
Clean up/homeostasis | Kupfer, alveolar, osteoclasts, microfilm, mesangial, sinusoidal
51
Inflammatory macrophage
``` M1 Blood —> tissue Arrive after neutrophils Activated by: INF-y, TNF, LPS, microbes Inhibited by: IL-13, IL-4, IL-10 Makes: ROS, NO, enzymes (microbicidal); IL-1,12,23, chemokines (inflammation) ```
52
Alternatively activated macrophages
``` M2 Downregulate inflammation —> repair Makes TGF-B, IL-10 (anti inflammatory) & GFs (tissue repair) Not antimicrobial Induced by: IL-4, IL-10, IL-13 Inhibited by: TNF, LPS, microbes, IFN-y ```
53
IFN-y
Type II Interferon T cells & NK cells Recruits/activates macrophages Stimulates adaptive immune response
54
Intrinsic Apoptosis
``` Outer membrane permeability Cytochrome C BCL2 proteins Cell injury: GF withdrawal, DNA damage, protein misfolding Activated caspase 9 ```
55
Extrinsic apoptosis
TNF-R death domain Fas (CD95) FasL on T cells Fas-FasL: FADD —> binds & activates caspace 8 / 10
56
Labile cells
Continuously dividing GI epithelium, hematopoietic cells Stem cell pool Not totipotent
57
Stable cells
Quiescent | Kidney, liver, pancreas, SM, lymphocytes
58
Permanent cells
Non dividing after injury | Neurons, cardiac m, skeletal
59
Angiogenesis
``` VEGF & NO Pericyte detachment BM degradation Endothelial cell migration & proliferation Periendothelial cells are recruited BM deposited ```
60
Nutrition & wound healing
Protein Vit C Copper T III —> T I collagen (collagenase MMP + Zinc)
61
First intention healing
D1 coagulation - fibrin, neutrophils D2 epithelial cells & BM D3 macrophages, fibroblasts, nearly thick epidermis D5 neovascularization peak - granulation tissue Wk2 fibroblasts & collagen Mo1 cellular CT scar
62
Second intention healing
Large wound, edges not in contact | Myofibroblast wound contraction over 6wks
63
Wound Strength
D7 10% strength low collagen D60-70 100% collagen, 30% strength (TIII) 3mo 100% collagen, 70-80% strength (inc TI) Never reaches 100%

FD1 (3 decks)

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